Heat stroke is a life-threatening condition defined as a core body temperature above 41°C with neurological dysfunction. It can be exertional, caused by strenuous physical activity in heat, or nonexertional, often affecting the elderly, chronically ill, or very young. Risk factors include impaired thermoregulation, dehydration, and medications that interfere with sweating. Complications involve multiple organ systems and can include delirium, seizures, hypotension, liver and kidney damage, and disseminated intravascular coagulation. Immediate cooling and medical care are crucial to prevent high mortality rates from heat stroke.

1. NEUROLOGICAL COMPLICATIONS OF HEAT STROKEDR.ANJANEYULU SRIRAMA

2. DEFINITION Elevation of the body temperature beyond 104 0 F . Most severe form of the heat-related illnesses Defined as a body temperature higher than 41.1°C (106°F) associated with neurologic dysfunction.

4. FORMS Exertional heatstroke (EHS) - young,strenuous physical activity, for a prolonged period of time, in a hot environment. Classic nonexertional heatstroke (NEHS) -sedentary elderly individuals, chronically ill, and very young persons. Both associated with a high morbidity and mortality, if therapy is delayed.

5. Pathophysiology Maintainence of constant body temperature by balancing heat gain with heat loss. Excessive heat denatures proteins, destabilizes phospholipids and lipoproteins, and liquefies membrane lipids leading to cardiovascular collapse, multi organ failure, and, ultimately, death.

6. HEAT GENERATION,INTERNAL At rest, basal metabolic processes produce a 100 kcal of heat per hr . Strenuous physical activity can increase heat production more than 10-fold(>1000 kcal/h) Fever, shivering, tremors, convulsions, thyrotoxicosis,sepsis, sympathomimetic drugs increase heat production.

7. HEAT GENERATION ,EXTERNAL Acquire heat from the environment through mechanisms involved in heat dissipation, including conduction, convection, and radiation. They occur at the level of the skin and require a properly functioning skin surface, sweat glands, and ANS , but may be manipulated by behavioral responses.

8. HEAT TRANSFER Conduction -transfer of heat between 2 surfaces with differing temp that are in direct contact. Convection - between the body's surface and a gas or fluid with a differing temperature. Evaporation, which refers to the conversion of a liquid to a gaseous phase Radiation - in the form of electromagnetic waves between the body and its surroundings. The efficacy of radiation depends on the angle of the sun, season, and the presence of clouds. During summer, lying down in the sun can result in a heat gain of up to 150 kcal/h.

9. HEAT LOSS/DESSIPATION Physiologic responses to heat Increase in the blood flow to the skin, major heat-dissipating organ. Dilatation of the peripheral venous system. Stimulation of the eccrine sweat glands to produce more sweat.

10. RISK GROUP When heat gain exceeds heat loss, the body temperature rises. AT RISK INDIVIDUALS who lack the capacity to modulate the environment (eg, infants). Elderly persons and patients with diminished cardiovascular reserves . Patients with skin diseases and those taking medications that interfere with sweating .

11. Frequency USA-CDC- 8,015 deaths were attributed to excessive heat exposure from 1979-2003, 334 deaths/yr. 3,442 deaths from exposure to extreme heat in US 1999–2003. 1998, worst heat waves to strike India in 50 years resulted in > 2600 deaths in 10 wks. Unofficial reports described the number of deaths as almost double .

12. INDIAN SCENAREO

13. Indian statastics

14. PRESENT SCENAREO INDIA,AP

15. Mortality/Morbidity Duration of the temperature elevation. Delayed theraphy- mortality rate may be as high as 80%; Early diagnosis and immediate cooling -10%. Highest among the elderly population, pts with preexisting disease, those confined to a bed, and those who are socially isolated.

16. causes Increased heat production Increased metabolism Infections Sepsis Encephalitis Stimulant drugs Thyroid storm Increased muscular activity Exercise((doubles ) Convulsions Tetanus Strychnine poisoning Sympathomimetics Thyroid storm Strenuous exercise and status epilepticus can increase heat production 10-fold . Stimulant drugs, including cocaine and amphetamines, can generate excessive amounts of heat by increasing metabolism and motor activity through the stimulatory effects of dopamine. Neuroleptic agents also may elevate body temperature by increasing muscle activity, but, occasionally, these agents may cause neuroleptic malignant syndrome(NMS. Idiosyncratic reaction characterized by hyperthermia, altered mental status, muscle rigidity, and autonomic instability and appears to be due to excessive contraction of muscles. Inhaled volatile anesthetics and succinylcholine, may result in malignant hyperthermia. MH- decreased ability of the sarcoplasmic reticulum to retain calcium, resulting in sustained muscle contraction.

17. Decreased heat loss Reduced sweating Dermatologic diseases Drugs Burns Reduced CNS responses Advanced age Toddlers and infants Alcohol Barbiturates Other sedatives Reduced cardiovascular reserve Elderly persons Beta-blockers Calcium channel blockers Diuretics Drugs Anticholinergics Neuroleptics Antihistamines Exogenous factors High ambient temperatures High ambient humidity Reduced ability to acclimatize Children and toddlers Elderly persons Reduced behavioral responsiveness: Infants, patients who are bedridden, and patients who are chronically ill are at risk for heatstroke –cannot control their environment and water intake.

18. Clinical features T> 41°C , anhidrosis associated with an altered sensorium. Classic heatstroke- during environmental heat waves-very young persons ,elderly population, individuals who are chronically ill-failure of the body's heat dissipating mechanisms. EHS –young-healthy individuals who engage in strenuous physical activity-increased heat production.

19. Exertional heatstroke Hyperthermia, diaphoresis, and an altered sensorium, manifest suddenly during extreme physical exertion in a hot environment. Abdominal and muscular cramping, nausea, vomiting, diarrhea, headache, dizziness, dyspnea, weakness commonly precede the heatstroke . Syncope and LOC observed commonly before the development of EHS. Occurs in young, healthy individuals (eg, athletes, firefighters, military personnel) who, while engaging in strenuous physical activity, overwhelm their thermoregulatory system and become hyperthermic. As their ability to sweat remains intact,EHS pts are able to cool down after cessation of physical activity and may present with T<41°C. Risk factors that increase the likelihood of heat-related illnesses include a preceding viral infection, dehydration, fatigue, obesity, lack of sleep, poor physical fitness, and lack of acclimatization. May occur because of increased motor activity due to drug use, such as cocaine and amphetamines, and as a complication of status epilepticus.

20. Nonexertional heatstroke Hyperthermia, anhidrosis, and an altered sensorium, which develop suddenly after a period of prolonged elevations in ambient temperatures (ie, heat waves). Core body temperatures greater than 41°C are diagnostic. CNS symptoms, ranging from minor irritability to delusions, irrational behavior, hallucinations, and coma . Anhidrosis due to cessation of sweating is a late occurrence. Other CNS symptoms - seizures, cranial nerve abnormalities, cerebellar dysfunction, and opisthotonos. Initially may exhibit a hyperdynamic circulatory state, but, in severe cases, hypodynamic states may be noted. Affects people who are unable to control their environment and water intake (eg, infants, elderly persons, individuals who are chronically ill),. people with reduced cardiovascular reserve (eg, elderly persons, patients with chronic cardiovascular illnesses). people with impaired sweating (eg, patients with skin disease, patients ingesting anticholinergic and psychiatric drugs). Infants - immature thermoregulatory system,. Elderly persons -impaired perception of changes in body and ambient temperatures and a decreased capacity to sweat.

22. Heat Stroke Col SR Mehta VSM*, Lt Col DS Jaswal+ MJAFI 2003; 59 : 140-143

23. Physical features Vital signs Temp->41°C( presence of sweating, evaporating mechanisms, and the initiation of cooling methods<41°C ). Pulse: Tachycardia to rates exceeding 130 . BP: normotensive, with a wide pulse pressure; ( hypotension due to vasodilation of the cutaneous vessels, pooling of the blood in the venous system,dehydration, myocardial damage and may signal cardiovascular collapse.)

24. Central nervous system Universal in persons with heatstroke. Range from irritability to coma. Pts may present with delirium, confusion, delusions, convulsions, hallucinations, ataxia, tremors, dysarthria, and other cerebellar findings, as well as cranial nerve abnormalities and tonic and dystonic contractions of the muscles. Pts also may exhibit decerebrate posturing, decorticate posturing, or they may be limp. Coma (electrolyte abnormalities, hypoglycemia, hepatic encephalopathy, uremic encephalopathy, and acute structural abnormalities, such as intracerebral hemorrhage due to trauma or coagulation disorders). Cerebral edema and herniation also may occur during the course of heatstroke.

25. Eyes Examination of the eyes may reveal nystagmus and oculogyric episodes due to cerebellar injury. The pupils may be fixed, dilated, pinpoint, or normal.

26. Cardiovascular Heat stress places a tremendous burden on the heart. Pts with preexisting myocardial dysfunction do not tolerate heat stress for prolonged periods. Pts commonly exhibit a hyperdynamic state, with tachycardia, low systemic vascular resistance, and a high cardiac index. A hypodynamic state, with a high systemic vascular resistance and a low cardiac index, may occur in patients with preexisting cardiovascular disease and low intravascular volume. A hypodynamic state also may signal cardiovascular collapse. High-output cardiac failure and low-output cardiac failure may occur.

27. Pulmonary Pts with heatstroke commonly exhibit tachypnea and hyperventilation caused by direct CNS stimulation, acidosis, or hypoxia. Hypoxia and cyanosis - atelectasis, pulmonary infarction, aspiration pneumonia, and pulmonary edema.

28. Hepatic Jaundice and elevated liver enzymes. Rarely, fulminant hepatic failure occurs, accompanied by encephalopathy, hypoglycemia, and disseminated intravascular coagulation (DIC) and bleeding.

29. RENAL Musculoskeletal Muscle tenderness and cramping ,rhabdomyolysis. The patient's muscles may be rigid or limp. Renal ARF - hypovolemia, low cardiac output, and myoglobinuria (due to rhabdomyolysis). Pts may exhibit oliguria and a change in the color of urine.

30. Differential Diagnoses Delirium Meningitis Delirium Tremens Neuroleptic Malignant Syndrome Diabetic Ketoacidosis Tetanus Encephalopathy, Hepatic&Uremic Toxicity, Phencyclidine Hyperthyroidism Toxicity, Salicylate

31. Work up Complete blood cell count Arterial blood gas analysis: res. alkalosis - direct CNS stimulation ; metabolic acidosis - lactic acidosis Glucose: Hypoglycemia electrolytes;Na,K,PO4,Ca,Mg. Hepatic function tests Muscle function tests Renal function tests CSF- nonspecific pleocytosis, and protein levels may be elevated as high as 150 mg/dL.

32. Imaging findings in heat stroke Early cerebral edema . loss of gray-white matter differentiation . Patchy high signal intensity of the white matter of cerebral hemispheres and corpus striatum . Central pontinemyelinolysis. Vascular boundary zone infarcts . later stages- diffuse cerebellar atrophy.

33. MR imaging in heat stroke;Carol T. McLaughlin etal; AJNR Am J Neuroradiol 24:1372–1375, August 2003

34. MR imaging in heat stroke;Carol T. McLaughlin etal; AJNR Am J Neuroradiol 24:1372–1375, August 2003

35. MR imaging in heat stroke;Carol T. McLaughlin etal; AJNR Am J Neuroradiol 24:1372–1375, August 2003

36. Treatment Rapid reduction of the core body temperature . Admission to the hospital for at least 48 hours . lowering the core temp to about 39°C , at least 0.2°C/min . Removal of restrictive clothing and spraying water on the body. Covering the patient with ice water–soaked sheets. Placing ice packs in the axillae and groin . Supplemental oxygen. Infusion of D50W should be considered in all patients

37. Optimal method of rapidly cooling Ice-water immersion -extremely effective method , increased thermal conductivity of ice water can reduce core body temp <39°C in 20-40 mts. Extremely uncomfortable , subcutaneous vasoconstriction, increases shivering, difficulty monitoring and resuscitating . Evaporative techniques –recent and equally effective without the practical difficulties. Intermittently spraying with warm water while a powerful fan blows across the body. Peritoneal, thoracic, rectal, and gastric lavage with ice water; cold intravenous fluids; cold humidified oxygen; cooling blankets; and wet towels.

38. TR……. Antipyretics-no role. Stop excessive production of heat -Agitation and shivering with benzodiazepines, Neuroleptics best avoided . Convulsions -Benzodiazepines and, if necessary, barbiturates ;refractory sz-paralysis and ventilation IV fluids-hypovolemia, preexisting medical conditions, and preexisting cardiovascular disease. Metabolic support and symptomatic treatment for ARF,hepatic failure and PE. Rhabdomyolysis -infusion of large amounts of intravenous fluids (fluid requirements may be as high as 10 L), alkalinization of the urine, and infusion of mannitol. Mannitol may improve renal blood flow and glomerular filtration rate, increase urine output, and prevent fluid accumulation in the interstitial compartment (through its osmotic action). Mannitol also is a free radical scavenger and, therefore, may reduce damage caused by free radicals.

40. CEREBELLAR ATROPHY The physiology of neurological involvement in heat stroke Increased intracranial pressure combined with autonomic dysfunction that leads to cerebral hypoperfusion and ischaemia . Tendency towards intracranial haemorrhage because of abnormal coagulation. The cerebellum is most susceptible to hyperthermia, followed by cerebral cortex, brainstem, and spinal cord. The cerebellar findings may be a combination of these factors coupled with or solely due to the directly destructive effects of hyperthermia on the Purkinje cells. Post-Heat Stroke CerebellarAtrophy,USudhiretal, JIACM 2009; 10: 60-2 Cerebellar syndrome following neuroleptic induced heat stroke ;DAVID LEFKOWITZetal, JNNP;1983;46:183-185