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Thread: Altered Mental Status in a Young Man Picked Up On the Street

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    Default Altered Mental Status in a Young Man Picked Up On the Street

    A 33-year-old man is brought by ambulance to the emergency department (ED) with altered mental status and agitation. He had called 911 from a pay phone, stating that people were trying to shoot him. Upon arrival of the police to the scene, the patient was reported to be visibly paranoid, so Emergency Medical Services (EMS) was called. En route to the hospital, the patient became more confused and combative. EMS requested and received authorization to give intramuscular midazolam. A total of 4 mg was given, but 8 people were still needed to control the patient and get him into the ED and onto a gurney. On arrival, the patient is unable to provide much meaningful history of his present illness, but he is coherent enough to deny any previous medical problems, allergies, or prescription medication use (other than methadone). He does admit to using cocaine.

    On physical examination, he is extremely diaphoretic and, soon after arrival, the patient begins convulsing. His pupils are dilated but equal and reactive to light. His vital signs are notable for a blood pressure of 80/40 mm Hg, a heart rate of 180-190 bpm, a respiratory rate of 32 breaths/min, and an oxygen saturation of 63% while using a nonrebreather mask. The patient's rectal temperature is measured at 108.1F (42.3C). While preparations are made to intubate the patient, his blood pressure drops to 60/40 mm Hg. Cardiac monitoring reveals the patient to be in a wide-complex tachycardia indicative of ventricular tachycardia vs supraventricular tachycardia with aberrancy. Because he is unstable, Advanced Cardiac Life Support (ACLS) guidelines are followed, and he is defibrillated with 50 Joules biphasic, without response. The initial defibrillation attempt is followed by a second attempt at 100 Joules, also without resolution of the tachycardia. A 3-lead rhythm strip is then obtained (Figure 1) that demonstrates a narrow-complex tachycardia. Rapid-sequence intubation is initiated with 20 mg intravenous (IV) etomidate and 10 mg IV vecuronium. Once the endotracheal tube is successfully placed and the position confirmed, 4 mg IV lorazepam is administered for ongoing sedation.

    A presumptive diagnosis of heatstroke caused by cocaine toxicity is made. Ice packs are applied to the patient's groin and axillae, and a cooling blanket is placed on the patient. Cooled IV saline is infused, and a Foley catheter with a temperature probe is placed. The patient's temperature drops to 102F (38.9C). After sedation, intubation, aggressive cooling measures, and IV hydration have been initiated, the patient's heart rate is noted to slow to around 130 bpm, and his blood pressure and oxygen saturation both normalize. The patient is admitted to the medical intensive care unit (ICU).



    What is the potentially life-threatening finding seen on the electrocardiogram (ECG) that is a result of this patient's condition?

    Hint: Play close attention to the T waves; the ECG computer will miss this every time.


    Acute myocardial infarction
    Hypomagnesemia
    Cerebral T waves
    Hyperkalemia
    Answer & Discussion



    [ CLOSE WINDOW ]Figure 1. The rhythm strip demonstrated sinus tachycardia, with peaked symmetric T waves that are consistent with hyperkalemia. In addition, hyperkalemia can often be associated with small or absent P waves and a widening of the QRS complex. In the setting of tachycardia, this can give the appearance of bundle branch block (BBB) (aberrancy) or ventricular tachycardia (as was the concern here, given the patient's hemodynamic instability). ECG abnormalities can reveal a cardiac effect of hyperkalemia, but they do not always correlate with the severity of the hyperkalemia; therefore, it is important to corroborate the ECG evidence with the laboratory values.

    The hyperthermia and convulsions in this patient likely led to a severe metabolic acidemia and rhabdomyolysis, with resultant hyperkalemia. The laboratory analysis showed a white blood cell count of 19.1 103/L (19.1 109/L), with no left shift. The coagulation tests and cardiac troponin results were normal. The urine microscopy and chest radiograph, both performed to investigate for a source of infection, were normal. A serum toxicology screen, including for aspirin and acetaminophen, was negative; however, a urine toxicology screen was positive for cocaine, methadone, benzodiazepines, and opiates (but it was negative for amphetamines, barbiturates, phencyclidine [PCP], and oxycodone). The chemistry panel showed a potassium level elevated at 6.9 mEq/L (6.9 mmol/L; normal range is < 5.0 mEq/L), a carbon dioxide level of < 5 mEq/L (< 5 mmol/L), and a creatinine of 1.7 mg/dL (150.28 mol/L). The patient's serum glucose was measured at 170 mg/dL (9.44 mmol/L), and his serum lactic acid was 25.23 mg/dL (2.8 mmol/L). The creatine kinase was elevated at 710 U/L, as were the aspartate transaminase (AST) at 86 U/L and the alanine transaminase (ALT) at 123 U/L. His urine, while initially negative, turned red on a repeat specimen (while still in the ED). Treatment for hyperkalemia was initiated with calcium gluconate, dextrose plus insulin, and sodium bicarbonate. Copious IV fluids were also given.

    The underlying etiology of the patient's problems was heatstroke. This condition is defined as the combination of hyperthermia (core temperature > 105F [40.6C]) and neurologic impairment.[1] There are 2 types of heatstroke: classic nonexertional heatstroke (NEHS) and exertional heat stroke (EHS).[1] From 1979 to 1997, the National Centers for Health Statistics (NCHS) reported 7046 deaths secondary to heat, or 371 deaths per year; this is presumed to underestimate the true numbers of deaths. Those older than age 65 years make up almost half of these cases.[1] Heatstroke is seen less often in subtropical areas than in temperate climates. The 2003 heat wave in France is attributed for the deaths of more than 10,000 people.[2]

    The 80% mortality rate associated with heatstroke can be reduced to as low as 10% if heatstroke is recognized early and cooling treatment is initiated promptly. The damage caused by this condition is directly related to the temperature and the length of time it remains elevated. The classic presentation is that of hyperthermia, anhidrosis, and neurologic deficit. Some patients, however, will still sweat, and others will begin to cool en route to the hospital; these patients might not meet the classic temperature criteria.[1]

    Classic NEHS occurs most frequently in very young and very old individuals during heat waves. Also at risk for NEHS are alcoholics, the chronically or mentally ill, and those who are dehydrated. Patients present with high temperatures, lack of sweating, and altered mental status. Neurologic complaints may include irritability, lethargy, confusion, ataxia, seizures, and coma. Psychiatric-type symptoms, such as delusions or hallucinations, can also occur. The classic triad is not always present. Sweating may occur, and patients may present with temperatures < 105.8F (41C).[1] Additional symptoms and signs may include vomiting, diarrhea, tachycardia, hypotension, and tachypnea.

    EHS typically occurs in healthy young patients participating in vigorous physical activity in hot environments,[1] but it can occur at ambient temperatures as low as 70F (21.1C) as well.[3] Those affected with EHS present with hyperthermia, altered mental status, and diaphoresis. They can exhibit strange behaviors or syncope during physical activity, as well as experience abdominal cramps, nausea, vomiting, diarrhea, headache, and dizziness. Because these patients retain their ability to sweat, their temperatures may drop after physical activity has stopped but before presentation at the ED. Risk factors for EHS include viral infections, fatigue, dehydration, the use of stimulants, and not being acclimatized to higher temperatures.

    In addition to elevated temperatures and neurologic signs and symptoms, other organ systems may also be affected in EHS, including the cardiovascular, pulmonary, gastrointestinal, hepatic, renal, and musculoskeletal systems.[1] The stress caused to the cardiovascular system can be particularly worrisome in the elderly. Tachycardia at 130-140 bpm and greater is common, as is hypotension resulting from dehydration, redistribution of blood to the skin, and collapse of vascular tone. Patients can be tachypneic and hypoxic for various reasons, including atelectasis, noncardiogenic pulmonary edema, and aspiration.[1] Liver and renal failure can pose serious risks to those surviving the neurologic insult.[3] Rhabdomyolysis is common and, along with hypotension, often leads to renal failure. Liver failure also commonly occurs, possibly secondary to direct heat injury and hypoxia.[2-5] Disseminated intravascular coagulation may also occur.[5]

    Multisystem damage is a result of the widespread deadly cellular effects of heat and the body's resultant inflammatory response. Multisystem injury leads to increased morbidity and mortality. In a retrospective study on heatstroke victims, Varghese and colleagues found that the overall mortality rate was 70% for all cases, but it was 85% in patients with multiorgan failure. These investigators found that elevation of creatine kinase, elevation of liver transaminases, and metabolic acidosis were each predictors of poor patient prognosis.[2]


    The differential diagnosis of heatstroke includes entities in many categories, including thyroid storm, pheochromocytoma, sepsis, meningitis/encephalitis, alcohol withdrawal, and abuse of stimulants (among others). Anticholinergic and antipsychotic drugs rarely cause fever, except in rare cases of neuroleptic malignant syndrome, but these agents can place a patient at risk for heatstroke by preventing sweating. Such drugs include antihistamines, antiparkinsonian drugs, neuroleptics, and others.[6] Another life-threatening condition secondary to exposure to certain drugs is malignant hyperthermia (MH). This condition can lead to an uncontrolled rise in body temperature in susceptible individuals from exposure to volatile anesthetics during general anesthesia, nearly all gas anesthetics, and the neuromuscular blocking agent succinylcholine. The clinician must keep a high level of suspicion for heatstroke because, in some cases, it may present insidiously, and valuable time may be lost to investigating other possible diagnoses (as shown in a study by Varghese and colleagues, in which patients presented a mean of 4.1 days after the onset of elevated temperature).[2]

    Given the possibility of multisystem failure, many diagnostic tests are appropriate for suspected heatstroke; these include complete blood cell count, chemistries, liver function tests, creatine kinase, troponin, urinalysis and urine culture, blood cultures, chest radiography, and ECG. A computed tomography scan of the brain may identify alternative causes of altered mental status.[1] A toxicology screen may, in some cases, be useful as well.

    Hypokalemia can occur early on in heatstroke; however, hyperkalemia can possibly occur secondary to muscle damage. Moreover, rhabdomyolysis can lead to creatine kinase levels greater than 100,000 U/L. A urinalysis showing marked hematuria on urine dipstick interpretation but few red blood cells on microscopic analysis is consistent with myoglobin in the urine and rhabdomyolysis. Blood urea nitrogen and creatinine measurements may detect renal failure, which may result from dehydration, heat injury to the kidney, and rhabdomyolysis (or even all three). Liver transaminases can be elevated into the thousands or even tens of thousands as a result of liver and/or muscle injury. A rise in troponin level is not uncommon in NEHS, particularly in the elderly; in fact, it was associated, among other parameters, with a higher level of mortality in a study of victims of the 2003 French heat wave.[7] The etiology of elevated troponin in this setting remains unclear.[8]

    Among illicit drugs, cocaine has been associated with a higher incidence of death secondary to hyperthermia. Marzuk and colleagues concluded that, of patients younger than 55 years dying from hyperthermia in New York City, one fourth had taken cocaine immediately beforehand. Moreover, these investigators showed that there were one third more deaths secondary to cocaine use on days hotter than 88F (31.1C). They concluded that cocaine is singular among drugs in its association with hyperthermia and mortality.[9] A small study of 8 patients presenting with heatstroke during the 1998 New Orleans heat wave found cocaine was associated more often with heat-related illness than were other drugs and medications.[6]

    Heatstroke requires emergent treatment with active cooling measures. Ice packs should be placed on the groin and axillae, and cooled IV saline should be given. The mainstay of treatment in most centers is through the process of evaporation; warm water is sprayed onto the patient, preferably as a mist, followed by the use of fans to evaporate the water. If no fans are available, a cooling blanket can be considered. Ice-water immersion is effective, but this technique introduces difficulties in monitoring and resuscitating patients, and it also has been criticized for potentially leading to peripheral vasoconstriction and preventing the core body temperature from dropping. Other more aggressive cooling techniques include cold lavage in the peritoneal, thoracic, rectal, and gastric cavities. In the most severe cases, cardiopulmonary bypass has been suggested. Antipyretics such as acetaminophen and ibuprofen are not useful in heatstroke; however, until other causes of disease (such as infection) are ruled out, antipyretics may be used. Dantrolene has not proven to be effective in lowering body temperature.[1] Benzodiazepines are helpful in preventing the generation of additional heat by shivering, agitation, or seizures.[1] Cooling measures should be stopped when the patient's temperature reaches 102.2F (39C) to prevent overshoot hypothermia.[1]

    In addition to cooling the patient, supportive care for other manifestations resulting from high temperatures is necessary. Hypovolemia should be treated with fluids. Rhabdomyolysis should be treated primarily with aggressive volume resuscitation. The addition of sodium bicarbonate can be considered, although no conclusive data exist supporting its use. Liver failure is usually mild or moderate and amenable to conservative therapy.[3,5] Expectant management of frank liver failure may be the best approach. Three patients with acute liver failure who met the criteria for transplantation underwent transplantation, and all had fatal outcomes. There are, however, case reports of patients meeting these same criteria who fully recovered after only conservative treatment.[3,5]

    The patient in this case was intubated and admitted to the medical ICU. After clinicians noted continued normalization of his temperature and an improved mental status, he was successfully extubated the next day. His chest radiographs continued to show clear lungs. Treatment for his rhabdomyolysis was continued with IV fluids containing bicarbonate. His creatine kinase continued to rise, peaking on day 2 at 130,000 units/L, then began to fall. His urine output remained adequate and, although his creatinine peaked at 2.5 mg/dL on hospital day 4, he never required dialysis. His troponin, within normal limits at first, peaked on hospital day 2 at 0.89 ng/mL (0.89 g/L), then began to fall. His liver enzymes peaked on hospital day 3, with an AST of 3870 unit/L (3870 U/L) and an ALT of 2080 units/L (2080 U/L), then began to resolve spontaneously. He eventually stabilized by hospital day 3, and then he began to improve; at discharge, he had no evidence of any permanent neurologic damage.


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    Default Self-Assessment

    You are examining a patient in the emergency department (ED) with a very high temperature and apparent heatstroke. Which of the following should NOT be guiding factors in your treatment of this patient?

    Damage to the tissues is caused by the thermal insult directly and the body's inflammatory response to the thermal insult
    Peaked T waves are possible on electrocardiogram (ECG)
    Before treating for heatstroke, the clinician should first rule out all other diagnoses
    Multiple organ system failure is a poor prognostic indicator
    Renal failure is a common complication of patients after heatstroke

    The key to success in treating heatstroke is rapid cooling as early as possible because any tissue damage incurred is directly related to the amount of time that hyperthermia is present. Other diagnoses must be considered, but priority should be given to rapid cooling of the patient. Tissue damage is caused directly by the thermal insult and indirectly by the body's response to the insult. Peaked T waves may be seen on a patient's ECG because the hyperthermia and muscle activity can lead to rhabdomyolysis and renal failure, which can then lead to hyperkalemia. Renal and liver failures are common complications of patients suffering from heatstroke, and multiple organ system failure leads to higher morbidity and mortality.


    Which of the following characteristics must your patient have in order to be diagnosed with heatstroke?


    The patient must have neurologic impairment
    The patient must have a core temperature > 105F (40.6C) at presentation
    The ambient temperature must be > 86F (30C)
    The patient must have stopped sweating
    The patient must have normal labs, tox screen, and computed tomography (CT) of the brain to rule out all other causes in order to attribute his symptoms to heatstroke

    The definition of heatstroke includes the manifestation of neurologic impairment, including states ranging from irritability to coma. Altered mental status may also present with psychiatric symptoms, such as hallucinations. Although the definition of heatstroke also includes hyperthermia, with a temperature of > 106F (41.1C), it is possible that at presentation the patient may already have begun to cool. Heatstroke can occur with vigorous activity at moderate ambient temperatures. Blood tests are useful in indicating multiple organ system failure and very well may be abnormal in the patient with heatstroke. A CT scan can be helpful in evaluating other possible causes of altered mental status. Heatstroke can be associated with some medications and illicit drugs, such as cocaine. These examinations should not delay the timely initiation of cooling.


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