Thats Hot Dr Kelly Kasteel Case Studyhyperthermia Hyperthermia

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That’s Hot! Dr. Kelly Kasteel Case Studyhyperthermia

That’s Hot! Dr. Kelly Kasteel Case Studyhyperthermia

Hyperthermia: Epidemiology l l 4, 000 heat related deaths yearly (US) 80% of the

Hyperthermia: Epidemiology l l 4, 000 heat related deaths yearly (US) 80% of the fatalities are elderly – l l Occurs in 5 per million over age 85 compared to 1 per million in the 5 -44 age group 2 nd leading cause of death among young athletes Very young (<4 yo) also at increased risk – Occurs in 0. 3 per million compared to 0. 05 per million in patients > 4 yo.

Case Study-History l l l l 36 y. o female Admitted-SPH 11/07/2007 (73 previous

Case Study-History l l l l 36 y. o female Admitted-SPH 11/07/2007 (73 previous visits) Vancouver is experiencing a rare heat wave where outside temperatures have ranged between 37 -39 degrees Brought in via EHS agitated, spitting, naked and running into traffic at the scene. Hx of ? 45 second seizure en route to the hospital which is not clearly documented. Remote history of foul stools over the previous week before admission Without complaint at arrival, but…had precipitous decrease in LOC and was intubated for airway protection

Case Study-History l PMHx 1. Hepatitis C. 2. BAD l Meds – l Allergies

Case Study-History l PMHx 1. Hepatitis C. 2. BAD l Meds – l Allergies – l None. Previously (1/12) on Risperidone-2 mg qhs via pharmanet None SHx – – – Prostitution – multiple STD’s in past Polysubstance abuse (cocaine/heroine IVDU). Last used this am

Case Study-On Examination l l HR-144 reg/ RR-22/ Temp-41 C/ BP-90/40/ Pressure support 15,

Case Study-On Examination l l HR-144 reg/ RR-22/ Temp-41 C/ BP-90/40/ Pressure support 15, PEEP of 5, Fi. O 2 of 0. 5, CPP was 11, mixed venous 81% and a MAP of 75 with no pressor support. Spent 8 hrs in ED before transfer to ICU

Case Study-On Examination l l l l CVS-s 1 s 2 no murmur no

Case Study-On Examination l l l l CVS-s 1 s 2 no murmur no s 3 s 4 Resp- eae no wheeze no crackles Abdo-soft non-tender GU – ++discharge, no FB Neuro- Initially the ED, the pt was confused and combative with a GCS E 3 M 5 V 2 = 10. Moving all 4. Pupils 3 reactive. MSK- Injection marks over antecubital space Derm- Warm and Dry

Case Study- Labs l l l l l Glucose-6. 8 Sodium-142 Potassium-5. 4 Chloride

Case Study- Labs l l l l l Glucose-6. 8 Sodium-142 Potassium-5. 4 Chloride 104 Bicarb 11 Urea 6. 3 Creatinine 147 Total Bili 8 Osmolality 319 Anion Gap-27 CK -405 Troponin 0. 19 Amylase-1018 TSH -0. 52 B-HCG- weakly positive Ethalene glycol/methanol- cancelled Tox serum screen (asa- weakly positive 0. 2, acetaminophen, etoh)-negative

Case Study- Labs l Infectious workup – – – l l l l l

Case Study- Labs l Infectious workup – – – l l l l l Genital C/S- Normal flora Stool C/S – Negative Sputum-Negative Urine –Negative Blood C/S- 1 bottle gram positive cocci in clusters-coag negative staphlococcus Hypoglycemia- Glucose-0. 7 (24 hrs after admission) Hyponatremia-Sodium-128 ARF-Creatinine-600 APTT-189 INR >9 (july 12) Fibrinogen-1. 0 D- dimmer >4000 Hepatitis-AST 1000, ALT 5573, GGT 66, BR 666(total)) Blood smear-schistocytes, burr cells

Case Study-Imaging CT head- July 24 th There is severe compression of structures in

Case Study-Imaging CT head- July 24 th There is severe compression of structures in the fourth ventricle. Fluid around the brainstem has been effaced and the fourth ventricle is compressed. The patient is at risk for developing transtentorial or tonsillar herniation. Severe cerebral edema. l CXR: small lung volumes, no obvious airspace disease

Case study- Course in Hospital l l l Treated presumptively as sepsis nyd- piptazo,

Case study- Course in Hospital l l l Treated presumptively as sepsis nyd- piptazo, flagyl Negative workups – no identifiable septic or obstetrical causes for DIC. July 23 -24 - Patient briefly extubated before reintubation and markedly decreased LOC. Brain Death Comfort care initiated July 24 th, patient deceased within the hour. Autopsy- Non-contributory to date-MOS

Now That’s HOT l What is your differential diagnosis for this pt? l What

Now That’s HOT l What is your differential diagnosis for this pt? l What are the potential complications that can occur in heat stroke? l What investigations should you order? l What otherapies should be considered?

Basic principles of Heat l 4 mechanisms that allow the body to maintain a

Basic principles of Heat l 4 mechanisms that allow the body to maintain a constant core temperature – – Radiation Convection Conduction Evaporation

Fever vs. Hyperthermia l Fever – l Elevation of body temp due to the

Fever vs. Hyperthermia l Fever – l Elevation of body temp due to the “resetting” of the hypothalamic set point in response to endogenous or exogenous pyrogens Hyperthermia – Elevation of body temp above the hypothalamic set point due to the failure of the body’s heat dispersing mechanisms

Diff Dx - Hi temp with altered mental state

Diff Dx - Hi temp with altered mental state

Heat Stroke l l Total breakdown of body’s thermoregulatory system Leads to multiorgan damage

Heat Stroke l l Total breakdown of body’s thermoregulatory system Leads to multiorgan damage if left untreated A true medical emergency 2 forms described – – Exertional Non-exertional/Classical

Exertional Heat Stroke l l Occurs in young, healthy individuals engaged in heavy exercise

Exertional Heat Stroke l l Occurs in young, healthy individuals engaged in heavy exercise during periods of high ambient temperature and humidity One series of 58 patients with heat stroke found an acute mortality rate of 21 percent (Ann Intern Med 1998 Aug 1; 129(3): 173 -81)

Non-exertional heat stroke l l Affects individuals with underlying chronic medical conditions that either

Non-exertional heat stroke l l Affects individuals with underlying chronic medical conditions that either impair thermoregulation or prevent removal from a hot environment. Conditions include: – – – Cardiovascular disease Neurologic or psychiatric disorders Obesity Anhidrosis Extremes of age Anticholinergic agents or diuretics

Diff Dx - Hi temp with altered mental state l INFECTIOUS – l DRUG/TOXIN

Diff Dx - Hi temp with altered mental state l INFECTIOUS – l DRUG/TOXIN INDUCED – – – l Overdose – anticholinergic, sympathomimetic Withdrawal – benzodiazepene, alcohol – delirium tremens Neuroleptic malignant syndrome malignant hyperthermia Serotonin syndrome ENDOCRINE – l Sepsis, Meningitis/Encephalitis, Falciparum malaria Thyroid storm, Pheochromocytoma CNS – Hypothalamic hemorrhage, status epilepticus esp nonconvulsive

Neuroleptic Malignant Syndrome Impaired thermoregulation in hypothalamus due to relative lack of dopamine l

Neuroleptic Malignant Syndrome Impaired thermoregulation in hypothalamus due to relative lack of dopamine l Caused by antipsychotic meds/neuroleptics l Distinguishing features – hyperthermia, – altered mental status – "lead pipe" muscle rigidity, choreoathetosis, tremors – autonomic dysfunction- diaphoresis, labile blood pressure, and dysrhythmias – Hx of psychotic disorder/neuroleptic medication use Treatment – Cooling, hydration, benzodiazepines – Bromocriptine, amantadine, dantrolene l

Malignant Hyperthermia l l l Rare (autosomal dominant) Genetic instability of sarcoplasmic reticulum causing

Malignant Hyperthermia l l l Rare (autosomal dominant) Genetic instability of sarcoplasmic reticulum causing massive calcium release Onset: 1 to 10 hours after exposure Triggered by inhalational anaesthetic or succinylcholine Distinguishing features – – l History of succinylcholine use Muscular rigidity Treatment – – Cooling, hydration Dantrolene

Serotonin syndrome l l l Excess serotonin and dopamine levels in CNS Triggered by

Serotonin syndrome l l l Excess serotonin and dopamine levels in CNS Triggered by any med that increases serotonin levels (eg. SSRI’s, demerol, dextromethorphan, lithium etc. ) Distinguishing features – – l Appropriate medication history Muscular rigidity Treatment – – Cooling, Hydration Cyproheptadine

Thyroid storm l l Hypermetabolic state from extreme thyrotoxicosis Distinguishing features – – –

Thyroid storm l l Hypermetabolic state from extreme thyrotoxicosis Distinguishing features – – – l History of thyroid disease Goiter Ophtho clues lid retraction/lag, exophthalmos, EOM palsy Treatment – – Cooling, Hydration PTU, iodide solution, propranolol etc.

Overdose l l Anticholinergics, sympathomimetics Distinguishing features – – l Hx of ingestion Toxidromes

Overdose l l Anticholinergics, sympathomimetics Distinguishing features – – l Hx of ingestion Toxidromes Treatment – – Cooling, hydration Benzodiazepine, Decontamination

Diff Dx cont’d l The differential for heat stroke contains many potentially life threatening

Diff Dx cont’d l The differential for heat stroke contains many potentially life threatening illnesses l It all comes down to your ABC Cooling Hemodynamic support l l l

Heat Stroke – Complications l CNS – – l Renal – l Cerebral edema

Heat Stroke – Complications l CNS – – l Renal – l Cerebral edema Permanent neuro damage eg. cerebellar deficits, hemiplegia, or dementia is possible after severe cases Myoglobinuric renal failurerhabdomyolysis Cardiopulmonary – – Heart failure Pulmonary edema

Heat Stroke - Complications l Electrolyte – – – l Hematologic – – l

Heat Stroke - Complications l Electrolyte – – – l Hematologic – – l Hypo or Hyperkalemia Hypernatremia Hypocalcemia, hypomagnesemia Thrombocytopenia DIC Hepatic – – Centrilobular necrosis – not permanent However, can be a useful diagnostic adjunct

Heat Stroke – Hepatic Damage l “ Hepatic damage is such a consistent feature

Heat Stroke – Hepatic Damage l “ Hepatic damage is such a consistent feature of heat stroke that its absence should cast doubt on the diagnosis “ From Rosen’s 5 th edition p 2003

Heat Stroke - Diagnostic Criteria l Classic triad – – – l Markedly elevated

Heat Stroke - Diagnostic Criteria l Classic triad – – – l Markedly elevated temp ( >40. 5 degrees ) CNS dysfunction Anhidrosis Caveats – Sweating seen 50% of the time esp. in exertional heat stroke

Investigations l l l CBC+diff , blood culture Infection, thrombocytopenia Electrolytes, ABG Electrolyte derangement,

Investigations l l l CBC+diff , blood culture Infection, thrombocytopenia Electrolytes, ABG Electrolyte derangement, acidosis Chemstrip/Glucose DKA BUN, Cr Renal failure U/A, urine for myoglobin Rhabdomyolysis Hepatic panel Liver damage INR, PTT, Fibrinogen etc DIC CT Head Intracranial event, pre-LP LP Meningitis/encephalitis Thyroid panel Thyrotoxicosis CXR Pulmonary Edema EKG Secondary ischemia

Initial management

Initial management

Treatment summary l The Basics… – – l Resusc room, oxygen, iv, monitors Vitals-including

Treatment summary l The Basics… – – l Resusc room, oxygen, iv, monitors Vitals-including continuous rectal temp monitoring The ABC’s… – – Airway, Breathing Cooling l – Evaporative/Immersive +/- adjuncts Circulation l l Cautious rehydration Pressor support as needed

Treatment summary cont’d l More ABCDE’s…. l +/- Antibiotics ? Sepsis, meningitis +/- Benzodiazepines

Treatment summary cont’d l More ABCDE’s…. l +/- Antibiotics ? Sepsis, meningitis +/- Benzodiazepines ? Withdrawal syndrome +/- Cyproheptadine ? Serotonin syndrome +/- Dantrolene ? Malignant Hyperthermia ? Neuroleptic Malig Syndrome +/- Decontamination ? Ingestion +/- Endocrinopathy tx ? Thyroid storm l l l

What about antipyretics? l Acetaminophen and ASA are not indicated in heat stroke –

What about antipyretics? l Acetaminophen and ASA are not indicated in heat stroke – – l l These drugs counteract fever caused by an elevated hypothalamic set point In heat stroke, the increased temperature is due to an entirely different mechanism ASA --> may worsen coagulopathy Acetaminophen --> may exacerbate hepatic damage

Cooling l The key to successful outcome in heat stroke Prognosis in heat stroke

Cooling l The key to successful outcome in heat stroke Prognosis in heat stroke is directly related to how quickly the body can be cooled down l Goal is to cool by 0. 1 -0. 2 degrees/min l

In the ER …. Cooling Methods l Immersion l Evaporation

In the ER …. Cooling Methods l Immersion l Evaporation

Ice Water Immersion l l Primary cooling mech = conduction Pt is undressed and

Ice Water Immersion l l Primary cooling mech = conduction Pt is undressed and placed into a tub of ice water deep enough to cover the trunk and extremities Can achieve cooling rates of 0. 13 degrees/min Can decrease core temp to 39 degrees in 1040 min

Ice Water Bath-Disadvantages l l Can’t perform defibrillation or resuscitative procedures while immersed Vasoconstriction

Ice Water Bath-Disadvantages l l Can’t perform defibrillation or resuscitative procedures while immersed Vasoconstriction Shunting of blood from the skin ? Heat exchange Induced shivering endogenous heat production Uncomfortable

Evaporative Cooling l l l Fans positioned beside an undressed pt while warm water

Evaporative Cooling l l l Fans positioned beside an undressed pt while warm water is sprayed/sponged on Pt kept continually wet for continued cooling Can achieve cooling rates comparable to immersive techniques

Evaporative Cooling-Advantages l l Easier patient access No induced peripheral vasoconstriction Less induced shivering

Evaporative Cooling-Advantages l l Easier patient access No induced peripheral vasoconstriction Less induced shivering More comfortable for the patient

Methods of Cooling l Br J Sports Med 2005 Aug; 39(8): 503 -7 l

Methods of Cooling l Br J Sports Med 2005 Aug; 39(8): 503 -7 l l Review of 17 journal articles. Modalities of reducing body core temperature in patients with exertional heatstroke l The most effective method is immersion in iced water – The practicalities of this treatment may limit its use

Cooling Goal l l Keep rectal temperature <39. 4ºC and skin temperature 30ºC-33ºC. Cooling

Cooling Goal l l Keep rectal temperature <39. 4ºC and skin temperature 30ºC-33ºC. Cooling should be discontinued when rectal temp hits 39 -40 degrees – l to avoid “overshoot” hypothermia Avoid: – – – antipyretic agents Alcohol sponge baths Alpha-adrenergic agonists

Main Predictors of Outcome l l l Duration and degree of hyperthermia Time to

Main Predictors of Outcome l l l Duration and degree of hyperthermia Time to cooling Indicators of organ dysfunction, such as transaminases, LDH and CK

Cooling methods cont’d l To counteract shivering… – – – Benzodiazepines Phenothiazines – advocated

Cooling methods cont’d l To counteract shivering… – – – Benzodiazepines Phenothiazines – advocated in the past, however may potentially lower seizure threshold If severe- non-depolarizing paralytic

Circulation – Main Issues l l Hypotension and dehydration are the main issues for

Circulation – Main Issues l l Hypotension and dehydration are the main issues for heat stroke patients Usually, more than one cause for hypotension – – Hypovolemia Increased peripheral vasodilatation

Circulation – Complicating factors l Heat stroke patients are at high risk of developing

Circulation – Complicating factors l Heat stroke patients are at high risk of developing pulmonary edema and renal failure l Cooling a patient will redistribute peripheral blood flow back to the core l Need careful balance between hydration and preventing fluid overload

Circulation-Approach to hypotension l 1 st line – cooling – l Will redistribute volume

Circulation-Approach to hypotension l 1 st line – cooling – l Will redistribute volume from periphery to core 2 nd line – judicious hydration – – – Most sources suggest 250 -500 cc/h Titrate to hemodynamic response, urine output, age and PMHx of patient etc. Invasive monitoring may be indicated for complicated cases

Circulation-Approach to hypotension l 3 rd line – pressors – Be cautious with primarily

Circulation-Approach to hypotension l 3 rd line – pressors – Be cautious with primarily alpha blocking agents (eg. Levophed) l – Will cause further vasoconstriction and could potentially decrease heat exchange No definitive evidence on which pressor is the “best” to use

Heat exhaustion vs Heat stroke l l Important to think of heat exhaustion and

Heat exhaustion vs Heat stroke l l Important to think of heat exhaustion and heat stroke as two ends of a spectrum The point at which heat exhaustion becomes heat stroke --> when thermoregulatory mechanisms fail or are overwhelmed Heat exhaustion can easily progress to heat stroke if not adequately treated Thus early recognition and treatment essential!

Heat exhaustion vs. Heat stroke Differentiation l l Vital signs – In general, heat

Heat exhaustion vs. Heat stroke Differentiation l l Vital signs – In general, heat exhaustion < 40 deg, heat stroke > 40 deg – Remember though that prehospital cooling may have occurred in the heat stroke patient Clinical exam – Heat stroke implies significant CNS dysfunction – seizures, coma, very altered mental state – Pts with heat exhaustion have less florid CNS dysfunction- eg. mild disorientation, clumsiness

Heat exhaustion vs. Heat stroke. Bottom line l If the possibility of heat stroke

Heat exhaustion vs. Heat stroke. Bottom line l If the possibility of heat stroke is entering your mind, initiate immediate tx (ie Airway, Breathing, Cooling, Diff Dx) l Hepatic transaminases may be a useful differentiating factor – but you must initiate immediate cooling while you wait for results

Take Home Points l l l Altered mental state + hyperthermia = heat stroke

Take Home Points l l l Altered mental state + hyperthermia = heat stroke until proven otherwise ABC’s = Airway, Breathing, Circulation, Cooling Treat hyperthermia early or patient dies

References l l l Rosen’s 5 th edition, pages 1997 -2009 Tintinalli’s 5 th

References l l l Rosen’s 5 th edition, pages 1997 -2009 Tintinalli’s 5 th edition, pages 1235 -1242 Khosla et al, “Heat-Related Illnesses”, Critical Care Clinics, 15(2), 251 -263 Tek et al, “Heat Illness”, Emergency Medicine Clinics of North America, 10(2), 299 -309 Wexler, Randall K, “Evaluation and Treatment of Heat-Related Illnesses”, American Family Physician, 65(11), 2307 -2313