Thats Hot! Dr. Kelly Kasteel Case Study- hyperthermia.
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Transcript of Thats Hot! Dr. Kelly Kasteel Case Study- hyperthermia.
That’s Hot!Dr. Kelly Kasteel
Case Study-hyperthermia
Hyperthermia: Epidemiology
4,000 heat related deaths yearly (US) 80% of the fatalities are elderly
– Occurs in 5 per million over age 85 compared to 1 per million in the 5-44 age group
2nd leading cause of death among young athletes Very young (<4yo) also at increased risk
– Occurs in 0.3 per million compared to 0.05 per million in patients > 4yo.
Case Study-History
36 y.o female Admitted-RCH 2011 (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
PMHx1. Hepatitis C.2. BAD
Meds– None. Previously (1/12) on
Risperidone-2mg qhs via pharmanet Allergies
– None SHx
– Prostitution – multiple STD’s in past– Polysubstance abuse (cocaine/heroine
IVDU).– Last used this am
Case Study-On Examination
HR-144 reg/ RR-22/ Temp-41 C/ BP-90/40/ Pressure support 15, PEEP of 5, FiO2 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
CVS-s1s2 no murmur no s3s4 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 E3M5V2 = 10. Moving all 4. Pupils 3 reactive.
MSK- Injection marks over antecubital space Derm- Warm and Dry
Case Study- Labs
Glucose-6.8 Sodium-142 Potassium-5.4 Chloride104 Bicarb 11 Urea 6.3 Creatinine 147 Total Bili 8 Osmolality 319 Anion Gap-27 CK -405 Troponin0.19 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
Infectious workup– 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 24th 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.
CXR: small lung volumes, no obvious airspace disease
Case study- Course in Hospital
Treated presumptively as sepsis nyd- piptazo, flagyl Negative workups – no identifiable septic or
obstetrical causes for DIC. July 23-24- Patient briefly extubated before re-
intubation and markedly decreased LOC. Brain Death Comfort care initiated July 24th, patient deceased
within the hour. Autopsy- Non-contributory to date-MOS
Now That’s HOT
What is your differential diagnosis for this pt?
What are the potential complications that can occur in heat stroke?
What investigations should you order?
What other therapies should be considered?
Basic principles of Heat
4 mechanisms that allow the body to maintain a constant core temperature– Radiation – Convection – Conduction– Evaporation
Fever vs. Hyperthermia
Fever– 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
Heat Stroke
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
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
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
INFECTIOUS– Sepsis, Meningitis/Encephalitis, Falciparum malaria
DRUG/TOXIN INDUCED– Overdose – anticholinergic, sympathomimetic– Withdrawal – benzodiazepene, alcohol – delirium tremens– Neuroleptic malignant syndrome– malignant hyperthermia– Serotonin syndrome
ENDOCRINE– Thyroid storm, Pheochromocytoma
CNS– Hypothalamic hemorrhage, status epilepticus esp nonconvulsive
Neuroleptic Malignant Syndrome
Impaired thermoregulation in hypothalamus due to relative lack of dopamine
Caused by antipsychotic meds/neuroleptics 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 useTreatment
– Cooling, hydration, benzodiazepines– Bromocriptine, amantadine, dantrolene
Malignant Hyperthermia
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
– History of succinylcholine use– Muscular rigidity
Treatment– Cooling, hydration– Dantrolene
Serotonin syndrome
Excess serotonin and dopamine levels in CNS Triggered by any med that increases serotonin levels
(eg. SSRI’s, demerol, dextromethorphan, lithium etc.)
Distinguishing features– Appropriate medication history– Muscular rigidity
Treatment– Cooling, Hydration– Cyproheptadine
Thyroid storm
Hypermetabolic state from extreme thyrotoxicosis Distinguishing features
– History of thyroid disease– Goiter– Ophtho clues lid retraction/lag, exophthalmos, EOM palsy
Treatment– Cooling, Hydration– PTU, iodide solution, propranolol etc.
Overdose
Anticholinergics, sympathomimetics Distinguishing features
– Hx of ingestion– Toxidromes
Treatment– Cooling, hydration– Benzodiazepine, Decontamination
Diff Dx cont’d
The differential for heat stroke contains many potentially life threatening illnesses
It all comes down to your ABC Cooling Hemodynamic support
Heat Stroke – Complications
CNS – Cerebral edema– Permanent neuro damage eg.
cerebellar deficits, hemiplegia, or dementia is possible after severe cases
Renal– Myoglobinuric renal failure-
rhabdomyolysis Cardiopulmonary
– Heart failure– Pulmonary edema
Heat Stroke - Complications
Electrolyte– Hypo or Hyperkalemia– Hypernatremia– Hypocalcemia, hypomagnesemia
Hematologic– Thrombocytopenia– DIC
Hepatic– Centrilobular necrosis – not permanent– However, can be a useful diagnostic adjunct
Heat Stroke – Hepatic Damage
“ Hepatic damage is such a consistent feature of heat stroke that its absence should cast doubt on the diagnosis “
From Rosen’s 5th edition p2003
Heat Stroke - Diagnostic Criteria
Classic triad– Markedly elevated temp ( >40.5 degrees )– CNS dysfunction– Anhidrosis
Caveats– Sweating seen 50% of the time esp. in exertional heat
stroke
Investigations
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
Treatment summary
The Basics…– Resusc room, oxygen, iv, monitors– Vitals-including continuous rectal temp monitoring
The ABC’s…– Airway, Breathing– Cooling
Evaporative/Immersive +/- adjuncts– Circulation
Cautious rehydration Pressor support as needed
Treatment summary cont’d
More ABCDE’s….
+/- Antibiotics ? Sepsis, meningitis +/- Benzodiazepines ? Withdrawal syndrome +/- Cyproheptadine ? Serotonin syndrome +/- Dantrolene ? Malignant Hyperthermia ? Neuroleptic Malig Syndrome +/- Decontamination ? Ingestion +/- Endocrinopathy tx ? Thyroid storm
What about antipyretics?
Acetaminophen and ASA are not indicated in heat stroke– 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
The key to successful outcome in heat stroke Prognosis in heat stroke is directly related to
how quickly the body can be cooled down
Goal is to cool by 0.1-0.2 degrees/min
In the ER ….Cooling Methods
Immersion
Evaporation
Ice Water Immersion
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 10-40 min
Ice Water Bath-Disadvantages
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
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
Easier patient access No induced peripheral vasoconstriction Less induced shivering More comfortable for the patient
Methods of Cooling
Br J Sports Med 2005 Aug;39(8):503-7
Review of 17 journal articles. Modalities of reducing body core temperature in
patients with exertional heatstroke
The most effective method is immersion in iced water
– The practicalities of this treatment may limit its use
Cooling Goal
Keep rectal temperature <39.4ºC and skin temperature 30ºC-33ºC.
Cooling should be discontinued when rectal temp hits 39-40 degrees
– to avoid “overshoot” hypothermia
Avoid:– antipyretic agents– Alcohol sponge baths – Alpha-adrenergic agonists
Main Predictors of Outcome
Duration and degree of hyperthermia Time to cooling Indicators of organ dysfunction, such as
transaminases, LDH and CK
Cooling methods cont’d
To counteract shivering…– Benzodiazepines– Phenothiazines – advocated in the past, however
may potentially lower seizure threshold– If severe- non-depolarizing paralytic
Circulation – Main Issues
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
Heat stroke patients are at high risk of developing pulmonary edema and renal failure
Cooling a patient will redistribute peripheral blood flow back to the core
Need careful balance between hydration and preventing fluid overload
Circulation-Approach to hypotension
1st line – cooling– Will redistribute volume from periphery to core
2nd 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
3rd line – pressors– Be cautious with primarily alpha blocking agents
(eg. Levophed) 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
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
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
If the possibility of heat stroke is entering your mind, initiate immediate tx (ie Airway, Breathing, Cooling, Diff Dx)
Hepatic transaminases may be a useful differentiating factor – but you must initiate immediate cooling while you wait for results
Take Home Points
Altered mental state + hyperthermia = heat stroke until proven otherwise
ABC’s = Airway, Breathing, Circulation, Cooling
Treat hyperthermia early or patient dies
References
Rosen’s 5th edition, pages 1997-2009 Tintinalli’s 5th 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