diving med overview - no slide title

Diving Medicine: An Overview

MAJ James Lynch, MD, MS

U.S. Army Diving Medical Officer

• Barotrauma• Decompression

Sickness• Flying After Diving• Rebreathers

Agenda

• Eustachian Tube– Connects middle ear with nasopharynx– Allows equalization of middle ear with ambient

pressure– Will “lock” closed with excessive pressure in

nasopharnyx– Most divers have to actively equalize on

descent– Equalization will occur passively on ascent

Barotrauma - Anatomy

• Four major sinus groups– Maxillary– Frontal– Sphenoid (pain in occipital region)– Ethmoid air cells

• Function– Lighten skull – Provide mucous for nasal cavity

Barotrauma - Anatomy

Boyle’s Law:

At constant Temperature, Volume varies inversely proportional to

Pressure

Barotrauma

• Elements needed to produce barotrauma– Membrane (vascular) lined space – Ambient pressure change – Rigid walls– Gas filled space– Enclosed space

Barotrauma

If rigid gas filled spaces are properly vented, barotrauma will not occur

• Predisposing factors– Wax impaction– Tight wet suit

hood– Ear plugs– Otitis externa

Barotrauma – External

• Signs and Symptoms– Ear pain on descent– Hearing loss until pressure is equalized– Hemorrhage in external canal

• Treatment– Stop descent– Relieve obstruction– Treat OE if present

Barotrauma - External

• Most common type of pressure-related injury

• More common in inexperienced divers– Ineffective valsalva

• Etiology is a blocked Eustachian Tube– Upper respiratory infection– Large adenoid tonsils, nasal septal deviation

Barotrauma - Middle

• Pathogenesis– Relative vacuum forms in middle ear resulting in

capillary leakage.– TM rupture will occur between 100-500 mmHg of

differential pressure• Signs and symptoms

– Fullness or pain– Mild transient conductive hearing loss– TM perforation in severe cases– May have blood in face mask– Transient vertigo and/or tinnitus

Barotrauma - Middle

• Treatment– Restrict diving until resolved– Mild (0-1) 8 to 72 hours– Moderate (2-3) 1 to 8 days– Severe (4-5) may take up to six weeks (for

perforations)

Barotrauma - Middle

Recurrent perforation is common if diving is resumed too soon after severe ear squeeze

• Treatment (continued)- Decongestants - Intranasal steroid- Systemic Steroids – if mod-severe (1mg/kg x 5

days + taper)– Antibiotics if perforated– Avoid topicals if perforated unless

recommended by ENT (use otic suspension not solution)

Barotrauma - Middle

• Prevention– Avoid diving with Eustachian Tube

Dysfunction– Topical and systemic decongestants– Stay ahead of pressure changes

Barotrauma - Middle

• May result in permanent damage to cochlea or vestibular system

• Occurs most commonly on descent– Generally starts as middle ear squeeze– Forceful Valsalva causes injury to inner ear

• Can be caused by implosion or explosion

Barotrauma - Inner

• Sites of injury– Oval window– Round window

Barotrauma - Inner

} Results in perilymph fistula

• Signs and symptoms– Vertigo (persistent)– Tinnitus (often described as “roaring”)– Nystagmus with positional testing– Bubbling sensation in ear– Neurosensory hearing loss– Otoscopic findings of middle ear barotrauma

Barotrauma - Inner

• Treatment– R/O AGE and DCS (covered later)– Strict bed rest– Avoid straining– Consider sedation– ENT referral, early in course if possible– Surgical exploration is often needed

Barotrauma - Inner

• Caloric Vertigo– Transient; common on descent (thermocline)– Caused by differing water temperatures in

external canals or TM rupture allowing water to enter middle ear

• Alternobaric Vertigo– Transient; common on ascent – Caused by rapid pressure change transmitted

into inner ear

Barotrauma – Inner DDX

• Predisposing factors– Infection or Allergy– Anatomic variations

• Signs and Symptoms– Pain in sinus area– Dental pain with maxillary sinus involvement– Blood in face mask– Tenderness on sinus percussion

Barotrauma - Sinus

• Treatment– No diving– Decongestants– Observe for infection– May require surgical correction

• Anatomical defects• Polyps• Mucus retention cysts

Barotrauma - Sinus

• Barodontalgia– Occurs on ascent or descent– Predisposing factors

• Dental disease• Failed dental restorations• Recent dental work

Barotrauma - Teeth

• Signs and Symptoms– Tooth pain– Maxillary sinus pain– Exploding or imploding tooth

• Treatment– Pain relief– Dental referral

Barotrauma - Teeth

• Predisposing factors– Failure to clear mask on descent– Diving with goggles

• Signs and Symptoms– Periorbital pain– Periorbital petechiae and swelling

• Treatment - observe

Barotrauma - Face mask

• Pulmonary Over-inflation Syndrome (POIS)• Expansion of gas trapped in lung during ascent

(decreasing ambient pressure) with rupture of lung tissue

• Causes:– Breath-holding during ascent– Inhaling while pushing purge button– Rapid uncontrolled ascent (blow-up)– Air trapped in lung

Pulmonary Barotrauma

Air trapped in lung due to:• Airway obstruction as in asthma• Thick secretions• Lung granulomas (sarcoidosis)• Cysts and blebs

• spontaneous pneumothorax


Clinical presentation• Initial rupture of lung tissue with release of gas• Gas may remain in lung tissue

- migrate to pulmonary circulation- move to the pleural space- dissect along the bronchial tree into the

mediastinum and subcutaneous tissues



Conditions resulting from POIS• Arterial gas embolism• Pneumothorax• Mediastinal emphysema• Subcutaneous emphysema• Pneumopericardium


Surface

3 FSW

96 FSW

99 FSW

Arterial Gas Embolism• Alveolar rupture with concomitant venous or

capillary rupture• Air traverses pulmonary vein to left heart• Emboli are pumped out to the systemic

circulation and distributed to all organs


Arterial Gas Embolism (AGE)

Arterial Gas Embolism • CNS and Heart most susceptible to injury• CVA sxs commonly caused by emboli to brain• Emboli to coronary arteries may cause

myocardial ischemia or infarction• Usually present within the first ten minutes of a

surface interval


AGE – Presenting Signs and Symptoms• Stupor or confusion• Coma with or without seizures• Unilateral motor deficits• Visual disturbances• Vertigo• Sensory abnormalities


AGE – Treatment• A, B, C’s ; check vital signs • Keep patient warm• Neutral position, not Trendelenberg• 100% O2 by facemask or ET tube• IV Fluids• Serial Neurological exams• Immediate recompression upon diagnosis• Cabin pressure below 1000 feet


Pneumothorax - SimpleSymptoms

• Chest pain (lateral or apical)• Cough• Shortness of breath

Signs• Decreased breath sounds• Typical CXR findings


Simple Pneumothorax

Pneumothorax – SimpleTreatment

• Needle thoracostomy, Chest tube• Observe if pneumo is small

Resumption of diving• Spontaneous - unsafe for diving• Traumatic - may return to diving after

resolution with proper evaluation


Pneumothorax - TensionSymptoms

• Chest pain and cough• Increasing SOB and tachypnea

Signs• Asymmetric chest wall movement• Tracheal deviation• JVD• Rapid pulse with decreasing pulse pressure• Mediastinal shift on CXR


Tension Pneumothorax

Pneumothorax - TensionTreatment

• Immediate needle decompression• Chest tube


Mediastinal EmphysemaSymptoms

• Substernal chest pain or burning• May be worsened by inspiration• Intensity of pain may vary greatly

Signs• Mediastinal air on CXR• May hear crepitus - Hamman’s sign


Mediastinal Emphysema

Subcutaneous EmphysemaSymptoms

• Substernal chest pain or burning• May be worsened by inspiration• Feeling of “Rice Krispies” under skin• Subjective voice changes

Signs• Crepitus in neck and supraclavicular area• Audible voice changes


Subcutaneous Emphysema

Mediastinal or Subcutaneous EmphysemaTreatment

• Surface O2• For cardiac or respiratory compromise

consider recompression• 5 - 10 FSW may be sufficient


POIS other than AGE –Treatment• Casualty with SOB, substernal chest pain, voice

change, but stable.• Signs of subcutaneous emphysema (“rice

krispies”)• Tx with 100% O2 on surface at least for 1 hour. • May obtain CXR / CT chest for confirmation /

documentation


Decompression Sickness

Definition

Pathologic response to the formation of bubbles from gas dissolved in tissue due to a reduction in ambient pressure.

Synonyms: DCS, Decompression Illness (DCI), dysbarism, bends, Caisson’s disease


• Robert Boyle, 1670– Decompressed a snake and noted visible bubble

formation in its eye vitreous—and that the snake was “tortured furiously.”

• Triger, 1841– French mining engineer first described

pressure-related limb pain and paralysis in 2 caisson workers—after a 7-hour dive in the Loire river.

History

Visible Bubbles in Tissue


Further experiences with Caisson’s Disease• Construction of Eads Bridge,

St. Louis, 1860s• Construction of Brooklyn

Bridge, NY, 1869-1883, 20 deaths

• Popularization of name, “bends”, because of the bent posture of some patients.

History

Paul Bert, French physiologist• 1878, publishes Barometric Pressure• States bubbles cause decompression sickness• Bubbles are composed primarily of N2

• Was the first to suggest recompression for DCS• Was first to suggest a slow decrease in pressure

to avoid DCS• Was first to suggest decompression with O2

History

J.S. Haldane, British physiologist• Developed the first

comprehensive decompression theory and applied it for the Royal Navy, 1905-7.

• His ideas still are utilized today (such as the initial formulation of the US Navy standard air decompression tables).

Haldanian Decompression Theory

• On the surface, our tissues are in equilibrium (balance) with the inert (non-metabolic, e.g. nitrogen) gases in our breathing mixture– Air is 78% N2, 21% O2 , and 1% Argon

• When we dive with this same breathing mix, what happens to the concentration of the inert gas in the mix????

Why Decompression?

“The amount of gas that will dissolve in a liquid is proportional to the partial pressure of that gas above the liquid”• What happens to the partial pressure of the inert

gas in our breathing mix when we dive?• What does this do to the amount of inert gas

dissolved in our tissues? By the second Law of Thermodynamics, tissues will equilibrate with the respired gas.

Henry’s Law

• Thus at depth, more inert gas than usual is pushed into our tissues.

• If we come up too quickly, then we may exceed the capacity for dissolved inert gas in our tissues, and the excess gas has no where else to go except to form…

BUBBLES!

Decompression

On ascent, the external (surrounding, ambient) pressure reduces, so . . .• The partial pressure of inert gas in our

breathing mix decreases• Correspondingly, per Henry’s Law, the amount

of inert gas that can be dissolved in our tissues will be reduced

• What happens to this excess dissolved gas when ascend?

Decompression

• Bubble formation (to the best of current knowledge) is the root cause of decompression sickness.

• By following ascent (or decompression) rules, such as slowing the rate of ascent, we can prevent significant bubble formation and reduce the risk of decompression sickness.

Decompression

• Everywhere the bubble bounces causes damage on walls of vasculature

• Eventually it becomes stuck and causes more damage and pain

• It damages capillaries and causes tissue hypoxia and injury

Bubble Damage

• Bubble size reduced IAW Boyles Law– If the pressure of the gas in the bubble is > than

the surrounding pressures the bubble grows. – If it is < than the surrounding pressures the

bubble will shrink.

Recompression

Hydrostatic Reduction

• During the ascent or decompression phase of a dive, inert gas, which has been dissolved under depth pressure into tissues, comes out of solution under lower pressure.

• This process can lead to inert gas in tissue becoming supersaturated, resulting in bubble formation.

Pathophysiology of DCS

• Not felt to be a major factor in the pathogenesis of DCS

• Autochthonous (formed or originating in the place where found, not carried there from somewhere else) bubble formation in CNS white matter: is this an example of extravascular bubbles? --we’re not sure.

Extravascular Bubbles

• Arterial, venous, capillary, lymphatic• Most of the evidence for the in vivo

presence of intravascular bubbles is based upon doppler ultrasound studies

• Usually observed on the venous side• Arterial bubbles rarely observed

–However, if present, is associated with serious DCS

Intravascular Bubbles

The pulmonary tissue bed usually is efficient in filtering bubbles, but the following may compromise it:• Pulmonary impairment (disease,

barotrauma)• Arterio-venous shunts• Intracardiac shunts

Arteriolization of venous bubbles

• Prevalence of patent foramen ovale (PFO) in the general population is as high as 30%

• 1998 meta-analysis shows OR = 2.5 for DCS with PFO (3.4 cases in 10,000 dives)

• 2003 Review of 145 articles shows no clear agreement to role of PFO in DCS

• Extremely low absolute risk of DCS: <0.08%

Intracardiac Shunts

• Embolization and blocked blood flow• Compression or distortion of tissue and

vessels• A bubble acts as a foreign body provoking

an inflammatory response– Aggregation of platelets and leukocytes– Activation of coagulation enzymes– Activation of the complement system

Bubble Effects

• Release of histamine and similar mediators• Inflammatory vasoactive plasma polypeptides

such as Kinin• Many effects

--Vasodilation

--Increased vascular permeability

--Decreased perfusion

--Increased pain via stimulation of nerve endings

Bubble Effects (Secondary)

DCS – Presenting Signs and Symptoms• Numbness or Pain• Dizziness• Fatigue or weakness• Headache• Nausea• Gait and Sensory abnormalities• Visual disturbance• Itching


• Develops within minutes after deep, brief dives; but may develop over hours to days after long, shallow dives

• CNS DCS may have shorter latency

> 90% become symptomatic < 3 hours• Pain-only DCS may have a longer latency

90% become symptomatic < 6 hours• A few cases of DCS have been reported 36 hours

after dive

Latency of DCS

Time of onset of initial symptoms in 591 DCS cases from 1999 Divers Alert

Network (DAN) data

Time of Onset %

Upon surfacing 30

< 1 hour 50

< 6 hours 67

< 24 hours 84

> 48 hours < 7%

• Musculoskeletal joint pain

• Skin itching and marbling

• Lymphatic edema and tender lymph nodes

Type I DCS

Musculoskeletal DCS• If isolated, also known as “pain only” DCS• Typically joint pain, usually outside the area

covered by shorts and a T-shirt• Peri-articular knees, shoulders, and elbows• No signs of inflammation• Usually dull, vague, deep, aching• Unaffected by movement

Type I DCS

Cause of musculoskeletal pain is unknown• Bubble formation in joint space?

– Bubbles artificially introduced don’t seem to cause pain

• Bubbles in the bone marrow?– Bubble formation in marrow of sheep caused ↑ intra-

medullary pressure and evidence of limb discomfort

• Bubble formation under periosteum?• Autochthonous bubble formation in perarticular soft

tissue (tendons, ligaments, joint capsule)?• Referred pain from central neurological injury?

Type I DCS

Minor musculoskeletal pain,“Niggles”• Refers to “odd fleeting aches and pains”• May herald typical limb pain DCS• Some experts recommend treating as a form

of Type I DCS

Type I DCS

Skin DCS• Itching and mild urticaria--no Tx needed• Cutis Marmorata—more serious

– Deep red or purple marbling or mottling– Blanches with pressure suggests vascular

etiology– May be associated with itching– Tends to be associated with subsequent

serious DCS, so some will treat as Type II DCS

Type I DCS

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Lymphatic bends• Usually presents as local edema with or without pain,

can involve nodes and wider lymphatic obstruction• Can get swelling of breast, abdominal areas, extremities• Can be accompanied by skin changes

--‘orange peel’ appearance• Treat with recompression

--associated pain should respond quickly, but swelling may persist for several days

Type I DCS

• Pulmonary (“chokes”)• Neurologic• Vestibular (Inner Ear)

Type II DCS

Navy diver in MK21 hard hat rig

Pulmonary DCS• 2% of DCS cases • Overwhelming load of venous, inert, gas bubbles in the

pulmonary circulation• Animal studies have shown:

• Pulmonary arterial and right ventricular pressure rise

• Cardiac output and O2 sat• blood vessel permeability• Pulmonary edema

Type II DCS

Common scenarios for Pulmonary DCS • Emergency ascents from long, deep dives

with large, omitted decompression• Altitude DCS • Caisson workers

Type II DCS

Signs and symptoms of Pulmonary DCS• Substernal discomfort• Cough• Pain with inspiration or expiration• May progress rapidly to cardiovascular

collapse

Type II DCS

Neurologic DCS• More common in recreational diving (up to

80% of reported cases to the Divers Alert Network)

• In contrast, Type I, pain-only DCS is the main type in military or commercial diving (approximately 86% of reported cases).

• Neurologic DCS tends to present rapidly as noted earlier

Type II DCS

Neurologic DCS• Spinal cord most affected (40-60% of cases),

then brain, then peripheral nerves• Distinction of cord v. brain doesn’t matter as far

as treatment is concerned• Paresthesias and numbness are the most

common symptoms

Type II DCS

Manifestations of Spinal cord DCS• Signs usually are multi-focal, not conforming

to a cord syndrome• May have extremity deficits corresponding to

a cord level and a dermatomal pattern• Bowel and/or bladder problems in severe

cases

Type II DCS

Manifestations of Cerebral DCS • Motor deficits including hemiplegia• Sensory changes• Mental status changes• Loss of coordination, ataxia• Upper motor neuron signs

–Hyperactive deep tendon reflexes–Spasticity

Type II DCS

Inner Ear DCS, “Staggers”• Mainly in heliox and saturation dives• Possible role of isobaric counter-diffusion

--With He and N2 at depth, He more readily diffuses into tissue than N2 diffuses out at the interface of the inner and middle ear, and bubbles form in the inner ear fluid

• Structural pathophysiology--Rupture of membranes of semicircular

canals and cochlea--Hemorrhage

Type II DCS

Signs and Symptoms of Inner Ear DCS• Severe vertigo• Severe nausea and vomiting• Nystagmus• Tinnitus• Hearing loss

Type II DCS

Differentiating inner ear DCS from barotrauma• Dive depth and time profile--shallow, no-D

dives are unlikely to result in DCS• Point of onset--during descent, unlikely inner

ear DCS• Sx with difficult Valsalva suggest baro-trauma• Other signs / Sx of DCS can go along with

inner ear DCS

Type II DCS

Ocular manifestations• Nystagmus• Diplopia• Visual field defects and scotomata• Homonymous hemianopsia• Central retinal artery occlusion• Optic neuropathy• Ocular muscle impairment• Eyelid muscle pain

Type II DCS

• Proposed term including all cases of reduced-pressure, bubble-related disorders, including AGE because distinguishing between neuro DCS and AGE can be very difficult.

• In practice, recompression treatment of most cases of neurologic DCS and AGE is the same

“Decompression Illness” (DCI)

• DCS/AGE: symptoms of confusion, drowsiness, fatigue, indifference. • AGE attacks brain directly & immediately. • Manifests as acute stroke with focal hemispheric or

brain stem injury. Seizure, aphasia, hemiparesis & CV arrest common.

• Divers on SCUBA may be susceptible for combination of DCS & AGE.

DCI: Brain Involvement

Localized pain 858 91.8 744 76.6Numbness or paresthesia 199 21.2 41 4.3Muscular weakness 193 20.6 8 0.8Skin rash 140 14.9 42 4.4Dizziness of vertigo 80 8.5 24 2.5Nausea or vomiting 74 7.9 8 0.8Visual disturbances 64 6.8 14 1.4Paralysis 57 6.1 2 0.2 Headache 37 3.9 5 0.5 Unconsciousness 26 2.7 6 0.6Urinary disturbances 24 2.5 0 -Dyspnea (“chokes”) 19 2.0 4 0.4Personality change 15 1.6 0 -Agitation or restlessness 13 1.3 0 -Fatigue 12 1.2 2 0.2Muscular twitching 12 1.2 0 -Convulsions 11 1.1 0 -Incoordination 9 0.9 0 -Equilibrium disturbances 7 0.7 0 -Localized edema 5 0.5 0 -Intestinal disturbances 4 0.4 0 -Auditory disturbance 3 0.3 0 -Cranial nerve involvement 2 0.2 0 - Aphasia 2 0.2 0 - Hemoptysis 2 0.2 0 -Emphysema-subcutaneous 1 0.1 0 -

Sign or Symptom Number of Percentage of Number of Percentage of Instances Within Instances Within Instances Manifested Initial 935 Cases 935 Cases Initially Manifestations

Frequency of Signs and Symptoms: 935 Cases of Decompression Sickness (Rivera, 1964)

Type Manifestation % CasesNeurological 47Pain 25Constitutional 18Skin 3Cardiopulmonary 1.5Lymphatic 0.4

DAN Survey Data

1110 cases of DCI from SCUBA divers (1987-99)

• If you don’t think of it, you won’t ask about recent diving

• The key is the clinical, “bedside,” diagnosis of DCS

• History: dive profile, latency, symptoms

• Exam: neuro findings

Diagnosis of DCS

• Short, deep dives—a large pressure change that happens quickly

• Omitted decompression• Patent foramen ovale• Cold conditions• Older age• Obesity• Dehydration• Previous episode of DCS

DCS Risk Factors

• The sooner the treatment initiated, the better the outcome

• Cases of improvement have occurred even after about a week following the pressure exposure

Timing of Treatment

• 3 Categories Of Urgency– Emergent: neurologic signs are present and obvious

even without an examination• “feet should not be elevated, nor head lowered”• Type II DCS or AGE

– Urgent: “only severe symptom is pain”• Can delay briefly for DMO or equipment• Start all normal chamber preps

– Timely: symptoms are not obvious without a detailed exam

• “only a DMO may make the decision not to treat”

Casualty Assessment

Treatment Table 6 (TT6)

0

30

60

30

Total Elapsed Time: 4 hrs 45 minutes (not including descent time)

O2

O2 O2 O2

O2

20 20 20 30 60 605 5 5 15 152.4

O2 O2Descent Rate = 20 fpm

Ascent 1 fpm

Time at depth, min

Air

• Indications– Type II symptoms– Type I symptoms not relieved in 10 minutes– Cutis marmorata– Asymptomatic omitted decompression with > 30 min

missed– Symptomatic, uncontrolled (> 20 fsw) ascent – Treatment of unresolved sxs following in-water

recompression– Severe CO poisoning, CN poisoning, or smoke

inhalation

TT6

• Considerations– Can be extended twice at 60 ft (20-5 cycle) and twice at

30 ft (60-15 cycle) (don’t extend for mild joint soreness)

– Tender breathes 100% O2 for last 30 minutes of last 30 ft O2 period and to the surface• If > 1 extensions then tender breathes all 60 minutes

of last O2 period• If tender has been under pressure in last 12 hours,

add 60 minutes 100% O2 at 30 ft to requirement

TT6

• Surface O2 at 15 liters/min for up to 12 hours• IV normal saline or lactated Ringer’s, goal of clear

urine output (BUT, limit fluids in cases of pulmonary DCS)

• Enoxaparin (Lovenox), 30 mg SQ every 12 hours for cases of low-extremity paralysis

• Aspirin / NSAIDs, lidocaine, and steroids are NOT recommended

Adjunctive Treatment

• 100 % O2 breathing should be initiated during transport to the recompression site

• Potential benefits of O2(1) Enhanced off-gassing of inert gasses(2) Improved tissue oxygenation(3) Decreased cerebral edema

Oxygen

• Dehydration decreases tissue oxygenation and off-gassing.

• Immersion diuresis, insensible water loss (breathing a dry air source), as well as minimal intake before / during the dive are all factors in dehydration.

• AGE/ /Type II DCS (brain) IV 80 - 100 ml/h• Type II DCS (non-brain) IV 200-250 ml/hr

Fluid Therapy

• Two options:– Transport to nearest chamber vs. in-water

recompression• Transport (preferred)

– position prone or left lateral if unconscious– 100% O2– monitor hydration and body temperature– unpressurized aircraft < 1000 ft if possible

• In-water recompression: “only when the delay in transporting to a chamber would cause greater harm”

No Chamber

• Climbing to altitude is like ascending to the surface and can bring on DCS

• If air transport is necessary, the cabin should be pressurized to 1 ATA: C-9, C-40 (and other commercial airliners), Citation jet, Learjet

• If only unpressurized aircraft such as helo’s are available, then the aircraft should be kept below 1000 ft.

• Transport on O2

Flying with DCS

Flying After Diving

Diver’s Alert Network (DAN) 2002 Consensus Guidelines for Flying After Recreational Diving

Applies to air dives followed by flights at cabin altitudes of 2000 to 8000 feet for divers without DCS symptoms

• For a single no-decompression dive: – Wait at least 12 hours before flying

• For multiple dives/day or multiple days of diving: – Wait at least 18 hours before flying

• For any decompression dives: – “substantially longer than 18 hours appears

prudent.”

Flying After Diving

• Weight: 25 pounds• Chest mounted• Oxygen bottle volume:

1.5 liters• Oxygen bottle working

pressure: 200 BARS• Canister duration: 115-

200 minutes

Rebreathers: Draeger LAR V

Rebreathers

• Decompression sickness• Nitrogen narcosis• Hypoxia• Oxygen toxicity• CO2 toxicity• Caustic cocktail• Draeger Ear

Medical Considerations in Rebreather Diving

• Caused by canister leak• Highly alkaline solution

– Sofnolime (a typical CO2 scrubber material)• >75% Calcium hydroxide• 3% Sodium hydroxide

– Lithium hydroxide is 10 times more toxic than Sofnolime/Sodasorb.

• Usually preceded by symptoms of hypercarbia

Caustic Cocktail

• Also known as “Draeger Ear”• Refers to the negative pressure that develops in

middle ear after long O2 dives.• Sxs: ear pain, pressure, hearing loss, crackling

sensation secondary to middle ear effusion.• Dx: may look like mild squeeze, +/- middle ear

effusion.• Tx: decongestants• Avoid by periodic valsalva post O2 dive.

Middle Ear Oxygen Absorption Syndrome

• Analgesics• NSAIDS• Decongestants• Antibiotics• Topicals• Antacids• Vitamins

Considered Safe in Diving

Questions?

Hang Loose!

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