VARIOUS

EMERGENCIES
(1)
Hypothermia Hyperthermia Injuries produced by
Electricity Injuries produced by lightning
HYPOTHERMIA
 HYPOTHERMIA
Central temperature decrease below 35C
Severity depends on High risk groups
Moderate Severe Major Patient Elders
Velocity of ability of cold perception
decreasing temp. Newborns
Etiology ratio > surface/volume
<32C 32-25C <25C Energy reserves
Volemia
Vascular reactivity

Thermogenesis Metabolic processes

40-60 kcal/m2/h

Convection skin/air
Radiation IR emission
Evaporation perspiration
Thermolysis
HYPOTHERMIA
Thermoregulation center is in the
hypothalamus
anterior hypothalamus orders
vasodilation and perspiration and
opposes to body overheating
Posterior hypothalamus is the
center of response to cold
Vasoconstriction
Chills
Increase heat production by 250-
1000 kcal/hour
 HYPOTHERMIA- CLASSIFICATION
SUPERACUTE
Immersion in cold water
Non-asphyxial avalanche
Injury produced by cold is
severe
Body cools before the
exhaustion of the adaptive
mechanisms
ACUTE
Within few hours
Means to fight the cold are
altered in the presence of
associated pathologies
(trauma)
Enough time for volume
changes to occur
SUBACUTE
Indemn victim stuck outside
in cold weather
Signs of hypothermia appear
only after the exhaustion of
energy reserves
SUBCHRONIC
In the elders/those with low
socio-economic status who
live in unheated spaces
Installation of hypothermia
slow
Inter-compartment fluid
exchanges important

Predisposing conditions to hypothermia

Exposure to a cold environment under conditions of wind and
rain
Improper clothing
Physical exhaustion
Immersion in cold water 16-21C
Metabolic causes (lower metabolic rate): hypothyroidism,
hypopituitarism, hypoadrenalism, hypoglycemia
Head injury, cerebral tumors, stroke can interfere with the
mechanisms of temperature regulation
Wernicke disease can involve hypothalamus reversible upon
parenteral administration of thiamine
Intoxications with ethanol or drugs (sedatives, hypnotic)
Sepsis afftects thermoregulation center; sign of poor outcome
Dermatological diseases exfoliative dermatitis, extensive burns
Diabetic ketoacidosis
Resuscitation with cold fluids or cold blood transfusions
 HYPOTHERMIA CLINICAL MANIFESTATIONS
The answer of different systems and organs to lowering the temperature varies
depending on the individual.
Mild hypothermia
Core T 32-35C
Excitation state
Chills increase the oxygen consumption & generates acidosis
Disappear when body T la 33-32C
HR, cardiac output & BP
Tachypnea & cold bronchospasm
 HYPOTHERMIA CLINICAL MANIFESTATIONS
Nervous system After the initial phase of agitation at 32C appears dysarthria
Coma is installed at 28C a quiet coma
Pupils initially miotic, at 28C become mydriatic & and so remain until death
Cerebrovascular self-regulation
Sustained up to 25C
Increasing resistance & blood redistribution to the brain
The heart Below 35C gradually tachycardia & high BP bradycardia & arterial hypotension
Bradycardia depolarization of pacemaker cells; refractory to atropine
Prolonged QRS&QT
ECG changes
T wave inversion Atrial fibrillation/flutter
Prolonged PR, QRS & QT Nodal rhythm
OSBORN wave Ventricular premature
Sinus bradycardia beats
AV block Ventricular fibrillation
asystole
 HYPOTHERMIA- CLINICAL MANIFESTATIONS
Hemodynamic Moderate hypothermia
effects Peripheral vasoconstriction volume redistribution to deep venous system ~ hypervolemia
x 3 diuresis
Hypothermia aggravates decreased distal tubular reabsorption & lack of sensitivity to ADH
hypovolemia
Fluids extravasation to the extravascular space
The importance of absolute hypovolemia (cold diuresis) and of relative hypovolemia (inter-
compartment) depends on hypothermia installation speed
The patient with hypothermia= hypovolemic & CVP
Respiratory tract Tachypnea breathing rate stops at 20C central temperature
dead space
current volume
Cold bronchorrhea
Decreased muco-ciliary activity
Decreased cough reflex
Predisposition to aspiration pneumonia
 HYPOTHERMIA CLINICAL MANIFESTATION
Electrolytes & ABB hypoK is associated with hypothermia
Reverses spontaneously when patient t increases
Sometimes extracellular K concentration due to decreased enzymatic activity of the pump
membrane Na/K
Frequently acidosis
Severe respiratory depression & CO2 retention
Lactic acid production by shivering and reduced tissue perfusion
alkalosis
Reduced production of CO2 with decreased metabolic rates
Sodium bicarbonate administration
Coagulation appear constantly disseminated intravascular coagulation
disorders Peripheral Tissue thromboplastin release into the blood
hypoperfusion Decreasing the enzymatic reactions in all coagulation
Trombocitopenia phases
Clinical obvious, but undetected by the common coagulation tests which are done at 37 C
Coagulation imbalance hypercoagulability state with increase risk of thrombosis
 HYPOTHERMIA- CLINICAL MANIFESTATIONS
Other manifestations Well supported endocrine function
Plasma cortisol & thyroid hormones N/
Hyperglycemia is common reduced insulin release, reduced glucose use
In a significant proportion of patients hypoglycemia occurs
pancreatitis (not just high blood amylase) may appear in case of hypothermia
anuria and ileus install progressively according to hypothermia severity
rhabdomyolysis and acute kidney injury caused by myoglobinuria and renal hipoperfusion
Impaired immunity and neutrophile dysfunction, predisposing to infections
 HYPOTHERMIA DIAGNOSIS & TREATMENT
Measure T with cu special thermometers tympanic, esophageal,
rectal/vezical
Differential
stroke para / tetraplegia(areflexia)
Traumatic or hypoxic coma (with bilateral mydriasis) Myocardial infarction
Ample J wave, it may be confused with Pardee wave

Not dead unless warm and dead!

At the place of the accident

Thermic isolation Mild heating
Full coverage Hot water containers
Change wet clothes with dry ones Thermal blanket
Careful mobilization Providing the hot air saturated with water vapor
Cardiac/respiratory arrest resuscitation
3 electric shocks of 200 J
The patient is warmed & start again when t>30C
Transport is done with the patient lying in the recovery position making sure there are no sudden movements
Reheating patient Electrolyte rebalancing

HIPOTERMIA TRATAMENT Depending

Passive (physiological)
Endogenous heat produced by metabolism
volemia
on

It takes time, it is not recommended to those who are CV Blood pH

compromised
Active (External)
Immersion in hot water
Hot air under pressure paper or plastic blankets at 40C
Peripheral vasodilation & venous stasis
Hypovolemia & hypotension (reheating shock)
Active (Internal)
Inhaled air/O2 through nasal cannula/mask at 40C
Prevents heat loss in the lungs
Fluids iv & blood heated at 40C
Gastro-intestinal lavage with heated saline solution
Peritoneal lavage with dialysis without potassium, heated at
40C
Pleural lavage (in the left pleural cavity ensures the heating of
the heart)
Reheating through extracorporeal circuit: patients blood
passes through a reheating circuit and then is re-infused in the
body
Serum K
Coagulation disorders
Blood glucose level
Normovolemia (circulating volume = active vascular bed)
Passive reheating the less risky
Hypovolemia (circulating volume < active vascular bed)
Fast vascular refilling with crystalloid solutions: 9 saline
together with bicarbonate 1.4% depending pH
Prevent ventricular fibrillation
Sometimes the association of dopamine & lidocaine is
necessary
Hypervolemia (circulating volume > active vascular bed)
Specific to sub-chronic hypothermia in the elderly
Passive reheating due to high risk of acute pulmonary edema
 HYPOTHERMIA TREATMENT

Other therapeutic measures Circulatory arrest?

I.V. thiamine administration 50 mg Fast reheating until 28C in order to allow defibrillation
Glucose 50% - 50-100ml, if blood glucose The hypothermic heart is resistent to athropine, pacing,
Antibiotics useful ( risk of infection) electric shock
Hormone replacement (depending on the clinical context)

Diagnosis of death is established depending on

The speed of installation of hypothermia if it is fast the chances of survival are low

The difference of temperature between two body locations (high gradient favors death)

K value over 10 mEg/L zero chance of recovery

 At the place of the accident

Is the victim breathing? Apparent death

T > 25C Central T T < 25C

Conscious or not? Available monitor

YES NO YES NO
Asystole, VFib

Insulation from the cold

Heating Cardiac massage
Careful mobilization Ventilation

Rapid transport to hospital

 MEDICAL
EMERGENCIES
INDUCED BY HEAT
EMERGENCIES INDUCED BY HEAT
Minor in the majority of cases / rarely potentially fatal

After prolonged exposure to heat

Extreme ages: elders or children under the age of 4

Effort hyperthermia
Thermic overload of endogene origin intense and prolonged muscular exercise

Native mechanisms of thermoregulation disrupt at <35C or >40C

Physiological response to thermic stress
Peripheral vasodilation Decreased heat production
(especially in the skin tissue) Thermal behavioral control
Increased production of sweat secretions
EMERGENCIES INDUCED BY HEAT
Inhibition of the
Unchanged
sympathetic
sympathetic efferents
Internal T increases efferents of the
in the anterior
posterior
hypothalamus
hypothalamus

HR increases to
compensate for Skin perfusion Decreases vascular
volume decrease & increases from tone (especially the
and maintain cardiac 0.2L/min to 8L/min skin)
output

Thermic stress may lead to arrhythmia, myocardial ischemia & heart failure

Increased cholinergic stimulation of the skin production of perspiration

Behavioral thermic control the patient looks for a cool environment

 Thermal load
Exogenous / Endogenous (muscular effect)

Hyperthermia
Skin vasodilatation Hydro-electrolyte losses CNS lesions Tissue lesions

PVR Volemia

Splanchnic
ischemia Endotoxemia
Shock Inflammation

Liver Kidney DIC

 EMERGENCIES INDUCED BY HEAT
The mechanism of lesions due to heat

Increased heat
Increased external heat Diminished heat losses
production

Adjuvant factors in producing lesions caused by heat

Obesity the adipose tissue vascularization & inhibits heat Drugs
dispersion due to blood flow Interfere with the mechanisms of heat loss (anticholinergics,
diuretics, phenothiazines, -blockers, calcium channel blockers,
Skin disorders: sclerodermia, eczema, psoriazis sympathomimetic)
Decrease sweat glands secretion
Alcohol inhibits ADH dehydration
Metabolic disorders: hyperthyroidism, pheocromocytoma Heroine, cocaine, amphetamines heat production
Increase the endogenous heat production
High ambient temperature, with high humidity
EMERGENCIES INDUCED BY HEAT
Indoor hyperpyrexia

Children left inside the cars in the sun

temperature inside can reach 54-60C in 10-15 minutes, affecting small children more
severely

Ilegal immigrants abandoned in cars or in wagons

The workers who work indoors at high temperatures

 EMERGENCIES INDUCED BY HEAT MINOR SYNDROMES
Edema, rash, cramps, physical exhaustion induced by heat, syncope
Edema Self-limiting process & resolves spontaneously in a few days 6 weeks
induced by Mild swelling of ankles or hands, within the first days of exposure
heat Skin vasodilation & orthostatic accumulation of fluid in the interstitial space
Diuretics are not efficient volume depletion & electrolyte imbalance

Rash provoked Itchy maculopapular rash, erythematous in the areas uncovered by clothes
by heat Acute inflammation of the sweat gland ducts
Itching is treated with antihistamines
Frequent infection with stafilococus aureus (oxaciclin/erythromycin)

Cramps Spasmodic muscular contractions of the striated muscle

induced by Usually in people who sweat a lot & replace losses with water or hypotonic solutions
heat During the physical effort/frequently during resting periods
Relative deficiencies of Na, K & fluids in the muscle cell
Treatment: fluids, sodium chloride p.o./i.v. & rest in a cool environment
 EMERGENCIES INDUCED BY HEAT MINOR SYNDROMES
Edema, rash, cramps, physical exhaustion induced by heat, syncope
Tetany induced hyperventilation & intensive heat stress
by heat Respiratory alkalosis, parethesia of the extremities & perioral, unsignificant muscle spasms
treatment: removal from the warm environment& decrease respiratory rate

Physical Important volume depletion temperature

exhaustion due Weakness, dizziness, fatigue, nausea, vomiting, frontal headache, myalgia
to heat Orthostatic hypotension, sinus tachycardia, tachypnea, diaphoresis, syncope
Internal temperature N to 40C
muscular cramps and/or rhabdomyolysis
Secondary to water and salt deficiency hemoconcentration, secondary electrolyte
abnormalities
Treatment
Orally electrolyte solutions and rest
Isotonic sodium chloride 1-2 L iv
Corect the deficiency of Na, Cl
Generally there is no need for hospitalization
 EMERGENCIES INDUCED BY HEAT MINOR SYNDROMES
Edema, rash, cramps, physical exhaustion due to heat, syncope
Syncope due to Secondary orthostatic arterial hypotension
heat Volume depletion
Peripheral vasodilation
Reduction in vasomotor tone

Elders/ non acclimatized in the initial periods of exposure to heat

Treatment: removal from the heat source, oral rehydration or i.v. & rest
 EMERGENCIES INDUCED BY HEAT MAJOR SYNDROMES
Extreme hyperthermia heatstroke
Heatstroke Internal T >40C
CNS alteration
Absence of sweating
Multiorgan damage
Increased mortality rate

Central Vulnerable at t especially the cerebellum ataxia early neurological sign)

nervous Instability, confusion, bizarre behavior, halucinations , seizures, coma
system Babinski +
involvement Decortication/decerebration by rigidity
Hemiplegia
Status epilepticus and coma

!!! Absence of sweating in presence of extreme hyperthermia appears due to important volume depletion or damage of
the sweat glands
 EXTREME HYPERTHERMIA DIAGNOSIS OF EXCLUSION
Diffrential diagnosis
Drug toxicity: anticholinergics, stimulantes (phencyclidine Generalized infections: sepsis, malaria, typhoid fever
cocaine, amphetamines, ephedrine), salicylates
Ethanol withdrawal syndrome CNS infections: meningitis, encephalitis, cerebral abscess
Serotonin syndrome Neuroleptic malignant syndrome
Endocrine disorders: diabetic ketoacidosis

Malignant hyperthermia also presents

Hemostasis disorders, DIC and rarely isolated fibrinolysis and thrombocytopenia
Liver disorders: citolysis and rarely cholestasis and liver failure
Kidney disorders: renal failure initially functional, but can progress rapidly to organic renal failure requiring
dialysis
 EMERGENCIES INDUCED BY HEAT TREATMENT
Prehospital treatment
undressing, positioning in a shaded area, application of wet clothes on the vascular axis and
positioning near a ventilator
Patient Antipyretics such as salicylates-aspirin to be avoided because they emphasize hemostasis
cooling disorders
Paracetamol is not efficient + risk of liver toxicity

Cold crystalloid solutions (1000-1500 ml in 1h)

Collapse
Dextran should be avoided (hemostasis disorders)
treatment

The
treatment of
Coma endotracheal intubation + MV
the
Seizures diazepam
neurological
Nasogastric tube
disorders
 EMERGENCIES INDUCED BY HEAT TREATMENT
Hospital treatment ICU with ECG monitoring, t, diuresis, SaO2, O2 therapy
Evaporating ventilator near the undressed patient
cooling Spraying with warm water

Cooling by Bathtub with ice water, so that the body and the extremities to be covered
immersion
Cooling on a The patient is positioned and sprayed with water at 15C.
special bed Skin temperature held at 32-33C with a flow of hot air
body cooling Proper evaporation
unit
Invasive Only in extreme conditions, when the other procedures have not been effective
cooling Cardio-pulmonary by-pass
Ice packs to the neck, axilla and groin (areas with rich vascularization)
Other Gastric lavage with saline and ice, bladder lavage or rectal lavage with saline and ice (laborious, not very
methods effective)
 EMERGENCIES TREATMENT
Treatment of complications
HR & cardiac contractility increased cardiac index, increased central venous pressure
Cardiovascular Peripheral vascular resistance (vasodilatation)
Arterial hypotension is not treated (N after rehydration 250ml/hour + body cooling)

Purpura, petechiae; conjunctival, gastrointenstinal, renal & pulmonary hemorrhage

Coagulation Trombocytopenia, decreased prothrombin and fibrinogen or DIC
Substitution treatment is the only efficient therapy: fresh frozen plasma, fibrinogen, platelets

Liver necrosis enzymes at 24-72h

Liver damage Always reversible, with complete recovery

Direct thermal injuries to the kidney

Rhabdomyolysis
Kidney damage Volume depletion
Treatment: proper hydration, furosemide, dialysis
INJURIES PRODUCED
BY ELECTRICITY
 INJURIES PRODUCED BY ELECTRICITY

Electric shock Electrocution Electric injury Electrical burns

Violent response caused by Death due to electricity Damage of a tissue caused by Skin lesions & necrosis, due
electrical current flowing the flow of electrical current to electric current flowing
through any part of the body through the skin
and head
INJURIES PRODUCED BY ELECTRICITY
When the circuit is connected to a person or a body part, the current gets in and out
of it through the points gate in & gate out

Jellineck electric mark

The effects on the structurethrough it passes depend on the intensity of the

electrical current

I=

Exemple
Current of 10 mA determines muscle contraction which stops when current
stops
Current of 50 mA may cause ventricular fibrillation which does not stop with the
interruption of the electrical current circuit
 INJURIES PRODUCED BY ELECTRICITY

Vital prognosis of the patient is influenced by

Asfixia Due to muscle contracture in the chest
Stops when the current is interrupted
Circulatory stop The risk starts from I=50mA for 1 sec in case of AC and from I 4x larger in case of
through VFib CC
Altered consciousness Through the inhibition of the nervous structures situated on the electric current
& autonomous circuit
disorders
 INJURIES PRODUCED BY ELECTRICITY

Electric burning produced by an electric arc when the electrical current does not cross the body
Electric energy thermal energy outside the body

Electric burning low voltage current

head & hands
Less severe compared to that caused by high voltage current ( 3rd degree burns)
No difference from classical thermal burns
Elements on which The body global resistance (muscle tone & organs with rich vascularization - resistance
the effects of the Dry skin (protector) versus wet skin (favors the flow of electricity)
electricity depend on The electricity way longitudinal/transverse cardiorespiratory risk & deep electrothermal burns
Time of exposure
Prolonged by freezing reaction to electricity
Shortened the patient is projected away from the source of electricity
Intensity, voltage of the electrical current, type of the electric current (continuos/alternating)
 INJURIES PRODUCED BY ELECTRICITY
Circulatory distress Myocardial damage = association of injuries
Disturbing the electric phenomena
Direct myocardial Coronary artery thrombosis
damage Direct myocardial injury through the Joule effect (electrothermal burning, due to
electricity crossing the human body)
Hypovolemia Anoxic myocardial injuries secondary to respiratory arrest
Myocardial contusion by the shock wave

Cardiac arrest = the cause of death VFib low voltage electric current vs Asystole high voltage electric current

Arrhythmias may occur even after a while => careful follow-up of the patient!
 INJURIES PRODUCED BY ELECTRICITY
Circulatory distress Mechanisms of hypovolemia
Fluid loss (deep burns)
Vascular injuries internal hemorrhage (! Evolution in two steps, after the detachment
of the eschar tissue)
Trauma (violent projection of the victim) important hemorrhage
Spinal trauma with high medullary section hypovolemia due to vasoplegia
Respiratory distress Damage of the respiratory center (electrical circuit through the brain)/severe cerebral
trauma
Spine fracture (medullary section) respiratory muscle paralysis
Obstruction of the upper airways
Tetany-like contracture of the respiratory muscles
Bronchial perforation, pneumothorax (electric injuries)
 INJURIES PRODUCED BY ELECTRICITY
Neurological 50% of the patients
dysfunction Temporary loss of conscious, agitation, confusion, coma, seizures,
Tetraplegia, hemiplegia,
Aphasia,
Visual disorders (homonymous hemianopsia due to occipital infarction, optic atrophia, electric cataract),
hearing problems (tympanic/labyrinthic trauma)

Skin lesions (contact areas) painless burns

Orthopedic injuries tetanic muscle contraction/trauma fractures
Gastrointestinal injuries have to be suspected in patients who have suffered burns of the abdominal wall

Disseminated intravascular coagulation secondary to hypoxia, vascular stasis, rhabdomyolysis & release of
procoagulants from the affected tissues.
 INJURIES PRODUCED BY ELECTRICITY- TREATMENT

APPARENTLY UNAFFECTED PATIENT PATIENT WITH SIGNS OF SEVERITY

Exacerbations may appear even after 24h Cardiac arrest immediate
Hospitalization & monitoring in the first 24h resuscitation measures +
Evaluation of myocardial and vascular damage Correction of hypovolemia (crystalloid
solutions) & alkalizing with caution
Repeated ECG

Dosing CKMB, myoglobin, troponin, Antibiotics (infectious complications)

echography Treatment of electric burns
Evaluation of muscle and kidney damage
Breaking (taking the patient away from) the electric circuit
CK, myoglobinuria, renal functional tests
! Even wood or rubber may conduct large amounts of
Evaluation of neurological damage electricity if the voltage > 600 V !
Cerebral CT, X-ray , electromyogram
 Algorithm for managing a victim with electricity injuries
Victim

Low voltage electric current < 1000V High voltage electric current > 1000V

Without symptoms Symptoms (Cardio, Neuro)

Without skin lesions Skin lesions

EKG Hospital

EKG(-) EKG(-) EKG(+) Without severe burns Severe burns

Clinical exam (-) Clinical exam (-) Clinical
Without Severity factors (+) exam (+)
severity factors

Home ICU CICU ICU

INJURIES PRODUCED
BY LIGHTNING
INJURIES PRODUCED BY LIGHTNING
Lightning = electrical discharge of DC at extremely high voltages

Lightnings emit short but intense thermal radiations which produce rapid
heating
Lightning = electrical energy, BUT injuries produced by lightning are
different from classic high voltage generated lesions
70-80% of people struck by lightning survive, BUT remain with
permanent sequelae
Lightning is usually attracted to metal objects of the victim (melted)

The nature and gravity of injuries vary depending on the lightning strike
INJURIES PRODUCED BY LIGHTNING
Direct strike
The victim is stroke by the lightning discharge and may suffer very serious injuries

Electric discharge with side sparks

When a nearby object is struck by the lightning, and the current transverses the air
and hits the victim

Contact strike
When the lightning hits an object kept in the victims hand (ex lightning damage by
using the phone)

Cloud-to-ground currents
When the lightning strikes the ground and the current is transferred through the
ground to a nearby victim. The voltage and current intensity decrease with the
increasing distance between the victim and the striking point
 INJURIES PRODUCED BY LIGHTNING
Cardiac tachycardia & high blood pressure (SNS activation)
Decreases the global myocardial contractility
Coronary artery spasm
Pericardial fluid
Atrial and ventricular arrhythmias

ECG ST elevation, prolonged QT, T wave inversion

Myocardial infarction due to injuries produced by lightning IS NOT common

Neurologic The majority are unconscious/temporary paralysis of the lower extremities
Potentially lethal lesions
Coagulation of the cerebral cortex (intense heat)
Epidural or subdural hematomas
Intracranial hemorrhage
Injuries
Immediate (temporary) disappear in 24h loss of consciousness, confusion, amnesia and paralysis of the
extremities
Late (permanent) seizures, spinal muscle atrophy, amyotrophic lateral sclerosis, Parkinsons syndrome,
progressive cerebellar ataxia, myopathy with paraplegia and chronic pain syndrome
 INJURIES PRODUCED BY LIGHTNING

Ocular cataract produced by lightning (bilateral) crystalline lesions produced by radiant energy (after
months/years)
Vitreous hemorrhage, uveitis, retinal detachment, optic nerve damage
Acoustic explosions tympanic membrane rupture
Persistent tinnitus , sensorial deafness ataxia, dizziness, nistagmus
Musculoske fractures
letal Intense myotonic contractures posterior shoulder dislocations/cervical spine fractures
Rhabdomyolysis less probable
Vascular Vasomotor spasm in one of extremities
Vasoconstriction vasodilation spontaneously solved)
 INJURIES PRODUCED BY LIGHTNING

Figures of Lichtenberg Specific

disappear in 24h, are not actual thermal burns
Alternating burns Mild erythema
May also affect cornea
Point burns Similar to those produced by cigarette, less than 1
cm
Contact burns When the lightning heats metallic objects close to
the skin
INJURIES PRODUCED BY LIGHTNING- TREATMENT
Usually lightning bolts produce more victims.

People stroke by lightning who seem dead must be immediately

resuscitated ( success rates).
Victims will be under close follow-up (late injuries).

Ophthalmological and neurological follow-ups.

Skin lesions will be treated according to classical algorithms.