DECOMPRESSION SICKNESS
Hyperbaric oxygen should begin during the acute episode. Several treatments may be necessary to completely clear symptoms.
RATIONALE: This disease is caused by nitrogen bubble formation in the vascular system and in tissues, in volumes sufficient to interfere with the function of an organ or cause alterations in sensation. Secondary surface active effects of the nitrogen bubbles include activation of the complement system, lyophobic effects, and increased blood viscosity, to name just a few. Protocols for hyperbaric treatment of decompression sickness have been available for nearly 100 years. Recompression of gas bubbles in the hyperbaric chamber is the only definitive form of treatment known. The clinical manifestations range from skin eruptions and joint pain to neurological dysfunction and profound fatigue, and rarely to an end stage of shock and death. Prompt treatment is important to mechanically reduce bubble size and to help reduce activation of the complement system and the clotting cascade that occur at the blood-bubble interface.
SOURCE: UHMS Publication CR(HBO) 1996
CLOSTRIDIAL MYONECROSIS (Gas Gangrene)
Hyperbaric oxygen is used as an adjunct to surgery and antibiotics in the treatment of clostridial myositis, myonecrosis or spreading clostridial cellulitis with systemic toxicity (or a presumptive diagnosis of any of the three).
RATIONALE: Gas gangrene is caused by a number of pathogenic clostridial organisms which multiply, producing necrotizing tissue toxins and a characteristic picture of pain, fever, and tachycardia out of proportion to the clinical presentation. Ninety percent of cases are caused by Clostridium perfringens which grow rapidly in low oxygen tensions. Restricted growth and a halt in alpha toxin production is evident at tissue oxygen tensions above 250 mmHg. Experimentally, hyperbaric oxygen therapy should be started early and continued until progress of the anaerobic infection is completely halted. It is recommended that a patient with gas gangrene receive 3 treatments in the first 24 hours, then twice a day treatments for the next 4 to 5 days. Hyperbaric oxygen must be started on the basis of clinical impression and gram stain results, without delays for bacterial confirmation. Elevation of oxygen tensions in the region of functioning capillaries in the infected wound halts alpha toxin production. Necrotic tissue can be debrided more conservatively, salvaging more viable tissue than would otherwise be possible. Although surgery and antibiotics remain the primary treatment, the need for emergency, life saving ablative surgery is often obviated as hyperbaric oxygen effects a chemical barrier to progression of the disease.
SOURCE: UHMS Publication CR(HBO) 1996