National Resident Review Course

Ian Rigby

What’s New in Environmental Emergencies?

Diving EmergenciesHigh Altitude Illness

SnakesSpiders

On the downloadable presentation is presentation notes for Heat Illnesses and Cold Illnesses

www.ianrigby.net - under Presentations

Not much!These topics are admirably covered in

standard text books and very little is groundbreaking since they’ve been written.

Great reference is EMCNA May 2004

Cochrane Protocol for “Recompression and adjunctive therapy for decompression illness”. 2007

Recompression therapy is standard for the treatment of DCI, but there is no randomized controlled trial evidence. Both the addition

of an NSAID or the use of heliox may reduce the number of recompressions required, but neither improves the odds of recovery. The

application of either of these strategies may be justified. The modest number of patients studied demands a cautious interpretation.

Benefits may be largely economic and an economic analysis should be undertaken. There is a case for large randomized trials of high

methodological rigour in order to define any benefit from the use of different breathing gases and pressure profiles during recompression

therapy.

Diving InjuriesDiving Injuries

Diving InjuriesDiving Injuries

Gas LawsGas Laws

• Boyle’s LawBoyle’s Law

• Dalton’s LawDalton’s Law

• Henry’s LawHenry’s Law

Gas Laws – Boyle’s LawGas Laws – Boyle’s Law

• PV=k @ constant tempPV=k @ constant temp

• For every 10m of depth For every 10m of depth you increase pressure you increase pressure by 1 atmby 1 atm

• So the size of bubbles in So the size of bubbles in solution increases as solution increases as pressure decreasespressure decreases

• That’s why bubbles are That’s why bubbles are small at the bottom of small at the bottom of the glass and get bigger the glass and get bigger at the topat the top

Dalton’s LawDalton’s Law

• What is (DaltWhat is (Daltinin) in the beer bubbles.) in the beer bubbles.

• The pressure of a gas is the sum of the partial The pressure of a gas is the sum of the partial pressures of all it’s gassespressures of all it’s gasses

• PPairair = P = PPPOO22 + P + PPPNN22 + P + PPPCOCO22 …etc …etc

• Let’s assume 20% 0Let’s assume 20% 022 and 80%N and 80%N22 in air in air

• At 1 atm of air (i.e. sea level) you are inspiring At 1 atm of air (i.e. sea level) you are inspiring 0.2 atm pressure of O0.2 atm pressure of O22 and 0.8 atm of N and 0.8 atm of N22

Dalton’s LawDalton’s Law• At 30m depth (underwater) you At 30m depth (underwater) you

are being subjected to 4 atm of are being subjected to 4 atm of pressurepressure

• Now breathing compressed air Now breathing compressed air at 4 atmat 4 atm

• (20% O(20% O22 and 80% N and 80% N22))

• PPairair = PO = PO22 + PN + PN22

• At 4atm you are getting 0.8atm At 4atm you are getting 0.8atm OO22 and 3.2 atm of N and 3.2 atm of N22

• So, at depth you are breathing So, at depth you are breathing in more molecules of the gassesin more molecules of the gasses

Henry’s LawHenry’s Law

• The number of beer The number of beer bubblesbubbles

• The amount of any The amount of any given gas that will given gas that will dissolve in a liquid at a dissolve in a liquid at a given temperature is a given temperature is a function of the partial function of the partial pressure of that gas in pressure of that gas in contact with the liquidcontact with the liquid

• The higher the The higher the pressure, the more gas pressure, the more gas is dissolved in the is dissolved in the solutionsolution

So….So….

• If Dalton’s Law means we are inhaling If Dalton’s Law means we are inhaling more of a gas with increasing pressure more of a gas with increasing pressure and….and….

• Henry’s law says with increased pressure, Henry’s law says with increased pressure, more gas dissolves into a liquid and…more gas dissolves into a liquid and…

• Our tissues (muscle, nerves, blood) are Our tissues (muscle, nerves, blood) are mostly liquid then….mostly liquid then….

• As pressure increases more gas is As pressure increases more gas is dissolved into our tissuesdissolved into our tissues

• We’ll see how this works out in a bitWe’ll see how this works out in a bit

Diving EmergenciesDiving Emergencies

Key Question in Hx

Descent – Facial BarotraumaDescent – Facial Barotrauma

• Failure to equalize Failure to equalize pressure in maskpressure in mask

• Leads to traction Leads to traction on face, eyes due on face, eyes due to relative negative to relative negative pressurepressure

• See edema and See edema and petechial petechial hemorrhages of hemorrhages of skin, scleraskin, sclera

Middle Ear BarotraumaMiddle Ear Barotrauma

• Failure to equalize Failure to equalize pressures of pressures of eustasian tube and eustasian tube and the outer ear canalthe outer ear canal

• Leads to squeeze Leads to squeeze on the TMon the TM

• Most common Most common disorder of divingdisorder of diving

Middle Ear BarotraumaMiddle Ear Barotrauma

• Various grades of Various grades of injury of TMinjury of TM– 1 – Capilary dilation1 – Capilary dilation– 2 – Mucosal edema2 – Mucosal edema– 3 – Hemorrhage into 3 – Hemorrhage into

TMTM– 4 – Hemorrhage or 4 – Hemorrhage or

serrous exudateserrous exudate– 5 – TM rupture5 – TM rupture

• Treat conservativelyTreat conservatively

External Ear BarotraumaExternal Ear Barotrauma

• Due to plug of the Due to plug of the external canal with external canal with a patent a patent eustachian tubeeustachian tube

• Develops a relative Develops a relative negative external negative external pressure and pressure and bowing of the TM bowing of the TM outwardsoutwards

Inner Ear BarotraumaInner Ear Barotrauma

• RareRare• Occurs with rapid Occurs with rapid

pressurization of the pressurization of the inner ear leads to a inner ear leads to a pressure wave that pressure wave that disrupts the cochlear disrupts the cochlear round windowround window

• Presents with Presents with sensorineural hearing sensorineural hearing loss and severe vertigoloss and severe vertigo

• Usually requires ENT Usually requires ENT f/uf/u

Sinus BarotraumaSinus Barotrauma

• Same theory with Same theory with the ear can lead to the ear can lead to sinus pain either in sinus pain either in descent or ascent if descent or ascent if the sinuses fail to the sinuses fail to equalize pressureequalize pressure

• Treat with Treat with pseudophed or pseudophed or other OTC other OTC decongestantsdecongestants

Injuries at DepthInjuries at Depth

• Nitrogen NarcosisNitrogen Narcosis

• HypothermiaHypothermia

• Oxygen ToxicityOxygen Toxicity

Nitrogen NarcosisNitrogen Narcosis

• Rapture of the DeepRapture of the Deep

• Dalton’s law says….Dalton’s law says….

• At depth inspiring more NAt depth inspiring more N22

• Henry’s law says….Henry’s law says….

• More NMore N22 diffusing into tissues diffusing into tissues

Nitrogen NarcosisNitrogen Narcosis

• Nitrogen has a special affinity for Nitrogen has a special affinity for fatty tissuefatty tissue

• Diffuses into neural membranes and Diffuses into neural membranes and acts like an anesthetic gasacts like an anesthetic gas

• Causes euphoria, poor judgment and Causes euphoria, poor judgment and impaired motor skillsimpaired motor skills

• Injury occurs due to lack of judgmentInjury occurs due to lack of judgment• Treatment is ascentTreatment is ascent

DCS – Decompression DCS – Decompression SicknessSickness

DCS I – ‘the bends’DCS I – ‘the bends’

• Occurs with ascent from depthOccurs with ascent from depth• Especially with long times at depthEspecially with long times at depth• Presents with periarticular joint painPresents with periarticular joint pain• Can also see skin itching and marbling in DCS ICan also see skin itching and marbling in DCS I

• Occurs when NOccurs when N22 forms bubbles in tissues forms bubbles in tissues• Leads to obstructive and inflammatory changesLeads to obstructive and inflammatory changes

– DCS is more than just bubblesDCS is more than just bubbles

• Is DCS I if symptoms limited to MSK system onlyIs DCS I if symptoms limited to MSK system only• Relief when joint compressed with BP cuff at Relief when joint compressed with BP cuff at

200mmHg200mmHg

DCS I – TreatmentDCS I – Treatment

• Treat by recompression therapy Treat by recompression therapy (hyperbaric O(hyperbaric O22))

• Can utilize 100% OCan utilize 100% O22

• Search for DCS II symptoms….Search for DCS II symptoms….

DCS IIDCS II

• Decompression sickness involving Decompression sickness involving anything more than the MSK systemanything more than the MSK system

• Treatment for all is supportive care Treatment for all is supportive care and recompression therapy and recompression therapy (hyperbaric)(hyperbaric)

DCS II - CNSDCS II - CNS

• CNS – nitrogen dissolves easily into the fatty CNS – nitrogen dissolves easily into the fatty myelinated tissues of the nervous system myelinated tissues of the nervous system

• So has predilection for formation of bubbles So has predilection for formation of bubbles with decompressionwith decompression

• Spinal cord findings common especially in the Spinal cord findings common especially in the thoracolumbar areathoracolumbar area

• Presents as paresthesias, weakness, etc.Presents as paresthesias, weakness, etc.• Can present as CVACan present as CVA• Inner Ear DCS gives vertigo – ‘the staggers’Inner Ear DCS gives vertigo – ‘the staggers’• LOC is uncommon (as opposed to AGE)LOC is uncommon (as opposed to AGE)

DCS II – ‘the chokes’DCS II – ‘the chokes’

• Pulmonary circulation is a low pressure Pulmonary circulation is a low pressure systemsystem

• Large volume/size bubbles can cause venous Large volume/size bubbles can cause venous gas emboligas emboli

• Get progressive cough, chest pain, dyspnea Get progressive cough, chest pain, dyspnea in the 1in the 1stst 24hr of surfacing 24hr of surfacing

• What gas laws?What gas laws?

• Tx with supportive care, 100% O2 & Tx with supportive care, 100% O2 & recompressionrecompression

Rapid Ascent–Acute Gas Rapid Ascent–Acute Gas EmbolismEmbolism

• 22ndnd leading cause of death in diving leading cause of death in diving• Rapid ascent causes bubble formation in Rapid ascent causes bubble formation in

pulmonary circulationpulmonary circulation• These can traverse the L atrium and ventricle and These can traverse the L atrium and ventricle and

are sent to the systemic circulationare sent to the systemic circulation• 60% of those who suffer AGE have demonstrated 60% of those who suffer AGE have demonstrated

right to left shunts (i.e. patent foramen ovale, etc.)right to left shunts (i.e. patent foramen ovale, etc.)• Bubbles cause mechanical obstruction and then Bubbles cause mechanical obstruction and then

inflammatory rxninflammatory rxn• Onset of symptoms occurs within 10min of Onset of symptoms occurs within 10min of

surfacing (90% of the time)surfacing (90% of the time)

AGE – CNS/CVSAGE – CNS/CVS

• Predilection for Predilection for cerebral and cerebral and cardiovascular cardiovascular circulationcirculation

• Altered LOCAltered LOC

• SeizuresSeizures

• Visual changesVisual changes

• CN deficitsCN deficits

• Focal weaknessFocal weakness

• Predilection for Predilection for cerebral and cerebral and cardiovascular cardiovascular circulationcirculation

• IschemiaIschemia

• MIMI

• DysrhythmiasDysrhythmias

AGE - TreatmentAGE - Treatment

• Supportive careSupportive care

• 100% O100% O22

• Recompression therapy (only Recompression therapy (only definitive tx)definitive tx)

PneumothoraxPneumothorax

• Occurs with alveolar Occurs with alveolar damage and gas damage and gas crossing the visceral crossing the visceral pleurapleura

• Treat as standard Treat as standard pneumopneumo

• Needs chest tube Needs chest tube (not just aspiration) (not just aspiration) if patient undergoing if patient undergoing recompression txrecompression tx

PneumomediastinumPneumomediastinum

• Air bubbles dissecting Air bubbles dissecting into pulmonary into pulmonary interstitiuminterstitium

• Goes into neck, Goes into neck, pericardium, pericardium, mediastinummediastinum

• Unless Unless hemodynamically hemodynamically unstable, treat unstable, treat conservatively and gas conservatively and gas will absorb on ownwill absorb on own

Alternobaric VertigoAlternobaric Vertigo

• RareRare• Failure to equalize pressure of the inner ear Failure to equalize pressure of the inner ear

on ascent.on ascent.• Occurs with blockage of unilateral eustacian Occurs with blockage of unilateral eustacian

tubetube• Develops pressure difference from middle Develops pressure difference from middle

ear and cochlear organear and cochlear organ• Get profound vertigo, nauseaGet profound vertigo, nausea• Once pressures equalize symptoms Once pressures equalize symptoms

disappeardisappear

Diving Comes Down to Beer Diving Comes Down to Beer BubblesBubbles

Boyle’s Law describes size of bubbles

Dalton’s Law describes what’s in the bubbles

Henry’s Law describes the gas dissolvedin the liquid and the number of bubbles

High Altitude IllnessesHigh Altitude Illnesses

Am I High Yet?Am I High Yet? No absolute No absolute

definition for high definition for high altitudealtitude

The most accepted The most accepted is altitudes greater is altitudes greater than 2500 mthan 2500 m

Very high is 3500-Very high is 3500-5500 m5500 m

Extreme is >5500 mExtreme is >5500 m

Where Can I Go To Get High?Where Can I Go To Get High? High altitude (>2500 m) is High altitude (>2500 m) is

found only in western found only in western Alberta, British Columbia Alberta, British Columbia and the Yukonand the Yukon

Banff 1372 mBanff 1372 m Lake Louise 1646/2637mLake Louise 1646/2637m Sunshine 1658/2729mSunshine 1658/2729m Whistler 652/2182mWhistler 652/2182m Mt.Columbia 3747mMt.Columbia 3747m Mt. Logan 5959mMt. Logan 5959m

More About Gas!More About Gas!

At sea level we are At sea level we are underneath an underneath an ocean of airocean of air

%O%O22 is always 21% is always 21% But as you climb But as you climb

higher, the Phigher, the Patmatm drops and thus your drops and thus your POPO22 drops drops

PiPiO2O2 = 0.21(P = 0.21(PBB-47)-47) PPBB=barometric pressure=barometric pressure

At sea levelAt sea level PiPiO2O2= 160 mm Hg = 160 mm Hg

At 2500mAt 2500m PiPiO2O2 = 119 mm Hg = 119 mm Hg

Aconquilcha,Chile 5340mAconquilcha,Chile 5340m PiPiO2O2 = 82 mm Hg = 82 mm Hg

On top of Everest On top of Everest (8848m)(8848m)

PiPiO2O2 = 43 mm Hg = 43 mm Hg

Respiratory AdaptationsRespiratory Adaptations Hypoxia sensed by carotid body Hypoxia sensed by carotid body

(Pa(PaO2O2<60) and signals the brain for an <60) and signals the brain for an increased respiratory rate (hypoxic increased respiratory rate (hypoxic ventilatory response - HVR)ventilatory response - HVR)

After 30 minutes, the resulting After 30 minutes, the resulting respiratory alkalosis is sensed in the respiratory alkalosis is sensed in the brain stem and the medullary brain stem and the medullary respiratory centre limits HVRrespiratory centre limits HVR

The respiratory alkalosis is sensed by The respiratory alkalosis is sensed by the kidney, which begins to excrete the kidney, which begins to excrete HCO3HCO3--, allowing the HVR to increase , allowing the HVR to increase over the next week.over the next week.

Circulatory AdaptationsCirculatory Adaptations Hypoxia stimulates increased Hypoxia stimulates increased

catecholaminescatecholamines Thus a transient increase in cardiac Thus a transient increase in cardiac

output, heart rate, venous tone, and output, heart rate, venous tone, and blood pressureblood pressure

Hypoxia signals an increased cerebral Hypoxia signals an increased cerebral blood flow (CBF)blood flow (CBF)

Hypoxia causes pulmonary Hypoxia causes pulmonary vasoconstrictionvasoconstriction

Cardiac function returns to baseline Cardiac function returns to baseline quickly but shows a decreasing ability to quickly but shows a decreasing ability to generate higher cardiac output with generate higher cardiac output with exerciseexercise

Hematologic ChangesHematologic Changes

Within 2 days of ascent plasma Within 2 days of ascent plasma volume falls due to diuresis and volume falls due to diuresis and fluid shifts causing fluid shifts causing hemoconcentrationhemoconcentration

Erythropoetin is released rapidly Erythropoetin is released rapidly on ascent and a few days later RBC on ascent and a few days later RBC mass increasesmass increases

Some DefinitionsSome Definitions

AMSAMS - Acute Mountain Sickness- Acute Mountain Sickness HAPEHAPE - High Altitude Pulmonary Edema- High Altitude Pulmonary Edema HACEHACE - High Altitude Cerebral Edema- High Altitude Cerebral Edema HAFEHAFE - High Altitude Flatus Expulsion- High Altitude Flatus Expulsion

Acute Mountain Sickness (AMS)Acute Mountain Sickness (AMS)

Onset 12-24 hours after arrival at Onset 12-24 hours after arrival at altitude (can be 2-96 hr)altitude (can be 2-96 hr)

Very CommonVery Common– 66% of Climbers on Mt. Rainier66% of Climbers on Mt. Rainier– 50% of visitors to Khumbu region of 50% of visitors to Khumbu region of

NepalNepal– 20% of visitors to Colorado ski resort20% of visitors to Colorado ski resort

AMS DiagnosisAMS Diagnosis1991/93 Lake Louise Consensus1991/93 Lake Louise Consensus

Recent gain in altitudeRecent gain in altitude HeadacheHeadache 2 of the following:2 of the following:

– Fatigue or weaknessFatigue or weakness– GI symptoms GI symptoms

(nausea/vomiting/anorexia)(nausea/vomiting/anorexia)– Dizziness or lightheadednessDizziness or lightheadedness– Difficulty sleepingDifficulty sleeping

AMS Risk FactorsAMS Risk Factors

Higher risk populations include:Higher risk populations include:– Rapid altitude gainRapid altitude gain– Previous AMSPrevious AMS– Children and teenagersChildren and teenagers– People taking alcohol or other People taking alcohol or other

respiratory depressantsrespiratory depressants

What Causes AMS?What Causes AMS?

Bottom line is we don’t truly knowBottom line is we don’t truly know AMS is likely due to mild cerebral AMS is likely due to mild cerebral

edema and a generalized high edema and a generalized high sympathetic tone sympathetic tone

It is very likely that AMS/HAPE/HACE It is very likely that AMS/HAPE/HACE are a continuum of the same are a continuum of the same pathophysiological processpathophysiological process

Prevention of AMSPrevention of AMS

Gradual ascent beginning below 2500mGradual ascent beginning below 2500m Rest on the first day above 2500mRest on the first day above 2500m Gain no more than 300-600m per day Gain no more than 300-600m per day

(sleeping altitude)(sleeping altitude) Two nights at same altitude every three Two nights at same altitude every three

daysdays Avoid ETOH, sedatives, etc as they depress Avoid ETOH, sedatives, etc as they depress

HVR especially at nightHVR especially at night

Prevention of AMSPrevention of AMS

AcetazolamideAcetazolamide 125 – 500 mg BID 125 – 500 mg BID beginning 24h prior to departure and beginning 24h prior to departure and continued for 3-4dcontinued for 3-4d

Causes a metabolic acidosis that allows for Causes a metabolic acidosis that allows for greater HVRgreater HVR

Diuresis helps with fluid shiftsDiuresis helps with fluid shifts Well designed trials demonstrating Well designed trials demonstrating

acetazolamide as effective in preventionacetazolamide as effective in prevention

Prevention of AMSPrevention of AMS

DexamethasoneDexamethasone 4 mg q6h 4 mg q6h Will prevent AMSWill prevent AMS Unknown physiology but likely relieves Unknown physiology but likely relieves

minor cerebral edema and produces minor cerebral edema and produces euphoriaeuphoria

Has side effects (hyperglycemia/psychosis)Has side effects (hyperglycemia/psychosis) Rebound common when drug stoppedRebound common when drug stopped Generally not used in prophylaxisGenerally not used in prophylaxis

Treatment of AMSTreatment of AMS Mild SymptomsMild Symptoms Does not need Does not need

descent if mild Sx descent if mild Sx and constant and constant supervisionsupervision

Stop ascent until Stop ascent until betterbetter

AcetazolamideAcetazolamide Tylenol/ASA for SxTylenol/ASA for Sx Consider OConsider O22 at 1-2 at 1-2

LPMLPM

Moderate or Moderate or Unresolving AMSUnresolving AMS

Descent 500 mDescent 500 m Consider:Consider:

– OO22 at 1-2 LPM at 1-2 LPM– Hyperbaric Hyperbaric

therapytherapy– Dexamethasone Dexamethasone

4mg PO q6h until 4mg PO q6h until able to descendable to descend

May ascend after May ascend after symptoms resolvesymptoms resolve

High Altitude Pulmonary EdemaHigh Altitude Pulmonary Edema

HAPE DiagnosisHAPE Diagnosis Recent gain in altitudeRecent gain in altitude 2 of the following (symptoms):2 of the following (symptoms):

– Dyspnea at restDyspnea at rest– CoughCough– Weakness or decreased exercise Weakness or decreased exercise

performanceperformance– Chest tightness or congestionChest tightness or congestion

2 of the following (signs):2 of the following (signs):– Central cyanosisCentral cyanosis– Audible rales in at least one lung fieldAudible rales in at least one lung field– TachypneaTachypnea– TachycardiaTachycardia

Pathophysiology of HAPEPathophysiology of HAPE Radiologically Radiologically

demonstrates a patchy demonstrates a patchy edema of the lungsedema of the lungs

This edema is protein This edema is protein rich and contains large rich and contains large amounts of inflammatory amounts of inflammatory mediatorsmediators

Cardiac catheter studies Cardiac catheter studies demonstrate pulmonary demonstrate pulmonary hypertension with normal hypertension with normal wedge pressures and wedge pressures and slightly decreased slightly decreased cardiac outputcardiac output

Pathophysiology of HAPEPathophysiology of HAPE

Over Perfusion ModelOver Perfusion Model Nonuniform hypoxic vascular congestion Nonuniform hypoxic vascular congestion

in the pulmonary bed in the pulmonary bed Areas with high precapillary constriction Areas with high precapillary constriction

are sparedare spared This shunts excessively high pressures This shunts excessively high pressures

to areas of lesser constriction in the to areas of lesser constriction in the lungslungs

The pressure and volume overload leads The pressure and volume overload leads to capillary wall damage and leakageto capillary wall damage and leakage

Pathophysiology of HAPEPathophysiology of HAPE

Neurogenic ModelNeurogenic Model Swelling and distortion of brain matter elicit an Swelling and distortion of brain matter elicit an

increased sympathetic tone and increased sympathetic tone and neurogenicneurogenic pulmonary edemapulmonary edema

Increased sympathetic tone causes increased Increased sympathetic tone causes increased pulmonary arterial and venous constriction pulmonary arterial and venous constriction forcing edema into the lungsforcing edema into the lungs

Some evidence that sympathetic tone also Some evidence that sympathetic tone also modulates the vascular permeabilitymodulates the vascular permeability

Few animal studies show neurogenic Few animal studies show neurogenic pulmonary edema can be stopped with pulmonary edema can be stopped with adrenergic blockade - only one human study adrenergic blockade - only one human study showing no effectshowing no effect

Is neat as it attempts to link HAPE and HACEIs neat as it attempts to link HAPE and HACE

Prevention of HAPEPrevention of HAPE

Gradual ascent as with all AMSGradual ascent as with all AMS Nifedipine 20 mg TID will help Nifedipine 20 mg TID will help

prevent HAPEprevent HAPE Unknown if acetazolamide helps Unknown if acetazolamide helps

prevent HAPEprevent HAPE

NifedipineNifedipine

CaCa2+2+ channel blocker that causes channel blocker that causes vasodilation in the pulmonary systemvasodilation in the pulmonary system

Helps reduce the hypoxic pulmonary Helps reduce the hypoxic pulmonary vasoconstiction seen at altitudevasoconstiction seen at altitude

2 trials demonstrating its 2 trials demonstrating its effectiveness in preventing HAPEeffectiveness in preventing HAPE

Treatment of HAPETreatment of HAPE

DescentDescent DescentDescent Oxygen at 4-6 LPMOxygen at 4-6 LPM Nifedipine 10mg SL then 20 mg TID Nifedipine 10mg SL then 20 mg TID Hyperbaric Oxygen (i.e. Gamow Bag)Hyperbaric Oxygen (i.e. Gamow Bag) PEEPPEEP

NifedipineNifedipine

CaCa2+2+ channel blocker that causes channel blocker that causes vasodilation in the pulmonary systemvasodilation in the pulmonary system

Helps reduce the hypoxic pulmonary Helps reduce the hypoxic pulmonary vasoconstiction seen at altitudevasoconstiction seen at altitude

4 reasonable trials demonstrating its 4 reasonable trials demonstrating its effectiveness in treating acute HAPEeffectiveness in treating acute HAPE

Gamow BagGamow Bag

Temporizing measure Temporizing measure to allow for descentto allow for descent

Using a pump Using a pump creates hyperbaric creates hyperbaric pressurepressure

Places 1/8th an atm Places 1/8th an atm of pressure above of pressure above ambientambient

6000m-> 3975m in 6000m-> 3975m in bagbag

High Altitude Cerebral EdemaHigh Altitude Cerebral Edema

Diagnosis of HACEDiagnosis of HACE Recent gain in altitudeRecent gain in altitude In a person with AMS:In a person with AMS:

– Mental status changes Mental status changes oror– Ataxia (tandem gait)Ataxia (tandem gait)

In a person without AMS:In a person without AMS:– Mental status changes Mental status changes andand– AtaxiaAtaxia

Progression of HACEProgression of HACE Occurs in 2-3% of those trekking >5500m Occurs in 2-3% of those trekking >5500m Usually takes 1-3 days at altitude to Usually takes 1-3 days at altitude to

developdevelop Ataxia is usually the earliest signAtaxia is usually the earliest sign May rapidly progress to coma in hoursMay rapidly progress to coma in hours Mortality in untreated patients is 13%Mortality in untreated patients is 13% If progresses to coma, mortality is 60%If progresses to coma, mortality is 60% Recovery to completely normal neurological Recovery to completely normal neurological

function usually takes weeksfunction usually takes weeks

Pathophysiology of HACEPathophysiology of HACE Vasogenic edema modelVasogenic edema model CT/MRI data shows prediliction for CT/MRI data shows prediliction for

white mater tractswhite mater tracts Some limited animal studies Some limited animal studies

support a nonuniform increased support a nonuniform increased cerebral blood flow (like the HAPE cerebral blood flow (like the HAPE model) and loss of cerebral model) and loss of cerebral autoregulationautoregulation

Human studies with doppler flow Human studies with doppler flow suggest that increased CBF alone suggest that increased CBF alone is not the causative factoris not the causative factor

Prevention of HACEPrevention of HACE

Gradual ascent as per AMSGradual ascent as per AMS Acetazolamide thought to help (no Acetazolamide thought to help (no

studies)studies) Nifedipine ineffective (1 study)Nifedipine ineffective (1 study) Prophylactic dexamethasone not Prophylactic dexamethasone not

studiedstudied

Treatment of HACETreatment of HACE

Descent, descent, descent!Descent, descent, descent! DescentDescent Oxygen at 2-4 LPMOxygen at 2-4 LPM Dexamethasone 4mg PO/IM/IV q6hDexamethasone 4mg PO/IM/IV q6h Hyperbaric therapyHyperbaric therapy

DexamethasoneDexamethasone Considered very helpful temporizing Considered very helpful temporizing

measure to assist in descentmeasure to assist in descent Thought to reduce cerebral edemaThought to reduce cerebral edema CT/MRI studies have not demonstrated CT/MRI studies have not demonstrated

significant radiological decreases in significant radiological decreases in edema in AMS/HACEedema in AMS/HACE

Symptom scores in AMS/HACE are Symptom scores in AMS/HACE are improved, and tests of neurological improved, and tests of neurological function do improvefunction do improve

To Wrap It UpTo Wrap It Up Altitude illnesses are common to Altitude illnesses are common to

travelers in the rockiestravelers in the rockies Prevention is key with slow accentPrevention is key with slow accent Treat AMS with cessation of ascent, Treat AMS with cessation of ascent,

acetazolamide, oxygen, symptomatic tx. acetazolamide, oxygen, symptomatic tx. Descend if worseningDescend if worsening

Treat HAPE with descent! Consider OTreat HAPE with descent! Consider O22, , hyperbaric therapy, nifedipine and hyperbaric therapy, nifedipine and acetazolamideacetazolamide

Treat HACE with descent. Consider OTreat HACE with descent. Consider O22, , hyperbaric therapy and dexamethasonehyperbaric therapy and dexamethasone

Flashback!Flashback!

35 yr old diver comes to see you35 yr old diver comes to see you 6 hours ago had a very long and deep dive6 hours ago had a very long and deep dive He has now developed pleuritic chest pain He has now developed pleuritic chest pain

(onset 1.5 hr after dive) and cough(onset 1.5 hr after dive) and cough His vitals HR 80, RR14, BP 120/80 and His vitals HR 80, RR14, BP 120/80 and

OO22Sat 98%Sat 98% Chest is clear to auscultate and CXR is Chest is clear to auscultate and CXR is

normalnormal

FlashbackFlashback

What is your DDx?What is your DDx? What would you do to treat this What would you do to treat this

person?person?

Altitude…Where Else?Altitude…Where Else?

Air Transport and the Medical Air Transport and the Medical PatientPatient

All contraindications are relativeAll contraindications are relative

Weigh risk of altitude with the benefit or Weigh risk of altitude with the benefit or rapid transport.rapid transport.

Open Intracranial Wounds

Open Globe Injuries

ETT Cuffs

Pneumothorax

Pneumomediastinum

Pneumoperitoneum

Bowel Obstruction

Altitude TroubleAltitude Trouble

Snakes! I Hate Snakes!

North American Poisonous Snakes

• Croatalids/Viperidae (Pit Vipers)• Account for 98% of reported bites

• Elapidae (Coral Snakes)

Another Great Reason to Be Canadian!

Western RattlerMassasaga Rattler

Timber Rattler

The USA

Hey Doc! Is This Snake Poisonous?Identifying the Pit Viper

Hey Doc! Is This Snake Poisonous?

Hey Doc! Is This Snake Poisonous?Identifying Coral Snakes

“Red on Yellow Kills a Fellow”

Sonoran Coral Snake

Hey Doc! Is This Snake Poisonous?

Milk Snake - nonvenomous

“Red on Black, Venom Lack”

Pathophysiology of Poison Bites

• Digestive Enzymes• Cause local pain, erythema,

swelling, petechia, hemorrhagic blisters

• Hematologous Proteins• Lead to coagulopathies

• Neurotoxins• Cause muscle weakness, nerve

palsies, etc.

Pit Vipers

Coral Snake

Pit Viper Bites

• 20% are dry bites (no evenomation)

• Primary problem for humans is the local effect of the digestive enzymes

• Can also have hematological effects, seen more often in children or with direct arterial envenomation.

Field Treatment of Pit Viper Bites

• Don’t get bit

• Immobilize the limb.• Med J Aust. 1982;1:212-214• Aust Fam Phys. 1983;12:365-368

• Gentle tourniquet (should be able to get 2 fingers under tourniquet) - debatable. • Ann Emerg Med. 1992;21:1086-1093

• Don’t use:cryotherapy, electric shock, arterial tourniquets, excision, or incision

ER Treatment of Pit Viper Bites

• ABCs as usual• Local wound care• Draw off CBC, coags, CK, fibrinogen,

Type&Hold in anticipation of potential coagulopathies

• Grade your evenomation and consider use of antivenom.

Grading Evenomations - N Engl J Med

2002;347(5):347–56 • Minimal Envenomation

• Local: swelling, erythema, and/or ecchymosis confined to the site of the bite

• Systemic: no systemic signs or symptoms• Coagulation: no coagulation abnormalities; no other significant

laboratory abnormalities• Moderate Evenomation (consider antivenom)

• Local: progression of swelling, erythema, and/or ecchymosis beyond the site of the bite

• Systemic: non–life-threatening signs/symptoms (nausea, vomiting, perioral paresthesias, fasciculations, mild hypotension)

• Coagulation: mildly abnormal coagulation profile without clinically significant bleeding; mild abnormalities on other laboratory tests

• Severe Envenomation (likely giving antivenom)• Local: rapid swelling, erythema, and/or ecchymosis involving the

entire extremity• Systemic: markedly severe signs and symptoms (hypotension [systolic

blood pressure <80 mmHg], altered sensorium, tachycardia, tachypnea, or respiratory distress)

• Coagulation: markedly abnormal coagulation profile with evidence of bleeding or threat of spontaneous hemorrhage (markedly prolonged prothrombin time, unmeasurable activated partial thromboplastin time, severe hypofibrinogenemia, severe thrombocytopenia with platelet count <20,000/mm3, and the presence of fibrin degradation products)

AntiVenoms – There are now Two!

• Antivenin Crotalidae Polyvalent • (ACP) (equine) • Wyeth

• Crotalidae Polyvalent Immune Fab • CroFab (Ovine)• Savage Laboratories

Dosing Antivenoms• ACPACP• Guide dosing by

severity of effects• Give over 1 hour

• Moderate envenomations get 10-15 vials of ACP

• Severe get 15 vials

• Profound circulatory collapse get 20 vials

• FabAV/CroFabFabAV/CroFab

Notes on Antivenoms

• ?Which is best?• There is a high percentage of allergic rxns

to both ACP and FabAV.• This includes anaphylactic/anaphylactoid

rxns as well as delayed serum sickness rxns

• Recent studies have documented a significant rebound effect in the 1st 24 hours after evenomation, so patient may require more antivenom

• Antivenoms work well on systemic symptoms, but poorly on local symptoms.

Local Injury

Local Injury

• Local wound care• Consider admission for blister

management and delayed debridement• Antivenom not very effective for local

injury• Often appears to be compartment

syndrome, but most often compartmental pressures are normal, so…..

• DON’T LET THE SURGEONS DO FASCIOTOMY WITHOUT MEASURING COMPARTMENT PRESSURES!

Coral Snakes (Elapidae)

• These guys are different than the pit vipers

• Their bite contains neurotoxins only, so local reactions are rarely seen (i.e. can look like a dry bite).

• Do not have hematological effects• Neurotoxic effects can be delayed,

with case reports of up to 12 hr delay

Coral Snakes

• EMS/First Aid is the same as for the pit vipers• Even if asymptomatic, admit for 24hrs

observation• For any eastern coral snake bite with possible

envenomation, three to five vials of Antivenin (Micrurus fulvius) should be administered immediately.

• Note this is antiCoral antivenom, not ACP or FabAV!

• If systemic manifestations are present, at least six to 10 vials should be administered.

• One exception is the Arizona coral snake (Micruroides), which is not associated with human fatality and for which no antivenin exists

Review

• EMS – immobilize limb/2 finger tourniquet• ABCs – people survive with supportive care• ? What type of snake was it ?• If pit viper – grade evenomation and consider

indications for antivenom• 2 types of pit-viper antivenom, ACP and CroFab• Don’t allow fasciotomy without compartmental

pressure monitoring

• For coral snakes, bites may look dry• Admit and consider antiCoral antivenom even if

no current signs of toxicity (depends on history of snake bite)

Itsy Bitsy Spider….

Spider Stuff

• Most spiders are venomous, but most lack apparatus tough enough to penetrate human skin

• Difficult diagnosis as often spider not seen or obtained

• Very few deaths yet over 10000 US reported bites/yr

ED Presentations – Canadian, eh!

• Local Reactions– Nearly all spider bites can present like this

• Necrotic Arachnidism– Brown Recluse, Hobo Spider in N. America– Question if Wolf Spider and Jumping Spiders can

cause this. Only questionable reports in South America and Australia

• Systemic– Classically Black Widow– Can occur with others too (less well described)

Culprits – Black Widow• Latrodectus mactans• Only the female can

envenomate humans• Classically black and

glossy with red abdominal markings (hourglass)

• Commonly found under rocks, woodpiles, etc

• Both local and systemic rxns

Culprits – Black Widow

• Worldwide distribution, including southern Canada

The Bite of the Black Widow

• Black widow venom has a multitude of agents but alpha-latrotoxin is most likely culprit

• This acts at the presynaptic membrane of the neuronal and the neuromuscular junctions and causes the opening of nonspecific cation channels

• results in increased neurotransmitter release and decreased reuptake of neurotransmitter

• primary symptom of envenomation is muscle cramping due to release of acetylcholine at the neuromuscular junction

Bite of the Black Widow – Local Presentation

• Pinprick bite• In 30-120 minutes get crampy pain at

site

• Local rxn causing a flat erythematous ring 5 to 15 mm away from a central macule which fades in 12 hours (halo lesion)

• No local cytotoxic necrosis

Bite of the Black Widow – Systemic

• Proximal muscle cramping pain begins.• Pain in back, chest, or abdomen occurs

depending on the anatomic location of the bite. Pain may wax and wane.

• Autonomic nervous system symptoms include nausea, vomiting, sweating, hypertension, tachycardia, and, rarely, priapism.

• These symptoms persist for 36 to 72 hours.• Milder symptoms and a sensation of being

“not quite right” may last for 1 to 2 weeks.• Usually not life threatening unless large

evenomation of small child

Black Widow Bite Treatment

• Local wound care & tetanus as indicated• Analgesic (often require parental opiods)• Benzodiazepines as second line agents if

considerable cramping symptoms (one retrospective study only)

• Calcium gluconate long touted as treatment, but studies do not demonstrate much success so Ca falling out of favor.– Am J Trop Med Hyg 1981; 30:273–277

– Ann Emerg Med 1992; 21:782–787

Black Widow Bite Treatment - Antivenom

• There is a horse serum derived antivenom

• Indications:– severe pain that is refractory to opioid

analgesics – life-threatening hypertension and

tachycardia uncontrolled with supportive care

• Problems:– Approximately 10% have acute allergic rxn

Culprits – Brown Recluse

• Loxosceles reclusa• Range from tan to dark

brown• Classic marking is the

violin shaped dark area on the cephalothorax

• Have 3 pairs of eyes (most spiders with 4)

• 1-5cm length (leg to leg)

Culprits – Brown Recluse

Southern USA

But bear in mind that can get stragglers transported.

We have a documented case in Calgary

Culprits – Hobo Spider• Relatively large. 1-1.5 cm

body and up to 5cm including legs

• Usually tan to brown• No true identifying marks for

us non-entymologists• Fast – run up to 1m/sec• Bites and venom usually

only cause local damage, but few case reports of systemic toxicity exist

Culprits – Hobo Spider

• Tegenaria agrestis• Leading cause of necrotic arachnidism in

western states/provinces

Bite of the Brown Recluse (and Hobo)

• Causes both local and systemic toxicity by means of endothelial cell damage, lysis of red blood cells, coagulopathy, and complex activations such as calcium-dependent systems

• Sphingomyelinase D is unique to Loxosceles venom and appears to be the major dermonecrotic factor

• SMD causes platelet aggregation & thrombosis, leading to ischemic and inflammatory tissue damage

Bite of the Brown Recluse

• Almost painless bite at first• Within few hours pain increases and gets

erythematous• In more severe cases may see necrotic

blebs develop• Are “Red, White, Blue” areas of Erythema,

Vasoconstriction, Necrosis• Progresses to ulcers that may not

maximize for 2 weeks• Then eschar formation that take months to

heal

Bite of the Brown Recluse

Photo Courtesy of Dr. M. Francis

Bite of the Brown Recluse – Local Tx

• Local wound care and tetanus• Analgesics as indicated• No proven treatments for necrotism• Dapsone touted, but little evidence and can lead to

methemoglobinemia and hemolysis on its own• Treatments tried: Steroids, hyperbaric oxygen,

cyproheptadine• None with convincing results

• Ulcer may progress for weeks!• Corrective surgery, such as skin grafting or

debridement with closure, should be delayed for 4 to 8 weeks

Bite of the Brown Recluse – Systemic

• Systemic Toxicity is quite rare• Thought to occur in children or with arterial

delivery of venom.• Systemic symptoms onset in 24-96 hrs• Leads to:

– Nausea/Vomiting/Arthralgias and Myalgias– Severe evenomations lead to hemolysis,

coagulopathy and DIC– Coagulopathy and DIC are leading causes of

death

Bite of the Brown Recluse• Serial hemoglobin, hematocrit, platelet, urinalysis• Obtained based on clinical picture: type and

crossmatch (perform early), LFTs and coagulation studies

• Analgesic/antipyretic agents• Systemic corticosteroids for hemolysis

– Methylprednisolone, 10–40 mg IV q6h for 3–5 days• Disseminated intravascular coagulation—specific

management• Packed red blood cell transfusions as needed for

anemia• Other blood products/components as indicated• Dialysis as needed for renal failure• Symptomatic and supportive care• No commercially available antivenom

Spider Review• Black Widow

– Red Hourglass on underside– Venom causes release of neurotransmitters– Symptoms are cramps/pain– Treat symptomatically/supportively– There is an antivenom. Use if life threatening tachycardia and

hypertension unresponsive to usual ICU care• Brown Recluse

– Has violin on back and 3 pairs of eyes– Bite can lead to necrotic skin lesions– Supportive care with prn skin grafting in 4-8 wks– Can have systemic toxicity with hemolysis and DIC– Steroids and supportive care for this

• Hobo– If see necrotic arachnidism in Canada, it is likely the hobo– Treat like the Brown Recluse bite, but less likely to see

systemic symptoms

Flashback

• 27 yr old male presents with a snake bite to his lower leg (out in the badlands of Alberta)

• His Vitals: HR 90, RR12, BP120/80 afebrile, Sat 99%

Flashback

• There is slowly spreading area of inflammation and edema on his leg

• He has nausea and perioral tingling

• His coag profile is normal.

• What grade of evenomation is this?

• Outline how you would treat this patient.

Fin

Dowload has Hot/Cold injuries

Cold Injuries

Cold Injuries

• Local

• Systemic / Hypothermia

Local Cold Injuries

• Frostnip– Cold injury without tissue loss

• Frostbite (most common)– Cold injury with tissue loss

• Chilblain / pernio– Cold injury due to chronic dry cold

• Immersion / Trench Foot– Cold injury due to cycles of near freezing in wet

environment

Physiology

• See marked vasospasm

• Skin pallor

• Episodes of cold induced vasodilation (Hunting Reflex)

15oC

Physiology - Prefreeze

• Vasospasm and endothelial dysfunction• Causes plasma leakage to extracellular space• Intracellular fluid shifts to extracellular space and

intracellular dehydration particularly in endothelial cells

<10oC

Physiology - Freeze• Ice crystal formation intra & extracellularly• Disruption of cellular function, especially the

endothelial cells leading to large amounts of edema

• Stasis and microthrombosis – leads to ischemic tissue damage and inflammatory responses

<0oC

Presentation

Painful White/blanching with times oferythema

Loss of sensation

Appears white / mottledLoss of fine motor control

Loss of gross motor control

Frozen tissue

Tissues appear rigid and waxy

Degrees of Frostbite

• Seen after rewarming

• 1st Degree– Erythema, paresthesias

• 2nd Degree– Clear fluid filled blisters, erythema

• 3rd Degree– Deep frostbite, develops hemorrhagic blistering

• 4th Degree– Involves muscles, tendon, bone

Treatment

• Immersion in 40-42oC water• Treat until tissues become pliable and capillary

refill returns• Will require analgesia as rewarming hurts• Local wound care• Update Td

• Most severe frostbite is admitted and given BID-TID whirlpool sessions and ROM therapy

• No surgical amputation for 8-12 wks minimum (until shows extent of tissue loss)

• Frostbite in January, amputate in June

I’m OK, right doc?

Oh, it must be Summer now…

Long Term Tx

• Autoamputation in severe cases

• Neuropathic Pain Syndromes

• Autonomic Dysfunction

• Anatomical restriction of movement

Hypothermia

Physiology of Heat Loss

Definitions

• Hypothermia <35oC

• Mild 32-35oC– Characterized by mild changes and shivering

thermogenesis

• Moderate 28-32oC– Loss of shivering– presence of atrial arrythmias

• Severe <28oC– Ventricular arrythmias

Pathophysiology

• CNS

• CVS

• Renal

• Mild Resp/GI

Hypothermic Brain

• 34oC Amnesia&Dysarthria• 33oC Ataxia• 32oC Stupor

• 29oC Marked LOC

• 27oC Loss of reflexes and voluntary motor

• 25oC CNS blood flow 1/3 of norm due to loss of autoregulation

• 23oC No corneal or oculocephalic reflexes

• 19oC Flat EEG

Hypothermic Heart

• >32oC May see tachycardic or bradycardic response

• <32oC Bradycardia due to prolonged depolarization phase of pacemaker cells

• <32oC Atrial arrythmias• <32oC Osbourne J-Waves

• <28oC Ventricular arrythmias• <24oC Significant hypotension• <18oC Asystole

Osbourne J-Waves

Cold Kidneys

• Peripheral vasoconstriction initially leads to an increased effective circulatory volume

• This leads to diuresis (cold diuresis)• May lead to naturesis (not in all)

• Then see progressive decreased GFR as temperature drops (GFR is 50% normal at 30oC)

• Leads to fluid/salt abnormalities

Resp and GI

• Be aware of cold bronchorrhea due to decreased ciliary function

• Decreased GI motility as core temperature drops

Investigating Hypothermia

• Use rectal temperature probe – best correlates with core temperature

• Need low temperature thermometer• Most of our TM probes, etc only go to 35oC

• If you see a low temp, think of checking with a low temperature thermometer

Investigating Hypothermia

• EKG– May see prolongation of almost any

EKG intervals– Cardiac arrythmias– Osbourne J-Waves

Investigating Hypothermia

• ABGs– Often see metabolic acidosis due to lack of

perfusion and oxygenation– Much debate in literature about warming/not

warming ABGs on analyzer. It doesn’t really matter

• CBC– Increased Hct due to cold diuresis– 2% in Hct for every 1oC drop in temp

• Electrolytes– Most common abnormality is hypokalemia– Due to shift of K+ into muscles not a kaliuresis– Most often corrects with rewarming

Hypothermia and ACLS

• ACLS care is different

• Hypothermic patient has markedly abnormal circulation

• Has impaired receptor functions

• Decreased liver metabolism

Hypothermia and ACLS

• Airway management as usual– Shown to be safe and does not induce

arrythmias– Paralytics may not work in severe hypothermia

• Breathing as usual– Be aware of cold bronchorrhea

• Circulation– If an arrest rhythm and temp <30oC then

consider defib at 200J x1 only (some guides say up to x3)

– CPR ‘You’re not dead until warm and dead’– No drugs recommended until temp >30-32oC– Fluid trial of 250-500cc NS/D5W

Rewarming Strategies

Passive Active

Active External Rewarming (AER)

Active Core Rewarming (ACR)

Simple

(Warmed IV/O2)

Invasive

(lavage, CPB)

Passive Rewarming

• Remove wet clothing• Cover in blankets, etc• Allow patient to rewarm on own (i.e.

shivering)

• Appropriate for mild hypothermia as patient has intact shivering thermogenesis

• Often not enough for moderate to severe hypothermia

Active External Rewarming

• Provide external heat source• Warmed blankets, radiant heat

sources, ‘Bair Hugger’

• Appropriate for mild and moderate hypothermia

• Get core temp rises of about 0.5 - 1oC/hr

Active Core Rewarming-Simple

• Warmed, humidified O2

• Warmed IV fluids (Level I blood warmer for fluids)

• Appropriate for mild/mod/severe hypothermia

• Get temp rises of 0.5-2oC/hr with each

Active Core Rewarming-Invasive

• Warmed Bladder Irrigation• Gastric Lavage• Peritoneal Irrigation• Closed Thorasic Lavage• Each modality will raise temp ~ 1oC/hr

• Cardiopulmonary Bypass• Can raise temp by 1-2oC / 5 min• Hemodialysis

Active Core Rewarming-InvasiveAnn Emerg Med 16:1042, 1987

ACR - Active core rewarmingAER - Active external rewarmingET - Endotracheal tubeGBC - Gastric-bladder-colon lavageIV - Intravenous

NT - nasotracheal tubeP - peritoneal lavagePER - passive external rewarming

Indications for Extra Corporeal Rewarming (Bypass)• Severe hypothermia

• Cardiovascular instability

• Failure to rewarm by conventional techniques

• Completely frozen extremity

• Rhabdomyloysis with severe hyperkalemia

Approach

Temp Passive AER ACR-Simple

ACR-

Invasive

32-35 C Yes Yes Yes/No No

28-32 C Yes Yes Yes Usually no

<28

Or <32 and unstable

Yes Yes Yes Yes

Core Temperature Afterdrop

• Theory is that as you warm the patient’s extremities the vascular beds open up and cold blood returns to the circulation

• Consider truncal rewarming in mod to severe hypothermia

• True clinical relevance is uncertain

Note on study of self cooling/rewarming in bath w temp probes in self

Summary

• Local cold injuries– Frostnip, frostbite, immersion, Chilblain– Rewarming and local care– Delayed amputation

• Hypothermia– mild, moderate, severe– Effects: CNS, CVS, Kidney– Rewarming

• Passive• Active External• Active Core Rewarming

10 minute break!

Flashback

• You’re in the south on a camping trip after your ‘little three day quiz’ and you find that this critter has nibbled you when you venture to the outhouse.

Flashback

• The Doc at the local ED scratches his head and says ‘I dunno…’

• What do you advise him about your expected course and treatment?

Heat Illness

Heat Loss

• We are biochemical furnaces

• Without heat management mechanisms we would see body temp rise of >1oC/hr

Heat Management

The Heating-Cooling System

Heat Illnesses

• Minor Illnesses– Miliaria (Heat Rash)– Heat Edema– Heat Syncope– Heat Cramps

• Major Illnesses– Heat Exhaustion

• Water Depletion• Salt Depletion

– Heat Stroke• Classical• Exertional

Miliaria/Heat Rash/Prickly Heat

• Plugging of eccrine sweat glands

• Occurs under clothing area

• Itchy at first then get inflammatory eruptions

• Sometimes secondary staph infection

• Treat with cooling, cleaning

• May last 1-2 weeks

Heat Cramps

• Occur with work in hot environments• Copious sweating during exertion• Usually fluid replacement with insufficient

sodium• Often after exertion get cramps (i.e. after

work, not during activity)

• Treat oral Na/water replacement or IV NS

Major Heat Illness

Heat Exhaustion Heat Stroke

Mild Severe

Heat Exhaustion

• Volume depletion under conditions of heat stress

• Presents with malaise, fatigue, headache• Temp usually <40oC• NEURO FUNCTION is NORMAL

• If unsure if this is heat exhaustion or heat stroke, treat it as heat stroke

• Classically described as either salt or water deficiency. Usually a combo of both

Heat Exhaustion – Water & Salt

• Water Deficit– Occurs with inadequate fluid replacement when

working in hot environment– See progressive hypovolemia– Treat with cooling and fluid replacement

• Salt Deficit– Takes longer to develop and occurs with sweat loss

and hypotonic fluid (water) replacement– Characterized by hyponatremia, hypochloridemia– Treat with cooling and hyponatremia therapy

Heat Stroke

• Exogenous hyperthermia

• Loss of thermoregulatory function

• Signs of severe CNS dysfunction– Coma, seizures, other neuro defects

• Temp usually >40oC

• Often see dry hot skin (but not always)

Classic vs. Exertional Heat StrokeClassicClassic ExertionalExertional

Age Elderly Younger

Health Impaired Good

Activity Sedentary Strenuous

Drug Use Diuretics, anticholinergics, antipsychotics, antihypertensives

Usually none

Sweating No Profuse

Lactic Acidosis Usually no, but poor prognosis if present.

Yes, is not prognostic

Rhabdo Unusual Often

Hyperuricemia Modest Severe

Acute Renal Failure <5% ~30%

Hypocalcemia Uncommon Common

DIC Mild Marked

CK Mild Elevation Severe Elevation

Hypoglycemia Unusual Common

Cause Poor Heat Dissipation Excess Heat Production

Treatment

• ABCs as usual– Consider hyperK+/rhabdo in exertional heat stroke

contraindicating succinylcholine

• Rapid Cooling– Cool Water Immersion– Evaporative Cooling (wet skin and fans)– Adjuncts: ice packs, lavage, etc.

• Judicious Fluids– Most only require modest IV fluids (i.e. 500cc NS)

Cooling• Ice Water Immersion• Likely faster cooling• Challenges to patient

management if:– Decreased LOC– Seizure

• Evaporative Cooling• Spray with tepid

water and use fans• May be slower

cooling• Better patient access

for treatment

Cooling

Cooling

• Aim for a temperature of 39oC

• Then stop active cooling (don’t want hypothermia)

• If severe shivering (such that cannot cool) consider chlorpromazine 25mg IV

Heat Stroke’s Complications

• It doesn’t take long to fry and egg or a brain

• Hypotension is common and tricky as can be from multiple causes– Dehydration responds to fluids– Hypodynamic heart (increased CVP, PCWP, low CO) may

require pressors– Hyperdynamic heart (increased CVP, PCWP,CO) require

modest fluid and very aggressive cooling– So consider CVP/SwannGanz monitoring in hypotensive heat

stroke patient not responding to judicious fluids

Heat Stroke’s Complications

• May get pulmonary edema of lungs

• Centrilobar necrosis of the liver almost always evident by 24-72hr post with large increases of LFTs

• Renal Failure– Due to poor perfusion and rhabdo

Heat Stroke’s Complications• Coagulopathies

– Poor prognostic sign– See with purpura, bleeding (CNS, lung, GI)– Manage with cooling and supportive care

Review

• Minor: Miliaria, Heat Cramps

• Major: Heat Exhaustion and Stroke

• IF ANY DOUBT TREAT AS HEAT STROKE

• Cooling to 39oC

• Supportive care