VARIOUS

EMERGENCIES
(2)
Drowning Strangulation Altitude related illness
Diving related disorders
 SUBMERSION
INJURIES
Drowning & Imminent
drowning
PATHOLOGY OF SUBMERSION
For submersion injuries which cause death in less than 24 hours we use
the term drowning
Imminent drowning is defined as survival more than 24 hours after
suffocation by submersion
Risk populations: small children, teenagers and elders
 PATHOLOGY OF SUBMERSION
Inability to keep the head above the water (cannot swim)
Circumstances
Inability to react to stimuli medical causes: seizures, stroke or head trauma
predisposing to
Muscle exhaustion (associated with hypothermia)
drowning
Hydrocution syncope
Plunging accident

Spinal trauma (plunging in shallow water)

Other injuries /
disorders which can Hypothermia
predispose to Syncope (exp. hyperventilation before diving)
drowning Seizures
 PATHOLOGY OF SUBMERSION
Aspiration of a Laryngeal
few mL of spasm Hypoxia
liquid Diving reflex
(1-2 min)
(< 6 months)

Stomach fills
Laryngeal with Deglutition
spasm stops submersion reflexes Initial protection
liquid Parasympathetic activation
Bradycardia
Apnea
Peripheral vasoconstriction
Invasion of the
respiratory tract with
submersion liquid
 PATHOLOGY OF SUBMERSION

Injury of alveolar-capillary membrane

Sea water Proteins & interstitial fluid in alveoli
Solid particles
(hypertonic 3x plasma) Lesion pulmonary edema

Inactivation of surfactant
Micro-atelectasis
Fresh water Temporary haemodilution Septic complications
Important hemolysis hiperK VFib
 PATHOLOGY OF SUBMERSION
Anoxia the major consequence of drowning Pulmonary injuries &
CNS damage
Cerebral hypoxia cerebral edema & vascular endothelial injuries

Volume disorders & electrolyte disorders

Water & ions pass through the injured alveolar-capillary membrane

Metabolic acidosis the consequence of tissue anoxia

Hypothermia depends on duration of immersion & liquid temperature

Coagulation disorders
Trombocytopenia, DIC, due to hypoxia, hemolysis, septic complications

Final outcome
 PATHOLOGY OF SUBMERSION- DIAGNOSIS
Group I Stress induced by water Predictors of favorable outcome
Victim did not inhale water Age > 3 years, female
Group II Mild hypoxia Water T < 10C
Water entered the airways, but the victim was quickly Duration of submersion short (minutes)
removed Absence of inhalation
Respiratory discomfort, cough, tachypnea, rapid pulse, Resuscitation within the first 10 minutes
few bronchial rales Mild hypothermia (35-33C)
Preserved consciousness Rapid recovery of the spontaneous
Group III Severe hypoxia obnubilation/coma cardiac activity
Respiratory distress, tachypnea, dyspnoea, cianosis Arterial pH > 7.10
Diffuse bronchial rales GCS > 6, conscious patient
Pupillary reflex - present
Group IV anoxia circulatory arrest of anoxic origin
 PATHOLOGY OF SUBMERSION - TREATMENT
AT THE PLACE OF THE ACCIDENT IN THE HOSPITAL
Drying & covering with an isothermal Group I Heated victim
blanket glucose & hospitalized follow-up 24h
Evacuation of swallowed water Group II Gastric drainage
through a nasogastric tube O2/mask
Admission for 48h & follow-up (clinical situation
Heimlich maneuver only for foreign may worsen)
respiratory bodies
Group III O2/mask
Endotracheal intubation + assisted ventilation
INDICATIONS FOR ENDOTRACHEAL
INTUBATION Group IV Cardio-respiratory resuscitation
1. Disorders of consciousness (GCS <8) / External defibrillation is possible without risks
important agitation
2. Hypoxemia (SaO2<90%) which does not
correct with oxygen administration
3. Hypothermia < 38C
4. Exhaustion
 PATHOLOGY OF SUBMERSION - TREATMENT

Group I water Hospital admission for 24h

induced stress HR, BP, RR, O2Sa, state of consciousness
Blood glucose, blood gases, blood alcohol, X-rays (chest X-ray mandatory)
Group II - mild ICU admission
hypoxemia Lab tests: urea, creatinine, glucose, blood ions, CBC, inflammation, coagulation tests,
blood gases, alcohol, urine toxicology
ECG
Chest X-ray
Treatment: O2, antibiotics, LMWH (prophylactic dosages)
Group III, IV ICU with supporting vital functions
Shock therapy
Correction of hyponatremia
Preserving the neurological statusmajor objective, restoration hematosis key factor
STRANGULATION
 STRANGULATION
Severity and rapid evolution of injuries depends on
The type of Complete 70%, the legs are in the air & all the body weight is
stangulation transmitted to the rope
Incomplete 30%, feet touch the ground & only a part of the body
weight is transmitted to the rope
The node position Anterior/posterior 75%, sudden cerebral ischemia through the
compression of the carotid arteries the white hanged
Lateral 25%, arterial circulation is temporarily preserved around the
node, while the venous circulation is blocked the blue hanged

Compression of cervical structures results in

2kg: jugular veins compression Laryngo-tracheal injuries
5kg: carotid compression & laryngeal edema 25-45% of cases
15-25kg: tracheal compression & vertebral Fractures of the hyoid bone & thyroid cartilage
arteries
STRANGULATION

Hypoxia & Hypercapnia + Cerebral ischemia cerebral edema

constant, sudden & intense
Worsened by rapidly installed mixed acidosis

Acute pulmonary edema in 25% of cases

Central origin
Severe neurological injuries
Pulmonary arterial hypertension
Increased histamine release
 STRANGULATION - EVALUATION
Strangled patient in Clinical examination together with resuscitation
cardiac respiratory arrest
Strangled patient NOT in Clinical presentation
cardiac respiratory arrest Neurological syndrome constant, secondary to cerebral edema
Cerebral infarction, due to traumatic carotid thrombosis
Depth of coma in relation to the duration of anoxia
Signs of diffuse cerebral damage, without localization
agitation, pyramidal syndrome, seizures, decerebration, midriasis or miosis

Respiratory syndrome
constant, of different intensities: tachypnea/bradypnea, apnea
dyspnea, due to laryngeal edema
acute pulmonary edema, very severe

Autonomic nervous system syndrome vasomotor disorders, sweat, cardio-vascular

disorders: unstable BP and HR, collapse, arrhythmias (ventricular fibrillation),
thermoregulation disorders with hyperthermia
 STRANGULATION - EVALUATION
Laboratory X-ray of the cervical regional completed by CT
Ultrasound of cervical soft tissue
Chest X-ray & arterial gases
ECG
Toxicological exam: alcohol
Treatment Cervical collar
Cardio-pulmonary resuscitation
Shock therapy
Emptying the gastric content
O2 ( cerebral edema) in order to maintain paO2>80 mmhg & paCO2 ~ 35mmhg
Diazepam seizures, agitation
Moderate hypothermia (32-22C) helps cerebral protection
ALTITUDE RELATED
ILLNESS
Acclimation to high altitude
ACCLIMATION TO HIGH ALTITUDE
At high altitude the environment is hypoxic.

Atmospheric concentration of O2 remains constantly ~ 21%

Partial pressure of O2 drops depending on barometric pressure

Intermediary altitude Reduces exercise capacity
1500-2440m Increases alveolar ventilation
Without major changes in O2 transport
High altitude Rapid ascension could be dangerous
2440-4270m A period of acclimation is necessary
Very high altitude
4270-5490 m
Extreme altitude Accesible only for alpinists
over 5490 m Accompanied by severe hypoxia & hypocapnia
 ACCLIMATION TO HIGH ALTITUDE
Suddenly at high altitude hypoxia, dizziness, if SaO2<65%.
Weeks to reach this degree of hypoxia acclimation
Ventilation Increases in order to consume alveolar PO2
Ventilation response to hypoxia carotid bulb
Initial hyperventilation respiratory alkalosis acts as a brake on the respiratory center
Respiratory alkalosis compensated by renal excretion of bicarbonate
Process = ventilatory acclimation, maximum at 4-7 days
Blood After 2h serum erythropoietin polyglobulia (days)
The dissociation curve of HbO2 minimal changes
(hypoxia shifts the curveto the left, respiratory alkalosis shifts it to the right)
Liquid Oliguria, specific
balance Venous constriction cerebral blood volume stimulates the baroreceptors inhibits ADH &
aldosteron diuresis
 ACCLIMATION TO HIGH ALTITUDE

Cardiovascular Stroke volume initially

Cardiac output maintened through HR
BP ( sympathetic tone)
vasoconstriction in pulmonary circulation pulmonary HT high risk of acute pulmonary
edema
Cerebral flow temporarily during the ascension, O2 supply to the brain
response is limited by the increase of cerebral blood volume ( intracranial pressure)
Exercise capacity Decreases with aproximately 10% for every 1000m over 1500m
Inadequate oxygen supply of the muscle fiber
Limitation of the muscular activity by the CNS, in order to preserve its own oxygenation
Sleep quality Is affected at high altitudes,
Increased number of awakenings,
Decreased periods of rapid eye movement (REM) sleep
High altitude syndromes

Acute hypoxia severe & sudden hypoxic aggression

malfunction in the O2 system in alpinists, pilots
sudden depressurization in the cabin of a plane
dizziness, empty head feeling, decreased vision and loss of consciousness
quickly reversible by O2 administration
alteration of vascular endothelium in different organs: brain, lung, retina, subcutaneous
Acute mountain tissue
sickness altitude > 2000 m / 3500m, at an interval of hours or 3-4 days
(AMS) headache (96%), insomnia (70%), anorexia, nausea (30%)

Clinical exam: unsignificant & non specific changes

Peripheral edema: specific to AMS despite the normal diuresis
Neurological: ataxia, disorientation, signs that suggest the presence of cerebral edema

Treatment
Simple analgesics (aspirin, paracetamol, ibuprofen)
Acetazolamide is very useful when administered early
Dexametazone 4-8mg/6h
Bringing the patient to lower altitudes
High altitude syndromes
Pulmonary edema Main cause of death
Healthy young, at an altitude of 2000-7000m
Fast access to altitude, without acclimation
Non-cardiogenic pulmonary edema = pulmonary hypertension + injury of the alveolar-capillary
membrane hydric retention

Clinical diagnosis
Effort dyspnea rest dyspnea irritating cough + chest pains & intense asthenia
Typically during night, cough & pink mucous expectoration/ hemoptisis
Permanent & early cyanosis
Crackles in the lungs

ECG: right ventricular overload & tachycardia

Chest X-ray diffuse alveolar opacities unequally distributed.
Without signs of left heart failure (normal pulmonary capillary wedge pressure)

Treatment
Bringing the patient to lower altitudes 500-1000m remission of pulmonary edema
Necessary time for PE remission only with O2, without lowering altitude = 36-7h
Nifedipine 10mg sublingual/ 15 minutes PHT & O2Sa
Rarely necessary ETI+MV (PEEP)
High altitude syndromes
Cerebral edema Progressive neurological deterioration during the acclimation period at 3500-5000m
Frequently associated with high altitude pulmonary edema

Variations in blood flow & changes in vascular permeability

Hemodynamic changes + changes in vascular permeability + dysfunction of the cell membrane

Diagnosis
Rapidly installed
Altered mental status, ataxia, stupor coma
Headache, nausea, vomiting inconstant
Focal neurological signs (distorsion of brain structure & compresion)
Fundus examination: papillary edema retinal hemorrhages

Treatment
Immediate lowering of altitude
O2 therapy
Hyperosmolar solutions (manitol 0.25-0.5g.kgc in bolus / saline less sensitive to cold)
Dexametazone 8mg/6h
High altitude syndromes
Ischemic stroke, Secondary to changes in hemostasis, alteration of vascular endothelium, circulatory stasis
thromboembolic Lower extremities DVT, pulmonary embolism of high altitude
events and TIA which regresses after O2
bleeding aspirin 300mg/day + hydration & O2 therapy
Retinopathy of 9% of climbers (alpinists)
high altitude Retinal edema, papillary hyperemia, retinal hemorrhages
Injuries spontaneously cure within 10-14 days, only by adequate oxygenation
Peripheral edema Swelling of the face & lower extremities, spontaneous improvement or after descent
Pharyngitis & cough due to alterations of mucoasa (dry, fissures due to dehydration & ventilation )
bronchitis antibiotics do not help (injuries are not provoked by infectious agents)
Solar dermatitis Severe pain, photophobia, foreign body sensation in the eye, tearing, important conjunctive edema,
chemosis and palpebral edema
Spontaneously cures after 24 hours
Chronic Those who live at high altitudes
polycythemia of Important polycythemia (Hb 20-22 g/dl), headache, sleep disorders, alteration of peripheral
high altitude circulation, sleepiness
(Monge disease) Movement at a lower altitude, phlebotomy
Respiratory stimulants (acetazolamide 250mg x 2/day p.o. sau medroxiprogesterone acetate 20-60
g /day)
DIVING RELATED
DISORDERS
 DIVING RELATED DISORDERS
Barotrauma
Due to pressure variations influencing volume of free gas in the body, especially that within less compliant cavities.
Decending dive Ascending dive
Middle ear barotitis media or the cry of Middle ear the air expands, Eustachio tube opens pressure
the ear equalization, otherwise strong dizziness, but temporary
Pain, hemorrhage of tympanic
membrane it breaks Teeth cavities/improper treatments, the air inside the tooth -
Strong vertigo, syncope risk of pain/fracture
drowning Gastrointestinal abdominal colic (gas distension gastric rupture
Pulmonary barotrauma (pulmonary overinflation/lung explosion
Maxillary & frontal sinuses syndrome) pneumomediastinum; pneumothrorax
Previously damaged, NO pressure The air entering the pulmonary circulation gas embolism
equalization The brain the most vulnerable; cerebral artery gas embolism
pain & mucous edema, submucosal
hemorrhage & detachament of sinusoidal
lining from the bone mask epistaxis
 DIVING RELATED DISORDERS

Biochemical accidents
Provoked by the gas from the inhaled content, when its partial pressure reaches toxic levels
Hypercapnia PaCO2 > 0.05bar in the arterial blood
Favored by physical exercise, cold, anxiety
Stop physical exertion, ample exhalation

Nitrogen narcosis: disorientation, behavioral disorders, decrease in response to stimuli, alteration of the
neuromusculary coordination and global hypoesthesia
Risk of drowning
From a depth of 30 m, usually at 70m

Hyperoxygenation pulmonary toxicity with O2 at PaO2>0.5 bar, long time of exposure

Neurological manifestations: iritability, reduced visual field, sensation of fear, diplopia, tonic muscle
contractions, seizures associated with drowning risk
 DIVING RELATED DISORDERS
Decompression accidents or caisson disease
decompression sickness is caused by nitrogen bubbles released from tissues & blood during/after decompression
more frequent than those of diving
Bubbles migrate into the veins, and block part of the pulmonary capillary circulation opening shunts migration of
bubbles in the arterial circulation acute ischemia
Persistent foramen ovalae = predisposing factor for the decompression accidents

Decompression sickness
Type I pain, involve the joints, the extremities and the skin + possible lymphatic obstruction with lymphedema
Type II severe form with
Neurological manifestations (involvment of CNS and especially of spine)
vestibulary (dizziness)
cardio-vasculary (dyspnea)

Usually the symptoms of the decompression sickness appear at a few minutes or hours after returning to the surface,
but may appear within days after diving.
 DIVING RELATED DISORDERS - DIAGNOSIS
THE FORM WITHOUT NEUROLOGICAL
DAMAGE
Skin manifestations: maculopapular rash,
often erythematous or livid, mottled, situated
periumbilical or lumbar, may be painful.
Osteoarticular manifestations (bubble
attachment on a tendon/bone capillary
osteonecrosis. Clinic: pain, unrelieved by
analgesics, relieved only by hyperbaric chamber.
The most commonly affected are the knees and
the shoulders.
General & pulmonary manifestations: intense
asthenia, headache, faintness, chest pain,
paroxysmal cough
THE FORM WITH NEUROLOGICAL
DAMAGE
Over 50% in the first 10 min.
Cerebral injuries appear before the muscle
injuries.
Ist manifestation spinal pain punch , then
urine retention, paresthesia, ataxia or paraplegia.
Strokes vary in clinical manifestations depending
on territory affected by ischemia (uni-/bilateral
carotid artery, vertebro-basilar embolism).
Arterial gas embolism. 4% of gas embolisms are
immediately followed by apnea & cardiac arrest.
DIVING RELATED DISORDERS - TREATMENT
I.V. fluids (to maintain tissue perfusion)

Quickly return to atmospheric pressure after decompression

Normobaric oxygen therapy 15L/min accelerates the elimination of

bubbles
Hyperbaric oxygen therapy tissue oxygenation & dissolution of nitrogen
bubbles
Aspirin 500 mg p.o. or i.v. risk of thrombosis by platelet aggregation
phenomena