Week 24: Earth, Wind, Fire, and Bites

Heat emergencies represent a continuum of disorders that range in severity from heat cramps to heat exhaustion to life-threatening heat stroke. In most circumstances, heat emergencies can be avoided through common sense, public education, and prevention. People most at risk for heat injuries include athletes, military personnel, and laborers who work outdoors in the heat. Classic heat injury, as is the case with this patient, usually occurs during periods of high environmental heat stress. Physical exertion is not required if environmental temperatures and humidity create a situation where heat gain overwhelms native heat losses. Exertional heat injury usually affects individuals who are participating in athletic events in conditions of high heat stress. Clinical features are what determine the severity of heat illness. This patient is presenting with symptoms characteristic of heat exhaustion. Other symptoms can include muscle cramps, headache, and vomiting. On physical examination of patients with heat exhaustion, the temperature may be normal or elevated. However, patients with heat exhaustion will not have mental status changes. Mental status changes are a sign of heat stroke which can be life-threatening.

Dry skin, or anhidrosis (A), can classically be found in patients with heat stroke but this is not a requirement for the diagnosis since patients with severe heat illness can also present with diaphoresis. Heat exhaustion is characterized by the inability to maintain adequate cardiac output due to strenuous exercise and environmental heat stress. Acute dehydration may be present. Athletes with heat exhaustion have difficulty continuing with exercise. Other signs of heat exhaustion include hypotension (B), syncope, and tachycardia (D). The presence of these factors does not necessarily portend severe complications from the illness. Severe heat illness, heat stroke, presents with neurological symptoms such as hallucinations, seizure, mental status changes, or coma.

The class Arachnida contains the largest number of venomous species known, but most are not harmful to humans. Humans fear spiders and scorpions, but of this class of species ticks probably cause the greatest morbidity. One of the more venomous spiders known is the black widow spider or Latrodectus species. They are found throughout the United States, except Alaska. Symptoms of a black widow spider bite include a pinprick sensation followed by local redness and swelling, but sometimes the bite is not felt. Over the next hour, patients develop dull cramping in the area of the bite that eventually spreads to the entire body. Pain is centered in the chest in patients who suffer an upper extremity bite, and pain is centered in the abdomen in patients who suffer a lower extremity bite. The abdomen may become boardlike and can mimic pancreatitis, appendicitis, or a perforated peptic ulcer. Signs and symptoms usually abate within a few hours and definitely resolve in two to three days. Management is supportive with benzodiazepine treatment for muscle spasms.

Symptoms of a brown recluse spider (B) bite include local burning pain at the site of the bite. After a few hours, a bleb forms in the center of the bite with a surrounding erythematous ring. The area can look like a target sign or a bull’s eye. Over the next few days, the bleb darkens and begins to necrose with eventual involvement of the underlying subcutaneous fat along with the skin. Systemic symptoms such as fever, malaise, vomiting, and rash can develop and lead to shock in severe cases, although fatalities are rare. This patient does not have a bite characteristic of a brown recluse spider. A scorpion (C) sting is characterized by immediate pain at the site of the sting. Over some time, patients can develop numbness and weakness locally and will have heightened sensitivity in the sting area. Systemic symptoms such as restlessness, vomiting, muscle spasms, nystagmus, and myoclonus can develop in severe cases but are more rare. Scorpion sting symptoms can mimic those found in patients with black widow spider bites but are much less common. Most tarantulas (D) are nontoxic. They are unusual in that their abdominal hairs can be thrown and embedded in human skin, leading to allergic reactions. There is not a toxic bite. The patient in this question is not presenting with allergic reaction symptoms.

Decompression sickness occurs due to the liberation of gas bubbles associated with a decrease in ambient pressure. This can occur in divers breathing compressed air as well as high altitude pilots or astronauts. The gas bubbles likely obstruct blood flow, leading to direct tissue ischemia. They also activate a variety of inflammatory processes, leading to thrombosis and capillary leaking. Symptoms of decompression sickness typically occur minutes to hours after surfacing. Decompression sickness can include pain syndromes involving the joints (“the bends”) as well as more serious manifestations including pulmonary (“the chokes”), cardiovascular, and neurologic symptoms (“the staggers”). Treatment of decompression sickness is similar to the treatment of an arterial air embolism and includes administration of oxygen, increasing tissue perfusion with intravenous fluids, and rapid decompression with hyperbaric oxygen.

Arterial air embolism (A) is an example of a barotrauma of ascent and results from entry of air into the arterial system with resultant embolization. The brain is the most commonly affected organ. Arterial air embolism should be suspected in any diver with loss of consciousness upon surfacing. Inner ear barotrauma (C) is an example of barotrauma of rapid descent or ascent and results from rupture of the round window or tearing of the vestibular membrane due to a forceful Valsalva maneuver done during descent to clear the ears. Symptoms include vertigo (as seen in the patient above) but this condition is easily differentiated from decompression sickness due to the onset of symptoms during descent rather than after surfacing. Nitrogen narcosis (D) occurs with deep dives and includes symptoms such as loss of fine motor skills and higher-order brain functions, resulting in bizarre and dangerous behavior. Presentation is similar to alcohol intoxication.

Atrial fibrillation in hypothermia tends to be relatively benign and resolves spontaneously with rewarming. Persistent atrial fibrillation after complete rewarming is unlikely to be due to hypothermia and may suggest an underlying medical pathology. Cardioversion increases the risk of ventricular fibrillation and is contraindicated unless the patient is unstable. Anticoagulation for temporary atrial fibrillation is not indicated and could worsen the coagulopathy already present in hypothermia.

This patient presents with rhabdomyolysis after an electrical injury and should be treated with aggressive intravenous hydration. Electrical injuries are common and are the cause of about 5% of burn unit admissions and 6% of occupational fatalities. The extent of the injury is related to the type of circuit (alternating current (AC) versus direct current (DC)), the resistance, amperage, duration of contact and voltage. The initial exposure to electricity can cause severe burns spreading from the point of impact. Additionally, the energy from the shock is transmitted into the body and can cause significant muscle breakdown. Breakdown is increased if the patient experiences tetany or prolonged exposure to the electrical source. The classic finding of rhabdomyolysis is a urine dip that is positive for blood with only scant or no RBCs on microscopy. The urine dipstick falsely reports myoglobin as hemoglobin in this case. A serum creatinine kinase level should be obtained. Initial treatment is with aggressive fluid resuscitation to maintain urinary output as myoglobin accumulation can lead to renal failure. Electrolyte abnormalities (specifically hyperkalemia from cellular breakdown) should be closely monitored and treated as well.

A CT scan of the abdomen (A) is not necessary to look for a bleeding source. Intravenous antibiotics (B) are not necessary as this urinalysis does not indicate the presence of infection. Packed red blood cells (D) are not needed at this time as the patient does not exhibit signs of bleeding.

The partial pressure of oxygen decreases as barometric pressure decreases at altitude. At 8,000 feet or greater above sea level, the environment becomes hypoxic and high-altitude syndromes can occur due to hypoxia. These include acute mountain sickness (AMS), high-altitude pulmonary edema, high-altitude cerebral edema, retinopathy, and certain neurologic syndromes. High-altitude cerebral edema (HACE) is the most severe form of acute mountain sickness. At altitude, cerebral vasodilation occurs and leads to increased blood flow and blood volume. This is due to a leaky blood-brain barrier either from lack of autonomic autoregulation or increased vascular permeability, or a combination of the two. HACE is characterized by progressive global cerebral dysfunction and causes confusion, altered mental status, and ataxia. Ataxia is a cardinal and early sign of HACE, and all patients with acute mountain sickness should be monitored for ataxia. Other features, such as headache, nausea, or vomiting, may be absent. Retinal hemorrhages are also common, and cranial nerve palsies of the third and sixth cranial nerves may occur due to increased intracranial pressure. Concomitant pulmonary edema is common. Death from HACE is due to brainstem herniation, so early identification and management are critical. The highest priority is descent. If this is not possible, temporizing measures (though often unavailable) include supplemental oxygen, corticosteroids, and use of a portable hyperbaric oxygen chamber. Computed tomography of the head may demonstrate white matter hyperattenuation more than gray matter with effacement of the sulci and flattening of the gyri.

This patient presents with signs and symptoms consistent with a left middle cerebral artery stroke as well as subcutaneous emphysema that developed during ascent from diving. Any focal neurologic deficit that results during ascent or immediately thereafter should be considered a cerebral arterial air embolism until proven otherwise. Rapid uncontrolled ascent against a closed glottis causes the volume of gas in the lungs to expand according to Boyle’s law (pressure and volume of a gas are inversely related at a constant temperature). As this gas expands, it can lead to pulmonary barotrauma, including pneumothorax, pneumomediastinum, (as indicated by this patient’s subcutaneous emphysema on exam), and alveolar rupture. Alveolar rupture leads to gas leakage into the pulmonary veins, which can then move into the systemic circulation and lodge in distal arterioles as arterial gas emboli. Cerebral gas embolism presents with typical stroke symptoms and is one of the most serious complications of pulmonary barotrauma. Air embolization can be prevented by exhaling during ascent, which prevents the rapid expansion of volume within the lungs as pressure decreases. Treatment includes fluid resuscitation and rapid recompression with 100% hyperbaric oxygen. Hyperbaric oxygen works by decreasing the size of the air embolism as well as easing washout of other gases by increasing the diffusion gradient for nitrogen from the air embolism to plasma.

Barotitis (B), or ear barotrauma, is the most common diving disorder and results from unequalized increasing pressure on the tympanic membrane on descent. Symptoms include unilateral ear pain and fullness, as well as vertigo and disorientation from rupture of the tympanic membrane and uneven caloric stimulation of the middle ear. Treatment is conservative. Decompression syndrome (C), or “the bends,” usually occurs within six hours after ascent. It results from the expansion of inert gas that dissolved in tissues during descent. As the pressure of these inert gases exceeds atmospheric pressure, it can exit tissue in the form of bubbles, which often lodge in veins, leading to localized venous obstruction and inflammatory cascades. Patients either present with significant pain (type I) or ascending paresthesias or paralysis (type II). Treatment is the same as for arterial gas embolization. Nitrogen narcosis (D) results from the increased partial pressure of nitrogen in CNS tissue and therefore occurs at significant depth. Symptoms are similar to alcohol intoxication and include altered coordination and impaired judgment.

The ECG demonstrates the presence of J waves or Osborn waves which are seen in hypothermia. One of the first cardiac effects of hypothermia is bradycardia secondary to decreased firing of the cardiac pacemaker cells in cold temperatures. Osborn waves may appear at any temperature below 32°C. The waves are an upward deflection at the terminal portion of the QRS complex. They may represent abnormal ion flux in cold temperatures along with delayed depolarization and early repolarization of the left ventricular wall. As temperatures continue to drop, the ECG will demonstrate prolonged intervals: PR, followed by QRS and then QTc.

Both diabetic ketoacidosis (A) and digoxin toxicity (B) may lead to hyperkalemia. In diabetic ketoacidosis, hyperkalemia develops as a result of the acidic pH in the blood and the transport of hydrogen ions intracellularly in exchange for a potassium ion. Digoxin toxicity poisons the cellular Na+/K+ ATPase resulting in elevated extracellular levels of potassium. The ECG manifestations of hyperkalemia begin with peaked T waves. Multiple other findings eventually develop including a shortened QT interval, ST depression, bundle branch blocks, widened QRS, prolonged PR interval, flattened T wave and ultimately a sine wave. Hyperparathyroidism (C) may lead to hypercalcemia. In hypercalcemia, the ECG shows a shortened QT interval, flattened T waves and QRS widening at very high levels.

Hepatic injury, as denoted by aspartate aminotransferase 2100 U/L, alanine aminotransferase 1900 U/L, is so extremely common in heat stroke that its absence should push one to reconsider the diagnosis. The hallmarks of heat stroke include severe hyperthermia (> 40.5oC) and neurologic dysfunction. Neurologic dysfunction occurs due to a progressive increase in heat stores because of the body’s decreasing ability to perfuse the distal extremities. As the heat stores increase, intracranial pressure increases with a subsequent decrease in cerebral blood flow. There are two types of heat stroke, each with their own patient population and clinical presentation. Classic heatstroke is due to exogenous heat production, while exertional heatstroke is due to endogenous heat production. Patients with classic heat stroke are commonly elderly with chronic diseases or those with limited access to shelter against the heat or oral hydration that present with symptoms usually in the setting of a prolonged, severe heat wave. Patients with exertional heat stroke are commonly young, athletes, or military personnel that present with symptoms after strenuous exercise in the heat. Classic heat stroke patients are usually anhidrotic, while those with exertional heat stroke tend to present diaphoretic. Diagnosis is primarily clinical, though laboratory testing should always be performed, as end-organ damage is common and can help further differentiate the types of heat stroke. Classic heat stroke tends to cause respiratory alkalosis, mild coagulopathies, mild creatinine kinase elevations, and elevated troponin. It is more common to see lactic acidosis, disseminated intravascular coagulation, rhabdomyolysis, and hypoglycemia in those with exertional heat stroke. With a mortality rate of 21–63%, treatment must be immediate and aggressive. Cooling is the mainstay of treatment with the primary goal to maximize evaporative cooling and prevent heat-generating shivering. Antipyretics are not useful in cooling, as they counteract hypothalamic-mediated hyperthermia and not environmental hyperthermia. Alongside cooling, immediate supportive treatment with intravenous fluids, supplemental oxygen, and reversal of coagulopathies should be started.

Acute kidney injury, as denoted by blood urea nitrogen 30 mg/dL, creatinine 1.5 mg/dL (B), and elevated troponin 0.8 ng/mL (D) can occur in classic heat stroke but are rare in exertional heat stroke. Rhabdomyolysis, as denoted by creatinine kinase 2500 U/L (C), is common in exertional heat stroke and less so in classic heat stroke. While each of these laboratory findings is possible in heat stroke, hepatic damage is still the most common finding.