Pathophysiology and Hyperbaric Effects
Decompression illness (DCI) is an affliction of gas separation causing bubbles (foreign bodies) in the tissues and blood resulting from a decrease in ambient pressure. The gas separation results in a number of responses ranging from an immune “foreign body” response, ischemia, and finally a reperfusion injury. The separation of gas, to form bubbles in the blood or tissue, impedes blood and lymphatic flow by direct mechanical obstruction, as well as directly disrupts or distorts tissues when intratissue bubble formation occurs. Intravascular gas perturbs the vessel’s endothelial surface and the cell surfaces of the platelets and white blood cells. Should recompression relieve the bubble(s), a reperfusion injury in the affected area will likely occur.
Often, intravascular gas embolism (IGE) complicates DCI and may result from either a variant of DCI or a complication arising from separate, concurrent pulmonary barotrauma with gas embolization. Intravascular gas embolic occlusion potentially blocks off-gassing tissue areas during decompression and may potentiate the local DCI injury in the involved area.
All tissues, including bone, are susceptible to DCI. When the involvement includes the nervous system or heart, a potential life threatening condition exists. The spectrum of DCI symptomatology extends from simple malaise to full cardiovascular collapse. Central nervous system (CNS) injury may be subtle or blatant and peripheral nerves may be involved. DCI may also present as a variant of the systemic inflammatory response syndrome.
DCI has classically been categorized into Type I and Type II (and recently Type III when the injury occurs concurrent with and is complicated by intravascular gas embolism. Type I involves joints and their ligaments, lymphatics, and skin. Type II involves the central nervous system (brain and spinal cord, autonomic nervous system, and peripheral nervous system), the lungs (chokes), and the cardiovascular system.
A more recent proposal would classify DCI into a descriptive format that imparts more historical information about the injury. The evolution, manifestation, time of onset, gas burden and any evidence of barotrauma are fused into one diagnostic run-on sentence. This classification at first appears cumbersome, but the approach is useful in packaging vital, pertinent patient information at the time of admission to a treatment facility.
Recompression treatment in acute DCI has three main effects: bubble compression, aerobic support for ischemic tissues, and an anti-inflammatory effect. Recompression causes reduction of the size of bubbles in tissues and in vessels in accordance with the ideal gas law. Besides shrinking the bubbles mechanically to improve liquid flow, their resulting smaller size forces them back into solution. Recompression provides aerobic support by filling the plasma fraction of blood with an increased content of dissolved oxygen to support the oxygen needs of downstream tissues. This also promotes the diffusion of the inert gas out of the separated gas phase bubble, and facilitates the blockade of potential inflammatory mediators. Hyperbaric oxygen therapy blunts leukocyte adhesion and blocks lipid peroxidation. Thus, hyperbaric oxygen therapy recompression allows dissolution of the separated gas and attenuates the inflammatory response which occurs during reperfusion of acutely injured ischemic tissue.
DCI may involve the spinal cord or the brain. DCI can produce a spectrum of injury ranging from a transient ischemic attack-like event (TIA), a small stroke, or a major stroke. CNS ischemia produces two zones of injury. The umbra, is a region of ischemically destroyed or infarcted tissue and is surrounded by the penumbra, a region of viable, yet functionally impaired tissue. Penumbral regions of a CNS injury have been found to fill with polymorphonuclear leukocytes (PMN’s) and macrophages. In the early post DCI period, extravasated leukocytes in an ischemic CNS tissue function as an oxygen sink. The goal of hyperbaric oxygen therapy is to minimize conversion of penumbral to umbral tissue in regions of marginal oxygenation in the brain or spinal cord.
The DCI injury involves acute, subacute, and chronic phases. Further understanding of the immune/ inflammatory processes may lead to modifications of current treatments or new treatment modalities. Thus far, the use of pharmacologic agents has been disappointing in DCI patients. Drugs have failed to ameliorate acute, subacute, and chronic neurologic DCI injury. Recompression is the only effective treatment of this devastating disease.
Lymphocytes can be immunomodulated by different oxygen tensions. Subacutely and chronically they may roam the penumbra much as they would in a healing wound. If perfusion of the penumbra is not re-established, then dysfunctional regions of poorly perfused neuronal tissue may never again become functional. Successful reperfusion modulated by lymphocytes, macrophages and fibroblasts may account for the accelerated recovery in neurologically injured DCI patients undergoing a “tailing” series of hyperbaric oxygen treatments. New capillary growth in the ground substance matrix can be accelerated in ischemically injured CNS tissue undergoing hyperbaric oxygen therapy. However, the gradual recovery in a few patients with untreated severe neurological injuries from DCI was observed at the turn of the century.
Archer J, Rhodes V: The grief process and job loss: A cross-sectional study. Br J Psychol 1993;84:395-410.
Barghage TE, Vorosmarti J, Barnard EEP: An evaluation of recompression treatment tables. Naval Med Res Inst Bethesda, MD, 1978;1-82.
Barnett HJM, Elasziw M, Meldrum HE: Drugs and surgery in the prevention of ischemic stroke. N Engl J Med 1995;332(4):238-248.
Blick G: Notes on divers paralysis. Brit Med J 1909;2:1796-1798.
Bove AA: The basis for drug therapy in decompression sickness. Undersea Biomed Res 1982;9(2):91-111.
Boysen G, Overgaard K: Thrombolysis in ischemic stroke—how far from a clinical breakthrough? J Intern Med 1995;237:95-103.
Brom JR, Dutka AJ, McNamee GA: Exercise conditioning reduces the risk of neurologic decompression illness in swine. Undersea Hyperbaric Med 1995;22(1):73-85.
Burkard ME, Van Liew HD: Simulation of exchanges of multiple gases in bubbles in the body. Respir Physiol 1994;95(2):131-145.
Carlton PW, Hallenbeck JM, Flynn ET, Bradley ME, Evans DE: Pathogenesis and treatment of cerebral air embolism and associated disorders. Bethesda: US Naval Medical Research Institute Report 84-20, 1984.
Cohen SN: The neurologic examination: Practical points part 1 & 2. Hospital Med 1987;23(9)(10):21-42.
Cross MR, Pimlott JK: Pressure induced changes in blood cell rigidity; a mechanism for causing aseptic bone necrosis. In: Bove AA, Bacharach AJ, Greenbaum LJ, eds: Underwater and Hyperbaric Physiology IX. Bethesda, MD: Undersea Hyperbaric Medical Society; 1987: 345-358.
Cummins RO: Advanced Cardiac Life Support Textbook. Dallas, TX: American Heart Association; 1994:1-17.
Curley MD, Schwartz HJ, Zwiingleberg KM: Neuropsychologic assessment of cerebral decompression sickness and gas embolism. Undersea Biomed Res 1988;15:223-236.
Dart, TS, Butler W: Towards new paradigms for the treatment of hypobaric decompression sickness. Aviat Space Environ Med 1998;69)4):403-409.
Davis PE, Piantadosi CA, Moon RE: Treatment of severe neurological DCI with saturation vs. multiple short tables. UHMS J 1994;21(Sup):93.
Eastman AB: Advanced Trauma Life Support®, Student Manual. Chicago, IL: American College of Surgeons Committee on Trauma; 1993:19-37.
Fitzpatrick DT: Visual manifestations of neurologic decompression sickness. Aviat Space Environ Med 1994;65(8):736-738.
Fuerdi GA, Czarnecki DJ, Kindwall EP: MR findings in the brains of compressed air workers: Relationship to psychometric results. Am J Neuroradiol 1991;12:67-70.
Gersh I, Hawkineon GE, Rathburn EN: Tissue and vascular bubbles after decompression from high pressure atmospheres—correlation of specific gravity with morphological changes. J Cellular Compar Physiol 1994;24:55-61.
Goldenberg I, Shupak A: Oxy-helium treatment for refractory neurological decompression sickness: a case report. Aviat Space Environ Med 1996;67(1):57-60.
Golding FC, Griffiths PD, Hempleman HV, Patron WD, Walder DN: Decompression sickness during the construction of the Dartford Tunnel. Br J Ind Med 1960;17:167-180.
Gorman DF: A proposed classification of the decompression illness. In: Francis TJR, Smith DJ, eds: Describing Decompression Illness (Undersea Hyperbaric Medical Society Workshop, Alverstoke, United Kingdom). Bethesda, MD: Undersea Hyperbaric Medical Society; 1990:6-9.
Hall ED, Braughler JM, McCall JM: Role of oxygen radicals in stroke: Effects of the 21-aminosteroids (lazaroids). A novel class of antioxidants. Prog Clin Biol Res 1990;351-362.
Hallenbeck JM, Dutka AJ, Tanishima T: Polymorphonuclear leukocyte accumulation in brain regions with low blood flow during the early postischemic period. Stroke 1986;17:246-253.
Heimbecker RO, Lemire G, Chen CH: Role of gas embolism in decompression sickness—a new look at “the bends.” Surgery 1968;64(1):264-272.
Hossman KA: Viability thresholds and the penumbra of focal ischemia. Ann Neurol 1994;36:557-565.
Isakov AP, Broome JR: Acute carpal tunnel syndrome in a diver: evidence of peripheral nervous system involvement in decompression illness. Ann Emerg Med 1996;28(1):90-93.
Kerut E, Truax W, Borreson T, Van Meter K: Patent foramen ovale (PFO) and decompression sickness. Undersea Hyperbaric Med 1995;22(Suppl):36.
Kihara M, McManus PG, Schmelzer JD: Experimental ischemic neuropathy: salvage with hyperbaric oxygen. Ann Neurol 1995;37(1):89-94.
Lee AK, Hester RB, Coggin JH: Increased oxygen tensions modulate the cellular composition of the adaptive immune system in BALB/c mice. Cancer Biotherapy 1993;8(3):241-252.
Lee AK, Hester RG, Coggin JH, Gottlieb SF: Increased oxygen tensions influence subset composition of the cellular immune system in aged mice. Cancer Biotherapy 1994;9(1):39-54.
Lee HC, Miu KC, Chen SH: Therapeutic effect of type II decompression sickness, a comparative study between United States Navy treatment table 6A and modified treatment table 6A1. J Hyperbaric Med 1988;3(4):235-242.
Levin LL, Stewart GJ, Lynch PR, Bove AA: Blood and blood vessel wall changes induced by decompression sickness in dogs. J Appl Physiol 1981;50:944-949.
Longoni C: Preliminary diagnostic measures for performing hyperbaric oxygen therapy in a diving accident. Schweiz Z Sportmed 1993;41(4);175-177.
McCulloch J: Excitatory amino acid antagonists and their potential for the treatment of ischemic brain damage in man. Br J Clin Pharmacol 1992;34:106-114.
Mackay CR: Honing of naïve, memory and effector lymphocytes. Curr Opin Immunol 1993;5:423-427.
Madsen J, Hink J, Hyldegaard O: Diving physiology and pathophysiology. Clin Physiol 1994;14:547-626.
Mebane GY, McIver NKI: Fitness to dive. In: Bennett P, Elliot D, eds: The Physiology and Medicine of Diving. London, England: WB Saunders; 1993:53-76.
Miller JN, Fagraeus L, Bennett PB: Nitrogen-oxygen saturation therapy in serious cases of compressed air decompression sickness. Lancet 1978;2:169-171.
Moon RE, Camporesi EM, Erwin CW: Use of evoked potentials during acute dysbaric sickness. In: Halsey MJ, Elliot DH, eds:Diagnostic Techniques in Diving Neurology. London, England: Medical Research Council; 1987:63-69.
Moon RE, Sheffield PJ; Guidelines for treatment of decompression illness. Aviat Space Environ Med 1997;68(3);234-43.
Muir KW, Lees KR: Clinical experience with excitatory amino acid antagonist drugs. Stroke 1995;26:503-513.
Myers R, Monjil LG, Cullen BM: Macrophage and astrocyte populations in relation to [3H]PK 11 195 binding in rat cerebral cortex following a local ischemic lesion. J Cereb Blood Flow Metab 1991;11:314-322.
Myers RAM: Hyperbaric Chambers, United States and Canada. Bethesda, MD: Undersea and Hyperbaric Medical Society; 1993.
Neuman TS, Bove AA: Combined arterial gas embolism and decompression sickness following no-stop dives. Undersea Biomed Res 1990;17(S):429-436.
Philip RB: A review of blood changes associated with compression-decompression: relationship to decompression sickness. Undersea Biomed Res 1974;1:117-150.
Shields TG, Lee WB: The incidence of decompression sickness arising from commercial offshore air-diving operations in the UK Sector of the North Sea Diving 1982-83. Robert Gordon’s Institute of Technology and National Healthboard Report. United Kingdom: National Healthboard.
Shupak A, Melamed Y: Helium and oxygen treatment of air diving induced neurologic decompression sickness. Arch Neurol 1997;54(3);305-311.
Smith LA, Hardman JM, Sandberg GD, Beckman EL: Is acute bone decompression sickness initiated by bubbles and hemorrhages? Undersea Biomed Res 1992;19(Suppl):69.
Sub Sea Medical Manual. Ecosystem treatment table 7A. Sub Sea Publications; 1992:7-19 to 7-20.
Taylor WF, Chen S: Enhanced aggregability of human red blood cells by diving. Undersea Hyperb Med 1998;25(3);167-170.
Teasdale G, Jennett B: Assessment of coma and impaired consciousness: A partial scale. Lancet 1974;2:81-84.
Thom SR, Elbuken ME: Oxygen dependent antagonism of lipid peroxidation. Free Radical Biol Med 1991;10:413-426.
Thom SR, Mendiguren I, Nebolon M: Temporary inhibition of human neutrophil B2 integrin function by hyperbaric oxygen (HBO). Clin Res 1994;42:130A.
Thom SR: Hyperbaric Oxygen Therapy, A Committee Report. Bethesda, MD: Undersea and Hyperbaric Medical Society; 1992:71-80.
Thomsen T, Ovsteda IT, Vereide A, Holmsen H: Effects of platelet antagonists on the reduction in platelet density caused by microbubbles in vitro. Undersea Biomed Res 1986;13(3):289-303.
Thorsen T, Dalen H, Bjerkvig R, Holmsen H: Transmission and scanning electron microscopy of N2 microbubble-activated human platelets in vitro. Undersea Biomed Res 1987;14(1):45-66.
United States Navy Diving Manual. NAVSEA 0994-LP-001-9110. United States Navy; 1993:8-29 to 8-72.
Van Meter K: Medical field management of the injured diver. In: Moon RE, Camporesi EM, eds: Problems in Respiratory Care: Clinical Applications of Hyperbaric Oxygen. Philadelphia, PA: J.B. Lippincott Co.; 1991:253-268.
Van Meter K: Edgar End Memorial Lecture: A better end: high dose/low dose sequential hyperbaric oxygen therapy respectively in acute and convalescing CNS injury. Presented at: 1991 American College of Hyperbaric Medicine Annual Scientific Meeting; Ft. Lauderdale, FL.
Van Meter K: Medical field management of the injured diver. Problems Respiratory Care 1991;4(2):253-268.
Van Meter K, Harch P, Gottlieb S: Use of hyperbaric oxygen to improve patient placement on the oxygen dose response curve during advanced cardiac life support during resuscitation from cardiopulmonary arrest. In: Jain KK, ed: Hyperbaric Oxygen Therapy (in press).
Van Meter K, Harch P, Weiss L: 14 year experience of the use of a tailing of hyperbaric oxygen treatments to lessen or resolve neurologic residual injury in arterial gas embolism (AGE) or decompression illness (DCI) in the acute 0-15 day and sub-acute 16 day to 6 month post-injury period. In: Proceedings of the 1995 Gulf Coast Chapter of the Undersea and Hyperbaric Medical Society. Gulf Coast Chapter, Undersea and Hyperbaric Medical Society; New Orleans, LA: 1995.
Van Meter KW: Two diving accident case histories. In: Miller JN, Parmentier JL, eds: Rehabilitation of the Paralyzed Diver(Undersea Hyperbaric Medical Society Workshop #30, Point Clear, Alabama). Bethesda, MD: Undersea Hyperbaric Medical Society; 1984:25-30.
Vann RD: Hypobaric decompression sickness workshop. In: Pilmanas AA, ed: Proceedings of Workshop Held at Armstrong Laboratories; October 16-18, 1990; Brooks AFB, TX.
Warren LP, Djang WT, Moon RE: Neuro imaging of diving injuries to the central nervous system. Am J Neuroradiol 1988;9:933-938.
Zamboni WA, Roth AC, Russel RC: Morphologic analysis of the microcirculation during reperfusion of ischemic skeletal muscle and the effect of hyperbaric oxygen. Plast Reconstr Surg 1993;91:1110-1123.