tag:blogger.com,1999:blog-37498840894155168792024-03-06T12:02:25.581-08:00Emergency MedicineEmergency Medicinehttp://www.blogger.com/profile/06606398346130594987noreply@blogger.comBlogger16125tag:blogger.com,1999:blog-3749884089415516879.post-48352595594758456882009-04-05T06:15:00.000-07:002009-04-05T06:23:34.173-07:00ANESTHETIC AGENTS<p style="text-align: justify;" class="MsoNormal">A number of diverse drugs are routinely used in the ED to induce anesthesia prior to intubation. These include thiopental, methohexital, ketamine, etomidate, and propofol. Midazolam and fentanyl may also be used; these two agents are more commonly used at low doses as conscious sedation agents (see Analgesia and Sedation). The choice of a particular anesthetic agent depends to a great extent on the experience and training of the physician and to a<o:p></o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"> <o:p></o:p></p><div style="text-align: justify;"> </div><table class="MsoTableGrid" style="border: medium none ; border-collapse: collapse; text-align: left; margin-left: 0px; margin-right: 0px;" border="1" cellpadding="0" cellspacing="0"> <tbody><tr style=""> <td colspan="2" style="border: 1pt solid windowtext; padding: 0in 5.4pt; width: 498.15pt;" valign="top" width="664"> <p class="MsoNormal" style="text-align: center;" align="center">TABLE 3-1 -- Rapid-Sequence Induction Protocol</p> </td> </tr> <tr style=""> <td style="border-style: none solid solid; border-color: -moz-use-text-color windowtext windowtext; border-width: medium 1pt 1pt; padding: 0in 5.4pt; width: 54.8pt;" valign="top" width="73"> <p class="MsoNormal">1.</p> </td> <td style="border-style: none solid solid none; border-color: -moz-use-text-color windowtext windowtext -moz-use-text-color; border-width: medium 1pt 1pt medium; padding: 0in 5.4pt; width: 443.35pt;" valign="top" width="591"> <p class="MsoNormal" style="text-align: justify;">Preoxygenate (denitrogenize) the lungs by providing 100% oxygen by mask. If ventilatory assistance is necessary, bag gently while applying cricoid pressure.</p> </td> </tr> <tr style=""> <td style="border-style: none solid solid; border-color: -moz-use-text-color windowtext windowtext; border-width: medium 1pt 1pt; padding: 0in 5.4pt; width: 54.8pt;" valign="top" width="73"> <p class="MsoNormal">2</p> </td> <td style="border-style: none solid solid none; border-color: -moz-use-text-color windowtext windowtext -moz-use-text-color; border-width: medium 1pt 1pt medium; padding: 0in 5.4pt; width: 443.35pt;" valign="top" width="591"> <p class="MsoNormal">Assemble required equipment:<o:p></o:p></p> <p class="MsoNormal"> Bag-valve-mask connected to an oxygen delivery system<o:p></o:p></p> <p class="MsoNormal"> Suction with Yankauer tip<o:p></o:p></p> <p class="MsoNormal"> Endotracheal tube with intact cuff, stylette, syringe, tape<o:p></o:p></p> <p class="MsoNormal"> Laryngoscope and blades, in working order<o:p></o:p></p> <p class="MsoNormal"> Cricothyrotomy tray</p> </td> </tr> <tr style=""> <td style="border-style: none solid solid; border-color: -moz-use-text-color windowtext windowtext; border-width: medium 1pt 1pt; padding: 0in 5.4pt; width: 54.8pt;" valign="top" width="73"> <p class="MsoNormal">3.</p> </td> <td style="border-style: none solid solid none; border-color: -moz-use-text-color windowtext windowtext -moz-use-text-color; border-width: medium 1pt 1pt medium; padding: 0in 5.4pt; width: 443.35pt;" valign="top" width="591"> <p class="MsoNormal">Check to be sure that a functioning, secure IV line is in place.</p> </td> </tr> <tr style=""> <td style="border-style: none solid solid; border-color: -moz-use-text-color windowtext windowtext; border-width: medium 1pt 1pt; padding: 0in 5.4pt; width: 54.8pt;" valign="top" width="73"> <p class="MsoNormal">4.</p> </td> <td style="border-style: none solid solid none; border-color: -moz-use-text-color windowtext windowtext -moz-use-text-color; border-width: medium 1pt 1pt medium; padding: 0in 5.4pt; width: 443.35pt;" valign="top" width="591"> <p class="MsoNormal">Continuously monitor the cardiac rhythm and oxygen saturation.</p> </td> </tr> <tr style=""> <td style="border-style: none solid solid; border-color: -moz-use-text-color windowtext windowtext; border-width: medium 1pt 1pt; padding: 0in 5.4pt; width: 54.8pt;" valign="top" width="73"> <p class="MsoNormal">5.</p> </td> <td style="border-style: none solid solid none; border-color: -moz-use-text-color windowtext windowtext -moz-use-text-color; border-width: medium 1pt 1pt medium; padding: 0in 5.4pt; width: 443.35pt;" valign="top" width="591"> <p class="MsoNormal">Premedicate as appropriate:<o:p></o:p></p> <p class="MsoNormal"> Fentanyl: 2 to 3 mug/kg given at a rate of 1 to 2 mug/kg/min IV for analgesia in awake patients<o:p></o:p></p> <p class="MsoNormal"> Atropine: 0.01 mg/kg IV push for children or adolescents (minimum dose of 0.1 mg recommended)<o:p></o:p></p> <p class="MsoNormal"> Lidocaine: 1.5 to 2.0 mg/kg IV over 30 to 60 seconds</p> </td> </tr> <tr style=""> <td style="border-style: none solid solid; border-color: -moz-use-text-color windowtext windowtext; border-width: medium 1pt 1pt; padding: 0in 5.4pt; width: 54.8pt;" valign="top" width="73"> <p class="MsoNormal">6.</p> </td> <td style="border-style: none solid solid none; border-color: -moz-use-text-color windowtext windowtext -moz-use-text-color; border-width: medium 1pt 1pt medium; padding: 0in 5.4pt; width: 443.35pt;" valign="top" width="591"> <p class="MsoNormal">. Induce anesthesia with one of the following agents administered intravenously: thiopental, methohexital, fentanyl, ketamine, etomidate, or propofol.</p> </td> </tr> <tr style=""> <td style="border-style: none solid solid; border-color: -moz-use-text-color windowtext windowtext; border-width: medium 1pt 1pt; padding: 0in 5.4pt; width: 54.8pt;" valign="top" width="73"> <p class="MsoNormal">7.</p> </td> <td style="border-style: none solid solid none; border-color: -moz-use-text-color windowtext windowtext -moz-use-text-color; border-width: medium 1pt 1pt medium; padding: 0in 5.4pt; width: 443.35pt;" valign="top" width="591"> <p class="MsoNormal">Give succinylcholine 1.5 mg/kg IV push (use 2.0 mg/kg for infants and small children).</p> </td> </tr> <tr style=""> <td style="border-style: none solid solid; border-color: -moz-use-text-color windowtext windowtext; border-width: medium 1pt 1pt; padding: 0in 5.4pt; width: 54.8pt;" valign="top" width="73"> <p class="MsoNormal">8.</p> </td> <td style="border-style: none solid solid none; border-color: -moz-use-text-color windowtext windowtext -moz-use-text-color; border-width: medium 1pt 1pt medium; padding: 0in 5.4pt; width: 443.35pt;" valign="top" width="591"> <p class="MsoNormal">Apnea, jaw relaxation, and decreased resistance to bag/mask ventilations indicate that the patient is sufficiently relaxed to proceed with intubation.</p> </td> </tr> <tr style=""> <td style="border-style: none solid solid; border-color: -moz-use-text-color windowtext windowtext; border-width: medium 1pt 1pt; padding: 0in 5.4pt; width: 54.8pt;" valign="top" width="73"> <p class="MsoNormal">9.</p> </td> <td style="border-style: none solid solid none; border-color: -moz-use-text-color windowtext windowtext -moz-use-text-color; border-width: medium 1pt 1pt medium; padding: 0in 5.4pt; width: 443.35pt;" valign="top" width="591"> <p class="MsoNormal">Perform endotracheal intubation. If unable to intubate during the first 20-second attempt, stop and ventilate the patient with the bag-mask for 30 to 60 seconds. Follow pulse oxymetry readings as a guide.</p> </td> </tr> <tr style=""> <td style="border-style: none solid solid; border-color: -moz-use-text-color windowtext windowtext; border-width: medium 1pt 1pt; padding: 0in 5.4pt; width: 54.8pt;" valign="top" width="73"> <p class="MsoNormal">10.</p> </td> <td style="border-style: none solid solid none; border-color: -moz-use-text-color windowtext windowtext -moz-use-text-color; border-width: medium 1pt 1pt medium; padding: 0in 5.4pt; width: 443.35pt;" valign="top" width="591"> <p class="MsoNormal">Treat bradycardia occurring during intubation with atropine 0.5 mg IV push (smaller dose for children; see item 5).</p> </td> </tr> <tr style=""> <td style="border-style: none solid solid; border-color: -moz-use-text-color windowtext windowtext; border-width: medium 1pt 1pt; padding: 0in 5.4pt; width: 54.8pt;" valign="top" width="73"> <p class="MsoNormal">11.</p> </td> <td style="border-style: none solid solid none; border-color: -moz-use-text-color windowtext windowtext -moz-use-text-color; border-width: medium 1pt 1pt medium; padding: 0in 5.4pt; width: 443.35pt;" valign="top" width="591"> <p class="MsoNormal">Once intubation is completed, inflate the cuff and confirm endotracheal tube placement by auscultating for bilateral breath sounds and checking pulse oxymetry and capnography readings.</p> </td> </tr> <tr style=""> <td style="border-style: none solid solid; border-color: -moz-use-text-color windowtext windowtext; border-width: medium 1pt 1pt; padding: 0in 5.4pt; width: 54.8pt;" valign="top" width="73"> <p class="MsoNormal">12.</p> </td> <td style="border-style: none solid solid none; border-color: -moz-use-text-color windowtext windowtext -moz-use-text-color; border-width: medium 1pt 1pt medium; padding: 0in 5.4pt; width: 443.35pt;" valign="top" width="591"> <p class="MsoNormal">Release cricoid pressure and secure endotracheal tube.</p> </td> </tr> </tbody></table><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal">certain extent on institutional protocols governing use of these agents. Drugs commonly used and their doses are listed in Table 3-2 .<o:p></o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal">Barbiturates: Thiopental and Methohexital<o:p></o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal">The barbiturates, in particular thiopental, have been the traditional agents used for RSI in the operating room. These agents are used less often in the ED setting because of their<o:p></o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p><div style="text-align: justify;"> </div> <table class="MsoTableGrid" style="border: medium none ; border-collapse: collapse; text-align: left; margin-left: 0px; margin-right: 0px;" border="1" cellpadding="0" cellspacing="0"> <tbody><tr style=""> <td colspan="2" style="border: 1pt solid windowtext; padding: 0in 5.4pt; width: 498.15pt;" valign="top" width="664"> <p class="MsoNormal" style="text-align: center;" align="center">TABLE 3-2 -- Recommended Anesthetic Doses for Rapid-Sequence Induction<o:p></o:p></p> <p class="MsoNormal" style="text-align: center;" align="center"><o:p> </o:p></p> </td> </tr> <tr style=""> <td color="-moz-use-text-color windowtext windowtext" style="border-style: none solid solid; padding: 0in 5.4pt; width: 249.05pt;" valign="top" width="332"> <p class="MsoNormal" style="text-align: center;" align="center">Drug *</p> </td> <td style="border-style: none solid solid none; padding: 0in 5.4pt; width: 249.1pt;" valign="top" width="332"> <p class="MsoNormal" style="text-align: center;" align="center">Dose</p> </td> </tr> <tr style=""> <td color="-moz-use-text-color windowtext windowtext" style="border-style: none solid solid; padding: 0in 5.4pt; width: 249.05pt;" valign="top" width="332"> <p class="MsoNormal" style="text-align: center;" align="center">Thiopental</p> </td> <td style="border-style: none solid solid none; padding: 0in 5.4pt; width: 249.1pt;color:-moz-use-text-color windowtext windowtext -moz-use-text-color;" valign="top" width="332"> <p class="MsoNormal" style="text-align: center;" align="center">3-5 mg/kg IV</p> </td> </tr> <tr style=""> <td color="-moz-use-text-color windowtext windowtext" style="border-style: none solid solid; padding: 0in 5.4pt; width: 249.05pt;" valign="top" width="332"> <p class="MsoNormal" style="text-align: center;" align="center">Methohexital</p> </td> <td style="border-style: none solid solid none; padding: 0in 5.4pt; width: 249.1pt;color:-moz-use-text-color windowtext windowtext -moz-use-text-color;" valign="top" width="332"> <p class="MsoNormal" style="text-align: center;" align="center">1-3 mg/kg IV</p> </td> </tr> <tr style=""> <td style="border-style: none solid solid; border-color: -moz-use-text-color windowtext windowtext; border-width: medium 1pt 1pt; padding: 0in 5.4pt; width: 249.05pt;" valign="top" width="332"> <p class="MsoNormal" style="text-align: center;" align="center">Fentanyl</p> </td> <td color="-moz-use-text-color windowtext windowtext -moz-use-text-color" style="border-style: none solid solid none; padding: 0in 5.4pt; width: 249.1pt;" valign="top" width="332"> <p class="MsoNormal" style="text-align: center;" align="center"><span style="" lang="FI">5-15 mug/kg IV</span></p> </td> </tr> <tr style=""> <td style="border-style: none solid solid; border-color: -moz-use-text-color windowtext windowtext; border-width: medium 1pt 1pt; padding: 0in 5.4pt; width: 249.05pt;" valign="top" width="332"> <p class="MsoNormal" style="text-align: center;" align="center"><span style="" lang="FI">Ketamine</span></p> </td> <td color="-moz-use-text-color windowtext windowtext -moz-use-text-color" style="border-style: none solid solid none; padding: 0in 5.4pt; width: 249.1pt;" valign="top" width="332"> <p class="MsoNormal" style="text-align: center;" align="center"><span style="" lang="FI">1-2 mg/kg IV</span></p> </td> </tr> <tr style=""> <td style="border-style: none solid solid; border-color: -moz-use-text-color windowtext windowtext; border-width: medium 1pt 1pt; padding: 0in 5.4pt; width: 249.05pt;" valign="top" width="332"> <p class="MsoNormal" style="text-align: center;" align="center">Etomidate</p> </td> <td style="border-style: none solid solid none; border-color: -moz-use-text-color windowtext windowtext -moz-use-text-color; border-width: medium 1pt 1pt medium; padding: 0in 5.4pt; width: 249.1pt;" valign="top" width="332"> <p class="MsoNormal" style="text-align: center;" align="center">0.3 mg/kg IV</p> </td> </tr> <tr style=""> <td style="border-style: none solid solid; border-color: -moz-use-text-color windowtext windowtext; border-width: medium 1pt 1pt; padding: 0in 5.4pt; width: 249.05pt;" valign="top" width="332"> <p class="MsoNormal" style="text-align: center;" align="center">Propofol</p> </td> <td style="border-style: none solid solid none; border-color: -moz-use-text-color windowtext windowtext -moz-use-text-color; border-width: medium 1pt 1pt medium; padding: 0in 5.4pt; width: 249.1pt;" valign="top" width="332"> <p class="MsoNormal" style="text-align: center;" align="center">2.0 mg/kg IV</p> </td> </tr> </tbody></table> <div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal">reputation as cardiorespiratory depressants. Of these two agents, methohexital is used more commonly in the ED because of its extremely rapid onset and short duration of action.</p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><b style=""></b></p><div style="text-align: justify;"><span style="font-weight: bold;">Pharmacology </span><br />Following IV injection,the ultrashort-acting barbiturates bind rapidly to plasma proteins, particularly albumin. Unbound barbiturate quickly accumulates in highly vascular organs, reaching peak brain levels in as short a time as 50 seconds. The drugs then diffuse from the brain, ultimately reaching equilibrium between the intracerebral and plasma concentrations. Degradation occurs primarily in the liver, producing inactive metabolites that are excreted in the urine or gut, depending on the drug used. Single-pass hepatic clearance is substantially higher for methohexital than for thiopental, which accounts for the former drug's shorter duration of action. The period of anesthesia following a single IV dose of methohexital is 4 to 6 minutes, compared with 5 to 10 minutes for thiopental. [13] [14]<o:p></o:p> </div><p style="text-align: justify;" class="MsoNormal">The barbiturates are central nervous system (CNS) depressants that are capable of producing mild sedation to deep coma. They do not block afferent sensory impulses to a significant extent and therefore should be used in conjunction with an analgesic agent such as fentanyl if a painful procedure is to be performed. However, it is common practice to intubate patients who have received only barbiturates. [14]<o:p></o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal">The advantages of barbiturates as adjuncts to intubation include their high potency, rapid onset, and short duration of action, traits they share with fentanyl and midazolam. The barbiturates are also known to reduce cerebral metabolism and oxygen consumption and, secondarily, cerebral blood flow and intracranial pressure (ICP). [15] [16] For this reason, thiopental is considered the agent of choice for anesthesia induction and maintenance in patients with elevated ICP. Some have stated that thiopental is the drug of choice to temporarily anesthetize the patient with a head injury before intubation. It has not been proved, however, that barbiturates exert a protective effect on the CNS when used for a short period of time during RSI. Moreover, their use in trauma patients may lead to systemic hypotension and impaired cerebral perfusion pressure that may offset the theoretic advantages of barbiturate therapy.</p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><b style=""></b></p><div style="text-align: justify;"><span style="font-weight: bold;">Dose </span><br />The recommended doseof thiopental is 3 to 5 mg/kg IV administered as a 2.5% solution over 60 seconds. Normal saline should be used as a diluent. Methohexital is given at 1 to 3 mg/kg IV over 30 to 60 seconds. </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><b style=""></b></p><div style="text-align: justify;"><span style="font-weight: bold;">Adverse Effects </span><br />It has been stated that barbiturates are "fatally easy" to use. [14] This is an overstatement that reflects improper use of the drugs more than an inherent danger associated with their proper use. The most significant complication of barbiturate therapy is depression of the vasomotor center and myocardial contractility leading to significant hypotension. This may be particularly pronounced in the presence of hypovolemia or cardiovascular disease.<o:p></o:p> </div><p style="text-align: justify;" class="MsoNormal">Barbiturates also depress the brainstem respiratory centers when given rapidly or in large doses. This effect may be accelerated by simultaneous treatment with opioids. Patients<o:p></o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal">with asthma or chronic bronchitis may experience bronchospasm. Laryngospasm may occur in patients who were anesthetized lightly with barbiturates during manipulation of the upper airway. Laryngospasm usually responds to positive-pressure ventilation or paralysis with succinylcholine. In addition, the high pH of the barbiturate solution can cause tissue necrosis following extravascular administration and severe pain, vessel spasm, and thrombosis following intraarterial infusion.</p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><b style=""></b></p><div style="text-align: justify;"><span style="font-weight: bold;">Etomidate </span><br />Etomidate is an ultrashort-acting nonbarbiturate hypnotic agent that has been used successfully as an anesthesia induction agent in Europe since the mid-1970s and in the <st1:place st="on"><st1:country-region st="on">United States</st1:country-region></st1:place> since 1983. Only recently has it been used as an adjunct to intubation in the ED. A potentially significant benefit of etomidate in the emergency setting is its lack of cardiodepressant effects. [17] Although experience in this setting is limited, etomidate's potency, rapid onset, short duration of action, and minimal side effects suggest that it will become much more widely used. </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><b style=""></b></p><div style="text-align: justify;"><span style="font-weight: bold;">Pharmacology </span><br />Etomidate is a carboxylated imidazole that is both water and lipid soluble. The drug rapidly accumulates in vascular organs, reaching peak brain concentrations within 1 minute of IV infusion. [18] Sleep is produced within 1 arm-brain circulation time and lasts less than 10 minutes following a single bolus infusion. [19] Redistribution of the drug is quite rapid (distribution half-life, 2.6 minutes), which accounts for the short duration of action. Etomidate is rapidly hydrolyzed in the liver and plasma, forming an inactive metabolite excreted primarily in the urine. [18]<o:p></o:p> </div><p style="text-align: justify;" class="MsoNormal">Etomidate acts on the CNS to stimulate gamma-aminobutyric acid receptors and depress the reticular activating system. After IV infusion, etomidate produces electroencephalographic changes similar to those produced by barbiturates as patients pass rapidly through light to deep levels of surgical anesthesia. Because etomidate has no analgesic activity, [18] it should be used in conjunction with an analgesic such as fentanyl when painful conditions are being treated. Etomidate decreases cerebral oxygen consumption, cerebral blood flow, and ICP but appears to have minimal effects on cerebral perfusion pressure. [20]</p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><b style=""></b></p><div style="text-align: justify;"><span style="font-weight: bold;">Dose </span><br />The recommended dose is 0.3 mg/kg IV.There is virtually no accumulation of the drug, and anesthesia may be maintained through repeated or continuous dosing. [21] </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><b style=""></b></p><div style="text-align: justify;"><span style="font-weight: bold;">Adverse Effects </span><br />The most common side effectsof etomidate are nausea and vomiting, pain on injection, and myoclonic jerks. [22] Pain on injection occurs in up to two thirds of cases. Use of a large vein, simultaneous saline infusion, and opioid premedication are reported to reduce this side effect. [23] Myoclonic activity has been reported in about one third of cases and is believed to be caused by disinhibition of subcortical activity rather than CNS stimulation. [18] </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><b style=""></b></p><div style="text-align: justify;"><span style="font-weight: bold;">Ketamine </span><br /><span style="font-weight: bold;">Pharmacology </span><br />Unique among anesthetic agents currently in use, ketamine produces a dissociative anesthesia characterized by excellent analgesia and amnesia despite the appearance of wakefulness. As a drug that is potent and relatively safe and possesses a rapid onset and brief duration of action, ketamine fits the profile of a drug that could be used effectively to facilitate intubation. It does, however, possess a number of pharmacologic properties that limit its use to selected circumstances.<o:p></o:p> </div><p style="text-align: justify;" class="MsoNormal">Ketamine is a water- and lipid-soluble drug with rapid penetration into the CNS. Like the barbiturates, ketamine accumulates rapidly in highly vascular organs and then undergoes redistribution. The half-life of redistribution from plasma to peripheral tissues is 7 to 11 minutes, and the half-life of elimination is 2 to 3 hours. Degradation occurs primarily in the liver. [24]<o:p></o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal">Unlike other anesthetic agents that depress the reticular activating system, ketamine acts by interrupting association pathways between the thalamocortical and limbic systems. Characteristically, the eyes remain open, and patients exhibit spontaneous, although not purposeful, movements. Increases in blood pressure, heart rate, cardiac output, and myocardial oxygen consumption are seen--effects that are most likely mediated through the CNS. In vitro studies indicate that ketamine is a myocardial depressant, but the CNS-mediated pressor effects generally mask the direct cardiac effects. [25] [26] Respirations are initially rapid and shallow after ketamine administration, but they soon return to normal.<o:p></o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal">Other features of ketamine anesthesia include increased skeletal muscle tone, preservation of laryngeal and pharyngeal reflexes, hypersalivation, and relaxation of bronchial smooth muscle. ICP is increased, most likely as a consequence of increased cerebral blood flow. [24]<o:p></o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal">Ketamine has been recommended for anesthesia induction in children because of its relative safety and infrequency of postanesthesia emergence reactions in this group. There is no evidence, however, that it offers any advantage over commonly used agents. Ketamine also has been recommended for the unstable critically ill patient, because it does not depress the cardiovascular system. This recommendation is too vague to be useful to the clinician, and it ignores the fact that ketamine is potentially harmful in patients with cardiac ischemia (because it can increase myocardial oxygen consumption) or acute intracranial pathology (because it can increase ICP). Ketamine may be useful during hemorrhagic shock because of its cardiostimulatory effect. Its administration to patients in shock has been reported to cause a fall in blood pressure only when the shock state has been prolonged. [29] [30]<o:p></o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal">The most promising use of ketamine as an intubation adjunct has been in the setting of acute bronchospastic disease. Ketamine relaxes bronchial smooth muscle either directly, through the enhancement of sympathomimetic effects, or through the inhibition of vagal effects. Ketamine also increases bronchial secretions, which may decrease the incidence of mucus plugging commonly reported in autopsies of asthmatic patients. [31] Clinical studies have demonstrated a reduction in airway resistance and an increase in pulmonary compliance that occur within minutes of ketamine administration. L'Hommedieu and Arens [8] reported<o:p></o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal">prompt improvement in respiratory acidosis in 5 asthmatics intubated with ketamine and succinylcholine.</p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><b style=""></b></p><div style="text-align: justify;"><span style="font-weight: bold;">Dose</span> <br />The recommended dose of ketamine before intubation is 1 to 2 mg/kg administered IV over 1 minute. Anesthesia occurs within 1 minute of completing the infusion and lasts approximately 5 minutes. A small dose (0.5 to 1.0 mg/kg) may be given 5 minutes after the initial dose if there is a need to maintain anesthesia. The simultaneous administration of succinylcholine and midazolam is recommended to provide adequate muscle relaxation and to decrease the incidence of postanesthesia emergence reactions. </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><b style=""></b></p><div style="text-align: justify;"><span style="font-weight: bold;">Adverse Effects </span><br />A side effect that has greatly limited the use of ketamine is its tendency to produce postanesthesia emergence reactions, a characteristic that it has in common with the structurally similar drug phencyclidine. The reactions may be marked and distressing to the patient; symptoms include floating sensations, dizziness, blurred vision, out-of-body experiences, and vivid dreams or nightmares. The reported incidence of these reactions varies from 5 to 30%. They are less common in children than in adults.<o:p></o:p> </div><p style="text-align: justify;" class="MsoNormal">Of the drugs that have been evaluated for their ability to suppress postanesthesia emergence reactions, the benzodiazepines show the most promise. Both diazepam and lorazepam are useful, but the latter is more effective, most likely owing to its enhanced amnestic effect. Midazolam has not been evaluated as thoroughly as have the other benzodiazepines, but it has potent amnestic effects and offers the advantage of a short duration of action. White [40] reported a 55% incidence of postemergence dreaming in patients receiving ketamine and complete suppression of dreaming with the addition of midazolam. Evidence also suggests that midazolam may inhibit the cardiostimulatory effects of ketamine.<o:p></o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal">Although ketamine produces excellent analgesia and is relatively safe, its use as an agent to facilitate intubation is somewhat limited. The widely held belief that aspiration does not occur with ketamine because of preservation of pharyngeal and laryngeal reflexes is incorrect. Moreover, ketamine does not relax skeletal muscle. The production of desired intubation conditions often requires the simultaneous administration of a paralytic agent, thereby removing any upper airway reflexes.</p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><span style="font-weight: bold;"></span></p><div style="text-align: justify;"><span style="font-weight: bold;">Propofol </span><br />Emergency department experience with propofol is limited, and it is uncertain whether it will have a significant role as an adjunct to intubation in this setting. </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><b style=""></b></p><div style="text-align: justify;">Pharmacology <br />Propofol is an alkylphenol sedative-hypnotic recently introduced for induction and maintenance of general anesthesia. The drug has no analgesic activity, but it does have an amnestic effect. It produces dose-dependent depression of consciousness ranging from light sedation to coma. Propofol is a highly lipophilic, water-insoluble compound that undergoes rapid uptake by vascular tissues, including the brain, followed soon afterward by redistribution to the muscle and fat. The drug is metabolized by the liver and excreted in the urine. </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><b style=""></b></p><div style="text-align: justify;"><span style="font-weight: bold;">Dose </span><br />Following an induction dose of 2 mg/kg IV, hypnosis occurs within 1 minute and lasts for 5 to 10 minutes. A smaller dose (1.0 to 1.5 mg/kg) is recommended in the elderly and when simultaneously administering other CNS depressants. Because propofol has a short duration of action and patients rapidly regain consciousness, repeat bolusing is not a practical way to maintain a desired level of anesthesia or sedation. A slow drip infusion of 3 to 5 mg/kg/hour titrated to effect is the preferred technique. Conscious sedation may be achieved using a drip infusion beginning at 6 mg/kg/hour and decreasing the rate as the desired level of sedation is obtained. </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p><div style="text-align: justify;"> </div><p style="text-align: justify;" class="MsoNormal"><b style=""></b></p><div style="text-align: justify;"><span style="font-weight: bold;">Adverse Effects </span><br />Side effects of propofol include direct myocardial depression causing a moderate fall in blood pressure, particularly in the elderly, in hypovolemic patients, and when administered simultaneously with opioids. Propofol reduces cerebral blood flow and may cause mild CNS excitation activity (e.g., myoclonus, tremors, hiccups) during anesthesia induction. Pain on injection occurs commonly, even when the drug is infused slowly. </div><p style="text-align: justify;" class="MsoNormal"><o:p> </o:p></p>Emergency Medicinehttp://www.blogger.com/profile/06606398346130594987noreply@blogger.com3tag:blogger.com,1999:blog-3749884089415516879.post-13398794078355807992009-03-13T03:27:00.000-07:002009-03-13T03:29:41.574-07:00CHANGING TRACHEAL TUBES<div style="text-align: justify;">The tracheal tube with a leaking cuff is a vexing problem, especially if the original intubation was difficult. A method of replacing the tube without losing control of the tracheal lumen is preferred. This can be achieved by passing a guide down the defective tube, withdrawing the tube while leaving the guide in place, and introducing a new tube over the guide and into the trachea.<br />A number of different guides have been described (e.g., simple nasogastric tubes, 18 Fr Salem sump tubes , feeding tubes), but they are poor substitutes for a designated tube exchanger such as the TTX "tracheal tube exchanger" (Sheridan Catheter Corporation, Argyle, NY) or a similar commercially available device. The advantages of the designated tube exchanger are that it is stiff enough to prevent dislodgment when the endotracheal tube is introduced, it is ready to use without modification, it has a printed scale to aid in determining depth of placement, and if replacement is prolonged, the patient may be oxygenated using the exchanger and wall oxygen.<br /><br /><span style="font-weight: bold;">Procedure</span><br />Prior to the procedure, the patient is properly sedated or restrained. The patient is hyperventilated before placing the guide through the existing tube. The guide is lubricated and advanced into the defective tube so that it is well within the tracheal lumen (adults, 30 cm). While applying cricoid pressure (Sellick maneuver), the defective tube is withdrawn over the guide, and care is taken not to dislodge the guide when removing the tube. The replacement tube is then slid over the guide and is gently advanced into the trachea . At this juncture, it may be helpful to perform a jaw thrust or chin lift to facilitate passage through the pharynx. Resistance may be encountered at the laryngeal inlet or vocal cords; if this occurs, withdraw the tube 1 to 2 cm, rotate it 90° counterclockwise, and readvance it. With the tube clearly in the trachea, remove the guide, inflate the cuff, and ventilate the patient. After correct placement has been verified, the new tube can be secured.<br />Complications are related to the time required to change the tube. A successfully performed procedure can be accomplished within 30 seconds. Laryngeal injury from forcing the guide or the tube is a possibility to consider when replacing a tube<br /><br /></div>Emergency Medicinehttp://www.blogger.com/profile/06606398346130594987noreply@blogger.com0tag:blogger.com,1999:blog-3749884089415516879.post-77890661368141790022009-03-13T03:16:00.000-07:002009-03-13T03:25:59.267-07:00GUIDED INTUBATION TECHNIQUES<div style="text-align: justify;"><span style="font-weight: bold;">Digital Intubation</span><br /><br />Digital intubation is a technique that uses the index and middle finger to blindly direct the endotracheal tube into the larynx. It is particularly well adapted to the out-of-hospital situation in which a trapped victim cannot be positioned for intubation. An out-of-hospital series of 66 digitally intubated patients demonstrated an 89% success rate.<br /><br /><span style="font-style: italic; font-weight: bold;">Indications and Contraindications</span><br />Digital intubation is indicated in the deeply comatose patient whose larynx cannot be visualized and who has a contraindication to nasotracheal intubation. Advantages include speed and ease of placement, immunity to anatomic constraints and other difficulties visualizing the larynx, and little neck movement. Contraindications are primarily precautions to protect the operator: digital intubation should not be attempted on any patient who presents a significant risk of biting. This includes the calm and awake patient as well as the agitated patient.<br /><br /><span style="font-weight: bold; font-style: italic;">Procedure</span><br />The patient's head and neck are placed in neutral position. The operator stands at the patient's right side, facing the patient. The operator's left index and middle fingers are introduced into the right angle of the patient's mouth and are slid along the surface of the tongue until the epiglottis is palpated. The tip of epiglottis is palpated at 8 to 10 cm from the corner of the mouth in the average adult. The use of a stylet in the tube is optional; the largest reported series had good success without a stylet. For the operator with short fingers or a patient with an anterior larynx, a stylet is advantageous. If a stylet is used, it is placed in the tube and bent into the form of an open "J" with the distal end terminating in a gentle hook. A lubricated tube is introduced from the patient's left between the tongue and the rescuer's 2 fingers . The tube is cradled between 2 fingers and the tip is guided beneath the epiglottis. Gentle anterior pressure directs the tube into the larynx. If the operator has sufficiently long fingers, they can be placed posterior to the arytenoids, acting as a "backstop" for the tube to both avoid esophageal passage and to assist in laryngeal placement. If a stylet has been used, it is withdrawn at this time while simultaneously advancing the tube. An alternative to using a stylet for directing the tube anteriorly is to select an endotracheal tube with a controllable tip (Endotrol, Mallinckrodt Medical Inc, St Louis).<br />A variation on the technique of digital intubation has been described for intubating the newborn. Only the index finger is used to guide the tube intraorally into the larynx. The end of the tube is bent and both the tube and the finger are moistened with sterile water. The index finger of the nondominant hand follows the tongue posteriorly to easily palpate the epiglottis and paired arytenoid. The thumb of the same hand may be used to apply cricoid pressure to steady the larynx. The endotracheal tube is held in the dominant hand and advanced using the nondominant index finger as a guide . The tube snugs up (encounters subtle resistance) as it enters the trachea, and palpation of the tube through the trachea provides further confirmation of correct placement. A styletted tube, shaped in the form of a J, is usually desired until familiarity with the procedure is achieved.<br /><br /><span style="font-weight: bold; font-style: italic;">Complications</span><br />The risk of esophageal intubation is always present and, being a blind procedure in deeply comatose or cardiac arrested patients, the potential for esophageal misplacement is increased. If used in patients with a gag, induction of emesis with aspiration is a possibility. A high incidence of left main stem intubations was noted in a cadaveric study, but clinical confirmation is lacking. The greatest risk seems to be to the operator, whose fingers may be bitten.<br /><br /><span style="font-weight: bold; font-style: italic;">Summary</span><br />While most of the recent experience with digital intubation in adults has been out of hospital, there is no reason why it should be confined to this setting. The majority of moribund emergency department patients who defy orotracheal intubation are never given a trial of digital intubation. This omission undoubtedly deprives some patients of expeditious airway management.<br /><br /><br /><span style="font-weight: bold;">Lighted Stylet Intubation</span><br /><br />This technique uses a battery-operated lighted stylet that is placed in an endotracheal tube and used to guide the tube into the trachea by transilluminating the soft tissues of the neck. First described in 1957 by MacIntosh and Richards, it was designed to aid in intubating the difficult airway. It has also been shown to be a useful means of determining the position of the tracheal tube.<br />In the operating room, the Tube Stat lighted stylet (Concept Corp, Clearwater, Fla) has been 99 to 100% successful. The requirement that the overhead lights be dimmed during the procedure has limited its use in most emergency settings. In a small out-of-hospital study, 88% of patients were successfully intubated by physicians using a lighted stylet. The majority of the failures occurred in the setting of bright sunlight and in patients who had vomited. A new device (Trachlight, Laerdal, Inc, Starger, Norway) with a brighter light source and adjustable length, appears to have solved this problem. In a series of 96 patients, many with a history of difficult intubation, all but 1 were successfully intubated in ambient light with this device using either the oral or nasotracheal route. Consistent with other series, the only failure was in a morbidly obese patient.<br /><br /><span style="font-style: italic; font-weight: bold;">Indications and Contraindications</span><br />The patient with a difficult airway in whom direct laryngoscopy has failed is a candidate for light-guided tracheal intubation. A multiple trauma patient with airway bleeding is a prime example. The patient who has been pharmacologically paralyzed and cannot be intubated with direct laryngoscopy is another example. The lighted stylet may also be helpful in successfully completing a difficult nasotracheal intubation. One advantage of this technique over nasotracheal intubation is that it can be used in the apneic patient.<br />Because lighted stylet intubation is a blind approach, it should be avoided in patients with expanding neck masses and patients with airway compromise presumed due to a foreign body. Massive obesity has been shown to be the most common cause for failure with this technique because of the impossibility of transilluminating through the generous soft tissue.<br /><br /><span style="font-weight: bold; font-style: italic;">Preparation</span><br />The function of the bulb of the lighted stylet should be checked before use. The patient's head should be placed in a neutral or, if cervical spine injury is not a concern, the sniffing position. The awake patient should have the oropharynx and hypopharynx sprayed with lidocaine and sedation should be administered as indicated.<br /><br /><span style="font-weight: bold; font-style: italic;">Procedure</span><br />The lubricated lighted stylet is inserted into a tracheal tube (5.5 mm or larger) until the bulb lies just distal to the side port, not protruding from the end of the tube. This unit is bent in the shape of a hockey stick that approximates a 90° curve beginning just proximal to the tube cuff. The operator stands at the head of the patient. When this is not possible, the patient can be approached from the right or the left side. The tongue is grasped with gauze and pulled forward. Another means of exposing the oropharynx is to grasp the jaw between the thumb and the fingers . The light is turned on and the unit is inserted into the mouth, following the curve of the tongue into the oropharynx. A transilluminating glow indicates the location of the tube tip. Application of cricoid pressure may enhance transillumination. The overhead light should routinely be dimmed if feasible. Positioning is optimal when the glow emanates from the midline at the level of the hyoid bone. Holding the lighted stylet steady, the tube is slid off and advanced into the trachea. If the glow is located elsewhere, the unit should be withdrawn 2 cm or cocked back and repositioned as indicated by the light. If no light is seen, the tube is in the esophagus and should be pulled back, laryngeal pressure applied, and, if necessary, the head extended slightly. After passage, the tube should be checked for correct positioning and then secured.<br /><br /><span style="font-weight: bold; font-style: italic;">Complications</span><br />Earlier reports noted complications resulting from an equipment failure and lost bulbs, but these problems have been corrected. No complications have been noted in the recent literature, but this may only reflect the limited use of this technique in uncontrolled settings.<br /><br /><span style="font-weight: bold; font-style: italic;">Summary</span><br />Lighted stylet intubation is a safe, rapid, and highly successful method that has a definite place in the management of the difficult airway. Recent improvements in the device will increase its applicability to most settings in which emergency airway control is required.<br /><br /><br /><span style="font-weight: bold;">Intubation over a Fiberoptic Bronchoscope</span><br /><br />The use of the flexible fiberoptic bronchoscope as an aid to tracheal intubation is a recent addition in airway management in the emergency department. In this setting, success approximates 80%, with the most common cause of failure being the inability to visualize the glottis secondary to blood and secretions.<br />Flexible fiberoptic endoscopy is the best method for intubating the awake patient with a difficult airway. It can be accomplished using the nasal or oral route and is better tolerated than direct laryngoscopy. It also may be effective in the comatose patient when more conventional methods have failed. It provides excellent visualization of the airway and permits the evaluation of the airway prior to tube placement. The greatest obstacle to success is the inability to see through the scope secondary to blood, secretions, or fogging. The expense of the equipment, its fragility, and the time required to achieve technical proficiency are three other drawbacks.<br /><br /><span style="font-weight: bold; font-style: italic;">Indications and Contraindications</span><br />Common indications for emergency fiberoptic intubation include the unstable cervical spine, expanding neck masses, upper airway infection, facial and airway burns, and anticipation of a difficult intubation due to anatomic constraints. It may also be helpful in guiding blind nasotracheal intubation that is initially unsuccessful.<br />Contraindications to fiberoptic nasotracheal intubation are those ascribed to nasotracheal intubation in general: severe midface trauma and coagulopathy. Although there are no clear contraindications to fiberoptic orotracheal intubation, active airway bleeding and vomiting are relative contraindications because successful fiberoptic intubation is rarely achieved in this setting. If the operator is inexperienced in fiberoptic intubation, apnea is another relative contraindication to its use.<br /><br /><span style="font-weight: bold; font-style: italic;">Equipment</span><br />Fiberoptic scopes are graded according to their external diameter (in millimeters). A convenient intubating scope is 3.5 mm. Although it is physically possible to pass a 4.0 mm (0.5 mm larger) tracheal tube over the scope, the fit is quite tight. As a rule, the tracheal tube should be at least 1 mm larger than the intubating scope. The size of the working channel--the port to which suction or oxygen is applied and through which fluid or catheters may be passed--is another important dimension when evaluating fiberoptic scopes. Large working channels are desirable.<br /><br /><span style="font-weight: bold; font-style: italic;">Procedure</span><br />The optimal positioning of the neck is in extension, as opposed to the cervical flexion desired when using direct laryngoscopy. Extension allows for better visualization of the<br />glottis by elevating the epiglottis off the posterior pharyngeal wall. This is especially pertinent in the comatose patient who lacks the muscle tone necessary to maintain an open airway. Problems with the tongue and soft tissues falling back and obscuring fiberoptic scope view are effectively managed by applying a jaw lift or pulling the tongue forward and away from the soft palate and posterior pharyngeal wall. This maneuver also moves the epiglottis away from the posterior pharyngeal wall facilitating exposure of the cords. Extending the head on the neck may accomplish the same objective.<br /><br /><span style="font-weight: bold; font-style: italic;">Nasotracheal approach.</span><br />The nasal approach is preferred to the oral approach because the angle of insertion allows for easier visualization of the larynx and because patient cooperation is not as critical. Also, in the unconscious patient, the tip of the scope is less likely to impinge on the base of the tongue with a nasal approach.<br />The nose is prepared using a vasoconstrictor and topical anesthetic agent as described for nasotracheal intubation. Using an aerosolized anesthetic agent, it is important to obtain sufficient hypopharyngeal anesthesia to minimize gagging and laryngospasm once the procedure begins. The well-lubricated endotracheal tube may be placed in the nostril first, and the scope passed through it, or the endotracheal tube can be mounted over the scope and the scope first passed through the nostril. The advantage of the former is that it avoids the possibility of nasal secretions covering the scope and obscuring the view. The disadvantage is that nasotracheal placement may cause bleeding as well as that in some patients, the tube may not make the bend into the nasopharynx.<br />The most patent nostril is prepped and the endotracheal tube is advanced until it makes the bend into the nasopharynx in the manner described under nasotracheal intubation. If negotiating this bend is difficult, a well-lubricated fiberoptic scope can be placed through the tube and into the oropharynx to serve as a guide for the endotracheal tube. Once the tracheal tube is in the oropharynx, thorough oropharyngeal suctioning should be performed prior to introduction of the scope into the endotracheal tube. The fiberoptic scope is then advanced toward the larynx; the epiglottis and vocal cords are seen with little or no manipulation of the tip of the fiberoptic scope in 90% of patients. As the scope is advanced, the cords are kept in view by frequent minor adjustments of the scope tip.<br />In the comatose or obtunded patient, the tongue and other soft tissue may obscure the view of the larynx; this can be alleviated by having an assistant pull the tongue forward or apply a chin or jaw lift. The scope is advanced through the larynx to the level of the midtrachea and the endotracheal tube is passed over the firmly held fiberoptic scope into the trachea . It is helpful to remember that in adults the average distance from the naris to the epiglottis is 16 to 17 cm; if the scope has been advanced much beyond this distance and the glottis is still not seen, the scope is probably in the esophagus. If the scope meets resistance at about this same level and only a pink blur is visible, the scope tip is probably in a piriform sinus; transillumination of the soft tissues may be present to confirm this as well as to indicate what corrective maneuvers are necessary.<br />The greatest impediment to successful fiberoptic intubation is the inability to visualize the larynx because blood or secretions have covered the optical element and cannot be removed. The best time to suction is before introducing the fiberoptic scope, actively suctioning the oropharynx just prior to scope insertion. Once the scope is in place, minor secretions can be suctioned through the fiberoptic suction port. Significant blood and secretions, however, are best removed by insufflation of oxygen through the suction port and out the tip of the scope, serving simultaneously to remove blood and secretions, defog the tip, and increase the inspired O2 content. The set-up required for insufflation should be immediately available, if not already attached to the suction port prior to scope insertion. Once the scope has entered the trachea, difficulty may be encountered in advancing the endotracheal tube into the trachea. The tip of the tube most commonly catches on the right arytenoid cartilage or vocal cord; withdrawing the tube 2 cm, rotating it counterclockwise 90°, and readvancing the tube should result in successful tracheal intubation.<br /><br /><span style="font-weight: bold; font-style: italic;">Orotracheal approach.</span><br />Oral fiberoptically guided intubation is indicated when contraindications to nasal intubation are present, the most common being severe midface trauma, or when the operator is more comfortable with this approach. The oral approach is more difficult than the nasal approach because the path of the scope is less defined by the surrounding soft tissue and the tip of the scope is more likely to impinge on the base of the tongue or vallecula. Attention to keeping the scope in the midline and elevating the soft tissue by pulling the tongue forward or applying the jaw lift will minimize this difficulty. Another disadvantage of the oral approach is that the oropharyngeal axis is not as well aligned with the laryngeal axis as in the nasal approach and thus requires more scope manipulation to visualize the larynx.<br />The drawbacks of the oral approach can be minimized by using an oral intubating airway. This adjunct resembles an oropharyngeal airway but is longer and has a cylindrical passage through which the fiberoptic scope and tracheal tube are passed. The tip of this airway lies just cephalad to the epiglottis and assures midline positioning and a predictable place from which to advance the scope.<br />The patient must be adequately anesthetized or obtunded to minimize the gag reflex. Topical anesthesia is achieved by spraying a 4 or 10% solution of lidocaine into the oropharynx. A degree of laryngeal and tracheal anesthesia may be achieved by a transoral spray using the laryngeal tracheal anesthetic (LTA) set. A well-lubricated fiberoptic scope, premounted with an endotracheal tube, is placed through the oral intubating airway and the trachea is fiberoptically intubated. The endotracheal tube is advanced over the scope into the trachea, frequently requiring the same counterclockwise manipulation as described with the nasal approach. After successful intubation, the intubating device can be left in place as a bite block, or it can be removed over the endotracheal tube after removal of the tube adapter. Some oral intubating airways can be removed from the mouth without disconnecting the endotracheal tube adapter.<br /><br /><span style="font-weight: bold; font-style: italic;">Complications</span><br />Complications of fiberoptic orotracheal intubation include prolonged intubation attempts and vomiting and laryngospasm in the underanesthetized patient. Oxygen saturation monitoring should alert the operator to hypoxemia from prolonged intubation attempts. The majority of complications seen with fiberoptically guided nasotracheal intubation are associated with the passage of the endotracheal tube through the nasopharynx. Epistaxis is most common, followed by other nasopharyngeal injuries seen with nasotracheal intubation in general. A rare but potentially significant complication may result if on blind advancement of the fiberoptic scope through the endotracheal tube, the tip of the scope inadvertently exits out through the distal side port (Murphy's eyes) as it is being advanced through the larynx into the trachea. [74] Attempts at passing the endotracheal tube through the larynx will fail because the tube tip, now extending off the midline, will catch on the laryngeal structures. This complication is avoided if the scope is introduced prior to tracheal tube placement.<br /><br /><span style="font-weight: bold; font-style: italic;">Summary</span><br />The primary advantage of fiberoptic intubation is its ability to negotiate difficult airway anatomy. It is noninvasive and well tolerated. Its major limitation in the emergency setting is lack of visibility in the presence of blood and secretions. The fiberoptic scope requires more practice than other methods of airway management; the first experience using the scope should not be in the setting of an emergency airway problem. Once familiarity and facility with the scope are acquired, fiberoptic intubation can be used early in the management of the difficult airway rather than as a last resort after repeated failed attempts using conventional techniques.<br /><br /><span style="font-weight: bold; font-style: italic;">Retrograde Intubation</span><br />Retrograde orotracheal intubation is a technique of guided endotracheal intubation using a wire or catheter placed percutaneously through the cricothyroid membrane or high trachea and exiting through the mouth or nose. An endotracheal tube is then passed over this guide and advanced through the vocal cords into the trachea. Introduced by Butler and Cirillo in 1960, the technique has undergone several recent modifications that have enhanced its value as a means of establishing a definitive airway when more conventional techniques have failed.<br /><br /><span style="font-weight: bold; font-style: italic;">Indications and Contraindications</span><br />Retrograde intubation is indicated when definitive airway control is required and less invasive methods have failed. Indications include trismus, ankylosis of the jaw or cervical spine, upper airway masses, unstable cervical spine injuries, and maxillofacial trauma. It can be used to convert transtracheal needle ventilation into a definitive airway. It has been described in a 1-month-old with developmental abnormalities. It is particularly helpful in the trauma patient with airway bleeding that prevents visualization of the glottis. A striking example of the efficacy of this technique is presented in an article by Barriot and Riou describing successful out-of-hospital retrograde intubation in a series of trauma patients in whom attempts at conventional intubation failed.<br />Contraindications to this procedure include the ability to control the airway by less invasive means. The inability to open the mouth is another contraindication. A relative contraindication is the apneic patient who cannot be effectively ventilated using the bag-valve-mask; in this setting it is advisable to first establish transtracheal needle ventilation before attempting retrograde intubation or to go directly to cricothyrotomy.<br /><br /><span style="font-weight: bold; font-style: italic;">Equipment</span><br />Needed materials include the following: (1) local anesthetic and skin preparation materials, (2) 18-ga needle, (3) 60 cm epidural catheter-needle combination or 80 cm (0.88 mm diameter) spring guide wire (J-tip preferred), (4) hemostat, (5) long forceps (e.g., Magill) for grasping wire in pharynx, (6) endotracheal tube of appropriate size, (7) syringe for tube cuff, and (8) materials for securing tube. A prepackaged alternative is the Cook Retrograde Intubation Set (Cook Critical Care, Bloomington, Ind), which also contains a sheath.<br /><br /><span style="font-style: italic; font-weight: bold;">Procedure</span><br />Three anatomic landmarks must be located by palpation: the hyoid bone, thyroid cartilage, and cricoid cartilage. The skin overlying the cricothyroid membrane is prepped and anesthetized. Next, the lower half of the cricothyroid membrane is punctured with a needle directed slightly cephalad. The bevel should also face cephalad. Air is aspirated to confirm needle tip position within the lumen of the larynx. An alternative entry point is the high trachea, usually through the subcricoid space, using the same steps as described for the cricothyroid membrane.<br />The syringe is removed and the wire is then passed through the needle and advanced until it is seen in the patient's mouth, with the help of the laryngoscope, or until it exits out the nose. If the wire is found in the hypopharynx, it is grasped with the Magill forceps and drawn out through the mouth. The needle is removed from the neck and the end of the wire is secured at the puncture site with a hemostat. The oral end of the wire is then threaded in through the endotracheal tube side port--not the end of the tube--and advanced up the tube until it can be grasped by a second hemostat. Threading the wire through the side port allows the tube tip to protrude 1 cm beyond the point at which the wire enters the larynx. The wire is then pulled taut and moved back and forth to ensure that no slack remains.<br />The endotracheal tube is then advanced over the wire until resistance is met. This is the most critical point in the procedure; because this is a blind technique, it may be difficult to determine whether the tube has entered the trachea or is hung up on more proximal structures. If the endotracheal tube has successfully passed through the vocal cords and it is being restricted by the guide wire as it traverses the anterior laryngeal wall, one should feel some caudally directed tension on the wire at its laryngeal insertion point. If this does not occur, the tip of the endotracheal tube may be proximal to the vocal cords, either in the vallecula, the piriform sinus, or abutting the narrow anterior aspect of the vocal cords. If in doubt, pull the tube back 2 cm, rotate it 90° counterclockwise, and readvance the tube. This will usually result in successful passage through the larynx. [73] When satisfied that the tube has entered the trachea, the tube should be stabilized and the guide wire pulled out through the mouth. The tube is then advanced further into the trachea.<br />The classic method of retrograde intubation, as described above, has undergone modifications that facilitate the passage of the endotracheal tube through the glottis. A significant advance has been the addition of a plastic sheath that is passed antegrade over the wire until it meets resistance at the point at which the wire penetrates the laryngeal mucosa . This sheath needs to be stiff enough to effectively guide an endotracheal tube, yet small enough to easily pass through the vocal cords without impinging on supraglottic or glottic structures. Once the sheath comes to rest against the anterior laryngeal wall, the wire is withdrawn from the mouth and the sheath is advanced. With the sheath well within the trachea, the endotracheal tube is passed over the sheath. Any resistance that may be encountered at the arytenoids or vocal cords can usually be remedied by pulling the tube back 1 to 2 cm and rotating it counterclockwise 90°. One advantage of the antegrade sheath is that it lies freely in the larynx, allowing for a more posterior passage through the widest distance between the cords. The wire, however, pulls the endotracheal tube anteriorly toward the narrow commissure of the vocal cords and is more likely to result in impingement of the tube on the cords. Also, the use of the sheath permits unrestricted advancement of the endotracheal tube, whereas a wire entering the larynx 1.0 to 1.5 cm below the vocal cords prevents the tube from advancing more than this distance prior to removal of the wire.<br />If no sheath is available, one should consider placing the needle inferiorly in the subcricoid space, thereby increasing the distance the endotracheal tube can be advanced before being stopped by the wire. This will decrease the likelihood of dislodging the endotracheal tube tip when the guide wire is withdrawn.<br />Up to this point, blind retrograde intubation has been described. A further modification of the technique allows for visualization using a fiberoptic scope. In addition to the scope, an extra long guide wire (e.g., 125 cm, 0.025 cm Teflon-coated J-wire) is also required. The procedure is the same as previously described up to the point at which the wire is withdrawn from the mouth. At that point, with a endotracheal tube mounted on a lubricated fiberoptic scope, the long guide wire is passed retrograde up through the end of the fiberoptic scope and out the suction port. The fiberoptic scope is then advanced over the guide wire and through the cords, coming to rest against the anterior laryngeal wall. The wire is withdrawn from the suction port and the scope is advanced into the trachea. The endotracheal tube is then passed over the fiberoptic scope, and visualization guarantees correct endotracheal placement. The scope is then withdrawn and the lungs are auscultated.<br /><br /><span style="font-style: italic; font-weight: bold;">Complications</span><br />The complications of retrograde intubation are largely related to cricothyroid membrane puncture. Hemorrhage is minimized by taking care to puncture the cricothyroid membrane in its lower half (to avoid the cricothyroid artery). Subcutaneous emphysema may occur, but it is of no clinical significance because no air is insufflated during this technique. A small incidence of soft tissue infection is reported with translaryngeal needle procedures, but this can be minimized by ensuring that the wire is withdrawn from the mouth rather than the neck.<br />The final complication, the failure to achieve intubation, has been mitigated by the addition of the antegrade sheath over the wire.<br /><br /><span style="font-weight: bold; font-style: italic;">Summary</span><br />Retrograde intubation is an underused technique for achieving endotracheal intubation in a patient who cannot be intubated by less aggressive means. It is more invasive than fiberoptic intubation but requires less skill. Whereas retrograde intubation usually takes several minutes to complete, [81] the patient can undergo bag-mask ventilation through much of the procedure. Recent modifications in the technique guarantee this method a prominent place in the management of the difficult airway, particularly when active bleeding compromises the airway.<br /><br /></div>Emergency Medicinehttp://www.blogger.com/profile/06606398346130594987noreply@blogger.com0tag:blogger.com,1999:blog-3749884089415516879.post-55989188038051028932009-03-13T03:09:00.000-07:002009-03-13T03:15:31.709-07:00NASOTRACHEAL INTUBATION<div style="text-align: justify;">Nasotracheal intubation was first described by Magill in the 1920s and the basic technique has changed little over the years. Modifications have been described that increase the success rate and limit complications. The tube may be placed blindly or with the aid of a laryngoscope or bronchoscope. Blind nasotracheal intubation can be one of the more technically demanding airway approaches, with the outcome being heavily dependent on the skill and experience of the operator. The primary advantage of blind nasotracheal intubation is that it minimizes neck movement and does not require opening the mouth.<br /><br /><span style="font-weight: bold;">General Indications and Contraindications</span><br />Nasotracheal intubation is technically more difficult than oral intubation, but it has definite advantages. It is especially suitable for the patient with a short, thick neck or other anatomic characteristics that would make orotracheal intubation difficult. Patients with clenched teeth or suspected cervical spine injury can be intubated with minimal preparation. Cervical spine films, jaw spreading, or paralyzing agents as preliminaries to airway control are unnecessary.<br />Blind nasotracheal intubation is possible with the patient in the sitting position, a distinct advantage when intubating the patient with congestive heart failure who cannot tolerate lying flat. In fact, patients in respiratory distress are the easiest to intubate blindly because their air hunger results in increased abduction of the vocal cords, which facilitates tube entry into the trachea. The drug overdose patient with a decreased level of consciousness is a candidate for nasotracheal intubation. These patients are often intubated before gastric lavage and may be sufficiently awake to make orotracheal intubation difficult without paralyzing agents.<br />A nasotracheal tube has advantages that extend beyond the immediate difficulties of airway control. The patient cannot bite the tube or manipulate it with the tongue. Oral injuries may be cared for without interference by the tube. A nasotracheal tube is more easily stabilized and generally easier to care for than an orotracheal tube. It is better tolerated by the patient, permitting easier movement in bed, and produces less reflex salivation than do oral tubes.<br />Nasal intubation should be avoided in patients with severe nasal or midface trauma. In the presence of a basilar skull fracture, a nasotracheal tube may inadvertently enter the brain through a basilar skull fracture. [41] The technique should be avoided in patients in whom thrombolytic therapy is being considered. Nasal intubation is relatively contraindicated if the patient is taking anticoagulants or is known to have a coagulopathy.<br /><br /><span style="font-weight: bold;">Blind Placement</span><br />Blind nasotracheal intubation is the most common form of nasotracheal intubation in the emergency setting. Danzl and Thomas reported a success rate of 92% in a large series of emergency department patients.<br /><br /><span style="font-weight: bold;">Indications and Contraindications</span><br />Any patient requiring airway control who has spontaneous respirations is a candidate for blind nasotracheal intubation. Specific indications that favor this approach over others are (1) short, thick neck, (2) inability to open the mouth, (3) inability to move the neck, (4) gagging or resisting the use of the laryngoscope, and (5) oral injuries.<br />Apnea is the major contraindication to blind nasotracheal intubation. Attempts to place the tube without respirations as a guide are futile. Relative contraindications include basilar skull fracture and nasal injury. Furthermore, significant bleeding may occur if the patient is receiving anticoagulants or has a coagulopathy. Blind nasotracheal intubation should be avoided in patients with expanding neck hematomas. Patient combativeness, if not controlled with sedation, is also a contraindication.<br />Some would argue that the inability to open the mouth is a relative contraindication, because emesis may be induced that could not be cleared. The operator must exercise judgment in the individual case and be prepared to use neuromuscular blocking agents or to bypass the upper airway with a surgical technique if such a complication develops.<br /><br /><span style="font-weight: bold;">Procedure</span><br />The patient is placed in the "sniffing" position with the proximal neck slightly flexed and the head extended on the neck. In preparation for intubation, the operator constricts the nasal mucosa of both nares, using either 0.25 to 1.0% phenylephrine drops, oxymetazoline (Afrin) spray, or 4% cocaine spray. Topical anesthesia of the nares, oropharynx, and hypopharynx with lidocaine spray (10%) is also indicated if time permits. If available, cocaine is ideal because it is both a vasoconstrictor and an anesthetic; caution is necessary in hypertensive patients. The most patent nostril is chosen. In the cooperative patient, this can be determined simply by occluding each nostril and asking the patient which one is easier to breathe through. The most patent nostril can also be identified by direct vision, or by gently inserting a gloved finger lubricated with viscous lidocaine, full length into the nostrils. If time is not an issue, an effective method to dilate the nasal cavity and administer the anesthetic is to pass a lidocaine gel-lubricated nasopharyngeal airway (nasal trumpet) into the selected nostril. This<br />airway is left in place for several minutes, and progressively larger trumpets are introduced.<br />After preparation of the nostril, a well-lubricated endotracheal tube with a 7.0 or 7.5 mm ID is inserted along the floor of the nasal cavity. The tube is not directed cephalad, as one might expect from the external nasal anatomy, but rather is directed straight back toward the occiput, corresponding with the nasal floor. Twisting the tube may help bypass soft tissue obstruction in the nasal cavity. It is sometimes recommended that the bevel of the tube be oriented toward the septum to avoid injury to the inferior turbinate. However, such an event is rare. At 6 to 7 cm, one usually feels a "give" as the tube passes the nasal choana and negotiates the abrupt 90° curve required to enter the nasopharynx. This is the most painful and traumatic part of the procedure and must be done gently. If resistance is encountered that persists despite continued gentle pressure and twisting of the tube, the passage of a suction catheter down the tube and into the oropharynx may allow for successful passage of the tube over the catheter. [44] If this fails, the other nostril should be tried. In an attempt to avoid this difficulty from the outset, a controllable-tip tracheal tube (Endotrol, Mallinckrodt Medical Inc, St Louis) may be used that allows the operator to increase the flexion of the tube and facilitates passage past this tight curve. One study found the Endotrol tube to enhance first attempt success with blind nasotracheal intubation.<br />As the tube is advanced through the oropharynx and hypopharynx and approaches the vocal cords, breath sounds from the tube become louder, and fogging of the tube may occur. At the point of maximal breath sounds, the tube is lying immediately in front of the laryngeal inlet. The tube is most easily advanced into the trachea during inspiration because that is when the vocal cords are maximally open. As the patient begins to breathe in, the tube is advanced in one smooth motion. If a gag reflex is present, the patient usually coughs and becomes stridulous during this maneuver, suggesting successful tracheal intubation. The absence of such a response should alert the operator to probable esophageal passage. If there is a delay in advancing the tube, oxygen can be added to the end of the tube to increase inspired oxygen. Once the tube is in the trachea, moaning and groaning should cease. If they continue, esophageal intubation is likely. Breath sounds coming from the tube and tube fogging are other signs of endotracheal placement. Reflex swallowing during blind nasotracheal intubation may direct the tube posteriorly toward the esophagus. If this occurs, the conscious patient should be directed to stick out the tongue to inhibit swallowing and prevent consequent movement of the larynx. Application of laryngeal pressure may also help avoid esophageal passage.<br />Following intubation, both lungs are auscultated while positive-pressure ventilation is applied. If only one lung is being ventilated, the tube is withdrawn until breath sounds are heard bilaterally. The optimum distance from the external nares to the tube tip is about 28 cm in males and 26 cm in females. After verification of tracheal placement, the cuff is inflated and the tube is secured.<br /><br /><span style="font-weight: bold;">Technical Difficulties</span><br />The nasotracheal tube may slide smoothly through the hypopharynx and into the trachea on the first pass. Unfortunately, this is not always the case; in the operating room, the first attempt was successful in <50% of cases. When the initial pass is unsuccessful, there are 4 potential locations of the tip of the tube: (1) anterior to the epiglottis in the vallecula, (2) on the arytenoid or vocal cord, (3) in the piriform sinuses, or (4) in the esophagus.<br />Observation and palpation of the soft tissues of the neck during attempted passage of the nasotracheal tube are helpful in determining the location of the misplaced tube. This is ideally done by the operator but may also be performed by an experienced attendant. Before reattempting placement, the tube is withdrawn slightly; it is not removed from the nose, because this will create additional trauma to the nasal soft tissues. The possibility of cervical spine injury must be kept in mind when considering corrective maneuvers. Any maneuver that moves the neck significantly should not be used if alternatives are available. Methods for achieving success when difficulties with tube placement are encountered include the following:<br /><br /><span style="font-style: italic;">Anterior to the epiglottis.</span><br />Difficulty advancing the tube beyond 15 cm or palpation of the tube tip anteriorly at the level of the hyoid bone suggests an impasse anterior to the epiglottis in the vallecula. Withdrawing the tube 2 cm, decreasing the degree of neck extension, and readvancing the tube will frequently remedy this problem.<br /><br /><span style="font-style: italic;">Arytenoid cartilage and vocal cord.</span><br />Contrary to the classic teaching, recent studies have demonstrated a propensity for a nasotracheal tube, when placed through the right nares, to lie posteriorly and to the right as it approaches the larynx. It is not surprising, then, that the most common obstacles to advancement of the nasotracheal tube are the right arytenoid and vocal cord. No data are available on the common obstacles encountered if the tube is placed in the left nares. If the tube appears to be hanging up on firm, cartilaginous tissue, withdraw the tube 2 cm, rotate it 90° counterclockwise, and readvance the tube. This maneuver orients the bevel of the tube posteriorly and frequently results in successful passage . Another technique is to pass a suction catheter down the tube; it often will pass through the larynx without difficulty and the tube can then be advanced over the catheter.<br /><br /><span style="font-style: italic;">Piriform sinus.</span><br />Bulging of the neck lateral and superior to the larynx indicates tube location in a piriform sinus. The tube should be withdrawn 2 cm, rotated slightly away from the bulge, and readvanced. An alternate method is to tilt the patient's head toward the side of the misplacement and reattempt placement.<br /><br /><span style="font-style: italic;">Esophageal placement.</span><br />Esophageal placement is indicated by a smooth passage of the tube with the loss of breath sounds. The larynx may be seen or felt to elevate as the tube passes under it. Assisted ventilation will usually produce gurgling sounds when the epigastrium is auscultated. The tube should be withdrawn until breath sounds are clearly heard, and passage should be reattempted while pressure is applied to the cricoid. Increased extension of the head on the neck during placement may help. If attempts continue to result in esophageal misplacement, the following maneuver may result in successful tracheal intubation: from the precise point at which breath sounds are lost, the endotracheal tube is withdrawn 1 cm. The cuff is inflated with 15 mm of air, resulting in an elevation of the tube off the posterior pharyngeal wall and angling it toward the larynx. The tube is then advanced 2 cm; continued breath sounds indicate probable intralaryngeal location. At this point, the cuff is deflated and the endotracheal tube is advanced into the trachea . This technique may be particularly useful in the patient with cervical spine injury, because it requires no manipulation of the head or neck. This maneuver, when used on the first pass in 20 patients in the operating room, was successful in 75% of cases. One should bear in mind, however, that these patients were paralyzed and thus did not experience the laryngospasm that may be encountered in a breathing patient. The use of topical anesthesia is recommended. Alternatively, if a controllable-tip endotracheal tube (Endotrol) is used, the tip can be flexed anteriorly to help avoid esophageal placement. Remember that the tip is very responsive to pulling on the ring. A common mistake is to exert too much force on the ring, resulting in the tube curling up short of the larynx, thus preventing tube advancement.<br /><br /><span style="font-style: italic;">Laryngospasm.</span><br />Laryngospasm is common when attempting nasotracheal intubation. It is usually transient. The tube is withdrawn slightly and the operator should wait for the patient's first gasp; advancement of the tube at this precise moment is frequently successful, as the vocal cords are widely abducted during forced inhalation. Laryngeal anesthesia should also be assessed, and if IV and nebulized lidocaine have already been administered without success, transcricothyroid anesthesia (e.g., 2 mL of 4% lidocaine) should be considered. Occasionally, a jaw lift is necessary to break prolonged spasm. Another option is to use a smaller tube.<br /><br /><span style="font-weight: bold;">Placement Under Direct Vision</span><br />This technique combines elements of oral and nasotracheal intubation. The indications and precautions are similar, and the importance of considering cervical spine injury is identical. Likewise, the need for jaw opening by physical or pharmacologic means is unchanged. This method is preferred to orotracheal intubation if the presence of an orotracheal tube might interfere with the repair of an oral injury. It is also useful when blind nasotracheal intubation has failed.<br />Preparation of the nose and nasopharynx and passage of the tube into the oropharynx are the same as described for blind nasotracheal intubation. It is with the introduction of the laryngoscope that the technique changes.<br />Laryngoscopy, as described with orotracheal intubation, is used to visualize the vocal cords and the tip of the endotracheal tube. With the Magill forceps in the right hand, the endotracheal tube is grasped proximal to the cuff (to avoid damage to the balloon) and directed toward the larynx . An assistant advances the tube gently while the operator directs the tip into the larynx and trachea. Cricoid pressure may facilitate the passage. Often the larynx can be manipulated sufficiently with the laryngoscope so that the physician can advance the tube with the right hand and guide it between the cords without using the Magill forceps. Occasionally, the natural curve of the tracheal tube guides it through the cords without any manipulation. The cuff is inflated, and both lungs are auscultated to ensure ventilation. When placement is satisfactory, the tube is secured.<br /><br /><span style="font-weight: bold;">Complications</span><br />Epistaxis is the most common complication of nasotracheal intubation. However severe epistaxis was encountered in only 5 of 300 cases reported by Danzl and Thomas. [42] Tintinalli and Claffey reported severe bleeding in 1 of 71 cases and less serious bleeding in 12 others. [54] Bleeding is usually not a problem unless it provokes vomiting or aspiration, a serious potential problem in obtunded patients with a clenched jaw or a decreased gag reflex. Other immediate complications include turbinate fracture, intracranial placement through basilar skull fracture, retropharyngeal laceration or dissection, and delayed or unsuccessful placement. Unsuccessful placement may be minimized by selection of a smaller tube and by gentle technique.<br />Sinusitis in patients with nasotracheal tubes is common and can be an unrecognized cause of sepsis. Rare but potentially fatal delayed complications include mediastinitis following retropharyngeal abscess and massive pneumocephalus.<br />Because most of the complications occur during tube advancement through the nasal passage and proximal nasopharynx, the complications of blind nasotracheal intubation and placement under direct vision are largely the same. However, retropharyngeal laceration and esophageal intubation are more of a threat in blind placement techniques because they are more likely to go unrecognized. One unique problem associated with nasotracheal intubation is damage of the tube cuff with the Magill forceps.<br />Delayed nasotracheal placement under direct vision deserves special discussion. Manipulation of the endotracheal tube through the nose and with the Magill forceps during the direct vision technique involves additional steps that require time. Because time is of the essence in the resuscitation of the critically ill patient, orotracheal intubation may be preferable.<br /><br /><span style="font-weight: bold;">Summary</span><br />Nasotracheal intubation is being used less frequently than in the past, because practitioners are increasingly comfortable using oral intubation in the patient with potential cervical spine injury. In addition, emergency physicians frequently use paralytics to facilitate orotracheal intubation. Nevertheless, nasotracheal intubation remains an effective and potentially life saving approach to the difficult airway and should be a dependable part of the armamentarium of all providers who are active in emergency airway management.<br /><br /></div>Emergency Medicinehttp://www.blogger.com/profile/06606398346130594987noreply@blogger.com3tag:blogger.com,1999:blog-3749884089415516879.post-27953938294597575842009-03-13T03:05:00.000-07:002009-03-13T03:09:10.138-07:00MODIFIED OROTRACHEAL INTUBATION<div style="text-align: justify;"><span style="font-weight: bold;">Intubation with an Intermediate Airway in Place</span><br /><span style="font-weight: bold;">Esophageal Obturator/Gastric Tube Airway in Place</span><br />The unconscious patient who requires ventilatory assistance may benefit from the temporary use of the esophageal obturator airway (EOA) or similar device. Although this may be an effective means of ventilation, it is at best a temporary measure. The patient experiencing upper airway hemorrhage with the EOA in place may have oropharyngeal blood insufflated into the trachea. Also, an endotracheal tube is the preferred airway, because with endotracheal intubation the airway is more secure and ventilation more convenient. Although the EOA may allow rapid airway support until cervical spine injury can be ruled out, it is recommended that the EOA not be left in place for more than 2 hours.<br />Replacement of the EOA with an orotracheal tube requires appropriate care. Removal of the esophageal cuff before placement of the endotracheal tube is fraught with danger. Spontaneous gastric regurgitation often occurs on EOA removal. The rescuer must therefore learn to perform endotracheal intubation around the EOA to protect the patient from aspiration.<br />The patient is hyperventilated through the EOA before intubation is attempted around it. The EOA mask is then removed, and the EOA tube is moved to the left side of the patient's mouth. Laryngoscopy and intubation are then performed in the usual fashion. If resistance to passage of the tracheal tube is met, the volume of the EOA balloon should be reduced, because the balloon may be producing distortion of the larynx. Next, the operator deflates the EOA balloon completely and slides it out of the patient's esophagus. If resistance is met, the operator must be sure that the esophageal cuff has been deflated completely.<br /><br /><span style="font-weight: bold;">Esophageal-Tracheal Combitube (ETC) in Place</span><br />Combitubes placed in the esophagus will generally require replacement with a tracheal tube. The inflated pharyngeal balloon prevents tracheal intubation around this airway. This proximal balloon must be deflated before attempting tracheal intubation. If intubation is still not possible, the ETC may need to be removed; the stomach should first be emptied via a gastric tube placed through the esophageal port of the airway. Suction is readied, the distal balloon is deflated, and the patient is quickly intubated. This maneuver poses an added risk over that associated with the esophageal obturator intermediate airway placement (i.e., EOA and EGTA) .<br /><br /><span style="font-weight: bold;">Laryngeal Mask Airway in Place</span><br />The trachea can often be intubated with the laryngeal mask airway (LMA) left in place.<br /><br /><span style="font-weight: bold;">Bullard Laryngoscope Use</span><br />A recent development for intubating the difficult airway is the Bullard laryngoscope, an anatomically shaped rigid fiberoptic laryngoscope that provides an indirect view of the larynx . It was design`ed to aid in intubating the difficult airway; and because no manipulation of the neck is necessary, it is especially well suited for the patient with potential cervical spine injury. Indeed, in the anesthetized patient, the Bullard laryngoscope has been found to cause less head extension and cervical spine extension than conventional laryngoscopes do. [36] The recent addition of an intubating stylet attached to the laryngoscope has resulted in increased ease and speed of intubation, and the technique appears to be effective regardless of the patient's head and neck anatomy. [37] Because alignment of the oropharyngeal and laryngeal axes is not required, the Bullard laryngoscope offers the advantage provided by a conventional fiberoptic scope but requires less training to gain proficiency in its use. [38]<br /><br /><span style="font-weight: bold;">Indications and Contraindications</span><br />The Bullard laryngoscope is indicated in patients with anticipated difficult airways who require definitive airway control. It can be used in awake as well as unresponsive patients. [39] The total inability to open the mouth is a contraindication to the use of this laryngoscope. However, because the Bullard laryngoscope follows the contour of the mouth and hypopharynx, only 2 cm of occlusal opening is necessary for the introduction of the scope plus endotracheal tube for intubation.<br /><br /><span style="font-weight: bold;">Procedure</span><br />The technique for introducing the Bullard laryngoscope blade is similar to that for direct laryngoscopy. The operator, who is at the head of the patient, opens the mouth with the left thumb while holding the head stable. As the scope blade is introduced into the oropharynx, the handle is rotated to follow the curve of the hypopharynx until the handle is fully vertical. The tip of the blade can be used to lift the epiglottis, but visualization of the larynx is usually possible without this maneuver. Only minimal force is exerted along the axis of the handle. Intubation of the larynx can be accomplished using a styletted endotracheal tube or an endotracheal tube with a directional tip (Endotrol; Mallinckrodt, Critical Care, Glens Falls, NY). The technique is generally successful when using the new Bullard intubating stylet. [37]<br />Awake intubation using the Bullard laryngoscope can be performed comfortably using topical anesthesia and light IV sedation. [39] Adult and pediatric Bullard laryngoscopes are available, and the scope has been used successfully in neonates. [38] The Bullard scope can also be used in conjunction with nasotracheal intubation and has the advantage of requiring only 6 mm of mouth opening through which to insert the blade. [40]<br /><br /><span style="font-weight: bold;">Complications</span><br />The major difficulty in using the Bullard laryngoscope is the inability to visualize the larynx because of blood, emesis, or secretions. Another reason for failure is the inability to place the blade tip under the epiglottis. [37]<br /><br /><span style="font-weight: bold;">Summary</span><br />The Bullard scope is useful in the difficult airway uncomplicated by blood and excessive secretions. In the all-too-common setting of blood and secretions, however, the inability to visualize the vocal cords significantly limits the utility of this device in emergency airway management.<br /><br /></div>Emergency Medicinehttp://www.blogger.com/profile/06606398346130594987noreply@blogger.com0tag:blogger.com,1999:blog-3749884089415516879.post-79472244680119416282009-03-13T02:50:00.000-07:002009-03-13T03:05:09.469-07:00OROTRACHEAL INTUBATION<div style="text-align: justify;"><span style="font-weight: bold;">Indications and Contraindications</span><br />Any clinical situation in which a definitive airway is necessary and limited neck motion is permissible is an indication for orotracheal intubation. Many of these situations, including cardiac arrest, airway compromise in infection and trauma, and airway obstruction are discussed in detail in Chapter 1 . Most orotracheal intubations are accomplished using a direct laryngoscope. An unstable cervical spine injury is a relative contraindication to direct laryngoscopy.<br /><br /><span style="font-weight: bold;">Equipment</span><br /><span style="font-weight: bold;">Laryngoscope</span><br />Facility in the use of the direct laryngoscope is a prerequisite for orotracheal intubation. Various adult and pediatric blade sizes are available. There are two basic blade designs-- curved (MacIntosh) and straight (Miller and Wisconsin). Slight variations in laryngoscopic technique follow from one's choice of blade design, which is often a matter of personal preference. The tip of the straight blade goes under the epiglottis and lifts it directly, whereas the curved blade fits into the vallecula and indirectly lifts the epiglottis via the hyoepiglottic ligament to expose the larynx. Special blades designed for the anterior larynx include the Siker and the Belscope (Avulunga Pty Ltd, New South Wales, Australia).<br />Each blade type has advantages and disadvantages. The straight blade is usually a better choice in pediatric patients, in patients with an anterior larynx or a long floppy epiglottis, and in individuals whose larynx is fixed by scar tissue. It is less effective, however, in patients with prominent upper teeth, and it is more likely to break teeth. Use of the straight blade is also more often associated with laryngospasm due to its stimulation of the superior laryngeal nerve, which innervates the undersurface of the epiglottis. A straight blade may inadvertently be advanced into the esophagus and initially present one with unfamiliar anatomy until it is withdrawn. The blade has a light bulb at the tip that may slightly hamper vision. The wider, curved blades are helpful in keeping the tongue retracted from the field of vision, allowing for more room in passing the tube in the oropharynx, and they are generally preferred in uncomplicated adult intubations. Aside from patient considerations, some clinicians prefer the curved blade because they find it requires less forearm strength than the straight blade.<br /><br /><span style="font-weight: bold;">Tracheal Tubes</span><br />The standard endotracheal tube is plastic and measures approximately 30 cm. Tube sizing is based on internal diameter (ID), measured in millimeters, and ranges from a 2.0 to a 20.0 mm tube, increasing in increments of 0.5 mm. The outer tube diameter is 2 and 4 mm larger than the internal diameter. Tube size is printed on the tube. There is also a scale, in centimeters, for determining the distance along the tube from the tip.<br />Adult men will generally accept a 7.5 to 9.0 mm orotracheal tube, whereas women can usually be intubated with a 7.0 to 8.0 mm tube. In most circumstances, tubes smaller than these should not be used, especially in patients with chronic obstructive lung disease who may be difficult to wean from the respirator due to excessive airway resistance from a small tube. However, in emergency intubations, particularly if a difficult intubation is anticipated, many clinicians<br />choose a smaller tube and change to a larger tube later if necessary. One exception is in the burn patient, in whom one places as large a tube as possible on the initial attempt because swelling may prohibit subsequent tube placement. For nasal intubation, a slightly smaller tube (by 0.5 to 1.0 mm) is chosen.<br />The cuff of a standard tracheal tube is high-volume and low-pressure. A clinical test for determining correct cuff inflation is to slowly inject air until no air leak is audible while the patient is receiving bag-tube ventilation. This usually occurs with 5 to 8 mL of air if the proper-sized tracheal tube has been selected. Many clinicians use the tension of the pilot balloon as a guide to cuff inflation; slight compressibility with gentle external pressure indicates adequate inflation for most clinical situations. For long-term use, cuff pressure should be measured and maintained at 20 to 25 mm Hg. Capillary blood flow is compromised in the tracheal mucosa when the cuff pressure exceeds 30 mm Hg.<br />In infants and children, the following formula is a highly accurate method for determining correct tracheal tube size:<br /><br /><span style="font-style: italic; font-weight: bold;">Tube size = [4 + age (years)]/4</span><br /><br />For most clinical situations, however, using the width of the nail of the little finger as a guide is sufficiently accurate and has been shown to be more precise than finger diameter 45911.<br />Correct tube size is especially important in the pediatric population, because most patients younger than 8 years are intubated with an uncuffed tube; adequate tube size is necessary to provide a good seal between the tube and the upper trachea and to prevent aspiration. A cuffed tube is used in children with decreased lung compliance who may require prolonged mechanical ventilation. In a child, the smallest airway diameter is at the cricoid ring rather than at the vocal cords, as in adults. Hence, a tube may pass the cords but go no farther. Should this occur, the next smaller sized tube should be passed after reoxygenation.<br />Adult endotracheal tubes will accept a standard adaptor on which the ventilator tubing will fit. Pediatric tubes require a special adaptor with a distal end small enough to accommodate the small tube size.<br /><br /><span style="font-weight: bold;">Preparing for Intubation</span><br />Before beginning intubation, a number of issues should be addressed. In chronologic order, they are (1) confirm that<br />the required intubation equipment is available and functioning; (2) position the patient correctly; (3) assess the patient for difficult airway; (4) establish intravenous (IV) access, time permitting; (5) draw up essential drugs, and; (6) attach the necessary monitoring devices. In the haste of the moment, it is a common error to fail to position the patient properly or to proceed with the procedure before the proper equipment is assembled and checked. Simple omissions, such as failing to restrain the patient's hands, removing dentures, or misplacing the suction device, can seriously hamper the performance of the procedure. A suggested pre-intubation checklist is presented in Table 2-2 .<br />In addition to the preparation necessary for optimum patient care, the operator should also minimize exposure to potentially infectious materials . Generally, the operator should be gloved and should wear eye and mouth protection to guard against exposure to patient secretions.<br />The endotracheal tube cuff should be checked for leaks by inflating the balloon before attempting intubation. The tube is prepared for placement by passing a flexible stylet down the tube to increase its stiffness and enhance control of the tip of the tube. The stylet should not extend beyond the end of the tube. The tube is then bent in a gradual curve with a more acute angling in the distal one-third to more easily access the anterior larynx. The tip and cuff of the tube are lubricated with viscous lidocaine or another water-soluble gel.<br />The patient should be positioned to optimally align the oral, pharyngeal, and laryngeal axes . The desired position was aptly described by Magill to make the patient appear to be "sniffing the morning air," with the head extended on the neck and the neck slightly flexed relative to the torso. A small towel under the occiput (to raise it 7 to 10 cm) may facilitate positioning. Positioning of the head and neck is a critical step; nonoptimal head positioning may be the sole reason for some intubation failures.<br /><br /><span style="font-weight: bold;">The Difficult Airway</span><br />The majority of difficult intubations are predictable. Perhaps the most frequently encountered condition associated with a difficult intubation is the agitated or combative patient. Fortunately, this condition can be readily eliminated through pharmacologic intervention. The classic parameters that predict a difficult intubation include a history of previous difficult intubation, prominent upper incisors, limited ability to extend at the atlanto-occipital joint, [5] poor visibility of pharyngeal structures when the patient extends the tongue (Mallampati's classification, or the tongue/pharyngeal ratio), [6] limited ability to open the mouth, [7] a limited direct laryngoscopic view of the laryngeal inlet, [7] and a short distance from the thyroid notch to the chin with the neck in extension . [8] Radiographic indicators of the ease of intubation include the mandibular length-to-height ratio [9] and the distance from the spine of the atlas to the occiput. [10] In emergency airway management, many of these predictors are not obtainable. An extensive history is rarely available, the patients are frequently uncooperative, and the presence of trauma limits movement of the neck. Fortunately, some of the key predictors are apparent simply by observing the external appearance of the patient's head and neck.<br />Patients with neck tumors, thermal or chemical burns, traumatic injuries to the face and anterior neck, angioedema and infection of the pharyngeal and laryngeal soft tissues, or previous operations in or around the airway suggest a difficult intubation because distorted anatomy or secretions may compromise visualization of the vocal cords. Facial or skull fractures may further limit airway options by precluding nasotracheal intubation. Patients with ankylosing arthritis or developmental abnormalities, such as a hypoplastic mandible or the large tongue of Down's syndrome, are difficult to intubate because neck rigidity and problems of tongue displacement can obscure visualization of the glottis.<br />Besides these obvious congenital and pathologic conditions, the short, thick neck poses the greatest difficulty for performing orotracheal intubation. In such individuals, the larynx is anatomically higher and more anterior, which makes it harder to visualize the vocal cords. These individuals are easily identified by observing the head and neck in profile. In such patients, apply laryngeal pressure and consider using the straight blade. Use of other options, including nasotracheal intubation, may be required.<br />It should be emphasized that some patients, despite normal-appearing anatomy and the absence of a complicating history, are unexpectedly difficult to intubate. One must be prepared for this rare but inevitable occurrence.<br /><br /><span style="font-weight: bold;">Procedure</span><br /><br /><span style="font-weight: bold;">Adults</span><br /><br /><span style="font-weight: bold; font-style: italic;">Direct laryngoscopy.</span><br />The operator is stationed at the patient's head . The patient is generally supine with the head at the level of the operator's lower sternum. To maintain the best mechanical advantage, the operator keeps his or her back straight and does not hunch over the patient; any bending should occur in the knees. The left elbow is kept relatively close to the body and flexed to provide better support. In the severely dyspneic patient who cannot tolerate lying down, direct laryngoscopy can be performed with the patient seated semi-erect and the laryngoscopist on a stepstool behind the patient. [11]<br />The laryngoscope is grasped in the left hand with the blade directed toward the patient from the hypothenar aspect of the operator's hand. The patient's lower lip is drawn down with the right thumb, and the tip of the laryngoscope is introduced into the right side of the mouth. The blade is slid along the right side of the tongue, gradually displacing the tongue toward the left as the blade is moved to the center of the mouth. If the blade is initially placed in the middle of the tongue, the tongue will fold over the lateral edge of the blade and obscure the airway. Placing the blade in the middle of the tongue and failure to move the tongue to the left are two common errors preventing visualization of the vocal cords.<br />As the blade tip approaches the base of the tongue, the operator exerts a force along the axis of the laryngoscope handle, lifting upward and forward at a 45° angle. The epiglottis should come into view with this maneuver. It may help to have an assistant retract the cheek laterally to further expose the laryngeal structures. Do not bend the wrist; bending the wrist can result in dental injury because the teeth may be used as a fulcrum for the blade.<br />The step following visualization of the epiglottis depends on which laryngoscope blade is used. With the curved blade, the tip is placed into the vallecula, the space between the base of the tongue and the epiglottis. Continued anterior elevation of the base of the tongue and the epiglottis will expose the vocal cords. If the blade tip is inserted too deeply into the vallecula, the epiglottis may be pushed down to obscure the glottis. [6] When using the straight blade, the tip is inserted under and slightly beyond the epiglottis, directly lifting this structure. The jaw and larynx are literally suspended by the blade. If the straight blade is placed too deeply, the entire larynx may be elevated anteriorly and out of the field of vision. Gradual withdrawal of the blade should allow the laryngeal inlet to drop down into view. If the blade is deep and posterior, the lack of recognizable structures indicates esophageal passage; gradual withdrawal should permit the laryngeal inlet to come into view.<br />Proper neck positioning and pressure (cephalad, dorsally, and rightward) on the larynx by an assistant will facilitate visualization and intubation of an anterior larynx. If needed, suctioning is performed at this point. If the vocal cords are still not seen, consider using a tracheal tube introducer (Smiths Industries Medical Systems, Keene, NH). This device, also known as the "elastic gum bougie," is a long, semirigid introducer that is placed, using the laryngoscope, through the laryngeal inlet and into the trachea. [12A] The tracheal tube is then passed over the introducer and the introducer is withdrawn. If resistance is met in passing the tracheal tube, rotate the tube 90° counterclockwise and advance the tube.<br /><br /><span style="font-weight: bold; font-style: italic;">Tube passage.</span><br />Once the vocal cords have been visualized, the final and most important step, tube passage under direct vision through the vocal cords and into the trachea, is performed. The tube is held in the operator's right hand and introduced from the right side of the patient's mouth. The tube is advanced toward the patient's larynx at an angle, not parallel with or down the slot of the laryngoscope blade. This way, the operator's view of the larynx is not obstructed by the hand or the tube until the last possible moment before the tube enters the larynx. The tube should be passed during inspiration, when the vocal cords are maximally open. It enters the trachea when the cuff disappears through the vocal cords. The tube is advanced 3 to 4 cm beyond this point. It is not enough to see the tube and the cords; the tube must be seen passing through the vocal cords to ensure tracheal placement.<br />When the vocal cords are stimulated, laryngospasm-- the persistent contraction of the adductor muscles of the vocal cords--may prevent passage of the tube. Inadequate anesthesia is often the cause. Pretreatment with topical lidocaine decreases the likelihood of this occurring. Two percent or 4lidocaine is sprayed directly on the cords. An infrequent but effective route for achieving tracheal anesthesia is via transtracheal puncture, injecting a bolus of 3 to 4 mL of lidocaine through the cricothyroid membrane. Laryngospasm is usually brief and is often followed by a gasp. The operator should be ready to pass the tube at this moment. Occasionally, the spasm is prolonged and needs to be broken with sustained anterior traction applied at the angles of the mandible--the jaw lift. At no time should the tube be forced, because permanent damage to the vocal cords may result. Consideration should be given to using a smaller tube. Prolonged, intense spasm may ultimately require muscle relaxation with a paralyzing drug . The pediatric patient is far more prone to laryngospasm than is an adult. [12] In a child, if vocal cord spasm prevents tube passage, a chest thrust maneuver may momentarily open the passage and permit intubation.<br /><br /><span style="font-weight: bold; font-style: italic;">Positioning and securing the tube.</span><br />The endotracheal tube should be secured in a position that minimizes both the chance of inadvertent endobronchial intubation and the risk of extubation. The tip should lie in the midtrachea with room to accommodate neck movement. Because tube movement with both neck flexion and extension averages 2 cm, the desired range of tip location is between 3 and 7 cm above the carina. [14]<br />On a radiograph, the tip of the tube should ideally be 5 ± 2 cm above the carina when the head and neck are in a neutral position. On a portable radiograph, the adult carina overlies the fifth, sixth, or seventh thoracic vertebral body. If the carina is not visible, it can be assumed that the tip of the tube is properly positioned if it is aligned with the T3 or T4 vertebra. In children, the carina is more cephalad than in the adult, but it is consistently situated between T3 and T5. In children, T1 is used as the reference point for the tip of the endotracheal tube. [15]<br />An estimate of the proper depth of tube placement can be derived from the following formulas, the lengths representing the distance from the tube tip to the upper incisors in children and from the upper incisors [18] or the corner of the mouth [19] in adults:<br />Adults: Tracheal tube depth (cm) = 21 cm (women)<br />Tracheal tube depth (cm) = 23 cm (men)<br />In adults, this method has been shown to be more reliable than auscultation in determining the correct depth of placement. [18]<br />The cuff is inflated to the point of minimal air leak with positive-pressure ventilation. In an emergency intubation, 10 mL of air is placed in the cuff, and inflation volume is adjusted after the patient's condition is stabilized.<br />After tracheal tube placement, both lungs are auscultated under positive-pressure ventilation. Care is taken to auscultate laterally because midline auscultation may lead to an erroneous impression of tracheal placement when the tube is actually in the esophagus. With the tube in position and the cuff inflated, the tube is secured in place. Commercial endotracheal tube holders, adhesive tape, or umbilical (nonadhesive cloth) tape can be attached securely to the tube and around the patient's head . The tube should be positioned in the corner of the mouth, where the tongue cannot expel it. This position is also more comfortable for the patient and allows for suctioning. A bite-block or oral airway to prevent endotracheal tube crimping or damage from biting is commonly incorporated into the system used to secure the tube.<br /><br /><span style="font-weight: bold;">Infants and Children</span><br />Appreciation of the anatomic differences between children and adults is helpful when intubating the pediatric patient . Infants' proportionately larger head naturally places them in the "sniffing position," so a towel under the occiput is rarely necessary. The large head can even result in a posterior positioning of the larynx that prevents visualization of the vocal cords; a small towel under the child's shoulders should correct this problem. The head also may be floppy, and it can be stabilized by an assistant during intubation. The child's increased tongue-to-oropharynx ratio and shorter neck hinder forward displacement of the tongue and, coupled with a long U-shaped epiglottis, can make visualization of the glottis difficult.<br />Consequently, direct laryngoscopy in the infant and young child is generally best performed with a straight blade: Miller size 0 for premature infants, size 1 for normal-sized infants, and size 2 for older children. The infant's larynx lies higher and relatively more anterior. One can have an assistant lightly apply laryngeal pressure, or the operator can use the little finger of the hand holding the laryngoscope blade for this purpose . If no laryngeal structures are visible after laryngeal pressure, the blade should be gradually withdrawn, because inadvertent advancement of the blade into the esophagus is a common error.<br /><br /><span style="font-weight: bold;">Confirmation of Tracheal Intubation</span><br /><br /><span style="font-weight: bold;">Clinical Assessment</span><br />The best assurance of tracheal placement is for the operator to see the tube pass through the vocal cords . Absent or diminished breath sounds, vocalization, increased abdominal size, and gurgling sounds during ventilation are clinical signs of esophageal placement. However, esophageal placement is not always obvious. One may hear "normal" breath sounds if only the midline of the thorax is auscultated. One way to clinically assess tracheal placement after a ventilation or during spontaneous respiration is to note whether air is felt or heard to exit through the tube following cuff inflation. If the tidal volume is adequate, the exit of air should be obvious. It is important to note that when an appropriately sized tube is placed in the trachea, the patient cannot groan, moan, or speak. Any vocalization suggests esophageal placement.<br />Asymmetrical breath sounds indicate probable main stem bronchus intubation. Due to the angles of takeoff of the main bronchi and the fact that the carina lies to the left of the midline in adults, right main stem intubation is most common and is indicated by decreased breath sounds on the left side. When asymmetrical sounds are heard, the cuff should be deflated and the tube withdrawn until equal breath sounds are present. Bloch and colleagues report accurate pediatric tracheal positioning if after noting asymmetrical breath sounds, the tube is withdrawn a defined distance beyond the point at which equal breath sounds are first heard--2 cm in children younger than 5 years and 3 cm in older children. [20]<br /><br /><span style="font-weight: bold;">Esophageal Detector Device</span><br />An aspiration technique used to determine endotracheal tube location was first described by Wee in 1988. [21] The technique takes advantage of the difference in tracheal and esophageal resistance to collapse during aspiration to determine location of the tip of the tracheal tube. Following intubation, a large syringe is attached to the end of the endotracheal tube and the syringe plunger is withdrawn. If the tube is correctly placed in the trachea, the plunger will pull back without resistance as air is aspirated from the lungs. However, if the tracheal tube is in the esophagus, resistance is felt when the plunger is withdrawn, because the pliable walls of the esophagus collapse under the negative pressure and occlude the end of the tube. Another device using the same principle as syringe aspiration is the self-inflating bulb (e.g., Ellick's device).<br />Wee first reported use of an esophageal detector device in the operating room. [21] The tube was correctly identified in 99 of 100 cases (51 esophageal, 48 tracheal). The device result was considered equivocal in the remaining tracheal tube. The tube was removed and found to be nearly totally occluded with purulent secretions. Slight resistance was noted in one patient with a right main stem intubation; resistance decreased when the tube was pulled back. Before use, the esophageal detector device must always be checked for air leaks. If any connections are loose, the leak may allow the syringe to be easily withdrawn, mimicking tracheal location of the tube.<br />Wee recommends the following guidelines in using the aspiration technique: apply constant, slow aspiration to avoid tube occlusion from tracheal mucosa drawn up under high negative pressure. If the tracheal tube is correctly placed, 30 to 40 mL of air can be aspirated without resistance. If air was initially aspirated and then some resistance is encountered, the tracheal tube should be pulled back between 0.5 and 1.0 cm and partially rotated. This takes the tube out of the bronchus, if it has been placed too deeply, and changes the orientation of the bevel if the tube has been temporarily occluded with tracheal mucosa. Air is easily aspirated if the tube was in the trachea, but repositioning will make no difference if the tube was in the esophagus. The syringe aspiration technique can be used before or after ventilation of the patient. Continuous cricoid pressure should be applied pending tube confirmation. Inflation of the tube cuff will have no effect on the reliability of the test. [22] This device is reliable, rapid, inexpensive, and easy to use. Jenkins reported good success with physician use of the aspiration technique to confirm placement of emergency department and out-of-hospital intubations. [23]<br />A squeeze-bulb aspirator can be used as an alternative to the syringe technique. [24] [25] The bulb is attached to the endotracheal tube and squeezed; if the tube is in the esophagus, it is often accompanied by a flatus-like sound followed by absent or markedly delayed refilling. Insufflation of a tube in the trachea is silent, with instantaneous refill. An early study with the Ellick's evacuator bulb device reported that 87% of esophageal tubes were identified. [24] A later study using a slightly different bulb device (Respironics, Murrysville,Pa) found that all 45 esophageal tubes were detected. [25] The device is cheap and easy to use and can be operated single-handedly in <5 style="font-weight: bold;">End-Tidal CO2 Detector Devices</span><br />A high level of CO2 in exhaled gas is the physiologic basis for capnography and the principle on which end-tidal CO2 (ETCO2 ) detectors was developed. The most commonly available devices for emergency use are colorimetric indicators responding to CO2 levels of gas flowing through the device when placed on the tracheal tube adapter. The typical device displays two extreme colors indicating a low level of CO2 in esophageal intubation and another color in tracheal intubation. An intermediate color is indeterminate. Hand-held quantitative or semiquantitative electronic CO2 monitors are also available.<br />A multicenter study of a colorimetric device demonstrated an overall sensitivity of 80% and a specificity of 96%. [26] In patients with spontaneous circulation and the tracheal tube cuff inflated, the sensitivity and specificity rose to 100%. The poor sensitivity seen in cardiac arrest (69%) is due to the fact that low exhaled CO2 levels are seen in both very-low-flow states and in esophageal intubation. The device must therefore be used with caution in the cardiac arrest victim. Levels of CO2 return to normal after return of spontaneous circulation in these patients. Further, colorimetric changes may be difficult to discern in reduced lighting situations, and secretions can interfere with the color change. Regardless of the monitoring device, patients in cardiac arrest should be ventilated for a minimum of 6 breaths prior to taking a reading, because recent ingestion of carbonated beverages can result in spuriously high CO2 levels with esophageal intubation. [27]<br /><br /><span style="font-weight: bold;">Comparison of Detector Devices</span><br />In the setting of spontaneous circulation, both syringe aspiration and ETCO2 detection are highly reliable means of excluding esophageal intubation. A comparison of the techniques with clinical assessment was carried out in the animal laboratory, with measurement of the speed and accuracy of determination of tube placement. [28] Both the syringe esophageal detector device and ETCO2 detection were highly accurate, approaching 100%. The esophageal detector device was more rapid with determination in 13.8 seconds vs 31.5 seconds for ETCO2 detection. The detector device remained accurate when air was insufflated into the esophagus for 1 minute, simulating unrecognized esophageal placement. Clinical assessment alone yielded an alarming 30% rate of misidentifying an esophageal tube as being in the trachea. In the setting of cardiac arrest, the aspiration method is more reliable than CO2 detection, because its accuracy is not dependent on the presence of blood flow.<br /><br /><span style="font-weight: bold;">Complications</span><br />Prolonged efforts to intubate may result not only in hypoxia but also in cardiac decompensation. Pharyngeal stimulation can produce profound bradycardia or asystole; when it is feasible, an assistant should view the cardiac monitor during intubation of a patient who has not suffered cardiac arrest. Atropine should be available to reverse vagal-induced bradycardia that may occur secondary to suctioning or laryngoscopy. Prolonged pharyngeal stimulation also may result in laryngospasm, bronchospasm, and apnea.<br />The maximum interval allowable for routine intubation of the apneic patient is 30 seconds. As a guide, one should limit the time of an intubation attempt to the amount of time a single deep breath can be held. This is especially important in a child, because the functional residual capacity of a child's lungs is less than that of an adult. Failure to achieve control within this time frame demands an interval of bag-valve-mask ventilation before intubation is attempted again. The use of preoxygenation to minimize hypoxia is strongly recommended. An oxygen saturation monitor can also be used to monitor explicitly for hypoxia. Assuming optimal preoxygenation of the patient to >98% O2 saturation, attempts at intubation should be halted until the patient is reoxygenated whenever the O2 saturation drops below 92%, equal to a PO2 of about 60 to 65 mm Hg. When ventilation is not achievable, irreversible brain damage can result within minutes. Therefore, the maximum interval allowable for conservative airway management maneuvers is about 3 minutes; one must then choose alternative methods .<br />One should check for loose or missing teeth before and after orotracheal intubation. Any avulsed teeth not found in the oral cavity warrant a postlaryngoscopy chest film to rule out aspiration of a tooth. Swallowed teeth are of no consequence. In a study of 366 patients, McGovern and coworkers found broken teeth to be the most common complication of laryngoscopy. [29] Laceration of the mucosa of the lips, especially the lower lip, may occur if adequate care is not taken. Tracheal or bronchial injuries are rare but serious, usually occurring in infants and the elderly as a result of decreased tissue elasticity. [30] Vomiting with aspiration of gastric contents is another serious complication that can occur during intubation.<br />The most devastating complication of tracheal intubation is unrecognized esophageal intubation. Assessment of tube position should be the first step in the emergency department evaluation of patients who have undergone out-of-hospital intubation. The best assurance of tracheal placement is for the operator to see the tube pass through the vocal cords. Techniques to assess tube placement are discussed earlier. Another method of reliably determining tracheal tube location uses the fiberoptic scope. Passage of the scope through the tube with visualization of tracheal rings confirms endotracheal placement as well as the position within the trachea. The placement of a lighted stylet down the tracheal tube and successful transtracheal illumination also reliably predicts tracheal positioning. [31]<br />A chest radiograph should be taken shortly after the intubation to confirm tube placement and position. Bissinger and coworkers noted that endobronchial intubation was clinically unrecognized without a chest film in 7% of out-of-hospital intubations. [32] In addition to hypoxia, delayed tube repositioning can lead to unilateral pulmonary edema. [33] Persistent asymmetrical breath sounds after appropriate tube positioning suggests unilateral pulmonary pathology (e.g., main stem bronchus obstruction, pneumothorax, or hemothorax).<br />If an endotracheal tube is removed from the esophagus, vomiting may occur. This should be anticipated and suction readied. Cricoid pressure should be applied during tube removal and maintained until intubation is successful. Alternatively, the first tube can be left in the esophagus to serve as temporary gastric venting until tracheal intubation is achieved.<br />A persistent air leak during ventilation usually means one of three things: (1) the cuff is leaking because of damage to the balloon, (2) the cuff is positioned above or between the vocal cords, or (3) the pilot balloon is leaking. If the cuff is leaking, the tracheal tube must be replaced (see Changing Tracheal Tubes). If the pilot balloon is determined to be leaking, however, this can usually be remedied without changing the tube. [34] An incompetent 1-way balloon valve can be fixed by placing a stopcock into the inflating valve. Reinflation of the cuff followed by shutting off the stopcock should solve the problem. If the leak involves the pilot balloon itself, or if the distal inflation tube has been inadvertently severed, cut off the defective part and slide a 20-ga catheter into the inflation tube. Then connect the stopcock to the catheter, inflate the cuff, and close the stopcock.<br />Tracheal stricture used to be a significant late complication of long-term intubation with low-volume high-pressure cuffs. The standard use of high-volume low-pressure cuffs has markedly decreased the incidence of this complication. [35] Tubes with high-pressure cuffs are obsolete and should be avoided.<br /><br /><span style="font-weight: bold;">Summary</span><br />Orotracheal intubation is the mainstay of definitive airway management. In the comatose patient, it is usually accomplished rapidly and without difficulty. The easy intubation is frequently successful in the hands of the novice; the difficult intubation often proves challenging even for the experienced operator. Rapid-sequence intubation has increased the use of orotracheal intubation as the first-line approach in a variety of clinical situations and settings (see Chapter 3) . Once the patient's breathing and protective reflexes are removed, however, the operator has the supreme responsibility of safely reestablishing them. A mastery of the technique of orotracheal intubation is essential.<br /><br /></div>Emergency Medicinehttp://www.blogger.com/profile/06606398346130594987noreply@blogger.com1tag:blogger.com,1999:blog-3749884089415516879.post-59591341797468671892009-03-13T02:47:00.000-07:002009-03-13T02:49:21.331-07:00Tracheal Intubation<div style="text-align: justify;">Tracheal intubation is generally considered the most definitive means of airway control. The decision to tracheally intubate must consider the patient's physiologic status, anticipated patient care needs, operator experience, and features related to preparation for the procedure. This chapter discusses the indications for tracheal intubation in greater detail as well as the preparation for intubation and the key steps and modifications of the actual procedure.<br /><br /><span style="font-weight: bold;">GENERAL PREPARATION</span><br />Preparation is the key to successful airway management. Two general areas of preparation should be addressed before undertaking the first attempt at definitive airway management in a clinical setting. The first is mental and physical preparedness. The second is the assembly of essential intubation equipment.<br />Mental and physical preparation comes from reading about the procedures, discussing the principles and details with instructors, practicing the techniques on intubation mannequins or in the animal laboratory, and finally performing the technique under supervision in a controlled clinical setting. Studies addressing various approaches to tracheal intubation are generally performed under optimal conditions (i.e., with equipment available and appropriate preparatory training). Also, often hidden within the study findings are individual learning curves. Therefore, it is overly optimistic to expect to match the success reported in the literature when first attempting a new intubation technique. However, the goal of preparation is to be as high on the learning curve as possible prior to the first clinical application of a new intubation technique. Further, continued rehearsal and application of the techniques that have been learned are important for skill maintenance.<br />Each approach to tracheal intubation has a preferred training format. Orotracheal intubation, for example, may be simulated with a mannequin, whereas retrograde intubation is best learned using an animal or cadaver model. Orotracheal intubation is likely to be successful on the first attempt, whereas considerable practice is required for facile use of the scope for fiberoptic intubation. In preparation for managing critical airway problems, maximal hands-on training is desirable.<br />The second general area of preparation is material preparedness (i.e., the immediate availability of all essential equipment required to optimally perform the airway maneuvers that are within the capabilities of the care provider). This may be accomplished by the wall-mounting of essential resuscitation equipment. [1] Alternatively, dedicated adult and pediatric airway carts may be used for placement of the equipment in an open, organized, and labeled manner that can be regularly checked. [2] The worst moment to realize that a vital piece of equipment is missing is when a patient's life depends on it. The importance of this concept cannot be overstated. Technical expertise cannot substitute for the lack of essential equipment.<br />In airway management, failure has ominous consequences. Mental, physical, and material preparation maximizes the chances of success.<br /><br /><span style="font-weight: bold;">AIRWAY ANATOMY</span><br />Requisite for a discussion of procedures in airway management is a common understanding of airway anatomy and its terminology . The following terms are used frequently :<br /><br /><span style="font-style: italic;">Arytenoid cartilages</span><br />the paired cartilages forming the posterior aspect of the laryngeal inlet nasal cavity, from the external nares to the choana.<br /><br /><span style="font-style: italic;">Nasopharynx</span><br />from the end of the nasal cavity (choana) to the level of the soft palate.<br /><br /><span style="font-style: italic;">Oropharynx</span><br />soft palate to the upper border of the epiglottis.<br /><br /><span style="font-style: italic;">Hypopharynx (laryngopharynx)</span><br />epiglottis to the lower border of the cricoid cartilage.<br /><br /><span style="font-style: italic;">Vallecula</span><br />the space at the base of the tongue formed posteriorly by the epiglottis and anteriorly by the anterior pharyngeal wall.<br /><br /><span style="font-style: italic;">Laryngeal inlet</span><br />the opening to the larynx bounded anterosuperiorly by the epiglottis, laterally by the aryepiglottic folds, and posteriorly by the arytenoid cartilages.<br /><br /><span style="font-style: italic;">Piriform fossae (recesses)</span><br />the pockets on both sides of the laryngeal inlet separated from the larynx by the aryepiglottic folds.<br /><br /><span style="font-style: italic;">Corniculate cartilage</span><br />the posteromedial portion of the arytenoid cartilage.<br /><br /><span style="font-style: italic;">Cuneiform cartilage</span><br />the anterolateral prominence of the arytenoid cartilage.<br /><br /><span style="font-style: italic;">Glottis</span><br />the vocal apparatus, including the true and false cords and the glottic opening.<br /><br /><span style="font-style: italic;">Glottic opening (rima glottidis)</span><br />the opening into the trachea as seen from above through the vocal cords.</div>Emergency Medicinehttp://www.blogger.com/profile/06606398346130594987noreply@blogger.com0tag:blogger.com,1999:blog-3749884089415516879.post-37330060360191759322009-03-05T05:32:00.000-08:002009-03-05T05:35:59.619-08:00SPECIAL CONSIDERATIONS<div style="text-align: justify;"><span style="font-weight: bold;">Cardiac Arrest</span><br />Mouth-to-mouth and BVM ventilation may suffice for out-of-hospital care with short transport times or for the initial few minutes of ventilation in cardiac arrest. However, optimal BVM ventilation during CPR is impossible. Mouth-to-mouth and BVM ventilation are adequate and effective in the anesthetized or paralyzed patient with an empty stomach in the absence of chest compression, but they are inadequate for prolonged ventilation in the patient in cardiac arrest.<br />Proper BVM ventilation is probably harder to master than tracheal intubation, and prolonged attempts during CPR usually only distend the stomach and give the uninitiated a false sense of security. Patients in cardiac arrest should be orotracheally intubated. Most cardiopulmonary arrests are not associated with cervical spine injury. When there is suspicion of cervical injury, the following precautions should be followed.<br /><br /><span style="font-weight: bold;">Potential Cervical Spine Injury</span><br />Any patient who has sustained a significant injury has the potential for cervical spine injury. Approximately 1.5 to 3.0% of initial survivors of all types of major trauma seen in emergency departments have significant cervical spine injury. It is interesting to note that this prevalence is not increased in the setting of significant head injury. Falls from heights and motor vehicle crashes are also common causes of spinal instability.<br />In patients with multiple injuries, the possibility of cervical spine injury warrants caution when considering tracheal intubation involving the use of the laryngoscope. It is prudent to provide adequate oxygenation while limiting neck extension until cervical spine injury is disproved. If the patient is severely hypoxic or apneic, immediate tracheal intubation may be necessary with in-line manual stabilization of the neck (without axial traction) by an assistant. When done cautiously, oral intubation of the unconscious spinal cord injured patient may be as safe as other techniques, including intubation with fiberoptic guidance.<br />Note that mouth-to-mouth and BVM ventilation frequently require some degree of neck extension to open the airway. A cadaver study demonstrated increased neck motion with BVM ventilation when compared to various intubation techniques, including oral intubation, lighted stylet guided oral intubation, and nasotracheal intubation. BVM techniques may, therefore, be less desirable than the other methods of securing the airway and ventilating the patient.<br />Many institutions and some out-of-hospital systems use pharmacologic adjuncts, in-line cervical stabilization, and orotracheal intubation before cervical spine films are initiated. In the patient who is comatose, combative, or in severe respiratory distress without definite evidence of spinal cord injury, this approach is advocated, because it may be life saving. Precautions during intubation of the patient with known cervical spine fracture or its potential should include in-line stabilization of the cervical spine with attempts to minimize traction or lateral neck motion during the intubation procedure. Clinical experience is accumulating that supports the safety of this approach.<br /><br /><span style="font-weight: bold;">Potential Epiglottitis/Supraglottitis</span><br />Epiglottitis is often considered a disease of children between the ages of 2 and 8 years, but it is being recognized in adults with increasing frequency. The typical presenting picture is that of an adult or child sitting upright, drooling, or spitting up oral secretions rather than swallowing. The voice may sound muffled. There is a history of a relatively abrupt onset of a sore throat that rapidly becomes more painful. Children commonly present with a high temperature, but adults usually are only mildly febrile. The disease is especially treacherous in children because of their small airways and their tendency to panic when an oral examination or insertion of an IV line is attempted.<br />Small children are most calm when allowed to sit on a parent's lap. An oxygen mask with oxygen flowing at 10 L/min can be held by the parent several centimeters from the child's face. If the child is using accessory muscles to breathe, every attempt should be made to keep the child calm. If a lateral radiograph of the neck taken on inspiration can be obtained without disturbing the child, it will often establish the diagnosis. On radiography, the inflamed epiglottis often appears thickened and rounded. The hypopharynx is dilated above the obstruction.<br />In cases of respiratory compromise, an epiglottitis protocol should be implemented rapidly. A preestablished protocol can save many minutes of time otherwise spent trying to reach all of the personnel needed to manage this critical emergency. When a child is suspected of having epiglottitis based on history and clinical presentation, the safest course of action to establish the airway should be pursued. The emergency physician should accompany the child at all times until the airway is secure and be prepared to intervene. Otolaryngologist notification should be included in the protocol because a tracheostomy may be necessary. When operating room space or personnel are not available immediately, emergency department personnel must be prepared to manage the airway.<br />If the child lapses into a coma or stops making ventilatory efforts, the first step is to attempt to force oxygen past the obstruction by using mouth-to-mouth respiration or a BVM apparatus. Because the obstruction is edematous supraglottic tissue and epiglottis, positive-pressure ventilation often can displace the edema enough to allow adequate ventilation. If this effort is unsuccessful, the emergency physician should attempt oral intubation. However, a normal larynx will not be visible because of the edema. The operator should attempt to pass an endotracheal tube through the slit-like opening that remains for the supraglottic airway. An assistant can compress the chest to force bubbles through the airway, as a means of locating the airway. The assistant can also palpate the larynx and the trachea to detect the tube's entry into the trachea. If orotracheal intubation fails, the intubator should go directly to transtracheal needle ventilation (TTNV) . The obstruction of epiglottitis is mainly inspiratory, so there should be no difficulty with chest hyperinflation with intermittent TTNV. This method should ease subsequent orotracheal intubation, because the path of the airway should be readily apparent as exhaled gases pass through it.<br />It is recommended that all children with acute epiglottitis receive tracheal intubation. If the child is not in distress, an IV line can be established before intubation for appropriate drug administration, although some operators prefer to delay IV placement until after inhalation anesthesia.<br />Adults and cooperative older children with suspected epiglottitis can be examined directly. It is good practice to visualize the epiglottis and the vocal cords of the stable older patient with laryngeal tenderness who is complaining of a severe sore throat or difficulty swallowing. A mirror, fiberoptic scope, or a right-angle scope can be used to do this. In epiglottitis, the pharynx and tonsils usually do not appear inflamed, a finding that might otherwise explain the symptoms. Adults with epiglottitis do not always<br />need to be intubated if rigorous monitoring can be accomplished, a skilled intubator is immediately available, and the patient is not in distress. Orotracheal intubation for epiglottitis is not as difficult in adults as it is in small children. Transtracheal needle ventilation can also be used in adults who are difficult to intubate.<br /><br /><span style="font-weight: bold;">Jaw Clenching</span><br />Hypertonus induced by neurologic dysfunction is a common complicating factor of airway management, especially in the patient with multiple injuries, drug overdose, or seizures. Jaw clenching may be a lethal complication when it prevents clearing of blood, vomitus, or foreign bodies in the airway. No more difficult airway problem exists than occlusion of the nasal and oral passages by vomitus while the patient's teeth are tightly clenched. Respiratory efforts may lead to severe aspiration, and although the hypertonus gradually gives way as the brainstem becomes progressively hypoxic, the cerebrocortical hypoxic insult sustained in the process may be irreversible. Various disease states can lead to a similar scenario in which the jaws are clenched in the presence of upper airway hemorrhage or the accumulation of secretions.<br />Jaw clenching and cervical spine injury can, of course, occur together. At times, the blind nasotracheal route of intubation may be adequate for airway management while minimizing the risk of further spine injury. However, at least a small degree of spontaneous air movement should be present for the blind nasotracheal approach to be successful. Although a serendipitous success may occur in the apneic patient, it is recommended that time not be wasted on this approach in the completely apneic patient.<br />Neuromuscular blocking agents are generally an effective means to overcome jaw clenching in the breathing patient. Both neuromuscular depolarizing and nondepolarizing agents may be administered IV to induce paralysis and allow orotracheal intubation.<br /><br /><span style="font-weight: bold;">Apnea with Airway Obstruction</span><br />Despite the many nonsurgical approaches to tracheal intubation discussed in this chapter, the patient who is apneic secondary to deep airway obstruction may be served best by a surgical airway. When maneuvers to relieve airway obstruction are unsuccessful and direct laryngoscopy is not possible or cannot rapidly alleviate the obstruction and permit ventilation, the operator should rapidly move to a surgical airway approach.<br /><br /><span style="font-weight: bold;">CONCLUSION</span><br />Airway management is the most fundamental aspect of emergency care. Every rescuer must know basic airway maneuvers and be able to use them instinctively. When basic maneuvers fail, airway management rapidly becomes more complex. Familiarity with the ingenious intermediate airway devices can often reverse a deteriorating situation and provide the rescuer with a temporary solution to an airway dilemma. When basic and intermediate maneuvers fail, complexity, risk, and exigency mount. Choices become more critical and complications more likely. Advance consideration of situations represented in the airway management algorithms is a wise practice for the emergency physician. It may hasten accurate decision-making when time becomes critical. In this chapter we have described basic and intermediate airway techniques and offered a logical schema for their use in the patient with an acutely compromised airway. Subsequent chapters deal with the more advanced airway techniques of tracheal intubation and cricothyrotomy.<br /><br /></div>Emergency Medicinehttp://www.blogger.com/profile/06606398346130594987noreply@blogger.com0tag:blogger.com,1999:blog-3749884089415516879.post-4917850772977016292009-03-05T05:25:00.000-08:002009-03-05T05:32:22.570-08:00INTERMEDIATE AIRWAYS<div style="text-align: justify;">Intermediate airways are those interventions that go beyond the maintenance of a patent airway. They represent a midpoint between airway establishment and true airway control. Airway control is secured by maneuvers such as tracheal intubation and tracheotomy, in which an endotracheal cuff isolates the trachea. The devices described in this section occlude the esophagus and allow ventilation across the larynx. The devices discussed are the esophageal obturator airway (EOA), the esophageal gastric tube airway (EGTA), the laryngeal mask airway (LMA) and the esophageal-tracheal Combitube (ETC) airway (Sheridan Catheter Corp., Argyle, NY). Two are designed to occlude only the esophagus (EOA and EGTA), one (LMA) seals the larynx at the hypopharynx level, and one ETC offers the versatility of use whether placed into the esophagus or the trachea. Each is designed for use in the unconscious patient who requires positive-pressure ventilation. The esophageal cuff or seal built into these devices reduces gastric content aspiration. The EOA and EGTA have fallen into general disfavor in recent years due to the gravity of errors in placement. Complications including esophageal rupture and tracheal intubation have led many to prefer the ETC or LMA as an intermediate airway.<br />Esophageal Obturator Airway and Esophageal Gastric Tube Airway<br />The EOA and the EGTA maintain airway patency in ways similar to the oral and nasal airways, but they also protect<br />the airway by occluding the esophagus to reduce gastric distention and regurgitation. The face mask permits use of these airways as positive-pressure ventilating devices. Air insufflated through the airway traverses the upper airway before crossing the larynx and entering the trachea. Ventilation from the EOA exits the airway through numerous ports in its hypopharyngeal portion . Ventilation from the EGTA is identical to mask ventilation, with the addition of esophageal occlusion. A port is available on the EGTA to vent the stomach. The attractiveness of the EOA and the EGTA for use in the apneic patient stems from their retention of much of the simplicity of the artificial airway with the addition of an important feature of more complicated airways--some protection against regurgitation and reduction of gastric distention.<br /><br /><span style="font-weight: bold;">Indications and Contraindications</span><br />Speed and simplicity are advantages of the esophageal airway over tracheal intubation. Trained individuals can successfully place an esophageal airway in an average of 5 seconds, whereas the same individuals may need 20 seconds to perform a tracheal intubation. In one out-of-hospital study, failure to intubate was much higher with the endotracheal tube (19.4%) than with the EOA (1.7%). [19] Neck motion is not as necessary with the esophageal airway as it is with tracheal intubation. For these reasons, the EOA may be an effective adjunct in the management of the unconscious injured patient who requires respiratory assistance. Hypercarbia may occur more commonly with EOA ventilation as compared with endotracheal ventilation. The most difficult aspect of this form of ventilation is securing a tight fit with the mask. Dentures should be left in place to give support to the lips. Adequate tidal volume must be delivered to ventilate the lungs.<br />There are various contraindications to the use of the EOA and the EGTA. Because the airway is not protected from pharyngeal secretions, the presence of active oropharyngeal bleeding and excessive secretions represent a relative contraindication to EOA and EGTA use. Because of attendant discomfort, the devices cannot be used in the awake patient. Size specifications preclude their use in the pediatric patient; 16 years is the age usually cited as the lower limit for EOA and EGTA use. The actual limiting factors are the size of the esophagus and the face; an adult-sized 14-year-old would certainly tolerate an EOA or EGTA if necessary. However, a small adult may not receive an appropriate fit. Other contraindications include esophageal injury or conditions predisposing to perforation. A patient who has ingested a caustic agent or one with a known esophageal stricture should not undergo esophageal intubation. As a precaution against pressure-related complications, it is recommended that the device not be left in place for longer than 2 hours. It must be recognized that the EOA and the EGTA are temporary forms of airway control. This form of airway control is most often used in out-of-hospital care.<br /><br /><span style="font-weight: bold;">Placement of EOA/EGTA</span><br />The head is in the neutral position during placement of the EOA and the EGTA. Neck motion is unnecessary. The rescuer grasps and pulls the jaw forward. At this point, the rescuer inserts the assembled airway with the mask attached. The obturator tip is directed into the patient's posterior pharynx with gentle, steady pressure. The obturator is advanced down the esophagus until the mask rests flush against the face of the patient. Figure 1-9 (Figure Not Available) A illustrates the correct position at placement. The cuff should lie in the esophagus just distal to the carina of the trachea. The rescuer postpones inflation of the balloon until proper position is confirmed. The patient is ventilated with a tight mask seal on the face, and the lungs are auscultated. For effective ventilation, the mask seal must be tight. Breath sounds should be audible bilaterally. Unilateral breath sounds or failure of auscultation should lead the rescuer to reassess the airway placement. Pneumothorax or hemothorax may explain unilateral sounds, as may inadvertent main stem bronchus intubation. Tracheal intubation will result in the absence of breath sounds. The possibility of bronchial or tracheal intubation requires removal and replacement of the airway. Once satisfactorily placed, the esophageal balloon is inflated to 20 to 25 mL.<br /><br /><span style="font-weight: bold;">Complications</span><br />A 5% incidence of inadvertent tracheal intubation has been reported by Don Michael in experience with 29,000 placements. In a subsequent smaller sample, a 2.9% (5 of 170) incidence was reported with a 100% mortality among the 5 patients. One study comparing out-of-hospital EOA placement with endotracheal tube placement found that the occurrence rate for complications of the EOA that prevented resuscitation (tracheal placement, tube kinking) was nearly three times higher for the EOA (8.7% vs 2.6%). If not quickly rectified, tracheal intubation with the EOA or tube kinking are disastrous complications that produce occlusion of the patient's airway. Disciplined examination for bilateral breath sounds is critical.<br />Esophageal lacerations of undetermined depth were found in 8.5% of autopsies of patients in whom the EOA was used.Esophageal rupture has been found and reported in case histories. Since Scholl and Tsai first reported esophageal ruptures in 1977, the recommended balloon inflation volume was reduced from 35 to 20 mL. No further ruptures or leakage around the cuff have been reported. However, factors other than balloon inflation volume that theoretically can contribute to rupture include careless balloon removal without deflation and forceful attempts at placement when obstruction is met.<br />Tracheal intubation should be performed BEFORE removal of the EOA, because vomiting often occurs following deflation of the balloon and EOA removal. If the EOA cuff has been overinflated, it may partially occlude the trachea and make intubation difficult. In such cases, the balloon is partially deflated to facilitate tracheal intubation.<br /><br /><span style="font-weight: bold;">The Laryngeal-Mask Airway</span><br />The laryngeal-mask airway (LMA) (Intavent International SA, Henley-on-Thames, England) functions intermediately between an oropharyngeal airway and an endotracheal tube. It was developed for use in the operating room as an alternative for endotracheal intubation, but it has also been recommended for use in difficult intubations. It consists of a tube fitted with an oval mask, rimmed with an inflatable cuff. Contrary to usual mask design, the mask is intended to reside in the hypopharynx rather than on the face. It is inserted digitally until its tip meets resistance in the upper esophageal sphincter. The cuff is then inflated, forming a seal around the glottic opening. The result is a relatively secure airway. However, it cannot be considered to protect against gastric regurgitation. Leakage of the hypopharyngeal mask allows aspiration of emesis and gastric distention may occur with misplacement. Although the device may be used for prolonged periods under appropriate conditions, it is usually considered a temporary adjunct until tracheal intubation is established.<br /><br /><span style="font-weight: bold;">Indications and Contraindications</span><br />The LMA is indicated for patients requiring an airway who cannot be endotracheally intubated. The most frequently cited example is a patient whose anatomy prevents visualization of the larynx. Contraindications include the inability to open the patient's mouth and vomiting.<br /><br /><span style="font-weight: bold;">Placement of LMA</span><br />The LMA is first checked for possible air leaks by inflating and deflating the cuff. If the patient has a gag reflex, deep oropharyngeal topical anesthesia or conscious sedation must be administered. With the patient's head in the sniffing position, the mask is lubricated and oriented so the mask opening is facing the tongue. With the index finger of the dominant hand placed on the proximal aspect of the mask, the mask is inserted into the mouth, firmly against the hard palate. The index finger (or thumb) may also be used as a guide during advancement. With one smooth motion, the mask is advanced until resistance is encountered. With the tip of the mask thus seated in the upper esophageal sphincter, the cuff is inflated. The lungs are auscultated to confirm correct placement.<br />While the sniffing position is desirable, it has been shown that LMA placement was 95% successful when the patient was placed in the neutral position with in-line immobilization, simulating a trauma setting.<br />After successful placement of the LMA, several methods are available to achieve subsequent endotracheal intubation. The first method is simply to pass an appropriately sized endotracheal tube down through the lumen of the LMA, rotate the tube 90° so that the tip easily passes through the fenestrations, and advance it through the larynx to the trachea . This has been found to be successful in 90% of attempted cases. The second method involves the use of a tracheal tube exchanger. The exchanger is passed blindly down the lumen of the LMA and into the trachea. The LMA is then removed and an endotracheal tube is passed over the tracheal tube exchanger. This method of tube placement must be combined with confirmation of exchanger location, because it has been shown to pass into the esophagus in up to 70% of attempts. Confirmation of endotracheal tube location should be made . The third and most dependable method of intubation with an LMA in place is via a fiberoptic scope. A lubricated, appropriately sized endotracheal tube is mounted over a fiberoptic scope, and this combination is advanced through the lumen of the LMA out through the mask and through the larynx. The scope is then removed, but the LMA may be left in place with the cuff deflated. If the LMA must be removed after a tracheal tube has been successfully placed through it, pass a tracheal tube exchanger down the tube, remove the tracheal tube/LMA combination, and replace it with a tracheal tube.<br /><br /><span style="font-weight: bold;">Complications</span><br />Although the LMA works well in most cases, this airway has several significant drawbacks. Aspiration is always a possibility, because the cuff does not provide a watertight seal. Laryngospasm can occur if adequate anesthesia is not achieved. A significant air leak around the cuff may occur when high airway pressures exist, leading to poor ventilation. Finally, success rates in the operating room range from 94 to 98%; success rates in difficult emergency airway management are unknown, but they are undoubtedly lower.<br /><br /><span style="font-weight: bold;">Conclusion</span><br />The LMA is a blindly placed intermediate airway that should be considered in patients who require establishment of an emergency airway but cannot receive endotracheal intubation. The technique is quick and simple, requires a minimum amount of training, and appears effective in the hands of paramedics, nurses, and respiratory therapists.<br /><br /><span style="font-weight: bold;">The Esophageal-Tracheal Combitube</span><br />The ETC is a noninvasive airway device that is placed blindly. It allows for effective ventilation and oxygenation when placed in either the esophagus or the trachea. The device has two lumina running parallel to each other. One is perforated at the level of the pharynx and occluded at the distal end, similar to the EOA. The second lumen is open at the distal end, resembling an endotracheal tube. The device has two balloons: a proximal pharyngeal balloon that occludes the oropharynx by filling the space between the base of the tongue and the soft palate and a smaller, distal cuff that serves as a seal in either the esophagus or trachea . The Combitube has compared favorably with the endotracheal tube with respect to ventilation and oxygenation in cardiac arrest situations. It is also placed more rapidly.<br /><br /><span style="font-weight: bold;">Indications and Contraindications</span><br />The ETC is superior to other intermediate airways, because no face mask seal is necessary. It may be preferable to tracheal intubation in certain situations, because it can be placed blindly and is also effective in the esophageal or tracheal position. It is, therefore, more easily placed than an endotracheal tube and is indicated in situations in which tracheal intubation is difficult, neck motion is impossible, or the rescuers are not skilled in tracheal intubation.<br />The ETC should not be used in patients with an intact gag reflex and is not recommended in patients younger than 16 years or less than 5 feet in height. It is contraindicated in suspected caustic poisonings or proximal esophageal disorders.<br /><br /><span style="font-weight: bold;">Placement of ETC</span><br />The device is held in the dominant hand and gently placed caudally into the pharynx while the nondominant hand grasps the tongue and jaw between the thumb and index finger. The tube is passed blindly to a depth where the printed rings on the proximal end of the tube lie between the patient's teeth or alveolar ridge. The pharyngeal balloon is then filled with 100 mL of air, and the distal cuff is subsequently filled with 10 to 15 mL of air. The large pharyngeal balloon serves to both securely seat the ETC in the oropharynx and to create a closed system in the case of esophageal placement. Because approximately three-quarters of placements are esophageal, ventilation is begun through the longer (blue plastic) connector associated with the esophageal lumen. Chest rise and good breath sounds without gastric insufflation confirms effective placement in the esophagus. However, gastric insufflation without breath sounds and chest rise indicate a tracheal positioning of the tube and require changing the ventilation to the shorter (clear plastic) tracheal lumen. Auscultation of breath sounds over the lateral lung fields confirms endotracheal placement of the Combitube. If the tube is in the esophageal position, gastric suctioning can be accomplished by passing a catheter through the open lumen into the stomach while the patient is being ventilated via the other port.<br />An alternative method to identify position is to attach an aspirating device to the tracheal or clear plastic shorter tube. The inability to easily aspirate air confirms esophageal placement necessitating ventilation via the longer blue esophageal tube. In the patient with ventilatory effort, CO2 detector devices also may be useful.<br />A patient who has been successfully resuscitated with an ETC positioned in the esophagus should ultimately receive a definitive airway. The steps required to place a tracheal tube in this setting are detailed in Chapter 2 but consist generally of deflating the large pharyngeal balloon and, with the distal balloon still inflated, intubating around the ETC.<br /><br /><span style="font-weight: bold;">Complications</span><br />Inappropriate balloon inflation and incorrect ETC placement can lead to air leaks during ventilation. The most common placement error is an improper insertion angle. A more caudal, longitudinal direction is recommended, as opposed to an anteroposterior direction of insertion. Another caveat is that the ETC must be maintained in the true midline position during insertion to avoid blind pockets in the supraglottic area, which prevent passage of the tube. Attention to the ring markings on the tube at the level of the incisors ensures proper positioning of the tube. One must remember to first inflate the oropharyngeal balloon before inflating the distal balloon. Although unlikely, esophageal injury is theoretically possible with the overinflation of the distal balloon.<br /><br /></div>Emergency Medicinehttp://www.blogger.com/profile/06606398346130594987noreply@blogger.com2tag:blogger.com,1999:blog-3749884089415516879.post-47877386714597153452009-03-05T05:22:00.000-08:002009-03-05T05:25:20.433-08:00BAG-VALVE-MASK VENTILATION<span style="font-weight: bold;">Indications and Contraindications</span><br />Correctly performed, the BVM method of ventilation appears to be simple and effective. Still, it is fraught with difficulty and therefore deserves special mention. Bag-valve-mask ventilation should be used by experienced individuals who are able to ensure a tight mask seal in situations requiring positive-pressure ventilation. The BVM is often used with an oropharyngeal or nasopharyngeal airway in place.<br />Inexperience is a relative contraindication to the use of a BVM. A rescuer who is not skilled with the BVM will achieve much better ventilation with mouth-to-mouth or mouth-to-mask breathing than with a BVM. However, concern regarding transmission of infectious diseases has reduced the willingness of the lay public and health professionals to perform mouth-to-mouth ventilations. Although BVM ventilation may provide excellent respiratory support in the anesthetized, paralyzed patient in the operating room, the device frequently is of marginal value during cardiopulmonary resuscitation (CPR), during an ambulance run, or in the combative patient. A tight mask seal is mandatory to prevent loss of air volume during ventilation. Another hazard of BVM ventilation occurs when vomitus, blood, or other debris is present in the mouth or pharynx. The foreign material may be insufflated down the trachea if it is not cleared before ventilation. The three major problems encountered with BVM ventilation are inadequate tidal volumes, inadequate oxygen delivery, and gastric distention.<br /><br /><span style="font-weight: bold;">Ventilation Technique</span><br />Achieving adequate tidal volume with BVM ventilation requires a tight mask seal and adequate compression of the bag. Even trained paramedics practicing on manikins have difficulty delivering tidal volumes above 650 mL, which is well below the 10-15 mL/kg recommended by the American Heart Association. A variety of mask configurations are available to facilitate a tight seal, but none substitutes for the practiced skill of the rescuer. For the single rescuer, only one hand can be used to achieve the seal because the other must squeeze the bag. The rescuer's hand must be large enough<br />to apply pressure anteriorly while simultaneously lifting the jaw forward. The thumb and index finger provide anterior pressure while the fifth and fourth fingers lift the jaw. Care must be exercised to deliver an adequate tidal volume by full compression of the bag. Dentures generally should be left in place to help ensure a better seal with the mask.<br />It has been suggested that effective BVM ventilation during CPR requires two hands and, therefore, two rescuers. We suggest using the two-rescuer technique whenever it is practical. The presence on the BVM device of a pop-off valve may further frustrate ventilation efforts in the patient with reduced compliance.<br />All BVM devices should be attached to a supplemental oxygen source (with a flow rate of 15 L/min) to avoid hypoxia. A significant problem with the BVM method is the low oxygen saturation achieved with various reservoirs. The amount of delivered oxygen is dependent on the ventilatory rate, the volumes delivered during each breath, the oxygen flow rate into the ventilating bag, the filling time for reservoir bags, and the type of reservoir used. The commonly used corrugated tube reservoir is the least effective of those examined by Campbell and colleagues. [14] It is too sensitive to ventilatory technique and does not alert the clinician to changes in oxygen flow. A 2.5-L bag reservoir and a demand valve are the preferred supplementation technique during BVM ventilation.<br />Pediatric BVM devices should have a minimum volume of 450 mL. Pediatric and larger bags may be used for ventilation of infants with the proper mask size, but care should be taken to administer only the volume necessary to effectively ventilate the infant. Pop-off valves should be avoided because airway pressure under emergency conditions may often exceed the pressure of the valve.<br /><br /><span style="font-weight: bold;">Complications</span><br />Hypoventilation often occurs because of the difficulty of carrying out the technique properly. Three mechanisms can result in complications: poor mask seal, failure to achieve airway patency, and low tidal volume. Practiced skill development is necessary to avoid these errors. Gastric distention can also result from poor airway patency. Air is insufflated down the esophagus, which inflates the stomach. Consequently, the risk of regurgitation and aspiration increases. When assistance is available, the application of firm posterior pressure on the cricoid ring helps reduce gastric inflation during BVM ventilation. [15] [16] The technique must be used carefully in infants, whose airway is more pliable and subject to obstruction with excessive cricoid pressure. Even with proper BVM technique, aspiration can occur. The rescuer must be vigilant to recognize complications early and take corrective action.Emergency Medicinehttp://www.blogger.com/profile/06606398346130594987noreply@blogger.com0tag:blogger.com,1999:blog-3749884089415516879.post-89902965045734180212009-03-05T05:15:00.000-08:002009-03-05T05:21:46.684-08:00ESTABLISHMENT OF AIRWAY PATENCY<div style="text-align: justify;">The first concern in the management of a patient in critical condition is adequacy of the airway. Partial or complete airway obstruction must be overcome quickly. In some cases, such as an airway obstructed by a tongue, simple maneuvers will suffice. In other cases, particularly those in which myriads of obstructing agents are combining to block the airway, the task will be formidable. The tongue, dentures, swollen or distorted tissues, blood, and vomitus are common obstructing agents that make intubation difficult. Clearing obstructing agents may be made more difficult by muscular activity due to reflex stimulation or patient efforts to improve oxygenation. Moreover, the neck motion required for suction and intubation must be carefully managed in the face of potential cervical spine instability.<br />The wide availability of pulse oximetry monitors has greatly improved our ability to monitor oxygenation for patients at risk of airway or ventilatory compromise. Clinically subtle deterioration is much more quickly and easily recognized using the monitors. They have become standard equipment in emergency departments, intensive care units, and operating rooms to allow early recognition of patient deterioration.<br /><br /><span style="font-weight: bold;">Airway Maneuvers</span><br />Partial or complete airway obstruction resulting from lax musculature and tongue occlusion of the posterior pharynx may be overcome by a variety of maneuvers. The relative benefits of various airway-opening maneuvers have been examined. In a study of 120 anesthetized patients whose airways were obstructed by their tongues, Guildner compared the ease of performance of the neck-lift and head-tilt method, the jaw-thrust method, and the chin-lift method. He concluded that the chin lift was the easiest to perform and produced the greatest airway patency of the three methods tested. Besides offering greater patency, the chin-lift method has the additional advantage that neck extension is unnecessary.<br />Partial airway obstruction in the patient with a decreased level of consciousness is commonly due to posterior displacement of the tongue. This may be recognized readily in the presence of snoring or stridor, but an apneic patient or one who is moving minimal air may not exhibit any audible evidence of airway obstruction. Some type of jaw-thrust or chin-lift maneuver should be performed on every unconscious patient to ensure airway patency. When uncertain about cervical spine status, the neck must be maintained in the neutral position. If the patient was found with a flexed or extended neck, the neck should first be restored to neutral position with gentle longitudinal traction. The chin-lift or jaw-thrust method is then performed. A combination of these maneuvers usually clears airways obstructed as a result of the position of the neck itself. The neck-lift and head-tilt maneuver, as described in cardiac life support courses, should not be used when cervical spine injury is suspected, because the extension of the spine produced during the maneuver endangers the spinal cord.<br />Clearing the airway of foreign material requires more than a simple jaw thrust. The occasional patient who presents with complete airway obstruction secondary to food aspiration may be treated with abdominal thrusts as described in basic cardiac life support.<br />Partial or complete airway obstruction can be the result of upper airway hemorrhage, accumulation of the patient's own secretions, vomitus, or fractured dentition. When deciding on airway-clearing maneuvers, one must take these circumstances into account. Neck extension must be avoided or carefully minimized if the probability of a cervical spine injury is high. When stability of the spine is a concern, application of the abdominal thrust should be limited to the supine method described for unconscious victims. The abdominal thrust carries significant risks, compelling the rescuer to weigh the benefits of its application.<br /><br /><span style="font-weight: bold;">The Chin-Lift Maneuver</span><br />The rescuer places the tips of the fingers, volar surface superiorly, beneath the patient's chin. The jaw is lifted gently forward. The patient's mouth is opened by drawing down on the lower lip with the thumb of the same hand. Mouth-to-mouth resuscitation or other means of positive-pressure ventilation is provided if the patient is not ventilating spontaneously.<br /><br /><span style="font-weight: bold;">The Jaw-Thrust Maneuver</span><br />The jaw-thrust maneuver is the second choice, again because neck extension is not necessary. Forward traction on the mandible is achieved by using two hands to grasp the mandibular rami and pull them forward.<br /><br /><span style="font-weight: bold;">The Abdominal Thrust</span><br />The abdominal thrust is a method to relieve a completely obstructed airway. The technique was popularized by Dr. Henry Heimlich and is commonly referred to as the Heimlich maneuver. The technique is most effective when a solid food bolus obstructs the larynx. Although a subject of controversy, a role for the maneuver has not been found for the resuscitation of near-drowning victims.<br />The conscious patient with an obstructed airway exhibits increased respiratory effort, anxiety, aphonia, and, occasionally, cyanosis. In the conscious patient, the maneuver is performed with the rescuer positioned behind the upright patient. The rescuer's arms are circled about the patient's midsection with the radial side of the clenched fist placed in the epigastrium of the patient. Care is exercised to position the fist midway between the umbilicus and the xiphoid of the patient. After proper positioning, the rescuer grasps the fist with the opposite hand and delivers an inward and upward thrust to the abdomen. A successful maneuver will cause the obstructing agent to be expelled from the patient's airway by the force of air exiting the lungs.<br />An unconscious, supine patient must be handled differently: the rescuer kneels next to the patient's pelvis facing cephalad. The palmar bases of the hands are placed in an overlapping fashion on the epigastrium at the same spot as that used in the upright patient. Inward, upward thrusts are delivered in this fashion with the same objective.<br />Abdominal thrusts are relatively contraindicated in pregnant patients and others with protuberant abdomens. A chest thrust similarly to that delivered in closed chest massage may be used instead. The upright patient may be delivered a chest thrust by placing the fist over the sternum. Experimental primate models of infant airway obstruction show higher peak airway pressures with chest thrusts than with abdominal thrusts; a combined (simultaneous) chest and abdominal thrust produce even higher peak airway pressures. [6] Hence, a combined maneuver should be considered in the case of total airway obstruction that is unresponsive to simple abdominal thrusts.<br />Visceral injury can occur with the Heimlich maneuver. Excessive force may be responsible in such cases. In others, incorrect placement of the hands may play a role. Nonetheless, the technique can be life saving and should be used when needed. Attention to proper execution may limit complications.<br /><br /><span style="font-weight: bold;">Positioning</span><br />Positioning the patient who has sustained multiple trauma can be a problem. Spinal injury and airway access priorities dictate that the patient should be kept in the supine position while immobilized on a backboard. Turning the patient on the side allows upper airway hemorrhage, secretions, and vomitus to drain externally rather than to collect in the patient's mouth, which can lead to aspiration and airway obstruction.<br />Guidelines for patient positioning must take into account the status of the patient's spine and the use of gravity to enable secretions to drain rather than accumulate in the airway. The following is a judicious approach to airway management in a patient with spontaneous respiration:<br /><br /><ol><li>Initial airway maintenance accomplished by the chin-lift maneuver and the application of cervical stabilization </li><li>Immobilization of the patient on a spinal backboard.</li><li>With the position of the neck controlled, transportation of the patient on the side to facilitate airway drainage.</li></ol><br /><span style="font-weight: bold;">Suctioning</span><br />Patient positioning and airway opening and clearing maneuvers are often inadequate to achieve the degree of airway patency desired. Ongoing hemorrhage, vomitus, and particulate debris often require suction to clear and maintain the respiratory passage. Three basic types of suctioning tips are available . Each is suited to different types of airway obstruction problems.<br />Dental tip suction is most useful for clearing particulate debris from the upper airway. Vomitus is most readily cleared with this tip because it is least likely to become obstructed itself by particulate matter. The tonsil tip (Yankauer) suction device is used most effectively to clear upper airway hemorrhage and secretions. Its design is intended to prevent the obstruction of its tip by tissue and clot. The rounded tip is also less traumatic to soft tissues.<br />Unfortunately, the catheter tip suction device is the one most readily available in many hospitals. Often it is the only type of suction available. This device is inferior to the other catheter tips for suctioning before the patient has been intubated. After intubation, it works well for suctioning the trachea and bronchi through the tracheal tube. The dental tip device should be used during the resuscitation period and should be ready at the bedside. The dental tip allows rapid clearing of both particulate matter and hemorrhage, thereby expediting airway control.<br />Optimally, stabilization of the patient with multiple injuries will involve use of all three types of suction tips. The tonsil or dental tip should be attached to the suction source during the interval between patient evaluations because it is most likely to be the one needed on short notice. Both the tonsil tip and catheter tip should be stored next to the suction source so they can be attached when needed. It is essential that all physicians and nurses know the location of suction equipment and know how to turn it on during an emergency. In the resuscitation rooms, the equipment should be connected and ready to operate and not kept in cabinets or wrapped in difficult-to-open packaging material . Interposition of a suction trap at the base of the dental tip suction device prevents clogging of the tubing with particulate debris. A trap that fits directly onto a tracheal tube has been described; use of this device allows effective suctioning during intubation.<br />Although no specific contraindications to airway suctioning exist, complications of incorrectly performed suctioning may be significant. Nasal suction is seldom required to improve oxygenation (except in infants), because most adult airway obstruction occurs in the mouth and oropharynx. Vigorous nasal suction can induce epistaxis and further complicate an already difficult situation. Suctioning that is prolonged may not be recognized during an emergency, but it should be avoided because it may lead to significant hypoxia, especially in children. Suctioning should not exceed 15-second intervals, and the provision of supplemental oxygen before and after suctioning should be routine . Basilar skull fractures can allow the inadvertent placement of nasal suction tubes in the brain. Extreme care should be exercised when a basilar skull or facial fracture is suspected, because communication between nasal and intracranial cavities may exist.<br />Generally, it is best to perform suctioning under direct visual inspection or with the aid of the laryngoscope. Forcing a suction tip blindly into the posterior pharynx can injure tissue or convert a partial obstruction to a complete obstruction.<br />Complications may be avoided by anticipating problems and providing appropriate care during suctioning maneuvers. Epistaxis may be avoided by limiting the force applied during suctioning. Vasoconstrictor drops or spray, such as 0.25% phenylephrine, constrict the nasal mucosa and reduce the injury potential in patients who require repeated nasopharyngeal suctioning. The rescuer must be aware that the patient may develop transient pupillary dilation if the vasoconstrictor solution drips into the conjunctival space. Naigow and Powasner found that suctioning induced hypoxia in dogs consistently and that it was best avoided by hyperventilating the animals before and after suctioning.<br /><br /><span style="font-weight: bold;">Artificial Airways</span><br /><span style="font-weight: bold;">Indications and Contraindications</span><br />Once the airway has been established through various maneuvers and suctioning, the patient may require further temporary support to maintain airway patency. The semiconscious patient who is breathing with an adequate rate and tidal volume at the time of the chin-lift maneuver may develop hypoxia because of recurrent obstruction if the maneuver is discontinued. Oxygen supplementation and an artificial airway may be all the support that is necessary. The use of an artificial airway also allows more efficient use of rescuer skills and relief from fatigue that is caused by the continuous application of chin-lift or jaw-thrust maneuvers.<br />Positive-pressure ventilation with a bag-valve-mask (BVM) device may be necessary to bolster the patient's inadequate ventilatory effort or to provide total ventilation in cases of apnea. By maintaining airway patency, artificial airways facilitate spontaneous and bag-mask ventilation.<br /><br /><span style="font-weight: bold;">Airway Placement Technique</span><br />The simplest artificial airways are the oropharyngeal and nasopharyngeal airways . Both are intended to prevent the tongue from obstructing the airway by falling back against the posterior pharyngeal wall. The oral airway may also prevent teeth clenching. The oropharyngeal airway may be inserted by either of two procedures. In the first procedure, the airway is inserted in an inverted position along the patient's hard palate. When it is well into the patient's mouth, the airway is rotated 180° and advanced to its final position along the patient's tongue, with the distal end of the airway lying in the hypopharynx. The second procedure involves the performance of a jaw-thrust maneuver, either manually or with a tongue blade, and the simple advancement of the airway into the mouth to its final position. No rotation is performed when the airway is placed in this manner. Once inserted, the oral airway may have to be taped in place to prevent expulsion by the patient's tongue.<br />The nasopharyngeal airway is placed by gently advancing the airway into a nostril, directing the tip along the floor of the nose toward the nasopharynx. When in final position, the flared external end of the airway should rest at the nasal orifice. Either of these two airways provides airway patency similar to that in a correctly performed chin-lift maneuver, but the nasal airway may be better tolerated by the semiconscious patient.<br /><br /><span style="font-weight: bold;">Complications</span><br />Few complications are encountered in the use of these airways. The oropharyngeal airway may cause obstruction if during its placement the tongue is pushed against the posterior pharyngeal wall. Care in placement will prevent this occurrence. In the patient whose reflexes are intact, the gag reflex may stimulate retching and emesis, and the semiconscious patient may not tolerate the oropharyngeal airway. If gagging is a persistent problem, the airway should be removed and a nasal airway or tracheal intubation should be considered. If the patient with airway compromise is comatose and lacks a gag reflex, the oropharyngeal airway should not be used as a definitive airway; tracheal intubation should be used instead. The oropharyngeal airway will keep the mouth partially open if an orogastric tube is placed for gastric lavage or suction, and it will prevent clenching of the teeth, which can obstruct an orotracheal tube.<br />The nasopharyngeal airway may offer an advantage over the oropharyngeal airway in that the nasopharyngeal airway is less likely to induce gagging. The same considerations that apply to nasal suctioning apply to placement of the nasopharyngeal airway. That is, care must be exercised not to induce epistaxis, and extreme caution is indicated in patients with a suspected basilar skull fracture or facial injury. All patients with oral or nasal pharyngeal airways should be observed constantly, because these devices are temporary measures and cannot substitute for tracheal intubation.<br /><br /></div>Emergency Medicinehttp://www.blogger.com/profile/06606398346130594987noreply@blogger.com0tag:blogger.com,1999:blog-3749884089415516879.post-20890641105387178932009-03-05T05:11:00.000-08:002009-03-05T05:14:35.556-08:00DECISION-MAKING IN AIRWAY MANAGEMENT<div style="text-align: justify;">The resuscitator must have many tools at hand to deal with the acutely compromised airway. Although proficiency may exist for all of the available maneuvers, the specific procedural choice often must be made in challenging circumstances. Rescuers should practice potential scenarios before facing actual airway management scenarios in the clinical situation. Failure to do so may lead to unnecessarily aggressive management in some situations or to irreversible hypoxic injury as a result of unnecessary hesitation in others.<br />Several parameters must be assessed quickly before an airway management choice can be made. The parameters to be considered are as follows:<br /><br />1. Adequacy of current ventilation<br /><br />2. Time of hypoxia<br /><br />3. Patency of airway<br /><br />4. Need for neuromuscular blockade (muscle tone, teeth clenching, severe obstructive pulmonary disease or asthma)<br /><br />5. Cervical spine stability<br /><br />6. Safety of technique and skill of operator<br /><br />Consideration of these factors should guide a choice among those techniques described. This initial choice is often straightforward. Difficulty rises precipitously when the initial choice fails. Time becomes critical and safety of technique less important as the risk of irreversible hypoxic injury rises. Anxiety increases and error potential compounds under these circumstances. Forethought and practice are invaluable when making these decisions.<br />Now that the decision to manage the airway surgically has been made, one need only choose among three available options. Consideration of patient condition, security of the airway approach, and invasive nature of the procedure are factors to be weighed in the final decision.<br /><br /></div>Emergency Medicinehttp://www.blogger.com/profile/06606398346130594987noreply@blogger.com0tag:blogger.com,1999:blog-3749884089415516879.post-25941723463969430862009-03-05T05:09:00.000-08:002009-03-05T05:10:27.021-08:00Basic Airway Management<div style="text-align: justify;">Airway management is widely preached as the first priority in the management of any seriously ill or injured patient. However, despite the lip service given to the importance of airway management, it is often overlooked and, consequently, can be a source of error in the care of the critically ill or injured patient. Although appropriate airway management is evident in all smoothly run resuscitations, inappropriate management often presages a cycle of patient deterioration and misguided therapeutic intervention.<br />Unfortunately, recognition of the need for airway management is only the first part of the problem in emergency resuscitation. Managing the airway may be one of the most difficult aspects of the entire resuscitation. Because of the sheer variety of airway difficulties possible, even the most skilled resuscitator can find the task challenging. Blood, loosened teeth, vomitus, swollen or distorted landmarks--all of these present formidable barriers to successful management. When obstruction occurs in conjunction with reflex clenching of the jaws and possible cervical spine injury, conventional airway management tools may be rendered useless. Time pressures imposed by the need to avoid cerebral anoxia force one to make difficult decisions concerning the use of risky maneuvers such as moving the neck, administering paralyzing agents, or using invasive procedures. Tools must be at hand, skills must be well practiced, and decision-making must be sharp if optimal emergency airway management is to occur.<br />Some solutions to the dilemmas faced in emergency airway management are presented in this and the following chapters. Decision algorithms are presented to help assemble the pieces of the airway management puzzle into a logical framework. Readers are encouraged to study the algorithms at their leisure to facilitate later decision-making when time is limited.<br /><br /></div>Emergency Medicinehttp://www.blogger.com/profile/06606398346130594987noreply@blogger.com4tag:blogger.com,1999:blog-3749884089415516879.post-31340944590336120262008-08-16T09:02:00.002-07:002008-08-16T09:35:53.660-07:00Nuclear, Biologic, & Chemical Agents; Weapons of Mass Destruction<div style="text-align: justify;"><span style="font-weight: bold;">INTRODUCTION</span><span style="display: block;" id="formatbar_Buttons"><span class="" style="display: block;" id="formatbar_JustifyFull" title="Justify Full" onmouseover="ButtonHoverOn(this);" onmouseout="ButtonHoverOff(this);" onmouseup="" onmousedown="CheckFormatting(event);FormatbarButton('richeditorframe', this, 13);ButtonMouseDown(this);"></span></span><br /><br />In the past, injuries resulting from nuclear, biologic, and chemical attack were largely dealt with only in the military sector. Society as a whole, and specifically the civilian medical community, felt it unlikely that such weapons would be used against civilian populations. Recent changes in the global political environment have forced changes in this thinking. Many smaller nations, some of which are judged unstable, are attempting to develop weapons of mass destruction. Likewise, many terrorist organizations are now actively attempting to purchase or develop such weapons. In addition to the risk of an overt attack, other sources of exposure could come from accidents involving many nuclear, biologic, and chemical agents stored in facilities throughout the United States. An accident at any of these facilities could result in a large number of civilian casualties. As with most mass casualty situations, emergency physicians will be at the forefront of patient care. This chapter attempts to provide specific information regarding the management of nuclear, biologic, and chemical weapons injuries.<br /><br /><br /><span style="font-weight: bold;"> NUCLEAR WEAPONS </span><br /><br />Several incidents in recent history, both military and civilian, have resulted in radiation injuries. The most notable, and in fact the only war-time use, involved the detonation of nuclear weapons over Hiroshima and Nagasaki, Japan. Unfortunately, many terrorist organizations have attempted to obtain nuclear weapons. A terrorist attack would most likely involve the detonation of a nuclear bomb or the detonation of a conventional explosive that also dispersed radioactive material (so-called dirty bomb).<br /><br /><span style="font-weight: bold;">General Considerations </span><br /><br />Radiation-induced injury occurs when various types of ionizing radiation interact with body tissues. Radiation exposure may be external or internal. Internal contamination can occur via wound contamination or via inhalation or ingestion of contaminated particles. Four types of radioactive particles may cause damage:<br /><br /><span style="font-weight: bold;">1. Alpha particles</span>—Alpha particles are large particles that are stopped by the epidermis. They cause no significant external damage. Internal contamination may cause local tissue injury.<br /><br /><span style="font-weight: bold;">2. Beta particles</span>—Beta particles are small particles that can penetrate the superficial skin and cause mild burnlike injuries.<br /><br /><span style="font-weight: bold;">3. Gamma rays</span>—Gamma rays are high-energy particles that can enter tissues easily and cause significant damage to multiple body systems.<br /><br /><span style="font-weight: bold;">4. Neutrons</span>—Neutrons are large particles that are typically produced only during nuclear detonation. Like gamma rays, they cause significant tissue injury.<br /><br />The effect that radiation will have on the body depends on the type of radiation, the amount of exposure, and the body system involved. Tissues that display higher rates of cellular mitosis, such as the gastrointestinal and hematopoietic systems, are more severely affected. At very high radiation doses, neurovascular effects will also be seen. Radiation injury may cause either abnormal cell function or cell death.<br /><br /><span style="font-weight: bold;">Clinical Findings </span><br /><br /><span style="font-weight: bold;">A. Symptoms and Signs </span><br />The symptoms and signs of radiation exposure occur in 3 phases: prodromal, latent, and symptomatic.<br /><br /><span style="font-weight: bold;">1. Prodromal phase</span>—Patients will develop nonspecific symptoms of nausea, vomiting, weakness, and fatigue. Symptoms generally last no longer than 24-48 hours. With higher radiation exposures, symptoms will occur more rapidly and last longer.<br /><br /><span style="font-weight: bold;">2. Latent period</span>—The length of the latent period depends on the dose of radiation and the body system involved (neurologic, several hours; gastrointestinal, 1-7 days; hematopoietic, 2-6 weeks).<br /><br /><span style="font-weight: bold;">3. Symptomatic phase</span>—Symptoms will depend largely on the body system affected, which will depend on the radiation dose. At doses of 0.7-4 gray (Gy),1 the hematopoietic system will begin to manifest signs and symptoms of bone marrow suppression. Because of their long life span, erythrocytes are less severely affected than are the myeloid and platelet cell lines. Neutropenia and thrombocytopenia may be significant and lead to infectious and hemorrhagic complications. At doses of 6-8 Gy, gastrointestinal symptoms develop. Nausea, vomiting, diarrhea (bloody), and severe fluid and electrolyte imbalances will occur. The neurovascular system becomes affected at doses of 20-40 Gy. Symptoms include headache, mental status changes, hypotension, focal neurologic changes, convulsions, and coma. Exposures in this range are uniformly fatal. If an explosive device was used to disperse radioactive material, patients may also have thermal and blast injuries.<br /><br /><span style="font-weight: bold;">1The gray</span>, a unit of measure for the dose of ionizing radiation, is equal to 1 J/kg of tissue. One gray is equal to 100 rad.<br /><br /><span style="font-weight: bold;">B. Laboratory and X-ray Findings </span><br />Obtain a complete blood count (CBC) with differential for all patients sustaining a radiation injury. Although symptomatic bone marrow suppression may not be evident for some weeks, a drop of the absolute lymphocyte count of 50% at 24-48 hours is indicative of significant exposure. Monitor electrolytes in patients with gastrointestinal symptoms.<br /><br /><span style="font-weight: bold;">Treatment </span><br /><br />In the absence of aggressive medical therapy, the LD50 (the dose of radiation that will kill 50% of those exposed) is approximately 3.5 Gy. Aggressive medical care affords improved survival. Treat all life-threatening injuries associated with blast or thermal effects according to standard advanced trauma life support protocols. Perform surgical procedures early to avoid the electrolyte and hematopoietic effects that will occur. Clean wounds extensively and close them as soon as possible to prevent infection. Treat nausea and vomiting with standard antiemetic medications (prochlorperazine, promethazine, ondansetron). Treat fluid and electrolyte abnormalities with appropriate replacement. Anemia and thrombocytopenia can be treated with transfusion therapy. Leukopenia may be treated with hematopoietic growth factors such as sargramostim and filgrastim. In some instances bone marrow transplantation may be utilized. Follow neutropenic precautions at absolute neutrophil counts below 500. Some authors recommend prophylactic antibiotics at counts below 100. Use broad-spectrum antibiotics to treat infections. Infection is the most common cause of death in radiation patients. Despite aggressive medical care, radiation exposures above 10 Gy are usually fatal.<br /><br /><span style="font-weight: bold;">Decontamination </span><br /><br />Remove all contaminated clothing. Change contaminated dressings and splints. Thoroughly clean the patient's skin with soap and water or a 0.5% hypochlorite solution. Hair should be washed and in some instances removed. Eyes may be washed with large amounts of water or sterile saline. All contaminated materials should be bagged if possible and sent for proper disposal.<br /><br /><span style="font-weight: bold;">Disposition </span><br /><br />Patients who have been decontaminated and have only mild transient symptoms can be safely discharged. Because of the variable and lengthy latent period involved with this disorder, early admission is not indicated. Patients should be closely monitored and admitted when warranted.<br /><br />Goans RE et al: Early dose assessment in criticality accidents. Health Phys 2001;81(4):446. [PMID: 11569639] (Describes techniques for estimating the severity of radiation exposure.)<br /><br />Military Medical Operations Office, Armed Forces Radiobiology Research Institute: Medical Management of Radiological Casualties, 1st ed. Military Medical Operations Office, Armed Forces Radiobiology Research Institute, 1999. (Produced by the U.S. Army, this text provides general information regarding all aspects of radiologic injuries.)<br /><br /><br /><span style="font-weight: bold;"> BIOLOGIC WEAPONS </span><br /><br />Many agents can be used as biologic weapons. The most likely pathogens are presented here. Biologic agents can be classified as bacterial agents (anthrax, plague, tularemia, brucellosis, Q fever, glanders), viral agents (smallpox, hemorrhagic fever, encephalitis), and biologic toxins (botulinum, ricin, T-2 mycotoxins, staphylococcal enterotoxin B). A high index of suspicion will be required in order to identify patients who have experienced a biologic attack. A large number of patients with severe febrile illnesses will be the most likely clue. Keep in mind the attack most likely occurred several days prior to patient presentation. Aerosol release of infectious material is the most common form of biologic attack.<br /><br /><span style="font-weight: bold;">BACTERIAL AGENTS</span><br /><br /><span style="font-weight: bold;">1. Anthrax </span><br /><br />Bacillus anthracis is a gram-positive, sporulating rod. Anthrax infection occurs naturally after contact with contaminated animals or contaminated animal products. A biologic attack would likely involve the aerosol release of anthrax spores. The spore form of anthrax causes infection. Clinically the disease occurs in 3 forms: inhalational anthrax, gastrointestinal anthrax, and cutaneous anthrax.<br /><br /><span style="font-weight: bold;">Clinical Findings </span><br /><br /><span style="font-weight: bold;">A. Symptoms and Signs </span><br /><span style="font-weight: bold;">1. Inhalational anthrax</span>—Inhalation anthrax is the form of disease most likely expected after a terrorist attack. After spores are inhaled, a variable incubation period occurs, usually lasting 1-7 days. Prolonged incubation periods of up to 60 days have been observed. Initially, nonspecific symptoms of fever, cough, headache, chills, vomiting, dyspnea, chest pain, abdominal pain, and weakness occur. This stage may last from a few hours to a few days. Following these nonspecific symptoms, a transient period of improvement may be seen. When the second stage of disease is reached, high fever, diaphoresis, cyanosis, hypotension, lymphadenopathy, shock, and death will occur. Often death will occur within hours once the second stage is reached. The average time from onset of symptoms to death is 3 days. Once the initial symptoms of inhalational anthrax develop, the overall mortality rate may be as high as 95%. Early diagnosis of anthrax infection and rapid initiation of therapy may improve survival.<br /><br /><span style="font-weight: bold;">2. Gastrointestinal anthrax</span>—Gastrointestinal anthrax occurs when spores are ingested into the digestive tract. Two forms of the disease occur: oropharyngeal and abdominal. Oropharyngeal disease occurs when spores are deposited in the upper gastrointestinal tract. An oral or esophageal ulcer develops followed by regional lymphadenopathy and eventual sepsis. In abdominal anthrax, the spores are deposited in the lower gastrointestinal tract. Symptoms include nausea, vomiting, diarrhea (bloody), and the development of an acute abdomen with sepsis. Mortality rates for gastrointestinal anthrax are in excess of 50%.<br /><br /><span style="font-weight: bold;">3. Cutaneous anthrax</span>—Cutaneous anthrax is the most common naturally occurring form of the disease. Cutaneous anthrax occurs when spores come in contact with open skin lesions. This usually occurs on the arms, hands, and face. Following exposure, a small, often pruritic papule will develop. Eventually this papule will turn into a small ulcer (over 2 days), then progress to a small vesicle, and ultimately to a painless black eschar with surrounding edema. Then, over a period of 1-2 weeks, the eschar will dry and fall off. Regional lymphadenitis or lymphadenopathy may also occur. In some case secondary sepsis may develop. Without treatment, cutaneous anthrax has a mortality rate of 20%; however, the mortality rate drops to 1% with treatment.<br /><br /><span style="font-weight: bold;">4. Anthrax meningitis</span>—Anthrax meningitis can occur as a complication of any other form of anthrax. Symptoms include headache and meningismus. Anthrax meningitis carries a mortality rate of nearly 100%.<br /><br /><span style="font-weight: bold;">B. Laboratory and X-ray Findings </span><br />Multiple laboratory studies can be used to identify anthrax. In fulminant cases, the organism may be seen on routine Gram stain. Blood cultures, wound cultures, and nasal cultures may be obtained. Given the lack of an infiltrate, sputum cultures are rarely useful. Notify laboratory personnel of a possible anthrax exposure. Often Bacillus spp. are thought to be the contaminant and are not pursued further. Confirmatory enzyme-linked immunoassay (ELISA) and polymerase chain reaction (PCR) tests are available at some national reference laboratories. Chest X-ray may also be useful. Patients with inhalational anthrax will display a wide mediastinum on chest x-ray. No infiltrate is typically observed.<br /><br /><span style="font-weight: bold;">Treatment & Prophylaxis </span><br /><br />Because anthrax has a rapid and fulminant course, do not delay treatment while awaiting confirmatory tests. Institute empiric therapy when the diagnosis is considered. Delaying treatment for even hours may significantly increase mortality.<br /><br /><span style="font-weight: bold;">A. Antibiotics </span><br />Most naturally occurring strains of anthrax are sensitive to penicillin. Some strains, however, are penicillin resistant. Weapons-grade anthrax is likely to be penicillin resistant. As a result, the first-line therapy is now ciprofloxacin; doxycycline is an acceptable alternative (see Table 3-1). Treatment should continue for 60 days. If cultures were obtained, later sensitivity testing may direct antibiotic use.<br /><br /><span style="font-weight: bold;">B. Supportive Care </span><br />Patients may require intensive medical support such as airway management, hemodynamic support, and various measures to manage multisystem organ failure.<br /><br /><span style="font-weight: bold;">C. Prophylaxis </span><br />Individuals thought to be at high risk for anthrax exposure should receive treatment as though infection has occurred. Later laboratory analysis may allow discontinuation of therapy. An anthrax vaccination is available and requires injections at 0, 2, and 4 weeks, followed by injections at 6, 12, and 18 months. An annual booster is also required. If a combination of vaccination and antibiotics is used during treatment, the course of antibiotics may be shortened to 30 days.<br /><br /><span style="font-weight: bold;">Infection Control </span><br /><br />No data indicate that anthrax is spread via person-to-person contact. Use standard precautions during patient care activities (Table 3-2).<br /><br /><span style="font-weight: bold;">2. Plague </span><br /><br />Yersinia pestis is a nonmotile, gram-negative bacillus. Plague occurs naturally after the bite of an infected arthropod vector. Biologic attack would most likely involve the aerosolized release of Y pestis. Plague occurs in 3 clinical forms: bubonic plague, septicemic plague, and pneumonic plague.<br /><br /><span style="font-weight: bold;">Clinical Findings </span><br /><br /><span style="font-weight: bold;">A. Symptoms and Signs </span><br />1. Bubonic plague—Bubonic plague is the most common naturally occurring form of the disease. Infection begins with the bite of a contaminated flea. A latent period then occurs and may last up to 1 week, followed by fevers, chills, and weakness. Eventually the organism will migrate to the regional lymph nodes where it causes destruction and necrosis. A swollen and tender lymph node called a bubo will develop. Bubo size ranges from 1 to 10 cm. Some patients may develop secondary sepsis. Without treatment, bubonic plague has an estimated mortality rate of 50%; however, with antibiotic therapy the mortality rate falls to 10%.<br /><br /><span style="font-weight: bold;">2. Septicemic plague</span>—Septicemic plague may occur either as a complication of other forms of plague or as a primary entity. Symptoms include fever, dyspnea, hypotension, and purpuric skin lesions. Gangrene of the nose and extremities may occur, hence, the name "black death." Complications of disseminated intravascular coagulation may also be evident. Without treatment, septicemic plague has an estimated mortality rate of 100%; however, with antibiotic therapy the mortality rate falls to 40%.<br /><br /><span style="font-weight: bold;">3. Pneumonic plague</span>—Pneumonic plague may occur either as a complication of other forms of plague or as a primary entity. It is the most likely form of the disease to result from a terrorist attack. A latent period of 1-6 days following exposure is likely. Patients will then develop signs and symptoms of severe pulmonary infection including fever, cough, dyspnea, hypoxia, and sputum production. Gastrointestinal symptoms of nausea, vomiting, and diarrhea may also occur. Pneumonic plague has an estimated mortality rate of 100% if antibiotic therapy is not begun within 24 hours.<br /><br /><span style="font-weight: bold;">B. Laboratory and X-ray Findings </span><br />Y pestis can be identified by several different staining techniques. Routine Gram stain may reveal the organism. Y pestis also has a characteristic bipolar staining pattern with Wright, Giemsa, and Wayson stains. Routine blood cultures, sputum cultures, and cultures of lymph node aspirates may be useful. Specialized rapid confirmatory tests are available at some laboratories. In patients with pneumonic plague, chest x-ray will display a patchy or confluent infiltrate.<br /><br /><span style="font-weight: bold;">Treatment & Prophylaxis </span><br /><br />Plague has a rapid disease progression, and any delay in treatment will cause significant increases in mortality. Institute treatment on empiric grounds, and do not delay treatment while awaiting confirmatory tests.<br /><br /><span style="font-weight: bold;">A. Antibiotics </span><br />Streptomycin is the drug of choice for the treatment of plague. Gentamicin may also be used and is thought to have equal efficacy (see Table 3-1). Alternative antibiotics include doxycycline, ciprofloxacin, and chloramphenicol.<br /><br /><span style="font-weight: bold;">B. Supportive Care </span><br />Patients may require intensive medical support such as airway management, hemodynamic support, and other measures to manage multisystem organ failure.<br /><br /><span style="font-weight: bold;">C. Prophylaxis </span><br />Patients in a community experiencing a pneumonic plague epidemic should receive antibiotic therapy if they develop a cough or a fever above 38.5 °C (101.2 °F). Any person who has been in close contact with an individual with plague should receive a 7-day course of antibiotics. Antibiotic choices are the same as for treatment.<br /><br /><span style="font-weight: bold;">Infection Control </span><br /><br />Pneumonic plague can be spread from person to person by aerosol droplets. Use droplet precautions, and either the patient or caregivers should wear masks (see Table 3-2). Once the patient has received 48 hours of antibiotics and has improved clinically, standard precautions may be used.<br /><br /><span style="font-weight: bold;">3. Tularemia </span><br /><br />Francisella tularensis is a nonmotile, aerobic, gram-negative coccobacillus. Two strains of tularemia are known to exist. F tularensis biovar tularensis is considered highly virulent, whereas F tularensis biovar palaearctica is more benign. Tularemia occurs naturally after the bite of an infected arthropod vector or after exposure to contaminated animal products. Biologic attack would most likely involve the release of aerosolized F tularensis. Tularemia displays multiple clinical forms including ulceroglandular, glandular, oculoglandular, oropharyngeal, pneumonic, and typhoidal forms. The form of disease depends on the site and type of inoculation.<br /><br /><span style="font-weight: bold;">Clinical Findings </span><br /><br /><span style="font-weight: bold;">A. Symptoms and Signs </span><br />Patients with any form of tularemia may present with the abrupt onset of fever, chills, headache, malaise, and myalgias. Often a maculopapular rash is seen.<br /><br /><span style="font-weight: bold;">1. Ulceroglandular tularemia</span>—Ulceroglandular tularemia usually occurs after handling infected animals or after the bite of an infected arthropod vector. At the inoculation site a papule will form that will eventually become a pustule and then a tender ulcer. The ulcer may have a yellow exudate and will slowly develop a black base. Regional lymph nodes will become swollen and painful.<br /><br /><span style="font-weight: bold;">2. Glandular tularemia</span>—Glandular tularemia displays signs and symptoms similar to ulceroglandular tularemia, except that no ulcer formation is noted.<br /><br /><span style="font-weight: bold;">3. Oculoglandular tularemia</span>—After ocular inoculation, a painful conjunctivitis will develop with regional lymphadenopathy. Lymphadenopathy may involve the cervical, submandibular, or preauricular chains. In some cases, ulcerations occur on the palpebral conjunctiva.<br /><br /><span style="font-weight: bold;">4. Oropharyngeal tularemia</span>—After inoculation of the pharynx, an exudative pharyngotonsillitis will develop with cervical lymphadenopathy.<br /><br /><span style="font-weight: bold;">5. Pneumonic tularemia</span>—Pneumonic tularemia occurs after inhalation of F tularensis or following secondary spread from other infectious foci. A terrorist attack will most likely cause this form of disease. The findings of pulmonary involvement are variable and include pharyngitis, bronchiolitis, hilar lymphadenitis, and pneumonia. Early in the course of disease, systemic symptoms may predominate over pulmonary symptoms. In some cases, however, pulmonary disease progresses rapidly to pneumonia, pulmonary failure, and death.<br /><br /><span style="font-weight: bold;">6. Typhoidal tularemia</span>—In this form of tularemia, systemic signs and symptoms of disease are present without a clear infectious site. Signs and symptoms include fever, chills, headache, malaise, and myalgias.<br /><br />Any form of tularemia may be complicated by hematogenous spread leading to pneumonia, meningitis, or sepsis. The overall mortality rates for untreated tularemia range from 10% to 30%; however, with antibiotic therapy, mortality rates drop to less than 1%.<br /><br /><span style="font-weight: bold;">B. Laboratory and X-ray Findings </span><br />F tularensis requires special growth media. Notify laboratory personnel of a possible tularemia specimen so that proper plating can be performed. Cultures may be obtained from sputum, pharyngeal, or blood specimens. Specialized ELISA and PCR confirmatory tests are also available at some reference laboratories. In the case of pneumonic tularemia, chest x-ray may demonstrate peribronchial infiltrates to bronchopneumonia. Pleural effusions are often present.<br /><br /><span style="font-weight: bold;">Treatment & Prophylaxis </span><br /><br /><span style="font-weight: bold;">A. Antibiotics </span><br />Streptomycin and gentamicin are considered the drugs of choice for the treatment of tularemia (see Table 3-1). Ciprofloxacin has also displayed efficacy against tularemia. Second-line agents such as tetracycline and chloramphenicol may be used, but these agents are associated with higher rates of treatment failure. A 10-day course of antibiotics should be used. For second-line agents, a 14-day course should be used.<br /><br /><span style="font-weight: bold;">B. Supportive Care </span><br />Rarely patients may require intensive medical support such as airway management, hemodynamic support, and other measures to manage multisystem organ failure.<br /><br /><span style="font-weight: bold;">C. Prophylaxis </span><br />Some data suggest that a 14-day course of antibiotics begun during the incubation period may prevent disease. Antibiotic choices are the same as for treatment. A live attenuated vaccine for tularemia also exists and is often used for at-risk laboratory workers. Vaccination decreases the rate of inhalational tularemia but does not confer complete protection. Given tularemia's short incubation period, and the incomplete protection of the vaccine, postexposure vaccination is not recommended.<br /><br /><span style="font-weight: bold;">Infection Control </span><br /><br />Significant person-to-person transmission of tularemia does not occur. Standard precautions are sufficient during patient care activities (see Table 3-2).<br /><br /><span style="font-weight: bold;">4. Brucellosis </span><br /><br />Brucellae are small aerobic, gram-negative, pleomorphic coccobacilli. Many Brucella spp. occur naturally; however, only 4 species are infectious to humans. Each species typically infects a particular host organism, and human infection follows contact with contaminated animal material. The Brucella spp. that are infectious to humans are B melitensis (found in goats), B suis (found in swine), B abortus (found in cattle), and B canis (found in dogs). B suis has been weaponized in the past.<br /><br /><span style="font-weight: bold;">Clinical Findings </span><br /><br /><span style="font-weight: bold;">A. Symptoms and Signs </span><br />The symptoms and signs of brucellosis are similar whether infection is contracted via oral, inhalational, or percutaneous routes. The usual incubation period following infection is 1-3 weeks. Because Brucella spp. infection can involve multiple body systems, a wide range of clinical findings is typical. Nonspecific symptoms are common and include fever, chills, malaise, and myalgias. Osteoarticular involvement may manifest as joint infections or vertebral osteomyelitis. Respiratory symptoms include cough, dyspnea, and pleuritic chest pain. Cardiovascular complications are numerous and include endocarditis, myocarditis, pericarditis, and mycotic aneurysms. Gastrointestinal symptoms include nausea, vomiting, diarrhea, and hepatitis. Multiple types of genitourinary infections can also occur. Neurologic involvement may cause meningitis, encephalitis, cerebral abscesses, cranial nerve abnormalities, or Guillain-Barre syndrome. Patients may also develop anemia, thrombocytopenia, or neutropenia. Central nervous system and cardiac involvement, although infrequent, accounts for most fatalities. Brucella spp. are not known for their lethality, and infection has an estimated mortality rate of less than 2%. Its interest as a biological weapon stems from the prolonged disease course and significant morbidity.<br /><br /><span style="font-weight: bold;">B. Laboratory and X-ray Findings </span><br />Brucella spp. will grow on standard culture media. Because of their slow growth, cultures may need to be maintained for at least 6 weeks. Specialized biphasic culture techniques may improve isolation. A more common diagnostic modality is a serum tube agglutination test. ELISA and PCR studies are available at some reference laboratories. If vertebral involvement is suspected, spinal x-rays, magnetic resonance imaging, computed tomography scanning, or bone scintigraphy may be helpful.<br /><br /><span style="font-weight: bold;">Treatment & Prophylaxis </span><br /><br /><span style="font-weight: bold;">A. Antibiotics </span><br />Because of the high rate of treatment failure, single drug therapy is no longer recommended. A prolonged course of multiple antibiotics is now considered to be the standard of care. The most common regimen involves the use of rifampin and doxycycline given for a 6-week period (see Table 3-1). Other antibiotics that have displayed efficacy against Brucella spp. include gentamicin, streptomycin, trimethoprim-sulfamethoxazole, and ofloxacin. Regardless of the antibiotics chosen, combination drug therapy should be used. In patients with serious infections, a 3-drug parenteral regimen is the norm.<br /><br /><span style="font-weight: bold;">B. Supportive Care </span><br />Rarely patients may require intensive medical support such as airway management, hemodynamic support, and other measures to manage multisystem organ failure.<br /><br /><span style="font-weight: bold;">C. Prophylaxis </span><br />No human vaccine against Brucella spp. currently exists. Some authors recommend a 3- to 6-week course of antibiotics following a high-risk exposure such as a biologic attack.<br /><br /><span style="font-weight: bold;">Infection Control </span><br /><br />Person-to-person spread of brucellosis is thought to be uncommon. Standard precautions are sufficient during patient care activities (see Table 3-2).<br /><br /><span style="font-weight: bold;">5. Q Fever </span><br /><br />Q fever is caused by a rickettsial organism known as Coxiella burnetii. C burnetii has a worldwide distribution and occurs naturally in many domesticated animals (dogs, cats, sheep, goats, cattle). The organism is shed in feces, urine, milk, and placental material. Much like anthrax, C burnetii produces a sporelike form. Humans become infected by inhaling contaminated aerosols.<br /><br /><span style="font-weight: bold;">Clinical Findings </span><br /><br /><span style="font-weight: bold;">A. Symptoms and Signs </span><br />After infection, a typical incubation period ranges from 5 to 30 days. The symptoms and signs of Q fever are nonspecific and may occur acutely or have an indolent course. Typical symptoms and signs include fever, chills, malaise, myalgias, headache, and anorexia. If cough occurs, it tends to occur late in the disease process and may or may not be associated with pneumonia. Various cardiac manifestations may occur and include endocarditis, myocarditis, and pericarditis. Gastrointestinal findings are common and include nausea, vomiting, diarrhea, and hepatitis. A nonspecific maculopapular rash may develop. Although not as common, various neurologic symptoms may also occur.<br /><br />In some patients, Q fever may become a chronic condition. Chronic Q fever is typically manifest as endocarditis and tends to affect previously diseased cardiac valves. Although Q fever can be debilitating, it is usually not fatal. Mortality rates are generally less than 2.5%.<br /><br /><span style="font-weight: bold;">B. Laboratory and X-ray Findings </span><br />C burnetii is difficult to grow in culture, and sputum analysis is equally futile. Several serologic tests are available and include indirect fluorescent antibody staining, ELISA, and complement fixation. These tests often must be conducted at specialized reference laboratories. Elevated liver enzymes are also common in C burnetii infection.<br /><br /><span style="font-weight: bold;">Treatment & Prophylaxis </span><br /><br /><span style="font-weight: bold;">A. Antibiotics </span><br />Most cases of C burnetii infection will resolve without antibiotic therapy. Regardless, antibiotics are recommended because treatment will lower the rate of complications. A 7-day course of either doxycycline or tetracycline is usually sufficient (see Table 3-1). Fluoroquinolones are an acceptable alternative.<br /><br /><span style="font-weight: bold;">B. Supportive Care </span><br />Rarely patients may require intensive medical support such as airway management, hemodynamic support, and other measures to manage multisystem organ failure.<br /><br /><span style="font-weight: bold;">C. Prophylaxis </span><br />Prophylactic antibiotics should be started 8-12 days after initial exposure. Antibiotics are ineffective if started sooner. A 7-day course of either doxycycline or tetracycline is usually sufficient. Fluoroquinolones are an acceptable alternative. An investigational vaccine exists but is not yet available to the general public.<br /><br /><span style="font-weight: bold;">Infection Control </span><br /><br />Person-to-person spread of the disease is unlikely. Standard precautions are sufficient while engaging in patient care activities (see Table 3-2).<br /><br /><span style="font-weight: bold;">6. Glanders & Melioidosis </span><br /><br />Glanders and melioidosis are similar diseases caused by related bacteria. The causal agent of glanders is Burkholderia mallei; the causal agent of melioidosis is Burkholderia pseudomallei. Both organisms are gram-negative bacilli. Glanders and melioidosis occur naturally. Glanders is a rare disease in humans; horses and other domesticated animals are often infected. Melioidosis occurs more commonly in humans and is endemic to Southeast Asia. Infection with either organism occurs via contact with open wounds or mucous membranes or by inhalation.<br /><br /><span style="font-weight: bold;">Clinical Findings </span><br /><br /><span style="font-weight: bold;">A. Symptoms and Signs </span><br />Both glanders and melioidosis can cause multiple clinical syndromes.<br /><br /><span style="font-weight: bold;">1. Localized disease</span>—A localized disease may be seen and typically occurs after wound contamination or mucous membrane exposure. With wound contamination, patients develop a small ulcer with associated cellulitis. Regional lymphadenopathy or lymphangitis is also common. If mucous membrane exposure occurs, patients develop a bloody purulent discharge from the infected area (eyes, nose, or mouth). If secondary systemic infection occurs, a pustular rash similar to smallpox may develop.<br /><br /><span style="font-weight: bold;">2. Pulmonary disease</span>—A pulmonary form of disease may also be seen. Pulmonary disease may occur after inhalation of aerosols or after hematogenous spread. An incubation period of 1-2 weeks occurs initially. Symptoms of pulmonary disease, including fever, chills, cough, chest pain, and dyspnea, develop eventually.<br /><br /><span style="font-weight: bold;">3. Septicemic disease</span>—The most severe form of infection is the septicemic form. Patients present with nonspecific symptoms and signs of fever, chills, malaise, myalgias, photophobia, rigors, diffuse body abscesses, pustular rash, and headache. This condition is usually fatal; death occurs in 7-10 days.<br /><br /><span style="font-weight: bold;">B. Laboratory and X-ray Findings </span><br />Both organisms can be identified by routine Gram stain and culture. Special staining with methylene blue or Wright stain may facilitate diagnosis. Growth may be enhanced by the addition of meat nutrient agar or glucose to the growth media. Specialized agglutination and complement fixation tests may also be used. If pulmonary involvement is suspected, chest x-ray may demonstrate lung abscesses, miliary nodules, or pneumonia.<br /><br /><span style="font-weight: bold;">Treatment & Prophylaxis </span><br /><br /><span style="font-weight: bold;">A. Antibiotics </span><br />Both glanders and melioidosis respond to various antibiotics. Appropriate antibiotic choices include amoxicillin-clavulanate, tetracycline, trimethoprim-sulfamethoxazole, rifampin, ciprofloxacin, and ceftazidime (see Table 3-1). Various combinations of antibiotics have been recommended depending on the type and severity of infection.<br /><br /><span style="font-weight: bold;">B. Supportive Care </span><br />Rarely patients may require intensive medical support such as airway management, hemodynamic support, and other measures to manage multisystem organ failure.<br /><br /><span style="font-weight: bold;">C. Prophylaxis </span><br />According to some authorities, a course of trimethoprim-sulfamethoxazole may prevent the onset of disease.<br /><br /><span style="font-weight: bold;">Infection Control </span><br /><br />Person-to-person spread of the disease is uncommon but can occur with improper handling of body fluids. Standard precautions are sufficient during patient care activities (see Table 3-2).<br /><br /><span style="font-weight: bold;">VIRAL AGENTS </span><br /><br /><span style="font-weight: bold;">1. Smallpox </span><br /><br />Smallpox is a disease caused by the variola virus. The variola virus is a DNA virus of the genus orthopoxvirus. It occurs in 2 strains: the more severe variola major and a milder form, variola minor. Smallpox was essentially eradicated by an aggressive treatment and vaccination campaign conducted by the World Health Organization. The last naturally occurring case was in Somalia in 1977. Two stockpiles of the virus remain, one in the Centers for Disease Control and Prevention in Atlanta, and the other in the Institute of Virus Preparations in Moscow. Concern now exists that the Russian stockpile may have been compromised.<br /><br /><span style="font-weight: bold;">Clinical Findings </span><br /><br /><span style="font-weight: bold;">A. Symptoms and Signs </span><br />Disease begins with inhalation of the variola virus. After an initial exposure, a 7- to 17-day incubation period begins, during which the virus replicates in the lymph nodes, bone marrow, and spleen. A secondary viremia then develops leading to high fever, malaise, headache, backache, and in some cases delirium. After approximately 2 days a characteristic rash will develop. The rash begins on the extremities and moves to the trunk. The palms and soles are not spared. The rash follows a typical progression beginning as macules, then papules, and eventually becoming pustular. Eventually lesions will form scabs that separate, leaving small scars. Unlike chickenpox, all the lesions in smallpox will be in similar stages of development. In unvaccinated individuals, mortality rates associated with variola major are approximately 30%. Variola minor has a similar progression to variola major, but toxicity and rash are not as severe. In unvaccinated individuals, the mortality rates associated with variola minor are approximately 1%. In 10% of cases, a variant form of rash will develop. A hemorrhagic rash displaying petechiae and frank skin hemorrhage may occur. This variant of smallpox carries a mortality rate of nearly 100%. Likewise, a malignant form exists in which the pustules remain soft and velvety to the touch.<br /><br /><span style="font-weight: bold;">B. Laboratory and X-ray Findings </span><br />Analysis of pustular fluid will yield virus particles. All samples should be sealed in 2 airtight containers. Variola can easily be recognized via electron microscopy. The virus itself can be grown in cell cultures or on chorioallantoic egg membranes. Further characterization of strains can be accomplished via biologic assays. PCR analysis is available at some reference laboratories.<br /><br /><span style="font-weight: bold;">Treatment & Prophylaxis </span><br /><br /><span style="font-weight: bold;">A. Specific Therapy </span><br />Currently there is no specific therapy for smallpox. Treatment is essentially supportive care. Many investigational drugs are currently under study. Strict patient isolation, preferably in the home, should be used. Any person having close contact with infected patients should be either quarantined or monitored for signs of infection. Antibiotics may be used if secondary bacterial infection occurs.<br /><br /><span style="font-weight: bold;">B. Prophylaxis </span><br />Data indicate that vaccination within 4 days of smallpox exposure may lessen subsequent illness. Because of the risk of possible terrorist attack, some authorities are recommending a preemptive initiation of smallpox vaccination. This would be problematic for several reasons. First, the current supply of smallpox vaccine is inadequate to protect a large populace. Second, many complications were known to occur with smallpox vaccination. Postvaccinial encephalitis occurred in approximately 1 in 300,000 vaccinations and was fatal in 25% of patients. Immunocompromised patients may develop a condition known as progressive vaccinia. In this condition, the initial inoculation site failed to heal, became necrotic, and necrosis spread to adjacent tissues. This complication was often fatal. In some patients with eczema, a condition known as eczema vaccinatum could occur. Here, vaccinial lesions would occur in areas previously involved with eczema. Fortunately, the eruption was usually self-limited. In some patients, a secondary generalized vaccinia could develop. In others, inadvertent autoinoculation of eyes, mouth, or other areas occurred. Many of these complications could be treated with vaccinia immune globulin. Unfortunately, vaccinia immune globulin is also in short supply.<br /><br />Cidofovir has also displayed some efficacy in preventing smallpox infection if given within 48 hours. There is no evidence to suggest that cidofovir is more effective than vaccine. Further, cidofovir is associated with significant renal toxicity.<br /><br />Individuals vaccinated prior to 1972 are likely no longer protected, given that immunity lapses over a 5- to 10-year period.<br /><br /><span style="font-weight: bold;">Infection Control </span><br /><br />Smallpox is highly infectious. Infection is spread by aerosol droplets. It is generally thought that each index case will subsequently infect 10-20 secondary individuals. The period of infectivity begins with the onset of rash and ends when all scabs separate. Use airborne precautions during patient care activities (see Table 3-2). Any material in contact with patients should be either autoclaved or washed in a bleach solution.<br /><br /><span style="font-weight: bold;">2. Hemorrhagic Fever </span><br /><br />Viral hemorrhagic fever represents a clinical syndrome caused by several RNA viruses. These viruses exist in 4 different families: the Arenaviridae, the Filoviridae, the Flaviviridae, and the Bunyaviridae. Numerous viruses in each family may cause slightly different forms of hemorrhagic fever. The different forms of hemorrhagic fever are often named by their geographic origin (Table 3-3). Human infection occurs after contact with infected animals or infected arthropod vectors. Many of these viruses are also highly infectious in the aerosol form. This characteristic makes them potential biological weapons.<br /><br /><span style="font-weight: bold;">Clinical Findings </span><br /><br /><span style="font-weight: bold;">A. Symptoms and Signs </span><br />Several clinical aspects of hemorrhagic fever are unique to the individual forms (Table 3-3). Many symptoms and signs, however, are common to all types of hemorrhagic fever. Alterations in the vascular bed and increased vascular permeability lead to the dominant features of this disease. Early symptoms and signs include fever, conjunctival injection, mild hypotension, prostration, facial flushing, vomiting, diarrhea, and petechial hemorrhages. Eventually some patients may develop shock and mucous membrane hemorrhage. In some instances, evidence of hepatic, pulmonary, and neurologic involvement will be present. Secondary bacterial infection is also common.<br /><br /><span style="font-weight: bold;">B. Laboratory and X-ray Findings </span><br />A number of nonspecific laboratory abnormalities may be seen, including leukopenia, thrombocytopenia, proteinuria, hematuria, and elevated liver enzymes. Definitive diagnosis is possible with various rapid enzyme immunoassays and with viral culture.<br /><br /><span style="font-weight: bold;">Treatment & Prophylaxis </span><br /><br /><span style="font-weight: bold;">A. Specific Therapy </span><br />Ribavirin is a nucleoside analog that has been shown to improve mortality in some forms of hemorrhagic fever. Dosing is as follows: 30 mg/kg intravenously as an initial dose, followed by 16 mg/kg intravenously every 6 hours for 4 days and then 8 mg/kg intravenously every 8 hours for 6 days. Ribavirin is usually most effective if begun within 7 days. Unfortunately, ribavirin is thought to be ineffective against the filoviruses and the flaviviruses. Convalescent plasma containing neutralizing antibodies is also effective in some cases.<br /><br /><span style="font-weight: bold;">B. Supportive Care </span><br />Intravenous lines and other invasive procedures should be limited. Use fluid resuscitation with caution. Because of increases in vascular permeability, peripheral edema and pulmonary edema are frequent complications of volume replacement. If frank disseminated intravascular coagulopathy develops, consider heparin therapy.<br /><br /><span style="font-weight: bold;">C. Prophylaxis </span><br />A vaccine against yellow fever is currently available. Many other investigational vaccines exist but are not currently available to the general public. Protocols also exist for the use of ribavirin in high-risk exposures.<br /><br /><span style="font-weight: bold;">Infection Control </span><br /><br />The causal agents of hemorrhagic fever are highly infectious. Use caution when using sharps or when coming into contact with body fluids. Some forms are spread via aerosol, and patients with significant cough should be placed under airborne precautions. All laboratory specimens should be double sealed in airtight containers.<br /><br /><span style="font-weight: bold;">3. Viral Encephalitis </span><br /><br />Much like viral hemorrhagic fever, viral encephalitis represents a clinical syndrome caused by numerous viruses. Of the pathogens that cause viral encephalitis, members of the family Togaviridae are thought to have potential as biologic weapons. The family Togaviridae includes the eastern equine encephalitis (EEE) virus, western equine encephalitis (WEE) virus, and Venezuelan equine encephalitis (VEE) virus. VEE virus has been weaponized in the past. In nature, these viruses are spread by infected arthropod vectors, and they infect humans as well as equines. They are also infectious in aerosol form, hence, their utility as biologic weapons.<br /><br /><span style="font-weight: bold;">Clinical Findings </span><br /><br /><span style="font-weight: bold;">A. Symptoms and Signs </span><br />Nearly all forms of infection will cause nonspecific symptoms and signs of fever, chills, malaise, myalgias, sore throat, vomiting, and headache. A large number of associated equine deaths may lead one to suspect equine encephalitis. The degree to which encephalitis develops depends on the pathogen involved. Although nearly all cases of VEE are symptomatic, encephalitis occurs in less than 5% of cases. If encephalitis does develop, and the patient recovers, residual neurologic sequelae usually do not occur. Without encephalitis, VEE has an expected mortality rate of less than 1%. Although uncommon, if encephalitis develops, the mortality rate increases to approximately 20%. In contrast, EEE tends to progress to neurologic involvement. Encephalitis is usually severe, and residual neurologic findings are common. With EEE, mortality rates range from 50% to 75%. WEE displays an intermediate degree of severity, with an overall estimated mortality rate of approximately 10%. If encephalitis develops, confusion, obtundation, seizures, ataxia, cranial nerve palsies, and coma may occur.<br /><br /><span style="font-weight: bold;">B. Laboratory and X-ray Findings </span><br />Although nonspecific, leukopenia and lymphopenia are common. In cases of encephalitis, cerebral spinal fluid analysis will display a lymphocytic pleocytosis. A number of serologic studies such as ELISA, complement-fixation, and hemagglutination inhibition may aid diagnosis. Although time consuming, the gold standard test for VEE involves viral isolation following inoculation of cell cultures of suckling mice. Additional specialized tests may be available only at regional reference laboratories.<br /><br /><span style="font-weight: bold;">Treatment & Prophylaxis </span><br /><br /><span style="font-weight: bold;">A. Specific Therapy </span><br />Unfortunately, no specific treatment for equine encephalitis exists. Supportive care is all that can be offered. Headache may be treated with typical analgesics. Seizures are treated with typical anticonvulsant medications.<br /><br /><span style="font-weight: bold;">B. Supportive Care </span><br />Patients may require intensive medical support such as airway management, hemodynamic support, and other measures to manage multisystem organ failure.<br /><br /><span style="font-weight: bold;">C. Prophylaxis </span><br />An investigational vaccine against VEE virus exists. It does not provide protection against all strains of VEE virus, and some patients will not display an effective antibody response. In 20% of patients receiving the vaccine, fever, malaise, and myalgias may develop.<br /><br /><span style="font-weight: bold;">Infection Control </span><br /><br />Infection is not spread by person-to-person contact. Standard precautions are sufficient during patient care activities. To limit the spread of disease, patient exposure to arthropod vectors should be prevented.<br /><br /><span style="font-weight: bold;">BIOLOGIC TOXINS </span><br /><br /><span style="font-weight: bold;">1. Botulinum Toxin</span><br /><br />Botulism is caused by a protein toxin produced by Clostridium botulinum. C botulinum is a gram-positive, spore-forming, obligate anaerobe found naturally in the soil. Many authorities consider botulinum toxin to be among the most potent naturally occurring poisons. The toxin occurs in 7 antigenic types, designated types A through G. Once absorbed, toxin will bind to motor neurons and prevent the release of acetylcholine, causing a flaccid muscle paralysis. Natural infection occurs in 3 forms: wound botulism, foodborne botulism, and intestinal botulism. Wound botulism occurs after C botulinum contaminates an open wound, subsequently producing toxin. Foodborne botulism occurs after ingesting food already contaminated by the toxin. Intestinal botulism, typically seen in infants, occurs after ingesting food contaminated by C botulinum, which in turn produces toxin. Although not occurring naturally, botulism can also be caused by inhalation of the toxin. This is the form of botulism that will likely occur following biologic attack. Contamination of food or water supplies also represents a possible terrorist threat. Food contamination, however, is unlikely to induce the large numbers of affected persons that would be seen following aerosol exposure. Water contamination would be difficult because current purification techniques are effective in neutralizing botulinum toxin.<br /><br /><span style="font-weight: bold;">Clinical Findings </span><br /><br /><span style="font-weight: bold;">A. Symptoms and Signs </span><br />After initial exposure, an incubation period ranging from 12 to 80 hours will occur. The duration of the incubation period depends on the type and amount of exposure. After the incubation period, a flaccid symmetric muscle paralysis will affect the bulbar musculature. Patients often display ptosis, diplopia, dysphagia, dysarthria, and dysphonia. Dilated, poorly reactive pupils are common. Eventually the paralysis will extend to the lower muscle groups, leading to paralysis. Airway compromise is common, and patients may lose respiratory function.<br /><br />If foodborne exposure is involved, gastrointestinal symptoms such as nausea, vomiting, and diarrhea may occur. Botulism does not cause altered sensorium, sensory changes, or fever.<br /><br /><span style="font-weight: bold;">B. Laboratory and X-ray Findings </span><br />A mouse bioassay is the definitive test for botulism. Specimens for evaluation may be obtained from suspected food, blood, gastric contents, or possibly stool. This type of diagnostic testing is not widely available, and specimens may need to be sent to specialized laboratories. In addition to laboratory studies, electromyograms may display patterns consistent with botulism.<br /><br /><span style="font-weight: bold;">Treatment & Prophylaxis </span><br /><br /><span style="font-weight: bold;">A. Specific Therapy </span><br />A botulinum antitoxin can be obtained from many state health departments or from the Centers for Disease Control and Prevention. Antitoxin therapy is most effective when given early in the disease course. It acts by binding free toxin but will not restore nerve terminals that have already been compromised. The civilian antitoxin is effective in neutralizing the 3 most common types of botulinum toxin found to affect humans (types A, B, and E). If other forms of toxin are utilized, an investigational heptavalent antitoxin may be available from the military. The military antitoxin is effective against all types of toxin (types A through G). Because some patients may develop allergic reactions to the antitoxin, a test dose is recommended.<br /><br /><span style="font-weight: bold;">B. Supportive Care </span><br />Patients may require intensive medical support such as airway management and ventilator support. Parenteral or tube feedings may be required. Treat secondary bacterial infections with antibiotics. Avoid clindamycin and aminoglycoside antibiotics because they may worsen neurologic blockade.<br /><br /><span style="font-weight: bold;">C. Prophylaxis </span><br />Some evidence suggests that initiation of antitoxin prior to the onset of symptoms may prevent disease. Unfortunately, large amounts of the antitoxin are not available. A more prudent course of action would be to institute antitoxin therapy at the first signs of illness.<br /><br /><span style="font-weight: bold;">Infection Control </span><br /><br />Person-to-person transmission of botulism does not occur. Standard precautions are sufficient during patient care activities (see Table 3-2). If food is suspected of being contaminated, thorough cooking will neutralize the toxin.<br /><br /><span style="font-weight: bold;">2. Ricin </span><br /><br />Ricin is a polypeptide toxin that causes cell death by inhibiting protein synthesis. Ricin occurs naturally as a component of the castor bean, from the castor plant, Ricinus communis. Accidental ricin toxicity has occurred following ingestion of castor beans. Although ricin is less toxic than many other potential biologic agents, it is inexpensive, easy to produce, and can be aerosolized. These characteristics make it a potential biologic weapon. Ricin may be delivered by parenteral injection, ingestion, or inhalation. Ingestion and inhalation are the likely modes of biologic attack.<br /><br /><span style="font-weight: bold;">Clinical Findings </span><br /><br /><span style="font-weight: bold;">A. Symptoms and Signs </span><br />The signs and symptoms of ricin intoxication depend on the type and amount of exposure. Parenteral exposure causes necrosis of local tissues and regional lymph nodes. As the toxin spreads, visceral organs become involved, manifested as a moderate to severe gastroenteritis. Parenteral exposure is an unlikely means of biologic attack. If ricin is ingested, symptoms of gastrointestinal exposure will occur and may include nausea, vomiting, hematemesis, bloody diarrhea, melena, or visceral organ necrosis. If death occurs following parenteral or gastrointestinal exposure, it is usually secondary to circulatory collapse.<br /><br />The most likely means of biologic attack involve aerosol exposure. Inhalation of ricin is manifested by direct pulmonary toxicity. Between 4 and 8 hours after exposure, the patient may develop fever, cough, chest pain, and dyspnea. Findings consistent with an aerosol exposure include bronchitis, bronchiolitis, interstitial pneumonia, and acute respiratory distress syndrome. If death occurs, it is usually secondary to respiratory failure and generally will occur within 36-72 hours.<br /><br /><span style="font-weight: bold;">B. Laboratory and X-ray Findings </span><br />Various laboratory tests including ELISA, PCR, and immunohistochemical staining may aid in the diagnosis of ricin toxicity. In the event of pulmonary involvement, chest x-ray may display bilateral infiltrates or noncardiogenic pulmonary edema.<br /><br /><span style="font-weight: bold;">Treatment & Prophylaxis </span><br /><br />The treatment of ricin toxicity depends largely on the mode of exposure.<br /><br /><span style="font-weight: bold;">A. Parenteral Exposure </span><br />With parenteral exposure, treatment is largely supportive.<br /><br /><span style="font-weight: bold;">B. Gastrointestinal Exposure </span><br />The treatment of gastrointestinal exposure primarily involves the elimination of toxin. This can be accomplished by vigorous gastric lavage and by the use of cathartics such as magnesium citrate or whole bowel irrigation. Activated charcoal may be considered. Correct electrolyte abnormalities, and maintain adequate volume status. Treat secondary bacterial infections with appropriate antibiotics.<br /><br /><span style="font-weight: bold;">C. Pulmonary Exposure </span><br />With pulmonary exposure, treatment involves providing adequate ventilatory support. Patients may require oxygen, intubation, and ventilator management. Treat secondary bacterial infections with appropriate antibiotics.<br /><br /><span style="font-weight: bold;">D. Prophylaxis </span><br />Ricin vaccines are under development.<br /><br /><span style="font-weight: bold;">Infection Control </span><br /><br />Ricin intoxication is not spread by person-to-person contact. Standard precautions are sufficient during patient care activities (see Table 3-2).<br /><br /><span style="font-weight: bold;">3. T-2 Mycotoxins </span><br /><br />Like penicillin, mycotoxins are a diverse group of compounds produced by fungi for environmental protection. These compounds are frequently toxic to many animal species including humans. The T-2 mycotoxins are a particular group of compounds produced by fungi in the genus Fusarium. Although the actions of the T-2 mycotoxins are not completely understood, they are known to inhibit DNA and protein synthesis. They are most toxic to rapidly dividing cell lines.<br /><br />Many properties of these compounds make them attractive as biologic weapons. Specifically, they are resistant to destruction by ultraviolet radiation and are heat stabile. T-2 mycotoxins confer toxicity after ingestion, inhalation, or dermal exposure. Unlike most other biologic agents, they can be absorbed directly though the skin.<br /><br /><span style="font-weight: bold;">Clinical Findings </span><br /><br /><span style="font-weight: bold;">A. Symptoms and Signs </span><br />With T-2 mycotoxin exposure, contamination via dermal, gastrointestinal, and pulmonary routes may occur simultaneously. The earliest symptoms and signs may begin within minutes to hours. Dermal exposure may be manifest as skin pain, erythema, blistering, and skin necrosis. Toxin exposure to the eyes and upper airway may cause ocular pain, redness, tearing, sneezing, rhinorrhea, oral pain, blood-tinged mucus, and epistaxis. Patients with pulmonary involvement will display chest pain, cough, and dyspnea. Signs and symptoms of gastrointestinal toxicity include abdominal pain, nausea, vomiting, and a bloody diarrhea. With systemic toxicity, patients may develop weakness, dizziness, and ataxia. Similar to radiation exposure, these toxins may also cause bone marrow suppression resulting in thrombocytopenia and neutropenia.<br /><br /><span style="font-weight: bold;">B. Laboratory and X-ray Findings </span><br />Two primary forms of laboratory testing may be used to identify T-2 mycotoxins. First, antigen detection can be performed on urine samples. The metabolites of the T-2 mycotoxins are eliminated primarily in the urine and feces. These metabolites are detectable in the urine up to 1 month after exposure. Second, mass spectrometric evaluation can be conducted on various body fluids. Appropriate samples include nasal secretions, pulmonary secretions, urine, blood, and stomach contents.<br /><br /><span style="font-weight: bold;">Treatment & Prophylaxis </span><br /><br /><span style="font-weight: bold;">A. Specific Therapy </span><br />The treatment of T-2 mycotoxin poisoning is essentially supportive care. Remove all contaminated clothing, and wash the patient's skin with large amounts of soap and water. Treat dermal burns with standard therapy. Treat secondary bacterial infections with appropriate antibiotics. Ocular involvement requires irrigation with water or sterile saline. Activated charcoal may aid in gastrointestinal decontamination. Patients with pulmonary involvement may require advanced respiratory techniques such as intubation or ventilatory support.<br /><br /><span style="font-weight: bold;">B. Prophylaxis </span><br />Vaccines against the T-2 mycotoxins are under study. The early use of soap and water may prevent skin toxicity.<br /><br /><span style="font-weight: bold;">Infection Control </span><br /><br />The T-2 mycotoxins are dispersed as an oily liquid. Contact with this liquid may cause cross contamination. Therefore, remove all contaminated clothing and wash the patient's skin with soap and water. Standard precautions are sufficient during patient care activities (see Table 3-2).<br /><br /><span style="font-weight: bold;">4. Staphylococcal Enterotoxin B </span><br /><br />Staphylococcal aureus produces a number of exotoxins that produce disease in humans. One such exotoxin, staphylococcal enterotoxin B (SEB), is a causal agent of the gastrointestinal symptoms seen in staphylococcal food poisoning. It is a heat-stabile toxin that belongs to a group of compounds known as super antigens. These compounds have the ability to activate certain cells in the immune system, causing a severe inflammatory response. This response causes injury to various host tissues. Aside from injury caused by SEB in natural infections, it can be aerosolized, making it a potential biologic weapon. Biologic attack could involve deliberate contamination of foodstuffs, although a more likely scenario would involve an aerosol release.<br /><br /><span style="font-weight: bold;">Clinical Findings </span><br /><br /><span style="font-weight: bold;">A. Symptoms and Signs </span><br />After exposure to SEB, a variable incubation period occurs, ranging from 4 to 10 hours for gastrointestinal exposure and from 3 to 12 hours for inhalational exposure. Regardless of the type of exposure, nonspecific symptoms and signs will develop and include fever, chills, headache, malaise, and myalgias. If the exposure occurred via the gastrointestinal route, then patients will also develop nausea, vomiting, and diarrhea. Conversely, if the exposure occurred via an inhalational route, the patient will also develop chest pain, cough, and dyspnea. Death is rare but in severe cases may occur from respiratory failure. Patients generally recover from symptoms after 1-2 weeks.<br /><br /><span style="font-weight: bold;">B. Laboratory and X-ray Findings </span><br />The presence of SEB can be confirmed by identifying specific antigens via ELISA testing. Obtain serum and urine samples. Urine samples are more productive because toxin tends to accumulate in the urine. In the case of aerosol exposure, respiratory and nasal swabs may also demonstrate toxin if samples are obtained within 1 day of exposure. With inhalational exposure, the chest x-ray is usually normal but in severe cases may demonstrate pulmonary edema.<br /><br /><span style="font-weight: bold;">Treatment & Prophylaxis </span><br /><br /><span style="font-weight: bold;">A. Specific Therapy </span><br />The treatment of SEB exposure is largely supportive. Correct electrolyte abnormalities, and maintain volume status. If pulmonary edema develops, patients may benefit from diuretic therapy and in some cases may require intubation and ventilatory support. Steroids may be given to lessen the inflammatory response, but this approach is controversial. Treat secondary bacterial infections with appropriate antibiotics.<br /><br /><span style="font-weight: bold;">B. Prophylaxis </span><br />Vaccines against SEB are under study.<br /><br /><span style="font-weight: bold;">Infection Control </span><br /><br />Person-to-person transmission of toxin is not a hazard. Standard precautions are sufficient during patient care activities (see Table 3-2).<br /><br /><br /><br /> <span style="font-weight: bold;">CHEMICAL WEAPONS </span><br /><br />Like radiation and biologic agents, many chemicals can be developed into weapons of mass destruction. Chemical weapons are particularly attractive to rogue governments and terrorist organizations because of their low cost, stability, and ease of production. In fact, chemical agents have already been used by terrorist organizations. The terrorist group Aum Shinrikyo released sarin gas in a Japan subway in 1995. Chemical agents can be delivered as liquids, vapors, or as components of explosive devices. Chemical agents are generally categorized as nerve agents, pulmonary agents, vesicants, and cyanide agents.<br /><br /><span style="font-weight: bold;">NERVE AGENTS </span><br /><br />The nerve agents are a diverse group of compounds that were developed by the Germans prior to World War II. An agent known as GA (tabun) was the first nerve agent produced, followed by several others including GB (sarin), GD (soman), GF, and VX. Each of these agents has different physical characteristics, of which volatility is the most critical. The G agents are more volatile than VX; as a result, the G agents form a vapor more readily.<br /><br />These agents are classified as organophosphates and induce toxicity by binding to and inhibiting various forms of the acetylcholine esterase enzyme. This causes increased levels of acetylcholine, leading to hyperstimulation of both central and peripheral muscarinic and nicotinic receptors. The stimulation of these receptors causes the clinical syndromes consistent with nerve agent toxicity. Toxicity can occur either from skin contact or from vapor exposure. Given their increased volatility, the G agents are more prone to cause vapor exposure.<br /><br /><span style="font-weight: bold;">Clinical Findings </span><br /><br /><span style="font-weight: bold;">A. Symptoms and Signs </span><br /><span style="font-weight: bold;">1. Latent period</span>—When nerve agent exposure occurs as a vapor, there is generally no significant latent period and symptoms will develop within minutes. Likewise, the clinical effects of vapor exposure do not tend to progress over time. In contrast, liquid contamination may have a significant latent period depending on the amount of skin exposure. With small exposures, latent periods of up to 18 hours may be seen. Further, with liquid contact, symptoms and signs may progress over a period of time.<br /><br /><span style="font-weight: bold;">2. Clinical syndromes</span>—The findings that will develop following nerve agent poisoning depend on the amount and type of exposure. As the degree of exposure increases, so does the severity of symptoms. The general clinical syndromes of nerve agent toxicity are as follows:<br /><br /><span style="font-weight: bold;">a. Central nervous system</span>—The effects on the central nervous system may range from mild to severe depending on the degree of exposure. Mild symptoms and signs include mood swings, difficulty concentrating, poor judgment, and sleep disturbances. With more significant exposures, coma, convulsions, and apnea may occur.<br /><br /><span style="font-weight: bold;">b. Peripheral nicotinic stimulation</span>—The symptoms and signs of peripheral nicotinic receptor stimulation are manifest primarily as alterations in skeletal muscle functioning. The degree of involvement depends on the degree of exposure. Initially muscle fasciculations or weakness will occur and may eventually progress to paralysis.<br /><br /><span style="font-weight: bold;">c. Peripheral muscarinic stimulation</span>—The symptoms and signs of peripheral muscarinic receptor stimulation are manifest primarily as increased exocrine gland and smooth muscle activity. Typical symptoms and signs of exocrine gland stimulation include rhinorrhea, salivation, sweating, increased gastrointestinal secretions, and increased pulmonary secretions. Increased pulmonary secretions may be severe enough to compromise the patient's airway. Increased smooth muscle activity will cause vomiting, diarrhea, increased urination, and abdominal pain.<br /><br /><span style="font-weight: bold;">B. Laboratory and X-ray Findings </span><br />Acetylcholine esterase exists in various tissues within the body. Two important subpopulations of acetylcholine esterase are the plasma cholinesterase and the erythrocyte cholinesterase. Decreased activity within either population may indicate nerve agent exposure. Of the two forms, the erythrocyte cholinesterase is the more sensitive indicator of exposure.<br /><br /><span style="font-weight: bold;">Treatment </span><br /><br /><span style="font-weight: bold;">A. Specific Therapy </span><br />The treatment of nerve agent toxicity involves the use of 3 primary medications. The first, atropine, is an anticholinergic medication used to counteract the hyperstimulation of peripheral muscarinic receptors. Atropine (1-2 mg intravenously; if no effect, double dose every 5 minutes until secretions dry) should generally be given until secretions begin to dry. Atropine will not prevent central nervous system or nicotinic toxicity. In contrast, pralidoxime chloride (2-PAM), 1-2 g intravenously given over 15-30 minutes, ameliorates nicotinic toxicity by breaking the bond formed between the nerve agent and the esterase enzyme. The nerve agent-esterase bond may be broken as long as the compound has not aged, a process by which the bond becomes irreversible. For most of the nerve agents, the aging process is not clinically significant. One notable exception is GD (soman), which ages after only 2 minutes and is refractory to 2-PAM therapy. Finally, a common complication of severe intoxication is seizure activity. Seizures may be treated with benzodiazepines.<br /><br /><span style="font-weight: bold;">B. Supportive Care </span><br />Patients may require intensive medical support such as airway management and ventilatory support. Frequent suctioning of secretions may also be required.<br /><br /><span style="font-weight: bold;">Decontamination </span><br /><br />For more specific information on decontamination, see Chemical Decontamination, below.<br /><br /><span style="font-weight: bold;">PULMONARY AGENTS </span><br /><br />Many different chemicals can be classified as pulmonary or lung agents. All have a similar mechanism of toxicity, producing delayed onset of pulmonary edema. Of these agents, carbonyl chloride (phosgene) has been the most studied. Because phosgene is the prototypical lung agent, most of the discussion here relates to phosgene; however, the principles of management can be applied to all lung agents. As a military agent, phosgene was first used during World War I and today can be found in numerous industrial applications. Because of its high volatility, phosgene forms a gas readily, often with the faint scent of freshly cut hay. It is not absorbed through the skin, but when inhaled, it causes toxicity. After inhalation, phosgene is deposited in the peripheral airways, where it undergoes acetylation reactions. Subsequent damage to the alveolar-capillary membrane will occur, resulting in pulmonary edema. Phosgene may also interact with mucous membranes, causing local irritation.<br /><br /><span style="font-weight: bold;">Clinical Findings </span><br /><br /><span style="font-weight: bold;">A. Symptoms and Signs </span><br />As noted previously, the primary effect of phosgene involves lung toxicity, although with some exposures, patients may have transient irritation to the eyes, nose, and mouth. In some cases, rhinorrhea and oral secretions may be significant. Patients may also complain of mild chest discomfort and cough secondary to bronchial irritation. In significant exposures, early death may occur secondary to laryngeal spasm. Despite these early effects, most of the toxicity of phosgene exposure is delayed. After inhalation, a variable latent period of up to 24 hours will ensue. The length of the latent period depends on the dose of phosgene delivered and will be shorter with higher exposures. Eventually the patient may develop symptoms and signs consistent with pulmonary edema, including dyspnea, hypoxia, chest pain, and cough. In some cases, pulmonary edema may be severe enough to cause hypotension. The degree to which each patient is affected depends on the severity of exposure. In severe exposures, death may occur.<br /><br /><span style="font-weight: bold;">B. Laboratory and X-ray Findings </span><br />No clinical test exists for the diagnosis of phosgene exposure. Appropriate studies such as arterial blood gas measurements and chest x-ray should be used to manage pulmonary edema. Hemoconcentration secondary to pulmonary edema may also be evident.<br /><br /><span style="font-weight: bold;">Treatment </span><br /><br /><span style="font-weight: bold;">A. Bed Rest </span><br />Any activity, even walking, may increase the severity of pulmonary edema. As a result, discourage patients from any physical activity.<br /><br /><span style="font-weight: bold;">B. Upper Respiratory Symptoms </span><br />In some cases, upper airway secretions may be significant. Nasal, oral, or bronchial secretions should be suctioned, if needed. If bronchospasm develops, it may be treated with intravenous steroids and inhaled bronchodilators. Treat secondary bacterial infections with appropriate antibiotics.<br /><br /><span style="font-weight: bold;">C. Lower Airway Symptoms </span><br />If pulmonary edema develops, it should be managed with standard medical interventions including supplemental oxygen, intubation, and ventilator management. Positive end-expiratory pressure is a useful ventilator adjunct. Treat secondary bacterial infection with antibiotics.<br /><br /><span style="font-weight: bold;">D. Hypotension </span><br />Secondary hypotension may develop in the event of severe pulmonary edema. Treatment of hypotension is problematic, given the increased permeability of the alveolar-capillary membrane. Supplemental crystalloid or colloid solutions can be used but may worsen pulmonary edema. Vasopressor agents such as dopamine may also be used.<br /><br /><span style="font-weight: bold;">Decontamination </span><br /><br />No specific decontamination is required except removing the patient from the phosgene gas.<br /><br /><span style="font-weight: bold;">VESICANTS </span><br /><br />Vesicants are a group of related compounds known to cause skin lesions, primarily blisters. Despite their predilection for skin involvement, multiple systemic effects are also seen. Although multiple agents may be used as vesicants, sulfur mustard and lewisite are the most common.<br /><br /><span style="font-weight: bold;">1. Sulfur Mustard </span><br /><br />Sulfur mustard (mustard) was first used as a chemical weapon during World War I. Mustard is a lipophilic compound that is readily absorbed through intact skin. It causes significant dermal toxicity and after systemic absorption will affect various body systems. Exposure can occur after contact with mustard vapor or liquid. At different ambient temperatures, mustard may exist in either form. It displays a characteristic odor of garlic or mustard, hence, its name. The exact mechanism of mustard toxicity is not known but appears to involve DNA alkylation. Mustard also displays mild cholinergic activity. After systemic absorption, cell lines undergoing active mitosis are affected the most.<br /><br /><span style="font-weight: bold;">Clinical Findings </span><br /><br /><span style="font-weight: bold;">A. Symptoms and Signs </span><br />The symptoms and signs of mustard toxicity depend on the dose and mechanism of exposure. Unfortunately, initial mustard exposure is not symptomatic, and the patient may be unaware of contamination. Given the initial lack of symptoms, patients may not decontaminate, thus increasing toxicity. Depending on the dose, the latent period after exposure may range from 2 to 48 hours. In mild exposures, patients may display only mild dermal injury; in severe exposures, death may occur within hours. The specific symptoms and signs of mustard toxicity depend on the body areas exposed and the degree of systemic absorption. As noted, the skin is typically affected and will display areas of erythema, burning, and blister formation. The blisters may become large and express a clear to straw-colored fluid. The fluid does not contain mustard agent.<br /><br />The eyes are one of the organs most sensitive to mustard exposure and may develop symptoms and signs first. Following ocular exposure, ocular pain, photophobia, conjunctivitis, and blepharospasm may occur. The superficial layers of the cornea may be denuded, leading to corneal clouding with visual changes.<br /><br />With injury to the respiratory tree, patients may develop oronasal burning, rhinorrhea, sore throat, or epistaxis. In more severe exposures, findings of cough, dyspnea, mucous membrane necrosis, airway muscular damage, pulmonary edema, and respiratory failure may be seen. Symptoms and signs of gastrointestinal exposure may result either from the direct toxicity of mustard exposure or from mustard's cholinergic affects. Nausea, vomiting, diarrhea, and constipation are common findings.<br /><br />Severe mustard exposure may also affect the central nervous system; mental status changes and seizure activity are the most common findings. Given mustard's interference with DNA activity, delayed findings of bone marrow suppression may also occur.<br /><br /><span style="font-weight: bold;">B. Laboratory and X-ray Findings </span><br />With exposure to mustard, an early leukocytosis is typical. If bone marrow suppression develops, later findings of anemia, leukopenia, and thrombocytopenia may be seen. If wound or pulmonary secretions become more purulent, a secondary bacterial infection should be suspected and Gram stain and culture obtained. Gastrointestinal symptoms may require electrolyte monitoring. The primary metabolite of mustard agent thiodiglycol may be detected in the urine in contaminated patients. Such specialized testing usually can be conducted only at reference or military laboratories. In the event of pulmonary involvement, chest x-ray may demonstrate a focal or diffuse pneumonitis and occasionally pulmonary edema.<br /><br /><span style="font-weight: bold;">Treatment </span><br /><br /><span style="font-weight: bold;">A. Decontamination </span><br />The most critical aspect in the treatment of mustard toxicity is removal of the chemical agent. This is problematic given the initial lack of symptoms. Even delayed decontamination, however, may lessen subsequent toxicity. Washing contaminated areas with either large amounts of soapy water or 0.5% hypochlorite solution is the preferred method of decontamination. For more specific information on decontamination, see Chemical Decontamination, below.<br /><br /><span style="font-weight: bold;">B. Specific Therapy </span><br />With skin injuries, leave small blisters intact and unroof larger lesions. Clean unroofed areas frequently and cover them with antibiotic cream (Polysporin, silver sulfadiazine). Treat other irritated areas of skin with systemic analgesics or topical lotions. With ocular exposure, use topical antibiotics to prevent secondary bacterial infections. Topical anticholinergics may prevent the discomfort of ciliary spasm. With pulmonary involvement, treat associated cough with typical antitussive medications. Treat episodes of bronchospasm with systemic steroids and inhaled bronchodilators. Treat secondary bacterial infection with appropriate antibiotics. Supplemental oxygen, intubation, or ventilator management may be required in some patients. Typical gastrointestinal antispasmodics may ameliorate the symptoms of gastrointestinal exposure. Bone marrow transplant, growth factor utilization, or factor replacement are alternatives for the treatment of bone marrow suppression.<br /><br /><span style="font-weight: bold;">Decontamination </span><br /><br />As noted above, toxin can be removed by washing contaminated surfaces with large amounts of soapy water or 0.5% hypochlorite solution. For more specific information on decontamination, see Chemical Decontamination, below.<br /><br /><span style="font-weight: bold;">2. Lewisite </span><br /><br />Much like sulfur mustard, exposure to lewisite causes injury to contaminated body surfaces and may lead to systemic symptoms. Unlike mustard, however, lewisite exposure causes symptoms and signs without a significant latent period. Lewisite is a volatile agent with the odor of geraniums. Its exact mechanism of action is unknown, but it is thought that the arsenic component of lewisite may inhibit various enzymes.<br /><br /><span style="font-weight: bold;">Clinical Findings </span><br /><br /><span style="font-weight: bold;">A. Symptoms and Signs </span><br />As noted above, the symptoms and signs of lewisite exposure begin without a significant latent period. Even though findings of exposure begin early, it may take several hours for symptoms to fully develop. The severity of clinical findings depends on the degree and method of exposure. Shortly after skin exposure, an area of dead skin will develop that will subsequently blister. These lesions may take up to 18 hours to fully develop. Skin necrosis may also be evident. Symptoms and signs of ocular exposure are similar to those associated with mustard toxicity and include conjunctivitis, iritis, edema, ocular pain, and corneal injury. If pulmonary toxicity develops, findings of cough, dyspnea, and pulmonary edema may occur. Lewisite causes increases in vascular permeability that may lead to third spacing of fluid with subsequent hypotension. In some cases, gastrointestinal, renal, and liver involvement may be seen.<br /><br /><span style="font-weight: bold;">B. Laboratory and X-ray Findings </span><br />No specific test for lewisite exposure is currently available.<br /><br /><span style="font-weight: bold;">Treatment </span><br /><br /><span style="font-weight: bold;">A. Decontamination </span><br />As with mustard exposure, the cornerstone of treatment involves early decontamination. Compared with mustard exposure, decontamination is usually more successful with lewisite exposure, given the early onset of symptoms. Standard washing with soap and water or 0.5% hypochlorite solution is sufficient.<br /><br /><span style="font-weight: bold;">B. Supportive Care </span><br />Patients may require intensive medical support such as airway management, hemodynamic support, and various measures to manage multisystem organ failure.<br /><br /><span style="font-weight: bold;">C. Specific Therapy </span><br />British anti-lewisite (dimercaprol), 2-3 mg/kg every 4 hours, is a compound that can be given intramuscularly to decrease the effects of lewisite exposure.<br /><br /><span style="font-weight: bold;">Decontamination </span><br /><br />As noted above, the toxin can be removed by washing contaminated surfaces with large amounts of soapy water or 0.5% hypochlorite solution. For more specific information on decontamination, see Chemical Decontamination, below.<br /><br /><span style="font-weight: bold;">CYANIDE AGENTS </span><br /><br />Historically, cyanide was classified as a blood agent. This classification is somewhat inappropriate because many other chemical agents exert their effects after being distributed within the vascular system. Nevertheless, this classification is still used occasionally. Once cyanide is absorbed, it distributes rapidly throughout the body. It has a high affinity for trivalent iron compounds and will bond to the cytochrome a3 complex within the mitochondria. The cytochrome a3-cyanide bond effectively blocks aerobic cellular respiration, and anaerobic metabolism ensues. Cyanide exposure most often occurs naturally after inhalation of smoke from burning synthetic materials. In a biologic attack, cyanide exposure would likely follow an aerosol release. Cyanide gas is known to exhibit the scent of bitter almonds.<br /><br /><span style="font-weight: bold;">Clinical Findings </span><br /><br /><span style="font-weight: bold;">A. Symptoms and Signs </span><br />After inhalation of cyanide gas, the cytochrome a3 enzyme is effectively blocked. Because cells can no longer utilize oxygen, they will convert to anaerobic metabolism, leading to a lactic acidosis. This inability to utilize oxygen effectively smothers the patient. Tachycardia, hypertension, and tachypnea will be seen initially. As symptoms and signs progress, anxiety, mental status changes, coma, seizures, cardiac arrest, and death will occur. Because cyanide does not alter oxygen-hemoglobin saturation, cyanosis will not develop. In fact, the inability to utilize oxygen increases the venous oxygen saturation, leading to a cherry red appearance to the skin. It generally takes 6-8 minutes for death to occur following cyanide exposure.<br /><br /><span style="font-weight: bold;">B. Laboratory and X-ray Findings </span><br />An elevated blood cyanide concentration confirms the diagnosis. Given the short time interval to death, such testing is not useful in the acute setting but may later confirm the diagnosis. Two rapid tests, an elevated venous blood oxygen saturation and an increased lactic acid level, are characteristic of cyanide poisoning.<br /><br /><span style="font-weight: bold;">Treatment </span><br /><br /><span style="font-weight: bold;">A. Specific Therapy </span><br />In addition to cyanide's affinity for certain iron compounds, it also has a high affinity for sulfhydryl groups and for the methemoglobin complex. These 2 characteristics are the basis of the cyanide antidote kit. The kit contains 3 components: amyl nitrite (used if no vascular access is available), sodium nitrite, and sodium thiosulfate. First, the patient is given a nitrite compound (inhalation of an amyl nitrate ampule or sodium nitrite), which will cause the formation of methemoglobin. The dose of sodium nitrite is based on the patient's weight and hemoglobin concentration although 300 mg IV is the usual dose for non-anemic adults. Given the high affinity of methemoglobin for cyanide, it will preferentially bind the compound and help to remove it from the cytochrome a3 complex. Second, the patient is given sodium thiosulfate, (typically 12.5 g IV for an adult), which interacts with cyanide, forming thiocyanate. Thiocyanate is then excreted in the urine.<br /><br /><span style="font-weight: bold;">B. Supportive Measures </span><br />Severe lactic acidosis may be treated with bicarbonate administration. Seizures may be treated with benzodiazepines. In many cases, patients require intubation and ventilator support.<br /><br /><span style="font-weight: bold;">Decontamination </span><br /><br />The only effective mode of decontamination involves removing the patient from the cyanide gas.<br /><br /><span style="font-weight: bold;">CHEMICAL DECONTAMINATION </span><br /><br />Because of the risk of cross contamination to health care workers, the need for patient decontamination should be emphasized. All patients suspected of experiencing a chemical weapons attack should be decontaminated as soon as possible. Optimally, patient decontamination should be conducted in the field. Often this is not practical, and a decontamination station should be established in a secure location adjacent to the health care facility. All persons conducting decontamination duties should be provided adequate protective clothing and should receive specialized training.<br /><br />Decontamination involves physical removal of toxin and chemical deactivation of toxin. The physical removal of toxin is usually the most effective means of decontamination in the acute setting. Remove all clothing, jewelry, dressings, and splints. Wash the patient with copious amounts of soap and water. Avoid vigorous scrubbing because this may facilitate toxin absorption.<br /><br />After physical removal of toxin, any remaining toxin can be chemically deactivated. This may take some time and thus is considered secondary to physical removal of toxin. The most common neutralizing solution is 0.5% hypochlorite solution, which detoxifies many chemical agents via oxidation reactions. Hypochlorite solution should not be used to decontaminate open peritoneal wounds, open chest wounds, exposed neural tissue, or ocular tissue. Irrigate these areas with copious amounts of normal saline. All contaminated materials should be bagged and sent for proper disposal.<br /><br /></div>Emergency Medicinehttp://www.blogger.com/profile/06606398346130594987noreply@blogger.com0tag:blogger.com,1999:blog-3749884089415516879.post-90528854528811795802008-08-16T08:45:00.000-07:002008-08-16T09:01:48.042-07:00Prehospital Emergency Medical Services<div style="text-align: justify;"><span style="font-weight: bold;">INTRODUCTION</span><br /><br />1This chapter is a revision of the chapter by Charles E. Saunders, MD, FACEP, & Thomas Hearne, PhD, from the 4th edition.<br /><br />The delivery of effective, organized, prehospital emergency medical services (EMS) is a development that dates to the 1960s in the United States. Although there were ambulance providers and even some local systems, there was no national approach to prehospital care until publication of the 1966 White Paper entitled "Accidental Death and Disability—The Neglected Disease of Modern Society" (National Academy of Sciences, National Research Council).<br /><br />When medical emergencies are reported, trained medical personnel arrive on the scene to provide emergency care within 6-10 minutes. The skills of these personnel range from basic first aid techniques and cardiopulmonary resuscitation (CPR) to advanced life support (ALS) techniques, including defibrillation, endotracheal intubation, and the use of emergency medications. Radio communications permit ongoing discussion of patient status and treatment between emergency medical personnel at the scene and the supervising physician at the base hospital. Air ambulances (fixed-wing aircraft or helicopters staffed with medically trained flight crews) can rapidly evacuate and transport patients from a remote emergency scene to a regional medical center.<br /><br /><span style="font-weight: bold;">COMPONENTS OF THE EMERGENCY MEDICAL SERVICES SYSTEM </span><br /><br />Modern EMS systems consist of several major components: (1) professional field personnel trained to provide specific levels or types of care, (2) a comprehensive emergency communications network, (3) hospital emergency department physicians and nurses who supervise the treatment provided by EMS field personnel, (4) hospitals categorized according to their relationship with EMS field personnel and according to the level of care they can provide, and (5) EMS administrative officials who manage and coordinate the elements of the system.<br /><br /><span style="font-weight: bold;">Professional EMS Field Personnel </span><br /><br />The health professionals and first responders who provide prehospital care are trained to carry out specific levels of care, ranging from basic first aid and CPR provided by first responders, through basic life support (BLS) given by emergency medical technicians (EMTs), to the ALS provided by advanced EMTs (paramedics). These personnel provide care only as extensions or agents of physicians and are not independently licensed to provide medical care. The care they deliver is authorized by standing orders (written authorization to administer certain treatments without prior attempt at base contact by radio) or protocols from physician directors or by orders transmitted by radio from supervisory physicians at the base hospital to EMS personnel at the scene. A critical element in the development of EMS since 1970 has been the recognition that personnel without prior medical training can be prepared through relatively short courses to provide effective prehospital care. The designations, levels of training, and skills of EMS personnel are now largely standardized according to United States Department of Transportation (DOT) curriculum and formal categories established in 1983 by the National Registry of Emergency Medical Technicians. The curriculum is regularly reviewed and updated to reflect changes in medicine and in the prehospital environment. The latest iteration released by the DOT was in 1998, with some modifications in 2000. Types of EMS field personnel and their training are described below and summarized in Table 2-1.<br /><br /><span style="font-weight: bold;">A. First Responders </span><br />First responders may include law enforcement officers, rescue squad members, firefighters, or volunteer EMS personnel. First-responder courses usually consist of about 40 hours of classroom instruction and clinical training in basic first aid and CPR. First responders are equipped with basic emergency care equipment (eg, bandages, dressings, tape, blanket and pillow, upper and lower extremity splint sets). Oxygen equipment and a self-refilling bag-valve-mask combination (eg, Ambu bag) are optional. First responders also carry basic tools to help them reach and extricate trapped individuals. Increasingly, first responders are being trained and equipped to perform defibrillation using automated external defibrillators (AEDs).<br /><br /><span style="font-weight: bold;">B. Emergency Medical Technicians (EMTs) </span><br />The National Registry of Emergency Medical Technicians currently recognizes 3 formal grades of EMTs according to the typical number of hours of training given, the breadth of skills covered, and the range of procedures authorized: EMT-A (basic), EMT-I (intermediate), and EMT-P (advanced, paramedic). Designations and levels of training may vary from state to state. Emergency physicians should be familiar with regional variations and deviations from the National Registry guidelines.<br /><br /><span style="font-weight: bold;">1. EMT-A</span>—Basic EMTs constitute the essential workforce of EMS systems throughout the United States. Most state laws require at least one certified EMT on board ambulance vehicles that transport patients.<br /><br />The basic EMT course requires at least 81 hours of training standardized by the DOT. Basic classes frequently exceed this minimum by up to 140 hours. Students learn basic principles of patient care, how to identify signs and symptoms central to patient assessment and diagnosis, and how to provide treatment in specific emergencies. The use of AEDs is now standard curriculum for EMTs in most regions. Optional modules for EMTs include advanced airway management, intravenous access, and assisting patients with self-administration of medications. Additionally, some states allow administration of medications, including epinephrine in anaphylaxis and aspirin in suspected cardiac chest pain.<br /><br /><span style="font-weight: bold;">2. EMT-I</span>—The intermediate EMT is trained to provide a level of advanced care in areas that are underserved by paramedics. The scope of practice has evolved since 1990 to incorporate many advanced cardiac life support procedures, including cardiac monitoring, treatment of arrhythmias, defibrillation, and advanced airway management with either endotracheal intubation or an alternative airway.<br /><br /><span style="font-weight: bold;">3. EMT-P</span>—Advanced EMTs (paramedics) receive over 1000 hours of training in ALS techniques. Their skills include the basic EMT procedures as well as intravenous cannulation, invasive airway management (including endotracheal intubation), recognition of cardiac dysrhythmias, defibrillation, and the use of specific emergency medications. In addition to extensive classroom training, EMT-P personnel also complete clinical training and a field internship with experienced paramedic teams.<br /><br />Paramedics operate under standing orders and treatment protocols developed by a physician medical director that are usually broader and more advanced than those guiding basic EMTs. These protocols determine the type and level of care administered at the emergency site. Physicians who provide on-line medical supervision of paramedics (by radio and telemetry) from base hospitals may permit paramedics to deviate from established protocols or to provide treatment not specifically covered in standing orders.<br /><br /><span style="font-weight: bold;">Special Qualifications </span><br /><br />Additional training is available at all levels of providers for specific care settings. At the first responder level, a Winter Emergency Care course has been developed for the National Ski Patrol to address special situations that occur in ski areas. Similarly there are Wilderness modules at all levels of training that provide additional training for care provided in a remote setting with anticipated long evacuations and transportation. EMT-Tactical courses train EMTs and paramedics to function in a tactical law enforcement situation in which they may support or be part of a police special tactics teams. Finally, Paramedic-Critical Care training enables the advanced provider to provide care to critically injured or ill patients who are being transferred from one facility to another.<br /><br /><span style="font-weight: bold;">Types of EMS Systems </span><br /><br />EMS systems can be delivered in various ways. There are 2 basic forms of EMS response: a single-response system and a layered-response (or tiered-response) system. In a single-response system, there is only one grade of EMS unit, and the closest available unit is dispatched to any nearby emergency. In a layered-response system, 2 or more grades of EMS personnel respond hierarchically (eg, first responder, then EMT-A, then EMT-P) as needed. Layered-response systems usually provide for an EMT-A response for all less severe reported medical emergencies, reserving an EMT-P response for severe or life-threatening incidents (Table 2-2).<br /><br /><span style="font-weight: bold;">Communications Network </span><br /><br />The communications network is important in tying together the components of an EMS system. A dispatcher at a communications center receives a telephone request from a caller at the site of the emergency and dispatches mobile EMS personnel via the radio network. Dispatchers may use a call triaging system (eg, Priority Medical Dispatching) to assign resources to a call. In many areas of the United States, an easily remembered emergency telephone number (9-1-1) provides the public with rapid access to the communications center. Many systems offer an "enhanced 9-1-1" service that provides immediate callback and location information to the dispatcher.<br /><br />Communications between the EMS unit and medical facilities varies from region to region. For many BLS transports, contact with the base station or receiving facility is not required. In the event of an ALS transport, contact must be made with a medical facility. In some areas, the facility is called a base station hospital, which provides on-line direction and supervision for an entire EMS region. Information called into the base station hospital is then relayed to the receiving facility. In other areas, the receiving facility is called directly.<br /><br /><span style="font-weight: bold;">Hospital Facilities & Staffing </span><br /><br />EMS systems typically include hospitals with a variety of treatment capabilities, ranging from local community hospitals with a limited emergency department staffing to large teaching hospitals in urban areas with emergency physicians, surgeons, anesthesiologists, and surgical teams available 24 hours a day. Hospital facilities are frequently classified according to their relationship to EMS mobile units and their ability to provide definitive care.<br /><br /><span style="font-weight: bold;">A. Base Station Hospitals </span><br />Physicians or specially trained nurses with physician backup in the emergency department of the base station hospital provide EMS units with on-line medical supervision during treatment. EMS units may be housed at the base station hospital, but this may not be necessary or feasible because the units are usually strategically deployed in the hospital's service area. In many EMS systems, the base station hospital may also be the one most capable of providing definitive follow-up care.<br /><br /><span style="font-weight: bold;">B. Receiving Hospitals </span><br />Receiving hospitals are facilities to which patients may be transported. For each patient, the receiving hospital is selected according to its proximity; its capability to provide definitive care; and the preference of the patient, family members, or family physician, as long as transport to the hospital does not draw the EMS unit away from its primary service area.<br /><br /><span style="font-weight: bold;">C. Hospitals Categorized by Capability </span><br />Hospitals may be categorized by their ability to provide acute care as determined by the availability of physicians, nurse, allied health personnel, and other hospital resources (eg, operating rooms, laboratory, blood bank). Many categorization schemes exist. The Joint Commission on Accreditation of Healthcare Organizations has established 4 levels of emergency service:<br /><br /><span style="font-weight: bold;">1. Level I</span>—This service offers emergency care 24 hours a day with at least one physician experienced in emergency care on duty in the emergency care area. In addition, there must be in-house physician coverage by residents at the senior level or higher for the medical, surgical, orthopedic, obstetric-gynecologic, pediatric, and anesthesiologic services.<br /><br /><span style="font-weight: bold;">2. Level II</span>—This service offers emergency care 24 hours a day with at least one physician experienced in emergency care on duty in the emergency care area. Specialty consultation should be available within 30 minutes.<br /><br /><span style="font-weight: bold;">3. Level III</span>—This service offers emergency care 24 hours a day with at least one physician on duty in the emergency care area available within 30 minutes through a medical staff call roster.<br /><br /><span style="font-weight: bold;">4. Level IV</span>—This service is capable of performing a triage function and can administer life-saving first aid until transportation to the nearest appropriate facility is available.<br /><br /><span style="font-weight: bold;">D. Hospitals Categorized by Areas of Care </span><br />Hospitals can also be categorized by special areas of care (eg, trauma, burns, neonatal intensive care), especially where regionalization of services in these areas is practiced. The American College of Surgeons, for example, has established the following categorization of trauma facilities:<br /><br /><span style="font-weight: bold;">1. Level I</span>—This designates a full-service trauma center that can provide optimal care of the trauma patient. One or more experienced emergency physicians, a general surgeon, anesthesiology services, laboratory, blood bank, and an operating room team must be available in-house 24 hours a day. All surgical subspecialty services should be immediately available on call. A commitment to education and research in trauma must also be demonstrated.<br /><br /><span style="font-weight: bold;">2. Level II</span>—This trauma center is similar to a level I center but does not necessarily include a commitment to education or research. Occasionally patients with the most severe injuries or those needing highly specialized care may be transferred from a level II center to a level I center.<br /><br /><span style="font-weight: bold;">3. Level III</span>—This trauma center does not have all of the resources available at a level I or level II center but may represent the highest level available in a given community. Usually, initial stabilization and life-saving procedures are performed and the patient is then transferred to a level I or level II center.<br /><br /><span style="font-weight: bold;">EMS Administration </span><br /><br />EMS systems may be administered through a variety of organizations, including local health departments, public safety agencies such as police or fire departments, hospitals, or privately owned provider agencies. Often several of these agencies operate EMS systems in the same area, and these agencies are coordinated through an EMS regional council, which interacts with hospitals, public safety agencies, and physician medical directors; sets operational standards; and monitors performance (quality assurance).<br /><br /><span style="font-weight: bold;">Operation of the EMS System </span><br /><br />One way to visualize the interplay between various components of the EMS system is to review the sequence of events surrounding a typical emergency medical incident. There are 4 major phases: (1) report of the emergency and activation of the EMS system, (2) dispatch of appropriate prehospital units, (3) medical evaluation and field treatment by EMS personnel, and (4) transport of the patient to the appropriate hospital.<br /><br /><span style="font-weight: bold;">A. Report of the Emergency </span><br />In many areas of the United States, a single, easily remembered telephone number (9-1-1) can now be used to request emergency help from the police and fire departments and to activate the EMS system.<br /><br /><span style="font-weight: bold;">B. Dispatch </span><br />Dispatchers receive the emergency call, interview the caller to determine the type and severity of the emergency, and dispatch the appropriate type of emergency medical response. In systems with heavy call volumes, calls may be priority ranked and then dispatched in order of urgency of need and resource availability. In some systems, dispatchers offer advice to callers to assist patients pending the arrival of emergency units (prearrival instructions). Algorithms may be employed to guide the dispatcher in decision making (Figure 2-1). Dispatchers in layered-response emergency medical systems frequently follow specific protocols in determining which type of EMS unit to dispatch (ie, ALS, BLS, first responder; see Table 2-2). Dispatchers may also be trained to provide CPR instructions by telephone to callers. Dispatch centers may also monitor hospital availability, manage the status and geographic deployment of EMS vehicles, and through computer-aided dispatch perform EMS management information and quality assurance functions.<br /><br /><span style="font-weight: bold;">C. Medical Evaluation and Treatment </span><br />Most EMS systems in urban and suburban areas are capable of responding within a few minutes of receiving an emergency call. First responders can frequently arrive at the scene within 3-6 minutes, and paramedics within 5-10 minutes of receiving the call. Survival following time-sensitive medical emergencies such as cardiac arrest is closely correlated with unit response time, especially when basic EMTs have been trained in defibrillation. In layered-response systems, paramedics are held in reserve for such critical or life-threatening incidents, where their advanced skills may provide definitive or stabilizing care to patients. Many systems have advanced-level first responders, such as engine companies manned with paramedics. These responders can provide the same interventions as ambulance-based paramedics but lack the means to transport patients. These assets can be additional resources in the single complex patient or in the multiple-patient incident.<br /><br />Upon arrival at the emergency scene, EMS personnel undertake patient assessment and examination. EMT-paramedics in most cases are authorized by standing orders to proceed with patient care. Following patient evaluation and treatment, the EMS unit contacts the supervising emergency medical physician (or, in some states, a nurse) at the base station hospital by radio or telephone to describe the patient's condition and any treatment undertaken. The physician may give specific instructions for further treatment at the scene or request transport to the hospital for care.<br /><br /><span style="font-weight: bold;">D. Transport </span><br />The mode of transport (ground or air, with or without sirens or lights) depends on availability, stability of the patient's condition, transport time and distance, risks, and the like. Hospital destination decisions are often guided by local protocols, with critically ill patients directed to the closest, most appropriate facility. For example, a community hospital may be bypassed in favor of the nearest designated trauma center in the case of a severely injured patient. Noncritical cases may be transported to the hospital of the patient's choice.<br /><br /><span style="font-weight: bold;">1. Ground transport</span>—Most patients are transported in surface ambulances. These vehicles vary slightly from state to state in their configuration and on-board equipment, but all follow guidelines set by the DOT. Emergency vehicle operators usually are allowed by local and state laws to violate certain traffic laws while responding to an emergency or carrying a patient in a life-threatening emergency. In the vast majority of cases, however, the patient's life is not in danger and posted speeds and traffic laws should be obeyed. The time gained in using red lights and sirens to get to the hospital is often outweighed by the additional risk of death and disability associated with rapid transport.<br /><br />In most EMS systems, the responding unit is also the transporting unit. In others, especially layered-response systems, the responding unit may primarily evaluate and stabilize the patient and may summon a lower-level unit to provide transport.<br /><br /><span style="font-weight: bold;">2. Air transport</span>—Some EMS systems and regional trauma hospitals, particularly those serving large outlying rural areas, use helicopters or fixed-wing aircraft with trained medical teams on board as additional resources for prehospital care and transportation. The majority of these aircraft are hospital based, but some are operated by municipal or state governmental agencies. Where these services are unavailable, or when search-and-rescue missions are required, aircraft equipped for medical evacuation may be sent from local military bases, operating within the Military Assistance to Safety and Traffic program.<br /><br />Air ambulances are usually integrated into the EMS system and are activated according to certain locally established criteria. The decision to transport a patient by air requires careful consideration of the risks and benefits of air versus ground transport (see below).<br /><br /><span style="font-weight: bold;">Medical Supervision </span><br /><br /><span style="font-weight: bold;">A. On-Line Medical Direction </span><br />On-line medical direction is the direction given by radio to EMS personnel at the scene while care is being provided. It is usually given by emergency physicians or nurses at the base station hospital or receiving hospital. In most systems, the use of standing orders is allowed (Figure 2-2). This approach allows treatment to begin as soon as possible. Systems that have changed over from on-line medical control to standing orders have not shown a decrement in medical care but have shown an increase in EMS provider morale.<br /><br />Even in systems that operate nearly exclusively by standing orders, some exceptions may require on-line direction. These may include cessation of CPR in a nonviable patient or the administration of restricted medications such as narcotics or paralytics. Systems that employ standing orders require effective monitoring, training, and quality assurance mechanisms.<br /><br /><span style="font-weight: bold;">B. Off-Line Medical Direction </span><br />Off-line medical direction is the overall direction of the activities of EMS personnel. It includes establishing protocols and standing orders, ensuring adequate training and skills, reviewing patient care records and voice tapes retrospectively, and reviewing performance and outcome data. Off-line medical direction is usually provided by a physician experienced in emergency services or by an agency in which physicians play an active role.<br /><br /><span style="font-weight: bold;">Performance Evaluation </span><br /><br />System performance evaluation has many aspects, including the evaluation of input resources and operating guidelines (eg, protocol validation, personnel review, training assessment), evaluation of the process of delivering care in the field (eg, response times, service volume, treatment audits for adherence to protocols), and evaluation of the outcome of prehospital care (eg, complications, complaints, success in the performance of procedures, and patient survival). Outcome data are the most difficult to obtain.<br /><br /><span style="font-weight: bold;">PREHOSPITAL SKILLS & TECHNIQUES </span><br /><br /><span style="font-weight: bold;">Field Assessment </span><br /><br />EMTs responding to a call usually have certain dispatch information, including the location, the nature of the complaint, and the number of patients. Upon arrival, they must quickly determine the presence of hazards to themselves and the patient, ascertain the probable mechanism of injury, and identify other patients, if any. Support can be summoned for hazard suppression or additional medical assistance. Patients who are conscious and in minimal distress may be able to provide historical information. Information may also be obtained from witnesses or family members.<br /><br />Patients who are very ill may require that interventions be performed simultaneously with assessment. Interventions aimed at stabilizing airway, breathing, or circulation (the ABCs) will take precedence over secondary assessment. The receiving physician should expect that, if the patient is seriously ill or injured, only life-saving measures may be performed prior to arrival. In the more stable patient, a more thorough primary and secondary survey should be performed.<br /><br /><span style="font-weight: bold;">Field Treatment </span><br /><br /><span style="font-weight: bold;">A. Airway Control </span><br />Methods of airway control depend on the EMT's level of skill and certification. Initial steps to provide an airway include positioning the jaw and suctioning secretions (taking care in the trauma victim not to hyperextend the neck). Should this fail to achieve and maintain airway patency, the basic EMT can insert an oral or nasal airway. Ventilation may be assisted by a bag-valve-mask.<br /><br />EMTs and paramedics may establish alternative airways, depending on local protocol. The Combitube, a dual lumen tube designed to be placed blindly, can be used to ventilate the patient regardless of whether the tube is placed in the esophagus or the trachea. The laryngeal mask airway (LMA) is designed to be placed without laryngoscopy. It has an inflatable cuff that sits over the glottis. This allows for ventilation while minimizing gastric insufflation and aspiration. It is not as secure an airway as the endotracheal tube. An improvement on the original LMA is the LMA-Fastrach, which allows for an endotracheal tube to be passed through the LMA. Both the Combitube and the LMA have been implemented successfully in the prehospital setting.<br /><br />Endotracheal intubation is the preferred method of airway control in patients with inadequate ventilation. Typically the success rate for prehospital intubation is greater than 90%. However, two recent papers have questioned the value of intubation in the field. A randomized trial involving pediatric intubation found that patients did as well with bag-valve-mask ventilation as they did with intubation. Another study found that over 25% of adult intubations in the prehospital setting were misplaced. When intubation is performed in the field it is suggested that end-tidal CO2 detection and an esophageal detector device be used in addition to more conventional means of confirming location. After the tube is confirmed in the correct location, the risk of dislodgement should be minimized by using a commercial endotracheal tube holder and by securing the patient in a cervical collar and to a long spinal board.<br /><br /><span style="font-weight: bold;">B. Emergency Cardiac Care </span><br /><span style="font-weight: bold;">1. Cardiopulmonary resuscitation</span>—The probability of survival for victims of sudden cardiac arrest is inversely related to the elapsed time before an effective cardiac rhythm is reestablished. CPR is a temporizing measure that, when initiated within 4-6 minutes, increases the chances of survival. In most systems, a paramedic unit cannot routinely reach the scene within this period. Many systems provide first responders with AEDs. AEDs have been successfully deployed with police and fire first responders. In addition, public access defibrillators provide AEDs to the public at busy venues such as sporting arenas and airports.<br /><br /><span style="font-weight: bold;">2. Defibrillation</span>—Ventricular fibrillation is the initial rhythm encountered in many victims of sudden death. The sooner defibrillation is performed, the higher the survival rate. AEDs (Laerdal Heartstart 2000, others) can recognize ventricular fibrillation (or tachycardia) and deliver a countershock. The rescuer need not be able to recognize dysrhythmias but must be able to recognize cardiac arrest and operate the device. AEDs have enabled nonparamedic first responders to provide rapid defibrillation and have consequently improved survival rates.<br /><br /><span style="font-weight: bold;">3. Electrocardiography</span>—In the treatment of acute coronary syndromes, the prehospital 12-lead electrocardiogram (ECG) significantly shortens the time from arrival in the emergency department to administration of thrombolytic therapy ("door to drug time"). Prehospital fibrinolytic therapy has had mixed results. In European trials, where prehospital care is typically provided by physician-staffed ambulances, 6-month and 1-year survival rates have increased. However, trials in the United States with paramedic-staffed units has not shown a significant improvement over 12-lead ECG in the field with hospital-administered fibrinolytics.<br /><br /><span style="font-weight: bold;">C. Invasive Procedures </span><br /><span style="font-weight: bold;">1. Venous catheterization</span>—(See Chapter 6.) The use of intravenous techniques by EMS field personnel is usually limited to cannulation of peripheral veins of the upper extremities. In most EMS systems, the procedure can be initiated under standing order by intermediate or paramedic EMTs. Basic EMTs who have had special training in intravenous techniques and fluid therapy may also initiate intravenous lines. Studies have demonstrated that skilled paramedics in the field are able to start an intravenous line in approximately 3 minutes and achieve a success rate greater than 90%. However, when transport times are short (ie, 10 minutes or less), venous catheterization is usually unnecessary because the volume of fluid infused or the medications administered during such a short period are unlikely to be life saving. Further, in penetrating trauma to the thorax, fluid boluses may be detrimental by disrupting the clotting process. In addition, field placement of intravenous lines may increase the chances of infection. Needlestick injuries, which may occur during venous cannulation under adverse circumstances, such as in the back of a moving ambulance, are an increasing concern. Intraosseous needles may be placed by paramedics in the event that vascular access cannot be obtained in the pediatric patient.<br /><br /><span style="font-weight: bold;">2. Needle thoracostomy</span>—Chest decompression for suspected tension pneumothorax may occasionally be life saving and is performed by paramedics in some systems. A 14- or 16-gauge catheter-clad needle is inserted into the second intercostal space along the midclavicular line immediately above the subjacent rib using sterile technique. The catheter is sealed with a Heimlich valve or a latex glove with the fingertip removed. (The open fingertip of the glove is secured around the catheter, allowing air to escape but preventing its reentry.)<br /><br /><span style="font-weight: bold;">3. Cricothyrotomy</span>—(See Chapter 6.) Emergency entry to the airway may be life saving in cases of supraglottic airway obstruction or laryngeal trauma. Cricothyrotomy may be performed by paramedics in some EMS systems, usually after approval by the base physician via radio. Cricothyrotomy may be performed using a surgical, needle, or Seldinger technique. Because the procedure can be unexpectedly difficult, it should be performed as a last resort and only by properly trained personnel.<br /><br /><span style="font-weight: bold;">D. Medications </span><br />Medications are a contentious area in the prehospital realm. Because of the lack of clinical trials, it is difficult to state what interventions are of benefit. The emergency physician should know what medications are available to their EMS providers and under what indications they may be used.<br /><br /><span style="font-weight: bold;">1. Advanced cardiac life support</span>—Most drugs for advanced cardiac life support are stocked on most ALS ambulances. Consistently, epinephrine, atropine, lidocaine, sodium bicarbonate, and adenosine are stocked. In addition, nitroglycerin, aspirin, and morphine are available for treatment of acute coronary syndromes. Amiodarone often is not used because of the ongoing debate about its effectiveness and because of cost issues. Some systems do not stock diltiazem because patients with a tachydysrhythmia that requires rate control are relatively stable. Fibrinolytics are rarely used because of their cost, the staffing needed to administer and monitor them, and the minimal benefit shown in prehospital use. Other medications such as labetalol, magnesium, procainamide, and calcium chloride are typically stocked at the discretion of the agency's medical director.<br /><br /><span style="font-weight: bold;">2. Pulmonary</span>—Albuterol should be available to all ALS EMS agencies. Ipratropium has been shown to be beneficial to patients with moderate to severe asthma and to those with chronic obstructive pulmonary disease. In addition to sublingual nitroglycerin, furosemide is typically stocked for treatment of pulmonary edema.<br /><br /><span style="font-weight: bold;">3. Other drugs</span>—Benzodiazepines are typically stocked for treatment of seizures, anxiolysis, and sedation. The use of prehospital benzodiazepines is beneficial to patients presenting with recurrent seizures. Agents stocked include diazepam, lorazepam, and midazolam.<br /><br />Glucose, in the form of 50% dextrose in water (D50W) and oral glucose solution (occasionally D25W or D10W for pediatric patients), is stocked for treating hypoglycemia.<br /><br /><span style="font-weight: bold;">E. Extrication </span><br />Extrication is the process of removing a patient from a condition of entrapment, usually from a motor vehicle. It requires considerable skill and experience. Often, special tools are necessary, such as heavy bolt and metal cutters or large, powered spreading devices (eg, Jaws of Life, Hurst Tool). In most EMS systems, when there is a report of a trapped victim, a fire rescue team is dispatched in addition to the EMS unit to clear fire hazards, wash away spilled gasoline, and provide additional heavy equipment and personnel.<br /><br />As soon as the patient is accessible with minimal risk to emergency workers, the primary survey should be initiated while further efforts to free the patient continue. Once the patient is immobilized in place, emergency resuscitation can begin.<br /><br /><span style="font-weight: bold;">F. Immobilization and Splinting </span><br /><span style="font-weight: bold;">1. Immobilization</span>—Victims of trauma may have injuries to the spine or extremities, which, if manipulated, can lead to spinal cord or limb damage. Upon reaching a trauma victim, the rescue team must stabilize the patient's cervical spine. Manual stabilization is maintained throughout extrication. A cervical collar is applied as soon as practicable. Spine boards are sometimes difficult to maneuver in closed spaces, but alternative devices are available, such as the Kendrick Extrication Device (KED). In a hemodynamically unstable patient, rapid extrication onto a long spine board can be accomplished by multiple rescuers manually supporting the spine without the aid of a KED. Immobilization is not considered complete until the patient is secured to the spine board with straps, the patient's head is secured to the spine board with tape across the forehead and beneath the chin, and a cervical collar and lateral neck rolls or head immobilization device are in place.<br /><br />If endotracheal control intubation is necessary, the cervical spine should remain immobilized while the procedure is performed. Should vomiting occur, the patient may be logrolled to face sideways while one rescuer maintains cervical spine traction.<br /><br /><span style="font-weight: bold;">2. Splinting</span>—(See Chapters 28 and 29.) In general, extremities should be placed in an anatomic position, especially if pulses cannot be felt below a suspected fracture. If the patient protests or if resistance is felt, extremities should remain in a position of comfort. Reduction of fracture dislocations at a joint should be attempted only if vascular compromise is impending, the duration of transport is long, and the rescuer is experienced in the technique. This usually requires the base physician's approval.<br /><br />A pillow, rolled-up blanket, or other material may often serve as a simple splint. Specific splinting devices include cardboard splints, inflatable air splints, the MAST (military antishock trousers) garment, and traction splints. If inflatable devices are used, care must be taken to monitor distal perfusion, because a compartment syndrome may occur with swelling of the extremity or changes in atmospheric pressure (eg, during air transport). Traction splints are used primarily with fractures of the femur.<br /><br /><span style="font-weight: bold;">G. Protocols and Standing Orders </span><br />Protocols are guidelines designed to assist the EMT in performing tasks in a complete and orderly fashion (Figure 2-3). Because situations vary widely and protocols cannot anticipate every variable, they are not meant to be absolute and must be accompanied by training, judgment, and experience. Each EMS system tailors its protocol to the training and skill of its EMTs and the needs of the local medical community.<br /><br />Standing orders are express authorizations for the performance of a specific task or procedure. Under the standing order, an EMT may be authorized to perform a task or procedure without first obtaining verbal authorization by radio. Standing orders are useful when radio contact is impractical or would delay life-saving intervention (eg, CPR, defibrillation). Standing orders usually contain a clear list of circumstances under which the authorization applies (indications) and detailed instructions on the manner in which the procedure should be performed. They are signed by the physician medical director, who shares legal responsibility for the outcome.<br /><br /><span style="font-weight: bold;">H. Communications </span><br /><span style="font-weight: bold;">1. Equipment and frequencies</span>—EMS units communicate with receiving hospitals by various methods. Three main radio systems exist: the HEAR network (in the 150-MHz range), the COR system (400 MHz), and the 800-MHz truncated system. The HEAR system is the oldest and has largely been replaced in urban areas by 800-MHz systems, which provide multiple frequencies for providers. In addition, cellular phones and landline telephones are used frequently for communications. Communication is simplex. Signals pass in only one direction at a time, and neither party can simultaneously speak and be heard. In rural areas, communication may be direct, via radio, without a relay station or ground lines.<br /><br /><span style="font-weight: bold;">2. Communication technique</span>—Radio communication must provide information in a concise, precise, and easily understood manner. To facilitate speed and understanding, a common format is followed, with slight variations depending on the community. However, no one should hesitate to ask for clarification, because misunderstandings may prove fatal.<br /><br /><span style="font-weight: bold;">a. The initial contact</span>—The caller always names the party being called first, followed by the caller's own identification:<br /><br />"Central Hospital, this is medic 19, how do you copy?"<br /><br /><span style="font-weight: bold;">b. The initial response</span>—The initial response confirms the contact in the same manner:<br /><br />"Medic 19, Central Hospital, receiving you loud and clear, over."<br /><br /><span style="font-weight: bold;">c. The report</span>—The caller gives a concise, orderly report containing pertinent history, physical findings, destination, estimated time of arrival (ETA), and any necessary request for instructions. It should be as brief as possible:<br /><br />"Central Hospital, medic 19 en route to your location, ETA 8 minutes, with a 20-year old male victim of multiple, small-caliber gunshot wounds to the left chest, right flank, and right thigh. Patient is lethargic; blood pressure 80, pulse 140, respirations 46. Breath sounds absent over the left chest, abdomen soft. We have an ET tube in place, 2 IVs with lactated Ringer's wide open, and MAST garment inflated. Requesting permission for needle decompression of the left chest."<br /><br /><span style="font-weight: bold;">d. The report acknowledgment</span>—This acknowledgment is kept brief; only essential queries should be made:<br /><br />"Medic 19, have you checked ET tube position?"<br /><br />"That's affirmative. Withdrawn 2 centimeters without improvement."<br /><br />"Okay, medic 19; needle thoracostomy, left chest, is approved. Will stand by for update."<br /><br /><span style="font-weight: bold;">e. The sign-off</span>—After receiving an order, the field personnel should repeat it to demonstrate that it was received accurately before signing off:<br /><br />"Central Hospital, understand needle thoracostomy, left chest, is approved. Stand by."<br /><br /><span style="font-weight: bold;">3. 10-Codes</span>—"Ten codes" are phrases represented by 2 numbers, the first being 10. In many areas, these are used to ensure precise communication and to add some measure of privacy to the conversation. Unfortunately, few EMS personnel have all of the possible 120 codes memorized. The result is often more confusion rather than less. Because mistakes may be dangerous, the codes should not be used unless thoroughly understood by all parties.<br /><br /><span style="font-weight: bold;">4. Telemetry</span>—Receiving hospitals and ambulances may have equipment designed for the transmission of electrocardiographic traces (telemetry). This equipment is seldom used, however, because well-trained paramedics have shown the ability to interpret unstable rhythms (eg, ventricular fibrillation, ventricular tachycardia, bradycardia, and asystole) with acceptable precision, and more complex rhythms (eg, supraventricular tachycardia) rarely require treatment that cannot be postponed until arrival at the hospital. As indicated above, the prehospital 12-lead ECG has shortened the door to drug time in patients with acute coronary syndromes.<br /><br /><span style="font-weight: bold;">I. Air Transport </span><br /><span style="font-weight: bold;">1. Indications</span>—As noted above, the benefits to the patient must outweigh the risks inherent in this mode of transport. Aeromedical transport is most advantageous when great distances must be covered rapidly, when ground transport is unavailable or impeded by geographic obstacles or dense traffic, or when specialized care (eg, trauma resuscitation) is needed at the scene or en route. Emergency medical helicopters serving rural areas often provide a higher level of care and more skilled procedures (eg, intubation, needle thoracostomy, cricothyrotomy) than are provided by localized services using basic EMTs. However, air transport is hazardous, and helicopters operating at night and in inclement weather have crashed.<br /><br /><span style="font-weight: bold;">2. Requesting service</span>—Helicopters equipped for medical evacuation can be requested, through the EMS communications network, from an area hospital that offers such services or from a local military base that participates in the Military Assistance to Safety and Traffic program.<br /><br /><span style="font-weight: bold;">3. Patient preparation</span>—Before departure, stabilize the patient on a spine board and immobilize the patient as clinically indicated. Secure airway tubes and intravenous catheters.<br /><br /><span style="font-weight: bold;">4. Anticipated physiologic consequences of air transport</span>—<br /><br /><span style="font-weight: bold;">a. Hypoxia</span>—Atmospheric pressure decreases with increasing altitude, as does the partial pressure of oxygen. Patients with existing heart or lung disease may suffer adverse consequences. Supplemental oxygen is required.<br /><br /><span style="font-weight: bold;">b. Expansion of trapped gas</span>—The volume of trapped gas increases with decreasing barometric pressure. Thus, as altitude increases, air may expand in endotracheal tube cuffs, air splints, MAST garments, the bowel lumen, the stomach, pneumothorax, abscess cavities, and the bottles and tubing of intravenous infusion apparatus. These compartments must be monitored frequently and vented as necessary. Intravenous flow rates should be adjusted accordingly.<br /><br /><span style="font-weight: bold;">c. Motion, noise, and vibration</span>—These may cause patient discomfort. Forward acceleration with the patient's head forward may cause transient hypotension. This may be prevented by positioning the patient with feet forward.<br /><br /><span style="font-weight: bold;">5. Helicopter safety</span>—<br /><br /><span style="font-weight: bold;">a. Site selection and lighting</span>—A helicopter landing site should be level, approximately 100 feet square, and free of obstacles (eg, trees, wires) to approach and departure. It should also be clear of loose debris. The site should be secure from bystanders. At night, the site should be well lighted (eg, with vehicle headlights), but lights should never be directed upward toward the approaching helicopter, because they might interfere with the pilot's vision.<br /><br /><span style="font-weight: bold;">b. Approaching a helicopter</span>—While the rotor blades are turning, approach the aircraft only from the front and only after prompting by the pilot. Avoid the tail rotor. Approach in a crouched position. Do not run. Never approach from uphill.<br /><br />Lower tall objects such as poles associated with intravenous infusion apparatus. Secure sheets, hats, and loose clothing. Extinguish all smoking material.<br /><br /></div>Emergency Medicinehttp://www.blogger.com/profile/06606398346130594987noreply@blogger.com2tag:blogger.com,1999:blog-3749884089415516879.post-89641143567989992682008-08-16T08:40:00.000-07:002008-08-16T08:44:58.362-07:00Approach to the Emergency Department Patient<div style="text-align: justify;"><span style="font-weight: bold;">WHAT IS EMERGENCY MEDICINE? </span><br /><br />An emergency is commonly defined as any condition perceived by the prudent layperson—or someone on his or her behalf—as requiring immediate medical or surgical evaluation and treatment. Based on that definition, the American College of Emergency Physicians (ACEP) states that the practice of emergency medicine has the primary mission of evaluating, managing, and providing treatment to these patients with unexpected injury and illness.<br /><br />So what does an emergency physician do? This specialist routinely provides care and makes medical treatment decisions based on real-time evaluation of a patient's history; physical findings; and many diagnostic studies, including multiple imaging modalities, laboratory tests, and electrocardiograms. The emergency physician needs an amalgam of skills to treat a wide variety of injuries and illnesses—ranging from the diagnosis of an upper respiratory infection or dermatologic condition to resuscitation and stabilization of the multiple trauma patient. Furthermore, these physicians must be able to practice emergency medicine on patients of all ages and not just in urban tertiary-care facilities. Clinical emergency medicine may be practiced in emergency departments, both rural and urban; urgent care clinics; and other settings such as at mass gathering incidents, through emergency medical services (EMS), and in hazardous material and bioterrorism situations.<br /><br />Emergency medicine serves as the United States's health care safety net. It provides valuable clinical and administrative services to the health care delivery system, including care for the indigent and others who lack access to health care, and has evolved as the most visible and vital component of a patchwork of health care providers and facilities. These emergency departments have become the routine, and often the only, source of care for many of the uninsured, thereby acting as a critical safety net for our fragmented health care delivery system.<br /><br />Finally, emergency departments are the only element of the health care system whose function has been delineated by federal law. Initially authorized in 1986, the Emergency Medical Treatment and Active Labor Act mandates that all emergency departments provide screening, stabilization, and appropriate transfer to all patients with any medical condition. Emergency medicine is often the last resort for many patients and frequently the access point for competent, comprehensive, and efficient medical care.<br /><br /><span style="font-weight: bold;">BIRTH & GROWTH OF EMERGENCY MEDICINE </span><br /><br />By current popular opinion based on reality and dramatic television productions, emergency medicine appears to be at the forefront of medicine, providing compassionate and competent care by residency-trained emergency physicians. Unfortunately, this has not always been the case. The profession of emergency medicine is still quite young and continues to grow and mature. A brief timeline of emergency medicine growth is shown in Table 1-1. Since the first emergency medicine residency program began in 1970, the number of approved residency programs has increased dramatically (Table 1-2). Despite the rapid growth in emergency medicine residencies, a significant number of practitioners of emergency medicine are not residency trained or board certified (Table 1-3).<br /><br /><span style="font-weight: bold;">SCOPE OF PRACTICE </span><br /><br />Emergency medicine physicians are faced with an ever-growing patient volume, decreasing inpatient bed availability, decreasing reimbursement, and increased litigation. However, these same physicians have the unique responsibility for being prudent stewards of a finite amount of health care resources. Based on that responsibility, the ACEP in 2002 endorsed the following:<br /><br />• The best medical interest of the patient should be foremost in any clinical decision making process.<br /><br />Criteria for appropriate use of finite resources should include:<br /><br />1. Urgency of the patient's medical condition<br /><br />2. Likelihood, magnitude, and duration of medical benefit to the patient<br /><br />3. Burdens and cost of care to the patient<br /><br />4. Cost to society<br /><br />• Emergency physicians should not allocate health care resources on the basis of a patient's ability to pay, contribution to society, past use of resources, or responsibility for their medical condition.<br /><br />In 2001, the ACEP Core Content Task Force II published its Model of Clinical Practice of Emergency Medicine. In this publication, the scope of practice of an emergency physician is well defined and yet quite expansive, to include care from the prehospital environment to prevention and education. Listed below are the tasks of the emergency physician as agreed upon by the task force.<br /><br /><span style="font-weight: bold;">Prehospital Care </span><br /><br />Participate actively in prehospital care and education, provide direct patient care or on-line or off-line medical direction or interact with prehospital medical providers, and assimilate information from prehospital care into patient assessment and management.<br /><br /><span style="font-weight: bold;">Emergency Stabilization </span><br /><br />Conduct primary assessment, and take appropriate steps to stabilize and provide treatment to patients.<br /><br /><span style="font-weight: bold;">Performance of Focused History & Physical Examination </span><br /><br />Communicate effectively to interpret and evaluate the patient's symptoms and history; identify pertinent risk factors in the patient's history; provide a focused evaluation; interpret the patient's appearance, vital signs, and condition; recognize pertinent physical findings; and perform techniques required for conducting the exam.<br /><br /><span style="font-weight: bold;">Modifying Factors </span><br /><br />Recognize age, gender, ethnicity, barriers to communication, socioeconomic status, underlying disease, and other factors that may affect patient management.<br /><br /><span style="font-weight: bold;">Professional & Legal Issues </span><br /><br />Understand and apply principles of professionalism, ethics, and legal concepts pertinent to patient management.<br /><br /><span style="font-weight: bold;">Diagnostic Studies </span><br /><br />Select and perform the most appropriate diagnostic studies, and interpret the results.<br /><br /><span style="font-weight: bold;">Diagnosis </span><br /><br />Develop a differential diagnosis and establish the most likely diagnoses in light of the history, physical examination, interventions, and test results.<br /><br /><span style="font-weight: bold;">Therapeutic Interventions </span><br /><br />Perform procedures and nonpharmacologic therapies, and counsel patients.<br /><br /><span style="font-weight: bold;">Pharmacotherapy </span><br /><br />Select appropriate pharmacotherapy, recognize pharmacokinetic properties, and anticipate drug interactions and adverse effects.<br /><br /><span style="font-weight: bold;">Observation & Reassessment </span><br /><br />Evaluate and reevaluate the effectiveness of a patient's treatment or therapy, including addressing complications and potential errors; and monitor, observe, manage, and maintain the stability of one or more patients who are at different stages in their workups.<br /><br /><span style="font-weight: bold;">Consultation & Disposition </span><br /><br />Collaborate with physicians and other professionals to evaluate and provide treatment to patients; arrange appropriate placement and transfer if necessary; formulate a follow-up plan; and communicate effectively with patients, family, and involved health care members.<br /><br /><span style="font-weight: bold;">Prevention & Education </span><br /><br />Apply epidemiologic information to patients at risk; conduct patient education; and select appropriate disease and injury prevention techniques.<br /><br /><span style="font-weight: bold;">Documentation</span><br /><br />Communicate patient care information in a concise manner that facilitates quality care and coding.<br /><br /><span style="font-weight: bold;">Multitasking & Team Management </span><br /><br />Prioritize multiple patients in the emergency department in order to provide optimal patient care; interact, coordinate, educate, and supervise all members of the patient management team; utilize appropriate hospital resources; and have familiarity with disaster management procedures.<br /><br /><span style="font-weight: bold;">Other "Tasks" </span><br /><br />Emergency medicine has evolved to include much more than the above-mentioned "tasks." For the profession of emergency medicine to continue to progress, physicians must embrace the following responsibilities:<br /><br />• Basic and clinical research<br /><br />• Multidisciplinary and continuous medical education<br /><br />• Injury prevention<br /><br />• Disaster management and mass-gathering medicine<br /><br />• Toxicology and regional Poison Control Center direction<br /><br />• Hazardous material and bioterrorism management<br /><br />• Hospital and EMS systems administration<br /><br /><span style="font-weight: bold;">PRINCIPLES OF EMERGENCY MEDICINE </span><br /><br />It is often said that emergency department patients "don't read the textbook," meaning that their presentations do not fit nicely into specific textbook diagnoses or classical presentations of illness. However, a cornerstone of an emergency physician's practice is the recognition of patterns in a patient's presentation; therefore, the prudent physician must be a detective and scientist to muddle through the muck of vague signs and symptoms to find the pattern.<br /><br />The principles of emergency medicine are simply questions that must be answered to provide effective care to patients who have entrusted emergency physicians with their care. The questions are not to be used as a cookbook approach to the management of these often complex medical and psychosocial issues but are a simple method to guide the prudent emergency physician through the quagmire of clinical emergency medicine.<br /><br /><span style="font-weight: bold;">A. Is the Patient About to Die? </span><br />Obviously, this is the first and most important question to answer. Every patient's presentation is quickly prioritized to one of the following acuities:<br /><br />1. Critical—Patient has symptoms consistent with a life-threatening illness or injury with a high probability of death if immediate intervention is not begun.<br /><br />2. Emergent—Patient has symptoms of illness or injury that may progress in severity if treatment is not begun quickly.<br /><br />3. Nonurgent—Patient has symptoms that have a low probability of progression to a more serious condition.<br /><br />Look for symptoms of a life-threatening emergency, not a specific disease entity. Anticipate impending life-threatening emergencies in the apparently stable patient.<br /><br /><span style="font-weight: bold;">B. What Steps Must Be Undertaken to Stabilize the Patient? </span><br />Act quickly to stabilize the critically ill or injured patient. Focus on the primary survey (airway, breathing, circulation, and neurologic deficits), and make necessary interventions as each issue is identified. Do not delay necessary primary interventions while awaiting completion of ancillary testing.<br /><br /><span style="font-weight: bold;">C. What Are the Most Potentially Serious Causes of the Patient's Presentation? </span><br />Thinking of the worst-case scenario, develop a mental list of the most deadly causes of the patient's presentation by asking, "What will kill my patient the fastest?" Once the list has been developed, the vital signs, history, physical examination, and ancillary assessments should identify or confirm those causes highest on the list.<br /><br /><span style="font-weight: bold;">D. Could There Be Multiple Causes of the Patient's Presentation? </span><br />In addition to constant reevaluation and reprioritization of the differential diagnosis, continually ask, "Is this all there is?" For example, is the new-onset seizure and hypoglycemia in an older diabetic patient from intentional or accidental medication overdose or perhaps worsening renal insufficiency? Is the near-syncope and abdominal pain in an apparently intoxicated college coed from a ruptured ectopic pregnancy or perhaps a ruptured spleen secondary to undisclosed physical abuse by her boyfriend? Frequent reassessment and thoughtful inquiry as to the multiple possibilities responsible for each patient's condition are imperative.<br /><br /><span style="font-weight: bold;">E. Can a Treatment Assist in the Diagnosis in an Otherwise Undifferentiated Illness? </span><br />Often in emergency medicine, treatment response foretells a diagnosis. A case in point is the unconscious patient with no available collateral history. The patient's response to empiric administration of naloxone will include or exclude narcotic overdose as a contributor to the obtundation. Referred to as the "diagnostic-therapeutic" concept, it underscores the emergency medicine philosophy that an established diagnosis is not a prerequisite to initiating appropriate treatment. Pitfalls can exist. For example, sublingual nitroglycerin and so-called GI cocktails can relieve symptoms of chest pain resulting from the same cause.<br /><br /><span style="font-weight: bold;">F. Is a Diagnosis Mandatory or Even Possible? </span><br />After emergent issues have been addressed, the patient and emergency physician are often left with an undifferentiated symptom complex. This frequently elicits an uncomfortable response by non-emergency-medicine-trained physicians. Become accustomed to and comfortable with the notion of determining the disposition for a nonemergent patient—having treated their symptoms and excluding emergency conditions-without a specific diagnosis.<br /><br /><span style="font-weight: bold;">G. Does This Patient Need To Be Admitted to the Hospital? </span><br />Having appropriately answered the preceding questions, make the bottom-line disposition decision. Once assessments and treatments are under way, decide whether an emergent condition exists. Consider other subtleties. Does the patient have timely, accessible follow-up? How far away from a medical facility does the patient live? Are unresolved abuse or self-care issues involved? Are you, as the emergency physician, comfortable discharging the patient?<br /><br /><span style="font-weight: bold;">H. If the Patient Is Not Being Admitted, Is the Disposition Safe and Adequate for the Patient? </span><br />More frequently than not, patients are discharged home from the emergency department. However, many patients do not receive a specific diagnosis, and some symptoms may persist. Recommend appropriate follow-up, and provide written discharge instructions. Invite the patient back. Instruct the patient when to return for further evaluation should symptoms change or worsen. Provide the patient with information regarding treatment and diagnosis as well.<br /><br /><span style="font-weight: bold;">CONCLUSION </span><br /><br />Since 1970, emergency medicine has seen a tremendous growth and increase in awareness of the unique aspects of the profession. It remains a challenging and fulfilling experience for many physicians and an appealing choice of specialties for medical students. As emergency medicine matures as a specialty, its importance as the United States's health care safety net and its integral status as front-line medicine will continue to expand and grow.<br /><br /></div>Emergency Medicinehttp://www.blogger.com/profile/06606398346130594987noreply@blogger.com2