Heat Related Illnesses: Strengthening Health System Preparedness DR VIVEK NIDHI, JR3 UNDER GUIDANCE OF: DR SUDHIR MEHTA SIR DEPARTMENT OF MEDICINE
World Meteorological Organization (WMO) defines heat wave as: Five or more consecutive days during which the daily maximum temperature exceeds the average max temperature by 5º C.
POINTS OF DISCUSSION Pathophysiology of thermoregulation Predisposing factors of heat related illnesses(HRI) Spectrum of syndromes Clinical Features Strategies for management Take Home Message
PHYSIOLOGY OF THERMOREGULATION The body dissipates heat into the environment via four mechanisms 1. Evaporation of skin moisture: Single most efficient mechanism of heat loss Becomes progressively ineffective as the relative humidity rises to >70%. 2. Radiation of heat directly into the surrounding environment: continuous, major source of heat gain in hot climates conversely. 3. Conduction — direct transfer of heat to a cooler object 4. Convection — loss of heat to air currents—become ineffective when the environmental temperature exceeds the skin temperature.
PHYSIOLOGY OF THERMOREGULATION
SPECTRUM OF SYNDROMES
MINOR HEAT EMERGENCY SYNDROMES
HEAT CRAMPS Intermittent, painful, and involuntary spasmodic contractions of skeletal muscles Unacclimated individual->humid, hot environment->during rest after vigorous exertion RISK FACTORS : Profession - Roofers, firefighters, military personnel, athletes, steel workers, and field workers . Insufficient sodium intake before intense activity in the heat and lack of heat acclimatization , replacing fluid losses with copious water or other hypotonic fluids .
HEAT CRAMPS PATHOPHYSIOLOGY
HEAT CRAMPS TREATMENT: without significant dehydration:- commercially available electrolyte solutions two 650-mg salt tablets dissolved in 1 Litre of water produce a 0.1% saline solution. Rhabdomyolysis is very rare with routine exercise-associated muscle cramps.
HEAT EXHAUSTION PATHOPHYSIOLOGY : Characterized by the inability to maintain adequate cardiac output due to strenuous physical exercise and environmental heat stress water-depletion heat exhaustion Laborers, athletes, and elderly individuals exerting themselves in hot environments, without adequate fluid intake salt-depletion heat exhaustion Slowly in unacclimated persons who have been consuming large quantities of hypotonic solutions.
Clinical criteria for heat exhaustion : ●Obvious difficulty continuing with exercise. ●Core body temperature is usually 101 to 104ºF (38.3 to 40.0ºC) at the time of collapse. ●No significant dysfunction of the central nervous system ( eg , seizure, altered consciousness, persistent delirium) is present. This is the key difference from exertional heat stroke.
HEAT EXHAUSTION LABORATORY REPORTS: Mixed sodium and water depletion. Sodium depletion heat exhaustion- hyponatremia and hypochloremia . Hepatic aminotransferases are mildly elevated. Urinary sodium and chloride concentrations are usually low.
MANAGEMENT: Aggressive cooling of patients till core temperature is 39°C (102.2°F). Except in mild cases , free water deficits should be replaced slowly over 24–48 h to avoid a decrease of serum osmolality by >2 mEq /h. Older patients with comorbidities (including cardiovascular disease)-> inpatient fluid and electrolyte replacement, monitoring, and reassessment
HEAT STROKE Heat stroke is a multisystem illness characterized by central nervous system (CNS) dysfunction (encephalopathy ) and additional organ and tissue damage ( eg , acute kidney injury, liver injury, rhabdomyolysis) in association with high body temperatures. total loss of thermoregulatory function DIAGNOSTIC TRIAD
HEAT STROKE The premonitory symptoms include weakness, dizziness, disorientation, ataxia, and gastrointestinal or psychiatric symptoms resembling heat exhaustion . The sudden onset of heatstroke occurs when the maintenance of adequate perfusion requires peripheral vasoconstriction to stabilize the mean arterial blood pressure. Cutaneous radiation of heat ceases and core temperature rises dramatically causing SIRS Typical vital-sign abnormalities include tachypnea, various tachycardias, hypotension, and a widened pulse pressure The definitive diagnosis should be reserved until the other potential causes of hyperthermia are excluded. If the patient’s mental status does not improve with cooling, toxicologic screening may be indicated, and cranial CT and spinal fluid analysis can be considered
HEAT STROKE
HEAT STROKE CLASSIC HEAT STROKE: old patient During summer heat waves Patients are HOT and DRY LABORATORY FINDINGS: Significant leucocytosis , Hypernatremia AST,ALT>100x Renal failure DIC(thrombocytopenia, hypofibrinogenemia, prolonged prothrombin time)
HEAT STROKE EXERTIONAL HEAT STROKE: young athelete , labour , military personnel Patients are PROFUSELY DIAPHORETIC LABORATORY FINDINGS: Significant leucocytosis Rhabdomyolysis-> hyperphosphatemia,hypocalcemia , hyponatremia, hypoglycemia, renal failure(pigment nephropathy), DIC(thrombocytopenia, hypofibrinogenemia, prolonged prothrombin time) Elevated CPK NAC, LDH. Urine shows hematuria, myoglobinuria, red cell casts.
HEAT STROKE CARDIOVASCULAR CONSIDERATIONS 1. Thermal Cardiomyopathy may cause CVP elevation despite significant dehydration. 2.Deceptive non cardiogenic pulmonary edema despite significant hypovolemia 3. ECG shows tachyarrythmias and ST-T changes, anti- arrythmics /electric cardioversion ONLY after rapid cooling. 4. Noradrenaline (alpha-agonist activity) can impede cooling, dopamine or dobutamine advised if low cardiac output
COOLING STRATEGIES Before cooling is initiated, endotracheal intubation, continuous core temperature monitoring to be done. Rectal temperature(C)=(0.94*axillary temperature(C))+2.92
MOHFW SOP for management of HRI
TARP ASSISTED COOLING WITH OSCILLATION
COOLING STRATEGIES Commercially available cooling blankets should not be the sole technique used, rate of cooling is far too slow. Less efficacious and rarely indicated:1. IV infusion of cold fluids 2. cold irrigation of the bladder or gastrointestinal tract. Efficient maneuvers but invasive and rarely necessary: Cold thoracic and peritoneal lavage.
RESUSCITATION 1. RESPIRATORY : a] Endotracheal intubation necessary due to aspiration, b]depolarizing agents to be avoided c] pneumonitis. Pulmonary infarction, hemorrhage, edema, ARDS to be managed. 2. CARDIOVASCULAR : CHS: modest fluid requirement EHS: zealous isotonic saline resuscitation 3. NEUROLOGICAL : Significant shivering, discomfort, or extreme agitation is preferably mitigated with short-acting benzodiazepines , which are ideal due to their renal clearance. Barbiturates are avoided.
4 .HEMATOLOGICAL : occur after first day, replacement therapy with platelets and FFP. Tranexamic acid to be avoided as it may cause rhabdomyolysis . 5. ANTIPYRETICS: NO THERAPEUTIC ROLE . Aspirin: uncouples oxidative phosphorylation , exacerbates coagulopathies Paracetamol stresses hepatic function .
TAKE HOME MESSAGES 1. Understanding of thermoregulation is necessary for categorizing patients to different heat related syndromes and manage accordingly. 2. Identification of predisposing factors can help us to take precautions and modify prescription drugs during a heat wave. 3. Oral isotonic fluid intake can worsen heat related illness, electrolyte solutions are advised. 4. Heat exhaustion does not cause CNS symptoms, older patients are advised admission and monitoring.
TAKE HOME MESSAGES 5. Classic heat stroke patients are typically old, hot and dry on presentation, require evaporative cooling, have mild coagulopathy. 6.Exertional heat stroke patients are young atheletes or doing other exertional activity, are profusely diaphoretic, require immersive cooling(TACO), have rhabdomyolysis and severe dyselectrolytemia and coagulopathy. 7.Drugs to be avoided in management of heat stroke include noradrenaline, anti pyretics , tranexamic acid. 8. Fluid administration to be given according to clinical judgement and varies from patient to patient.