Erwin Mulyawan, dr, SpAn, DPBA

Heat Related Illnesses

Case

• 32 year old bank employee reported feeling unwell to his colleagues and took a nap in the afternoon. Did not wake up. Had traveled extensively on his bike in the morning. No co-morbidities.

• On admission GCS 5/15, HR 150/min, BP 90/60, Temp 40 C, Skin dry. No rash, meningeal signs, localising signs.

• Diagnosed as heat stroke• Aggressive cooling measures, shifted to

ICU• Progressive severe vasodilatory shock –

maximum inotropes within 4 hours• Anuric-dialyzed• DIC and bleeding – product support• Progressive severe shock and lactic

acidosis-died on day 4

Nov 2006

“It does not take long either to boil an egg or to cook neurons.”

Hamilton D, Anaesthesia 32:271, 1976

• Common medical catastrophe during the summer

• Failure of thermoregulatory mechanism coupled with an exaggerated acute phase response

• Heat stroke demands urgent attention because– High mortality– Can cause permanent neurological damage

How common is it?

• Largely under diagnosed and under reported

• No reliable Indonesian data

• In India, we see about 30-40 patients per year, of which 12-15 come to the ICU – referral bias

Kishore P.Critical Care Conference 2006

Heat Loss

• Conduction

• Convection

• Radiation

• Evaporation

Acclimatization

Heat Injury Predisposition

3 Factors Influencing Heat Production

1. Increased Internal Heat Production.• Physical Activity• Febrile illness• Pharmacologic agents

2. Increased External Heat Gain• Exposure to high ambient temperature

3. Decreased Ability to Disperse Heat• Pharmacologic agents• Humidity

S S

Coolingevaporation

of sweat

Heat Balance

H

H

InternalHeat sources

muscle activity

H

ExternalHeat sources

hot weatherradiant heat sources

Heat Injury Predisposition

• Elderly

• Sick – in our

hospital wards

• Poor

• Infants

• Institutionalized

• Labourers

• Medications

• Athletes, Military

• Explorers

• Non-Acclimated

Spectrum of heat illnesses

Heat cramps Heat syncope Heat exhaustion Heat stroke

Heat cramps

• Cramps of most worked muscles

• After exertion

• Copious sweating during exertion

• Copious hypotonic fluid replacement during exertion

• Hyperventilation not present in cool environment

• Treat with NS or oral salt water

• Results from cumulative effect of peripheral vasodilatation, decreased vasomotor tone and relative volume depletion.

• Usually occurs in non acclimated pt’s in early stage of exposure.

• Dx includes excluding more serious causes of syncope

• Treatment includes rehydration, removal from heat, and rest

Heat Syncope

Heat exhaustion

• Vague malaise, fatigue, headache• Sensorium normal-poor judgment, vertigo• Core temperature < 40,6 °C• Tachycardia, dehydration• Rule out other disease states• If in doubt, treat as heat stroke• Treat - Rest, cool environment• Hydration-IV and oral

Heat stroke-clinical diagnosis

• Core temperature > 40.6 C

• Severe CNS dysfunction (coma, seizures, delirium)

• During periods of sustained high ambient temperatures

• Dry hot skin common but sweating may persist

Heat Stroke-types

• Classic

– “Summer Heat Waves”

– No sweat in 84-100% of patients

– More insidious onset

– Elderly, poor, debilitated patients

– Rhabdomyolysis and ARF rare

Heat Stroke-types

• Exertional

– 50% sweat

– Young, healthy, labourers, athletes, military

– Rhabdomyolysis and ARF common

– Usually have predisposing factor

Cellular level

• Denaturation of all proteins

• Membrane proteins become non functional

• This process leads to MOSF

• Endothelial damage - cytokine storm - sepsis like syndrome

• Gut mucosal barrier disruption – translocation of GNB – contributes to sepsis and MOSF

Heat stroke-organ dysfunctionCNS

• CNS– drowsiness, coma– delirium, Irritability, bizarre behavior, seizures,– Cerebral edema with raised intracranial pressure.

• Cerebellum– Highly sensitive to heat– Ataxia common

• Total breakdown of thermoregulation• Any neurological disturbance can occur with

heatstroke.

CVS

• Cardiogenic pulmonary edema– Myocardial hypofunction– Cooling related

• Endothelial dysfunction – profound capillary leak

Hepatic

• Liver injury

• SGOT, SGPT > 1000 IU/L

• Transaminases may not be elevated at presentation

• Jaundice

• Fulminant hepatic failure

Hematological

• Thrombocytopenia (aggregation)

• DIC – aPTT, PT prolonged, low fibrinogen (protein denaturation)

Pulmonary

• Type I respiratory failure– ARDS– Pulmonary edema

Musculoskeletal

• Rhabdomyolysis

Renal

• Acute renal failure– Volume depletion– Decreased cardiac output– Direct thermal tubular damage– Sepsis syndrome– Rhabdomyolysis

• Heatstroke has been reported to affect almost every organ in the body except for the pancreas.

Anyone with hyperpyrexia and altered mental state is considered heatstroke until

proven otherwise.

Differential diagnosis

• Acute CNS infection

• Cerebral malaria

• Severe sepsis

• Neuroleptic malignant syndrome

• Malignant hyperthermia

• Thyroid storm

Predictors of multi-organ dysfunction in heatstroke

G M Varghese, G John, K Thomas, O C Abraham, D Mathai

• 28 patients over 3 years

• Overall mortality 71%

• 85% in >2 organ failures

• Elevated CPK (>1000), liver enzymes > twice normal and metabolic acidosis were predictors of mortality

Emerg Med J 2005;22:185–187

Nov 2006

The golden hour of heat stroke

Am J Emerg Med. 1989 Nov;7(6):616-9

Nov 2006

Treatment-Cooling methods

• Evaporative• Immersion• Strategic ice packs• Ice cold IV fluids• Ice packing• Cooling blankets• Gastric lavage• Peritoneal lavage• Cardiac bypass• Endovascular cooling catheters

Ice immersion

• Most effective method• Large quantities of ice

should be readily available in a large tub

• Difficult to resuscitate• IV access difficult• Vasoconstriction may

limit heat exchange

Wet the body and clothes-spray

Evaporative

Precautions

• Wet sheets over a patient, without good air flow, will tend to increase temperature and should be avoided

• Slow down cooling once core temperature is less than 101°F

Cold IV fluids

• 15 ml/kg of ice cold IV fluids reduces temp by 1-2°C

• Patients need fluid resuscitation as they are usually dehydrated

• Cooling more effective in air conditioned environment

Dangers while cooling

• Pulmonary edema

• Overshoot hypothermia

Mil Med. 2003 Aug;168(8):671-3Resuscitation. 1991 Feb;21(1):33-9

Supportive treatment• Fluid resuscitation followed by inotrope

and vasopressor therapy

• Ventilation for ARDS

• Platelet, FFP and cryoprecipitate support as indicated

• Dialysis for ARF

• Manage like sepsis

Treatment of early complications

• Shivering– Chlorpromazine 25-50mgIV only if cooling is

not adequate because of shivering

• Convulsions– Diazepam, Phenobarbitone, Mannitol to

reduce edema

• Myoglobinuria– Mannitol and crystalloids

Late complications

• Nosocomial sepsis

• CIPN, GBS like picture

• Cerebellar degeneration

• Bickerstaff brainstem encephalitis

Ann Fr Anesth Reanim. 2006 Jul;25(7):780-3. Epub 2006 May 3J Neurol Neurosurg Psychiatry. 1999 Mar;66(3):408

Heat Stroke No-Nos

• Aspirin

• Paracetamol

• Alcohol baths

• Dantrolene

Take home

• Common and deadly

• Recognize early– Have a high index of suspicion, even in a

hospitalised patient

• Early aggressive cooling measures

• Rule out differentials

• Aggressive organ supportive therapy

© Copyright Texas Parks & Wildlife Department

“HEAT, HATEI hate to hate, but heat makes me hate. Therefore I hate heat, even though, I repeat, I hate to hate. “ Ramesh Gandhi