Hypothermia and cold injuries

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HYPOTHERMIA & COLD INJURIES Farooq Khan MDCM PGY-5 FRCP-EM February 28 th 2014

Transcript of Hypothermia and cold injuries

Page 1: Hypothermia and cold injuries

HYPOTHERMIA& COLD INJURIES

Farooq Khan MDCMPGY-5 FRCP-EM

February 28th 2014

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Background

• Definition: Core Temp <35°C• Severity:– Mild hypothermia: 32-35°C• Shivering thermogenesis, amnesia, dysarthria

– Moderate hypothermia: 28-32°C• Stupor, extinguished shivering, dysrhythmias

– Severe hypothermia: <28°C• V-fib risk, acid base disturbance, decreased CO and CBF

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DDx• Accidental (environmental)

exposure• Metabolic disorders

– Hypoglycemia– Hypothyroidism– Hypoadrenalism– Hypopituitarism

• Hypothalamic and CNS– Head trauma– Tumor– Stroke– Wernicke encephalopathy

• Drugs– Ethanol– Sedatives-hypnotics

• Sepsis• Dermal disease

– Burns– Exfoliative dermatitis

• Acute incapacitating illness• Massive fluid or blood

resuscitation• Malnutrition

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ECG

• Typical sequence is sinus brady > a fib w/ slow ventricular response > v-fib > asystole

• Other ECG findings:– Osborn (J) wave– T-wave inversions– PR, QRS, QT prolongation– Muscle tremor artifact– AV block– PVCs

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Typical ECG

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Supportive measures

• Handle pt gently– V-fib may be induced by rough handling of pt due to irritable

myocardium (anecdotal)• O2– Hypothermia causes leftward shift of oxyhemoglobin

dissociation curve• IVF– Hypothermia > impaired renal concentrating ability > cold

diuresis– Pts are prone to rhabdo– Intravascular volume is lost due to extravascular shift

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Specific therapies• Abx

– Give if suspect sepsis (e.g. hypothermia fails to correct w/ rewarming measures)

• Thiamine– Consider if Wernicke disease is possible cause of hypothermia

(e.g. alcoholic pt)• Hydrocortisone

– Consider if pt has history of adrenal suppression or insufficiency• Thyroxine

– Consider if any suspicion for hypothyroidism/myxedema coma

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Passive Rewarming

• Consider in pt w/ mild hypothermia (>32°C) who is able to generate intrinsic heat

• Techniques– Removal from cold environment– Remove wet clothing– Insulation with blankets

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Active rewarming• Indications

– Cardiovascular instability– Moderate to severe hypothermia (<32°C)– Inadequate rate or failure to rewarm– Endocrine insufficiency– Traumatic or toxicologic peripheral vasodilation– Secondary hypothermia impairing thermoregulation

• Rewarm trunk BEFORE the extremities– Otherwise may lead to hypotension ("core temperature

afterdrop")• Warmed vasodilated peripheral tissue allows cooler blood in extremities

to circulate back to core

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Active External Rewarming• Consider in:– Moderate-severe

hypothermia– Mild hypothermia in pt

who is unstable or cannot generate intrinsic heat

– Failure to respond to passive external rewarming

– May be ineffective in pts w/ poor perfusion or in cardiac arrest

• Techniques– Warm IV bags

applied to skin– Heating blankets– Radiant heat– Forced air - Bair

hugger

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Active Internal Rewarming

• Consider alone or along with active external warming in:– Cardiovascular instability

/ life-threatening dysrhythmias

– Severe hypothermia– Moderate hypothermia

which fails to respond to less aggressive measures

• Techniques– Warm humidified O2

– Heated IV fluids: 40-42°C• Level 1 infuser• Microwave on high x 2min

– Peritoneal lavage• Encourages liver function

– Pleural lavage• 2 large chest tubes

– GI tract lavage and bladder lavage• Limited area for heat exchange

and can cause Electrolyte shifts

– Bypass/ECMO/AV Dialysis

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ACLS

• CPR– Only perform if pt truly does not have a pulse

(unnecessary CPR may lead to V-fib)– Spend 30-45s attempting to detect respiratory

activity and pulse before starting CPR• Pt not dead until warm and dead: 30-32°C• Active internal rewarming indicated for cardiac

arrest– Mediastinal and direct cardiac lavage

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ACLS• Dysrhythmias (Occur <30°C)– Active rewarming is treatment of choice

• Most dysrhythmias (e.g. sinus brady, a-fib/flutter) require no other therapy

• Activity of antiarrhythmics is unpredictable in hypothermia• Hypothermic heart is relatively resistant to atropine, pacing, and

countershock– V-fib

• May be refractory to therapy until pt is rewarmed• Attempt a single defibrillation attempt

– If unsuccessful continue CPR and attempt defibrillation again once temp >30C (86F)

– IV medications: increase interval between doses

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FREEZING INJURIES

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Background

• Results from the freezing of tissue• It is a disease of morbidity, not mortality• Risk correlated with temperature and wind speed– Risk is <5% when ambient temperature (includes wind chill)

is > –15°C– Most often occurs at ambient temp < –20°C

• Can develop w/in 2-3sec when metal surfaces that are at or below –15°C are touched

• Most commonly affects distal part of extremities, face, nose, and ears

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Pathophysiology

• Freezing alone is usually not sufficient to cause tissue death– Thawing contributes markedly to the degree of

injury– Endothelial damage, beginning at the point of

thaw, is the critical event in frostbite• Resulting damage results in swelling, platelet

aggregation, vessel thrombosis

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Zones of Injury

• Zone of Coagulation• Most severe and usually most distal• Damage is irreversible

• Zone of Hyperemia• Least severe and usually most proximal• Generally recovers w/o treatment in <10d

• Zone of Stasis• Middle zone characterized by severe, but possibly

reversible, cell damage• It is this zone for which treatment may have benefit

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Classification

• First degree (frostnip)– Partial-skin freezing– Stinging and burning, followed by throbbing– Numbness, erythema, swelling, dysesthesia,

desquamation (days later)– Prognosis excellent

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Classification

• Second degree– Full-thickness skin freezing– Numbness followed by aching and throbbing– Skin blisters form w/in 6-24hr• Desquamate and form hard black eschars over several

days– Prognosis is good

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Classification

• Third degree– Damage extends into subdermal plexus– Extremity feels like a "block of wood" followed by

burning, throbbing, shooting pains– Hemorrhagic blisters form and are a/w skin

necrosis and blue-gray discoloration– Prognosis is often poor– Tissue loss involving entire thickness of skin

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Classification

• Fourth degree– Extension into subcutaneous tissues, muscle,

bone, and tendon; little edema– Deep, aching joint pain– Skin is mottled w/ nonblanching cyanosis and

formation of deep, dry, black eschar– Prognosis is extremely poor

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Pre-thaw

• Assess Doppler pulse and appearance• Protect part – no friction massage• Stabilize core temperature• Address medical and surgical conditions• Rehydrate patient• Prevent partial thaw and refreeze– Refreezing will cause even more severe damage

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Thaw• Analgesia

– Provide parenteral opiates• Blocking prostaglandin, thromboxane, and arachidonic cascade

• Ibuprofen 400mg po q8h

• Rapid rewarming is the core of therapy and should be initiated as soon as possible– Extremities

• Place in water w/ temperature of 37- 40°C (do not exceed 42°C)• Leave in for 20-30min, when the extremity should become pliable and

erythematous– Face

• Apply moistened compresses soaked in warm water

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Post-thaw

• Tetanus prophylaxis• Local wound care– Apply topical aloe vera cream q6hr (interrupts arachidonic

acid cascade)– Affected digits should be separated w/ cotton and wrapped

w/ sterile, dry gauze– Dry, elevate and splint– Blister removal is controversial

• Consider drainage of nonhemorrhagic bullae that interfere w/ movement

• Never debride hemorrhagic bullae

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Post-thaw

• Systemic care– Hydrotherapy at 37°C tid– Streptococcal prophylactic Pen G 500kU IV q6hr– Intra-arterial tPA reduces digit amputation rate– Phenoxybenzamine to reduce vasospasm

• Surgery– Monitor compartment pressures– Amputation

• May be required if wet gangrene or infection occurs• Usually not performed until full demarcation occurs (3-4 wk)

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Sequelae

• Acute– Rhabdomyolysis, ATN, Electrolyte fluxes – Core temperature afterdrop– Compartment syndrome

• Chronic– Neuropathic pain/dysesthesias, thermal sensitivity– Autonomic dysfunction (Hyperhidrosis, Raynaud’s)– MSK (atrophy, tenosynovitis, strictures, OA)– Derm (edema, ulcers, delayed cancers)

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NON-FREEZING INJURIES

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Pernio (Chillblains)

• Background• Mild but uncomfortable inflammatory lesions

of skin– Caused by long-term intermittent exposure to

damp, nonfreezing ambient temperatures

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Pernio• Symptoms

– Tingling, numbness, pruritus, burning paresthesias

– Cutaneous manifestations appear up to 12hr after acute exposure:

– Localized edema, erythema, cyanosis, plaques, nodules• May progress in rare cases to

ulcerations, vesicles, and bullae– Rewarming may result in

formation of tender blue nodules which may persist for days

• Treatment• Affected skin should be

rewarmed, gently bandaged, and elevated

• Nifedipine 20mg PO TID may be helpful as both prophylactic and therapeutic tx

• Topical corticosteroids and oral steroid burst have been shown to be useful

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Cold Panniculitis

• Prolonged exposure to temp >freezing leads to mild necrosis of subcutaneous fat tissue

• Seen in children (popsicles) and women involved in equestrian activities

• Resolution may result in adipose fibrosis w/ cosmetic defects– There is no treatment

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Trench Foot (Immersion Foot)

• Background• Develops slowly over hours-days when foot is

exposed to cold/wet conditions• Reversible injury may progress to irreversible

injury

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Trench Foot• Clinical Features

– Tingling/numbness is initial symptom– Foot appears pale, mottled, anesthetic, pulseless, and immobile

• Initially does not change after rewarming– Hyperemic phase begins w/in hr after rewarming

• Assoc w/ severe burning pain and reappearance of proximal sensation– As perfusion returns to foot over 2-3d edema and possibly bullae may form– Anesthesia persists for weeks and may be permanent; gangrene may occur

• Treatment– Keep feet clean, warm, dryly bandaged, elevated– Monitor for signs of infection