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Hyperbaric Oxygen Therapy for Brain Injury, Cerebral Palsy, and Stroke

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Agency for Healthcare Research and Quality

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Hyperbaric Oxygen Therapy for Brain Injury, Cerebral Palsy, and Stroke
The hyperbaric chambers. Photo taken by KOMUnews taken on December 3, 2007.

Overview

Hyperbaric oxygen therapy (HBOT) is the inhalation of 100 percent oxygen inside a hyperbaric chamber that is pressurized to greater than 1 atmosphere (atm). HBOT causes both mechanical and physiologic effects by inducing a state of increased pressure and hyperoxia. HBOT is typically administered at 1 to 3 atm. While the duration of an HBOT session is typically 90 to 120 minutes, the duration, frequency, and cumulative number of sessions have not been standardized.

HBOT is administered in two primary ways, using a monoplace chamber or a multiplace chamber. The monoplace chamber is the lesscostly option for initial setup and operation but provides less opportunity for patient interaction while in the chamber. Multiplace chambers allow medical personnel to work in the chamber and care for acute patients to some extent. The entire multiplace chamber is pressurized, so medical personnel may require a controlled decompression, depending on how long they were exposed to the hyperbaric air environment.

The purpose of this report is to provide a guide to the strengths and limitations of the evidence about the use of HBOT to treat patients who have brain injury, cerebral palsy, and stroke. Brain injury can be caused by an external physical force (also known as traumatic brain injury, or TBI); rapid acceleration or deceleration of the head; bleeding within or around the brain; lack of sufficient oxygen to the brain; or toxic substances passing through the blood-brain barrier. Brain injury results in temporary or permanent impairment of cognitive, emotional, and/or physical functioning. Cerebral palsy refers to a motor deficit that usually manifests itself by 2 years of age and is secondary to an abnormality of at least the part of the brain that relates to motor function. Stroke refers to a sudden interruption of the blood supply to the brain, usually caused by a blocked artery or a ruptured blood vessel, leading to an interruption of homeostasis of cells, and symptoms such as loss of speech and loss of motor function.

While these conditions have different etiologies, prognostic factors, and outcomes, they also have important similarities. Each condition represents a broad spectrum, from barely perceptible or mild disabilities to devastating ones. All three are characterized by acute and chronic phases and by changes over time in the type and degree of disability. Another similarity is that the outcome of conventional treatment is often unsatisfactory. For brain injury in particular, there is a strong sense that conventional treatment has made little impact on outcomes.

Predicting the outcome of brain injury, cerebral palsy, and stroke is difficult. Prognostic instruments, such as the Glasgow Coma Scale (GCS) for brain injury, are not precise enough to reliably predict an individual patient’s mortality and long-term functional status. Various prognostic criteria for the cerebral palsy patient’s function have been developed over the years. For example, if a patient is not sitting independently when placed by age 2, then one can predict with approximately 95 percent confidence that he/she never will be able to walk. However, it is not possible to predict precisely when an individual patient is likely to acquire a particular ability, such as smiling, recognizing other individuals, or saying or understanding a new word.

Mortality and morbidity from a stroke are related to older age, history of myocardial infarction, cardiac arrhythmias, diabetes mellitus, and the number of stroke deficits. Functional recovery is dependent on numerous variables, including age, neurologic deficit, comorbidities, psychosocial factors, educational level, vocational status, and characteristics of the stroke survivor’s environment.

The report focuses on the quality and consistency of studies reporting clinical outcomes of the use of HBOT in humans who have brain injury, cerebral palsy, or stroke. This information can be used to help providers counsel patients who use this therapy and to identify future research needs.

Reporting the Evidence

This review addresses the following questions:

  • Does HBOT improve mortality and morbidity in patients who have traumatic brain injury or nontraumatic brain injury, such as anoxic ischemic encephalopathy?
  • Does HBOT improve functional outcomes in patients who have cerebral palsy? (Examples of improved functional outcomes are decreased spasticity, improved speech, increased alertness, increased cognitive abilities, and improved visual functioning.)
  • Does HBOT improve mortality and morbidity in patients who have suffered a stroke?
  • What are the adverse effects of using HBOT in these conditions?

To identify the patient groups, interventions, and outcomes that should be included in the review, we read background material from diverse sources including textbooks, government reports, proceedings of scientific meetings, and Web sites. We also conducted focus groups and interviews to improve our understanding of the clinical logic underlying the rationale for the use of HBOT. In the focus groups, we identified outcomes of treatment with HBOT that are important to patients, caregivers, and clinicians and examined whether patients, caregivers, and clinicians who have experience with HBOT value certain outcomes differently from those who have not used HBOT. A broader goal of the focus groups was to better understand the disagreement between supporters and nonsupporters of HBOT.

The following interventions, populations, outcomes, and study design criteria were used to formulate the literature search strategy and to assess eligibility of studies.

  • Intervention. Hyperbaric oxygen therapy: any treatment using 100 percent oxygen supplied to a patient inside a hyperbaric chamber that is pressurized to greater than 1 atm.
  • Population. Patients with: brain injury from any cause and in any stage (acute, subacute, or chronic). cerebral palsy of any etiology. thrombotic stroke.

Summary, Evidence Report/Technology Assessment: Number 85. AHRQ Publication Number 03-E049, September 2003. Agency for Healthcare Research and Quality, Rockville, MD. Used with permission. www.ahrq.gov/clinic/epcsums/hypoxsum.htm.

Comments [1]

HBOT saved me from the TBI and changed my life forever. I was suffering from a severe TBI for 7 weeks which happened while playing college football. My life was completely stopped. I was barely able to handle a normal conversation let alone attend class or maintain any hope of a normal life. My brain struggled to connect with anything around me while in the haze of the TBI. The splitting headaches for days on end, sensitivity to light and sound, unstable emotions, foggy thoughts, exhaustion, and and overall disconnect to my surrounding was my daily struggle. I was lucky enough to be treated by a doctor who prescribed HBOT to me. After 5 HBOT sessions, I could already feel myself coming out of my TBI. I began to feel life coming back into me. Two months and countless HBOT sessions later, I am symptom free and loving life. I owe it all to the use of HBOT

Mar 30th, 2014 3:39pm


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