Intern Report Case Discussion 1.10


Presented by Ryan Phillips, MD

History of present illness:

A 76-year-old female was wheeled down to the first aid station during a 90 degree Thursday afternoon day game at Comerica Park. The patient is a member of an assisted-living home and is visiting the park as a part of “Senior Day” promotion at the assisted living home.   The patient is wheeled down by one of the nurses from the home.  She knows some of the patient’s medical history and knows the patient has been in good health and was her normal alert and orientated self before coming to the baseball park today.  She was sitting enjoying herself for the first few innings, but the patient was thought to be napping for the past three innings.  In the bottom of the 8th inning the patient was noticed to be unresponsive and not napping.  The patient now is not responding to verbal stimuli, which is not normal for her.

Past medical history (as provided by the nurse): hypertension, mentally impaired

Medications: Metoprolol and hydrochlorothiazide

Allergies: NKDA

Past surgical history: Unknown

Social history:  patient lives at a member assisted living home patient does not smoke drink or use any drugs as per the nurse with the patient

Family History: unknown

Review of systems: unobtainable

Physical examination

VS: T 40.5°C oral, HR 140 RR 28 BP 90/60

Gen: patient is obtunded, skin is hot and dry, pt is responding to painful stimuli but not responding to verbal

HEENT: pupils equal and reactive to light, no pallor, anicteric, there are no facial asymmetrys noted, head is normocephalic, atraumatic, nares have no discharge, oral pharynx appears dry, no erythema, + gag, neck is supple, no JVD, trachea midline

Respiratory: patient is tachypneic, lungs are clear to auscultation bilaterally with no expiratory wheeze rales or rhonchi, patient has equal chest rise

CVS: tachycardic with S1-S2 present, no murmurs or rubs

Abdomen: soft, nontender, nondistended, with positive bowel sounds, no masses, no organomegaly appreciated

Extremities: patient able to move all 4 extremities in response to pain, no asymmetric swelling or erythema patient has 1+ pulses bilateral radial and bilateral pedal, slightly decreased but symmetrical muscle tone

Skin: hot and dry, no rashes, no jaundice, no diaphoresis

Neurologically: patient responds to painful stimuli and pupils are equal and reactive to light no facial asymmetry is note, noted to move all 4 extremities, +1 DTRs, no clonus, no cogwheel rigidity

Laboratory studies

CBC Hb – 16, WBC – 12, hematocrit 51 platelets 416

Electrolytes Na – 134 K – 5.1, Cl 96, HCO3 26, BUN 62, Cr 2.1 glucose 90

AST 245 ALT 276

Chest x-ray no acute occult cardiopulmonary process

Question 1

What is this patient most likely diagnosis?

A. Acute renal insufficiency

B. Heat exhaustion

C. Heat stroke

D. Hepatitis

E. Meningitis

Question 2

After controlling ABCs what is your next step in management with this patient?

A. CT of the head followed by lumbar puncture and initiation of steroids, ampicillin, ceftriaxone

B. Exchange transfusion and plasmapheresis

C. Oral hydration with hypotonic solutions

D. Placing an NGT and giving the patient acetaminophen 1,000mg and ibuprofen 800mg via NGT

E. Rapid cooling by removing clothing, misting the patient with water and/or immersing the patient in a tepid water bath

Question 3

Despite the treatment given, the patient declines and requires rapid sequence intubation.  Following successful intubation, the patient develops muscle rigidity, acidosis and her temperature is now 42°C.  What medication is indicated?

A. Atropine

B. Physostigmine

C. Dantrolene

D. Lorazepam

E. Sodium bicarbonate



Question 1

What is this patient most lately diagnosis?

A.Acute renal insufficiency

B.Heat exhaustion

C.Heat stroke



This is an elderly patient that was in good health until she sat in the 90 heat for an extended period of time and is now suffering from heat stroke.  Heat stroke is the most severe form of a series of heat related illnesses.  It is a catastrophic life-threatening emergency with multiorgan system involvement and a high mortality rate that requires immediate intervention that occurs when the homeostatic mechanisms fail to alleviate extreme body temperatures usually greater than 40°C.  The classic definition is a core temperature greater than 40°C, anhidrosis and CNS dysfunction.  These criteria, however, are not absolute diagnostic criteria.  Absence of sweating may or may not be present as hyper-hidrosis is followed by anhidorsis, thus, there may still be sweat present at presentation.  CNS dysfunction is not specifically defined, however some alteration of mental status must be present and 40°C is not a diagnostic cutoff.

Prolonged heat stress causes an increase in blood flow via peripheral vasodilation.  As the body tries to release heat at the skin surface, this results in a decrease in blood flow to splanchnic and renal vasculature.  This decreased blood flow results in splanchnic and renal ischemia causing nausea, vomiting and diarrhea.  Further ischemia will cause hepatic damage.  Laboratory studies may show increased renal function and LFTs after prolonged heat exposure.  Further heat stress causes the compensatory splanchnic vasoconstriction to fail causing the core blood temperature to dramatically increase.  This causes elevated intracranial pressure with a reduction of mean arterial pressure leading to decrease cerebral blood flow and major CNS dysfunction.

The most important treatment for heat stroke is rapid cooling as described in answer to Question 2.

Other forms of minor heat related illness

Heat edema

Prickly heat

Heat Cramps

Painful involuntary spasmodic contractions of skeletal muscles usually involving the calves.  Found in individuals sweating profusely causing losses of water or other hypotonic solutions may occur during exercise or more likely rest. Heat cramps are self-limited and do not cause significant morbidity.  The pain of heat cramps do not respond to opiates alone.  Heat cramps are limited to definitive group of muscles and are not known to cause rhabdomyolysis.  Pathogenesis is due to depletion of sodium and potassium at the level of the muscle.  Treatment consists of fluid and salt replacement with oral rehydration or intravenous rehydration in more severe cases.

Heat Syncope

Heat Exhaustion
A dehydration induced heat retention insufficient to cause heat stroke.  It is characterized by a combination of salt depletion and water depletion.  Symptoms include weakness, malaise, lightheadedness, fatigue, dizziness, nausea or vomiting, frontal headache, and myalgias.  Signs in the ER include orthostatic hypotension, sinus tachycardia, tachypnea, diaphoresis and syncope.  The core temperature usually remains below 40°C. Mental status remains normal.  Heat cramps and/or rhabdomyolysis may also be present on rare occasion.  Treatment includes rest, remove the patient from the heat environment, assess volume status and replace fluid.  Choice of intravenous solutions should be guided by laboratory determinations, isotonic salt solutions may be used until specific electrolyte abnormalities are identified.  If there is a free water deficit,  free water should be replaced slowly over 48 hours or correction of hypernatremia associated with seizures caused by cerebral edema.  Patients can be treated as outpatients if appropriate, but may need admission with significant electrolyte abnormalities.

Exhaustion has a potential progress to heat stroke.  The major differences between heat stroke and heat exhaustion are that heat stroke classically involves anhidrosis, CNS dysfunction and core temperature of greater than 40°C.  Typically the degree of dehydration and volume loss is greater with heat exhaustion versus heat stroke.

Question 2

After controlling ABCs what is your next step in management with this patient?

A. CT of the head followed by lumbar puncture and initiation of steroids, ampicillin, gentamicin and metronidazole

B. Exchange transfusion and plasmapheresis

C. Oral hydration with hypotonic solutions

D. Perform synchronized cardioversion at 100 KJ followed by adenosine 6 mg

E. Rapid cooling by removing clothing, misting the patient with water and/or immersing the patient in a tepid water bath

This patient needs to be rapidly cooled.  The patient also needs fluids, but that is independent of rapid cooling.  Several ways are appropriate to reduce a patient’s temperature and the best way to understand how is by understanding the different mechanisms of heat transfer

Evaporation – Heat loss mechanism accounts for over 25% and heat lost in cooler settings and virtually 100% at high environmental temperatures.  Heat loss is impaired at higher levels of humidity as evaporation is impaired.  This method of heat loss is enhanced by misting the patient with water or sponge baths.  Heat is pulled from the patient to help the water evaporate.  Placing a fan on the patient will increase the rate of evaporation and make this method even more effective.

Conduction – Kinetic energy of moving molecules in warm skin is transferred to the less kinetically active molecules in cooler surface. Usually occurs at less than 3% total heat loss of the body, but can be enhanced when ice packs are placed in the patients groin and axilla.  Can also be enhanced by placing the patient in a tepid water bath.  A tepid water bath is used for patient comfort and to prevent patient shivering.

Radiation – Primary mechanism of heat lost when the environmental temperature is lower than the body temperature.  Body heat is lost through infrared range of the electromagnetic spectrum.  When the body heat is less than the environmental temperature the body will gain the infrared heat.  It is best to move the patient a cooler environment

A combination of all four cooling mechanisms should be utilized.  The environment will dictate which mechanism will be the most appropriate.  The most practical method will often be a combination of evaporation and ice bags.  It is important to remember that antipyretics are ineffective and therefore not indicated in a patient with environmental hyperthermia.

Question 3

Despite the treatment given, the patient declines and requires rapid sequence intubation.  Following successful intubation, the patient develops muscle rigidity, acidosis and her temperature is now 42°C.  What medication is indicated?

A. Atropine

B. Physostigmine

C. Dantrolene

D. Lorazepam

E. Sodium bicarbonate

Malignant hyperthermia can be induced in the emergency department after the administration of general anesthesia.  It is rare in the emergency department setting, but it can occur with neuromuscular blocking agents such as succinylcholine and if the person has the inherited muscle disorder.  Malignant hyperthermia causes hyperthermia, muscle rigidity and acidosis and is treated with dantrolene.  Malignant hyperthermia is caused by an instability of skeletal muscle sarcoplasmic reticulum and the release of calcium.  Dantrolene treats malignant hyperthermia by lowering myoplasmic calcium.

Other drug induced hyperthermias include neuroleptic malignant syndrome and serotonin syndrome.  Neuroleptic malignant syndrome symptoms include muscular rigidity, severe dyskinesia, akinesia, tachycardia, dyspnea, dysphagia and urinary incontinence.  It is caused by dopamine receptor blockade from haloperidol or other antipsychotic medications causing muscle spasticity and dystonia.  Treatment starts with withholding neuroleptic agents followed by supportive care against potential complications including dehydration,electrolyte imbalances, rhabdomyolysis, renal failure, cardiac arrhythmias, seizures, hepatic failure and sepsis.

Serotonin Syndrome is a condition associated with increased serotonergic activity in the CNS.  It can be caused by therapeutic medication use, drug interactions or intentional self-poisoning.  Symptoms can range from mild tremor to life threatening hyperthermia.  Other symptoms can include diaphoresis, tachycardia, hypertension, vomiting, diarrhea, tremor, muscle rigidity, myoclonus and hyperreflexia.  Treatment of serotonin syndrome includes discontinuation of all serotonergic agents, supportive care aimed at normalization of vital signs, sedation with benzodiazepines, and administration of serotonin antagonists.

It is important to recognize hyperthermia has a wide differential diagnosis.  This patient had strong clinical presentation for an environmental hyperthermia.  Other diagnoses that need to be in the differential for high fever include sepsis or meningitis, seizures, toxins, CNS hemorrhage, thyroid storm malignant hyperthermia, neuroleptic malignant syndrome or serotonin syndrome.  If the patient responds to rapid cooling and becomes more responsive further workup may be unnecessary.  However, if a person presents from an apartment without air conditioning  in mid-July without any more history available we would be unable to differentiate if this person is hyperthermic from environment versus other etiologies such as infection or ICH.  The infection or ICH may be preventing the patient from leaving the 100 degree apartment.  This patient would need extensive evaluation and treatment to rule out other etiologies such as a head CT and LP.


Boyer, E. W. M., PhD (2009) Serotonin Syndrome. UpToDate

Eelco FM Wijdicks, M. (2009) Neuroleptic Malignant Syndrome. UpToDate

Helman, R. S., MD and M. Rania Habal (2007) Heatstroke. eMedicine

Lin, J., MD, MPH, FACEP, M. Ralph Losey, FACEP, et al. (2009) An Evidence-Based Approach to Hyperthermia and Other Heat-Related Emergencies. Pediatric Emergency Medicine Practice 6, 1-16

Marx, J. A., R. S. Hockberger, et al. (2006). Rosen’s emergency medicine : concepts and clinical practice. Philadelphia, Mosby/Elsevier.

Tintinalli, J. E., G. D. Kelen, et al. (2004). Emergency medicine : a comprehensive study guide. New York, McGraw-Hill, Medical Pub. Division.

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