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Environmental Medicine expert topics
Heat related illness
Epidemiology
 Equal male to female ratio
 Higher risk at extremes of age <4yrs and >75yrs
 Major risk factors include
o In children – CNS or diarrheal disease
o Alcoholics
o Medications – antipsychotics, tranquilizers, anticholinergics, anti-parkinsonian drugs
o Cardiovascular medications – β-blockers, CCB and vasodilators
 Other risk factors for exertional heat illness include
o Obesity
o Dehydration
o Vigorous exertion in hot environment without acclimitisation
o Rare disorders – absence of sweat glands, systemic scleroderma, hyperthyroidism
and pheochromocytoma
 Mortality from heat stroke may range from 10-75%
Mechanisms of heat transfer
Body regulates heat content through four mechanisms:
 Radiation –
o Primary mechanism of heat loss when environmental temperature is lower than
body temperature.
o Radiative loss occurs through the infrared range of electromagnetic spectrum
o Accounts for 60% of body cooling in colder conditions
o When surrounding environment is hot, heat will be gained by radiation
o Direct sunlight accounts for 100-250 kcal/h of heat burden
 Conduction –
o Kinetic energy from warm surface directly transferred on to less active surface
molecules of cooler surface
o Usually accounts for <3% of total heat loss of body
 Convection
o Heat transfer to air or fluid around the body e.g. thin air layer between body and
clothes, use of fans and cooler layer of air around skin
o Can along with conduction be responsible for up to 15% of heat loss
 Evaporation
o Primary heat loss mechanism of the body in higher temperatures
o Each gram of water evaporating from skin and lungs removes about 0.58kcal of heat
o Even in the absence of sweating, a basal level of skin and respiratory evaporation
(insensible loss) accounts for about 600 mL of water daily and 12 to 16 kcal of heat
loss per hour.
o Evaporation accounts for over 25 percent of the heat lost in cooler settings and
virtually 100 percent at high environmental temperatures.
o Each 1 percent decrease in body weight from dehydration results in a core
temperature increase of 0.1°C to 0.3°C (0.18°F to 0.54°F).
o Highly acclimatized humans can achieve sweating rates that exceed gastric emptying
rates. Such sweating rates outstrip the ability of the gastrointestinal tract to absorb
water and result in dehydration and eventual hyperpyrexia.
o Sweating rates faster than 1L/hr are not sustainable with oral hydration alone
Response to heat stress
 Body tends to maintain its core temperature between 36 – 38˚C. native thermal regulation
mechanisms begin to fail at core temperatures below 35˚C and above 40˚C.
 Physiologic response to heat stress occurs through four primary methods:
o Dilatation of blood vessels
o Increased seat production
o Decreased heat production and
o Behavioral heat control
 The primary function of heat regulation mechanisms in the human body seems to be for
prevention of heat loss in the cold environments. It is by the release or reversal of these
heat conserving mechanisms that heat loss or gain is achieved.
 Skin blood flow can be increased from basal level of 0.2L/min to 8L/min in response to heat
stress. Cardiac output will thus increase by 3L/min for each 1˚ increase in core temperature
 Any patient with impaired CV status or medications that prevent this increase, may not be
able to maintain this output.
 Heat stress thus may also result in arrhythmias, ischemia and exacerbation of CCF.
Classification of heat-related illnesses
 Minor syndromes
o Heat edema
o Prickly heat
o Heat cramps
o Heat exhaustion
 Major syndromes
o Heat stroke
Heat stroke
The classic definition of heatstroke includes: presence of temperature >40˚C, CNS dysfunction and
anhidrosis. Lack of sweating may not be present and is not a absolute criterion for diagnosis.
Therefore anyone with temperature and CNS dysfunction should be considered to have a
heatstroke, which is a medical emergency with multiple organ system involvement and high
mortality rate requiring immediate intervention.
Clinical features
CNS symptoms –
 Very variable from irritability, confusion to seizures and coma.
 Cerebellum very sensitive to heat and ataxia can be early neurologic finding
The distinction between exertional and non-exertional heatstroke is not clinically important since
signs, symptoms and management are the same.
Definitive diagnosis is of exclusion and once made should be aggressively treated.
System effects of hyperthermia
 Cardiovascular
o Tacyarrhythmias and hypotension – may be hyperdynamic or hypodynamic
depending on patient’s baseline health status
 Neurological
o Due to metabolic disarray, cerebral edema or ischemia
o Symptoms as above
 Rhabdomyolysis
o Direct injury to cells with leaking of calcium and phosphate
o
o
Hyperphosphatemia and hypercalcemia
Hypokalemia due to
 Direct catecholamine effect
 Associated with hyperventilation and respiratory alkalosis
 Sweat losses and renal wasting from physiological hyperaldosteronism
Late hyperkalemia worsened by ARF and hypocalcemia
Hyperuricemia from release of purines from muscle breakdown
o
o
 Renal
o Renal failure
 Direct thermal injury
 Pre-renal insults from volume depletion, renal hypoperfusion,
Rhabdomyolysis and DIC
 Hematological
o Petechial hemorrhages, ecchymoses due to direct thermal injury and DIC from
consumptive coagulopathy
 Immunological
o Release of inflammatory mediators due to direct thermal injury and tissue injury
with a SIRS response
 GIT
o Blood redistribution from splanchnic circulation to periphery causing gut ischemia
and diarrhea with further fluid loss and poor absorption
Differential Diagnosis of Heatstroke
Drug toxicity: anticholinergic toxicity, stimulant toxicity (phencyclidine, cocaine, amphetamines,
ephedrine), salicylate toxicity
Drug withdrawal syndrome: ethanol withdrawal
Serotonin syndrome
Neuroleptic malignant syndrome
Generalized infections: bacterial sepsis, malaria, typhoid fever, tetanus
Central nervous system infections: meningitis, encephalitis, brain abscess
Endocrine derangements: diabetic ketoacidosis, thyroid storm
Neurologic: status epilepticus, cerebral hemorrhage
Investigations
Bedside
 BSL – may be elevated in 70% of patients
 ABG – if significant metabolic and respiratory compromise suspected
 ECG – evidence of primary arrhythmia due to hyperthermia or secondary to electrolyte
abnormalities
 Urinalysis – may show false positive blood due to myoglobinuria
Laboratory
 EUC –
o Hypokalemia
o Hyperphosphatemia
o Hypercalcemia
o Hyperkalemia and hypocalcemia
o Renal impairment
 Raised serum Uric acid level
 LFT – may be deranged in severe cases with multi-organ dysfunction
 CK – usually elevated severely
 Coagulation studies – may be deranged with impending DIC
 CXR – signs of aspiration, ARDS
 Toxicology screen – to rule out suspected causes
 Lumbar puncture and CT brain as indicated by clinical features
Management
Supportive care and monitoring
 Mortality approaches 100% if prompt and effective treatment not instigated
 Rapid cooling associated with improved outcomes
 Goals of treatment – rapid colling and supporting organ function
 adequacy of airway, breathing, and circulation; initiation of high-flowoxygen;
 use of continuous cardiac monitoring and pulse oximetry; and intravenous access
 central venous access and invasive arterial blood pressure monitoring indicated if elderly
patient requiring close monitoring of fluid status
Comparison of Cooling Techniques
Technique
Advantages
Disadvantages
Evaporative
Simple and readily available
Shivering
Spraying with tepid water and
Difficult to maintain monitoring
fanning
electrodes in position
Noninvasive, easy patient
access
Relatively effective
Immersion
Noninvasive
Shivering
Relatively effective
Cumbersome
More rapid than evaporative
Poorly tolerated
Logistically difficult to access
Difficult to maintain monitoring electrode
and temperature probes
Ice packing
Noninvasive
Shivering
Readily available
Poorly tolerated
Strategic ice packs
Noninvasive, readily available
Shivering, poorly tolerated
Can be combined with other
Medium efficiency
techniques
1˚ every 10minutes
Cold gastric lavage
Generally available
Invasive
Labor intensive
Potential for water intoxication
May require airway protection
Limited human experience
Cold peritoneal
Theoretically beneficial
Invasive
lavage
Limited human experience
Body cooling units
Accelerated evaporative losses
Same as evaporative
Cardiopulmonary
bypass
2-3 times more effective than
immersion
Used for resistant cases with
cardiac compromise
Highly invasive
Additional therapy:
 Cease cooling methods at 38.5 - 39˚ to avoid reverse hypothermia
 Diazepam 5-10mg IV to reduce shivering
 Chlorpromazine 25-50mg IV to inhibit shivering – second line
 Neuromuscular paralysis with non-depolarising agents if resistant to cooling
 Anti-pyretics not helpful
 Maintain urine output at 1 – 1.5ml/kg/hr with fluid boluses, diuretics
 Consider renal dialysis if anuria, hyperkalemia or sever metabolic acidosis
 Treat coagulopathy with FFP and platelets
Complications of heatstroke
 CNS - Encephalopathy, edema, neuronal injury and hemorrhages
 Hepatic damage – hallmark of heatstroke
 Cardiac – myocardial injury
 Renal – ARF due to heat damage, Rhabdomyolysis and hypotension
 Respirator – ARDS
 GIT – pancreatitis
 Hematologic – DIC and thrombocytopenia
Hypothermia
Hypothermia is defined as a core temperature of less than 35˚C. Individuals at extremes of age and
those with altered sensorium are at increased risk due to decreased ability to increase heat
production and to conserve heat.
Pathophysiology
 Heat loss from body occurs through:
o Radiation
o Conduction
o Convection and
o Evaporation
 Shivering increases metabolic rate by 2-5times and only maintained until glycogen stores last
and temperatures of 30˚C.
 Cardiovascular effects
o Initial tachycardia and peripheral vasoconstriction → increase in cardiac output
o Subsequent bradycardia, hypotension and fall in CO
o Loss of vascular tone at 24˚C
o Osbourne J waves in ECG below 32˚C
o Progressive bradycardia with progressive hypothermia due to decreased
automaticity of pacemaker cells
o Increased risk of VF at low temperatures
o Antiarrhythmic therapy ineffective at temperatures <30˚C, so are inotropes
 CNS
o Loss of fine motor and then gross motor skils
o Progressive decline in consciousness
o Cerebrovascular autoregulation lost at 24˚C
o Rigidity, pupillary dilatation and areflexia as temperature falls below 28˚C
o May simulate rigor mortis
 Respiratory system
o Early stimulation followed by depression as metabolism slows
o Significant fall in O2 consumption and CO2 production
o Initial left shift of O2 dissociation countered by lactic acidosis, with severe
hypothermia overall-right shift of O2 dissociation curve
 Renal system
o Cold induced diuresis initially with drop in temperature
o Further hypothermia causes reduced cardiac output and renal blood flow and thus
reduced GFR
o ARF develops in 40% patients
 Endocrine
o BMR reduced to 50% by 28˚C
o Hypoglyecemia in case of slow hypothermia and hyperglycemia with rapid cases
o Hypokalemia due to EC K flow into cells
o Hyperkalemia usually late from cell lysis
 GIT
o Reduced GI motility with reduced temperature, ileus at 28˚
o Pancreatitis and mesenteric artery thrombosis from reduced flow may occur
 Hematological
o ↑viscosity, fibrinogen and hematocrit
o Hematocrit ↑2% for every 1˚C decline due to hemoconcentration
o Coagulopathy may develop with thrombocytopenia and DIC reported
Causes of hypothermia
 Accidental – environmental
 Metabolic
 Hypothalamic and CNS dysfunction
 Drug-induced
 Sepsis
 Dermal disease
 Acute incapacitating illness
 Iatrogenic – fluid resuscitation
Classification on severity
 Mild (35-32˚C)
o ↑BMR, maximum shivering and thermogenesis
o Amnesia, dysarthria, ataxia, apathy
o Respiratory stimulation
o Normalblood pressure
 Moderate (32-28˚C)
o Stupor
o Shivering ceases
o AF and other dysrhythmias
o Poikilothermia – adopting temperature of surroundings
o Reduced pulse and cardiac output – 2/3rd of normal
o Progressive loss of consciousness, pulse and respiration, pupils dilated
o Susceptible to VF
 Severe (<28˚C)
o Loss of reflexes and voluntary motion
o Major acid-base derangements
o Pulmonary edema, significant hypotension may develop
o ↓CBF and CO
o Absent corneal and oculocephalic reflexes
o Maximum risk of VF at 22˚C
o Flat EEG at 19˚ and asystole at 18˚
Investigations
Bedside
 BSL – hypo- or hyperglycemia
 ABG – reflecting metabolic state
 ECG – many sequential changes – discussed later
Laboratory
 EUC – abnormal renal function, potassium disorders
 CK may be eleveated
 Pancreatitis – raised lipase and amylase
 FBC – raised hematocrit due to hemoconcentration
ECG Changes in Hypothermia
T-wave inversions
PR, QRS, QT prolongation
Muscle tremor artifact
Osborn (J) wave- J wave seen in inferior leads, may be seen with SAH, CHI and MI
Dysrhythmias:

Sinus bradycardia

Atrial fibrillation or flutter

Nodal rhythms

AV block

PVCs

Ventricular fibrillation

Asystole
Management
Supportive care and monitoring
 Airway must be secured in any patient with reduced level of consciousness, initial reports of
increased risk of VF with intubation have not been confirmed
 Intubation and ventilation with warm humidified air may be an adjunctive treatment and
improve hemodynamics
 Gain IV access since IM/SC routes not feasible since no peripheral blood usually present
 NGT, IDC insertion for monitoring and therapeutic use
 IV fluid therapy – warm fluids to correct dehydration and aid with temperature correction
 Antiarrhythmic drug and inotropes usually ineffective when <30˚C
 Defibrillation for VF also unlikely to succeed at low temperatures but should be tried initially
if needed
Specific management options
Endogenous rewarming
 Ideal for mild hypothermia
 Rewarming of about 0.5 – 2.0˚ per hour possible, more if able to exercise
 Warm environment, warm clothing and insulation
Passive external rewarming
 Suffiecent for stable patients with mild hypothermia
 Remove wet clothing, place in warm dry environment
 Cover with blankets
 Same as above
Active external rewarming
 For moderate hypothermia
 External application of heat – warm blankets, radiant heat or forced heated air system
 Up to 2˚C per hr increase achievable
Active core rewarming
 For severe hypothermia
 Warmed humidified inhaled oxygen
o Prevent further heat loss
o Modest heat gain
 Blood warmer for blood and IV fluids
o Prevents further heat loss with therapy rather than increase temperature
o Cardiopulmonary bypass or left pleural lavage – lifesaving in arrested hypothermics
o Mediastinal, gastric, peritoneal and bladder lavage – less effective, more adjunctive
Venomous bites and stings
Snakes – refer to toxinology notes
Spiders – refer to toxinology notes
Hymenoptera – bees, wasps, ants
Hymenoptera means membrane wings, and includes:
 Vespids (yellow jacket or European wasp and paper wasps)
 Aspids (honey bees)
 Ants
 Saw flies
Bees can only sting once, wasps may sting multiple times. Stinging causes local pain and irritation.
Reaction to a sting depends on prior exposure and sensitivity.
Bee stings cause approximately one death per year in Australia.
 Nearly all deaths due to anaphylaxis
 Occasionally due to massive envenomation
 Anaphylactic reaction to insect venom is an absolute indication for venom immunotherapy,
as this is protective against further severe reactions in >80-90% cases
Bee swarming
Venom contains
 Melittin
 Phospholipase A2
 Hyaluronidase
Assessment
 Vomiting, diarrhea, Shock
 Hemoglobinuria, rhabdomyolysis
 Multiple organ failure
 Signs of anaphylaxis if sensitive
Prognosis
 15% mortality with massive envenomation
 Death likely if >20stings/kg and mild illness if 1-4stings/kg.
Wasp stings
 European wasp lives on ground, earth banks and walls
 Attracted to sweet food, so tendency for oral stings
 Does not leave sting behind like bees, so can sting multiple times
 Most serious reactions due to allergic reactions
 Life threatening envenomation occurs when attacked by swarms and >50stings
 Death usually due to anaphylaxis as massive envenomation rare
Massive envenomation
 Hemolysis, myocarditis, hepatitis
Management
 Ice, analgesia, management of anaphylaxis if present
 Supportive management for all other manifestations
Ticks
Most fatalities from tick paralysis were recorded before 1945. Neuromuscular paralysis and death
from ticks is unique to Australia.
 3 of 19 Australian species known to secrete paralytic toxin
 Nearly all cases due to scrub tick (Ixodes holocyclus), found on eastern seaboard
 Only caused by the female tick
 Natural hosts – bandicoots and other mammals such as dogs
 Attaches to host via proboscis
 Attachment may cause local necrosis, tick digs further deeper to re-attach
 Larval forma may cause allergic reaction in infested host
Tick venom
 Holocyclotoxin – slows action potential and has botulinum like effect on Ach release
Effects of tick bites
 Local skin irritation, rash and tick paralysis
 Local and systemic allergic reaction
 Bite site infection and
 Tick borne diseases
Tick paralysis
 Paralysis and fatality more common in children <5yrs
 Consider tick paralysis in any child with
o ataxia or progressive weakness
o ascending symmetrical paralysis
 local paralysis well documented – e.g. facial
 untreated can progress to full respiratory paralysis – cause for most deaths
Assessment
 onset of symptoms 4-5 days after attachment
 longer the attachment – more likely the paralysis
 unsteady gait, ataxia, distal muscles first affected
 generalized weakness – unable to walk
 swallowing difficulties, Bell’s palsy
 ascending flaccid paralysis – GBS important DD
 paralysis may worsen for up to 48hrs after tick removal
Management
Tick removal
 unless removed intact, prolonged local inflammatory reaction is common
 don’t squeeze body
 many methods documented – knot method, forceps and other commercial devices
 do not crush or squeeze the tick’s body, do not apply heat or other substances to tick
 symptoms may improve immediately or worsen slightly after tick removal
 thus any symptomatic tick bite patient should be admitted for observation
Tick antivenom
 indicated in severe envenomation
 may confer some benefit but not reverse established paralysis
 made from dog IgG – one vial contains 1000 units f neutralizing capacity
 dose of 1-2 ampoules depending on severity, slow IV infusion over 15-30 minutes
 serum sickness may occur
Supportive management
 general supportive care and ventilatory support as indicated
 tetanus prophylaxis
 routine antibiotic prophylaxis not indicated
Jellyfish envenomation
Overview
 mixture of toxic and/or antigenic polypeptides and enzymes
 systemic or local reactions to venoms by humans
 envenomation on contact with jellyfish tentacle – release of venom coated tubule from
nematocysts on tentacle
 suspect envenomation in
o unexplained collapse in surf
o diving accidents and
o near drowning
 only available antivenom is for box jellyfish
Local reactions
 most common; results in linear urticarial and painful eruptions
 kinin like substances in venom may release exogenous and endogenous mediators
 lesions of variable duration and may be vesicular, hemorrhagic, necrotizing or ulcerative
 localized sweating, lymphadenopathy, subsequent fat atrophy, vasospasm, limb necrosis,
gangrene and contracture may develop – toxic reactions
 exaggerated reactions may last weeks with recurrent reactions or delayed persistent
reactions up to months may occur
 contact dermatitis and urticaria
Chronic or long term reactions
 keloids
 hyperpigmentation
 fat atrophy
 scarring
 vasospasm
 mononeuritis
 autonomic nerve paralysis
 ataxia
Systemic reactions
 malaise, weakness
 local cramping and muscle spasm
 ataxia and paraesthesia
 fever, nausea and vomiting
 toxic reactions to venom
Box-jellyfish
 Chironex fleckeri – most venomous sea creature and can cause death within 30 seconds
 Most stings are not life-threatening
 Found mainly off the coast of north Queensland and far west up to Darwin
Venom
 Toxins not yet characterized
 Cardiac, skeletal and smooth muscle conduction pathways ± central neurological pathways
affected
 Cardiotoxicity major concern – impaired cardiac contraction, hypertension then
hypotension, arrhythmias and decreased coronary flow
Assessment
 Sting intensely painful – victim screaming and irrational
 Toxic skin reaction – wheals, vesicles and red-brown whip like marks
 Hypertension and tachycardia
 Muscle spasms and paralysis
Management
 Retrieve from water and call for help
 ABC – oxygen, CPR as indicated
 Immediately apply vinegar liberally over affected area to paralyze nematocysts and
worsening of envenomation
 First aid
o Protect yourself, do not touch stingers without gloves
o Consider compression bandage in extensive limb stings – controversial
o Dried nematocysts may reactivate with water so do not wash them
 If unconscious or life threatening envenomation –
o Minimum 1 vial antivenom diluted 1 in 10 crystalloid as IV push up to 3 vials
o Magnesium sulphate 0.2mmol/kg up to 10mmol as bolus over 5-10 minutes
o Continue CPR until further antivenom available and
o Repeat Mg and cardioactive drugs as needed
 Analgesia
o Icepacks
o Narcotic analgesia
o MgSO4 and antivenom in lower doses than above for symptom relief – titrate to
response