Environmental Flashcards
Water rescue Submersion or immersion without evidence of respiratory impairment Nonfatal drowning Process of drowning interrupted Fatal drowning Death from drowning All other terms should be avoided
Drowning Definitions
One of top two leading causes of accidental death in children 2/3 of deaths are age < 30 Young children Inability to swim Surveillance Fencing and locks Pools, bathtubs Curiosity, play Teens and adults Seizures Alcohol Associated trauma Inability to swim Exhaustion Scuba
Epidemiology of Drowning
Bradycardia, apnea
Shunting of blood to CNS
Decreased metabolism
Children > adults
Mammalian diving reflex (sudden cold water immersion)
Primary factor is duration of immersion
Also water temperature, age, associated trauma, associated dysbaric problems, bystander CPR, water contamination
If submerged < 60 minutes and no obvious physical signs of death – initiate CPR
Not all patients need admission
Good oxygenation, scattered rales
Can discharge
All others should be admitted
Drowning Survival Factors
The amount of gas dissolved in a liquid is proportional to the partial pressure of the gas in contact with the liquid
Henry’s Law:
Partial pressure of a gas increases with increasing pressure
Both above - Decompression Sickness and Nitrogen Narcosis
Dalton’s Law:
The volume of a gas varies inversely with the pressure
Squeeze Syndromes and Barotrauma
Boyle’s Law
Asthma COPD Seizures Sinus and ear disease Syncope Panic disorder Vertigo Poor training
SCUBA DivingContraindications
Disorders of descent (Boyle’s Law)
Squeeze Syndromes
Barotitis Media: “Ear squeeze”
Pain from pressure on the TM, due to inability to equalize pressure (blocked Eustachian tube)
TM can rupture with severe vertigo, N&V
Treatment: Nasal decongestants, maneuvers to open Eustachian tube (Valsalva, et al.)
Other squeeze syndromes: Sinus squeeze, facemask squeeze, eye squeeze, suit squeeze, lung squeeze
Barotrauma from Diving
Due to blockage of external auditory canal by cerumen or ear plugs
External ear barotrauma
Hemorrhage or rupture of the inner ear round window with sensorineural hearing loss = labyrinthine window rupture
Severe vertigo, N/V, tinnitus, nystagmus, ataxia
Referral to ENT
Inner ear barotrauma
Rapid uncontrolled ascent (Boyle’s Law)
Dropped weight belt
BC malfunction
Panic and charge to the surface
Expansion of unvented lung gases on ascent results in a “burst lung”
Must exhale on ascent to “vent” the expanded gases
Clinical presentation
PTX, pneumomediastinum, pneumopericardium
Hemothorax from injured lung
Arterial gas embolism can occur (rarer)
Pulmonary Barotrauma Pulmonary Over Pressurization Syndrome
Pulmonary overpressurization causes alveolar gas to enter systemic circulation
Air emboli in coronary, cerebral and retinal arteries
Sudden and dramatic symptoms often with focal neuro findings
Presents on surfacing or within 10 minutes
Unlike decompression sickness, which occurs gradually
ALOC is the rule and seizures are common
Dive chamber “stat” for treatment
Arterial gas embolism or AGE (high morbidity and mortality)
A disorder at depth from breathing compressed air
High concentrations of nitrogen are neurotoxic
Symptoms
Euphoria
Confusion
Disorientation
Poor judgment – may result in drowning
Diminished motor control
Treatment is controlled ascent to decrease the amount of dissolved nitrogen in the brain
Nitrogen Narcosis
A disorder of ascent (gas comes out of solution)
At depth, increased amounts of nitrogen dissolve in blood and tissues
Ascending too quickly causes nitrogen bubbles to form in blood and tissues
Length and depth of dive are the primary determinants of risk
Obesity is a risk factor (nitrogen is lipid-soluble)
A spectrum of illnesses depending on location and severity
Two categories: I and II (II is more serious)
Treatment: Recompression in a chamber
Decompression Sickness
Affects musculoskeletal, skin, lymphatics
“The Bends” or “Caisson’s Disease”
Periarticular pain (especially elbows and shoulders) in 70% of all cases
Pruritus, erythema, skin marbling (“cutis marmorata”) from venous stasis
Intravascular nitrogen bubbles cause a wide variety of presentations
Type I Decompression Sickness
Central nervous system decompression sickness
High CNS concentration of nitrogen
Prickly sensations in the limbs
Low back and abdominal pain
Spinal DCS: Limb paresthesias, weakness
Dermatome sensory distribution is common
Incontinence, priapism
Headache, diplopia, dysarthria, inappropriate behavior
LOC is rare
Differs from arterial air embolism where is is common
Symptoms develop gradually hours after surfacing (unlike arterial gas embolism)
Type II Decompression Sickness
DCS of the lungs = “The chokes”
Decompression shock = Vasomotor DCS
DCS involving cerebellum or inner ear = “The staggers”
Symptoms the same as inner ear barotrauma
Cause: Gas bubbles in inner ear or cerebellum
All decompression syndromes develop slowly
Type II Decompression Sickness
Occurs on ascent
Caused by unequal middle ear pressures
Transient vertigo, nausea
Alternobaric vertigo
Air trapped in a dental cavity expands on ascent, causing tooth pain
Barodontalgia (squeeze and reverse squeeze)
Serious problems are rare
Eructation, flatulence, bloating, abdominal cramps
Avoid carbonated beverages and gas-generating foods prior to diving
Gastrointestinal barotrauma
Pulmonary over pressurization syndrome
Air embolism - sudden
Decompression illness - gradual
Disorders of diving ascent
Squeeze syndromes Nitrogen narcosis (at depth)
Disorders of diving descent
Recompression is the definitive treatment for decompression sickness and arterial gas embolism
Have a low threshold for treatment of DCS
Delayed onset of symptoms is common
More subtle symptoms may develop after treatment of major symptoms
Minor symptoms may progress
May recompress up to 14 days after symptom onset
Recompression Therapy
Commercial planes pressurized to 5,000-8,000’
May exacerbate all symptoms of decompression sickness
May result in new symptoms of decompression sickness for divers without any symptoms initially
Is why diving discouraged for 24 hours prior to flying
No flying for 3-7 days post-treatment of DCS-1
No flying for 1 month post-treatment of DCS-2
Diving Risks associated with flying
Commercial planes pressurized
Type I: Pulse of pressure (barotrauma)
Type II: Flying debris (penetrating trauma)
Type III: Flying humans (deceleration impact)
Type IV: Toxic gases, radiation, burns
Blast Injury Classification
Ear: TM rupture, ossicle disruption
Lung: Pneumothorax, air emboli
GI: Hollow viscus rupture
CNS: Concussion, air emboli
Top 4 organs
Type I blast injuries
Pathophysiology of high altitude illness
Hypoxia-induced over perfusion and increased hydrostatic pressure with capillary leak
Increased sympathetic activity
High-Altitude Illness
Manifestations Acute Mountain Sickness (AMS) High Altitude Cerebral Edema (HACE) High Altitude Retinopathy (HAR) High Altitude Pulmonary Edema (HAPE) High Altitude Flatulent Expulsion (HAFE)
Factors influencing development
Rate of ascent and final altitude
Physiology, acclimation, hydration
Sleeping at altitude (ventilation decreases)
High-Altitude Illness
Prior history of altitude illness
Residence at an altitude below 900 meters
Pre-existing cardiopulmonary conditions
R to L cardiac shunts (listen for a heart murmur) and intrapulmonary shunts
Pre-existing pulmonary hypertension / mitral stenosis
Exertion (physical fitness is not protective)
Women and age >50 have a lower incidence
High-Altitude Illness risk factors
Common with rapid ascent to 8-10,000 feet
Headache, nausea, fatigue, insomnia +/- GI sx
Worse with drugs, alcohol, sedatives, and any respiratory depressant
Prophylaxis: Acetazolamide (carbonic anhydrase inhibitor)
Renal bicarbonate diuresis and metabolic acidosis
Increases respiratory drive
Increases oxygenation since less sleep-related hypoventilation
Avoid in sulfa allergy
Can cause paresthesias
Treatment: Steroids, oxygen, descent
Acute Mountain Sickness
Responsible for most altitude-related deaths
Most commonly on the second night at altitude
Resting tachypnea and tachycardia
Most patients also have acute mountain sickness
Fever / rales / pink sputum
Normal heart size
Non-cardiogenic heart failure
Severe hypoxemia and respiratory alkalosis
High-altitude pulmonary edema (HAPE)
Environmental causes HAPE Thermal injury Drowning Other causes Toxins: ASA, phenobarbital, CO, opioids Strangulation Fat emboli, amniotic fluid emboli
Non-CardiogenicPulmonary Edema
Improve oxygenation with supplemental oxygen
If rapid reversal does not occur (failure to increase oxygen saturation to above 90% within five minutes) descent is mandatory
Portable hyperbaric chamber is another option
Noninvasive ventilation may help
Nifedipine to treat pulmonary hypertension
Consider inhaled beta-adrenergics for wheezing
Dexamethasone and/or tadalafil MAY be helpful in HAPE (some recent debate exists here)
Treatment of HAPE
