approved by the FDA in 2006 for use in cyanide poisoning Its mechanism of action is that the hydroxyl group of the vitamin binds to free cyanide, forming the nontoxic cyanocobalamin The dose is 70 mg/kg (max g) given over 15 minutes, with a repeat dose if necessary The minimal side effects of hydroxocobalamin make this an attractive alternative to the traditional nitrite therapy TABLE 90.3 Considerations for Hyperbaric Oxygen Therapy a Neurologic symptoms or signs (syncope, seizure, coma) either on presentation or that persist despite normobaric oxygen Signs of cardiac ischemia or metabolic acidosis Pregnancy a Consider early consultation with a poison control center or HBO facility Anemia (hemoglobin less than 10 g/100 mL) must also be corrected to maximize oxygen-carrying capacity If myoglobinemia or myoglobinuria is present, vigorous hydration and diuresis with furosemide (1 mg/kg intravenously) and/or mannitol (0.25 to g/kg intravenously) with close attention to urine output may preserve renal function If hydration and diuresis are ineffective, renal failure should be considered and fluids restricted accordingly (see Chapter 100 Renal and Electrolyte Emergencies ) Indications for Discharge or Admission Determination of disposition from the ED will depend on the history and clinical status Patients with significant respiratory distress or decreased neurologic status should be admitted to an ICU Patients who appear well on presentation to the ED but have a significant history (loss of consciousness at the scene) or elevated CO levels should be admitted for monitoring for other sequelae of smoke inhalation Severe disease course has been associated with low Glasgow Coma Scale score, high leukocyte count, and high troponin T levels at presentation ENVIRONMENTAL AND EXERTIONAL HEAT ILLNESS Goals of Treatment Treatment of heat stroke involves rapid reversal of hyperpyrexia, cardiovascular support, and correction of electrolyte imbalances CLINICAL PEARLS AND PITFALLS Heat cramps involving the abdominal musculature may mimic an acute abdomen Heat stroke is differentiated from heat exhaustion by the presence of hyperpyrexia and anhidrosis with circulatory failure and/or severe CNS dysfunction Active cooling may be achieved effectively using evaporation with fans after spraying with cool water Current Evidence In the United States alone, heat injury is responsible for approximately 650 preventable deaths every year Heat stroke remains the third most common cause (after head injury and cardiac disorders) of exercise-related mortality among U.S high school athletes, despite the fact that survival following acute heat stroke has improved over the last century from an estimated 20% to more than 90% Although athletes are at risk for heat illnesses, children and especially those with chronic conditions are generally more vulnerable because they produce more metabolic heat, their core temperature rises faster during dehydration, and their small organs are less efficient at heat dissipation Environmental and exertional heat illness occurs with excessive heat generation and storage These conditions arise when high ambient temperature prevents heat dissipation by radiation or convection, and humidity limits cooling by sweat evaporation The spectrum of illness is broad, including heat cramps, heat exhaustion, and heat stroke Heat stroke is an acute medical emergency with significant associated morbidity and mortality Children with increased risk include those with cystic fibrosis or congenital absence of sweat glands, children receiving medications that cause oligohidrosis, those with eating disorders, diabetes insipidus, obesity, or uncontrolled diabetes mellitus, infants left in automobiles on hot days, and young athletes Heat-sensitive centers of the posterior hypothalamus control sympathetic tone This tone regulates vasoconstriction of arterioles and subcutaneous arteriovenous anastomoses, which, in turn, controls heat conduction from the body core to the skin Flow through these areas may represent up to 30% of total cardiac output High flow provides efficient heat transfer from the body core to the skin, which is an effective radiator Low flow to the skin prevents radiation and allows only inefficient diffusion through the insulating skin and subcutaneous tissues When body temperature rises, blood in the preoptic area of the anterior hypothalamus is warmer than optimal Impulses from this area increase and are conducted through autonomic pathways to the spinal cord and then, through cholinergic fibers to the sweat glands, where sweat is released Exercise and certain emotional states release circulating epinephrine and norepinephrine to increase sweat production A 0.6°C increase in core temperature causes a 10% elevation in basal metabolic rate There are four different ways for the body to reduce excess heat: convection, conduction, radiation, and evaporation, with the latter being the most important thermoregulatory mechanism Clinical Recognition Three types of heat illnesses are recognized and represent different physiologic disturbances ( Table 90.4 ) Heat cramps refer to the sudden onset of brief, intermittent, and excruciating cramps in muscles after they have been subjected to severe work stress Cramps tend to occur after the work is done, on relaxing, or on taking a cool shower Occasionally, abdominal muscle cramps may simulate an acute abdomen The usual victim is highly conditioned and acclimatized Typically, these individuals can produce sweat in large quantities and provide themselves with adequate fluid replacement but inadequate salt replacement Electrolyte depletion is probably the cause of heat cramps Most spasms last less than a minute, but some persist for several minutes, during which a rock-hard mass may be palpated in the affected muscle Cramps often occur in clusters Rapid voluntary contraction of a muscle, contact with cold air or water, or passive extension of a flexed limb may reproduce a cramp Laboratory investigation reveals hyponatremia and hypochloremia and virtually absent urine sodium The blood urea nitrogen (BUN) level is usually normal but may be mildly elevated Heat exhaustion is less clearly demarcated from heat stroke than are heat cramps There are two types of heat exhaustion with significant overlap: water depleted and sodium depleted In most cases, water depletion predominates because individuals who live and work in a hot environment not always voluntarily replace their total water deficit Progressive lethargy, intense thirst, and inability to work or play progress to headache, vomiting, CNS dysfunction (including hyperventilation, paresthesias, agitation, incoordination, or actual psychosis), hypotension, and tachycardia Hemoconcentration, hypernatremia, hyperchloremia, and urinary concentration are typical Body temperature may rise but rarely to higher than 39°C (102.2°F) If unattended, heat exhaustion may progress to frank heat stroke Heat exhaustion may also occur because of predominant salt depletion As in heat cramps, water losses are replaced but without adequate electrolyte supplementation Symptoms include profound weakness and fatigue, frontal headache, anorexia, nausea, vomiting, diarrhea, and severe muscle cramps Tachycardia and orthostatic hypotension may be noted Hyponatremia, hemoconcentration, and significantly diminished urine sodium are consistent findings Children with cystic fibrosis, particularly those who are young and unable to meet increased salt requirements, are at risk for electrolyte depletion because salt losses in their sweat apparently not respond to acclimatization and aldosterone stimulation of the sweat gland Heat stroke is a life-threatening emergency Classic signs are hyperpyrexia (41°C [105.8°F] or higher); hot, dry skin that is pink or ashen (anhidrosis) depending on the circulatory state; and severe CNS dysfunction Often sweating ceases before the onset of heat stroke The onset of the CNS disturbance may be abrupt, with sudden loss of consciousness Often, however, premonitory signs and symptoms exist These include a sense of impending doom, headache, dizziness, weakness, confusion, euphoria, gait disturbance, and combativeness Posturing, incontinence, seizures, hemiparesis, and pupillary changes may occur Any level of coma may be noted Cerebrospinal fluid findings are usually normal The extent of damage to the CNS is related to the time and extent of hyperpyrexia and to the adequacy of circulation In severe cases, coma may persist even after the body temperature is lowered Patients able to maintain cardiac output adequate to meet the enormously elevated circulatory demand are most likely to survive Initially, the pulse is rapid and full, with an increased pulse pressure Total peripheral vascular resistance falls as a result of vasodilation in the skin and muscle beds, and splanchnic flow diminishes If hyperpyrexia is not corrected, ashen cyanosis and a thin, rapid pulse herald a falling cardiac output The cause may be either direct thermal damage to the myocardium or significant pulmonary hypertension with secondary right ventricular failure Even after body temperature is returned to normal, cardiac output remains elevated and peripheral vascular resistance remains low for several hours, resembling the compensatory hyperemia after ischemia noted in post-trauma, post-shock, and post-septic states Persistently circulating vasoactive substances probably account for this phenomenon ... broad, including heat cramps, heat exhaustion, and heat stroke Heat stroke is an acute medical emergency with significant associated morbidity and mortality Children with increased risk include... acclimatization and aldosterone stimulation of the sweat gland Heat stroke is a life-threatening emergency Classic signs are hyperpyrexia (41°C [105.8°F] or higher); hot, dry skin that is pink