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PGY1 Environmental Injuries Block > Environmental > Flashcards

Flashcards in Environmental Deck (190):

Four mechanisms of heat transfer

Conduction: direct physical contact
Convection: heat loss to air and water vapour
Radiation: heat transfer by electromagnetic waves
Evaporation: conversion of liquid to gaseous phase


What 3 distinct functions regulate body temperature

Thermosensors: located peripherally and centeally; skin and in periodic anterior hypothalamus
Central integrative area: CNS creates set point
Thermoregulatory effectors: sweating and peripheral vasodilation


What are predisposing factors for classic heat stroke

Advanced age
Psychiatric conditions
Chronic disease
Certain medications

Dehydration (vomiting, diarrhea, diuretics)

Drugs (anticholinergics), skin disease, occlusive clothing

Increased heat production: exercise, drugs (synpathpmimetics), fever, delirium, thyroid storm, MH, NMS, seizures

Cardiac disease, BB drugs

Hypothalamic hemorrhage

Atherosclerosis, diabetes


What percentage body weight loss represents moderately severe deficit



What percentage body weight loss represents severe water depletion

7% or more


What is prickly heat

Acute inflammatory disorder of skin that occurs in tropical climates due to blockage of sweat gland pores by macerated stratum Cornell and secondary staphylococcal infection - aka miliaria, lichen tropicus, heat rash


Clinical presentation of prickly heat

Prurituc vesicles on erythematous base confined to clothed areas, area often anhidrotic


Ddx of prickly heat

Contact dermatitis
Allergic reaction


Treatment of prickly heat

Chlorhexidine in a light cream or lotion

Salicylic 1% acid can be applied to localized areas to assist in discrimination but not use in children or large areas due to risk of salicylate intoxication

Aretha Myson can use for diffuse for posture the rest of us


What are heat cramps

Brief intermittent and often severe muscle cramps occurring and muscles fatigue by heavy work


Risk factors for heat cramps

He cramps typically caused by salt deficiency in person to produce large amount of thermal sweat and drink copious amounts of hypertonic fluid
Often occur after exercise and while relaxing
Occupations often affected our athletes roofers steel workers coal miners field workers and boil operators


Ddx for heat cramps

Hyperventilation tetany can be distinguished by the presence of carpopedal spasm's and paraesthesias in the distal extremities and Perioral areas


Essentials of diagnosis of heat cramps

Cramps of most worked muscles
Usually occur after exertion
Heavy sweating during exertion
Copiius hypertonic fluid replacement
Hyperventilation not present and cool environment


Investigations for heat cramps


They often have hyponatremia, hypochloremia


Treatment of heat cramps

Mild cases without dehydration treated or early with 0.1% or 0.2% salt solution or one quarter to one half teaspoon of salt all dissolved in 1 quart of water
Severe cases respond rapidly to IV NS


What is heat edema

Hydrostatic pressure and vasodilation of cutaneous vessels in heat resulting in accumulation of interstitial fluid in Lower extremities


Ddx of heat edema

CHF, liver disease states,lower extremity infections, DVT


What is heat syncope

Loss of consciousness and presence of heat exposure due to cutaneous vasodilation


What are the two types of heat exhaustion

Water depletion heat exhaustion and salt depletion heat exhaustion

Water caused by too little replacement

Salt caused by replacement of hypotonic fluid


Diagnosis of heat exhaustion

Symptoms of vague malaise fatigue and headache
Core temperature often normal and if elevated is under 40°C
Mental function essentially intact no coma or seizures
Tachycardia orthostatic hypotension and clinical dehydration may occur
Other major illness ruled out
If in doubt treat as heat stroke


Investigations in patient with heat exhaustion

Electrolytes: hyponatremia, hypochloremia, and the low urinary sodium and chloride concentrations
CPK in renal function, hepatic transaminases


Management of heat exhaustion

Cool environment
Assessment of volume status
Fluid replacement: normal Celine to replete volume if patient is orthostatic, replace slowly to avoid cerebral edema
Healthy young patients are treated as Outpatients
Consider admission efficient is older, has significant electrolyte abnormalities or would be at risk for recurrence if discharged


What is the difference between heat exhaustion and heatstroke

Homeostatic thermoregulatory mechanisms remain intact in heat exhaustion

Heat stroke is when mechanism fails


diagnosis of heat stroke

Exposure to heat stress, endogenous or exogenous
Signs of severe CNS disfunction (coma seizures delirium)
Core temperature usually above 40.5 Celsius but maybe lower
Hot skin calming and sweating may persist
Marked elevation of hepatic transaminase levels


What are the two forms of heat stroke

Classic and exertional


Characteristics of exertional heat stroke

Younger healthy individuals
Acute renal failure
Marked lactic acidosis


Features of classic heat stroke

Older individuals with predisposing factors or medications
Heat wave occurrence
Mild coagulopathy
Mild to CK elevation
Mild acidosis
Normal calcium


Ddx of heatstroke

CNS hemorrhage
Toxins, drugs - anticholinergic poisoning, sympathomimetics
Malignant hyperthermia
Neuroleptic malignant syndrome
Serotonin syndrome
Thyroid storm
High fever, sepsis
Encephalitis, meningitis
Typhoid fevers
Delirium tremens
Hypothalamic hemorrhage


Investigations for patient with heat stroke

ABG, CBC, lytes- extended, glucose, urea/Cr, CK, myoglobin and UA, transaminases, PTT, INR, lactate, troponin


How to cool patients with heat stroke

Preferred method : evaporative with large fans and skin wetting ; ice water immersion

Ice packs to axilla and groin
Cooling blanket
Peritoneal lavage
Recital lavage
Gastric lavage
Cardiopulmonary bypass


Resuscitation of a patient with heat stroke

Airway control - seizures and aspiration common

Crystalloid fluid resus

Tachyarrhythnias usually resolve with cooling - avoid cardio version until myocardium cooled, avoid used of alpha adreneriv agents becuase they promote vasoconstriction and decrease cutaneous heat exchange and may exacerbate renal and hepatic damage
Atropine and antichokinfeics that inhibit sweating should be avoided

If rhabdo keep urine output at least 2ml/kg/he

Urinary alkalinization considered in patients with acids is, dehydration, or underlying renal diseS

Can give mannitol after volume to increase intravasuckar volume and gfr but don't use if oliguria

Benzos for shivering


What percentage of dogbite get infected and which sites are at higher risk

2 to 30%
Hand bites are at higher risk for infection
Face and scalp or a lower risk for infection
Puncture wounds at higher risk for infection than avulsions and lacerations


What types of bacteria are typically involved in dogbite wound infection

Often polynicrobial
Other aerobics: strep, staph, Neisseria, Corynebacterium, Moraxella
Anaerobic: Fusobacterium, Bacteroides, Porphyromonas, Prevotella, and Propionibacterium

Capnocytophaga canimorsus


3 days typically (can be 1-10 after bite) pt develops fever, V/D, abdo pain, headache, confusion with purpuric lesions

Can also progress to endocarditis, meningitis

Capnocytophaga canimorsus


What patients typically affected by capnocytophaga canimorsus

Middle aged men
Underlying medical problems most often alcoholism, splenectomy, or immunosuppression


What factors are high risk for bite wound infection

Species: cat, human, monkey, pig, camel, bear
Location: hand, foot
Wound type: puncture, crush injury, presence of divitalized tissue, delayed presentation (6 hours later), closed primarily
Patient characteristics: age over 50, diabetes, renal failure, liver dz, alcoholism, immune disorder, malnutrition, use of steroids or immunosuppressants, peripheral vascular disease, chronic edema of bitten area


What antibiotics to use for dog bite and next lines if pen allergic

Clindamycin + septra or cipro


Antibiotics for dog and cat bites requiring hospital admission


Clindamycin + cipro or septra


Indications for admission after animal bite

- injury to deep structures (bones, joints, tendons, arteries, nerves)
- injury requiring reconstructive surgery
- injuries requiring GA for appropriate wound care

- rapidly spreading cellulitis
- significant lymphangitis or lymphadenitis
- infection of patients at high risk for complications
- infection with failed outpatient therapy


Antibiotic prophylaxis for human and monkey bites

Clindamycin plus penicillin or cipro


Antibiotics for human and monkey bite if requires admission

Clindamycin plus pen or cipro


Antibiotic prophylaxis and inpatient treatment of rodent bites

Not recommended


Treatment of ferret, pig, horse, bear, big cats, coyotes, wolves bites

Same as dog / cat


Abx prophylaxis after camel bite and treatment if admitted


And inpatient to same as cats and dogs


Rate of dog bite infection



Rate of cat bite infection



What is the major concern for exposure in monkey bites and what is it

B virus which is similar to HSV and causes vesicular lesions at site of exposure with flu like symptoms incubation period 2 days to 5 weeks

Can develop paresthesiS and muscle weakness

CNS involvement can occur which include AMS, CN palsies, ataxia, coma, respiratory failure

If left untreated mortality rate is 80%


Management of monkey bites

Area scrubbed with soap, or iodine, chlorhexidine then irrigated with running water for 15-20 mins

Prophylaxis with valacyclovir after high risk bites can be offered up to 5 days after bite but should be started ASAP


Treatment of suspected B virus infection

IV acyclovir or ganciclovir


When is prophylaxis for monkey B virus recommended

Skin exposure (with loss of skin integrity) or mucosal exposure to a high risk source (macaque that is ill, immunocompromised, known to be shedding virus or lesions compatible with B virus)

Inadequately cleaned skin exposure or mucosal exposure to any macaque

Deep puncture bite

Laceration of head, neck, torso

Needle stick associated with tissue or fluid from the nervous system, eyelids, mucosa, or lesions suspicious for B virus

Puncture or lacerations after exposure to objects contaminated with either fluid from monkey oral, genital, or nervous system tissues or any object known to be contaminated with B virus

A post wound cleaning culture is positive for B virus


What other situations can prophylaxis be considered for monkey virus B exposure

Mucosal splash that has been adequately cleaned
Laceration that was been adequately cleaned
Puncture or lac occurring after exposure to either objects contaminated with body fluid or potentially infected cell culture


Dosing for monkey virus B prophylaxis

Valacyclovir 1g TID for 14 days

Or acyclovir 800ng five times a day for 14 days


When is monkey virus B prophylaxis not recommended

Skin exposure when skin remains in tact

Exposure associated with non macaque species of non human primates


What is rat bite fever

Caused by Streptobacillus moniliformis or Spirillum minus

Can occur by bite, scratch or simply handling a rat
Incubation 3 days to 3 weeks

Fever, migratory polyarthralgias, maculopapular, petechial, or purpurin rash

Untreated has 10% mortality


Treatment of rat bite fever

IV penicillin

Streptomycin and tetracycline in penallergic patients


Rates of infection after clenched fist injury (fight bite)

Osteomyelitis- 16%
Septic arthritis- 12%
Tenosynovitis - 22%


Management of bites to oral mucosa or through and through injury

Prophylaxis of penicillin for lacs requiring primary closure and those that result in mucocutaneous communication


Bacteria found in human bites

Eikenella corrodens

Staph, strep, corynebacterium, fusobacterium


Work up of fight bite

Hand X-ray to look for retained teeth, deep structure injuries


When can you suture dog bites

Most except hands and feet


When to suture cat bite

Face only


When can you suture human bite or monkey

Fave only (up to 24 h after bite)


When to suture rodent bite

Any but rarely needed


When to suture ferret, pig, horse, camel, bear, big cats

Face only


Management of fight bite

Wound exploration through entire ROM, including closed fist when fingers are flexed, because extensor tendons and cartilage damage may not be evident in other positions

If joint, tendon or bone injury should be admitted for open debridenent and irrigation in OR - same if they present later with infected wound

think about post exposure prophylaxis if either party is known HIV positive or at high risk and blood exposure occurred, prophylaxis also indicated if HBV positive or high risk or blood/saliva exposure has occurred


Indications for admission for human bites to the hand

Infection at time of Presbyterian
Deep structure violations
Wound requiring OR
Patients at high risk for wound infection
Patients with likely social support or compliance issues


components of a focused Dive history

onset of symptoms?
type of equipment used - compressed air, mixed gas, enriched air, rebreather ? - what was source of gas
did dive approach or exceed decompression limits
was a dive computer used?
what were the number, depth, bottom time, total time and surface intervals for all dives in the 72 hours preceding symptoms
were decompression stops used? was in-water decompression attempted?
what was the time delay from last dive to air travel?
did diver experience difficulty with ear or sinus equilibration ? did pain occur n descent or ascent
was diver intoxicated, dehydrated, or working strenuously
how long after dive did symptoms start, were they present at surfacing, delayed? progressive?
is med hx of ear or sinus infections or abnormalities present? emphysema or asthma ? CAD? PFO ? neuro illness?


disorders that occur during descent when diving

middle ear barotrauma
external ear barotrauma
inner ear barotrauma
facial barotrauma


disorders that arise at depth when diving

nitrogen narcosis
oxygen toxicity
contaminated air


disorders that arise during ascent when diving

alternobaric vertigo
GI barotrauma
pulmonary barotrauma
decompressino sickness
arterial gas emoblism
pulmonary edema


What happens in middle ear barotrauma when diving

During descent - unsuccessful equalization causes pressure on tm,

Can cause tm rupture leading to cold water entering middle ear and causing caloric stimulation with transient nystagmus and vertigo - can also lead to 7th nerve palsy


What happens in external ear barotrauma when descent diving

When external auditory canal is obstructed by wax, stenosis, etc it can trap air and cause negative pressure leading to pain and or hemorrhage of the EAC


What happens in inner ear barotrauma upon descent when diving

Large negative pressure builds and inward deflection of tm transmits to oval window of cochlea which causes a pressure wave in perilymph which distended round window - sudden equlibratipn or valsalva and lead to hemorrhage in inner ear or tear the labyrinthine (reissner's) membrane

Symptoms are hearing loss, vertigo, nausea, tinnitus and fullness in affected ear
Signs bare nystagmus positional vertigo ataxia and vomiting

Can be challenging to distinguish from inner ear DCS


What is barosinusitis which occurs on descent in diving

Obstruction of sinus Ostia causes sinus barotrauma
Most often maxillary or frontal sinus and causes facial pain and epistaxis


What happens with facial barotrauma with descent from diving

Pressure within dive mask over eyes and nose - if don't equalize can cause facial and conjunctival edema, petechial hemorrhages on face and subconjunctival hemorrhage


What is nitrogen narcosis

Intoxicating effects of increased tissue nitrogen concentration at depth

Euphoria, false feeling of well being, confusion, loss of judgement or skill disorientation inappropriate laughter diminished motor control and tingling in the vague treatment numbness of the lips and gums and legs
Occurs typically at deptus below 150 feet


What happens with oxygen toxicity during descent in diving

Pulmonary oxygen toxicity can present with burning sensation or pain on inspiration and coughing ; pneumonitis and permanent fibrosis are possible

CNS toxicity also occurs


What are possible air contaminants in scuba

CO and CO2 can contaminate compressed air tank
Rebreathera have Ca(OH)2 which if inhaled the particles form a caustic liquid


What happens in alternobaric vertigo

On ascent, passive equalization of middle ear doesn't occur properly because of mucosal edema or thickening within the Eustachian tube

Pt gets vertigo, N/V


What is barodontalgia

Air gets trapped beneath poorly filled dental cavity or abscess and expands on ascent leading to dental pain


What occurs in GI barotrauma

On ascent , bowel gas expands
Predisposing factors: carbonated beverages, large meals or gas producing foods, valsalva in head down position

Symptoms- eructation, flatulence, bloating, cramps abdominal pain, can get trapped in hernia and gastric rupture possible


What occurs in pulmonary barotrauma

Gas bubbles forced across alveolar capillary membrane

Can cause pneumothorax , pneumomediastinum, subq emphysema, and alveolar hemorrhage

Suggestive dive features: fast ascent, panic, problems regulating buoyancy, or running out of air; pts with lung disease at risk


Factors that increase barotrauma in asthmatics

Bronchospasm and mucus plugging predispose local regions of lung to injury

When air is compressed it becomes denser, more turbulent flow in narrow airways

Reduction in breathing capacity with immersion

Air from compressor is cooled and may trigger bronchospasm in asthma

Exercise component of diving can trigger asthma

Compressed air may be contaminated by pollen and other allergens


Diving recommendations for asthma patients

Thorough h/p by physician
Asthma well controlled
Normal spirometry: FEV1 above 80%, FEV1/FVC > 75%
Succeafufl completionbof bronchial provocation challenge
Cold, exercise or emotion induced asthmatics shouldn't dive
Asthmatics requiring rescue med within 48 hours should not dive


What is decompression sickness

Spectrum of clinical illnesses resulting from formation of small bubbles of nitrogen gas in the blood and and tissues ascent


What are risk factors for decompression sickness

Increased length and depth of dive
Heavy exertion
Cold ambient temperatures after diving
Diving at high altitude
Flying after diving
Tobacco and alcohol use


What is difference between DCS type I and II

1 involves MSK, skin and lymphatic vessels

2 involves any other organ system


What is arterial gas embolism

When air bubbles escape pulmonary venous circulation and proceed to LA and LV into arterial circulation

Most common presentation is altered consciousness, dizziness, convulsions, visual changes

Can affect cerebral or cardiac circ


Dive history features to differentiate between DCS and AGE

DCS: depth and length dependent, decimpression limits approached , flying after diving, diving at altitude

AGE: independent of dive profile, rapid ascent, inexperience, out of air


Risk factors to differentiate DCS and AGE

DCS: fatigue, dehydration, fever, hypothermia, obesity, strenuous activity

AGE: obstructive lung disease, emphysema, mucus plugging, PFO


Symptoms and signs differentiating DCS and AGE

DCS: progressive onset, spinal symptoms predominate, ha, limb weakness or paralysis, paresthesias, abdo pain, urinary retention, fecal incontinence, periarticular joint pain, skin marbling,vertigo or nystagmus

AGE: rapid onset, cerebral symptoms predominate, ha, LOC, confusion, convulsions, motor or sensory loss, cardiac dysthymias or arrest


Why does DCS affect spinal Cord more than CNS

Nitrogen lipophilic and increased concentration of lipids in spinal cord


Extra physical exam maneuver to help with DCS I if complaining of joint pain

Put bp cuff over joint and inflate to 150-200 - pt may experience relief if due to bubble in joint


Management of patients with suspected dive injuries

100% O2 until pulmonary barotrauma or DCS ruled out if vitals stable

ACLS if unstable

Call DAN

Rehydration if suspected nonpulmonary DCS (chokes)

Recompression when indicated


Diving disorders that require recompression therapy

DCS I and II
Contaminated air (CO poisoning)


Management of external ear barotrauma, middle ear barotrauma and internal ear barotrauma

External ear- clean external canal and remove foreign bodies
Middle ear - topical nasal vasoconstrictors like phenylephroje and oxymetalozine and repeated maneuvers to displace fluid through the eustschian tube
If ruptured tm, prophylactic oral abx
Oral steroid if CN7 palsy

IEBT- bed rest for 5-7 days with head elevated, avoid straining, decongestants to facilitate draining of middle ear, refer to otolaryngology


define drowning

the process of experiencing respiratory impairment from submersion/immersion in liquid


define immersion syndrome

syncope resulting from cardiac dysrhythmias on sudden contact with water that is at least 5C lower than body temperature

proposed cause: vagal stimulation leading to systole and VF secondary to QT prolongation after massive release of catecholamines on contact with cold water


risk factors for drowning

age: toddlers and those over 75
boys account for 80% of victims older than 1 year old
aboriginal for all age groups
black 11-12 year olds drown 10x more often than white kids
EtOH consumption
time of year- May-August in US
more likely on weekends
medical conditions: seizure disorders, autism and other developmental/behavioural disorders
cold water - increased dysrhythmia in those with long QT


pathophysiology of drowning

submersion -> breath holding, panic --> air hunger and hypoxia develop --> victim swallows water

aspiration of -2ml/kg of fresh or salt water destroys pulmonary surfactant leading to alveolar collapse, atelectasis, noncardiogenic pulmonary deem, intrapulmonary shunting and VQ mismatch
profound hypoxia and metabolic and respiratory acidoses ensure, leading to CV collapse, neuronal injury and death


factors influencing the pathophysiology of drowning which may affect survival

age: children lower ratio of body mass to surface area and therefore develop hypothermia more quickly and to a greater degree
water temp: cold water speeds the development of exhaustion, altered consciousness, and cardiac dysrhythmias
duration and degree of hypothermia: hypothermia lowers cerebral metabolic rate and is neuroprotective; however hypothermia usually poor prognostic factor
diving reflex: infants/children- immersion of face in cold water shunts blood centrally to heart and brain - apnea and bradycardia ensue, prolonging the duration of submersion tolerated without CNS damage
effectiveness of resuscitation efforts


prognostic factors in drowning

hypoxia which is dependent on submersion time is most important factor affecting outcome and QOL

poor outcome: age under 3, submersion longer than 5-10 minutes, and initiation of CPR more than 10 mins after rescue

neuro findings on initial presentation + victims whose submersion or resus longer than 10 mins usually unfavourable outcome

objective findings with poor prognosis: hypothermia, severe acidosis, unreactive pupils, GCS 3, asystole, or need for ongoing CPR

children with abnormal head CT (ICH, cerebral deem) within first 24 hours have nearly 100% mortality rate

abnormal CT at any time correlated with poor outcome (death or persistent vegetative state)


DDX/considerations in drowning

precipitants of drowning: EtOH, cardiac arrest, hypoglycaemia, seizure, attempted suicide or homicide

peds: child abuse or neglect

potential head or C spine injury


work up of drowning

cardiac monitoring and ECG to look for dysrhythmias , QT prolongation or ischemia
pulse ox, capnography, and ABG to look for hypoxemia, hypercarbia, and acidosis

glucose, Cr, lytes
EtOH, urine tox

subsequently, evidence of renal failure, hepatic dysfunction and DIC may be noted (N on initial labs)

CXR - repeat as infiltrates and deem may be evident within hours

EEG to assess for seizure activity in obtunded drowning victims
CT head rarely contributory initially unless significant trauma

MRI not prognostic until 3 or 4 days elapse


which drowning patients at risk for C spine injury and who needs a collar

ones who have clinical signs of serious trauma or hx of MVC, fall from height or diving into water - collar these ones, not needed if none of these risk factors present


indications for intubation of drowning patient

apparent or developing respiratory distress, absence of protective airway reflexes, significant associated head or chest injuries, PaCO2 > 50, unable to maintain sat above 90 or PaO2 < 60 on high flow, requiring PPV


when to use empirical abx in drowning patient

they do not increase survival so only in patient who was submerged in grossly contaminated water or who shows signs of infection or sepsis


management of drowning patient after resus

rewarming should not go above 34C, followed by 24 hour mild hypothermic treatment before normothremia causes decreased pulmonary reperfusion injury and reduced secondary brain injury


which drowning patients can be discharged from ED

asymptomatic on presentation to ED, maininta normal O2 sat on room air, no CXR or ABG abnormalities after observing them for 6 hours


define hypothermia

core temp below 35C


factors predisposing to hypothermia

decreased heat production:
endocrine failure
insufficient fuel
extreme exertion
neuromuscular inefficiency
age extremes
impaired shivering
lack of adaptation

increased heat loss:
non immersion
induced vasodilation
exfoliative dermatitis
emergency deliveries
cold infusions
heat stroke treatment

impaired thermoregulation:
peripheral failure
acute spinal cord transection
central failure, neuro
CNS trauma
hypothalamic dysfunction
Parkinson's disease
anorexia nervosa
cerebellar lesion
congenital intracranial abnoramlities

miscellaneous associated clinical states:
recurrent or episode hypotehrmia
CP disease
vascular insufficiency
Paget's disease
shaken baby syndrome
multisystem trauma
Shapiro's syndrome
Wernicke-Korsakoff syndrome
Hodgkin's disease


heat conservation mechanisms by temperature range

30-37C - vasoconstriction, shivering, and non shivering basal and endocrinology thermogenesis create heat

24-30C- progressive depression of basal metabolic rate without shivering

below 24- autonomic and endocrinology mechanisms for heat conservation become inactive


physiologic effects of hypothermia on CV system

initial tachycardia followed by progressive bradycardia
pulse decreases by 50% at 28 C

atrial and ventricular dysrhythmias common in moderate or severe hypothermia


ECG findings of hypothermia

Osborn (J) wave seen at junction of QRS complex and ST segment

as hypothermia worsens PR interval, then QRS interval, then QTc become prolonged


DDX for J waves on ECG

local cardiac ischemia
CNS lesions


what is core temp afterdrop

decrease in individual's core temp after removal from cold, temperature equilibration by conduction and countercurrent cooling of blood perfusing cold tissues results in greater decrease in core temp


how to prevent core temperature afterdrop

active external rewarming of extremities abolishes peripheral vasoconstriction and reverses AV shunting


physiologic effects of hypothermia on CNS

hypothermia depresses CNS
EEG silence at 19-20C
cerebral auto regulation maintained with an increased in vascular resistance until 25C


physiologic effects of hypothermia on kidneys

exposure to cold induces a diuresis


physiologic effects of hypothermia on respiratory system

stimulates respiration followed by progressive decrease in respiratory minute volume

CO2 production decreased by 50% with an 8C decrease in temp

CO2 retention with resp acidosis can occur

vicious bronchorrhea, decreased ciliary motility, and noncardiogenic pulmonary edema


clinical presentation of hypothermia by system

HEENT: mydriasis, decreased corneal reflexes, EOM abnormalities, erythopsia, flushing, facial deem, epistaxis, rhinorrhea, strabismus

CV: initial tachycardia, subsequent bradycardia, dysrhythmias , decreased heart tones, hepatojugular reflux, JVD, hypotension

resp: initial tachypnea, adventist sounds, bronchorrhea, progressive hypoventilation, apnea

GI: ileus, constipation, abdo distension or rigidity, poor rectal tone, gastric dilation in neonates or in adults with myxoedema

GU: anuria, oliguria, polyuria, testicular torsion

neuro: depressed LOC, ataxia, hypesthesia, dysarthria, antinociception, amnesia, initial hyperreflexia, areflexia, central pontine myelinolysis

psych: impaired judgment, perseveration, mood changes, peculiar flat affect, AMS, paradoxical undressing, neuroses, psychoses, suicdie, organic brain syndrome

MSK: increased muscle tone, shivering, rigidity or pseudo-rigor mortis, opisthotonos, compartment syndrome

derm: erythema, pernio, pallor, frosting, cyanosis, frostbite, icterus, popsicle panniculutis, sclera, cold urticaria, ecchymosis, necrosis, deem, gangrene


what reflex is last to disappear and first to reappear in hypothermia

knee jerk


DDX of hypothermia

hypothyroidism, hypopituitarism, diabetes, hypoglycaemia, malnutrition, intracranial and spinal cord injuries and sedative/hypnotic and EtOH intoxication
infection: GN sepsis, pneumonia, meningitis, encephaltiis, endocarditis, brucellosis, malaria, syphillis, typhoid, military tb, trypanosomiasis
carcinoma, pancreatitis, peritonitis, and cerebrovascula disease
low CO from MI can cause hypothermia
MgSO4 during labour
delayed recovery from NM blockade


lab workup of hypothermic patient

glucose, CBC, lytes, lipase, coags, urea/Cr, VBG
EtOH level, urine too if LOC inconsistent with degree of hypothermia
thyroid functions, cardiac markers and serum cortisol may also be indicated


changes in heme labs in hypothermic patient

HCT increases 2% for every 1C fall in temp, so if pt HCT is low-normal, consider blood loss
decreased WBC and platelet counts due to sequestration

hyper coagulable state - can progress to DIC, enzymatic activity of activated clotting factors is depressed by the cold


what to suspect if hypothermic patient remains hyperglycemic during rewarming

hemorrhagic pancreatitis or DKA


how to interpret ABG in hypothermic patient

blood gases analyzer warms sample to higher O2 and CO2 samples and lower pH than in vivo

target to uncorrected pH of 7.4, PaCO2 of 40


how to treat coagulopathy in hypothermia patient

rewarm them is ONLY treatment
do not give clotting factors


management of hypothermic patient

monitor with continuous core temp - rectal 15cm or esophageal
cardiac US prior to startgin compressions
intubation as necessary, NG tube afterward
continuous cardiac monitoring
catheter for urine output
IV fluids- warm 500cc NS bolus
ACLS- CPR until warm, if pt in VF can defibrillate x 1 and then warm to above 30C and further attempts can be made, don't use epinephrine below 30
treatment of ventricular dysrhythmias - amio can increase torsades, procainamide can increase VF, but quinidine has been shown to prevent VF during induced profound hypothermia and during cardiac manipulation at 25-30C
pacing- transcutaneous pacing ; don't do transvenous because hazardous for bradydysrhythmias
abx: empirical if under 3 months, older adults as well, treat any cellulitis, myositis, bacteriuria or infiltrate on CXR in other ages
hydrocortisone 100mg IV if failure to rewarm and suspect adrenal insufficiency or steroid dependence
thyroid if pt thought to have myxoedema - or if hx hypothyroidism, neck scar or failure to rewarm


what is leading cause of failure to rewarm in hypothermic patietn



what is passive external rewarming and when is it used

used in patients with mild hypothermia and active rewarming is not available

covering the patient in an insulating material in a favourable atmospheric condition, ambient temp should exceed 21C


what is active rewarming

direct transfer of exogenous heat to the patient - can be internal or external


indications for active rewarming

CV instability
moderate or severe hypothermia (<32C)
inadequate rate of rewarming or failure to rewarm
endocrinologic insufficiency (hypopituitarism, hypothyroidism, hypoadrenalism, and Wernicke's)
traumatic or toxicological peripheral vasodilation (spinal cord transection )
secondary hypothermia impairing thermoregulation (i.e.. stroke) (DKA because insulin not effective until T > 30C)


how to rewarm hypothermic patients

AER - ie. bair hugger - forced air warming that transfers large amount of heat and minimizes after drop
heated humidified O2 and warmed IV fluids in addition to AER may help prevent hypoxia, metabolic acidosis, core temp after drop and hypotension

AER + 1 or more active core rewarming for moderate to severe hypothermia

airway rewarming - heated humidified O2
peritoneal dialysis with dialyste at 40-45C
heated irrigation- thoracic lavage
endovascular rewarming
extracorporeal blood rewarming


freezing injury cascade

prefreeze phase: superficial tissue cooling, increased viscosity of vascular contents, microvascular constriction, endothelial plasma leakage

freeze-thaw phase: ECF ice crystal fluid formation, water movement across cell membrane, intracellular dehydration an dheyperosmolality, cell membrane denaturation or disruption, cell shrinkage and collapse

vascular stasis and progressive ischemia:


predisposing factors for peripheral cold injury

physiologic: genetic, core temp, previous cold injury, acclimatization, dehydration, overexertion, trauma-multisystem, extremity, dermatologic disease, physical conditioning, diaphoresis, hyperhidrosis, hypoxia

mechanical: constricting or wet clothing, tight boots, vapour barrier, inadequate insulation, immobility or cramped position

psychological: mental status, fear, panic, attitude, peer pressure, fatigue, intense concentration on tasks, hunger, malnutrition, intoxicants

environmental: ambient temperature, humidity, duration of exposure, wind chill factor, altitude and associated conditions, quantity of exposed surface area, heat loss- connective, evaporative, aerosol propellants, CV, hypotension, atherosclerosis, arteritis, Raynaud's, cold-induced vasodilation, anemia, sickle cell disease, diabetes, vasoconstrictors, vasodilators


define frostnip

superficial freezing injury manifested by transient numbness and tingling that resolves after rewarming
no tissue destruction occurs


favourable initial symptoms after rewarming cold injury

normal sensnation, warmth and color

early formation of clear fluid filled blebs is more favourable and than delayed appearance of smaller, more proximal hemorrhagic vesicles that are produced by damage do to subdermal vascular plexi


work up of patient with frostbite

lab testing and imaging for coexisting conditions and injuries

Xray baseline of frostbite tissue - f/u in 4-10 weeks may begin to demonstrate specific frostbite abnormalities

pts being considered for lytics should undergo CTA or MRA


sequelae of frostbite and nonfreezing cold injuries

neuropathic: pain (phantom pain, CRPS, chronic pain), sensation (hypesthesia, dysesthesia, parenthesis, anesthesia), thermal sensitivity, autonomic dysfunction (hyperhidrosis, Raynaud's)

MSK: atrophy, compartment syndrome, rhabdomyolysis, tenosynovitis, stricture, epiphyseal fusion, OA, osteolytic lesions, subchondral cysts, necrosis, amputation

derm: edema, lymphedema, chronic or recurrent ulcers, epidermoid or squamous cell carcinoma, hair or nail deformities

misc: core temp afterdrop, ATN, electrolyte fluxes, psychological stress, gangrene, sepsis


prehospital mgmt of frostbite/cold injuries

remove constricting/wet clothing and insulate/immobilize affected area
massage NOT effective and increases tissue loss
frozen parts kept away from dry heat sources during transport
do not rewarm in field if any possiblign that thawing will be incomplete or that tissue will refreeze during evacuation
when evacuation not possible - rapid field rewarming in water at 37-39C


ED rewarming protocol of frostbite/cold injuries

prethaw: assess Doppler pulses and appearance, protect part - no friction massage, stabilize core temp, address med/surg conditions, administer volume replacement pre

thaw: provide parenteral opiate analgesia as needed, administer ibuprofen 400-600mg (or asa 325)
immerse part in water at 37-39C
encourage gentle motion but do not massage

dry and elevate, aspirate or debride clear vesicles, decried and apply topic antibiotic or sterile aloe vera q6h, leave hemorrhagic vesicles in tact
tetanus prophylaxis
provide strep prophylaxis if high risk
consider phenoxybenzamine in severe cases
performing imaging including angiography if lysis may be indicated
carrot out thrombolysis if indicated and available
obtain admission photographs


what is pernio/chilblains

cold sores appear with 24 hours of cold exposure usually on face, dorsal on hands and feet and pretibial areas


treatment of pernio

v. painful may need opioids
nifedipine 20-60mg daily used in severe pernio


treatment of immersion injury

rewarm slowly
local cooling lowers metabolic requirements and improves pain and deem - cooling should be continued until hyperaemia resolves


what is the leading cause of death from altitude illness

high altitude pulmonary edema


factors influencing acute mountain illness

elevation and rapidity of ascent
prior acclimatization
individual genetic susceptiblity
sleeping elevation
duration of stay


what heights are deemed moderate and high and very high and extreme altitude

moderate: 5000-8000 feet
high: 8000-14000 feet
very high: 14000-18000 feet
extreme: over 18000


why does O2 change at higher altitudes

hypobaric hypoxia

occurs because Patm decreases at elevation and therefore partial pressure of O2 decreases


physiologic changes with occur with acclimatization to altitude

increase in minute ventilation - carotid bodies detect hypoxia within minutes of elevation and signal response control centre in medulla to increase ventilation

respiratory alkalosis develops, kidneys begin to excrete bicarbonate - acetazolamide enhances this excretion

hypoxia leads to release of catecholamines which increases CO, HR, SV, BP and venous tone

heme: increased Hb and #RBCs

increased 2,3-DPG, shifting O2-Hb dissociation curve, favouring release of O2 from blood to tissues; leftward shift caused by respiratory alkalosis counteracts this


timing of typical development of HACE and HAPE

2-4 days after exposure to high altitiude


Lake Louise criteria for the diagnosis of acute mountain illness

pt to have recently ascended to an elevation of 8000 feet, with headache PLUS one of: GI upset (anorexia, N/V), general weakness or fatigue, dizziness or lightheadedness, or difficulty in sleeping

h/a typically worse during night and on awaking or on suddenly becoming upright

timing: few hours after arrival at altitude and reaches max severity between 24-48 hours


DDX for acute mountain sickness

tension headache
viral prodrome
EtOH intoxication/toxidrome
CO poisoning
caffeine withdrawal
migraine h/a
infectious (mengintis, encephalitis/ viral syndrome)
intracranial hemorrhage or mass
CNS aneurysm
venous sinus thrombosis
abdominal process (ie. gastro)
AACG/ocular process


treatment of acute mountain sickness

should not ascend to higher sleeping altitude until symptoms resolve to allow acclimatization to occur (may take 1-4 days)

if pt develops neuro abnormalities or evidence of severe pulmonary deem - immediate descent indicated

supplemental O2 - lifesaving in severe

h/a - tx with asa, ibuprofen, acetaminophen

N/V- prochlorperazine cause stimulates HVR (hypoxic ventilatory response)

acetazolamide - prevents periodic breathing and eradicates insomnia; accelerates acclimatization

dexamethasone - only use when rapid ascent needed or in people with acetazolamide intolerance, does not improve acclimatization


prevention of acute mountain sickness

gradual ascent to allow acclimatizaiton
high carb diet
avoidance of EtOH or smoking
acetazolmaide if ascent is rapid or known history of recurrent acute mountain sickness - 250mg BID 24 hours before ascent and continuing for first 2 days at high altitude is effective


Clinical presentation of HAPE

Dyspnea at rest, cough, anorexia, cyanosis, rales, tachypnea, tachycardia
Usually 2-4 days after arrival at high altitude


Treatment of HAPE

Mild - may recover with bed rest
Moderate- bed rest and supplemental O2
Severe - O2 and descent, hyperbaric if available; if O2 and descent not possible then nifedipine 30mg SR q12h, consider acetazolamide 125-250 and tadalafil 10mg q12h



CO poisoning
Pleural effusion
AE of preexisting PH
Acute asthma flare
Acute exacerbation of valvular disease (insufficiency and stenosis)


Ultrasound findings in HAPE

Lung comet tails - B lines indicate extravascular water

Demonstration of high pulmonary artery pressure with normal LV function


CXR findings in HAPE

Unilateral infiltrates may be seen in mild cases, bilateral in more advanced
Involvement of RML most common
Pleural effusion may be present in severe cases


ECG findings in HAPE

Evidence of R sided heart strain
Right axis deviation, P wave abnormalities, tall R waves in precordial leads, S wave in lateral leads


Hemodynamic findings in HAPE

Increased pulmonary vascular resistance
Elevated PA pressures
Normal pulmonary wedge pressures


How does nifedipine help in HAPE

Lowers PA pressure, pulmonary blood volume, and pulmonary vascular resistance or enhance alveolar fluid clearance


Clinical presentation of HACE

Ataxia, severe headache, N/V, altered mentation, seizures, coma
Although severe symptoms usually develop within 1-3 days, may not occur until 5-9 days


Ddx of HACE

Acute CVA
CO poisoning
Intracranial mass
Vertebral/ carotid dissection or stenosis
Acute toxidrome - EtOH or other
Acute EtOH withdrawal/ DTs
Transient global amnesia


Treatment of HACE

Immediate evacuation to lower altitude, O2, bedrest, dexamethasone 8mg IV or Po then 4mg q6h, hyperbaric therapy if unable to immediately descend


Medical conditions that make travel to altitude contraindicated

Sickle cell anemia
Severe COPD
Symptomatic PH
Uncompensated CHF


Medical conditions that require caution when traveling to altitude

Moderate COPD
Asymptomstic PH
Compensated CHF
Morbid obesity
Sleep apnea syndromes
Troublesome arrhythmia
Stable angina or CAD
High risk pregnancy
Sickle cell trait
Cerebrovascular diseases
Any cause of restricted pulmonary circulation
Seizure disorder (not on meds)
Radial keratotomy


what are the 3 main epidemiological groups who get electrical injuries

toddlaers/younger children: low voltage injuries in household as a result of contac t wit electric sockets and cords

adolescents and young adults: high voltage injury y from contact with electic lines outside of houes

men in 3rd/4th decade due to occupational injuries to due to high voltage encounters


factors affecting electrical injury

circuit type: AC more dangerous than DC
resistance: different tissues have different resistance
current pathway
current duration


physical effects of different amperage levels

1mA- barely perceptible
6-9mA- usually range of let-go current
16mA- max current that an average person can grasp and let go
20mA- paralysis of respiratory muscles
100mA- VF threshold
2A- cardiac standstill and internal organ damage


electrical formulae- Joule's law

P= I^2RT



resistance of body tissues from lowest to highest

blood vessels


tips to avoid lightnin strike

seek shelter inside an enclosed building or metal-toped car
avoid large flat, open areas or hilltops
avoid contact with metal objects and remove metal objects such as jewelry or hairpins
avoid trees, boats and open water
if caught on open ground, curl up on your side with hands and feet close together to reduce contact points or squat with feet together; if possible place rubber raincoat under your body ro feet to reduce ground current effects
if in a forest, seek shelter under a thick growth of short trees
if indoors, avoid use of wired phones and contact with plumbing or electrical appliances


types of burns associated with electrical injury

entrance/exit site burns
arc burns
thermal burns
flash burns


ECG changes seen with lightning strike

ST segment elevation
QT interval prolongation
atrial fib
inverted or flattened T waves
MI pattern without cardiac sequelae


effects on CV system following electrical injury

sinus tachy or brady, a fib, ectopic beats, VF, asystole
transient ST segment elevation or depression that does not correlate with myocardial ischemia
resp arrest can occur as a result of tetanic paralysis of thoracic respiratory muscles


effects on head/neck in electrical injuries

ocular involvement -cataracts most common
vitreous/anterior chamber hemorrhages
retinal detachment
macular lacerations
corneal/conjuntival burns
sensorineural deafness
orofacial injuries in toddlers that eat cords - complication of delayed labial artery bleeding can occur 2 days after injury


extremity injuries caused by electrical injury

muscle necrosis
vascular injury - intima - immediate coagulative necrosis and thrombosis; media- aneurysmal dilation and hemorrhage in a delayed fashion
risk of compartment syndrome
bone injury- periosteal burns and osteonecrosis
DC current causes strong muscle contraction throwing victim away from source can cause fracture/dislocations; AC causes muscular tetany which can cause similar skeletal


nervous system effects of electrical injuries

CNS: altered mental status, seizure, coma
transient spastic paralysis, delayed/chornic: ascending paralysis, transverse myelitis, ALS
peripheral neuropathies
neuropsych: anxiety, depression, mood lability, difficulty concentrating, insomnia


CV effects of lightning injury

cardiac/resp arrest
myocardial contusion (most common)


what are Lichtenberg figures

superficial fernlike burns that occur in lightning strike burns


what is keraunoparalysis

lightning strike victim wakes up to find themselves on the ground unable to move limbs


effect of lightning strike on ears

TM commonly ruptured
bleeding and CSF leaks may accompany this injury
other effects: avulsion of mastoid process, ossicle damage, rupture of Meissner's membrane, strial degeneration
symptoms: hearing loss, tinnitus, vertigo and nystagmus


findings suggestive of a lightning strike

clothing wet from rain
tears or disintegration of clothing
multiple victims
typical arborescent pattern of erythema or superficial linear or punctate burns
tympanic membrane injury
cataracts, especially in a younger patient
magnetization of metallic objects on body or clothing
ECG changes


which electrically injured patients need further investigations

those exposed to high voltage sound
any voltage with: LOC, altered mental status or neuro deficits, significant symptoms, entrance and exit wounds and/or burns assessed as being more than superficial partial thickness burns


work up required for electrical injury patients

CBC, lytes, Cr/urea, troponin, myoglobin, UA for myoglobin

if suspected intraabdominal injury: hepatic/pancreatic enzyme levels, coags

Xray of injured extremities
CT/MRI indicated when intracranial, spinal, intra-abdominal or pelvic injuries clinically suspected


workup of patient with lightning injury

ECG of strike victims with high risk indicators: suspected direct strike, LOC, focal neuro complaint, chest pain or SOB, associated traumatic injuries, pregnancy and burns of the cranium or legs or on more than 10%
complaints of diffuse muscle pain or findings of compartment syndrome - evaluation for rhabdo and vascular insufficiency bearing in mind lightning has unique effects on vascular system that often clear without sequelae
cardiac markers often elevated but don't correlate with myocardial injury and are not prognostic


management of electrical injury patients

arrest - resus regardless of rhythm -good outcomes seen with asystole

fluid mgmt similar to crush injuries - IV crystalloids titrated to maintain urine output over 100mL/r in adults and 1.5-2ml/kg/hr in young children

monitor serum K in patients with renal insufficiency or myoglobinuria

if hypotensive- look for possible blood loss from traumatic injuries

who needs extra monitoring: ECG signs of cardiac inury/dysrhymia, more than minimal local signs and symptoms; peds pt with oral injuries hospitalize for hydration, wound and pain mgmt, plastic surg consult; pregnant patients should receive period of fetal monitoring

can pull out taser barbs with firm in line traction


management of lightning injury patients

can get extensive catecholamine release or autonomic stimulation - transient hypertension and tachycardia can be treated with BB, hydrazine or with alpha blockers

DC curent - transient vasospasm that results in blue, mottled, pulseless extremities - think about this when planning surgical intervention - may be TRANSIENT only

central line to assess volume status correctly as pulses extremities may limit ability to detect hypotension

can get fixed pupils, etc in absence of irreversible brain injury, so don't use this to prognosticate in resuscitations

disposition: direct lightning strike or abnormal ECG - telemetry monitoring for minimum 24 hours
D/C instructions: seek care if develop delayed onset symptoms - CP, neuro, psych, optho or ENT in nature