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The Dosage of Hyperbaric Oxygen in Chronic Brain Injury

The Dosage of Hyperbaric Oxygen in Chronic Brain Injury

Paul G. Harch M.D.


The concept of dosage of hyperbaric oxygen therapy (HBOT) derives from the definition of HBOT as a drug. Using the broad definition of HBOT by Harch and Neubauer (1), HBOT is the use of greater than ambient pressure oxygen as a drug to treat basic pathophysiologic processes/states and their diseases. Drug dosage of HBOT, therefore, is a function of baseline or reference ambient pressure, depth of pressurization, duration, frequency, air breaks, surface interval, number of treatments, idiosyncratic genetic patient factors, and time to intervention in the disease process which determines the pathological targets. All of these factors cause HBOT to be a narrow-window drug in chronic brain injury similar to digoxin and coumadin: too litfie maybe ineffective and too much can be toxic. In addition, oxygen is a respiratory metabolite: ;too little has serious metabolic consequences and too much can cause metabolic fatigue. Determining the proper dosage in a given patient with a specific or multiple diseases can be difficult. Ultimately, one wants the best dosage that improves the patient while doing the least harm.

HBOT has both acute and chronic effects (2). This paper will address only the chronic effects. Chronic effects of HBOT include fibroblast stimulation, collagen deposition, anglogenesis, epithelialization, and bone remodeling. This is most evident in shallow perfusion gradient wounds such as the classic homogenous wound of external beam radiation. In this animal and human model, Marx (3) has shown that intermittent exposure to HBOT induces the aforementioned chronic trophic effects to cause wound healing. The final level of tissue oxygenation after HBOT is approximately 80% of normal tissue, but the effect is durable for years. The unproven mechanism of the effect is thought to be secondary to transient elevation of tissue oxygen levels that results in a steep oxygen gradient that causes anglogenesis. Since 1995 this effect has been better characterized as signal induction where the drug HBOT, by elevation of tissue oxygen pressures, alone or in combination with other factors, signals the DNA to begin transcription of various gene sequences to mRNA (4,5,6). The mRNA is translated to proteins which cause trophic tissue changes, i.e., wound healing. These mechanisms are thought to be responsible for the HBOT-induced wound healing that is seen in a large variety of chronic non-healing wounds, such as arterial insufficiency, venous insufficiency, diabetic, radiation, sickle cell, vasculitic, and other ulcers.

Argument for Medicare/Medicaid - Coverage of Hbot - Treatment of Diabetic Foot Wounds

Hyperbaric Oxygen Treatment of Diabetic Foot Wounds

Argument for Medicare/Medicaid

By Paul G Harch MD

Hyperbaric oxygen therapy (HBOT) was first defined as a drug in 1977 by Gottlieb (1). Unfortunately, this critical definition has been long forgotten and substitute definitions have mis-characterized HBOT as a therapy for "certain recalcitrant, expensive, or otherwise hopeless medical problems."(2) This mischaracterization has resulted in a confusing collectionHyperbaric Oxygen Chambers of different lists e.g., CMS, UHMS Accepted Indications, and international lists(3), of seemingly unrelated reimbursable diagnoses (chronic refractory osteomyelitis, air embolism, cyanide poisoning, compromised flaps and grafts, carbon monoxide poisoning, acute stroke, etc) supported by widely varying amounts of basic science and clinical evidence. In 1999 the drug definition of HBOT was refined and restated as the use of greater than atmospheric pressure oxygen as a drug to treat basic pathophysiologic processes and their diseases (4). With that definition the above lists could now be understood as cohesive sets of diagnoses connected by HBOT effects on the acute and/or chronic underlying pathophysiology common to the diseases. Furthermore, the definition suggested and argued for the application of HBOT to additional diseases that shared this pathophysiology. The 1999 drug definition of HBOT will be used in this paper to argue for HBOT effectiveness in the treatment of infected diabetic foot wounds, and hence, CMS reimbursement for the same. The argument will be constructed by identifying the underlying pathophysiology in diabetic foot wounds, presenting the evidence for the beneficial effects of HBOT on this pathophysiology, demonstrating a similar benefit in patients with diabetic foot wounds, and then showing the risk/benefit and cost/effectiveness evidence for HBOT in diabetic foot wounds. This argument will lead to the conclusion that CMS coverage of HBOT should be extended to diabetic foot wounds.

Effect of HBOT Tailing Treatment on Neurological Residual & PSCT Brain Images in Type II (Cerebral) DCI/CAGE

PG Harch, KW Van Meter, SF Gottlieb, P Staab. JoEllen Smith Hyperbaric Medicine Unit, New Orleans, LA 70131.

Background: No guidelines exist for HBOT tailing treatment of residual neurological injury and no studies document their effect on SPECT brain images and neurological condition in Type II/CAGE DCI as we report herein.

Controversies in the treatment of acute carbon monoxide intoxication

Acute carbon monoxide (CO) poisoning causes brain lipid peroxidation as well as an hypoxic injury. Traditional therapy has been 1 ATA oxygen but now includes hyperbaric oxygen therapy (HBOT) which hastens dissociation of COHgb, reverses anoxia, inhibits reperfusion injury, and has toxic effects. All of these are dose dependant and time sensitive. The human experience with HBOT is anecdotal cases, uncontrolled and controlled series, which are largely positive, and randomized, prospective e controlled studies with conflicting results. A controversy exists over the pressure and number of HBOTs.