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Decompression Sickness


Decompression Illness

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Decompression Sickness
Definition and Early Management
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This page is written and maintained by
Ernest S Campbell, MD, FACS

First described in 1841, decompression sickness has gradually become better understood. Sport divers have provided a large body of material to study causing us to be able to learn more about the illness. It's safe to say that DCS is caused by the production of nitrogen bubbles in the circulation, and this is related to the depthand time of a dive and to rate at which the diver ascends from depth. DCS and AGE combined form what is known as "decompression illness".

Called "bends" by early investigators, it is now classically divided into Type I, Type II and "Type III" (a phrase coined by Bove and Neumann to describe a combination of  DCS and arterial gas embolism). Type I DCS includes cutaneous manifestations and minor joint pain, or "pain only"; Type II includes severe symptoms related to the cardiopulmonary and neurological systems. Type III is a combination of AGE and DCS with neurologic symptoms.

Pain syndromes spot the pain in the limbs-not the central skeleton. It is dull, difficult to characterize and localize and is located in the shoulders, elbows and hands in divers. Compressed air workers have more pain in their lower extremities.

It is caused by bubbles, intravascular and extravascular with large gas stores in the fatty bone marrow. This is a cause of dysbaric osteonecrosis.

Neurologic Syndromes are increasing in sport divers and the spinal cord is the most commonly involved site. Symptoms include abdominal, low back, lower extremity pain, weakness and loss of feeling and function. Cerebral involvement is much more common than previously thought and may account for a portion of the "spinal cord" lesions. Peripheral nerves can also be involved causing numbness, limb pains and weakness.


Early Treatment

  • Recognition *Symptoms usually appear 15 minutes to 12 hours after surfacing*
  • Signs
        • Blotchy rash
        • Paralysis or weakness
        • Coughing spasms
        • Staggering or instability
        • Unconsciousness
  • Symptoms
        • Tired feeling
        • Itching
        • Pain, arms, legs or trunk
        • Dizziness
        • Numbness, tingling or paralysis
        • Chest compression or shortness of breath
  • Early Management
        • Immediate oxygen breathing, continue even if person improves 

        • markedly
        • Stabilize patient the same way as for Air Embolism
        • Urgent recompression after stabilization in trauma facility
        • Early recompression treatment for all forms of decompression sickness. There is a lightweight, portable recompression facility that would appear to be ideal for the liveaboard or dive operation far from a fixed-base chamber. This is the 'SOS Hyperlite Stretcher'. More information can be obtained at http://www.hyperlite.co.uk/  .

    Decompression Illness in Sports Divers: Part I
    Ernest S. Campbell, MD, FACS, Orange Beach, Ala.

     Medscape Orthopaedics & Sports Medicine eJournal 1(5), 1997. 1997 Medscape Portals, Inc

    *See also Board Preparation, Part I with self-grading quiz.

    Abstract and Introduction

    Abstract

    Decompression sickness (DCS) results from gas coming out of solution in the bodily fluids and tissues when a diver ascends too quickly. This occurs because decreasing pressure lowers the solubility of gas in liquid. Also, the expansion of gas in the lungs may lead to alveolar rupture, also known as "Pulmonary Overinflation Syndrome," which may, in turn, result in arterial gas embolism (AGE). DCS, AGE, and all of their presentations are grouped together under the heading "decompression illness." Joint pain is the most common complaint in DCS, especially in the elbow, shoulder, hip and knee. Blockage of vessels results in ischemia and infarction of tissues beyond the obstruction, and inflammatory changes can lead to extravasation into the tissues, resulting in edema and further compromising the circulation. Involved skin displays a mottled appearance known as "cutis marmorata." In the lymphatic system, bubbles may result in regional lymphedema. More severe cases may involve the brain, the spinal cord, or the cardiopulmonary system. Neurologic manifestations may include sensory deficits, hemiplegia, paraplegia, paresthesias, and peripheral neuropathies. Possible cardiopulmonary effects include massive pulmonary gas emboli or myocardial infarction. Decompression sickness is treated with recompression in a chamber to 60 FSW or deeper, associated with hyperbaric oxygen breathing. In the US, this therapy is usually guided by a Navy Treatment Table. These tables are very effective, especially when recompression is begun promptly.

    Introduction

    On the earth's surface, the human body is exposed to an ambient pressure which is the result of the combined partial pressures of all the gases in the earth's atmosphere. At sea level, the force of this pressure is described as 1 atmosphere absolute (ATA). As a diver descends, exposure to increasing pressure forces more gas to dissolve in the bodily fluids and tissues, as described by natural gas laws. Upon ascent through the water column, the solubility decreases again. Rapid ascent may lead to bubble formation and decompression sickness (DCS) or alveolar rupture ("Pulmonary Overinflation Syndrome" [POIS]), with resultant bubbles in the arterial circulation (arterial gas embolism [AGE]).[1]

    DCS, AGE, and all of their presentations are grouped together under the heading "decompression illness" (DCI).[2] Treatment consists of recompression in a chamber using air and 100% oxygen. Bubbles may form in blood vessels, where they may cause ischemia and infarct, and in tissues, where they may initiate an inflammatory response. Inflammatory changes can lead to extravasation into the tissues, further compromising the circulation and resulting in edema.

    Hyperbaric exposures (situations where there are elevated pressures) can occur during construction and tunneling projects, in hyperbaric oxygen treatment facilities and in aviation. (The airman is subject to the same problem as divers, except that the situation is reversed--bubbles form on ascent, due to a decrease in pressure and supersaturation. Returning to the ground increases pressure and is analogous to recompression. However, DCS symptoms may occur after returning to the ground and sometimes require additional recompression.)

    Recreational scuba diving is the most common type of hyperbaric exposure, especially since the explosive growth of sports scuba (self-contained underwater breathing apparatus) diving in the past decade. Hyperbaric oxygen (HBO) treatment is gaining popularity as the definitive therapy for a growing number of disorders, including decompression sickness, AGE, CO poisoning, clostridial infections, crush injuries, diabetic leg ulcers, skin graft failures, refractory osteomyelitis, thermal burns, necrotizing soft tissue infections, and osteoradionecrosis.

    It is incumbent on physicians to be fully conversant with the diagnosis and treatment of decompression illness, especially because the hyperbaric chamber is now widely recognized as effective in reversing the sometimes-deadly changes that take place with DCI.

    Hyperbaric Terminology and Physics

    At sea level, the body is exposed to 1 ATA of pressure. This is also expressed as 760 millimeters of mercury (mm Hg), 33 feet of sea water (FSW), or 14.7 pounds per square inch (psi). The normal atmospheric pressure of 1 ATA is actually a reference point. When one states that systolic blood pressure is 120 mm Hg, we are really saying that it is 120 mm Hg above that of the surrounding environment which is 880 mm Hg (absolute pressure). The systolic blood pressure is a "gauge" pressure, meaning that the pressure displayed is the actual pressure minus the constant 1 ATA of atmospheric pressure. By analogy, the depth gauge of a diver reads "0" on the surface but he is exposed to 1 ATA or the same as 33 FSW--at 33 feet underwater he will be under 2 atmospheres of absolute pressure.

    A fluid-filled space or a solid organ will not change in size as pressure changes because fluids are not compressible. A space with elastic walls that is filled with air will change shape according to Boyle's law,[3] which states that the volume of gas is inversely proportional to the absolute pressure (Fig. 1). For example, a balloon filled with one cubic foot of air on the surface (1 ATA) would shrink to a volume of one-half cubic foot if taken to a depth of 33 FSW (2 ATA), and to one-fourth of a cubic foot at 99 FSW (4 ATA).

    Figure 1. Boyle's law states that the volume of gas is inversely proportional to the absolute pressure when temperature is constant. Therefore, divers are taught to exhale on ascent--otherwise expanding air may rupture the delicate alveoli. Adapted from NOAA (1979).
    The gas-filled organs--such as the middle ear or the lungs--have only a limited capacity to change their volume. As long as the quantity of gas within the space is vented to compensate for changes in pressure, there are no problems. Thus, divers are taught to exhale on ascent--otherwise the expanding air may rupture the delicate alveoli--and to clear their ears on descent, which adds gas to the middle ears to prevent collapse. If this equalization is not performed, "barotrauma" occurs--an "ear squeeze" (Fig. 2) in the case of the ear, and ruptured alveoli or POIS and possibly AGE in the case of the lung.
    Figure 2. Divers are taught to clear their ears on descent, which adds gas to the middle ears to prevent collapse. If this equalization is not performed an "ear squeeze" may occur. Note that the eardrum is retracted and the Eustachian tube is blocked by blood and fluid. Reprinted with permission from Scuba Diving Explained: Questions and Answers on Physiology and Medical Aspects of Scuba Diving, Lawrence Martin, MD.
    Henry's law and Dalton's law are central to understanding decompression sickness. Henry's law states that, at a given temperature, the amount of gas that will dissolve in a liquid is directly proportional to the partial pressure of the gas. Dalton's Law states that the pressure of a gas is the sum of the partial pressures of all gases present.

    Nitrogen , which comprises 78% of atmospheric gas and is biologically inert, is the gas which leads to pathology as it follows the gas laws in the vessels and organs of a scuba diving human. As a diver breathing air from a tank descends, the increased pressure causes more nitrogen to enter his tissues than was present at the surface. If enough nitrogen enters into solution and the diver returns to the surface too quickly, the excess gas will not have a chance to be eliminated ("blown off") gradually through the lungs. The nitrogen will then come out of solution and go into a gas phase--bubbles, which form in the blood and tissues of the body. These bubbles account for the clinical entity that we call decompression sickness (DCS).

    Decompression Sickness

    Pathophysiology. The amount of nitrogen that diffuses into the bodily tissues during a dive depends on the depth of the dive and the duration of exposure. On ascent, as the body experiences a rapid reduction in ambient pressure, biologically inert gases that are dissolved in the tissues may come out of solution as bubbles if the diver does not allow adequate time for the excess nitrogen to be eliminated through respiration. (For repetitive dives, the diver must consider the nitrogen retained from previous dives in order to select a safe decompression schedule.) Visualize the bubbling froth of CO2 that rushes out of solution from the sudden decrease in pressure that occurs when you open a can of soda pop. The bubbles in the body may form in the venous blood, musculoskeletal system or other body tissues; decompression sickness is the clinical condition that results.

    Systemic manifestations. Decompression sickness, as would be expected, is a multisystem disease. Joint pain is the most common complaint in DCS, with pain in the elbow, shoulder, hip and knee joints being the most prevalent sites.[4,5,6] The skin may be involved, displaying a mottled appearance known as "cutis marmorata" (Fig. 3). Bubbles in the lymphatic system may result in regional lymphedema. Cases of decompression sickness limited to musculoskeletal, skin, or lymphatic manifestations are often referred to as Type I DCS.

    Figure 3. Cutis marmorata is a mottled appearance of the skin seen in type I decompression sickness.
    More severe cases may involve the brain, the spinal cord, or the cardiopulmonary system.[7] Neurologic manifestations may include sensory deficits, hemiplegia, paraplegia, paresthesias, and peripheral neuropathies.[8] Possible cardiopulmonary effects include massive pulmonary gas emboli or myocardial infarction. Decompression sickness with neurologic or cardiopulmonary symptoms is often referred to as Type II DCS.

    The presenting symptoms of DCS are influenced by the depth of the dive and the bottom time of the dive, the inert gas breathed, the adequacy of decompression, and the delay to presentation.

    The US Navy Diving Manual notes that the majority of DCS cases involve musculoskeletal pain.[8] Thalmann and colleagues[9-12] reported that even relatively risky experimental dive series conducted by the navy to develop new decompression tables and decompression computer programs had a predominance of Type I symptoms (106 cases of Type I as compared to 37 cases of Type II DCS).

    In contrast to this, recreational reports have a higher incidence of more serious symptoms. Kizer[13] published a series of 50 cases and noted 24 patients with Type I and 26 with Type II DCS. Diving fishermen in Singapore with a significant delay in recompression had a much higher incidence of serious cases than previous reports, with 47 out of 58 patients experiencing Type II DCS.[14]

    Prevention. Important questions for divers include "how quickly should I rise?" and "how long should I stay on the surface between dives?" The various dive tables developed by governmental and diving instruction agencies attempt to answer these questions. The US Navy Decompression Tables were compiled after studying the effect of decompression on young, fit men and have been found in some cases not to apply to the average recreational diver. These tables are being revised; the training agencies PADI (Professional Association of Diving Instructors), in Canada, the DCIEM (Defense and Civil Institute of Environmental Medicine) (Table I), and the NAUI (National Association of Underwater Instructors) (Table II, III, IV, and V), all have different diving tables which attempt to meet this need for more conservative decompression schedules. This is accomplished in part by shortening the allowable bottom time for no-decompression diving (No-D diving).

    Adherence to appropriate decompression tables and dive computers reduces the risk of DCS, but does not eliminate it entirely. Many cases of DCS have been reported in divers who have been decompressed in strict compliance with published tables. In the navy, the incidence of DCS is variously reported between 0.01% and 1.25%.[3]

    Both dive computers and tables are tools that can help the diver understand the dive profiles they are conducting. Adherence to dive schedules does not guarantee DCS will not occur. "It doesn't matter which dive tables you don't use" is an apt phrase coined by Neuman. Shallow divers are at less risk, but they can still become saturated with nitrogen if they use more than one tank of compressed air, and will still need to off-gas as they ascend in the water column.

    Treatment. Decompression sickness is treated with recompression in a chamber to 60 FSW or deeper associated with hyperbaric oxygen breathing.[15] In the US, this therapy is usually guided by a Navy Treatment Table.[8] These tables are very effective, especially when recompression is begun promptly.[16]

    The purpose of the therapy called for in the Navy Treatment Tables is two-fold: to promote inert gas elimination and to help cause a decrease in bubble size. The treatment outlined by the tables also provides oxygen to the damaged tissues, treats platelet and clotting damage and allows excretion of harmful metabolites. The oxygen reduces CNS edema and provides a high oxygen gradient (2000 mm Hg) for the ischemic tissues.[17]

    Specifics: Recompression treatment of decompression sickness. First, it is important to take the time for a careful clinical exam, because true Type I DCS without other manifestations is very rare, and diagnostic tests are of little value.

    The initial therapy for Type I and Type II DCS is treatment in a chamber with Navy Treatment Table 6 ( Table VI ). Table 6 indicates recompression to 60 feet for 285 minutes, with intermittent oxygen breathing periods and slow "ascent to the surface." (The diving tables indicate increases in pressure with the word "descent" and decreases with "ascent." They also give their pressure values in depth-equivalents.) The periods of oxygen breathing are broken up into intervals to prevent O2 toxicity ( Table VI ). If O2 seizures occur, turn off the O2 for 15 minutes and continue the treatment.

    In the case of poor response to standard Navy Treatment Tables 6A ( Table VII ) or 6 ( Table VI ), Treatment Table 6 ( Table VI ) can be extended for additional oxygen breathing periods at 60 or 30 feet. If you are following Treatment Table 6A ( Table VII ) and there is no resolution or the patient is getting worse on ascent, try Treatment Table 4 ( Table VIII ) , which indicates staying at 165 feet for 2 hours--then go to Table 6 at 60 feet with extensions, if necessary.

    Treatment Table 7 ( Table IX ) is used for worsening or unresolved DCS or AGE. It is a long, involved and dangerous treatment and should not be used unless adequate support is available. If all else fails, call Divers Alert Network (DAN) at (919) 684-9111, rather than creating your own treatment table.

    Even after "successful" treatment, some people experience relapse of symptoms. Recurrences are treated with Treatment Table 5 ( Table X ) or Treatment Table 6 ( Table VI ) once or twice-daily until no further improvement is observed by the medical director of the facility. Recent evidence indicates that persistent neurologic defects may be lessened by repetitive treatments on Navy Treatment Tables 5, 6 (Tables X , VI ) or even with 100% oxygen at 30 FSW for 90 minutes bid. Flying should be avoided for a period of 72 hours after treatment for DCS or AGE.

    Equipment which might be needed in the altered pressure environment includes ventilators, bubble traps and pumps for use with intravenous catheters, endotracheal tube cuffs which inflate with water, and if chest tubes are required, the patient must be vented during descent using #18 gauge 1 1/2 " needle.

    Arterial Gas Embolism

    Pathophysiology. Arterial gas embolism (AGE) is another disorder in which bubble formation may occur in the vascular system.[18] The bubbles in AGE originate not from supersaturation of gases in the blood and tissues but from rupture of the alveoli due to the barotrauma of ascent. The bubbles enter the pulmonary venous system and are carried to the heart and arterial systemic circulation.

    Systemic symptoms. As might be expected, most symptoms from this disorder are localized to the cerebral circulation (Fig. 4), with occasional embolization to the coronary arteries causing cardiac arrest. Classically, the presentation is that of sudden onset of unconsciousness within minutes of reaching the surface after a dive--there having been some reason why the diver ascended with his glottis closed (unconsciousness, panic, dry suit blowup, loss of weights, malfunction of buoyancy compensator). Other possible presentations include hemispheric motor and/or sensory deficits, confusion and convulsion. Peripheral nerve changes and musculoskeletal pain are not part of the symptom complex of AGE.[19-21]

    Figure 4. Most symptoms from arterial gas embolism are due to the effect of air bubbles in the cerebral circulation, with occasional embolization to the coronary arteries, causing cardiac arrest. Pathway for the development of cerebral gas embolism is shown. Reprinted from the NOAA.
    Treatment. Management is generally similar to that of DCS--recompression and HBO are indicated in all cases as quickly as possible.[22]

    Specifics: Recompression treatment of gas embolism. In contrast to the treatment of decompression sickness, one should not delay for diagnostic work-up or extensive clinical evaluation. Instead, the first question is whether to use Treatment Table 6A or 6 (Tables VII , VI ). If there is a delay greater than 4 hours, Treatment Table 6 ( Table VI ) should be used initially and then proceed to 6A ( Table VII ) depending on the clinical response. Treatment Table 6A ( Table VII ) allows for rapid compression to 165 feet and is used for major air embolisms. If such a chamber is not available, then one should use a 3 ATA chamber.

    For those patients not responding to Navy Table 6 ( Table VI ), other choices are available: US Navy Table Treatment 4 ( Table VIII ) or the Comex Table, which prescribes 30 minutes breathing 50/50 O2/N2 mix at 100 feet. Unproven treatment schedules should be avoided, but extensions to the tables are not experimental and should be used as necessary.

    Tables

    Table I. Short Form of the DCIEM Tables (front)

     


    Table II. NAUI Dive Tables

     


    Table III. NAUI Dive Table 1

     


    Table IV. NAUI Dive Table 2

     


    Table V. NAUI Dive Table 3

     


    Table VI. US Navy Treatment Table 6: Oxygen Treatment of Type II Decompression Sickness*

     
     
    Depth
    (feet)
    Time
    (minutes)
    Breathing
    Media
    Total
    Elapsed
    Time (hr:min)
    60 20 O2 0:20
    60 5 Air 0:25
    60 20 O2 0:45
    60 5 Air 0:50
    60 20 O2 1:10
    60 5 Air 1:15
    60 to 30 30 O2 1:45
    30 15 Air 2:00
    30 60 O2 3:00
    30 15 Air 3:15
    30 60 O2 4:15
    30 to 0 30 O2 4:45
    * Treatment of Type II or Type I decompression sickness when symptoms are not relieved within 10 minutes at 60 feet.
    Descent rate--25 ft/min. Ascent rate--1 ft/min. Do not compensate for slower ascent rates. Compensate for faster rates by halting the ascent.
    Time at 60 feet begins on arrival at 60 feet.
    If oxygen must be interrupted because of adverse reaction, allow 15 minutes after the reaction has entirely subsided and resume schedule at point of interruption.
    Caregiver breathes air throughout unless he has had a hyperbaric exposure within the past 12 hours, in which case he breathes oxygen at 30 feet.
    Extensions to Table 6: Table 6 can be lengthened up to 2 additional 25 minute oxygen breathing periods at 60 feet (20 minutes on oxygen and 5 minutes on air) or up to 2 additional 75 minute oxygen breathing periods at 30 feet (15 minutes on air and 60 minutes on oxygen) or both. If Table 6 is extended only once at either 60 or 30 feet, the tender breathes oxygen during the ascent from 30 feet to the surface. If more than one extension is done, the caregiver begins oxygen breathing for the last hour at 30 feet during ascent to the surface.
    Adapted from the US Navy Diving Manual.


    Table VII. US Navy Treatment Table 6A - Initial Air and Oxygen Treatment of Arterial Gas Embolism*

     
     
    Depth
    (feet)
    Time
    (minutes)
    Breathing
    Media
    Elapsed
    Time
    (hrs:min)
    165 30# air 0:30
    165 to 60 3ft/min air 0:34
    60 20 O2 0:54
    60 5 air 0:59
    60 20 O2 1:19
    60 5 air 1:29
    60 20 O2 1:44
    60 5 air 1:49
    30 15 air 3:49
    30 60 O2 4:49
    60 to 30 30 O2 2:19
    30 15 air 2:34
    30 60 O2 3:34
    30 to 0 30 O2 5:19
    * Treatment of arterial gas embolism where complete relief obtained within 30 min at 165 feet. Use also when unable to determine whether symptoms are caused by gas embolism or severe decompression sickness. 
    Descent rate--as fast as possible. Ascent rate--1 ft/min. Do not compensate for slower ascent rates. Compensate for faster ascent rates by halting the ascent.
    Time at 165 feet-- includes time from the surface.
    If oxygen breathing must be interrupted as a result of adverse reaction, allow 15 minutes after the reaction has subsided and resume schedule at the point of interruption.
    Caregiver breathes oxygen during ascent from 30 feet to the surface unless he has had hyperbaric exposure within the past 12 hours, in which case he breathes oxygen at 30 feet. 
    Extensions: Table 6A can be lengthened up to 2 additional 25 minute periods at 60 feet (20 minutes on oxygen and 5 minutes on air) or up to 2 additional 75 minute oxygen breathing periods at 30 feet (15 minutes on air and 60 minutes on oxygen), or both. If Table 6A is extended either at 60 or 30 feet, the tender breathes oxygen during the last half at 30 feet and during ascent to the surface.
    # If complete relief is not obtained within 30 min at 165 feet, switch to Table 4, consulting with a Diving Medical Officer if possible.
    Adapted from the US Navy Diving Manual.


    Table VIII. US Navy Treatment Table 4 - Air or Air and Oxygen Treatment of Type II Decompression Sickness or Arterial Gas Embolism*

     
     
    Depth
    (feet)
    Time Breathing
    Media
    Total
    Elapsed
    Time (hrs:min)
    165 _ to 2 hr# Air 2:00
    140 _ hr Air 2:31
    120 _ hr Air 3:02
    100 _ hr Air 3:33
    80 _ hr Air 4:04
    60 6 hr Air or Oxygen/Air 10:05
    50 6 hr " 16:06
    40 6 hr " 22:07
    30 12 hr " 34:08
    20 2 hr " 36:09
    10 2 hr " 38:10
    0 1 min " 38:11
    * Treatment of worsening symptoms during the first 20 minute oxygen breathing period at 60 feet on Table 6, or when symptoms are not relieved within 30 minutes at 165 feet using treatment Table 3 or 6A.
    Descent rate--as rapidly as possible. Ascent rate--1 minute between stops. 
    Time 165 feet--includes time from the surface.
    If only air available--decompress on air. If oxygen available, patient begins oxygen breathing upon arrival at 60 feet with appropriate air breaks. Both tender and patient breathe oxygen beginning 2 hours before leaving 30 feet. 
    Ensure life support considerations can be met before committing to a Table 4. Internal chamber temperature should be below 85 degrees F 29.4 C.
    If oxygen breathing is interrupted, no compensatory lengthening of the table is required.
    # If switching from treatment table VIA at 165 feet, stay the full 2 hours at 165 feet before decompressing.
    Adapted from the US Navy Diving Manual.


    Table IX. US Navy Treatment Table 7- Oxygen/Air Treatment of Unresolved or Worsening Symptoms of DCS or AGE *@

     
     
    Depth (feet) Time (hours) Breathing Media Total
    Time (hours)
    60 12 hr minimum -no maximum Oxygen 20 min, air 5 min 12 hours
    Ascend 3 ft/hr or two ft every 40 min  6 hours   18 hours
    Ascend 2 ft/hr# 10 hours   28 hours
    Ascend 1ft/hr 16 hours   44 hours
    4 feet 4 hour stop   48 hours
    Ascend 1 ft/hr 4 min   48 hours/4 min
    * Used for treatment of unresolved life threatening symptoms after ini valign=toptial treatment on Table 6, 6A, or 4.
    Use only under the direction of a Diving Medical Officer.
    Table begins on arrival at 60 feet. Arrival at 60 feet is accomplished by initial treatment on Table 6, 6A or 4. If initial treatment has progressed to a depth shallower than 60 feet, compress to 60 feet at 25 ft/min to begin table 7. 
    Maximum duration at 60 feet is unlimited. Remain at 60 feet a minimum of 12 hours unless overriding circumstances dictate earlier decompression.
    Patient begins oxygen breathing periods at 60 feet. Caregiver need breathe only chamber air throughout. If oxygen breathing is interrupted, no lengthening of the table is required. 
    Minimum chamber O2 concentration: 19%. Maximum chamber CO2 concentration: 1.5% SEV (12 mm). Maximum temperature: 29.4C.
    # Decompression starts with a 2 foot upward excursion from 60 to 58 feet. Decompress with stops every 2 feet for the times shown on the above profile. Ascent time between stops is approximately 30 seconds. Stop time begins with ascent from deeper to next shallower step. Stop at 4 feet for 4 hours and then ascend to the surface at 1 ft/minute.
    @ Ensure chamber life support requirements can be met before committing to this table.
    Adapted from the US Navy Diving Manual.


    Table X. US Navy Treatment Table 5 - Oxygen Treatment of Type I DCS*

     
     
    Depth
    (feet)
    Time
    (minutes)
    Breathing
    Media
    Total
    Elapsed
    Time (hrs:min)
    60 20 O2 0:20
    60 5 Air 0:25
    60 20 O2 0:45
    60to30 30 O2 1:15
    30 5 Air 1:20
    30 20 O2 1:40
    30 5 Air 1:45
    30 to 0 30 O2 2:15
    * Treatment of Type I decompression sickness when symptoms are relieved within 10 minutes at 60 feet and a complete neurological exam is normal.
    Descent rate--25 ft/min. Ascent rate--1 ft/min. Do not compensate for faster rates by halting the descent.
    Time at 60 feet begins on arrival at 60 feet.
    If oxygen breathing must be interrupted, allow 15 minutes after the reaction has entirely subsided and resume schedule at point of interruption.
    If oxygen breathing must be interrupted at 60 feet, switch to Table 6 upon arrival at the 30 foot stop. 
    Caregiver breathes air throughout unless he has had a hyperbaric exposure within the past 12 hours, in which case he breathes oxygen at 30 feet.


    Table XI. US Navy Treatment Table 3 - Air Treatment of Type II DCS or Arterial Gas Embolism*

     
     
    Depth
    (feet)
    Time
    (minutes)
    Breathing
    Media
    Total
    Elapsed
    Time
    (hrs:min)
    165 30 min Air 0:30
    140 12 min Air  0:43
    120 12 min Air 0:56
    100 12 min Air 1:09
    80 12 min Air 1:22
    60 30 min Air 1:53
    50 30 min Air 2:24
    40 30 min Air 2:55
    30 720 min Air 14:56
    20 120 min Air 16:57
    10 120 min Air 18:58
    0 1 min Air 18:59
    * Treatment of Type II symptoms or arterial gas embolism when oxygen unavailable and symptoms are relieved within 30 minutes at 165 feet.
    Descent rate--as rapidly as possible. Ascent rate--1 minute between stops.
    Time at 165 feet--includes time from the surface.
    Adapted from the US Navy Diving Manual.


    References

    1. Polak B, Adams H: Traumatic air embolism in submarine escape training. U.S. Naval Med. Bull. 30: 165-177, 1932.
    2. Francis TJR, Smith D (eds): Describing Decompression Illness. Bethesda, Undersea and Hyperbaric Medical Society, 1987.
    3. Boyle R: New pneumatic experiments about respiration. Phil. Trans. R. Soc. London 5: 2011-2031, 1670.
    4. Vann RD, Thalmann ED: Decompression physiology and practice, in Bennett PB, Elliott DH (eds): The Physiology and Medicine of Diving. London, WB Saunders, 1993, ed 4, pp 376-432.
    5. Elliott DH, Moon RE: Manifestations of the decompression disorders, in Bennett PB, Elliott DH (eds): The Physiology and Medicine of Diving. London, WB Saunders, 1993, ed 4, pp 481-505.
    6. Flynn ET: Decompression sickness, in Camporesi EM, Barker A (eds): Hyperbaric Oxygen Therapy: A Critical Review. Bethesda. Undersea and Hyperbaric Med. Soc. , 1991, pp 55-74.
    7. Francis TJR, Gorman DF: Pathogenesis of the decompression disorders, in Bennett PB, Elliott DH (eds): The Physiology and Medicine of Diving. London, WB Saunders, 1993, ed 4, pp 454-480.
    8. US Navy Diving Manual. Commander Naval Sea Systems Command Publication 0994-LP-001-9010. Washington DC, US Government Press, 1993, Revision 3, Vol 1, Chapter 8.
    9. Thalmann ED, Buckingham IP, Spaur WH: Testing of Decompression Algorithms for Use in the US Navy Underwater Decompression Computer (Phase I). US Navy Experimental Diving Unit Report 11-80, 1980.
    10. Thalmann, ED: Phase II Testing of Decompression Algorithms for Use in the US Navy Underwater Decompression Computer, US Navy Experimental Diving Unit Report 1-84, 1984.
    11. Thalmann ED: Development of a Decompression Algorithm for Constant 0.7 ATA Oxygen Partial Pressure in Helium Diving. US Navy Experimental Diving Unit Report 1-85, 1985.
    12. Thalmann ED: Air-N2O2 Decompression Algorithm Development. US Navy Experimental Diving Unit Report 8-85, 1986.
    13. Kizer KW: Delayed treatment of dysbarism: A retrospective review of 50 cases. JAMA 247: 2555-2558, 1982.
    14. Yap CL: Delayed decompression sickness--the Singapore experience, in Proc Joint S Pacific Underwater Med Soc and Republic Singapore Navy Underwater Med Conf. SPUMS J Suppl, 1981.
    15. Kindwall EP: Decompression sickness. In: Davis JC, Hunt TK (eds): Hyperbaric Oxygen Therapy. Bethesda, Undersea Medical Society, 1977, pp 125-140.
    16. Butler FK, Pinto C: Progressive Ulnar Palsy as a late complication of decompression sickness. Annals Emerg Med 15: 738-741, 1986.
    17. Air decompression, in Department of the Navy: US Navy Diving Manual, NAVSHIPS 0994-001-9010, Vol 1. Air Diving. Washington, DC: Department of the Navy, 1991 pp 7-1 to 7-24.
    18. Behnke, AR: Analysis of Accidents occurring in training with the submarine "lung". U.S. Naval Medical Bull. 30: 177-184, 1932.
    19. Schaefer KE, Nulty WP, Carey C, et al: Mechanisms in development of interstitial emphysema and air embolism on decompression from depth. J. Appl. Physiol. 13: 15-29, 1958.
    20. Malhotra MC, Wright CAM: Arterial air embolism during decompression and its prevention. Proc. R. Soc. Med. B154: 418-427, 1960.
    21. Mader JT, Hulet WH: Delayed hyperbaric treatment of cerebral air embolism. Arch. Neurol. 36: 504-505, 1979.
    22. Catron PW, Dutka AJ, Biondi DM, et al: Cerebral air embolism treated by pressure and hyperbaricoxygen. Neurology. 41: 314-315, 1991

    Suggested Readings

    Arthur DC, Margulies RA: A short course in diving medicine. Annals Emerg Med 16: 689-701, 1987.

    Ball R. Effect of severity, time to recompression with oxygen, and retreatment on outcome in forty-nine cases of spinal cord decompression sickness. Undersea and Hyperbaric Medicine 20:133-145, 1993.

    Berghage TE, Durman D: US Navy Air Decompression Schedule Risk Analysis. Bethesda, MD: Naval Medical Research Institute Technical Report, NMRI #80-1, 1980.

    Boettger ML. Scuba diving emergencies: Pulmonary overpressure accidents and decompression sickness. Annals Emerg Med 12: 563-567, 1983.

    Boussuges A, Thiriion P, Molenat F, et al: Neurologic decompression illness: A gravity score. Undersea and Hyperbaric Medicine 23:151-155, 1996.

    Boycott AE, Damant GCC, Haldane JS: The prevention of compressed-air illness. J Hyg Camb 8: 342-443, 1908.

    Bove AA, Moon RE, Neuman TS: Nomenclature of pressure disorders. Classification of the decompression disorders: time to accept reality. DCI/DCS: Does it matter whether the Emperor wears clothes? Undersea and Hyperbaric Medicine 24:1-4, 1996. Editorials.

    Bove AA: The basis for drug therapy in decompression sickness. Undersea Biomed Res 9: 91-111, 1982.

    Bracken MB, et al: A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal injury. New Eng J Med 322: 1405-1412, 1990.

    Catron PW, Flynn ET Jr: Adjuvant drug therapy for decompression sickness: A review. Undersea Biomed Res 9: 161-74, 1982.

    Cross SJ, Thomson LF, Jennings KP, et al: Right-to-left shunt and neurological decompression sickness in divers.

    Lancet ii 568, 1989. Letter.

    Cross SJ, Lee HS, Thomson LFet al: Patent foramen ovale and subaqua diving . BMJ 304: 1312, 1992. Letter.

    Davis JC, Kizer KW: Diving medicine, in: Auerbach PS, Geehr EC (eds): Management of Wilderness and Environmental Emergencies, 2nd edition. St. Louis, The C.V. Mosby Co., 1989.

    Dewey AW, Jr: Decompression sickness, an emerging recreational hazard. N Engl J Med 267: 759-65; 812-20, 1962.

    Dick APK, Massey EW: Neurologic presentation of decompression sickness and air embolism in sport divers. Neurology 35: 667-671. 1985

    Edmonds C. Barotrauma, in Strauss R.(ed): Diving Medicine. New York, Grune & Stratton, 1976.

    Gorman DF: Decompression sickness and arterial gas embolism in sports scuba divers. Sports Medicine 8: 32-42, 1989.

    Green RD, Leitch DR: Twenty years of treating decompression sickness. Aviat Space Environ Med 58: 362-6, 1987.

    Hall ED: Lazaroids: Mechanisms of action and implication for disorders of the CNS. Neuroscientist, 3:42-51, 1997.

    Johnston RP, Broome JR, Hunt PD, et al: Patent foramen ovale and decompression illness in divers. The Lancet 348: 1515, 1996. Letter.

    Kelleher PC, Pethybridge RJ, Francis TJR: Outcome of neurological decompression illness: development of a manifestation based model. Aviat, Space, and Environ Med 67: 654-658, 1996.

    Kindwall EP: Diving emergencies, in Kravis TC (ed): Emergency Medicine Aspen Systems Corporation, Rockville, Maryland, 1983.

    Kizer KW: Dysbaric cerebral air embolism in Hawaii. Ann Emerg Med 16: 535-41, 1987.

    Knauth M, Ries S, Pohlmann S, et al: Cohort Study of multiple brain lesions in sport divers: Role of a patent foramen ovale. BMJ 314: 701-705, 1997.

    Krzyzak J: A case of delayed-onset pulmonary barotrauma in a scuba diver. Undersea Biomed Res 14: 553-61, 1987.

    Mebane GY, Dick AP: DAN Underwater Diving Accident Manual. Divers Alert Network, Duke University, 1985.

    Mitchell SJ: The role of lignocaine in the treatment of decompression illness: A review of the literature. SPUMS Journal 25:182-194, 1995.

    Moon RE, Sheffield PJ: Guidelines for Treatment of Decompression Illness. Aviat Space Environ Med 68:234-43, 1997.

    Moon RE, Camporesi EM, Kisslo JA: Patent foramen ovale and decompression sickness in divers. Lancet

    1: 513-514, 1989.

    Moon RE, Sheffield PJ, (eds.): Treatment of Decompression Illness. 45th Workshop of the Undersea and Hyperbaric Medical Society, June 1996.

    Neblett LM: Otolaryngology and sport scuba diving. Update and guidelines. Annals Otology, Rhin and Laryng. Supplement 115: 1-12, (a great article) 1985.

    Rivera JC. Decompression sickness among divers: An analysis of 935 cases. Military Medicine, pp 314-334, April 1964.

    Roydhouse N: 1001 disorders of the ear, nose and sinuses in scuba divers. Can J Appl Spt Sci 10: 99-103. 1985.

    Schaefer KE, McNulty WP Jr., Carey C, Liebow AA. Mechanisms in development of interstitial emphysema and air embolism on decompression from depth. J Appl Physiol 13: 15-29, 1958.

    Strauss RH. Diving Medicine: State of the Art. Amer Rev Resp Dis 119: 1001-1023, 1979.

    Thalmann ED in Moon RE, Sheffield PJ eds. Treatment of Decompression Illness. 45th Workshop of the Undersea and Hyperbaric Medical Society, June 1996; pp 75-95.

    Weeth JB. Management of underwater accidents. JAMA 192: 215-219, 1965.

    Wilmshurst P, Byrne JC, Webb-Peploe MM. Relation between interatrial shunts and decompression sickness in divers.

    Lancet II: 1302-1306, 1989.

    Weathersby PK, Homer LD, Flynn ET: On the likelihood of decompression sickness. J Appl Physiol 57: 815-25, 1984.

    Weathersby PK, Survanshi SSM, Homer LD, Parker E, Thalmann ED: Predicting the time of occurrence of decompression sickness. J Appl Physiol 72:1541-1548, 1992.

    Weathersby PK, Survanshi SS, Hays JR, et al: Statistically based decompression tables III. Comparative Risk Using US Navy, British, and Canadian Standard Air Schedules. Bethesda, MD: Naval Medical Research Institute Technical Report, NMRI #86-50, 1986.

    Wilmshurst: Patent foramen ovale and subaqua diving . BMJ 1312, 1992. Letter.

    Wilmshurst P: Transcatheter occlusion of foramen ovale with a button device after neurological decompression illness in professional divers. The Lancet 348: 752-753, 1996.

    Wilmshurst P: Brain damage in divers (editorial). BMJ 314: 689-690, 1997.



    Decompression Illness in Sports Divers: Part II
    Ernest S. Campbell, MD, FACS, a resident of Orange Beach, Ala.

     Medscape Orthopaedics & Sports Medicine eJournal 1(5), 1997. 1997 Medscape Portals, Inc

    Abstract and Introduction

    Abstract

    Decompression sickness (DCS) results from gas coming out of solution in the bodily fluids and tissues when a diver ascends too quickly. This occurs because decreasing pressure lowers the solubility of gas in liquid. Also, the expansion of gas in the lungs may lead to alveolar rupture, also known as "Pulmonary Overinflation Syndrome," which may, in turn, result in arterial gas embolism (AGE). DCS, AGE, and all of their presentations are grouped together under the heading "decompression illness". Joint pain is the most common complaint in DCS, especially in the elbow, shoulder, hip and knee. Blockage of vessels results in ischemia and infarction of tissues beyond the obstruction, and inflammatory changes can lead to extravasation into the tissues, resulting in edema and further compromising the circulation. Involved skin displays a mottled appearance known as "cutis marmorata." In the lymphatic system, bubbles may result in regional lymphedema. More severe cases may involve the brain, the spinal cord, or the cardiopulmonary system. Neurologic manifestations may include sensory deficits, hemiplegia, paraplegia, paresthesias, and peripheral neuropathies. Possible cardiopulmonary effects include massive pulmonary gas emboli or myocardial infarction. Decompression sickness is treated with recompression in a chamber to 60 FSW or deeper, associated with hyperbaric oxygen breathing. In the US, this therapy is usually guided by a Navy Treatment Table. These tables are very effective, especially when recompression is begun promptly.

    Introduction

    On the earth's surface, the human body is exposed to an ambient pressure which is the result of the combined partial pressures of all the gases in the earth's atmosphere. At sea level, the force of this pressure is described as 1 atmosphere absolute (ATA). As a diver descends, exposure to increasing pressure forces more gas to dissolve in the bodily fluids and tissues, as described by natural gas laws. Upon ascent through the water column, the solubility decreases again. Rapid ascent may lead to bubble formation and decompression sickness (DCS) or alveolar rupture ("Pulmonary Overinflation Syndrome" [POIS]), with resultant bubbles in the arterial circulation (arterial gas embolism [AGE]).[1]

    DCS, AGE, and all of their presentations are grouped together under the heading "decompression illness" (DCI).[2] Treatment consists of recompression in a chamber using air or a combination of helium-oxygen. Bubbles may form in blood vessels, where they may cause ischemia and infarct, and in tissues, where they may initiate an inflammatory response. Inflammatory changes can lead to extravasation into the tissues, further compromising the circulation and resulting in edema.

    Hyperbaric exposures (situations where there are elevated pressures) can occur during construction and tunneling projects, in hyperbaric oxygen treatment facilities and in aviation. (The airman is subject to the same problem as divers, except that the situation is reversed--bubbles form on ascent, due to a decrease in pressure and supersaturation. Returning to the ground increases pressure and is analogous to recompression. However, DCS symptoms may occur after returning to the ground and sometimes require additional recompression.)

    Recreational scuba diving is the most common type of hyperbaric exposure, especially since the explosive growth of sports scuba (self-contained underwater breathing apparatus) diving in the past decade. Hyperbaric oxygen (HBO) treatment is gaining popularity as the definitive therapy for a growing number of disorders, including decompression sickness, AGE, CO poisoning, clostridial infections, crush injuries, diabetic leg ulcers, skin graft failures, refractory osteomyelitis, thermal burns, necrotizing soft tissue infections, and osteoradionecrosis.

    It is incumbent on physicians to be fully conversant with the diagnosis and treatment of decompression illness, especially because the hyperbaric chamber is now widely recognized as effective in reversing the sometimes-deadly changes that take place with DCI.

    Medical Management of DCS and AGE

    Early response at the dive site. As with other emergency life support situations, the ABCs come first: maintain an airway, assure ventilation and accomplish circulation. The standard left decubitus head down position should be avoided because it may promote cerebral edema; the patient should be placed in a supine position. Other measures include:
    • Provide 100% oxygen through a tight-fitting mask. This helps to off-gas inert gases. Resuscitation equipment should be available on all dive boats and in all dive facilities. Divers should refuse to dive if this equipment is not readily available.
    • Give copious fluids as needed to maintain good urinary output. Fluids should be administered at a rate greater than 0.5ml/kg/hr--usually 1 L qhr or 1 L q4hr, titrated against the hematocrit, which should be maintained at less than 50%. The hemoconcentration associated with decompression sickness is the result of increased vascular permeability mediated by endothelial damage and kinin release.[3] The fluids can be given orally if the diver is conscious--if not, give fluids by intravenous, if available. Avoid using hypotonic fluids, such as D5W, using 0.9% saline instead. Insert a urinary catheter if there is spinal cord DCS.
    • Give steroids if there is neurological DCS; dexamethasone 10 to 20 mg IV initially, followed by 4 mg every 6 hours; diazepam (5 to 10 mg) controls the dizziness, instability and visual disturbances associated with labyrinthine (vestibular) damage to the inner ear.
    • Seizure activity is treated with a loading dose of Dilantin. Seizures result from damage incurred from cerebral bubbles formed from DCS or air embolism (resulting from pulmonary barotrauma); they can also result from oxygen toxicity associated with the treatment schedule. Dilantin (phenytoin) is given IV at 50 mg/min for 10 minutes for the first 500 mg and then 100 mg every 30 minutes thereafter. Blood levels of Dilantin should be monitored to maintain a therapeutic concentration of 10 to 20 mcg/mL. Levels over 25 mcg/mL are toxic.[4]

    •  

       

      Some people provide aspirin, 600 mg, for its anti-platelet effects; this modality is debatable because of the possibility of associated spinal cord hemorrhage. Lidocaine has been shown to be protective in animal models but has not been studied adequately in humans.[5]

    Attempting to treat the diver by returning him/her to the water, (known as in-water recompression), is hazardous not only to the diver, but to the caregivers who have to be re-subjected to pressure. This should not be attempted unless special arrangements have been made to do so. For example, in Australia, because of the great distances and time lags involved in reaching a recompression chamber, dive operators have a system of surplus air and oxygen tanks ready for in-water recompression.

    Transportation. Ascending to an altitude greater than 1000 feet should be avoided. Sea level aircraft that are acceptable for transportation include the military C9, the Cessna Citation and the Lear Jet. Commercial aircraft fly at 5000 to 8000 feet cabin pressure. The "ABCs" initiated at the dive site should be continued while in transport.

    Treatment in the chamber.[6] The treatment of choice for decompression illness, whether DCS or AGE, is recompression in a multiplace, hands-on chamber. It should have the capability of locking personnel and equipment in or out with trained attendants available for critical care monitoring.

    Multiplace chambers. These units (Fig. 1) can accommodate between 2 to 18 patients, depending upon configuration and size. They incorporate a minimum pressure capability of 6 atmospheres absolute. Patients are accompanied by hyperbaric staff members, who may enter and exit the chamber during therapy via an adjacent access lock or compartment. The multiplace chamber is compressed on air and patients are provided with oxygen via an individualized internal delivery system. A dedicated compressor package and high volume receivers provide the chamber's air supply.

    Advantages include constant patient attendance and evaluation (particularly useful in treating evolving diseases such as decompression sickness), and multiple patients treated per session; disadvantages include high capitalization and staffing costs, large space requirements and risk of decompression sickness in the attending staff.

    Figure 1. Multiplace chambers accommodate between 2-18 patients, depending upon configuration and size. They have a pressure capability of 6 atmospheres absolute. Reprinted from Hyperbaric Medicine, Brooks Airforce Base.
    Duoplace chambers include the Reneau (Proteus) and the Sigma II with pressurization capabilities to 6 ATA and 3 ATA respectively. The chambers are compressed with air, and the patient breathes oxygen by an individualized internal delivery system. Advantages include constant patient attendance, with access limited to the head and neck; disadvantages include relatively high capitalization cost for single patient treatments and risk of decompression sickness in the attending staff.

    The multiplace chamber is not always possible, however, and the monoplace chamber is sometimes the only alternative. Hart and coworkers,[7] as well as Kindwall and colleagues[8] have developed protocols with the monoplace chamber, utilizing Navy Treatment Table 6 (Table I) which can be used with air breaks.

    Monoplace chambers. These units (Fig. 2), first introduced in the 1960s are designed for single occupancy. They are constructed of acrylic, have a pressure capability of 3 atmospheres absolute and are compressed with 100% oxygen. Recent technical innovations have allowed critically-ill patients to undergo therapy in the monoplace chamber. The high flow oxygen requirement is supplied via the hospital's existing liquid oxygen system.

    Figure 2. Recent technical innovations have allowed critically-ill patients to undergo therapy in the monoplace chamber. Monoplace chambers are designed for single occupancy. They have a pressure capability of 3 atmospheres absolute and are compressed with 100% oxygen. Reprinted from Hyperbaric Chambers Systems & Management.
    Advantages of this chamber include that it provides the most cost efficient delivery of hyperbaric oxygen (capitalization and operating costs), and that it presents essentially no risk of decompression sickness to the attending staff. Disadvantages include relative patient isolation and increased fire hazard.

    Treatment goals in all instances are to reduce bubble size and surface area while providing hyperbaric oxygenation (HBO). HBO reduces edema, blocks WBC adherence, protects and preserves the microcirculation, corrects hypoxia (100% oxygen under pressure produces 7 volume % in the plasma), blocks reperfusion injury, and facilitates the removal of dissolved gas from the lungs through perfusion.[9]

    Outcome. The most recent DAN (Divers Alert Network) report (1994 data) suggests that complete resolution of symptoms occurred in only 56% of cases while 28% of divers had neurologic sequelae and 17% continued to experience pain.[10] Travel after treatment of DCS should be delayed for at least 48 hours; 72 hours for arterial gas embolism. Recurrence of symptoms has occurred with flying more than one week after the initial event. Diving should not be resumed if there is any residual neurological damage.

    Summary

    Decompression illness is the combination of decompression sickness and arterial gas embolism; DCS is a disorder resulting from the reduction of ambient pressure with the formation of bubbles from supersaturated dissolved gas in the blood and tissues, usually associated with pain and/or neurologic manifestations; AGE is the result of air being forced through ruptured alveoli caused by ascent with a closed glottis and results in air bubbles blocking arteries in the brain and heart. Both entities are treated by recompression with oxygen in a chamber. Before initiating a dive vacation to a remote location, it would be wise to check on the availability of a recompression chamber and surface oxygen. Many dive sites pay little attention to pre-dive planning[11]and evacuation can often be prolonged, resulting in permanent damage.

    Tables

    Table I. US Navy Treatment Table 6: Oxygen treatment of Type II Decompression Sickness*

     
     
    Depth
    (feet)
    Time
    (minutes)
    Breathing
    Media
    Total
    Elapsed
    Time
    (hr:min)
    60 20 O2 0:20
    60 5 Air 0:25
    60 20 O2 0:45
    60 5 Air 0:50
    60 20 O2 1:10
    60 5 Air 1:15
    60 to 30 30 O2 1:45
    30 15 Air 2:00
    30 60 O2 3:00
    30 15 Air 3:15
    30 60 O2 4:15
    30 to 0 30 O2 4:45
    * Treatment of Type II or Type I decompression sickness when symptoms are not relieved within 10 minutes at 60 feet.
    Descent rate--25 ft/min. Ascent rate--1 ft/min. Do not compensate for slower ascent rates. Compensate for faster rates by halting the ascent.
    Time at 60 feet begins on arrival at 60 feet.
    If oxygen must be interrupted because of adverse reaction, allow 15 minutes after the reaction has entirely subsided and resume schedule at point of interruption.
    Caregiver breathes air throughout unless he has had a hyperbaric exposure within the past 12 hours, in which case he breathes oxygen at 30 feet.
    Extensions to Table 6: Table 6 can be lengthened up to 2 additional 25 minute oxygen breathing periods at 60 feet (20 minutes on oxygen and 5 minutes on air) or up to 2 additional 75 minute oxygen breathing periods at 30 feet (15 minutes on air and 60 minutes on oxygen) or both. If Table 6 is extended only once at either 60 or 30 feet, the tender breathes oxygen during the ascent from 30 feet to the surface. If more than one extension is done, the caregiver begins oxygen breathing for the last hour at 30 feet during ascent to the surface.
    Adapted from the US Navy Diving Manual.


    References

    1. Polak B, Adams H: Traumatic air embolism in submarine escape training. U.S. Naval Med. Bull. 30: 165-177, 1932.
    2. Francis TJR, Smith D (eds): Describing Decompression Illness. Bethesda, Undersea and Hyperbaric Medical Society, 1987.
    3. Boussuges A: Hemoconcentration in neurological decompression illness. Int J Sports Med 17 (5): 351-55, 1996.
    4.  Neurological Disorders (Section 11) and Seizure Disorders (Section 121) in Berkow R (ed): The Merck Manual of Diagnosis and Therapy, ed 16, Whitehouse Station, NJ, 1996-1997; http://www.merck.com/!!tMSNq2zF6tMSOn1CAu/pubs/mmanual/html/hjinkcff.htm.
    5. Gorman, D. The pathology and clinical features of decompression illness, DAN 21st Diving Accidents and Hyperbaric Medicine Course, Sharm-el-Sheik, Egypt, 1992.
    6. Berghage TE, Vorosmarti J JR, Barnard EEP: Background, in: Davis JC (ed): Treatment of Serious Decompression Sickness and Arterial Gas Embolism. Rep 34 WS (SDS). Bethesda, Undersea Medical Society, 1979, pp xi-xvii.
    7. Hart GB, Strauss MB, Lennon PA: The treatment of decompression sickness and air embolism in a monoplace chamber. J Hyperbar Med 1: 1-7, 1986.
    8. Kindwall EP, Goldman RW, Thombs PA: Use of the monoplace chamber in the treatment of diving diseases. J Hyperbar Med ; 3: 5-10, 1988.
    9. Zamboni WA: The microcirculation and ischemia-reperfusion: mechanisms of HBO, in: EP Kindwall (ed): Hyperbaric Medicine Practice, Flagstaff, AZ Best publishing, 1994, pp 551-564.
    10. Cianci, Paul: Pathophysiology of Decompression Sickness, Medical Seminars, Palua, May, 1996.
    11. Campbell ES: Danger! At Hotel Scuba. Scuba Times Online. http://www.scubatimes.com/medcntr/med_hotl.html. 1996.

    Suggested Readings

    Arthur DC, Margulies RA: A short course in diving medicine. Annals Emerg Med 16: 689-701, 1987.

    Ball R. Effect of severity, time to recompression with oxygen, and retreatment on outcome in forty-nine cases of spinal cord decompression sickness. Undersea and Hyperbaric Medicine 20:133-145, 1993.

    Berghage TE, Durman D: US Navy Air Decompression Schedule Risk Analysis. Bethesda, MD: Naval Medical Research Institute Technical Report, NMRI #80-1, 1980.

    Boettger ML. Scuba diving emergencies: Pulmonary overpressure accidents and decompression sickness. Annals Emerg Med 12: 563-567, 1983.

    Boussuges A, Thiriion P, Molenat F, et al: Neurologic decompression illness: A gravity score. Undersea and Hyperbaric Medicine 23:151-155, 1996.

    Boycott AE, Damant GCC, Haldane JS: The prevention of compressed-air illness. J Hyg Camb 8: 342-443, 1908.

    Bove AA, Moon RE, Neuman TS: Nomenclature of pressure disorders. Classification of the decompression disorders: time to accept reality. DCI/DCS: Does it matter whether the Emperor wears clothes? Undersea and Hyperbaric Medicine 24:1-4, 1996. Editorials.

    Bove AA: The basis for drug therapy in decompression sickness. Undersea Biomed Res 9: 91-111, 1982.

    Bracken MB, et al: A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal injury. New Eng J Med 322: 1405-1412, 1990.

    Catron PW, Flynn ET Jr: Adjuvant drug therapy for decompression sickness: A review. Undersea Biomed Res 9: 161-74, 1982.

    Cross SJ, Thomson LF, Jennings KP, et al: Right-to-left shunt and neurological decompression sickness in divers.

    Lancet ii 568, 1989. Letter.

    Cross SJ, Lee HS, Thomson LFet al: Patent foramen ovale and subaqua diving . BMJ 304: 1312, 1992. Letter.

    Davis JC, Kizer KW: Diving medicine, in: Auerbach PS, Geehr EC (eds): Management of Wilderness and Environmental Emergencies, 2nd edition. St. Louis, The C.V. Mosby Co., 1989.

    Dewey AW, Jr: Decompression sickness, an emerging recreational hazard. N Engl J Med 267: 759-65; 812-20, 1962.

    Dick APK, Massey EW: Neurologic presentation of decompression sickness and air embolism in sport divers. Neurology 35: 667-671. 1985

    Edmonds C. Barotrauma, in Strauss R.(ed): Diving Medicine. New York, Grune & Stratton, 1976.

    Gorman DF: Decompression sickness and arterial gas embolism in sports scuba divers. Sports Medicine 8: 32-42, 1989.

    Green RD, Leitch DR: Twenty years of treating decompression sickness. Aviat Space Environ Med 58: 362-6, 1987.

    Hall ED: Lazaroids: Mechanisms of action and implication for disorders of the CNS. Neuroscientist, 3:42-51, 1997.

    Johnston RP, Broome JR, Hunt PD, et al: Patent foramen ovale and decompression illness in divers. The Lancet 348: 1515, 1996. Letter.

    Kelleher PC, Pethybridge RJ, Francis TJR: Outcome of neurological decompression illness: development of a manifestation based model. Aviat, Space, and Environ Med 67: 654-658, 1996.

    Kindwall EP: Diving emergencies, in Kravis TC (ed): Emergency Medicine Aspen Systems Corporation, Rockville, Maryland, 1983.

    Kizer KW: Dysbaric cerebral air embolism in Hawaii. Ann Emerg Med 16: 535-41, 1987.

    Knauth M, Ries S, Pohlmann S, et al: Cohort Study of multiple brain lesions in sport divers: Role of a patent foramen ovale. BMJ 314: 701-705, 1997.

    Krzyzak J: A case of delayed-onset pulmonary barotrauma in a scuba diver. Undersea Biomed Res 14: 553-61, 1987.

    Mebane GY, Dick AP: DAN Underwater Diving Accident Manual. Divers Alert Network, Duke University, 1985.

    Mitchell SJ: The role of lignocaine in the treatment of decompression illness: A review of the literature. SPUMS Journal 25:182-194, 1995.

    Moon RE, Sheffield PJ: Guidelines for Treatment of Decompression Illness. Aviat Space Environ Med 68:234-43, 1997.

    Moon RE, Camporesi EM, Kisslo JA: Patent foramen ovale and decompression sickness in divers. Lancet

    1: 513-514, 1989.

    Moon RE, Sheffield PJ, (eds.): Treatment of Decompression Illness. 45th Workshop of the Undersea and Hyperbaric Medical Society, June 1996.

    Neblett LM: Otolaryngology and sport scuba diving. Update and guidelines. Annals Otology, Rhin and Laryng. Supplement 115: 1-12, (a great article) 1985.

    Rivera JC. Decompression sickness among divers: An analysis of 935 cases. Military Medicine, pp 314-334, April 1964.

    Roydhouse N: 1001 disorders of the ear, nose and sinuses in scuba divers. Can J Appl Spt Sci 10: 99-103. 1985.

    Schaefer KE, McNulty WP Jr., Carey C, Liebow AA. Mechanisms in development of interstitial emphysema and air embolism on decompression from depth. J Appl Physiol 13: 15-29, 1958.

    Strauss RH. Diving Medicine: State of the Art. Amer Rev Resp Dis 119: 1001-1023, 1979.

    Thalmann ED in Moon RE, Sheffield PJ eds. Treatment of Decompression Illness. 45th Workshop of the Undersea and Hyperbaric Medical Society, June 1996; pp 75-95.

    Weeth JB. Management of underwater accidents. JAMA 192: 215-219, 1965.

    Wilmshurst P, Byrne JC, Webb-Peploe MM. Relation between interatrial shunts and decompression sickness in divers.

    Lancet II: 1302-1306, 1989.

    Weathersby PK, Homer LD, Flynn ET: On the likelihood of decompression sickness. J Appl Physiol 57: 815-25, 1984.

    Weathersby PK, Survanshi SSM, Homer LD, Parker E, Thalmann ED: Predicting the time of occurrence of decompression sickness. J Appl Physiol 72:1541-1548, 1992.

    Weathersby PK, Survanshi SS, Hays JR, et al: Statistically based decompression tables III. Comparative Risk Using US Navy, British, and Canadian Standard Air Schedules. Bethesda, MD: Naval Medical Research Institute Technical Report, NMRI #86-50, 1986.

    Wilmshurst: Patent foramen ovale and subaqua diving . BMJ 1312, 1992. Letter.

    Wilmshurst P: Transcatheter occlusion of foramen ovale with a button device after neurological decompression illness in professional divers. The Lancet 348: 752-753, 1996.

    Wilmshurst P: Brain damage in divers (editorial). BMJ 314: 689-690, 1997.




    DCS Prevention
    This page is compiled and maintained

    by Ernest S Campbell, MD, FACS

    Prior to 1980, there was an organization known as "Leofast", located at Brooks A.F.B., TX , where divers consulted with hyperbaric physicians concerning possible diving injuries.

    In the twelve years prior to 1980 there were 62 cases of DCS reported and described . Here are some of the suspected causes of the illnesses thought to be DCS:

        • Repititive dive
        • Exceeded No-decompression limits
        • Running out of air, rapid ascent
        • Diving on the edge of No-decompression limits
        • Deep or repetitive dives using computer outside the limits of the tables or no-decompression limits
        • Flying after diving
        • Diving at altitude
        • Vigorous exercise before and after a dive
    There are other factors that are thought to increase the chances of getting DCS but have little data in support; some of these are:
    • Age; risk increases in proportion to increase in age
    • Obesity
    • Sex ? (Possibly more frequent in females )
    • Fatigue, Hard physical work
    • Dehydration, due to any cause (coffee, oral diuretics, alcohol, vomiting and diarrhea states, failure to drink non-alcoholic liquids)
    • Alcohol and hangover state (related to dehydration)
    • Medical problems increasing the viscosity of the blood (Sickle cell anemia and trait)
    • Injury to muscle, bone or joint (due to increased blood flow to inflamed area)
    • Rate of ascent
    • Repetitive, multiday dives after a long lay-off; deep prolonged air diving
    • Failure to do safety stops
    • Patent foramen ovale
    • Smoking habits
    • Adaptation or recent diving history
    • Conditioning
    • Underestimated depth
    • Table "fudging"

    There is no good evidence that shows that a hot shower after diving increases the rate of decompression sickness.


    Some believe that the use of aspirin might help prevent the adherence of blood platelets to bubbles, thereby reducing the chance of bubble damage.



    Risks for DCS
    Compiled and maintained
    by Ernest S Campbell, MD



    Self-grading Quiz  for Prevention of Decompression Accidents

    Some Causes of Decompression Accidents

    The best way to categorize the various ways a diver can prevent the occurrence of DCS is by looking for the causes of the accident.

    Some predisposing causes for DCS are as follows:

    • Inadequate decompression or violating the no-decompression limits. By surfacing too rapidly and not taking safety stops a diver allows bubbles to form and to get larger as the pressure differential decreases. Nitrogen loads in all the tissues at different pressures and times and violation of the NDL (no-decompression limits) is a major cause of DCS. 
    • Inadequate surface intervals (failure to decrease accumulated nitrogen). Surface times are outlined for various diving profiles and failure to adhere to the prescribed length of time does not allow "off-gassing" of onboard nitrogen. The accumulated nitrogen is then added to by the next dive, increasing the risk of DCS. 
    • Flying or going to higher altitude soon after diving (12-24 hours), which  increases the pressure gradient. This in reality is a continuation of an ascent from a dive. This allows any nitrogen that is in the tissues to come out of solution and form bubbles, leading to DCS. 
    • Individual physiological differences that have been traditionally thought of as increasing the risk of DCS are as follows:
      • Dehydration: This is probably the most important of the predisposing factors. Taking in adequate quantities of water (8-10 glasses/day).This is needed to counteract the drying effect of compressed air and the obligatory diuresis that all divers get from immersion. Dehydration, due to any cause (coffee, oral diuretics, alcohol, vomiting and diarrhea states, failure to drink non-alcoholic liquids) 
      • Pre-existing illness affecting lung or circulatory efficiency: The lung acts as a filter for the buubles that occur in all divers. Chronic lung disease, heart failure both tend to increase the risk of DCS. Decreased perfusion from any source can increase the possibility of DCS. Intracardiac septal defect (PFO) bypasses the filtering effect of the lungs and increases risk of bubbles. Undeserved DCS (DCS that has no other causative factors) should have investigation for this entity. 
      • Scar tissue from previous injury: (scar tissue decreases diffusion). Areas of decreased and increased blood flow have been incriminated in leading to DCS. Whether this is operative in the growth plates of teenagers is unknown. Nitrogen off-gassing is influenced by factors that alter perfusion. 
      • Gender; women have been shown to have a slightly higher rate of DCS, particularly during the menses. 
      • Obesity (nitrogen is lipid soluble). Several studies have incriminated obesity as a factor in increasing the risk of DCS. Fat is poorly supplied with blood vessels and decreased perfusion (ability to off-gas) can lead to DCS. 
      • Fatigue: This clouds the decision making process, often leading to mistakes and DCS. Fatigue is also a subtle symptom of decompression sickness. Exertion during the deep part of the dive is a risk factor. 
      • Age: The older diver has long been thought to be have increased tendencies to have DCS. Studies done by the Navy show a definite increase in DCS in older divers (all under 50 years of age). Other studies have not borne this out. Older divers have a higher percentage of body fat. Age and obesity: risk possibly increases in proportion to increase in age. Greater age and higher fat content are traditionally associated with  increased incidence of DCS but the evidence is not consistent, recent reports showing no relationship. 
      • Poor physical condition: Good physical fitness increases perfusion and ensures good gas exchange. 
      • Exercise after diving increases the incidence of DCS from 22% to 46%. Exercise at depth is detrimental, increasing nitrogen uptake. (Requiring three times the decompression). Immersion in cold water with exercise causes increased incidence of DCS. Exercise while decompressing is beneficial. 

    Environmental factors that are important include the following:

    • Cold water (vasoconstriction decreases nitrogen off-loading). Warm water immersion (vasodilation) and the head down position increases nitrogen elimination.
    • Heavy work (vacuum effect in which tendon use causes gas pockets). Exercise at depth increases nitrogen uptake and is detrimental.
    • Rough sea conditions
    • Heated diving suits (leads to dehydration)
    • Divers who have been chilled on decompression dives (or dives near the no-decompression limit) and take very hot baths or showers may stimulate bubble formation.

    Sport divers mainly need to avoid dehydration, dive shallower, ascend slower and spend more time between dives eliminating nitrogen.

    Here are some of the factors found to increase the risk of decompression accidents:

        • Repetitive diving
        • Exceeded No-decompression limits
        • Running out of air, rapid ascent
        • Diving on the edge of No-decompression limits
        • Deep or repetitive dives using computer outside the limits of the tables or no-decompression limits
        • Flying after diving
        • Diving at altitude
        •  


    There are other factors that are thought to increase the chances of getting DCS but have little data in support; some of these are:
    • Alcohol and hangover state (related to dehydration)
    • Medical problems increasing the viscosity of the blood (Sickle cell anemia and trait)
    • Injury to muscle, bone or joint (due to increased blood flow to inflamed area)
    • Rate of ascent
    • Repetitive, multiday dives after a long lay-off; deep prolonged air diving
    • Failure to do safety stops
    • Patent foramen ovale
    • Smoking habits
    • Adaptation or recent diving history
    • Underestimated depth
    • Table "fudging"
    • Neurological DCS symptoms are most common after short, deep dives. less common after altitude exposure, slow saturation decompression and low-pressure caisson exposure.
    • Slow ascent near the surface more effective in reducing neurologic DCS than was slow ascent from depth.
    • Fewer VGE with short safety stops. (venous gas emboli)
    • Off-gassing greatest in subjects tilted head down, immersed in warm water and exercising. Increasing venous return to the thorax increases off-gassing.(Head down tilt)
    • Exercise in warm water immersion decreases DCS (decrease by about 30%)
    • Some believe that the use of aspirin might help prevent the adherence of platelets to bubbles, thereby reducing the chance of bubble damage.


    References:
    Gorman,  Pearce and Webb, Dysbaric illness treated at the Royal Adelaide Hospital, 1987: A factorial analysis. SPUMS Journal 18:95-101, 1988


    Wilmshurst PT, Byrne JC, Webb-Peploe MM: Relation between inter-atrial shunts and decompression sickness in divers. Lancet, 2:1302-1306, 1989.

    Moon RE, Camporesi EM, Kisslo JA: Patent foramen ovale and decompression sickness in divers. Lancet 1: 513-514, 1989.



    Exercise and Decompression Accidents

    The inveterate runner or hiker on a dive trip often wants to know if there is any harm in exercising before or after diving. Of course, the problem is whether or not bubbles are induced by pre-dive exercise or by exercise immediately after a non-saturation dive.

    The scientists at NASA are understandably interested in this aspect of decompression and have done studies to elucidate this problem with their extra-vehicular activity astronauts. To determine the answer to these questions, an elegant study was done by Dervay, J, MR Powell, and CE Fife, " Effective lifetimes of tissue micronuclei generated by musculoskeletal stress" in Aviat. Space and Environ. Med., 68 (Suppl), A12. (1997); Dervay, J, MR Powell BD Butler, and CE Fife. From Doppler bubble determinations in this study the following can be deduced:

    All strenuous activities for about four hours prior to scuba diving will increase micronuclei, thereby increasing venous gas emboli. Musculoskeletal activity will definitely increase the number of tissue micronuclei. That is an experimental fact. These micronuclei will persist for about two to five hours again an experimental fact. There are no studies that show clearly what happens to these bubbles when they are compressed by a dive.

    It is thought that if one were to put four restful hours between exercise and diving and six between diving and exercise, a diver should be in good shape in terms of absent bubbles. That is probably sufficient for non-decompression dives.

    A web site that has some diagrams and explains bubble growth can be found at:

    http://www.cisatlantic.com/trimix/emaiken/bubble.htm


    If one were to schedule their exercise activities in the morning and diving in the afternoon, there should not be a problem with this situation. One would not need to take off a whole day as far as exercise is concerned.

    In regard to the hot shower or hot tub question post-dive, there is an increase in blood flow to the skin to eliminate body heat. When this happens, blood is shunted away from muscles (a steal) and flows to the skin. We have increased perfusion to the skin but that is not of much help in prevention of DCS.

    This is thought to be harmful to the diver attempting to off-gas due to the shunting of blood away from the musculoskeletal areas that need to have blood flow promoted. This is done by moderate, non-straining exercise, avoiding running, climbing ladders and lifting SCUBA tanks. However, non-strenuous movement is thought to be helpful - sleeping should be avoided..

    There are mixed reports of exercise causing increased DCS in altitude exposed individuals (Pilmanis). On the contrary, there is evidence that exercising while decompressing is helpful in reducing decompression accidents. Muth et al, have found that exercise increases the elimination of nitrogen post-dives that are non-DCS producing. Jankowski has shown that exercise during decompression reduces the amount of venous gas emboli.



    Here are two other pages on our site related to exercise.
    http://www.scuba-doc.com/exhrt.htm
    http://www.scuba-doc.com/travexer.htm



    Patent Foramen Ovale
    Download Web Page PDF
     

    PFO (Patent foramen ovale) is a persistent opening in the wall of the heart which did not close completely after birth (opening required before birth for transfer of oxygenated blood via the umbilical cord). This opening can cause a shunt of blood from right to left , but more often there is a movement of blood from the left side of the heart (high pressure) to the right side of the heart (low pressure).

    People with shunts are less likely to develop fainting or low blood pressure with diving than are obstructive valve lesions (such as mitral valve stenosis or aortic stenosis), but are more likely to develop fluid accumulation in the lungs from heart failure and severe shortness of breath from the effects of combined exercise and water immersion.

    Ordinarily, the left to right shunt will cause no problem; the right to left shunt, if large enough, will cause low arterial O2 tension (hypoxia) and severely limited exercise capacity. In divers there is the risk of paradoxical embolism of gas bubbles (passage of bubbles into the arterial circulation) which occur in just about all divers in the venous circulation during decompression.

    Blood can flow in both directions with Intra-atrial shunts at various phases of the cardiac cycle and some experts feel that a large atrial septal defect (PFO) is a contra-indication to diving. In addition, a Valsalva maneuver, used by most divers to equalize their ears during descents and ascents, can increase venous atrial pressure to the point that it forces blood containing bubbles across the PFO into the arterial circulation. Thus the usual filtering process of the lungs is by-passed.

    Dr. Fred Bove, a Temple University cardiologist, did a search of the literature for patent foramen ovale in relation to diving and diving risks. His conclusion of a meta analysis of 1400 injured divers in about 2.5 million divers (DAN, 1991) in whom the risk of DCS is about 0.05% in the diving population, was that the risk ratio for decompression sickness is increased by a factor of about three for individuals with PFO, and is reduced by a factor of about 2 in individuals who do not have a PFO. It would appear that the risk is low and the significance of the small differences is questionable.

    Echocardiography is the tool of choice in making the diagnosis of PFO. However, it's probably not a good idea to do an echocardiogram on all divers because of the cost/benefit ratio. If you personally are concerned or are having some of the symptoms of decompression illness that are undeserved,  then a bubble contrast echocardiogram should be done. Bubble contrast echocardiography appears to be the most sensitive method for detecting a shunt while color flow doppler appeared to be a poor means of detecting the shunt in a transthoracic echo.

    There have been recent reports of an association between cerebral emboli, migraines with aura and right to left shunts (PFO).

    Philip Foster et al, in the Journal of the Aerospace Medical Association, has an elegant article "Patent Foramen  Ovale and paradoxical Systemic Embolism: A Bibliographic Review" in which is presented in a single document a summary of the original findings and views from authors in this field. It is a comprehensive review of 145 peer-reviewed journal articles related to PFO that is intended to encourage reflection on PFO detection methods and on the possible association between PFO and stroke.

    The article abstract and related articles can be seen at this address:
    http://snipurl.com/4sao

    Patent  Foramen Ovale Closure - A button closure (Amplatzer) is performed trans venously without entering the chest. About four weeks  after the surgery, another echocardiogram is done to verify that the device is still in position.

    After two-three weeks there is an overgrowth of endothelial cells covering the device, reducing the risk of infection.

    After six to eight weeks the connective tissue has completely filled the spaces in the device and it becomes invisible to ultrasound. Return to diving is usually in six weeks (Wilmshurst), given the full recovery to the satisfaction of the cardiologist/surgeon. Others require a longer wait of twelve weeks.




    DCS References



    Web Links to DCI:2006[Google]


    1. Boyle R. New pneumatic experiments about respiration. Phil. Trans. R. Soc. London 5: 2011-2031, 1670

    2. Polak B and Adams H: Traumatic Air Embolism in Submarine Escape Training. U.S. Naval Med. Bull. 30: 165-177, 1932 (Related Articles)

    3. Vann RD, Thalmann ED: Decompression physiology and practice, in Bennett PB, Elliott DH (eds): The Physiology and Medicine of Diving. London, WB Saunders, 1993, ed 4, pp376-432 (Related articles)

    4. Francis TJR, Smith D (eds): Describing Decompression Illness. Bethesda, Undersea and Hyperbaric Medical Society, 1987.

    5. Elliott DH, Moon RE: Manifestations of the decompression disorders, in Bennett PB, Elliott DH (eds): The Physiology and Medicine of Diving. London, WB Saunders, 1993, ed 4, pp 481-505. (Related articles)

    6. Flynn ET: Decompression Sickness, in Camporesi EM, Barker A: Hyperbaric Oxygen Therapy: A Critical Review. Bethesda. Undersea and Hyperbaric Med. Soc. , 1991, pp55-74 (Related articles)

    7. Francis TJR, Gorman DF: Pathogenesis of the Decompression disorders, in Bennett PB, Elliott DH (eds): The Physiology and Medicine of Diving. London, WB Saunders, 1993, ed 4, pp 454-480 (Related articles)

    8. US Navy Diving Manual. Commander Naval Sea Systems Command Publication 0994-LP-001-9010. Washington DC, US Government Press, 1993, Revision 3, Vol 1, Chapter 8

    9. Thalmann ED, Buckingham IP, Spaur WH: Testing of Decompression Algorithms for Use in the US Navy Underwater Decompression Computer (Phase I). US Navy Experimental Diving Unit Report 11-80, 1980

    10. Thalmann, ED: Phase II Testing of Decompression Algorithms for Use in the US Navy Underwater Decompression Computer, US Navy Experimental Diving Unit Report 1-84, 1984.

    11. Thalmann ED: Development of a Decompression Algorithm for Constant 0.7 ATA Oxygen Partial Pressure in Helium Diving. US Navy Experimental Diving Unit Report 1-85, 1985

    12. Thalmann ED: Air-N2O2 Decompression Algorithm Development. US Navy Experimental Diving Unit Report 8-85, 1986.

    13. Kizer KW: Delayed Treatment of dysbarism: A retrospective review of 50 cases. JAMA 247: 2555-2558, 1982

    14. Yap CL: Delayed decompression sickness- the Singapore experience, in Proc Joint S Pacific Underwater Med Soc and Republic Singapore Navy Underwater Med Conf. SPUMS J Suppl, 1981 (Related Articles)

    15. Butler FK, Pinto C: Progressive Ulnar Palsy as a late complication of decompression sickness. Annals Emerg Med 15:738-741, 1986. (Related Articles)

    16. Behnke, AR: Analysis of Accidents occurring in training with the submarine "lung". U.S. Naval Medical Bull. 30: 177-184, 1932

    17. Schaefer KE, Nulty WP, Carey C, et al: Mechanisms in development of interstitial emphysema and air embolism on decompression from depth. J. Appl. Physiol. 13: 15-29, 1958 (Related articles)

    18. Malhotra MC, Wright CAM,: Arterial air embolism during decompression and its prevention. Proc. R. Soc. Med. B154: 418-427, 1960

    19. Mader JT, Hulet WH: Delayed hyperbaric treatment of cerebral air embolism. Arch. Neurol. 36: 504-505, 1979 (Related articles)

    20. Catron PW, Dutka AJ, Biondi DM, Flynn ET, Hallenbeck JM: Cerebral Air Embolism treated by pressure and hyperbaric oxygen. Neurology. 41: 314-315, 1991 (Related articles)

    21. Berghage TE, Vorosmarti J JR, Barnard EEP. Background. In: Davis JC, ed. Treatment of serious decompression sickness and arterial gas embolism. Rep 34 WS (SDS). Bethesda, Undersea Medical Society, 1979, pp xi-xvii.

    22. Kindwall EP. Decompression sickness. In: Davis JC, Hunt TK, eds. Hyperbaric Oxygen Therapy. Bethesda, Undersea Medical Society, 1977, pp 125-140.

    23. Hart GB, Strauss MB, Lennon PA. The treatment of decompression sickness and air embolism in a monoplace chamber. J Hyperbar Med 1: 1-7, 1986 (Related articles)

    24. Kindwall EP, Goldman RW, Thombs PA: Use of the monoplace chamber in the treatment of diving diseases. J Hyperbar Med ; 3: 5-10, 1988. (Related Articles)

    25. Campbell ES: Danger! At Hotel Scuba. Scuba Times Online. http://www.scubatimes.com/medcntr/med_hotl.html. 1996


    References for further reading

    Arthur DC, Margulies RA. A short course in diving medicine. Annals Emerg Med ; 16:689-701. 1987(Related Articles)

    Boettger ML. Scuba diving emergencies: pulmonary overpressure accidents and decompression sickness.

    Annals Emerg Med ;12:563-567. 1983

    Boycott AE, Damant GCC, Haldane JS. The prevention of compressed-air illness. J Hyg Camb ;8:342-443. 1908

    Bove AA. The basis for drug therapy in decompression sickness. Undersea Biomed Res ;9:91-111. 1982 (Related articles)

    Catron PW, Flynn Et, Jr. Adjuvant drug therapy for decompression sickness: a review. Undersea Biomed Res ;9:161-74. 1982(Related articles)

    Cross SJ, Thomson LF, Jennings KP, Shields TG. Right-to-left shunt and neurological decompression sickness in divers. (Letter). Lancet ;ii;568. 1989 (Related articles)

    Cross SJ, Lee HS, Thomson LF, Jennings K. Patent foramen ovale and subaqua diving (letter). BMJ ;304:1312. 1992

    Davis JC, Kizer KW. Diving Medicine. In: Auerbach PS, Geehr EC, editors. Management of Wilderness and Environmental Emergencies, 2nd edition. The C.V. Mosby Co., St. Louis, 1989.

    Dewey AW, Jr. Decompression sickness, an emerging recreational hazard. N Engl J Med : 267:759-65; 812-20. 1962

    Dick APK, Massey EW. Neurologic presentation of decompression sickness and air embolism in sport divers. Neurology; 35:667-671. 1985 (Related articles)

    Edmonds C. Barotrauma. In Strauss R., editor. Diving Medicine. New York, Grune & Stratton, 1976.

    Green RD, Leitch DR. Twenty years of treating decompression sickness. Aviat Space Environ Med ;58:362-6. 1987 (Related articles)

    Gorman DF. Decompression sickness and arterial gas embolism in sports scuba divers. Sports Medicine ;8:32-42. 1989 (Related articles)

    Johnston RP, Broome JR, Hunt PD, et. al. Patent foramen ovale and decompression illness in divers (letter). The Lancet ; 348: 1515. 1996 (Related articles)

    Kindwall EP. Diving emergencies. In: Kravis TC, editor. Emergency Medicine; Aspen Systems Corporation, Rockville,Maryland, 1983.

    Kizer KW. Dysbaric cerebral air embolism in Hawaii. Ann Emerg Med ;16:535-41. 1987 (Related articles)

    Krzyzak J. A case of delayed-onset pulmonary barotrauma in a scuba diver. Undersea Biomed Res ;14:553-61. 1987 (Related articles)

    Mebane GY, Dick AP. DAN Underwater Diving Accident Manual. Divers Alert Network, Duke Univesity, 1985.

    Moon RE, Camporesi EM, Kisslo JA. Patent foramen ovale and decompression sickness in divers. Lancet ;1:513-514. 1989 (Related articles)

    Neblett LM. Otolaryngology and sport scuba diving. Update and guidelines. Annals Otology, Rhin and Laryng. Supplement ; 115:1-12. (A great article)1985 (Related articles)

    Roydhouse N. 1001 disorders of the ear, nose and sinuses in scuba divers. Can J Appl Spt Sci ;10:99-103. 1985 (Related articles)

    Schaefer KE, McNulty WP Jr., Carey C, Liebow AA. Mechanisms in development of interstitial emphysema and air embolism on decompression from depth. J Appl Physiol ;13:15-29. 1958

    Strauss RH. Diving Medicine: State of the Art. Amer Rev Resp Dis ;119:1001-1023. 1979

    Weeth JB. Management of underwater accidents. JAMA ; 192: 215-219. 1965

    Wilmshurst P, Byrne JC, Webb-Peploe MM. Relation between interatrial shunts and decompression sickness in divers. Lancet ;II;1302-1306. 1989 (Related articles)

    Wilmshurst. Patent formen ovale and subaqua diving (letter). BMJ ;1312. 1992 (Related articles)

    Wilmshurst P. Transcatheter occlusion of foramen ovale with a button device after neurological decompression illness in professional divers. The Lancet ;348:752-753. 1996 (Related articles)

    Wilmshurst P. Brain damage in divers (editorial). BMJ ; 314: 689-690. 1997 (Related articles)

    Knauth M., Ries S, Pohlmann S, Kerby T, Forsting M, Daffertshofer M, Hennerici M, Sartor K. Cohort Study of multiple brain lesions in sport divers: role of a patent foramen ovale. BMJ ; 314:701-705.1997


     Links to Decompression Accidents

    Scottish Diving Medicine - DCS

    DCS, Women and the bends

    Treating DCS, Bove in Skin Diver



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