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Audio Program
Ninth Edition Selected Transcripts References
Carol S. Rivers, M.D.

Comprehensive Preparation Program

Part I Text Part II Audio


200 TechneCenter Drive, Suite 103, Milford, Oh 45150 (800) 878-5667

Audio Program
Selected Transcripts (Intro,!^, 7)

Due to the amount of detailed information contained in four of the CDs, transcripts of this material have been enclosed for your easy reference to specific information. The key points of the introductory CD have been summarized on a single sheet. CDs 1, 6 and 7 have been transcribed in their entirety.

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Topic Key to a Good Performance Meeting the Challenge of Difficult Cases ACLS Differential Diagnosis of Headache Pediatric Resuscitation Pediatric Resuscitation (continued) Case Management Checklist Key Points in Text and CDs 3 4 25 33 37 40 45 49

Intro CD1 CD6

1 2 3 1 2 3


Copyright 2007 Emergency Medicine Educational Enterprises, Inc. All rights reserved. No part of this publication may be reproduced without permission. Printed in the United States of America. Disclaimer Emergency Medicine Educational Enterprises, Inc. cannot be assumed to guarantee the user of The Oral Board Comprehensive Preparation Program (text and audio program) success in the oral boards. Recommendations regarding diagnosis, treatment and drug therapy are not intended to be instructional in the practice of Emergency Medicine.

"KEY TO A GOOD PERFORMANCE" Your "Key to a Good Performance" is the development of "Test-Taking Skills for the Oral Board Exam." These skills are essential for Oral Board Candidates. Many of those who had previously failed the exam (and subsequently learned these skills) went on to pass it the next time around. In the next 20 minutes, I'm going to teach you rules and strategies to use as you take the exam. There are four rules and four strategies for you to learn. When I use the word "rule", I mean something you MUST do all the time. If I use the word "strategy", I'm referring to something you CAN do when confronted with a problem. The four strategies I will give you, are in my opinion, the ones you will need to know to effectively deal with the problems you may be confronted with during the Oral Board Exam process. First, I'm going to enumerate the rules and strategies and then I'm going to explain how to use them. Here are the four rules: Rule #1 Rule #2 Rule #3 Rule #4 All patients with abnormal vital signs or an altered level of consciousness require IMMEDIATE STABILIZATION.

If you are dealing with potentially serious illnesses or injuries, be management. control of the case yourself.. .and


up on your concentration.

Now, here are the four strategies: Strategy #1 - If you feel intimidated by an Examiner, deal with this feeling; failure to do so may adversely effect your performance. Strategy #2 - In the early part of the case, if a patient is not responding to usual stabilization or therapeutic measures, you have missed an important clue; you need to methodically retrace the case and look for that clue. Strategy #3 - If a suspected diagnosis is not materializing, your differential diagnosis is incomplete; review the clinical presentation again and develop a good working differential diagnosis...and Strategy #4 - If you make a mistake during the exam, admit it openly and declare your intent to correct it immediately.

CD1 "MEETING THE CHALLENGE OF DIFFICULT CASES" The cases that challenge you in the Emergency Department, are those you can expect to encounter during the Oral Board Exam. This may make you feel a little uncomfortable at first, particularly since you will be meeting this challenge in front of your peers. However, the review that follows will sharpen your clinical acuity, in managing these difficult cases. And, like many of us who have passed this exam, you will find it beneficial to your clinical practice as well. In this session, Fm going to enumerate the major categories that deserve special attention in preparation for this exam.. .and I'm going to talk about the challenges you'll face, in managing them. I have also included the case management check list found in the oral board book. Because of its importance in managing difficult cases, I have repeated it here and added comments. There are nine MAJOR categories of cases that pose special problems to the Oral Board Candidate. Here they are: 1 - Major trauma that involves multiple injuries 2 - Cardiopulmonary emergencies at high risk for cardiac arrest 3 - Substance abuse with complicating illnesses or injuries 4 - Poisoning and overdose 5 - Pediatric emergencies 6 - Acid-base disorders 7 - Environmental emergencies 8 - Vascular emergencies... and 9 - Diabetic emergencies. In my judgment, these nine represent the core case categories of the Oral Exam. Now let's go back through these categories and determine the critical decision points that can make or break a clinical performance. The first category is MAJOR TRAUMA THAT INVOLVES MULTIPLE INJURIES. The critical decision points in Advanced Trauma Life Support are the following: 1 - Choosing appropriate airway control measures, while establishing and maintaining in-line cervical spine immobilization 2 - The timing of chest tube insertion, once the diagnosis of pneumothorax has been established clinically 3 - Determining the size and placement of IV catheters 4 - Choosing appropriate methods for gastric emptying and bladder decompression.. .and 5 - Determining the need for peritoneal lavage, abdominal CT or focused abdominal ultrasonography for trauma (the FAST exam). The first three critical decision points revolve around the ABCs. Let's begin with the


Deciding which airway control measure is indicated in a given patient is the first challenge in managing the severely traumatized patient...and it is the most crucial. An error in judgment here, can lead to dire consequences. Before taking definitive steps, however, be sure the cervical spine is adequately immobilized. This includes a backboard, a semirigid (Stif-Neck) collar and sandbags or similar bolstering device, with chin and forehead straps anchored to the backboard. For the patient with airway compromise or one with an altered level of consciousness, intubation is indicated. If the patient is not deeply unconscious, rapid sequence induction may also be required. The majority of RSIs can be safely and effectively performed with the combination of etomidate and succinylcholine. Other agents can be used of course, but the literature still supports the use of these combined agents for most situations. A notable exception is infants and children, where the one proven pretreatment measure is atropine (0.02mg/kg), since succinylcholine can produce a profound bradycardia and, possibly, asystole. In any case, adequate preoxygenation is the first step: if the patient has spontaneous respirations, apply a non-rebreather with high-flow oxygen; if respirations are inadequate, the patient needs to be bag-valve masked with 100% oxygen. This should be followed by the induction agent (etomidate) or, in kids, pretreatment with atropine... 15-30 seconds later, the paralytic agent (succinylcholine) can be given. If you are unable to intubate the patient as described above, a surgical airway is indicated unless you are skilled in rescue airway management with the intubating laryngeal mask airway or combitube. If one of these procedures cannot be performed quickly and easily, surgical cricothyroidotomy is the procedure of choice in adults, and needle cricothyroidotomy is the preferred procedure in children, less than 12 years-old... Next is

When you suspect a pneumothorax on clinical grounds, should you wait for x-ray confirmation, prior to chest tube thoracostomy? Well, here's a guideline that should help you make that decision: If there is evidence of tension or if the patient is in obvious respiratory distress or if the breath sounds aresignificantly decreased or absent on one sideinsert a large-bore catheter into the second intercostal space above the rib at the midclavicular line and follow with chest tube decompression; THEN order an x-ray to confirm tube placement, as well as re-expansion of the lung... Next is

The size and placement of IV catheters in the severely traumatized patient is a critical decision, since the estimated blood and fluid loss is frequently underestimated. Two large-bore peripheral catheters (14-16 gauge) should be inserted in all patients in whom the potential for hypovolemic shock exists. A central line may subsequently be inserted to help guide fluid resuscitation, but should not be used as a primary IVfluidresuscitation route unless peripheral access is NOT possible... Next is


Gastric emptying to prevent aspiration and determine the presence of blood is usually accomplished with a nasogastric tube. There can be no objection to that with most patients, but those with facial or basilar skull fractures should have OROgastric tubes. In this group of patients, nasogastric tubes can penetrate the cranial vault, if the cribriform plate has been injured. Foley catheterization is usually required in patients with multiple injuries if they cannot void spontaneously. This is contraindicated however, in patients with suspected urethral injury.. .that is, those with blood at the urethral meatus, scrotal hematoma or a high-riding or "boggy" prostate. Therefore, a rectal exam and an exam of the urethral meatus and scrotum should always precede Foley insertion in multiple trauma patients. If urethral injury is suspected, a retrograde urethrogram should be done to rule out this diagnosis. In the male, urethral rupture should alert the clinician to possible associated pelvic fractures. In the female, urethral injury in the presence of pelvic fractures is also associated with vaginal rupture. A question I have been frequently asked is this: "Don't patients with urethral tears require bladder decompression?" Well, yes, they do. But if the bladder is not distended, suprapubic catheterization is done by the urologist in the OR, at the time of the urethral repair. However, if the bladder is found to be distended while the patients in the Emergency Department, suprapubic catheterization should be done there...either by you or the urologist. This can be accomplished with a percutaneous cystotomy set or a peritoneal dialysis trocar and catheter... Next is ABDOMINAL INJURY Peritoneal lavage, CT or ultrasonography are procedures that may be overlooked in the din of activity surrounding a seriously injured patient. If circumstances dictate the need to confirm or rule out a surgical abdomen in the multiple trauma patient with unreliable abdominal exam AND a history or physical findings which suggest the possibility of an intra-abdominal injury, one of these procedures needs to be done. Specific indications include: Head or spinal cord injuries An altered level of consciousness due to drug or alcohol abuse A history of blunt abdominal trauma, in a patient with unexplained hypotension A negative exam in a patient who has sustained blunt abdominal trauma and who will be unavailable for sequential exams...and An equivocal or unreliable exam in a patient with multiple injuries.

For the hemodynamically unstable patient, the procedure of choice is peritoneal lavage because it is readily available, can be rapidly performed and (most of all) has a sensitivity of 98%. The major pitfalls of DPL are that it can miss significant retroperitoneal bleeding and isolated hollow viscus perforation. The single most useful test for evaluating retroperitoneal organs (that is ... the kidney, colon and pancreas) is CT with contrast; however, it misses some injuries of the bowel and pancreas (as well as the diaphragm and bladder). In addition, the use of CT is reserved for the hemodynamically stable patient. An alternative to DPL and CT for evaluating both hemodynamically stable and unstable patients with blunt abdominal trauma is ultrasonography. The major disadvantage of this procedure is that it can miss bowel and retroperitoneal injuries. Also, a negative (or equivalent) ultrasound does not rule out the need for further testing. The second major category of cases is CARDIOPULMONARY EMERGENCIES AT HIGH RISK

Examples of such cases include the following: The Acute MI The Acute MI with AV block The Acute MI with cardiogenic shock Supraventricular tachycardia with shock Ventricular tachydysrhythmias... and Pulmonary edema in the absence of an MI If you get one of these cases, or a similar one, you'll get the feeling that he's going to arrest...and he usually does. Critical decision points in these cases can be divided into two groups: those that occur before the arrest and those that occur at the time of arrest. Right now, let's look at these patients, before the arrest:
ATELY with

The patient with an obvious or apparent ACUTE MI should be stabilized IMMEDIan IV, O2, pulse oximeter and cardiac monitor; chest pain should be treated with nitroglycerin; morphine is indicated for continuing pain that is unresponsive to nitroglycerin and other anti-ischemic agents as well as anti-platelet agents. Those patients who meet criteria for thrombolytic agents (and have no known contraindications) should receive one of them as quickly as possible (preferably within 30 minutes of arrival in the Emergency Department); aspirin should be given immediately, unless contraindications exist. Adjuvant therapy with IV heparin, Betablockers, glycoprotein Ilb/IIIa receptor inhibitors and ACE inhibitors, should also be initiated when appropriate.

New-onset ventricular ectopy that occurs in association with an acute MI that is frequent, repetitive and associated with circulatory compromise should be treated. In the patient with an uncomplicated MI, lidocaine may be used; for a complicated MI (one with pump dysfunction) amiodarone is a better choice. The appropriate intervention sequence for symptomatic bradycardia that occurs in association with an acute MI is atropine or transcutaneous pacing. Initial treatment with atropine is indicated only when serious signs and symptoms are occurring with a heart rate greater than 50 in a patient who has anlV in place or when

a transcutaneous pacer is not immediately available. Hemodynamically unstable bradycardia (that is, a rate less than 50) is a clear indication for placement of transcutaneous patches with provision for immediate pacing. The patient with an ACUTE MI AND AV BLOCK is at high risk for ventricular asystole. Do NOT GIVE THIS PATIENT LIDOCAINE OR PROCAINAMIIDE, since either of these drugs may suppress his normally functioning rhythm. Bretylium should not be given either, and it has been removed from the ACLS guidelines because of a high occurrence of side effects and the limited supply and availability of the drug. In the presence of an advanced blockthat is, Mobitz II or a wide complex third-degree AV Blocka transvENOUS pacemaker should be inserted, even if the patient is asymptomatic. While preparations for insertion of a transvenous pacemaker are being made, symptomatic patients should be temporized with a transcutaneous pacemaker. Atropine should be avoided in these patients because it decreases the proportion of beats conducted in infranodal block. Atropine works BEST in nodal blockthat's first degree, Mobitz I and narrow complex third-degree AV Blockby shortening the P-R interval and/or increasing the proportion of conducted beats. The patient in CARDIOGENIC SHOCK SECONDARY TO AN ACUTE MI requires aggressive management. Ideally, Swan-Ganz catheterization should be done to guide therapy, but only if the time, equipment and expertise are available. The Board will probably not require you to perform the procedure yourself, but you should know the indications for emergency Swan-Ganz catheterization. In any case, the patient in cardiogenic shock should be intubated early, to ensure adequate ventilation and oxygenation. The goals of therapy in the treatment of cardiogenic shock are reduction of pulmonary congestion and increased cardiac output. These goals are achieved by the use of agents that reduce preload and afterload, inotropic [pronounced'eye-no-tropic'] agents and vasopressors. Assuming that Swan-Ganz catheterization is not done, the choice of drugs is dictated by the patient's systolic blood pressure. If the patient's blood pressure is greater than 100 mm mercury, use agents that reduce preload and afterload and provide inotropic support: IV nitrates such as nitroglycerin and sodium nitroprusside produce the most predictable reduction in preload. In addition, both drugs decrease the afterload and help to increase cardiac output. In the setting of an Acute MI, IV nitroglycerin is especially useful because it also alleviates pain and reduces myocardial ischemia. However, it should be avoided in the presence of bradycardia or extreme tachycardia. The dose of IV nitroglycerin is 10-20 meg/minute; the dose of IV nitroprusside is 5-10 meg/minute every 5-10 minutes until a favorable response occurs. A further increase in cardiac output can be achieved with inotropic agents such as dopamine or dobutamine. The dose of both dopamine and dobutamine is 5-20 meg/kg/minute. Now let's talk about those patients whose systolic blood pressure is between 70 and 100 mm mercury. What these patients need is inotropic support...use dopamine, dobutamine or both. Agents that reduce preload can be used in combination with these inotropes, but in reduced dosages.

Finally, let's consider the patient whose systolic blood pressure is less than 70 or those who have not responded to pharmacologic therapy so far. These patients are obviously in real trouble. Chances are that at least 40% of the myocardium has been damaged and cardiac arrest is imminent. Try a norepinephrine drip (4mg in 250cc D5W). The initial infusion rate is 0.5lmcg/minute which can be titrated to a maximum dose of 30mcg/min. When the systolic blood pressure rises to 80mm mercury, try dopamine. Start the infusion at 5mcg/kg/minute and titrate up to 20mcg/ kg/minute as needed. When the systolic pressure reaches 90mmHg, add dobutamine to reduce the requirement for dopamine. For those patients in cardiogenic shock accompanied by severe pulmonary edema unresponsive to diuretics, vasodilators and conventional inotropic agents, consider the administration of amrinone which has similar hemodynamic properties to those of dobutamine; like dobutamine, it improves myocardial contractility through its positive inotropic action but it also has a direct vasodilatory effect, which makes it a very potent agent - so potent, in fact, that it may even be cardiotoxic. However, if nothing else has worked, and the patient's clinical condition is running a downhill course, it's worth a try. The dose is 0.75mg/kg IV over 2-3 minutes followed by an infusion of 5-15mcg/kg/min. An additional bolus may be given in 30 minutes. An amrinone infusion requires hemodynamic monitoring to titrate the dose properly because hemodynamic improvement is not necessarily associated with changes in heart rate or blood pressure. For patients with atrial fibrillation of acute onset (that's less than 48 hours) and hypotension, rate control is probably best achieved with amiodarone, particularly if there is any question of an underlying Wolff-Parkinson-White syndrome. DC cardioversion may also be required to convert the rhythm. In patients with cardiogenic shock secondary to an Acute MI, keep in mind the possibility of mechanical lesions which may predispose the patient to shock. These include: Mitral regurgitation secondary to rupture of the papillary muscle Ventricular septal rupture... and Left ventricular aneurysm formation. Aortic balloon counterpulsation, may be useful in these cases. Early surgical consultation is mandated, if a mechanical lesion is suspected. The next case SUPRAVENTRICULAR TACHYCARDIA WITH SHOCK requires IMMEDIATE SYNCHRONIZED CARDIOVERSION. The initial dose is 50 joules; most patients respond to a low dose but, if initial cardioversion is unsuccessful, increase the voltage to 100 joules...and try again. If there is still no response, the energy level can be increased to 200 joules before making a third attempt.

should be treated according to ACLS protocols. These are reviewed on the sixth CD.

MI, in my opinion, is a unique challenge in every case, since the response to therapy varies from patient to patient. I believe this is due to several factors, including age, general physical condition, previous cardiac history and medications the patient is taking. A major critical decision point in these patients is reached if the patient is not responding well to a high oxygen concentration, IV nitrates and an adequate Lasix dose (1 mg/kg). Continued administration of these agents is not likely to work. 9

At this point, you have to consider possible causes of the patient's failure to respond to conventional therapy; these include: paroxysmal atrial fibrillation, systemic arterial hypertension, acute bronchospasm (also known as "cardiac asthma"), respiratory acidosis, metabolic acidosis and anemia. Paroxysmal atrial fibrillation is treated initially by controlling the ventricular rate; the drug of choice (in the absence of hypotension) is diltiazem. Once the ventricular rate is slowed, chemical conversion with amiodarone can usually be achieved. However, if the patient's clinical condition is seriously compromised, consider DC cardioversion. The dose of diltiazem is 0.25mg/kg IV over 2 minutes, followed in 15 minutes by a second bolus of 0.35mg/kg if the first bolus was tolerated, but ineffective. IV amiodarone is administered as 150mg over 10 minutes, followed by a lmg/minute infusion for 6 hours and then 0.5mg/minute. Note that the role of amiodarone in the treatment of atrial fibrillation is different in the setting of left ventricular dysfunction with hypotension and without hypotension. Amiodarone is the agent of choice in the patient with pulmonary edema and cardiogenic shock in controlling the ventricular rate. But, in the patient with atrial fib and pulmonary edema without shock, diltiazem is the drug of choice to slow the ventricular rate with amiodarone being used in this setting to convert the y This is an important distinction for you to understand. Systemic arterial hypertension is best treated with IV nitroglycerin since it acts rapidly to reduce preload. Sometimes, this is all that is needed; however, if the blood pressure remains elevated, switch to nitroprusside which is a stronger agent. Patients with respiratory acidosis unresponsive to high oxygen concentrations should be intubated and continued on high oxygen concentrations. Ventilatory assistance with the use of continuous positive airway pressure, or "CPAP" can improve oxygenation AND it can also reduce preload by inhibiting venous return. If the patient also has severe METABOLIC acidosis (that is, an arterial pH less than 7.1) despite correction of respiratory acidosis, sodium bicarbonate can be given as well. Administer half the calculated deficit and then repeat the ABGs to determine the efficacy of therapy and the need for any additional bicarb. The patient found to have significant anemia (which may have precipitated pump failure) should be treated with slow infusion of packed red cells. For the patient in pulmonary edema with shock, follow the treatment guidelines discussed in the section on "Cardiogenic Shock Secondary to an Acute MI." Now I want to talk briefly about cardiopulmonary patients who arrest during the course of treatment. For the purposes of the exam, the arrest is likely to be witnessedeither by you, a nurse or an EMT. Critical points to remember are these: 1 - Patients with witnessed ventricular fibrillation who do not convert with a single defibrillation attemptrequire immediate CPR (beginning with chest compressions) and intubation, followed by epi10

nephrine IV (or endotracheally if an IV is not in place) prior to further defibrillation attempts. Check the rhythm again after five cycles of CPR or after two minutes have passed. Defibrillation doses are determined by the type of defibrillator being used (either the standard monophasic device or one of the newer biphasic devices). For a monophasic defibrillator the dose is 360 joules. If you are using a biphasic device, it is more complicated (unless you do not know the type of biphasic wave form device being used, in which case, the dose is 200 joules). But if you do know, you will be expected to know the correct dose for each type. There are two types of biphasic waveforms: truncated and rectilinear. If you are using a biphasic defibrillator with a truncated waveform, the dose is 150-200 joules; for a rectilinear waveform, it is 120 joules. 2 - When a patient is not responding to ACLS measures, recheck and confirm placement of the endotracheal tube (using a confirmation device). Poor oxygenation is one reason medications may not be working. 3 - The current recommendations for sodium bicarbonate in the arrest situation are restricted to the presence of any of the following: Known pre-existing hyperkalemia or hypermagnesemia Sodium channel blocker toxicity Severe metabolic acidosis with adequate ventilation A cyclic antidepressant or phenobarbital overdose An overdose of a drug that responds to urine alkalinization.. .and A long arrest interval. The third major category of cases that presents a challenge to the Emergency Physician is SUBSTANCE ABUSE WITH COMPLICATING ILLNESSES OR INJURIES. By "substance abuse" I mean street drugs such as: heroin, cocaine, PCP, etc.; the alcohols (ethanol, methanol and ethylene glycol); over-the-counter drugs; and prescription drugs. There are several critical decision points in managing these patients: is the decision to evaluate and treat him as you would any other patient. Many of us have an aversion to these patients, some are uncomfortable interviewing and managing them, and a few look for a quick way to dump these cases on another service.. .and these are the very reasons you are likely to be confronted with one of these patients sometime during the exam. The Examiner wants to know that you will act professionally, obtain an adequate history, perform a thorough physical exam, diagnose and treat all associated illnesses and injuries that are appropriate for Emergency Department management and, finally, assure an appropriate disposition for him.

The SECOND CRITICAL DECISION hinges on your ability and willingness to deal with the substance abuse patient, in a manner that is APPROPRIATE for him. If he's obnoxious, will you become angry? If he says he wants to leave, will you let him? If he's uncooperative, will you simply note that fact on the chart and then abandon your intent to do a thorough H & P? 11

Do not plan to write a complete history and physical after an initial interview and exam since those patients are frequently unwilling, uncooperative and unfriendlya single interview is unlikely to disclose the total picture. Plan to make two or three separate visits in that room, each time obtaining a little more history and performing a more extensive exam. Substance abuse patients, for the most part, tend to become more comfortable and cooperative if they see you frequently during the time they are in the Emergency Department. Specific diagnostic tests and treatment can be going on, in between these assessments. Here are some points in dealing with these patients that may help you deal with this difficult situation: 1Accept the fact that you have to spend some time with this patient. You may also have to search for "significant others" in order to obtain necessary information to determine all the problems he has. 2Never confront the patient with his unacceptable behavior. Instead, deal with what he is saying. If you respond to what he is saying, he will know that you are at least listening to him and he is more likely to become cooperative.

The THIRD CRITICAL DECISION is determining the extent of the physical exam. A cursory exam will not do. Substance abusers can have a multitude of complicating illnesses and injuries, many of which can have subtle presentations. Always perform a complete physical exam in these patients. This is a rule to which there are NO EXCEPTIONS. A complete physical exam will uncover most of his medical problems. A good history and appropriate diagnostic studies will uncover any others. The FOURTH CRITICAL DECISION is determining what diagnostic tests to order. The most common error in clinical practice, in this respect, is an inadequate work-up. I believe this is due to erroneous interpretation of the patient's affect and complaints. Here are some examples: an abrupt change in an alcoholic's behavior may be because he's a "drunk" or it may be secondary to an expanding subdural hematoma. Weakness and malaise in a heroin addict are common complaints of a "junkie" but they may also be symptoms of sepsis or an occult [pronounced 'OC-CULT'] abscess. There is no standard battery of tests for these patients. In general, it's best to base diagnostic studies on historical and physical exam findings. The FIFTH (and final) CRITICAL DECISION is disposition of the patient. Do not let him sign out AMA, and do not discharge him if he has no place to go. Most of the substance abuse cases presented at this exam, will require admission, since they are likely to have significant associated illnesses, injuries or both. The fourth category of exam cases is POISONING AND OVERDOSE. There are three critical points in these cases: #1 - Consider a toxicologic emergency in the differential diagnosis of ANY patient with vague complaints or an altered sensorium. Specifically, there are eight subgroups of patient types or presentations that are highly suspect:

Children, ages one through five The elderly The psychiatric or depressed patient Young trauma victims, especially males in their late teens or early twenties The patient exposed to a fire The comatose patient The young patient with a cardiac dysrhythmia.. .and The patient with metabolic acidosis of uncertain etiology #2 - Consider more than one diagnosis in these patients: MULTIPLE drug ingestions are frequent Associated injuries occur commonly Metabolic derangements such as acid-base or electrolyte imbalance are possible complications, particularly in the OD patient who is also diabetic and the alcoholic who just appears to be "drunk." #3 - Be very resourceful in determining what was ingested. Clues will be given to you if every historical source is pursued and a complete physical exam performed. Pay particular attention to the skin, breath odor, lung sounds and cardiac rhythm. For example: Diaphoresis is common in poisoning from organophosphates, salicylates and sympathomimetics Needle tracks point to a narcotic or cocaine overdose Pressure sores indicate poisoningfrombarbiturates, carbon monoxide or meprobamate A fruity breath odor suggests ketoacidosis An odor of silver polish or bitter almonds may be detected in poisoning from cyanide, but remember only 50% of the population can detect this A strong garlic or insecticide odor should suggest organophosphate poisoning Non-cardiogenic pulmonary edema may be the clinical presentation of a narcotic or salicylate overdose Cardiac dysrhythmias, may indicate toxicity from one of the following: Cyclic antidepressants Phenothiazines Carbon monoxide Cyanide Cocaine Digitalis Beta-blockers.. .and Chloral hydrate Now let's go to the next category. The PEDIATRIC EMERGENCY is the fifth major category, with "child abuse" heading the list as the most frequently encountered case. Any child with a burn,fractureor toxicologic presentation should be suspect.


Other topics that merit review are these: Pediatric arrest and trauma resuscitation Fluid resuscitation in the dehydrated child AsthmaSeizuresNear drowningNew onset diabetes FeverMeningitisSepsisand Reye's Syndrome Congenital and hereditary disorders should also be kept in mind when dealing with the pediatric age group. Two of the ones we see more commonly in the Emergency Department are: a slipped capital femoral epiphysis presenting as knee pain and the hemophiliac presenting with bleeding problemsoften secondary to occult trauma. Critical decisions in managing pediatric emergencies, emerge from situations such as these: 1 - Aggressive airway support for severe respiratory distress or depression, since this is the leading cause of arrest in children.. .the critical decision is WHEN to intubate. 2 - Aggressive circulatory support in shock syndromes, since a sudden severe drop in blood pressure occurs more frequently in children, than adults.. .the critical decisions here are.. .which fluid to use, how much and where to obtain venous access...and 3 - Correct medication doses, since too little or too much can make a crucial difference in resuscitative efforts...The critical decision is knowing which doses must be committed to memory. Remember the axiom we learned in training about LPs and meningitis? The axiom was this: if you're thinking about the possibility of doing a spinal tapdo it. We've all learned how true that statement is. Well, I have another axiom for you. This one concerns intubation and respiratory compromise in kids: if you're thinking the child might benefit from intubation, then do it. And remember the following when you intubate an infant or small child: Do NOT hyperextend the neck.. .place the child's head and neck in the sniffing position. The correct tube size is estimated based on the following formula: the age of the child plus sixteen divided by four. Use an uncuffed tube for children up to seven or eight years old. Don't worry if the correct-sized laryngoscope blade is an emergency situation, one can usually intubate with a straight blade that is larger than what is indicated. Now, the opposite is true for the size of the endotracheal tube.. .if you're having trouble passing it, try a size smaller...associated laryngeal edema can narrow the laryngotracheal opening. Fluid resuscitation in the treatment of the pediatric shock syndromes (including dehydration) is usually accomplished with Ringer's Lactate or Normal Saline. Fluid boluses of 20 cc/kg can be given as needed to support shock. Children in hypovolemic shock from blood loss should be given blood if there is no clinical improvement following the first two boluses. Those with dehydration who do not respond well to two fluid boluses should be given a third 20cc/kg fluid bolus, but it 14

should be given more slowly (over 20-30 minutes). Remember to use a Pediatric Microdrip IV set-up. Determining the site of venous access is another critical decision in the management of pediatric emergencies. The following guidelines may be helpful to you: If a child is dehydrated or in early shock, percutaneous PERIPHERAL venous cannulation is the procedure of is the safest, simplest and most rapid method of obtaining venous access (be sure to flush the catheter with at least 5cc of saline so that medications may reach the central circulation)...if peripheral venous cannulation is unsuccessful, central venous access via the femoral, internal jugular, axillary, subclavian or external jugular may be attempted. If venous access is NOT obtained within a few minutes in a child who is in profound shock or cardiac arrest, intraosseous cannulation or a venous cutdown should be performed. In a child less than 6 years of age, intraosseous cannulation of the proximal tibia is the procedure of choice, whereas a saphenous cutdown is preferred for a child 6 years of age or older. A WORD OF CAUTION HERE. Time spent securing vascular access at the expense of airway management is a common mistake in the management of pediatric emergencies, and nowhere is it more costly. A significant number of children will respond to airway management ALONE. In addition, once the child has been intubated, this route may be used to administer epinephrine, atropine, lidocaine and naloxone. Calculating pediatric doses, in my opinion, is a detriment to efficient emergency care, since time is of the essence in these situations. Unless you are a Pediatric Emergency Physician, you do not see these cases often enough to readily remember multiple dosage schedules. Most of you now use wall charts, index cards or a pocket reference in the Emergency Department where the doses are precalculated based on the child's age or weight. Since you won't have any of these tools available at the exam, let me give you a few of the critical medications and dosage schedules here. The most commonly observed rhythms in the pediatric patient with cardiac arrest are asystole and bradydysrhythmias. About 10-20% arrests in children are due to V-Fib or pulseless V-Tach. Remember that cardiac arrest in children is usually secondary to respiratory depression, so do three things early in the code: 1 - Check for foreign body obstruction 2 - Intubate and ventilate with a high O2 concentration ... and 3 - Give naloxone O.lmg/kg IV push if there is any possibility that a narcotic was ingested It is also important to note here that the 2005 ACLS Guidelines state that if, despite adequate oxygenation or ventilation (or delivery of two rescue breaths in an unresponsive child) with a heart rate less than 60 and signs of poor systemic perfusion, you should begin chest compressions. Why? Because bradycardia is a common terminal rhythm in infants and children. So don't wait for development of pulseless arrest to begin chest compressions. 15

Essential medications commonly used in pediatric resuscitation are: epinephrine, atropine, lidocaine, amiodarone and dopamine. The dosages of these drugs MUST be committed to memory. Epi, atropine and lidocaine may be given by the intravenous, intraosseous or endotracheal route, but the intravenous and intraosseous routes are preferred. For atropine and lidocaine, the dosages for these three routes are the same, but epinephrine may require higher dosing (at least 2-2V2 times the peripheral IV dose if given endotracheally) keep this in mind if Epi doesn't seem to be working...and use the dosings for the 1:1000 solution. In the ARREST situation, epinephrine is given in a dose of .01 mg/kg of the 1:10,000 solution for the first dose; for subsequent dosing, you may repeat the initial dose or increase the concentration tenfold by administering O.lmg/kg of the 1:1000 solution. However, for bradycardia, the dose of epinephrine is .01 mg/kg of the 1:10,000 solution for all doses. Atropine is indicated for a bradyasystolic arrest due to AV block. The dose is .02 mg/kg (and remember, the minimum dose of atropine, regardless of weight, is .1 mg since bradycardia may worsen with a lower dose) Lidocaine may protect against refibrillation after successful defibrillation; it should also be considered in children with shock-resistant V-Fib or pulseless V-Tach. The dose is lmg/kg. A drip is prepared by adding 120 mg of lidocaine into lOOcc DgW ... lcc/kg/hr. delivers 20 mcg/kg/minute. Start at l-2.5cc/hr. You may use lidocaine, but the AHA and ACLS Guidelines 2005 advocate the use of amiodarone if the dysrhythmia is resistant to defibrillation and epinephrine. So, here's the way it would go: Defibrillation CPR Epinephrine shock Amiodarone shock The dose of amiodarone in this setting is 5mg/kg and it should be given rapidly IV push. Again, if the endotracheal route is used, the dose of atropine is doubled, but the dose of lidocaine and epinephrine is the same for IV and IO routes. Amiodarone and dopamine should not be given through the tracheal tube. If bradyasystolic arrest persists or recurs after adequate epinephrine doses have been given, consider an epinephrine infusion: 0. l-0.2mcg/kg/minute titrated to effect. If a bradyasystolic arrest persists or recurs after administration of adequate atropine doses have been given, consider a dopamine infusion. Prepare as follows: multiply the child's weight in kilograms by 6 to determine the number of milligrams of dopamine; add this amount to D5W to make 100 cc... lcc/hr delivers lmcg/ kg/min. Titrate to effect starting at 5mcg/kg/min... and do not exceed 20mcg/kg/min.


"MEETING THE CHALLENGE OF DIFFICULT CASES" The sixth major category is ACID-BASE DISORDERS, particularly those complicated by electrolyte imbalance. Patients with an altered mental status, a vague clinical presentation, or a combination of symptoms suggesting involvement of multi-organ systems should be suspect. A careful history may uncover an underlying medical illness or a medication that has kindled the acid-base disorder. The basic challenge in these cases is determining the CAUSE of the chemical derangement and then providing appropriate therapy. Here are some of the critical points you need to consider in making your assessment and management decisions: 1 - Arterial blood gas analysis and serum electrolyte determinations should be ordered on all patients in whom the clinical diagnosis is unclear. 2 - Accurate interpretation of these lab values (plus a good H&P) should lead you to the cause of the chemical imbalance. 3 - Appropriate management means treating the CAUSE when possible, as well as the acid-base and electrolyte imbalance. One of the greatest challenges you have is the patient with metabolic acidosis of unknown etiology. There are three parameters that can help sort out this problem: The anion gap The serum chloride level.. .and The serum potassium level The anion gap is calculated by subtracting the concentration of chloride and bicarb from the concentration of sodium. The normal gap is 8-16 mEq/liter. Metabolic acidosis may be associated with a normal anion gap or a high anion gap. If the anion gap is normal, look at the serum chloride and potassium levels. The serum chloride level should be elevated. Now take a look at the serum potassium level. If it is low...that is, less than 3.5... consider the following causes: Diarrhea (either acute or chronic) Carbonic anhydrase inhibitors (such as acetazolamide which is Diamox)... and Renal tubular acidosis I doubt that you would be given a case of primary renal tubular acidosis but you might be given one that is secondary to ingestion of paraldehyde, out-dated tetracycline or amphotericin B. Hypercalcemia can also be associated with renal tubular acidosis. All of these conditions are caused by impairment of tubular reabsorption of bicarbonate. The most common clinical presentation of renal tubular acidosis is chronic weakness and fatigue which is secondary to the associated hypokalemia.


If the anion gap is normal with metabolic acidosis but the serum potassium is ELEVATED, consider the following as possible causes: Ammonium chloride toxicity (and remember that ammonium chloride is found in some of the antitussive, expectorant and antihistamine prescription drugs) Chronic pyelonephritis Obstructive uropathy... and Adrenal insufficiency Now, if the anion gap is high.. .that is, greater than 16 mEq/L.. .consider the following causes: Diabetic ketoacidosis Alcoholic ketoacidosis Lactic acidosis Salicylate toxicity Ingestion of methanol, ethylene glycol, isoniazid, iron or paraldehyde... and Renal failure (which is uremia) Note that paraldehyde ingestion can produce metabolic acidosis associated with either a normal or high anion gap. Metabolic alkalosis is another challenging situation. You don't see it as often as metabolic acidosis but, when you do see it, determining the cause can be a challenge indeed. There are multiple causes of metabolic alkalosis with complex clinical pictures, but I don't believe you'll be given such a case at the Oral Exam. There ARE causes, however, that are simpler to diagnose and one of them may very well appear on the exam. The serum chloride level can help you sort them out. I think the most common cause of HYPOchloremic metabolic alkalosis seen in the Emergency Department is secondary to the use of diuretics. A careful history will reveal this diagnosis. The second most common cause is vomiting. Some causes of metabolic alkalosis are associated with a HIGH serum chloride level. These include the following: Severe hypokalemia (usually less than 2.5) Cushing's Syndrome... and Licorice ingestion Of the three, Cushing's Syndrome is probably the one most difficult to diagnose. A common clinical presentation of the patient with Cushing's Syndrome is the triad of fatigue, weakness and depression. Significant historical findings are weight gain, menstrual irregularities, polyuria and polydipsia. On physical exam, there may be mild hypertension, hirsutism and acne, unexplained bruises, and of courseedema. The laboratory picture in the patient with Cushing's Syndromein addition to the hyperchloremic metabolic alkalosisincludes the following: a mild leukocytosis with less than 20 lymphs and no eosinophils on the differential and a normal or elevated serum glucose with glycosuria detected on urinalysis.


Metabolic acid-base disorders are among the most difficult clinical problems to assess in the Emergency Department. Mapping out the possibilities in a methodical, systematic manner is the key to uncovering the source. The seventh major category is ENVIRONMENTAL EMERGENCIES. Included in this category are Hypothermia Heat-related disorders (such as heatstroke and heat exhaustion) Carbon monoxide poisoning...and Near-drowning Hypothermia is easy to diagnose IF you think of it and IF you use a rectal probe that is calibrated to accurately determine subnormal temperatures. Unfortunately, most hypothermic patients present with illnesses or injuries that tend to divert your attention. The critical point in these cases is to obtain an accurate temperature recording. If you suspect this diagnosis, be sure to request that the temperature be taken with a rectal probe. Heat-related disorders are usually straightforward. But an important point to consider is this: many heat disorders are triggered by one or more medications the patient is taking. Frequent offenders include drugs with anticholinergic properties, especially cyclic antidepressants and atropine, as well as phenothiazines and cocaine. The critical point in assessing patients with heat-related disorders is to determine WHAT medications they have taken. If you are not sure whether a particular medication may have triggered the hyperthermia, check the PDR, consult with the hospital pharmacist or, if you have it in your ER, look at the package insert for more information. Drugs that have been known to precipitate a heatstroke include the following: Anticholinergic agents such as antihistamines, atropine, scopolamine and Cogentin Phenothiazines (particularly Thorazine) Cyclic antidepressants Cocaine Diuretics Phencyclidine and ephedrine Beta-blockers and calcium-channel blockers LSD (which is important to consider in the patient with apparent "acute psychosis").. .and Amphetamines.. .which are commonly used by dieters. You do not need to memorize these drugs for the Oral Exam. I listed them here in the event that you might be given a heatstroke patient on one of these medications. Your score would go up if you were able to tell the examiner that the heatstroke may have been precipitated by the medication. Carbon monoxide poisoning should be considered in all patients who have been exposed to a fire. Improperly vented heating systems are another source of exposure.. .particularly at the beginning of the heating season. A clue here, is the presence of concurrent illness in other family members and pets. Exposure to gasoline fumes, either intentional or accidental, is yet another, and usually the most

obvious cause of carbon monoxide poisoning. All of these patients typically present with headache, nausea, dizziness and/or a behavioral change. Of all the environmental emergencies, the near-drowning victim is probably your greatest challenge. Critical points to remember are these: 1 - Aggressive airway management with intubation and mechanical ventilation is indicated in the unconscious or obtunded patient. 2 - Cervical spine injury should always be considered. Immobilize the C-spine and order a portable lateral C-spine film. Remember that all seven cervical vertebrae AND the C7-T1 interspace, must be visualized. 3 - Substance abuse or medical emergencies may have precipitated the event. Administer Narcan and glucose when an IV line has been establishedorder appropriate lab studies and pursue historical sources that can provide you with the information you need. Always consider an MI as a possible cause of the drowning in the older adult patient and order an ECG. 4 - Hypothermia and noncardiogenic pulmonary edema are frequent complications. Ask the nurse to use a rectal probe in order to obtain an accurate core temperature. Aspiration may be confused with incipient pulmonary edema on clinical exam. Auscultation of the chest may reveal wheezing, rales or rhonchi and the patient may produce large amounts of frothy sputum. The chest x-ray may or may not be helpful. A diffuse alveolar or interstitial infiltrate may be seen with aspiration OR edema. However, a segmental or lobar infiltrate, particularly on the right side, is diagnostic of aspiration pneumonia. The cornerstone of therapy for the patient with fluid aspiration OR noncardiogenic pulmonary edema is the sameand that ismechanical ventilation and the use of positive end-expiratory pressure. Lasix is not likely to be effective since the pulmonary capillary wedge pressure in NONcardiogenic pulmonary edema is LOW. It should be noted here that pulmonary edema is more commonly associated with salt water drowning. 5 - Associated injuries are common in near-drowning victims, particularly skull fractures. But search for other injuries as well. Assess this patient as you would any major trauma victim...and 6 - In patients with a history of prolonged submersion renal failure, disseminated intravascular clotting and cerebral edema, may occur. Laboratory assessments and repeated physical exams are indicated.

constitute the eighth major category of cases. Aneurysms, pulmonary emboli and hypertensive emergencies are the cases most frequently encountered. Dissecting thoracic aneurysms and ruptured abdominal aortic aneurysms have one critical management point in common: both of these catastrophic events are associated with abnormal blood pressures that require treatment. Thoracic dissections are commonly associated with an elevated blood pressure that should be lowered to prevent progressive dissection. The most frequently used drug regimen is propranolol in combination with nitroprusside...following a

test dose of 0.5 mg of propranolol IV, 1 mg of propranolol is administered every 5 minutes until the heart rate is between 60 and 80. Then an infusion of sodium nitroprusside is started and titrated to a systolic pressure of approximately 100-120mmHg. Single-agent therapy with IV labetalol is another option. Abdominal aortic ruptures, on the other hand, are associated with low blood pressures and are frequently accompanied by a syncopal episode. In these cases, shock treatment consists of IV fluids and blood transfusion. The diagnosis of pulmonary embolus poses a unique challenge to Emergency Physicians because signs and symptoms are nonspecific and clinical presentations are frequently vague and misleading. Critical points in patient evaluation are these: 1 - Smaller emboli produce a clinical picture of predominately PULMONARY symptomsmost notablydyspnea, pleuritic chest pain and cough. Tachycardia is also frequently present. Remember, too, that "hyperventilation" is a common clinical presentation with these patients. 2 - Large or massive pulmonary emboli produce a clinical picture of predominately CARDIOVASCULAR symptoms which may appear similar to those of a patient having an MI; severe chest pain with shortness of breath and diaphoresis is not uncommon. Unlike the MI patient, however, onset of symptoms is usually abrupt rather than gradual. 3 - A ventilation-perfusion lung scan should be ordered for any patient with a suspected pulmonary embolism. In some hospi-tals, the spiral CT has been used in conjunction with an abnormal chest film to detect a PE. The major advantage of spiral CT over a V/Q scan is that it can identify other pulmonary pathology. However, neither of these studies can accurately detect subsegmental defects. This picture may change in the future as spiral CT angiography evolves as a diagnostic modality. 4 - If the lung scan or spiral CT is nondiagnostic, but the clinical picture is highly suggestive of pulmonary embolism, the patient needs further evaluation with either peripheral venous studies or CT angiography. Peripheral vascular studies are often done first because they are less invasive. If positive, they provide indirect evidence of a pulmonary embolus sufficient enough to initiate heparinization. If, however, these studies are negative or uncertain, an angiogram MUST be done. Angiography should also be done in those patients who are at high risk for bleeding complications from anticoagulation therapy and in those whom you anticipate thrombolytic therapy or surgical embolectomy (in other words, the unstable patient in whom you suspect a massive embolus). CT angiography is likely to replace pulmonary angiography (especially since CT images can be reconstructed to produce a resolution of 2mm, which is smaller than the resolution of pulmonary angiography). 21

Assessment of patients with hypertension revolves around two focal points: a CLINICAL focus and a CRITICAL focus. The clinical focus is determining whether or not the patient's clinical presentation is the result of a hypertensive crisis. The critical focus is determining how quickly the blood pressure should be lowered. Consider the following in your evaluation of these patients: 1 - A diastolic blood pressure of 130 or more is usually present in the u r g e n t and emergent cases...although it can be less, particularly in toxemia of pregnancy. 2 - More important than the absolute number is the presence or absence of signs and/or symptoms of end-organ damage or dysfunction. 3 - Hypertension that is associated with signs of end-organ damage...such as encephalopathy, myocardial ischemia or intracranial hemorrhage... is a hypertensive EMERGENCY. In these patients, the goal of therapy is to lower the blood pressure by 30% of their pretreatment levels, over the first hour of therapy...and then admit them to the ICU or CCU. 4 - Patients who have significant hypertension (that is, a diastolic blood pressure of 115 to 130 or more) WITHOUT signs of end-organ damage are classified as URGENT cases. In these patients, the goal is to lower their blood pressure more gradually, over a period of 24-48 hours. The ninth and last major category of cases is DIABETIC EMERGENCIES. Diabetic ketoacidosis, hyperosmolar nonketotic hyperglycemia and hypoglycemia are all cases we've managed with some frequency in the Emergency Department. What's important about these cases, in addition to their management, is the CAUSE of the problem. The hypoglycemic patient should also be checked for any possible injuries sustained, after losing consciousness. The most common cause of diabetic ketoacidosis is infection. Urinary tract infections and pneumonia are the most frequent precipitating infectionsbut ANY infection, even minor ones such as a cold or gastroenteritis, can trigger this metabolic derangement in the insulin-dependent diabetic. Other causes to consider are an Acute MI, a CVA, trauma, pregnancy, hyperthyroidism, pancreatitis, steroid usage, emotional upset andof courseomission of insulin. A careful history and physical exam will provide clues. If initial lab studies, ECG and chest x-ray are unrevealingmethodically rule out the possible causes in the following manner: Order cardiac enzymes, a serum amylase AND a pregnancy test when appropriate Consider a CT scan if the history and physical suggest the possibility of a CVA Search for evidence of occult trauma If hyperthyroidism is a possibility, clues to the diagnosis can be found on physical examfor example: Warm, moist, smooth skin An enlarged thyroid gland A wide pulse pressure... and


Brisk tendon reflexes. (Thyroid studies can be ordered but results are not likely to be available for several hours.) A history of emotional instability should be sought if organic causes of DKA have been ruled out. This is a likely possibility, if there is also a history of a recent emotional crisis. Diabetic ketoacidosis is usually precipitated rather suddenly (within a few hours to a few days) and occurs in the insulin-dependent diabetic. Nonketotic hyperosmolar hyperglycemic coma, on the other hand, develops over a period of many days to several weeks and is seen in the non-insulin-dependent diabetic. These latter patients are taking an oral hypoglycemic agent or they are on a diet-control program only. Some are not even aware of their diabetic condition. The majority of patients who present with hyperosmolar coma have chronic debilitating illnesses. Examples are the nursing home patient, the patient with a chronic renal or cardiovascular disorder and the patient with chronic dementia. A variety of drugs have been implicated as well. Thiazide diuretics and oral diazoxide are both well-recognized causes of non-ketotic hyperosmolar coma. ORAL diazoxide, by the way, is not used as an antihypertensive agent, but as a hyperglycemic agent that is used in the management of hypoglycemia due to hyperinsulinism. Other drugs that can induce hyperosmolar coma are furosemide, steroids, phenytoin, cimetidine, Beta and calcium-channel blockers, immuno-suppressive agents and chlorpromazine. Again, you don't need to memorize these drugs. They are simply clues to the possible cause of hyperosmolar coma. As in diabetic ketoacidosis, infection is a common precipitating cause of hyperosmolar coma with gram-negative pneumonia or sepsis being the most common cause. Other medical illnesses that have been implicated are: Myocardial infarction CVA or subdural hematoma GI bleeding Acute pyelonephritis Acute pancreatitis Uremia.. .and Thrombophlebitis Environmental exposure can also precipitate hyperosmolar coma. Included here are: extensive burns, heatstroke and hypothermia. The challenge of hypoglycemia lies in its recognition. Clinical presentations of hypoglycemia are variable, so strict adherence to the following principle, is imperative: any obtunded or comatose patient should be given an IV glucose bolus immediately after blood has been drawn for lab analysis. Acutely psychotic patients WITHOUT A PRIOR HISTORY OF A MENTAL DISORDER should also be suspect, particularly young adult males. Since hypoglycemia tends to occur suddenly, the patient may experience a syncopal episode. Significant injuries may result and should be sought.


Meeting the challenge of difficult cases gives you an edge during this exam. Listen to this CD two or three times because these are the cases that require skill and expertise for successful management. There are others, of course, but I believe these nine represent the core case categories of the Oral Exam. This the end of the first CD.


CD 6 "LAST-MINUTE CLINICAL REVIEW" In the last week before the exam, you will have finished studying the text, you will have practiced the exam process and you will have listened to the preceding CD. At this stage of your preparation, I thought you might find a last-minute review, useful. There are three topics I have chosen for the clinical review: ACLS, the differential diagnosis of headache and pediatric resuscitation. This may seem like an unusual combination to you, so let me explain the rationale of these choices. You MUST know the ACLS protocols. New guidelines were issued by the American Heart Association in December of 2005. These guidelines are available at the American Heart Association web page. ACLS changes are outlined in a concise manner listing the old standard, the new standard and why the changes were made. Though too numerous to be listed here, they are reasonable in length and content; you should be familiar with these changes before taking the oral examination. Some of them are reviewed here, but you should get a copy of ALL the ACLS revisions and review them. The witnessed arrest is more frequently encountered, so I will review the WITNESSED arrest situations that are most likely to appear on this exam. Pediatric resuscitation is a topic that has appeared on this exam...and you will need to know correct drug dosages, at least for the arrest situation. Both arrest and non-arrest clinical situations are reviewed here. ACLS and pediatric resuscitation protocols are frequently complex and difficult to learn, so I separated these reviews for easier learning. The differential diagnosis of headache is right between them. The headache patient may or may not appear on ths exam. However, it's a topic that I think merits review because if it DOES appear, certain pathologic entities should be ruled out. In addition to this clinical review, I have also included a last-minute review of key points in the exam process. This includes a case management checklist, critical actions, diagnostic clues and exam techniques. I will start with an ACLS review of the WITNESSED CARDIAC ARREST in the adult patient. This review reflects the revisions published in the Guidelines 2000 as well as those published in the December 2005 issue of Currents in Emergency Cardiac Care. All of these patients are on a monitor and have an IV established. Specific management of the following dysrhythmias will be reviewed: #1 #2 #3 #4 #5 Monitored ventricular tachycardia in a patient WITH a pulse Monitored ventricularfibrillation(which also includes monitored ventricular tachycardia in the unconscious, pulseless patient) Persistent or recurrent ventricular fibrillation Pulseless electrical activity.. .and Asystolic cardiac arrest

Specific management of monitored VENTRICULAR TACHYCARDIA in patients WITH A PULSE, is determined primarily by the presence of symptoms and the level of hemodynamic stability. An unstable patient is one with symptoms (especially chest pain or shortness of breath), hypotension (that is, a systolic blood pressure less than 100), congestive heart failure, myocardial ischemia or infarction or an altered level of consciousness. An unstable patient in V-Tach with a ventricular rate > 150 should be prepared immediately for synchronized cardioversion.Start with 100 joules and pretreat with a sedating agent, such as Versed or Valium. If delays in synchronization occur, switch to unsynchronized shocks, using equivalent energy. If the V-Tach does not convert, then increase the energy level to 200, then 300 and, finally, 360 joules as needed. Remember to reset the synch mode after each synchronized cardioversion because most defibrillators default back to the unsynchronized mode. Once cardioversion is achieved, antidysrhythmic therapy should probably be given. The ACLS Guidelines favor the use of amiodarone over lidocaine and I think this is a good choice (especially in the elderly and those with progressive decline in cardiac pump function). IV amiodarone is administered as 150mg over ten minutes followed by a lmg/minute infusion for six hours and then, 0.5mg/minute. If the patient's pulse and blood pressure are dropping after therapy has been initiated, slow down the infusion rate. Occasionally, it's difficult to distinguish V-Tach from SVT with aberrancy.The odds strongly favor V-Tach rather than aberrant SVT in a patient who is having or has had an MI. If the diagnosis of a wide complex tachycardia is in doubt (and the patient is stable), obtain a 12-lead ECG; an esophageal lead may be helpful if the origin of the dysrhythmia remains in doubt. SVT with aberrancy is diagnosed only if QRS morphology is typical of bundle-branch block; any other morphology of the QRS in leads Vx and V6 is assumed to represent V-Tach by default. Also, look for the following ECG findings that support the diagnosis of V-Tach: AV dissociation associated with fusion or capture beats and/or QRS concordance. Now, if you are looking at a rhythm strip with wide QRS complexes, look for dissociated P waves followed by relatively normal-looking QRS complexes; they will be interspersed between one or two wide QRS complexes. These P waves are capture (or fusion) beats. QRS concordance is another finding that strongly suggests V-Tach. In this situation, all the QRS complexes are either upright or inverted in the precordial leads or the QRS complexes are predominantly negative in leads Vi - V6. If the patient is unstable, treat with DC cardioversion or amiodarone. For the patient in V-Tach, who has a pulse (and is conscious and stable) the first thing you need to do is to determine whether it is monomorphic or polymorphic V-Tach. If the QRS morphology is the same, then the V-Tach is monomorphic; varying QRS morphology is called polymorphic V-Tach. If the patient has monomorphic V-Tach, which drug you give will be based on the integrity of cardiac function. If there is no evidence of pump failure, then procainamide is the drug of choice. Begin an infusion at 20mg/minute and continue until one of the following occurs: suppression of the dysrhythmia, hypotension, widening of the QRS complex or a total of 17mg/kg has been given. If the rhythm converts at this point, follow with a procainamide infusion drip run at 14mg/minute. If there is still no change in rhythm, amiodarone or lidocaine are other acceptable alternative agents. Now if the cardiac function is impaired in the presence of monomorphic V-Tach, administer amiodarone (a 150mg IV bolus over


ten minutes) or lidocaine (0.5 - 0.75mg/kg IV push) followed by synchronized cardioversion; if the patient is conscious, he should be premedicated with Versed or Valium. If repeated cardioversion attempts are needed, then use 200 - then 300 then 360 joules respectively as needed. Polymorphic V-Tach is treated differently .. . and depends on the duration of the QT interval, the history, physical exam and lab evidence suggesting myocardial ischemia or infarction, electrolyte abnormalities or a known (or suspected) toxic ingestion or exposure. Order an ECG - lytes (including magnesium and calcium) - cardiac enzymes and, if a specific toxin is suspected - a stat tox level for that substance. Now, look at a rhythm strip and examine the QT interval. Is it normal or prolonged? If the QT interval is prolonged, is the rate slow? Bradycardia associated with a prolonged QT suggests Torsades-de-Pointes and should be treated immediately with IV magnesium. If this is not the problem, you may go directly to cardioversion; if this option is not feasable, evaluate the diagnostic tests you ordered. Correct any electrolyte abnormalities. If the patient's history, physical exam, ECG or enzymes suggest an acute coronary syndrome go back to the QT interval again. If it is normal, a beta-blocker and anti-ischemic agents should be given; however, avoid beta-blockers if the rate is slow. If the QT interval is prolonged, strongly consider cardioversion starting at 200 joules; overdrive pacing may be required to shorten the QT interval. While this is being set up, a trial of lidocaine or phenytoin may be helpful. .. and may actually suppress the dysrhythmia. Lidocaine is a good choice if there is evidence of ischemia on the ECG. Phenytoin may work if the V-Tach is secondary to a cyclic anti-depressant or phenothiazine overdose. Monitored ventricular tachycardia (with a ventricular rate > 150) in the unstable patient with a pulse who is unconscious, hypotensive or in pulmonary edema, must be treated immediately with UNSYNCHRONIZED cardioversion to avoid delay associated with synchronization. Once ventricular tachycardia has resolved, begin an IV infusion of the anti-dysrhythmic agent that aided the resolution of the V-Tach. The infusion rate for lidocaine is 2-4mg/minute, phenytoin is 100-400mg/day and procainamide is l-4mg/minute. If cardioversion alone led to resolution of the V-Tach, the patient should be given a loading dose of lidocaine (not phenytoin or procainamide) followed by a lidocaine infusion. Administering a continuous infusion of a propylactic antidysrhythmic agents is controversial, but unless or until data becomes available that negates its potential theoretical advantages, it is reasonable to continue an infusion of the drug associated with restoration of a stable rhythm. After conversion to a stable rhythm, examine the ECG for signs of ischemia or a prolonged corrected QT interval. Also, examine the ECG for downsloping elevation of the ST segment in leads V!-V3 with or without a right bundle-branch block. These findings suggest a diagnosis of the "Brugada syndrome", a recently recognized inherited syndrome characterized by this typical ECG appearance and a history of syncope. Management of MONITORED VENTRICULAR FIBRILLATION AND PULSELESS V-TACH is as follows (parenthetically if your patient is in V-Tach, substitute the phrase "unsynchronized cardioversion" for "defibrillate"). Here we go:


Establish unresponsiveness and pulselessness. Confirm presence of V-Pib or V-Tach on the defibrillator. Using a monophasic manual defibrillator, deliver a single dose of 360 Joules. If unsuccessful, start CPR (beginning with chest compressions). Check the rhythm after 5 cycles of CPR or two minutes have passed. Intubate the patient during this time. Make sure an IV or 10 line is in place. If the patient remains in V-Fib or pulseless V-Tach, defibrillate again at 360 Joules. If unsuccesful, continue CPR and initiate drug therapy with epinephrine lmg (which may be repeated every 3-5 minutes). Defibrillation with 360 joules should be carried out within 30-60 seconds of an administered epinephrine dose. If the patient converts to a rhythm that is accompanied by return of spontaneous circulation, then do the following: Obtain and assess vital signs Check the upper airway for patency and support breathing Administer medications appropriate for blood pressure, heart rate and rhythm If the patient still does not convert to a stable rhythm, then one of the following is likely to be present: Persistent or recurrent V-Fib or V-Tach Pulseless electrical activity.. .or Asystole Management of these catastrophic, post-arrest conduction disturbances will be discussed here but, before I get into that, there are two points about the V-Fib and pulseless V-Tach protocol just reviewed, that I want you to remember: First Second Rapid defibrillation remains the MAIN determinant of survival in cardiac arrest due to V-Fib or pulseless V-Tach...and Sodium bicarbonate should not be used routinely in cardiac arrest. Adequate ventilation remains the mainstay for control of acidosis in cardiac arrest. However, if the arrest occurred in a patient with pre-existing hyperkalemia, bicarb is DEFINITELY indicated. It is also indicated if the arrest was associated with either a pre-existing acidosis that is bicarbonate-responsive or a cyclic antidepressant or phenobarbital overdose.

Metabolic alkalosis is easily induced when bicarb is given early in a WITNESSED arrest. With an airway and IV established and early CPR performed, acidosis does not usually occur for several minutes. RESPIRATORY acidosis occurs much more commonly than METABOLIC acidosis and is treated by improving oxygenation. The administration of bicarbonate should be guided by the bicarb concentration or the calculated base deficit obtained from ABG analysis or lab measurement... and only half of the calculated deficit should be given.


often the result of inadequate oxygenation and/or acid-base imbalance. If ventricular fibrillation or pulseless V-Tach persists or recurs after the usual ACLS protocol has been followed, consider metabolic abnormalities such as hyperkalemia and hypomagnesemia, as possible causes of persistent ventricular fibrillation: Treat presumed severe hyperkalemia with sodium bicarb in a dose of lmEq/kg. If the patient has a history of congestive heart failure, diabetes or alcoholism, administration of magnesium sulfate is worth a try the dose is l-2gm IV. Other potentially reversible causes of persistent ventricular fibrillation should be ruled outthese include: Hypothermia Digitalis toxicity Quinidine toxicity... and Myocardial irritation from a pacemaker or intracardiac catheter If V-Fib or V-Tach persists or recurs after the above measures, administer one of the following medications: (a) AMIODARONE ... which is initially administered in this setting as a rapid infusion with 300mg diluted in 20-30cc of D5W or Normal Saline. Follow in 30-60 seconds with defbrillation at 360 joules. Supplementary infusions of 150mg can be repeated for recurrent or resistant dysrhythmias to a maximum manufacturer-recommended total daily dose of two grams. Amiodarone is now considered the drug of choice unless the V-Tach is Torsade-de-Pointes or there is evidence of hypomagnesemia. (b) MAGNESIUM SULFATE in l-2gm in 50-100cc D5W over 5-60 minutes IV is indicated for ECG evidence of Torsade-de-Pointes (which is an atypical V-Tach) or suspected (or documented) hypomagnesemia. (c) PROCAINAMIDE 20mg/minute may be given for recurrent or refractory V-Fib. The total dose should not exceed 17mg/kg. (d) LIDOCAINE 1-1.5 mg/kg IV may be given if all else fails. Once considered a first-line drug, evidence-based studies have not demonstrated its superiority over the aforementioned agents. An additional bolus of 0.5-0.75mg/kg can be given over 3-5 minutes if necessary. For any med used, defibrillate with 360 joules after each dose. The pattern should be drug-shock- - CPR. Here is a summary of the V-FLb/pulseless V-Tach sequence: - Shock - CPRintubateIV - EpinephrineshockCPR -AmiodaroneshockCPR - Magnesium (if indicated) thenshock then CPR - Procainamide (if indicated) thenshockthen CPR - LidocaineshockCPR



(e) SODIUM BICARB should also be reconsidered at this time: Did this patient have metabolic acidosis, prior to arrest? Is this an "overdose patient?" Any of the following overdoses require alkalinization therapy: Cyclic antidepressants Salicylates Long-acting barbiturates... and Chlorpropamide The dose of bicarb is lmEq/kg. (f) Another overdose to consider (especially in the older patient) is a calcium-channel blocker. In this case, administration of CALCIUM CHLORIDE would probably be effective. The dose is lOcc of a 10% solution given IV over 10 minutes. Hypocalcemia, of course, is another indication for this drug. Does this patient have a history of a chronic bowel disorder (such as chronic diarrhea or malabsorption syndrome)? Other causes of hypocalcemia include renal failure, hypoparathyroidism and acute pancreatitis. Now, let's move on to the patient with PULSELESS ELECTRICAL ACTIVITY. What Tins means is that the electricity is still on but the pump is functioning poorly (if at all). PEA includes any of the following electrical disturbances: Electromechanical dissociation (also known as EMD) Pseudo-EMD Idioventricular rhythms Ventricular escape rhythms Bradyasystolic rhythms.. .and Post-defibrillation idioventricular rhythms If you have identified any of these situations in your patient, then do the following: Continue CPR and intubate the patient. While you are intubating, ask the nurse to start an IV. Ventilate the patient with 100% O2. Listen for breath sounds in both lung fields and assess the ease of manual ventilation to rule out tension pneumothorax. Administer a fluid bolus to correct hypovolemia and assess peripheral perfusion using Doppler ultrasound. Check the patient's ECG for evidence of hypo - or - hyperkalemia or an acute MI ...and Obtain a core body temperature, to rule out hypothermia. While these steps are being taken, consider the possible causes of this patient's problem (as well as their appropriate therapy). It will be helpful, in this respect, to have a nurse or EMT obtain more history from significant others (family, friends, etc.). Your approach will be guided by your clinical findings, the patient's medical history and the circumstances which preceded the development of pulseless electrical activity. Among the possible causes are these: Hypovolemia: appropriate therapy here is volume infusion Hypoxia: appropriate therapy is ventilation Cardiac tamponade: appropriate therapy is pericardiocentesis Tension pneumothorax: appropriate therapy is needle decompression

Hypothermia (which should be treated accordingly) Massive pulmonary embolus: appropriate treatment here is surgery and thrombolytics Drug overdoses with cyclic antidepressants, digitalis, Beta-blockers and calcium channel blockers (all of which may respond to appropriate drug therapy) Hyperkalemia or acidosis (both of which may respond to bicarb).. .and, finally Massive acute myocardial infarction (in which case, PEA is an ominous finding, since it is frequently associated with at least 40% myocardial injury) If PEA persists after BCLS measures have been carried out and you have considered possible causes, then administer epinephrine lmg IV push repeated every 3-5 minutes as needed. If this approach fails, higher doses may be used (up to 0.2mg/kg) but, as mentioned before, they are not recommended. If pulseless bradycardia exists, administer atropine lmg IV and repeat every 3-5 minutes as needed up to a total of .04mg/kg. These shorter atropine dosing intervals are possibly helpful in cardiac arrest. Now let's review the ASYSTOLE treatment algorithm. In managing an asystolic arrest, it is important to first confirm the diagnosis. Ventricular fibrillation, which is a more responsive dysrhythmia, may masquerade as asystole if only one lead is checked. Always check TWO leads. If doubt still remains, treat as ventricular fibrillation. The sequence for treating asystole is as follows: Continue CPR, intubate and obtain IV access Confirm asystole in more than one lead. This can be accomplished in one of two ways: First Move the positive chest electrode at the left shoulder to the substernal area OR Second Put on limb leads Rule out any of the following as a possible cause of asystole: Hypoxia Hyperkalemia Hypokalemia Pre-existing acidosis Drug overdoses... and Hypothermia If these conditions have been ruled out, then consider transcutaneous pacing. To be effective, transcutaneous pacing must be performed early, simultaneously with drugs. However, clinical evidence does not support the routine use of TCP for asystole.


Drug therapy for asystole is as follows: First Administer epinephrine lmg IV push every 3-5 minutes. Bicarb should also be given, if the patient has known pre-existing hyperkalemia...and Second Atropine should be given if epinephrine fails. The dose is lmg IV every 3-5 minutes up to a total of .04mg/kg. Consider bicarb again at this point... if there is pre-existing bicarb-responsive acidosis

for an overdose with cyclic antidepressants oj to alkalinize the urine in drug overdoses QS for those patients who have been in arrest for a long time (this is only acceptable for the patient who is intubated or who has return of spontaneous circulation).

If the patient still remains in asystole after all of these measures have been taken (and no reversible causes are identified) consider termination of resuscitation efforts. This completes the ACLS review of those dysrhythmias and clinical settings most frequently encountered at the Oral Board Exam. I recommend that you obtain a copy of the new 2005 guidelines from the American Heart Association website since there are some fairly significant changes I have alluded to on this CD.


Now let's review the differential diagnosis of "headache." There are nine potentially serious causes of headache that should be considered: 1 - Subdural hematoma 2 - Meningitis 3 - Subarachnoid hemorrhage 4 - Hypertension 5 - Glaucoma 6 - Mastoiditis 7 - Uremia 8 - Carbon monoxide poisoning.. .and 9 - Temporal arteritis Other poisonings (as well as cerebral tumors) can also cause headache, but the headache in these cases is usually not the predominant complaint. A SUBDURAL HEMATOMA should always be considered in the substance abuse patient, particularly the alcoholic. Children who are victims of abuse and hemophiliacs are also candidates for intracranial bleeding. Important clues are these: a history of trauma, a behavioral change, an altered level of consciousness, aphasia, vomiting, convulsions and unilateral weakness. In the young male child, be sure to ask the parent if there is a history of hemophilia. On physical exam, look for evidence of head injury and take note of the pulse. Patients with an expanding intracranial hematoma are often bradycardic. If a plain CT scan of the head appears normal (but you still suspect a subdural) then order a contrastenhanced CT or an MRI.
MENINGITIS classically presents with headache, neck pain, fever and vomiting. Very young and very old patients frequently do not have this classic presentation. In this latter group of patients, always consider the diagnosis of meningitis when the clinical presentation is UNFOCUSED. . .that is, signs and symptoms are vague or generalized. Almost all patients with meningitis appear acutely ill, often in disproportion to physical findings which may be sparse or even absent. The patient may be confused, irrational or excited. Positive findings on physical exam are: fever, nuchal rigidity, Kernig's and Brudzinski's signs. Absence of these findings does NOT rule out the diagnosis. CT scan of the head should be done first to rule out a mass lesion in patients who are obtunded or unconscious and those who have focal neurological signs, papilledema or seizures, as well as those with a history of AIDS or risk factors for HIV. If the CT is negative, then lumbar puncture is clearly indicated as it is THE definitive diagnostic study. Countercurrent immunoelectrophoresis or latex agglutination may help identify the causative organism; these tests are especially useful in cases of partially treated meningitis. Antibiotic therapy should be initiated without delay, especially in patients with acute presentations. Currently, third-generation cephalosporins (such as ceftriaxone and cefotaxime) are preferred by many for initial therapy of meningitis, particularly if therapy is initiated empirically. These agents have good CSF penetration and are effective against Strep, pneumoniae, Neisseria meningitidis, Haemophilus influenzae and most gram negative enteric organisms. They do not, however, cover Listeria or methicillin-resistant Staph. Empirical therapy, if instituted early (that is, within 30-60 minutes of presentation) significantly reduces the morbidity and sequelae associated with acute meningitis. The following regimens are appropriate:


For neonates (that is, those < 1 month of age) ampicillin and cefotaxime are commonly used; an alternative regimen is ampicillin and Gentamicin. Infants ( that is, those between 1 and 3 months of age) can be given ampicillin and cefotaxime or ampicillin and ceftriaxone. Children older than 2 months should be given cefotaxime or ceftriaxone along with vancomycin. Adults 18-50 years old should receive ceftriaxone along with vancomycin . . . a n d Adults older than 50 should be given ceftriaxone and ampicillin. A good oral board topic would be meningitis due to the West Nile Virus...which should always be considered as a possibility in patients with fever, headache, vomiting, mental status change and stiff neck. Additional findings of proximal muscle weakness or flaccid paralysis should heighten your suspicion. CSF findings reveal lymphocytes, an elevated protein and absence of bacteria. Emperic treatment for bacterial meningitis and/or herpes simplex encephalitis is appropriate until results of testing for the West Nile Virus have been clarified in serum and CSF studies. The headache associated with spontaneous SUBARACHNOID HEMORRHAGE is sudden in onset and frequently severe, sometimes described by the patient as "the worst headache I've ever had" but, more often described as "different" from any he or she has ever had. Most often, spontaneous subarachnoid hemorrhages are due to rupture of an intracranial aneurysm, referred to as a "berry aneurysm." Patients with these bleeds usually look sick and nausea and vomiting are prominent associated symptoms. If the patient has only had a small warning bleed, referred to as a "sentinel bleed", his presentation may be more subacute. This is also true of patient's whose aneurysms are expanding, but have not yet leaked. These patients sometimes present with a headache that has been present for several days and is different from any headache, they have had before. The headache of subarachnoid hemorrhage is also sometimes associated with a painful eye, and examination may reveal ptosis on that side. Patients with a history of migraine can have this clinical picture as well, but their headache is usually gradual in onset, rather than the abrupt SUDDEN onset characteristic of a subarachnoid hemorrhage. I think it's important to note here that patients with subarachnoid hemorrhage have been misdiagnosed as migraine headache. You should be suspicious if a known migraine patient tells you that THIS headache is "different" from the others. Be sure to perform a complete neurologic exam on your migraine patients. Physical findings associated with a subarachnoid hemorrhage, include drowsiness or coma, hypertension, nuchal rigidity, positive Kernig's and Brudzinski's signs, bilateral Babinskis and cranial nerve palsy (especially the third cranial nerve). Definitive diagnosis is usually made by CT scan. However, some patients with a subarachnoid hemorrhage have a negative scan. In these cases, an LP needs to be done to establish the diagnosis.


is a common cause of headache in patients with a history of hypertension, heart disease and kidney disease. Keep in mind, however, that uncontrolled hypertension may be associated with intracranial bleeding, so a CT scan should be considered, before attributing the headache to hypertension alone. A history of recurring headaches should make the clinician suspicious of this diagnosis. In addition to a high blood pressure recording, a characteristic finding is retinal changes. Signs of ventricular hypertrophy on physical exam, support this diagnosis. These include a deep S wave in Vi and a tall R wave in V5.

Patients with GLAUCOMA usually present with eye pain, but not always. Headache alone may be the single presenting complaint. Other associated symptoms are blurred vision and vomiting. Physical exam reveals a tense red eye, steamy cornea and a dilated pupil. Tonometry should be performed in these patients; elevated intraocular pressure establishes the diagnosis...immediate treatment is required. If the patient is not vomiting, have him drink glycerol 50% over ice, in a dose of l-2cc/kg. If he is vomiting, start an IV and administer acetazolamide 500mg followed by 20% mannitol 500cc or l-2gm/kg over one hour. A 2% solution of pilocarpine should be instilled into the eye every fifteen minutes. A topical Betaadrenergic agent should also be given: Timolol, one drop - - repeated in 10 minutes - - decreases the secretion of aqueous humor by the ciliary body. Immediate consultation with an ophthalmologist is required. Patients who present with a headache and a history of persistent ear drainage, should be evaluated for MASTOIDITIS. On physical exam, there is a purulent aural drainage with a small perforation of the tympanic membrane. There is tenderness over the mastoid and you'll also notice a thickening of the skin over the area of the mastoid. The diagnosis should be confirmed with mastoid x-rays or a CT if available. An ENT specialist should be called for immediate consultation. Patients with UREMIA can also present with headache. Other associated symptoms should be sought. These include: fatigue, decreased mental sharpness, laziness, muscle cramping and twitching, nausea and vomiting, anorexia, an unpleasant taste in the mouth and itching. On physical exam, the patient may be hypertensive and exhibit a yellowish-brown skin discoloration and/or a uremic frost. Lab findings consistent with the diagnosis of uremia are the following: an elevated BUN and c r e a t i n i n e , hyponatremia, hypocalcemia, hyperkalemia, hyperphosphatemia, a mild acidosis (with the CO2 usually in the range of 10-15) and a urine specific gravity that is around 1.010. Headache is the initial symptom of CARBON MONOXIDE POISONING and generally occurs with a carboxyhemoglobin level of 20%. The headache is described as "throbbing." As the carboxyhemoglobin level increases to 30%, patients may also complain of dizziness, nausea, vomiting, confusion and irritability. At the onset of cold weather, when furnaces and fireplaces are being used for the first time, people often present in clusters from the same house or apartment building. Suspect carbon monoxide poisoning and draw a carboxyhemoglobin level, whenever there is a history of exposure to:


exhaust fumes smoke methylene chloride... or poorly ventilated heaters. Therapy for carbon monoxide poisoning should be based primarily on the patient's clinical condition, as carboxyhemoglobin levels may be deceptively low, despite significant poisoning. Any patient with known or suspected CO poisoning should receive 100% oxygen therapy. Hyperbaric oxygen therapy produces a more rapid resolution of the acute effects of CO poisoning, but is both expensive and relatively unavailable. Given these restrictions, hyperbaric oxygen therapy is generally reserved for: Patients with coma or a history of coma A carboxyhemoglobin level greater than 25% at any time Severe metabolic acidosis (that is, a pH less than 7.2) Symptoms persisting after 4 hours of 100% oxygen therapy Seizure activity An altered mental status Neonates...and Pregnant patients who are symptomatic or have a carboxyhemoglobin level greater than 10%. In addition, patients with cardiovascular instability manifested by ischemia, infarction or dysrhythmias (as well as those with associated thermal, inhalation or chest wall injuries) are also candidates for hyperbaric oxygen therapy. Arrangements should be made to transfer these patients to the nearest facility with a hyperbaric chamber. The headache of TEMPORAL ARTERITIS may be confused with that of migraine because the patient is usually female and the headache is severe and frequently unilateral. At times, there is a low-grade fever and diminished vision on the affected side, but these signs are frequently absent. The classic finding on physical exam is tenderness over the site of the inflamed artery. Temporal arteritis is one of the few headaches whose diagnosis is aided by a laboratory testthe sed rate is ALWAYS substantially elevated. The suspicion of temporal arteritis constitutes a medical emergency because failure to diagnose and treat it may result in permanent neurologic loss. Visual impairment is the most common sequelae of temporal arteritis, but basilar and cerebellar infarcts have also occurred. High-dose steroids are indicated as soon as the diagnosis is suspected (oral Prednisone 60-80mg/day or IV methylprednisolone 250mg every six hours). For severe pain, narcotic analgesia may be required. Nonsteroidal anti-inflammatory agents can be used in other patients. If the patient has an impending vascular complication (or is unable to care for herself) she should be admitted. Those with less severe symptoms, who are able to care for themselves (and have an identified physician), may be discharged if close follow-up can be arranged for them.


The next topic for review is PEDIATRIC RESUSCITATION. Included in this review are: Medical emergencies in the newborn Acute asthma and epiglottitis Cardiac dysrhythmias Shock Isolated head injuries Blunt abdominal trauma Poisoning and overdose...and Fluid resuscitation All drug dosages and life support procedures and equipment are found in the PEDIATRIC ADVANCED LIFE SUPPORT SECTION of the Guidelines 2000 and they include both ACLS and ATLS measures. Let's begin with medical emergencies in the neonate. Metabolic acidosis (associated with a pH less than 7.0) may be treated with sodium bicarbonate lmEq/kg IV of a 4.2% solution infused slowly at a rate of lmEq/kg over ten minutes. Remember that IVfluids(and correction of any respiratory or metabolic component) are the mainstays of therapy in neonates with metabolic acidosis. Subsequent doses should be based on ABG analysis in patients with a pulse; in the absence of a pulse, empiric doses of 0.5mEq/kg may be given every 10 minutes slowly (over 1-2 minutes) IV push. Hypotension secondary to volume depletion is treated with either Ringer's lactate or normal saline lOcc/kg IV over 5-10 minutes. Bradycardia in the newborn is initially managed with ventilation and oxygenation. If, after administration of 100% oxygen for 30 seconds with good air movement and chest rise, the heart rate is less than 60, begin chest compressions and initiate drug therapy with epinephrine. The recommended IV or endotracheal dose is 0.1-0.3cc/kg of the 1:10,000 solution repeated every 3-5 minutes as needed. Endotracheal tube sizes for newborns are based on weight: if the newborn weighs less than lkg, use a 2.5 mm uncuffed tube; if the weight is l-2kg, use a 3 mm uncuffed tube; a weight of 23kg requires a 3.5 mm uncuffed tube. Larger newborns may need a 4mm uncuffed tube. For the newborn with respiratory depression secondary to narcotic abuse by the mother, give naloxone O.lmg/kg of a 0.4mg/cc (or lmg/cc) solution IV or (if perfusion is inadequate) IM or Sub-Q. According to the 2005 AHA guidelines, naloxone administration is not recommended during the primary steps of resuscitation (but may be given if initial resuscitation efforts fail). In addition, endo-tracheal administration is no longer recommended and naloxone should not be given to babies whose mothers are suspected of having had long-term exposure to opioids. Oxygen administration in the newborn and young infant is best accomplished with a small hood at a rate of 10-15 liters per minute. However, if cyanosis, bradycardia or other signs of distress are noted in a breathing newborn during stabilization, administration of 100% oxygen is indicated while determining the need for

additional intervention. Free-flow oxygen can be delivered through a face mask and flow-inflating bag, an oxygen mask or a hand cupped around the oxygen tubing. Hypoglycemia in the newborn (that is, a serum glucose less than 40), is treated with DioW 2-4cc/kg. Bolus infusions of dextrose in 25% or 50% concentrations should not be given to the neonate since they can induce rebound hypoglycemia and hypertonicity. Now let's move on to the child older than three months and review selected emergencies in this age group. With acute epiglottitis, the initial goal is to PREVENT respiratory arrest, so that a definitive airway can be established in the OR. Agitation of the child should be minimized. The child should remain in the company of his parents, allowed to assume a comfortable position and given humidified oxygen by mask. Equipment for airway management should be set up nearby and someone experienced in airway management should remain with the child at all times. While this is being accomplished, assembly of a team composed of an anesthesiologist, ENT specialist and pediatrician should proceed without delay. Antibiotic therapy is usually initiated once the airway has been secured by the anesthesiologist or ENT specialist. Acceptable antibiotic regimens include the following: cefuroxime lOOmg/kg/day divided in 3 doses; OR ampicillin-sulbactum 100200mg/kg/day divided in 4 doses PLUS chloramphenicol 75-100mg/kg/day divided in 6 doses. Ceftriaxone 50-100mg/kg/day divided in 2 doses is another alternative. All of these antibiotics are administered IV, and of the regimens just described, the cephalosporins are more commonly used today. The next topic is "acute asthma". This is a prime topic for the Oral Board Exam and it should be reviewed. If you get a case of pediatric asthma, it's likely to appear in one of the multiple encounters and the emphasis will be on your therapeutic approach to this patient. Another possibility is a single encounter with a child presenting with near-fatal asthma. This will be discussed separately after the general management of acute asthma has been reviewed. Administer oxygen to ALL asthmatics, put them on pulse oximetry and obtain a peak expiratory flow rate. Most asthmatics are hypoxic and treatment with Beta-adrenergic agents may initially worsen the hypoxia by increasing the ventilation-perfusion mismatch. The initial treatment of choice is aerosolized therapy with a Beta-adrenergic agent; it is associated with fewer systemic side effects and superior dilation when compared to parenteral therapy. The preferred agent is albuterol (0.5%solution); administer 0.15mg/kg in 2-3cc normal saline every 20 minutes for three doses then 0.15-0.3mg/kg up to lOmg every 1-4 hours as needed. Parenteral adrenergic therapy is usually reserved for the very young and the very sick who may not be able to cooperate or provide the necessary inspiratory effort. You can use either epinephrine or terbutaline: the dose of epinephrine is .Olmg/kg (up to .3mg) of a 1:1000 solution given subQ every 20 minutes as needed (up to 3 doses); the dose of terbutaline is .01mg/kg (up to .25mg) given subQ every 30 minutes as needed (up to 3 doses) then every 2-6 hours as needed.

For those patients who continue to wheeze despite adequate Beta-adrenergic therapy, consider using aerosolized anticholinergic therapy. When used in combination with Beta-adrenergic agents, their effects are ADDITIVE. The agent of choice is Ipratropium bromide 0.25mg in children every 20 to 30 minutes combined with the first three albuterol treatments. Corticosteroids are useful in treating the INFLAMMATORY aspect of asthma and are being used earlier and with greater frequency than in the past. They should be administered to any of the following patients: 1- Those who are currently taking or who have recently discontinued a steroid preparation. 2- Those who show only MILD improvement following initial sympathomimetic therapy. 3- Those with signs of severe OBSTRUCTION (in other words, the "tight" wheezer who can't seem to open up). 4- Those with a history of asthma-related RESPIRATORY FAILURE 5- Those whose attack has been PROLONGED...and 6- Those who RELAPSE...that is, those who return to the Emergency Department for the SAME attack. Patients in severe distress (or those who are vomiting) will need methylprednisolone l-2mg/kg IV. If the child does not require IV steroids, liquid Prednisone (or prednisolone) is rapidly absorbed from the GI tract and should be given in a dose of l-2mg/kg. Patients who receive steroids in the Emergency Department (and are subsequently discharged) SHOULD BE CONTINUED ON ORAL STEROIDS for 310 days. This is the end of the sixth CD. Pediatric Asthma will continue on CD 7.


CD 7 "LAST-MINUTE CLINICAL REVIEW" Now, lets' talk about the child presenting with near-fatal asthma. As soon as he is brought in, you will recognize him. He'll either be obtunded, agitated, confused or fighting against the oxygen mask; and he will probably need to be intubated. While the equipment is being set up, see if he can tolerate an albuterol treatment-if not, order parenteral therapy with epinephrine or terbutaline; then, administer IV steroids. Now, is he getting better, staying the same or getting worse? If you are not sure (based on his level of consciousness), look for other signs. Is he as diaphoretic as he was before? Is his muscle tone still poor... or is it better? If he is not better (and isn't getting worse) administration of Heliox may delay the need for intubation by decreasing the work of breathing while the other medications are beginning to take effect. Another thing you can try is bilevel positive airway pressure. This provides intermittent assisted ventilation which helps to abort or delay the need for tracheal intubation. For infants and small children, Heliox and BiPAP are probably not viable options so, if they are not getting better, intubation is indicated. For older children in whom these measures have failed, intubation is definitely in order. Critical points regarding tracheal intubation in patients with life-threatening asthma are these: (1) Adequate sedation is a must; most experts think ketamine is the agent of choice for severe asthmatics-the initial dose is 0.5-1.5mg/ kg repeated 20 minutes later; atropine should also be given because ketamine increases bronchial secretions-the dose is O.Olmg/kg with a minimum dose being O.lmg. (2) Paralyze the patient with succinylcholine or vecuronium; if you use succinylcholine, you will need to pretreat with atropine: if you sedated with ketamine and used atropine O.Olmg/kg to reduce bronchial secretions, you need to administer another O.Olmg/kg dose, but if you did not use atropine (because you were using another sedating agent) then you need to administer a full dose of atropine (0.02mg/ kg). (3) Immediately following intubation, check correct placement by visualizing the tube past the vocal cords; listen for adequate breath sounds in all lung fields; watch the chest wall rise ... and look for condensation in the tube. Confirm correct placement using one of the following devices or measurements: A qualitative end-tidal CO2 detector An esophageal detector device Dynamic pulse oximetry readings ... or Quantitative and continuous CO2 measurements using capnometers or capnographs (4) Once correct tube placement has been confirmed, inject an albuterol dose directly in the the tracheal tube because the patient may not have inhaled an adequate amount of this agent prior to intubation. Now let's move on to the treatment protocols for cardiac dysrhythmias that occur in infants and children.

Clinically significant bradycardia is a heart rate < 60 that most often results from hypoxemia. Therefore, initial therapy is aimed at ensuring adequate ventilation and oxygenation. Bradydysrhythmias that are unresponsive to these measures are treated with epinephrine (unless the bradycardia is vagally mediated, in which case, atropine is the drug of choice). The dose of epinephrine is O.Olmg/kg of the 1:10,000 solution repeated every 3-5 minutes as needed. Epi can also be given through the tracheal tube at a dose of O.lmg/kg of the 1:1000 solution. Atropine should be used (instead of epinephrine) in the presence of AV block or increased vagal activity (such as a rapidly dropping heart rate that may occur during attempts at intubation). Before giving atropine, R/O hypothermia as a cause of the bradycardia and make sure that oxygenation and ventilation are adequate. The dose of atropine is 0.02mg/kg; the maximum single dose allowed is 0.5mg in children and lmg in adolescents. The hazard of a low dose is paradoxical slowing of the ventricular rate which would necessitate temporary pacing. Supraventricular tachycardia is often well-tolerated for long periods of time in children. The rate is age-dependent and varies from 220-300 in infants, greater than 180 in children and between 150+250 in adolescents. Initial treatment in the stable child should consist of vagal maneuvers. Induction of the diving reflex, which is particularly sensitive in infants and young children, is one technique that is often effective. To do this, apply an ice pack on the child's face or briefly immerse his face in a basin of cold water. Other vagal maneuvers (such as carotid massage and gagging) may also be tried. If unsuccessful, the next step in the hemodynamically stable child with a narrow-complex SVT is drug therapy with adenosine which is the drug of choice. The initial dose is O.lmg/kg RAPID IV push with a (maximum 6mg) followed by a flush of normal saline. If this fails to convert the rhythm, repeat the dose at 0.2mg/kg; if the SVT persists, a third dose (using 0.3mg/kg) may be given; the maximum single dose should not exceed 12mg . . . and remember, adenosine MUST be administered RAPIDLY IV push to be effective. If adenosine fails to work (and the patient is still hemodynamically stable) other agents may be tried, but they have their drawbacks. Verapamil has been shown to have disastrous side effects in infants (such as hypotension, profound bradycardia and even asystole). Therefore, verapamil should not be used to treat SVT in infants or in children with congestive heart failure, myocardial depression, those on beta-adrenergic blockers or with a bypass tract. If you use it, the dose is 0. lmg/kg. Procainamide and amiodarone are alternative agents that are acceptable and possibly effective. Only one agent should be used however, and it should not be used concurrently with any agent that may prolong the QT interval... which is most of the "blockers." In children with Wolff-Parkinson-White Syndrome and a wide-complex SVT, verapamil and other "blockers" can increase conduction through accessory pathways and thereby increase the ventricular rate. Verapamil is also contraindicated in ventricular tachycardia (as well as in children less than a year old) because cardiovascular collapse has been associated with its use in these circumstances. Therefore, to avoid complications, ALL wide-complex SVTs should be treated with amiodarone or procainamide in the stable child...and hemodynamically UNSTABLE children should be cardioverted with 0.5 joules/kg REGARDLESS of the width of the QRS complex. If the initial attempt to cardiovert is unsuccessful, then double the dose.. .and try again.


Premature ventricular contractions in kids are only treated if they are frequent. The drug of choice is lidocaine and the dose is lmg/kg IV. The treatment of ventricular tachycardia is determined by the child's clinical condition. Ifthe child is unconscious or hypotensive, DC cardioversion at 0.5 joules/ kg is indicated. If the rhythm persists, check to see if it is Torsade-de-Pointes; if so, administer IV magnesium 25mg/kg slowly over 10-20 minutes (50mg/kg can be used for older children, especially the pre-teen and adolescent patients). If Torsades is not present, attempt DC conversion again at 1 joule/kg. If the child is conscious and normotensive, obtain a 12-lead ECG and a careful history, looking especially for a reversible cause such as drug toxicity, electrolyte imbalance or hypothermia. If a pharmaceutical agent is used to convert the rhythm (in the absence of a reversible cause) amiodarone is probably the best choice: 5mg/kg over 20-60 minutes. Alternative agents are procainamide (15mg/kg over 30-60 minutes) or lidocaine (lmg/kg over 2-4 minutes). The child with ventricular fibrillation should be defibrillated at 2 joules/kg. Double the dosage if initial defibrillation is unsuccessful. The paddle size for infants is 4.5cm; for the older child, use a paddle with an 8-10cm diameter. Pediatric shock may be difficult to assess if one relies on the blood pressure measurement. When the blood pressure drops, it will drop FAST because peripheral vasoconstriction and tachycardia both tend to maintain blood pressure until late. The clue to ongoing blood loss and progressive shock is a rising pulse rate. The rule for obtaining IV access in the child with shock is, "anything, anywhere." The external jugular is a good spot if you can get it (especially in older children and adolescents); be careful not to insert the needle or catheter beyond the level of the clavicle. If the child has injuries to the chest or upper extremities, try to obtain an IV line in a lower extremity; if the child has abdominal injuries, go for an upper extremity vein. If a peripheral vein cannot be accessed with a large-bore catheter, cannulation of the femoral vein is the procedure of choice in infants and young children. If a central line cannot be rapidly established, a saphenous cutdown or intraosseous infusion should be done. The anterior tibia, just below and medial to the tibial tuberosity, is the preferred site for intraosseous infusions. The IV fluids of choice in pediatric shock are Ringer's Lactate or normal saline; 20cc/kg (administered over 5-20 minutes) should be given. If the child is still in shock after THREE boluses, order packed red blood cells in the amount of 80cc/kg; an additional TWO bolusesof fluid can be given (if needed) while awaiting blood. If packed RBCs ARE given, warm them first and then give lOcc/kg boluses according to patient response. In children with a serious isolated head injury, the IV should be "keep open" only in the absence of shock. If shock is present, use normal saline; more importantly, if shock is present, you are not dealing with an ISOLATED head injurythere are other injuries as wellLOOK FOR THEM! Shock treatment takes precedence over treatment of head injury.


If, in fact, you are dealing with an isolated head injury and there is an altered level of consciousness, obtain a CT scan and contact the neurosurgeon. Hyperventilation is no longer routinely recommended. However, if there are definitive signs of increased intracranial pressure (such as transtentorial herniation) hyperventilation to a pCO2 of 35 mmHg is certainly justified and it should be done because it is the fastest way to reduce intracranial pressure. If furosemide, mannitol or hypothermia are used, they should be in consultation with the neurosurgeon. Mannitol is administered IV in a dose of 0.5-lgm/kg over 10-15 minutes; the dose of furosemide is 0.5-lmg/kg. Hypothermia induction is a last-ditch effort to reduce intracranial pressure when all other measures have failed.

Children with blunt abdominal trauma have a 50-70% chance of having other associated injuries. Be sure to examine these kids carefully. One method of determining the presence of intra-abdominal bleeding is to take serial girth measurements; an expanding abdomen that is measurable is a reliable sign of continuous abdominal bleeding. Diagnostic peritoneal lavage is a more precise method for detecting intraabdominal bleeding. DPL should be considered for the hemo-dynamically unstable child or one with an unreliable abdominal exam: for example, a child with head or spinal cord injury who also has a history or physical findings which suggest the possibility of an intra-abdominal injury. It is performed with lOcc/kg of Ringer's lactate. Aspiration of more than 5cc of free blood (or the presence of 100,000 RBCs/cc) of lavage fluid is considered positive. Computed tomography is the modality most often used to evaluate a child who has sustained significant abdominal trauma, but maintains stable vital signs. However, abdominal ultrasonography may provide important information early in the course of management. Data from the adult literature shows that the sensitivity for detection of intraperitoneal fluid is high (ranging from 85-98%) and will likely become a part of pediatric trauma protocols in the near future. The management of poisoning and overdose in adults (as well as in children) continues to change. A critical decision is whether to give Ipecac, activated charcoal and/or perform gastric lavage or do none of the above. If the ingested substance is known to be nontoxic and the child is alert, removal is not usually necessary. However, if the agent ingested is known to be toxic, or there is some question as to what the child ingested, activated charcoal, gastric emptying or both may be indicated. Administration of activated charcoal has become firstline therapy in GI decontamination and is most effective if given within one hour. While the use of Ipecac has become controversial, it is still considered an option in the alert child who ingested a moderate or highly toxic agent within 60 minutes of presentation (and for which there is no contraindication to emesis). If there is any doubt as to how to proceed, contact Poison Control for the most current recommendations. If Poison Control is not available to you at the exam, make a reasonable decision and explain your rationale to the Examiner. A reasonable explanation of your choice is likely to be acceptable.

Gastric lavage should be considered in children known (or suspected) to have ingested agents within 60 minutes of presentation that are highly toxic or in those who have ingested a toxic or potentially toxic substance that is not absorbed by charcoal, such as iron or lithium.. .and lavage should also be used in any child who is not alert or who does not have an intact gag reflex. Airway protection is a must in lavaged patients. If emesis is indicated, the dose of Ipecac is lOcc in infants 6-12 months; 15cc in children 1-12 years old; and 30cc in children over twelve. If the child does not vomit after this dose, repeat it, and encourage the child to drink several cups of water and then walk him around the room (increased activity promotes emesis in most kids). If there is still no vomiting, gastric lavage is indicated if the agent ingested is highly toxic (such as a calcium-channel blocker or cyclic antidepressant); use a 15-28 French orogastric tube in children, choosing the largest one that can be easily passed; smaller tubes may not recover large pill fragments. When inserting the gastric tube in an alert child with an adequate gag reflex, place him on his right side with the head lower than the body to minimize the risk of aspiration. If the child is not alert and has a depressed or absent gag reflex, intubation is necessary prior to lavage. The comatose child always needs to be intubated prior to lavage. When lavaging, use isotonic or 1/2 isotonic physiologic saline that is warmed; in a child, lavage in small amounts (lOcc/kg) to prevent passage of the stomach contents into the small intestine, where it can be absorbed. Contraindications for the use of Ipecac and gastric lavage are ingestions of: Caustics or strong acids Low-viscosity hydrocarbons (because they are easily aspirated) ...and Non-toxic substances IV fluid therapy in children is not difficult to remember, if you use a few simple guidelines: First The rate for maintenance fluids is as follows: 4cc/kg/hour for the first 10 kilograms, 2cc/kg/hour for the next 10 kilograms and Ice/ kg/hour for the remaining kilograms so for a 10kg child, this is 40cc/hour; a 20kg child would receive 60cc/hour and a 30kg child would receive 70cc/hour. Children who are hypoglycemic should be given a glucose solution; infuse 2-4cc/kg of 25% glucose or use a 10% glucose solution and give 5-10cc/kg. Children with shock or burns should be given Ringer's lactate; for the burned child, estimate the percent of body burn by using the Lund and Browder chartsmultiply that number times the weight in kilograms times four and you have the amount of fluid required in the first 24 hours, starting from the time the burn occurred. Give one-half of this amount in the first 8 hours and the second half over the next 16 hours. Daily maintenance fluids need to be administered as well. Always remember to order a pediatric microdrip IV set-up.

Second Third -

This completes the pediatric resuscitation review. Drug therapy for pediatric cardiac arrest was reviewed in the First CD.

Now I want to review with you the case management checklist I developed for this exam. A case management checklist is a valuable tool in the assessment of your clinical performance. It not only assures a thorough evaluation, but it's also very helpful in the event that you are in trouble. If a diagnosis isn't materializing or if a patient isn't responding to normal therapeutic measures, this can be a life saver...literally. The checklist I have prepared is a long one, but it is divided into six segments for easier learning. I recommend that you learn one segment at a time. I also recommend that you use this checklist in the Emergency Department as you are writing up a patient's chart. This is an ideal risk management tool; and repeated use will make it habitual for you so that it will be there with you in the Exam. If you are listening to this tape / CD while sitting in a room, I recommend that you take a pencil and paper and write down key words and phrases as you listen. This will facilitate the learning process. If you are driving your car, listen to one segment at a time, turning off the tape / CD and mentally reviewing what you have heard, before proceeding to the next segment. Repetition will reinforce the message. Now let's begin with the first segment of the checklist, which is the history. The first rule of good case management is this:

#1 - Define the present illness or injury, including events leading up to the illness or injury. #2 - What was the patient's condition before the present illness or injury? B. J. Brown, the paraplegic in Case Study #7 in the text, is a case in point. Ascertaining her neurologic status BEFORE her injury was necessary to determine any NEW neuro deficits. #3 - Have there been any recent illnesses or injuries? #4 - Listen carefully to the patient. Is he apathetic or depressed? Does he have a history of mental illness or an emotional disorder? The Examiner may present a patient with a flat affect. Some candidates are so intent on the specifics of the case, that they don't pick this up...and do not rely on the patient who denies a history of mental illness if you suspect otherwise. #5 - What medications is he taking? Have there been any recent changes in dosages or medications? #6 - Does he have any allergies? #7 - Talk to family members, friends, EMTs.. .ANY "significant others" if the patient gives a poor history or is unwilling or unable to give a

good history. I cannot stress too much the importance of this point. In one of the cases I use in tutorials, a 5-year-old boy is brought to the hospital by his parents and 7-year-old brother. The child is obviously very ill and the mother doesn't have some of the important information. Guess who does? About half of the physician candidates do not question the 7-year-old brother. #8 - Decode positive historical findings and formulate a good working differential diagnosis. #9 - If a history is not coming into focus, ask open-ended questions such as: How have you been feeling lately? When were you last well? What happened then? What did you do today? Patients with vague complaints or unusual clinical presentations often don't reveal what you want to know when you ask specific questions. General questions, on the other hand, allow the patient to tell you what he knows about his illness. This is the end of the first segment. The next segment of the checklist is the physical exam and the second rule of good case management, is this: PERFORM A COMPLETE PHYSICAL EXAM #1 - Do a complete physical exam INITIALLY on all patients WITHOUT lifethreatening illnesses or injuries, especially those with an apparently obvious diagnosis. The exception to this rule is the multipleencounter situation in which case you will be managing three patients at one time. Whenever you are dealing with more than one patient, use the case management format previously discussed, performing the H&P in a piecemeal fashion to maximize your efficiency and effectiveness. #2 - Beware of clinical presentations that appear to be clear-cut: a patient who arrests and (is successfully resuscitated) may have sustained chest or abdominal injuries secondary to chest com- pressions; likewise, an unconscious patient with hypoglycemia may have sustained injuries after losing consciousness. #3 - For patients with apparent or possible life-threatening illnesses or injuries, do a brief physical exam initially and then go back later and thoroughly examine the patient. #4 - Initial vital signs are clues to the clinical problem when they are decoded. Always recheck them throughout the case to monitor the effectiveness of your management. If they change unexpec-tedly, for no apparent reason, look for another cause of the patient's condition. If your patient's vital signs continue to deteriorate in spite of specific treatment, you are expected to try something elseeither a different medication or procedure. Accurate interpretation of vital signs is a problem with some candidates. They tend to focus on


the blood pressure alone. This should always be correlated with the pulse. Hypotension and tachycardia mean hypovolemia; hypotension and bradycardia suggest AV block, a poisoning or an overdose with a calcium channel blocker, a Beta-blocker or a digitalis preparation. #5 - Perform a neurologic exam in any patient with a CNS presentation. Determine the level of consciousness, pupil size and reactivity, respiratory pattern, spontaneous motor activity and deep tendon reflexes. And always check the rectal sphincter tone in majortrauma victims. #6 Learn the physical exam litanies in the appendix at the back of the book. When you are examining patients at this exam, how you ask the questions can be very important. It can help you obtain all the positive findings in the least amount of time. This is the end of the second segment. The third rule of good case management is this:

#1 - Let the chief complaint dictate some automatic lab work such as a CBC and urinalysis in patients with abdominal pain or ABGs glucose, lytes, BUN and creatinine in patients with an acute behavioral change. Also, in any woman of child-bearing age who presents with abdominal pain, a beta-HCG should also be ordered. #2 - In patients without a life-threatening illness or injury, in whom a complete history and physical exam can be done at one time, order all lab studies at one time. #3 - In patients with apparent or possible life-threatening illnesses or injuries, order stat tests first and other lab later as indicated. #4 - Order special diagnostic studies such as scans and angiography studies and perform diagnostic procedures such as orthostatic blood pressure measurements and peritoneal lavage as indicated. Some candidates hesitate to order these things because they are not sure that they are CLEARLY indicated. The rule here is: if you are thinking about itdo it! #5 - Make sure all pertinent diagnostic tests have been ordered returnedinterpretedand acted upon. #6 - Before speaking with a consulting or admitting physician, make sure you have the results of all diagnostic tests and procedures. The exception here is the unstable patient who requires EMERGENT specialty consultation. In this case, do not wait for lab results before calling a consulting physician. If he asks about pending lab results, tell him they are pending and discuss how the results will affect your management. This is the end of the third segment. The fourth rule of good case management is this:



#1 - Take time to get your thoughts organized. Occasionally, I see a candidate jump right into a case without actually focusing his attention on those things he should do first. In the trauma patient, failure to immobilize the cervical spine at the beginning of the case, is the most frequent error. In the cardiac patient with bradycardia and hypotension, look at a monitor strip but don't wait for an ECG before giving meds or initiating transcutaneous pacing. #2 - Always start with the ABCs (airwaybreathingand circulation) in ANY patient with abnormal vital signs. #3 - Stabilize seriously ill or injured patients with an IV, O2, pulse oximeter and monitor (if indicated) as SOON as possible. A chest pain patient will require all four, whereas a patient with abdominal pain may only need an IV. #4 - Be AGGRESSIVE with emergency measures when they are indicated. Do not hesitate to put in a chest tube or pacemaker in patients who clearly need them. Decide NOW under what circumstances you would perform a cricothyroidotomy and when you are confronted with one of those circumstancesdo it. #5 - Avoid giving any narcotic analgesia (except when indicated, such as the chest pain patient with an MI) until AFTER you have conducted a complete physical assessment. When indicated, however, it should be given in adequate doses. #6 - Listen carefully to the examiner. He is giving you clues to the patient's problem and expected management...and #7 - Before finalizing case management, order Tetanus prophylaxis, IV antibiotics, an NG tube and Foley catheter in patients who need them.

This is the end of the fourth segment.

The fifth rule of good case management is this: ENSURE APPROPRIATE DISPOSITION OF YOUR PATIENT #1 #2 #3 #4 Any patient with a possible life-or-limb-threatening condition should not be sent home when the diagnosis is in question. Any patient who has not been evaluated, or one who requires immediate therapy or a diagnostic work-up, should not be permitted to leave the hospital. Obtain immediate specialty consultation as indicated. Admit all patients who require admission to an attending physician with appropriate in-house consultations and designate special care unit placement as indicated.

This is the end of the fifth segment.


The sixth and final rule of good case management is this:


#1 - Briefly explain to the patient any procedures you need to do and the need for them.. .using terminology that is appropriate for the patient's age and level of education.. .and #2 - When wrapping up a case, explain the diagnosis and the plan to the patient and his family and provide reassurance. This completes the case management checklist. Whether you learn this checklist by reading it, listening to it or both, is unimportant. But it is VERY important that you DO learn it because, in my experience with Oral Board Candidates in tutorial sessions, most of the errors made were due to the omission of one or more of these rules.

In the final week prior to the exam, you are likely to reach a point where you have completed your study program and are wondering what to do next. At this time, a review of the key points covered in the book and tapes, CDs will be very useful. These key points will be presented now with added comments. I have divided this final review into three sections: Critical actions Diagnostic clues... and Exam techniques The critical actions are subdivided into six categories: Surgical Medical Pediatric Obstetric Orthopedic... and Diagnostic or therapeutic procedures In each category, there are ten or fewer key points enumerated, since a longer list would be difficult to remember. I have selected the most important key points on which to focus your attention. They are based on errors that have been made during this exam. The ten key points that are critical actions in the management of SURGICAL EMERGENCIES are these: 1 - The initial treatment of all major trauma patients includes C-spine immobilization and airway assessment with appropriate management. 2 - Insert large-bore IV catheters in all patients with suspected or documented hypovolemic shock. 3 - Perform immediate chest tube thoracostomy in the multipleinjured patient in whom you suspect a pneumothorax or a small or moderate hemothorax.

4 - If you suspect a massive hemothorax on clinical grounds (that is, absent breath sounds and dullness on percussion), initial management is NOT chest tube placement unless there is significant respiratory compromise, in which case, put the chest tube in immediately. But in the absence of significant respiratory compromise, treat shock FIRST with large bore IV lines. Order eight units of whole blood. While you are treating his hypovolemia, order a stat portable chest x-ray to confirm the diagnosis. Plan to use an autotransfusion device, if available. When you are ready to perform chest tube thoracostomy, use a large bore chest tube and insert it at the nipple level, just anterior to the midaxillary line, and direct it posteriorly. If the patient becomes hypotensive, clamp the tube and contact the thoracic surgeon for immediate thoracotomy. 5 - Perform immediate cricothyroidotomy in the presence of severe, ongoing tracheobronchial hemorrhage or massive midfacial injuries. A cricothyroidotomy should also be performed if intubation is contraindicated or impossible due to mechanical upper airway obstruction, facial or cervical trauma or uncontrollable oral hemorrhage. 6 - Perform peritoneal lavage in unstable trauma patients with multiple injuries, shock or those with an altered level of consciousness. 7 - Perform suprapubic bladder aspiration to relieve acute urinary tract obstruction when unable to pass a Foley catheter and a urologist is unavailable. 8 - Include "myocardial contusion" in your differential diagnosis of any patient presenting with signs or symptoms of chest injury. An ECG and cardiac enzymes should be part of your diagnostic work-up. 9 - In a major trauma case, make sure you examine the patient's back and flanks. If there are significant injuries anteriorly, log-roll the patient so that these areas will be protected. If there is possible Cspine injury, do not move the patient until the lateral C-spine film has been cleared... and if the lateral film demonstrates a fracture or dislocation, examine the back by sliding your hand under the patient. Do not log-roll him to see what is there; this can be done once the neurosurgeon has definitively stabilized the neck ... and 10 - In burn victims with intraoral burns, intubate early in the course of treatment, since laryngeal edema with airway obstruction is a frequent complication. This concludes the ten key points that are critical actions in the management of surgical emergencies. The ten key points that are critical actions in the management of MEDICAL EMERGENCIES, are these: 1 - Treat chest pain in MI aggressively with nitroglycerin and other anti-ischemic agents as needed. 2 - Activated charcoal can be given to patients who might need Mucomyst. Lavage until clear, if Mucomyst is indicated after giving charcoal.







If visual acuity is markedly reduced in a patient with acute glaucoma, administer ail topical agents immediately: this includes: Pilocarpine, Apraclonadine and Prednisone as well as a topical betablocker such as timolol or Timoptic. Acetazolamide should be given IV along with mannitol. Patients with intraocular pressures < 50mmHg without significant visual acuity impairment, do not require IV mannitol (unless they are vomiting) or acetazolamide; glycerol can be given orally and acetazolamide can be given topically. In radio communications with paramedics, never treat a monitor strip without asking for the patient's blood pressure, pulse and level of consciousness... and always ask about allergies before ordering medications. In overdose patients, always remember the following points: First If you decide to use Ipecac, it should be given only to patients who are fully conscious; and if your patient is drowsy, lethargic or unconsciousdo not use it. Second - Always suspect a multi-drug ingestion or overdose. Third Insist on a STAT tox level of a specific substance that is clinically suspected. Fourth If you are managing a poisoning or overdose that is not commonly seen in the Emergency Department, and you don't remember the specific therapy, call Poison Control for this information. If the Examiner tells you that Poison Control is "unavailable", be resourcefulcheck Poisindex, a toxicology text, or call the hospital pharmacist for this information. Now, if you know the specific therapy, but you don't remember the dose, then check the package insert that you have in the pharmacy in the emergency department. Fifth Fluid RESTRICTION is indicated with overdoses of cyclic antidepressants, heroin and methaqualone. The Cyanide Antidote Kit containsamyl nitrite, sodium nitrite and sodium thiosulfatethese drugs must be given in THAT order. The use of physostigmine is condemned by most Emergency Physicians and is contraindicated in a cocaine overdose because it may precipitate seizures; it is also contraindicated in acute cyclic antidepressant overdose due to the high risk of inducing severe bradycardia, AV Block and asystole. Other contraindica-tions exist as well (bowel obstruction, cardiovascular disease, asthma, COPD and pre-existing urinary tract obstruction). If none of these contraindications exist, use of physostigmine may be considered (in consultation with a toxicologist) for severe agitation and delirium in patients necessitating physical restraints and unresponsive to benzodiazepines.. Electrolyte disorders to consider in the adult patient withseizures are: Hyponatremia Hypocalcemia...and Hypomagnesemia In the infant or small child with seizures, hyponatremia is the one most commonly encountered.

9 - Urinary alkalinization for PCP intoxication may reduce deposition of myoglobin in the renal tubules which causes acute tubular necrosis...and 10 - If your patient arrests, and does not respond to BCLS and ACLS measures, check for endotracheal tube placement and a postarrest pneumothorax. This completes the medical critical actions list. The ten key points that are critical actions in PEDIATRIC EMERGENCIES are these: 1 - Always think of child abuse where injuries, poisoning or an unexplained illness is found. 2 - Always administer glucose and Narcan to all unconscious children. 3 - Think of lead poisoning if the peripheral blood smear demonstrates basophilic stippling. 4 - When estimating body surface area burns in kids, use the Lund and Browder charts. 5 - The Ipecac dose for children 1-12 years of age is 15cc; for infants 612 months old, the dose is lOcc. Ipecac should always be followed by one to two glasses of water, especially warm water, since this seems to work better. 6 - In children who present with seizures, rule out Reye's Syndrome order a serum ammonia and SGOT. 7. Rule out theophylline toxicity in children on theophylline therapy if the medication history or doses taken is unclear or unreliable. 8 - When performing CPR in children, the compression/ventilation ratio is 5:1and the compression rate is 100/minute. 9 - Rule out sepsis and meningitis in any infant who appears ill.. .and 10 - If you suspect epiglottitis in a child, do NOT attempt direct or indirect visualization of the larynx; instead, order a portable soft tissue lateral neck film; assemble emergency airway equipment at bedside; and provide constant supervision by someone experienced in airway management. This is the end of the critical actions list for pediatric emergencies. The six key points that are critical actions in the management of OBSTETRIC EMERGENCIES are these: 1 - Always perform culdocentesis in patients with suspected ectopic pregnancy when ultrasound is not available, unless the patient is in shock with peritoneal findings, in which case, culdocentesis is clearly unnecessary. 2 - The dose of magnesium sulfate for eclamptic seizures is 4-6 grams IV push over 5-15 minutes followed by a l-2gm/hr infusion drip. Stop the infusion if a post-treatment serum magnesium level is 10-12mEq/liter or the patellar tendon reflex disappears or the patient stops breathing. The antidote for magnesium toxicity is calcium gluconate, given in a dose of lgm slow IV push. Magnesium sulfate may not stop an eclamptic seizure; if there is no response to 52




magnesium sulfate, phenytoin or diazepam may be given; however, a lower-than-normal loading dose of phenytoin should be used due to the potential for toxicity during pregnancy and diazepam can produce maternal and fetal depression. The dose of phenytoin is lOmg/kg over one minute; the dose of diazepam is 5mg/minute IV every 5 minutes as needed, up to a maximum dose of 30mg. When evaluating fetal viability in an obstetric emergency, remember that the normal fetal heart rate is 120-160/minute. Continuous fetal monitoring is a critical action in third trimester patients with serious illnesses. The drug of choice for an eclamptic hypertensive emergency that does not improve with magnesium therapy is hydralazine; the dose is 5-10mg IV repeated every 20 minutes, as needed, to keep the diastolic pressure between 100 and 110mm Hg. Labetalol is also safe and effective in controlling hypertension in eclamptic patients. It should be used if hydralazine is ineffective or unavailable; the initial dose is 20mg IV... and can be doubled every 10 minutes until blood pressure control is achieved or 300mg has been given. Rule out placenta previa and ectopic pregnancy in all women of childbearing age who present with hemorrhagic shock.. .and Rule out placenta abruptio and ectopic pregnancy in all women of child-bearing age who present with abdominal pain. Also, rule out placenta abruptio in all pregnant patients involved in auto accidents, especially if the airbag was deployed.

This is the end of the critical actions list for obstetric emergencies. The seven key points that are critical actions in ORTHOPEDIC EMERGENCIES are these: 1 - Always perform a neurovascular exam in the presence of injuries to the spine and extremities. 2 - Know the differential diagnosis of non-traumatic joint pain. 3 - Know the indications for joint aspiration, what fluid studies to order, and how to interpret them; also be able to identify crystals on a slide by microscopy. 4 - Order a lactic acid level on aspirated fluid of a hot joint (usually the knee) to rule out a septic joint if the diagnosis is not apparent after microscopic examination and gram stain of the fluid; levels greater than 30mg/dL are diagnostic. 5 - Rule out a slipped capital femoral epiphysis in a teenage boy who presents with knee pain. 6 - Supracondylar fractures of the distal humerus may be complicated by a compartment syndrome of the forearm, due to entrapment of the brachial artery or median nerve; diagnostic clues are weak wrist flexion and weak thumb opposition.. .and 7 - Humeral shaft fractures may be associated with radial nerve injury; check for wrist drop. This completes the critical actions list for orthopedic emergencies.


The seven key points that are critical actions for INVASIVE AND NON-INVASIVE DIAGNOSTIC AND THERAPEUTIC PROCEDURES are these: 1 - When you are cardioverting a patient, be sure to turn on the synchronized mode unless otherwise indicated. 2 - For patients with persistent vomiting, order an NG tube with continuous nasogastric suctioning. 3 - In conscious patients in whom you are going to perform invasive or extraordinary procedures, explain to the patients the need for and the nature of the procedures. 4 - Ask that orthostatic blood pressure measurementsthat is, the Tilt Testbe taken in patients who present with weakness, dizziness or a possible ectopic pregnancy. 5 - Lumbar puncture is indicated ONLY in patients with suspected meningitis or those with a negative CT scan in whom a subarachnoid hemorrhage is suspected. 6 - Conscious patients who require endotracheal intubation must be sedated prior to using muscle relaxants or rapid sequence induction... and 7 - Insert a CVP line in trauma patients with persistent hypotension and tachycardia, particularly if there is evidence of a serious chest injury. CVP measurements reflect rapid changes in intravascular volume and are particularly useful in confirming the diagnosis of pericardial tamponade in a hypotensive patient. In the face of persistent hypotension (despite adequate shock therapy) the usual signs of pericardial tamponade will be absent. A CVP reading >15cm H2O in a hypotensive patient strongly suggests this diagnosis and is a clear indication for pericardiocentesis. This completes the critical actions list for procedures. The second category in this final review is groups that will be covered: Historical clues Physical exam clues Laboratory clues... and X-ray clues

There are four sub-

There are eight HISTORICAL CLUES that are key points in evaluating patients: 1 - If a temperature reading is not included in the initial vital signs, ask that it be taken. If you suspect hypothermia, ask that a rectal probe be used. 2 - Always ask about a history of hemophilia in male children with headaches and a history of migraine in the patient with recurring headaches. 3 - In black patients, ask about a history of sickle cell disease; if the patient is uncertain, order a sickle cell prep if his clinical condition suggests the possibility of a sickle cell etiology. 4 - In infants, ask about birth weight, feeding habits, immunization and fluctuations in weight. 5 - In all cases of bleeding, ask about anticoagulant use (including aspirin).


6 - In cases of suspected poisoning or overdose, send someone to the patient's home to look for empty bottles and a suicide note. 7 - Historical clues are frequently provided by EMTs and family members or friends; be sure to talk to them.. .and 8 - Always ask about a history of allergies. This completes the list of historical clues. The next category is PHYSICAL EXAM CLUES. There are seven clues in the physical exam that can bring the clinical picture in focus, when the diagnosis eludes you: 1 - The most important initial question is this: "What does the patient look like?" or "What do I see, as I walk up to this patient?" 2 - Rule out posterior shoulder dislocations in all postictal patients. 3 - When evaluating the optic fundi in patients with a cerebral event, look for spontaneous venous pulsations, retinal hemorrhages and exudates, and papilledema. Remember that the absence of spontaneous venous pulsations is the FIRST SIGN of increased intracranial pressure. 4 - In patients in whom you suspect a diagnosis of appendicitis, check for a Psoas sign and an Obturator sign: With the patient lying on his left side, extend the right leg at the hip; pain in the right lower quadrant is a positive Psoas sign. With the patient lying on his back, flex the right knee 90 and then externally rotate the right leg at the hip; pain in the right lower quadrant is a positive Obturator sign. 5 - In patients you suspect having meningeal irritation, check for a Kernig's sign and a Brudzinski's sign: With the patient supine, flex the leg at the hip and knee; then straighten the knee. If resistance or pain is elicited, this is a positive Kernig's sign. Again with the patient supine, flex the neck forward; spontaneous flexion of the knees and thighs is a positive Brudzinski's sign. 6 - To rule out constrictive pericarditis in a patient with chest pain, check for a pulsus paradoxuswhich is a drop of 10mm or more in the systolic blood pressure during normal inspiration...and 7 - Patients with suspected hypocalcemia or hypomagnesemia should be checked for Chvostek's sign and Trousseau's sign. When the facial nerve is percussed in front of the ear, twitching at the corner of the mouth is a positive Chvostek's sign. When the blood pressure cuff is inflated to a level midway between the patient's diastolic and systolic pressures and allowed to remain there for three minutes, carpal spasm is a positive Trousseau's sign. This completes the list of physical exam clues. The next category is LABORATORY CLUES. There are ten key points to note here: 1 - Order maximal laboratory tests ONLY when they are warranted; as a general rule, order only those tests that are clearly indicated.


2 - A Tylenol overdose that requires treatment with Mucomyst is characterized by a serum level greater than 140mcg/cc drawn four hours or more, after the ingestion. 3 - In all patients in whom you suspect a toxicologic or metabolic derangement, order ABGs, glucose, lytes (including calcium and magnesium), BUN and creatinine "stat." You need this information to calculate the anion gap and the osmolal gap. The anion gap is the difference between the cations (sodium) and the anions (chloride and bicarbonate). The osmolal gap is the difference between the measured osmolality and the calculated value determined by the following formula: (2 X serum Na+) + (glucose /18) + (BUN / 2.8) + (ETOH / 4.6) 4 - Red blood cell casts, reported in the urinalysis, are found in patients with glomerulonephritis. 5 - Basophilic stippling on a peripheral blood smear suggests lead poisoning. 6 - A zero bicarb level on the blood gas report suggests methanol or ethylene glycol toxicity. 7 - Order anticonvulsant levels on all seizure patients, even if there is a history of drug compliance. 8 - Hemophilia is characterized by a normal PT and an abnormal FIT. 9 - Synovial fluid that is clear and contains calcium pyrophosphate crystals is diagnostic of pseudogout. Synovial fluid with leukocytes and uric acid crystals is diagnostic of gout... and 10 - Laboratory clues to dehydration in infants are reflected in a CBC and urinalysis; hemoconcentration with a high hematocrit, ketonuria and a high urine specific gravity, all support the diagnosis. This completes the list of laboratory clues. The final category of diagnostic clues is RADIOGRAPHIC STUDIES AND INTERPRETATION. There are five key points to note when ordering and reading x-rays: 1 - X-ray findings are clues, but the patient's welfare should not be jeopardized to find them. Do portable films on critical patients; and if an emergency scan is ordered on a critical patient, send an RN WITH the patient to the radiology department. 2 - On all wrist films, look for lunate and perilunate dislocations on the lateral view; the lunate is dislocated if it is displaced volarlyif the capitate is displaced dorsally, there is a perilunate dislocation. 3 - Positive findings of a pulmonary infarction on chest x-ray include the following: A pleural effusion A wedge-shaped pleural-based density Cropped-off hilar vessels... and Rounded densities near the costophrenic angle above an elevated diaphragm. 4 - Positive findings of a traumatic tear of the aorta on chest x-ray include the following: A wide mediastinum


An indistinct aortic knob Tracheal deviation to the right NG tube displacement to the right On the LEFT side of the chest, look for A pleuroapical cap A pleural effusion... and Depression of the left mainstem bronchus... and 5 - The LeForte Classification of midfacial fractures is the following: LEFORTE I is a horizontal fracture of the maxilla above the level of the palate, but below the attachment of the zygoma. LEFORTE II is a pyramidal fracture with bilateral vertical fractures of the maxilla extending through the maxillary sinuses and infraorbital rims; there is also a horizontal fracture across the glabella (which is the bridge of the nose). LEFORTE III is characterized by complete craniofacial dysjunction; fractures extend through the frontozygomatic suture lines bilaterally, across the orbits horizontally, through the base of the nose and ethmoid. Aflat,"dish-pan" appearance is seen on the lateral view of the facial film. This completes the list of radiographic clues. The final section of this review is EXAM TECHNIQUES. Included here are key points that pertain to the exam process. There are ten techniques or key points that may be useful to you, as you are taking the exam. 1 - The only information ROUTINELY volunteered in the opening clinical presentation is the chief complaint and vital signs. In most cases, you will need to ascertain ALL pertinent information. The Examiner is not likely to waste time by giving you detailed information that is not relevant to case management. Only PERTINENT normal or abnormal historical points, exam findings and lab values are given. If any of this information is abnormal, this is significant. 2 - Always ask for a temperature recording, if it is not volunteered in the opening scenario. 3 - If you are presented with a trauma victim who has the POTENTIAL of developing hypovolemic shock, he is likely to remain stable unless you fail to insert two or more large bore IV catheters and order blood for type and crossmatch. 4 - If a patient presents with hip or leg pain of uncertain etiology, do not allow him or her to walk. An example here is an elderly woman who asks to go to the bathroom. If she has an undiagnosed hip fracture, the Examiner may lower your score, if you allow her to go to the bathroom. 5 - When providing specific treatment, adhere to established methods and modalities. Avoid NEW drugs and treatment protocols that have been advocated in recent literature or adopted by your hospital. Along the same lines, perform those procedures normally expected from an Emergency Physician. Examples are: central venous cannulation, CVP lines, emergency needle or surgical cricothyroidotomy, chest tube thoracostomy,pericardiocentesis,





peritoneal lavage, culdocentesis, joint aspiration, reduction of shoulder dislocations.. .and so on. In some community hospitals, the Emergency Physician defers these procedures to a specialist. At the Oral Exam, however, you will be expected to do them because they are established standards of care in our specialty. If you are not sure whether a specific procedure is expected to be performed by you, I recommend that you refer to one of the Emergency Medicine texts for direction. During the exam, if you call for a specialist for a specific procedure and the Examiner tells you he's "unavailable," he probably wants you to do it. When ascertaining physical signs in a specific area, try to ask for them all at once, rather than one at a time. For example, if you have a patient who has sustained a crush injury to the foot, the litany would be something like this: "I'm looking for swelling, deformity, and discoloration. Ill also check the skin color and temperature, evaluate the pedal pulses, and check for neurologic impairment. On palpation, 111 feel for bony crepitus and deformity." The case will move along more quickly and smoothly, if you are able to do this. Your interpersonal skills will be tested, either with the patient's family or the patient himself. Be sure to address the concerns of the patient or his family and offer assistance with social problems, when possible. When in doubt about specific management of a poisoning or overdose, call Poison Control, look it up, or obtain the information you need from someone who would know (such as the hospital Pharmacist or a Toxicologist). When you perform a complete physical exam, be sure to ask for specific signs and findings or you may miss pertinent information. For example, if you are examining the abdomen and don't ask if it's distended, that information may not be volunteered by the Examiner, even if it's present. So if you want specific information, ask for it. Also, review and learn the physical exam litanies at the back of the book. How you ask questions is a very important strategy for this exam. As a rule, all single-encounter patients will require admission. Occasionally, a patient from a multiple encounter will have an injury or illness that can be followed up, on an outpatient basis.

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This completes the last-minute clinical review. I've given you a lot of information in this last minute review. I recommend that you listen to this CD several times. Each time you listen, you will learn a little more than you did before. Repeated listening and practice through simulation will fortify your preparation for this exam. Above all, remember to think positively during your preparation. I've worked with physicians who did not believe they could pass this exam, but they did.. .and so can you... I wish you success at the Oral Exam.