HYPOTHERMIA, FROSTBITE AND HEAT ILLNESS Mark Bromley PGY3

Outline Heat Stroke Hypothermia Frostbite

HEAT STROKE

Case 68 M is brought into the ED for decreased LOC Found in bed in his apartment Freezer door was left open

PMHx: CAD, CHF, DMII

Meds: Metoprolol, Altace, Lipitor, ASA, NTG Patch, Gluconorm

OE: 42oC HR: 65 GCS:3

What are this patients HS risk factors?What other diagnoses are you concerned about?How would you like to manage?

Perspective Disease of the young and the old

Outdoor laborers Athletes, children, and the elderly

Proportional to climate US

20 cases per 100,000 people 240 deaths annually #1 cause of death among US soldiers in the 1st gulf war

Heat wave in 2003 (France) caused 14,802 deaths

Life-threatening emergency needing immediate treatment

Heat Generation

Thermoregulation

Respiration

TerminologyHeat wave

Three or more consecutive days during which the air temperature is >32.2°CHeat stress

Perceived discomfort and physiological strain associated with exposure to a hot environment, especially during physical workHyperthermia

A rise in body temperature above the hypothalamic set point when heat-dissipating mechanisms are impaired (by drugs or disease) or overwhelmed by external (environmental or induced) or internal (metabolic) heatHeat exhaustion

Mild-to-moderate illness due to water or salt depletion that results from exposure to high environmental heat or strenuous physical exercise; signs and symptoms include intense thirst, weakness, discomfort, anxiety, dizziness, fainting, and headache; core temperature may be normal, below normal, or slightly elevated (>37°C but <40°C)Heat stroke

Severe illness characterized by a core temperature >40°C and central nervous system abnormalities such as delirium, convulsions, or coma resulting from exposure to environmental heat (classic heat stroke) or strenuous physical exercise (exertional heat stroke)Multiorgan-dysfunction syndrome

Continuum of changes that occur in more than one organ system after an insult such as trauma, sepsis, or heat stroke

Progression of Disease

Perceived discomfort and physiological strain

A rise in body temperature above the hypothalamic set point

Mild-to-moderate illness due to water or salt depletion

Severe illness characterized by a core temp >40°C and CNS abnormalities

Changes in more than one organ system

Symptomatic

SickHot InsideHot Outside

Clinical and Metabolic Manifestations Hyperthermia CNS Dysfunction

Tachycardia, Hyperventilation (CO2 < 20) Respiratory Alkalosis / Metabolic Acidosis Hypophosphatemia / Hypokalemia Rhabdomyolysis (↑PO4, ↑K, ↓Ca) MODS

encephalopathy, rhabdomyolysis, acute renal failure, acute respiratory distress syndrome, myocardial injury, hepatocellular injury, intestinal ischemia or infarction, pancreatic injury, and hemorrhagic complications, DIC, with pronounced thrombocytopenia

Exertional vs ClassicExertional Classic Healthy Predisposing factors/medications Younger Older Exercise Sedentary Sporadic Heat wave occurrence Diaphoresis Anhidrosis Hypoglycemia Normoglycemia DIC Mild coagulopathy Rhabdomyolysis Mild CPK elevation Acute renal failure Oliguria Marked Lactic acidosis Mild acidosis Hypocalcemia Normocalcemia

Case 68 M is brought into the ED for decreased LOC Found in bed in his apartment Freezer door was left open

PMHx: CAD, CHF, DMII

Meds: Metoprolol, Altace, Lipitor, ASA, NTG Patch, Gluconorm

OE: 42oC HR: 65

What are this patients HS risk factors?What other diagnoses are you worried about?How would you like to manage?

Case 37 F presents altered and hot Post-op Day 1

PMHx: Graves

OE: 135 39oC 143/62 (widened pulse pressure) Moist skin Loose stools

Case 45-year-old man who had been outside mowing grass. EMS later found him unresponsive, and he arrived at the

emergency department with a GCS of 3

OE: His skin was warm and dry Rectal temperature 42.2°C HR:170/min. Pupils are 7mm and

reactive.

Urine tox screen was positive for cocaine and marijuana

He was admitted to the ICU, and rhabdomyolysis developed. He recovered with supportive care and was discharged 1 week

later.

What are his risk factors?Why is he dry?

Case 67 F with dementia Increased confusion and agitation, requiring

haloperidol 1mg at bedtime for ~5 months Agitated in the ED Found on the roof of her building

Progressively became minimally responsive, rigid, and incontinent, with a temp of 40.5oC

Case 58 M with Hyperthermia Feeling unwell for the past 48h Shaking Chills – Altered

OE: 40oC 120 75/52 25 Flushed/warm peripherally

Classic Heat Stroke (non-exertional)

Results from exposure to high temperature Unable to compensate

Thoughts?Approach? Consider:

Alternate Diagnoses Hepatic Transaminase elevations may be useful Treating presumptively (sepsis)

Case 42 F collapsed just shy of the finish line It was her first marathon, and a hot day.

But according to her friend she had been keeping “pretty well hydrated.”

Brought to the ED via EMS confused Tonic-clonic in the trauma bay

Risk Factors?Concerns?Management?

Exertional Heat Stroke

Results from strenuous exercise Typically young healthy people

(athletes/workers)

Thoughts? Consider:

Hydration Hyponatremia

Treatment Cooling

Active cutaneous vasodilation ↑ temperature gradient b/w skin and environment (conduction) ↑ gradient of water-vapor pressure b/w skin and environment

(evaporation) ↑ velocity of air adjacent to the skin (convection) How would you like to do it?

Evaporation / Convection Cool water or wet sheets applied to the

skin Fan Spritz or Mist

This rarely causes shivering

Conduction

†Internal cooling, which has been investigated in animals, is infrequently used in humans. Gastric or peritoneal lavage with ice water may cause water intoxication.

Cold water immersion has been linked with asystolic arrestsUsed by the military without incidentMay be more significant in “classic” heat stroke (14% mortality study of 28 patients with CHS)

Rectal lavage

ConductionThis may cause shivering

How can you stop it? If the pt is shivering:

Vigorous massage spray with tepid water (40°C) expose to hot moving air (45°C)…either at the same time as cooling methods

are applied or in an alternating fashion

Case A buddy recently back from visiting out east,

tells us it was way hotter than anything we’ve experienced here.

According to the Canadian Weather Services the average temperature was exactly the same.

“Yeah but it was a wet hot! It was way hotter!”

What do you think?Does humidity make a difference?

Case 68 M with Heat Stroke You continue to cool His BP falls to 68/40

How would you like to manage?

Resuscitation

Fever vs Hyperthermia Fever does not cause primary pathologic

or physiologic damage Fever does not require therapeutic

intervention…unless the patient has limited physiologic

reserve

Infectious agents / Toxins / Mediators of inflammation(Pyrogens)

stimulateMonocytes / Macrophages / Endothelial cells / Other cell types

releasePyrogenic cytokines - IL- 1, TNF, IL- 6, IFNs

stimulateAnterior hypothalamus (Mediated by PGE2)

results inElevated thermoregulatory set point

leads toIncreased Heat conservation

(Vasoconstriction/ behaviour changes)Increased Heat production

(involuntary muscular contractions) result in

F E V E R

(Antipyretics/ NSAIDs act here) 

Decreasing the Set Point Antipyretics

Not useful in true Heat Shock May be useful in mixed presentations (ie.

Sepsis/Heatshock)

Prevention Acclimatize yourself to heat Schedule outdoor activities during cooler times ↓ level of physical activity Drink additional fluids Consume salty foods ↑ amount of time spent in air-conditioning Automobiles should be locked, and children

should never be left unattended in an automobile during hot weather

AcclimatizationSuccessive exposures over weeks… Enhanced CV performance Activation of Renin-Angiotensin-Aldosterone

Axis Salt conservation by sweat glands Increased capacity to secrete sweat Expansion of plasma volume Increase in GFR Increase in ability to resist rhabdomyolysis

HYPOTHERMIA

Case 48 F presents with decreased LOC Found outside by police talking strangely to

passers-by Complaining about her bulky coat Undressing despite the cold

What is your approach? Differential Diagnosis? Why is this lady at risk? How is she losing heat?

Pathophysiology Evaporation

Vaporization of water through both insensible loss and sweat

Radiation Emission of infrared electromagnetic energy

Conduction Direct transfer of heat to an adjacent, cooler

object Convection

Direct transfer of heat to convective air currents

PathophysiologyCell membrane dysfunction

Efflux of intracellular fluid

Enzymatic dysfunction

Electrolyte imbalances

CaseOE: 48 10 110/62 34oC CNS Depression (GCS 5) – No focal findings Reflexes globally reduced Not shivering But she feels cold!

What would you like to do?

Assessment Thermometer

Need a “low” reading thermometer Oral temps influenced by respiration Tympanic temps unreliable

Rectal Probe “Core” temp Altered if adjacent to cold/frozen stool

Esophageal Probe Next to the Aorta

Bladder Probe

CaseOE: Repeat temperature via rectal probe =

28oC

What’s going on Doctor? Is Hypothermia a diagnosis? How would you classify?

Clasification Mild: 32-35oC

tachypnea, tachycardia, ataxia, dysarthria, impaired judgement, shivering, “cold diuresis”

Moderate: 28-32oC decreased heart rate, hypoventilation, CNS

depression, hyporeflexia, decreased renal blood flow, loss of shivering, paradoxical undressing, AFIB, junctional bradycardias

Severe: <28oC pulmonary edema, oliguria, areflexia, coma,

hypotension, bradycardia, ventricular arrhythmias, asystole

Differential Diagnosis

Differential Diagnosis

Why is this patient hypothermic?

CaseWhat investigations would you like to

order?

Investigations C/S (hypoglycemia) CBC, Lytes, INR/PTT ABG EKG

Anything else you’d like?

Coagulopathy Clotting factors are temperature

dependant…they don’t work when they’re cold

Coags are performed in the lab at 37°C...thus, clinical coagulopathy → “N” INR

and PTT

ABG Lactate Metabolic screen

pH, pCO2, pO2 Gas tension and H+ decline with the

temperature Use uncorrected values

EKG

•Rhythm abnormalities•AFIB/Sinus Bradycardia

•Intervals•PR/QRS/QTc prolonged

•Osborn J waves

CaseHow would you like to manage this

patient?

Management Passive External Rewarming

remove wet clothing blankets

Active External Rewarming warmed humidified O2 forced air warming systems

Active Internal Rewarming warmed IV fluids (42oC) pleural/peritoneal/bladder irrigation Extracorporeal (dialysis/bypass/continuous

venous)

Case You begin Initially by covering the

patient in warmed blankets while someone set’s up the Bair Hugger.

Patient goes into VFIB

How would you like to proceed?

Modifications of BLS for Hypothermia If not in cardiac arrest,

warm the patient Handle the victim gently for all procedures Physical manipulation may precipitate VF

If in cardiac arrest, Assess pulse/respirations for 30-45s (may be

difficult) Bag with warmed O2 If shockable (ie. VF) shock once them resume CPR

defer further attempts till warm

“Hypothermic heart may be unresponsive to cardiovascular drugs, pacemaker stimulation, and defibrillation. Drug metabolism is reduced.”

Modifications of ACLS for Hypothermia Intubation

ventilation with warm, humidified oxygen isolate the airway to reduce the likelihood of aspiration

Difibrilation try initial shock if unsuccessful, defer until core temperature > 30°C

IV meds may accumulate to toxic levels (decreased metabolism) < 30°C hold > 30°C give at increased intervals

Re-warming as discussed above

Volume patients who have been hypothermic for 45-60 min are likely to require volume

because the vascular space expands with vasodilation

Routine use of steroids, barbiturates, and antibiotics has not been shown to increase survival or decrease post-resuscitation damage.

Severe hypothermia is often preceded by other disorders (eg, drug overdose, alcohol use, or trauma). The clinician must look for and treat these underlying conditions while simultaneously treating the hypothermia.

CaseInitial shock converts briefly to sinus then

pt becomes asystolicContinue CPR for 30 minutes with no ROS

When do you stop?

Withholding and Cessation of Resuscitative Efforts In the field

resuscitation may be withheld if the victim has obvious lethal injuries or if the body is frozen so that nose and mouth are blocked by ice and chest compression is impossible

“you’re not dead until you’re warm and dead” hypothermia may exert a protective effect on the brain and organs

if the hypothermia develops rapidly in victims of cardiac arrest. it may be impossible to distinguish 1o from 2o hypothermia

stabilize the patient with CPR basic maneuvers to limit heat loss rewarming interventions

Once the patient is in the hospital, physicians should use their clinical judgment to decide when resuscitative efforts should cease in a victim of hypothermic arrest.

FROSTBITE

Case

16-year-old male attempted to "get high" by inhaling airbrush propellant which contained a fluorinated hydrocarbon

The patient lost consciousness and upon waking his lips and tongue were frozen

His main complaints on presentation were dyspnoea and pain in the oral/peri-oral areas

Case

OE: 159/94 101 24 37.1oC Alert and Appropriate Severe edema of the tongue and lips, with

blisters on the lips and frozen saliva in the oral cavity

What else would you like to know? Initial management/approach?

Case 4 hours after presentation develops

acute respiratory distress Nasally intubated – stabilized

- admitted (ICU) Endoscopy showed 1st and 2nd degree burns

of the larynx with vocal cord involvement and 1st degree burns of the trachea, main stem bronchi, and esophagus.

The oral cavity had 2nd and 3rd degree burns which required debridement

Pathophysiology

Classification

Classification

Classification1st Degree:

Central pallor and anesthesia of the skin Surrounding edema

2nd Degree: Blisters containing clear/milky fluid Surrounding edema/erythema

3rd Degree: Deeper injury Hemorrhagic blisters progressing to black eschar

4th Degree: Injury extends to muscle/bone Involves complete tissue necrosis

Who is at risk for frostbite?

Behavioural Physiologic

Risk Factors Increased Conductive Heat Loss

Contact with metal or water Increased Convective Heat Loss

Exposure to wind Alcohol

Behavioural Changes Vasodilation

Smoking Hx of Frostbite African Americans / Women Ice Packs (iatrogenic)

Diagnosis Clinical

Numbness (sensory deficit) Distal extremeties

Plain Radiographs Coincidental fractures Soft tissue swelling

Technetium (Tc)-99 scintigraphy Predicts long-term tissue viability Allows early debridement

MRI/MRA Predicts tissue variability Visualize occluded vessels – demarcate ischemic tissue

Management?

TreatmentPrehospital Transport the patient to a warm environment Remove wet clothing Insulate affected areas Avoid walking on frostbitten feet

...Don`t re-warm if there is a possibility of re-freezing use of stoves (tissue is insensate) use friction

TreatmentHospital Re-warming

Immerse affected area in water bath (40-42oC) 30 min – tissue is purple and soft Analgesia - opiods

Analgesia Dressing

Bulky dressing to decrease oedema Splint to prevent contractures

Tetanus (consider) Rehydration

Cold diuresis – increases blood viscosity and sludging

Thrombolysis

Design: Single institution retrospective review of clinical outcomes and resource use.

Setting: Burn unit of a tertiary academic referral center. Patients: 2001-2006, patients with severe frostbite admitted within 48 hours of

injury underwent digital angiography and treatment with intra-arterial tPA if abnormal perfusion was demonstrated. These patients were compared with those treated from 1995 to 2006 who did not receive tPA.

Interventions: tPA vs traditional management of frostbite injury. Main Outcome Measures: Number and type of surgery were recorded, along

with amputations of digits (fingers or toes) and more proximal (ray, transmetatarsal, or below-knee) amputations. Resource utilization including length of stay, total costs, cost per involved digit, and cost per saved digit were analyzed.

Results: 32 patients with digital involvement (hands, 19%; feet, 62%; both, 19%) were identified. 7 patients received tPA, 6 within 24 h of injury. The incidence of digital amputation in patients who did not receive tPA was 41%. In those patients who received tPA within 24 hours of injury, the incidence of amputation was reduced to 10% (P.05).

Conclusions: tPA improved tissue perfusion and reduced amputations when administered within 24 hours of injury. This modality represents the first clinically significant advancement in the treatment of frostbite in more than 25 years.

Treatment of experimental frostbite with pentoxifylline and

aloe vera cream OBJECTIVE: To compare the therapeutic effects of systemic

pentoxifylline and topical aloe vera cream in the treatment of frostbite.

DESIGN: The frostbitten ears of 10 New Zealand white rabbits were assigned to one of four treatment groups: untreated controls, those treated with aloe vera cream, those treated with pentoxifylline, and those treated with aloe vera cream and pentoxifylline.

MAIN OUTCOME MEASURES: Tissue survival was calculated as the percent of total frostbite area that remained after 2

weeks. RESULTS: The control group had a 6% tissue survival. Tissue

survival was notably improved with pentoxifylline (20%), better with aloe vera cream (24%), and the best with the combination therapy (30%).

CONCLUSION: Pentoxifylline is as effective as aloe vera cream in improving tissue survival after frostbite injury.

Arch Otolaryngol Head Neck Surg 1995; 121:678

Miller MB, Koltai PJ

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