<%server.execute "isdev.asp"%> Role of hyperbaric oxygen therapy in severe head injury in children Prakash A, Parelkar SV, Oak SN, Gupta RK, Sanghvi BV, Bachani M, Patil R - J Pediatr Neurosci
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ORIGINAL ARTICLE
Year : 2012  |  Volume : 7  |  Issue : 1  |  Page : 4-8
 

Role of hyperbaric oxygen therapy in severe head injury in children


Department of Pediatric Surgery, King Edward Memorial Hospital, Parel, Mumbai, India

Date of Web Publication28-Jun-2012

Correspondence Address:
Advait Prakash
302, Nirmal Kunj, Parel Village, Mumbai, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1817-1745.97610

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   Abstract 

Aim: A brain injury results in a temporary or permanent impairment of cognitive, emotional, and/or physical function. Predicting the outcome of pediatric brain injury is difficult. Prognostic instruments are not precise enough to reliably predict individual patient's mortality and long-term functional status. The purpose of this article is to provide a guide to the strengths and limitations of the use of hyperbaric oxygen therapy (HBOT) in treating pediatric patients with severe brain injury. Materials and Methods: We studied total 56 patients of head injury. Out of them 28 received HBOT. Only cases with severe head injury [Glasgow Coma Scale (GCS) < 8] with no other associated injury were included in the study group. After an initial period of resuscitation and conservative management (10-12 days), all were subjected to three sessions of HBOT at 1-week interval. This study group was compared with a control group of similar severity of head injury (GCS < 8). Results: The study and control groups were compared in terms of duration of hospitalization, GCS, disability reduction,and social behavior. Patients who received HBOT were significantly better than the control group on all the parameters with decreased hospital stay, better GCS, and drastic reduction in disability. Conclusion: In children with traumatic brain injury, the addition of HBOT significantly improved outcome and quality of life and reduced the risk of complications.


Keywords: Children, head injury, hyperbaric oxygen therapy


How to cite this article:
Prakash A, Parelkar SV, Oak SN, Gupta RK, Sanghvi BV, Bachani M, Patil R. Role of hyperbaric oxygen therapy in severe head injury in children. J Pediatr Neurosci 2012;7:4-8

How to cite this URL:
Prakash A, Parelkar SV, Oak SN, Gupta RK, Sanghvi BV, Bachani M, Patil R. Role of hyperbaric oxygen therapy in severe head injury in children. J Pediatr Neurosci [serial online] 2012 [cited 2019 Apr 26];7:4-8. Available from: http://www.pediatricneurosciences.com/text.asp?2012/7/1/4/97610



   Introduction Top


Hyperbaric oxygen therapy (HBOT) is the administration of high concentrations of oxygen within a pressurized chamber. HBOT has become the definitive therapy for patients with decompression illness, gas embolism, and severe acute carbon monoxide poisoning. It is now widely accepted in treatment of osteoradionecrosis, soft tissue radionecrosis and delayed wound healing. However, the role of HBOT in the treatment of patients with brain injuries is controversial.

Brain injury can be caused by an external physical force (traumatic brain injury, or TBI) with rapid acceleration or deceleration of the head and bleeding within or around the brain leading to cerebral hypoxia and passage of toxic substances through the blood-brain barrier. These result in a temporary or permanent impairment of cognitive, emotional, and/or physical functioning.

For brain injury there is a strong sense that conventional treatment has had little impact on outcome. [1] The use of various diagnostic and therapeutic interventions, viz, prehospital intubation, intracranial pressure (ICP) monitoring, ICP-directed therapy, and brain computed tomography scan utilization vary considerably among different centers. [2] Such variation signifies a lack of consensus on clinical effectiveness. Predicting the outcome of pediatric brain injury 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 in pediatric patients. The purpose of this article is to provide a guide to the strengths and limitations of HBOT in treating children with brain injury.


   Materials and Methods Top


We studied a total of 54 patients of head injury. Out of them 28 received HBOT (study group, n = 28). Only cases with severe head injury (GCS < 8) with no other associated injury were included in the study group. After an initial period of resuscitation and conservative management (10 days), all were subjected to three sessions of HBOT at 1-week interval each. This study group was compared with a matched control group of similar severity of head injury (GCS < 8) selected by randomization.

HBOT is the inhalation of 100% oxygen inside a hyperbaric chamber pressurized to greater than 1 atmosphere (atm). HBOT causes both mechanical and physiologic effects by inducing a state of increased pressure and hyperoxia. Hyperbaric oxygen pressure is expressed in multiples of atmospheric pressure at sea level, where 1 atm is about 760 mm Hg or 1 kg/cm 2 . The oxygen dissolved in blood at 1 atm (sea level) in room air is 0.3 ml/dL, and this is in addition to hemoglobin-bound oxygen. Inhalation of 100% oxygen at 1 atm increases blood oxygenation to 1.5 ml/dL. Increasing the pressure to 3 atm increases the blood oxygen (dissolved oxygen, not carried by hemoglobin) to 6 ml/dL. At rest and with good perfusion, tissues require 5-6 ml/dL of oxygen, whether from dissolved or hemoglobin-bound oxygen. Hence, in situations where hemoglobin-bound oxygen is limited (e.g., carbon monoxide poisoning), tissue oxygen needs can be met in this manner.

In addition, the increased pressure reduces the volume of gases in the blood by virtue of Boyle's law (in an enclosed space, the volume of a gas is inversely proportionate to the pressure exerted upon it). This very mechanism is relied upon in decompression illness and arterial gas embolism to reduce the size of the gas bubbles and allow replacement of inert gas in the bubbles with oxygen, which can be metabolized by tissues.

HBOT can be administered by two ways, using monoplace chamber or multiplace chamber. The monoplace chamber, which we used in our study, serves one patient at a time. The initial cost of setup is less but it provides limited opportunity for patient intervention while in the chamber. These chambers are generally constructed of acrylic or with view ports that allow for patient observation. These chambers are pressurized with 100% oxygen.

Multiplace chambers allow medical personnel to work in the chamber. Each patient is given 100% oxygen through a facemask, tight-fitting hood or endotracheal tube. The entire multiplace chamber is pressurized with air, so medical personnel may require a controlled decompression, depending on the duration of exposure to the hyperbaric environment.

The duration of an HBOT session in common practice is about 90-120 minutes, however, the duration, frequency, and cumulative number of sessions have not been standardized. The dose received by the patient may be affected by the type of chamber used. Monoplace chambers using face masks or hoods that do not fit snugly may result in dilution of 100% oxygen with room air.


   Results Top


The study and the control groups were compared on various clinical, social and functional parameters where study group (receiving HBOT) showed distinct advantage over the control group [Table 1].
Table 1: Comparison of study and control groups on various parameters

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On contrasting the GCS of both the groups; observed at the time of admission, after 10 days of conservative management and then at 1-week interval, it was quite evident that patients who recieved HBOT showed marked improvement as compared to the study group [Figure 1].
Figure 1: Comparison of improvement in Glasgow Coma Scale in study group (with hyperbaric oxygen therapy) and control group

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   Discussion Top


Each year, approximately 1.5 million Indians sustain traumatic brain injuries, ranging in severity from mild to fatal. [3],[4] The disability covers the entire spectrum of physical, social, and emotional function. No single instrument can measure all of the consequences of TBI. The oldest formal scale, the Glasgow Outcome Scale, categorizes patients into five broad categories: good recovery, moderate disability, severe disability, persistent vegetative state, and death. [5] This measure, although convenient and widely used, is insensitive to many cognitive and emotional deficits which strongly affect the quality of life. Since the 1970s, the GCS which ranges from 3 to 15 has been the most widely used measure of the severity of an acute brain injury. [6],[7] A GCS between 3-5 indicates serious injury with grave outcome, while GCS between 13 and 15 represents mild injury with the best prognosis. "Severe" injury is often defined as a GCS score of 8 or less indicating a mortality rate of 50% and high likelihood of suffering from severe long-term disabilities. [8],[9],[10],[11]

In addition to GCS, factors such as age, associated injuries, intracranial hypertension, and the presence of mass effect are also predictors of mortality and severe disability. [12],[13],[14],[15],[16],[17],[18] Preinjury productivity and education also help in predicting the functional outcome in survivors. [19],[20] Hypoxia (PaO 2 less than 60 mm Hg, or apnea or cyanosis) and hypotension (systolic blood pressure less than 90 mm Hg) are also strong predictors of death and severe disability. [17],[21],[22],[23]

HBOT in acute brain injury

In acute TBI, hypoxia and hypotension are independently associated with increased mortality and morbidity. Thus, secondary ischemia and oxygen deficiency are thought to be important mechanisms of cell death in TBI. [24] Aggressive management of trauma significantly reduces the hypoxic and ischemic episodes, but does not eliminate it. For this reason, there is renewed interest in finding more effective strategies for ensuring adequate oxygenation and redistributing cerebral blood flow (CBF) to injured areas of the brain.

The metabolic effects of brain injury are not easily demonstrated and are by no means fully understood. Immediately after a brain injury, brain cells can be inactivated temporarily by ischemia and edema which compromise local perfusion. This observation forms part of the rationale for the use of HBOT, which increases blood flow to the damaged areas of the brain, as documented by serial single photon emission computed tomography (SPECT) scans and other techniques. [25],[26],[27],[28]

In some experimental models of acute cerebral ischemia and acute carbon monoxide poisoning, HBOT prevents cell death. [29] The mechanism is unclear, but effects of oxygen on the cellular and inflammatory response to injury are considered important. [29] Recently, in a rat model of focal cerebral ischemia, HBOT reduced brain leukocyte myeloperoxidase (MPO) activity, which is produced by white blood cells (polymorphonuclear neutrophils) and is a marker of the degree of inflammation. Rats randomized to HBOT had reduced infarct size and improved neurological outcomes compared with untreated rats, and the degree of neurologic damage was highly correlated with the level of MPO activity. [30] In a separate model of cardiac arrest and resuscitation, the same investigators found that dogs treated with HBOT had better neurological outcomes and, histologically, fewer dying neurons than dogs treated conventionally. [31] The magnitude of neuronal injury correlated well with the neurological outcomes, but was not related to cerebral oxygen delivery or to the rate of oxygen metabolism. Another recent study showed that early HBOT increases cerebral adenosine 5?-triphosphate (ATP) production in rats following lateral fluid-percussion injury, offering strong mechanistic support for an O 2 delivery hypothesis in TBI. [32] It has also been reported that perilesional neurons have increased vulnerability to mitochondrial impairment, and attempts to augment regional CBF and oxygenation of this tissue may be very beneficial. [33] Tolias et al. reported that early and prolonged hyperoxia improved TBI, which was evident by improvements in microdialysate indices of brain oxidative metabolism and decrease in ICP. [34]

Sarah Rockswold and coworkers noted that in severely brain injured patients the cerebral metabolic rate of oxygen (CRMO 2 ) is typically reduced by up to 50% and only 45% of patients exhibited normal coupling of CBF and CRMO 2 . [35] In addition to decreased cerebral metabolism, most patients with severe brain injury have increased lactate production. The authors concluded that increased CRMO 2 and decreased CSF lactate levels after HBO treatment indicate a shift toward aerobic metabolism in severely brain injured patients, especially in those with reduced CBF or with ischemia. They also found that HBOT promotes blood-brain barrier integrity, reducing cerebral edema and hyperemia, which in turn helps to lower elevated ICP. [35] The authors also recommended shorter and more frequent HBOT sessions to sustain the beneficial effects and avoid elevations in the ICP. [35]

HBOT in chronic brain injury

Many brain-injured patients progress spontaneously from coma to consciousness and eventually recover some of the cognitive functions. This phenomenon of spontaneous recovery from brain injury implies that some brain cells that have lost function can regain it, sometimes after long periods of time. Several theories of recovery after injury in the central nervous system invoke the concept of temporary, reversible inactivity of brain tissue to explain this phenomenon.

The use of HBOT for chronic brain injury is based on the theory that, in any brain injury, there are inactive cells that have the potential to recover. According to this theory, these "idling neurons" exist in the ischemic penumbra, a transition area of dormant neurons between areas of dead tissue and the unaffected healthy tissue. [28],[29],[36],[37],[38] The oxygen availability to these cells stimulates the cells to function normally, reactivating them metabolically or electrically.

In contrast with the cognitive stimulation theory, the "idling neuron" theory views neuron inactivity denervation as the result of chronic hypoxia and postulates that restoring oxygen stimulates the growth of blood vessels and of new synaptic connections among previously dormant neurons. Supporters of the use of HBOT in brain injury argue that this theory has a stronger experimental base than the theory underlying restorative cognitive therapies. [29]

In contrast to the theoretical effects of cognitive stimulation, the effects of the proposed treatment-pressurized oxygen-can be observed directly in animal models. As noted above, animal studies have examined HBOT's effects on physiologic and anatomic endpoints, including neuronal death, infarct size, and, in some models, development or preservation of synapses. The physiologic effects of hyperbaric oxygen have also been examined in before-after treatment case studies in humans using SPECT imaging and markers of cerebral metabolism. [26],[28],[29]

Adverse effects of HBOT

Adverse events can occur during compression, treatment, and decompression and are related to the increased pressure and the increased oxygen concentration. [39] Complications such as pulmonary barotrauma or seizures can occur immediately, but more subtle adverse effects may emerge after a series of treatments. The findings of a recent study of HBOT for acute carbon monoxide poisoning (not covered in this report) raise concerns over worse cognitive outcomes in patients receiving HBOT compared with normobaric oxygen. [40]


   Conclusion Top


In children with TBI, the addition of HBOT significantly improved outcome and quality of life and reduced the risk of complications. HBOT for brain injury is not likely to gain acceptance in routine clinical use until a clinical method of assessing its effectiveness in the individual patient is validated. Specifically, the diagnostic value of SPECT scans and of other intermediate indicators of the effects of HBOT should be examined by large and high-quality studies. A longitudinal cohort study in which all patients undergo proper diagnostic evaluation as well as standardized follow-up tests would be a more prudent and ideal approach.

 
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    Figures

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