Faculty Bibliography

BACKGROUND: In the urban setting, hypothermia is commonly associated with illness or intoxication, with death often secondary to infection. OBJECTIVES: To evaluate factors that affect the rewarming rate (RWR) and the ability of the RWR and other clinical markers to predict the presence or absence of underlying infection in an adult urban population. METHODS: This was a prospective observational study of hypothermic patient visits to a large emergency department. Serial temperatures were obtained during rewarming to construct rewarming curves. Rewarming modalities selected by emergency physicians were correlated with admission temperatures. Univariate associates of RWR and infection were assessed. RESULTS: The authors identified 96 patient visits. The median temperature was 89.5 degrees F (31.9 degrees C; range, 73.0 degrees F to 95.0 degrees F [22.8 degrees C to 35.0 degrees C]). Thirteen patients had temperatures of < 80.0 degrees F (26.0 degrees C). Seven died within 14 hours of presentation; six, of infection. No patient experienced ventricular fibrillation. Potential candidate predictors of infection from a multivariate analysis were a RWR of < 1.80 degrees F (1.0 degrees C) per hour and a serum albumin of < 2.7 g/dL. Rapid rewarming was associated with the absence of infection and a temperature below 86.0 degrees F (30.0 degrees C). In patients without significant underlying illness, rewarming rates appeared to be independent of the modality of rewarming. CONCLUSIONS: Rewarming rates reflect intrinsic capacity for thermogenesis. Increased RWRs were associated with the absence of infection. The achievement of normothermia did not prevent death in infected patients. Initiation of invasive rewarming in urban patients with hypothermia who have not had hypothermic cardiac arrest may be unwarranted. Management of this population should emphasize support, detection, and treatment of underlying illness

Traumatic retrobulbar hemorrhage may result in acute loss of vision that is reversible when recognized and treated promptly. A case of traumatic retrobulbar hemorrhage is presented. The technique of emergent orbital decompression by lateral canthotomy and cantholysis is described. The anatomy of the lateral canthus and the surgical procedure are illustrated by gross dissection

OBJECTIVE: To determine the effects of body temperature, ethanol use, electrolyte status, and acid-base status on the electrocardiograms (ECGs) of hypothermic patients. METHODS: Prospective, two-year, observational study of patients presenting to an urban ED with temperature < or =95 degrees F (< or =35 degrees C). All patients had at least one ECG obtained. Electrocardiograms were interpreted by a cardiologist blinded to the patient's temperature. J-point elevations known as Osborn waves were defined as present if they were at least 1 mm in height in two consecutive complexes. RESULTS: 100 ECGs were obtained in 43 patients. Presenting temperatures ranged between 74 degrees F and 95 degrees F (23.3 degrees C-35 degrees C). Initial rhythms included normal sinus (n = 34), atrial fibrillation (n = 8), and junctional (n = 1). Osborn waves were present in 37 of 43 initial ECGs. Of the six initial ECGs that did not have Osborn waves present, all were obtained in patients whose temperatures were > or =90 degrees F > or =32.2 degrees C). For the entire group, the Osborn wave was significantly larger as temperature decreased (p = 0.0001, r = -0.441). The correlation between temperature and size of the Osborn wave was strongest in six patients with four or more ECGs (range r = -0.644 to r = -0.956, p = 0.001). No correlation could be demonstrated between the height of the Osborn waves and the serum electrolytes, including sodium, chloride, potassium, bicarbonate, BUN, creatinine, glucose, anion gap, and blood ethanol levels. CONCLUSIONS: The presence and size of the Osborn waves in hypothermic patients appear to be a function of temperature. The magnitude of the Osborn waves is inversely correlated with the temperature

In summary, a number of pharmacologic agents interfere with the body's ability to maintain normal body temperature during exercise or under conditions of environmental heat stress. Life threatening elevation of body temperature may occur. Regardless of the predisposing cause of heatstroke, the final common pathway is heat injury to tissues causing cell death. Rapid cooling of the patient must take precedence and elucidation of the pathophysiologic disturbance is secondary to the accomplishment of this goal.