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    Diving Med Overview - No Slide Title Diving Med Overview - No Slide Title Presentation Transcript

    • 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
      Otitisexterna
      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
    • Barotrauma – Inner DDX
      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
    • 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
      Periorbitalpetechiae 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
      Pulmonary Barotrauma
    • 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
      mediastinumand subcutaneous tissues
      Pulmonary Barotrauma
    • Pulmonary Barotrauma
      Conditions resulting from POIS
      • Arterial gas embolism
      • Pneumothorax
      • Mediastinal emphysema
      • Subcutaneous emphysema
      • Pneumopericardium
    • Surface
      3 FSW
      96 FSW
      99 FSW
      Pulmonary Barotrauma
    • 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
      Pulmonary Barotrauma
    • 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
      Pulmonary Barotrauma
    • AGE– Presenting Signs and Symptoms
      • Stupor or confusion
      • Coma with or without seizures
      • Unilateral motor deficits
      • Visual disturbances
      • Vertigo
      • Sensory abnormalities
      Pulmonary Barotrauma
    • 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
      Pulmonary Barotrauma
    • Pneumothorax - Simple
      Symptoms
      Chest pain (lateral or apical)
      Cough
      Shortness of breath
      Signs
      Decreased breath sounds
      Typical CXR findings
      Pulmonary Barotrauma
    • Simple Pneumothorax
    • Pneumothorax – Simple
      Treatment
      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
      Pulmonary Barotrauma
    • Pneumothorax - Tension
      Symptoms
      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
      Pulmonary Barotrauma
    • Tension Pneumothorax
    • Pneumothorax - Tension
      Treatment
      Immediate needle decompression
      Chest tube
      Pulmonary Barotrauma
    • Mediastinal Emphysema
      Symptoms
      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
      Pulmonary Barotrauma
    • MediastinalEmphysema
    • Subcutaneous Emphysema
      Symptoms
      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
      Pulmonary Barotrauma
    • Subcutaneous Emphysema
    • Mediastinal or Subcutaneous Emphysema
      Treatment
      Surface O2
      For cardiac or respiratory compromise consider recompression
      5 - 10 FSW may be sufficient
      Pulmonary Barotrauma
    • 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
      Pulmonary Barotrauma
    • 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
      Decompression Sickness
    • 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
    • Decompression Sickness
      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%
      IntracardiacShunts
    • 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
      Decompression Sickness
    • 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 DCScases from 1999 Divers Alert Network (DAN) data
    • 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
    • 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
    • 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
    • PulmonaryDCS
      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
    • NeurologicDCS
      • 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
    • NeurologicDCS
      • 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
    • Sign or Symptom Number of Percentage of Number of Percentage of
      Instances Within Instances Within Instances Manifested Initial
      935 Cases 935 Cases Initially Manifestations
      Localized pain 858 91.8 744 76.6
      Numbness or paresthesia 199 21.2 41 4.3
      Muscular weakness 193 20.6 8 0.8
      Skin rash 140 14.9 42 4.4
      Dizziness of vertigo 80 8.5 24 2.5
      Nausea or vomiting 74 7.9 8 0.8
      Visual disturbances 64 6.8 14 1.4
      Paralysis 57 6.1 2 0.2
      Headache 37 3.9 5 0.5
      Unconsciousness 26 2.7 6 0.6
      Urinary disturbances 24 2.5 0 -
      Dyspnea (“chokes”) 19 2.0 4 0.4
      Personality change 15 1.6 0 -
      Agitation or restlessness 13 1.3 0 -
      Fatigue 12 1.2 2 0.2
      Muscular 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 -
      Frequency of Signs and Symptoms: 935 Cases of Decompression Sickness (Rivera, 1964)
    • 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)
      Time at depth, min
      30
      20
      20
      20
      30
      60
      60
      5
      5
      5
      15
      15
      2.4
      0
      O2
      O2
      O2
      O2
      O2
      O2
      O2
      30
      Descent Rate = 20 fpm
      Ascent  1 fpm
      Air
      60
      Total Elapsed Time: 4 hrs 45 minutes (not including descent time)
    • 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 sxsfollowing 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
    • Dehydrationdecreases 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: DraegerLAR V
    • Rebreathers
    • Decompression sickness
      Nitrogen narcosis
      Hypoxia
      Oxygen toxicity
      CO2 toxicity
      Caustic cocktail
      DraegerEar
      Medical Considerations in RebreatherDiving
    • 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!