CORRESPONDENCE
phylaxis by sensitization to albumin. Dr Orlowski further suggests that some of the "inconsistencies" in the rabbit model may be the result of our method for determining cardiac output. He states that pulmonary edema as part of the anaphylactic reaction could possibly give a falsely low cardiac output using our thermodilution method. Certainly there is a margin of error using a thermodilution cardiac output technique in low flow states. Warren and Ledingham8 describe that in low cardiac output states in rabbits, thermodilution cardiac output measurements from a right atrial injection may be in error by 10% to 12% compared with thermodilution outputs determined by left atrial injections. The right atrial injections tended to be high. Also, pulmonary edema is not a common finding in rabbits with anaphylaxis. We believe that our animal model is a useful one to evaluate new treatment procedures for anaphylactic shock. It is consistent with the hemodynamic alterations found in primate models of anaphylactic shock. The exact hemodynamic alterations and their sequence during anaphylactic shock in human beings still is undetermined; however, it would appear that the manifestations of anaphylactic shock in human beings may vary considerably. Some cases of anaphylactic shock appear to affect primarily the upper airway, whereas other cases result in cardiovascular collapse. It is possible that the primary cause for hypotension in human beings may differ from case to case.
William G Barsan, MD Jerris R Hedges, MD Department of Emergency Medicine University of Cincinnati Medical Center Cincinnati, Ohio 1. Hanashiro P, et al: Anaphylactic shock in man. Arch Intern Med 1967;119:129-140. 2. Silverman H, et al: Hem.dynamic changes in human anaphylaxis. Am J Med 1984;77:341-344. 3. Nordstrom L, et al: Shock of anaphylactoid type induced by protamine: "A continuous cardioresEiratory record. Acta Anesth Scan 1978;22:195-201. 4. Ravenas B, et al: Anaphylaxis in the monkey. Acta Anesth Scand 1979;23:435-443. 5. Smedegard G, et al: Anaphylactic shock in the monkey: Here.dynamics and blood flow distribution. Acta Physiol Scand 1979;106:191-198. 6. Pavek K: Anaphylactic shock in the monkey: Its hem.dynamic and mediators. Acta Anesth Scand 1977;21:293-307. 7. Smedegard G, et al: Anaphylactic shock in monkeys passively sensitized with human reaginic serum: I. Hem.dynamics and cardiac performance. Acta Physiol Scand 1981;111:239-247. 8. Warren DJ, Ledingham JG: Cardiac output in the conscious rabbit: An analysis of the thermodilution technique. J Appl PhysioI 1974;36:246-251.
"Ortho Consult" With "Another Doctor" To the Editor: An interesting conversation occurred in our emergency department that in its simplicity raised several poignant issues in our practice of emergency medicine. A senior resident in emergency medicine and a senior medical student interested in making emergency medicine his career asked me to review a radiograph of an injured elbow, as it had several classic findings. The radiograph revealed classic signs of a radial head fracture, the anterior and posterior fat pad signs. I asked both of the young physicians what they wanted to do and in unison they answered, "Ortho consult." Herein lies the issue: As good emergency physicians and educators of future practitioners we know that the definitive care for this patient is a sling, analgesics, and proper followup with his orthopedist or family physician. If it were a reasonable time of the day, a phone call to that physician would certainly be courteous. But to have the patient wait any longer than necessary for "another doctor" to see him, an orthopedic resident who will render the same care and
make the same follow-up arrangements, is in my opinion improper care for the patient. Moreover, it gives those skeptics of emergency medicine more ammunition to hurl at us that we are only glorified "triage officers." Most of our emergency medicine training programs indude several months of orthopedic training. What is the purpose of such training? So that we may pick up a phone and call a consult when a bone is injured, or is it to learn to render care of many minor orthopedic injuries, such as this one, and ensure proper follow-up care for the patient? It is for those who believe the former to be proper, that one must "cover one's derriere" with an ortho consult, that I have taken the time to write this letter. George E Goldman, MD, FACEP Akron City Hospital Akron, Ohio
CSWO, Not COWS, in the Unresponsive Patient To the Editor: The brief letter by Charles Webb, MD, "COWS Caloric Test" [September 1985; 14:938] nicely summarizes the traditional teachings about this procedure. However, this test as described is of very limited use clinically. The magnitude of caloric-induced nystagmus is highly dependent on the de170/981
gree of visual fixation permitted during the test procedure; electronystagmography is necessary for accurate results.l,2 Caloric testing in the emergency department is much more valuable in evaluating the unresponsive patient. After inspection of the auditory canals to verify that the tyro-
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panic membrane is intact and the canal not impacted with cerumen that may impair stimulation, cold water is introduced into the canal. Normal nystagmus is regular, rhythmic, and lasts two to three minutes in response to caloric stimulation. As consciousness is lost acutely from metabolic or supratentorial brain disease, the fast component progressively disappears and the slower reflex eye movements carry the eyes tonically toward the irrigated ear.2,3 When present this reaction indicates intact brainstem function. Severe brainstem injury or deep metabolic depression of brainstem traction may alter or obliterate the caloric response. If normal nystagmus is elicited, the patient is physiologically awake, and the unresponsiveness cannot be caused by structural or metabolic disease of the nervous system. Conversion disorders, catatonia, malingering, and other causes of psychogenic unresponsiveness should be considered. In summary, in the unconscious patient with intact
brainstem hmctions, cold water irrigation produces slow deviation of the eyes to the same side of stimulation. Warm water irrigation should produce deviation to the side opposite the site of irrigation. Not "COWS" but cold - - same, warm - - opposite in the unresponsive patient.
J Stephen Huff, MD Department of Emergency Medicine University of Cincinnati Cincinnati, Ohio l. Baloh RW, Honrubia V: Clinical Neurophysiology of the Vestibular System. Philadelphia, FA Davis Company, 1979, p 134. 2. Baker PB: Caloric testing, in Roberts JR, Hedges JR (eds): Clinical Procedures in Emergency Medicine. Philadelphia, WB Saunders Company, 1985. 3. Plum F, Posner JB: The Diagnosis of Stupor and Coma. Philadelphia, FA Davis Company, 1980, pp 54-56.
Beta Blocker Overdoses To the Editor: The following case studies present two patients with beta blocker overdoses. Case 1: A 27-year-old woman who had ingested 40 80-mg Inderal ® tablets less than one hour before was admitted to the emergency department. She was given ipecac and within minutes suffered cardiovascular decompensation. Her pulse was 40 and blood pressure was 55/30 m m Hg. She was given 7.5 mg glucagon IVP Within minutes her pulse and blood pressure were restored to normal range. They remained stable for the duration of her emergency treatment. She was transferred to the MICU on a continuous infusion of glucagon at 2.5 mg/h. She was weaned from the infusion after 12 hours and was discharged within the next 72 hours without incident. Case 2: Paramedics were called to a residence because of a report that a young woman had taken 100 40-mg Inderal ® tablets. When they arrived, the patient was semiconscious, had a weak pulse, and no apparent blood pressure. An IV line was started and she was transported to the ED. On arrival CPR was in progress and the rhythm had deteriorated from sinus bradycardia to asystole. After extensive resuscitation techniques were applied the patient was pronounced dead. Only 3 mg glucagon were available in the ED. Two more were obtained 30 minutes after the patient arrived. These cases point out several clear lessons. First, the rapidity of onset of cardiovascular compromise in overdose of beta-blocking agents, particularly Inderal ®, should cause the emergency physician to be very cautious in the use of ipecac in these patients. Ipecac is relatively contraindicated
in beta blocker overdoses. Second, glucagon, which has been recognized since 1980 as effective in reversing bradycardia and hypotension, should be available for immediate use on all paramedic vans and in all EDs. The recommended dosage of glucagon is 100 to 150 ~g/kg IVP followed by a continuous infusion of 1 to 5 mg/h for the duration of four to five half-lives of the specific beta blocker. This should be accompanied by standard overdose therapy of lavage with large-bore orogastric tube with 3 to 5 L sodium chloride. Charcoal should be administered in a dose of 1 gm/kg or five times the ingested dose of the beta blocking agent. Because of enterohepatic circulation pulse charcoal should be administered in a dose of 20 to 40 g every two to four hours. A cathartic should be used as well. Glucagon should be approved for paramedic usage in the field according to poison center guidelines. Similarly, IV pyridoxine has been shown to be extremely effective in treatment of seizures due to isoniazid overdose. The IV dose of pyridoxine is 1 mg pyridoxine IV push for every 1 mg of isoniazid ingested. If the quantity of isoniazid ingested is unknown, then 5 g should be used. A recent survery of the EDs in our area shows that neither of these drugs are readily available. We believe it advisable that all directors check their drug supplies.
John Wilkinson, DO Clinical Toxicology Associates of San Diego Poway, California
Manual Intubation: Transmitter of Disease? To the Editor: While practicing the technique of manual oral endotracheal intubation on the intubation m a n n e q u i n we 15:8 August 1986
noticed a disturbing fact. Every successful intubater was noted to have abrasions over the second and third metacar-
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