From the website of the Brain Injury Association of America

Anoxia



Question: My seven-year-old son recently sustained an anoxic brain injury from a near drowning incident in a pool. Although I have found much information on traumatic brain injury (TBI), I have had difficulty finding information specifically pertaining to anoxic brain injuries. What is the difference between the two types of injuries and how does the treatment and rehabilitation differ? Finally, what types of outcomes can I expect from my child, and what can I do to increase his success when he returns to school?

Answer: Brain Injury Source, Volume 3, Issue 3, Ask the Doctor
By Nathan D. Zasler, MD, FAAPM&R, FAADEP, DAAPM, CIME

Thank you for your question. Since you did not provide any information to allow me to determine how severely impaired or disabled your son is as related to the magnitude of his anoxic/hypoxic brain injury I only can answer your question in general terms.

I would start off by stating that the literature on neurologic rehabilitation, as it relates to hypoxic and/or anoxic brain injuries, is rather sparse. So that other readers are clear on terminology, many different phrases are used to describe insults to the brain that result in lack of oxygen or blood flow to the brain, both of which may produce brain injury. A relative lack of oxygen is known as hypoxia, whereas an absolute lack or deprivation of oxygen is known as anoxia. A lack of blood flow to the brain is termed ischemic insult. There are various scenarios that may lead to hypoxic ischemic brain insults. These include drowning incidents, heart attacks, intra-operative complications leading to cardiopulmonary arrests, respiratory arrests, carbon monoxide poisoning and other toxic exposures, among a multiplicity of other mechanisms.

There have been various classifications for these types of injuries, including the one used by Barcroft, which divided hypoxic/anoxic injuries into four categories:


anoxic anoxia - due to inadequate oxygen supply

anemic anoxia - due to inadequate oxygen carrying capacity of the blood

stagnant hypoxia - due to the critical reduction of cerebral blood flow or pressure

toxic anoxia - due to toxins or metabolites that may interfere with oxygen utilization


As with traumatic brain injury, hypoxic ischemic brain injury may occur along a spectrum from very mild to very severe, the latter potentially so devastating that it results in the death of the individual. There are certainly individuals with very subtle insults who make excellent recoveries. In general, the little literature that exists on this type of injury suggests that with more significant injuries requiring inpatient rehabilitation the general outcome is, as a rule, poorer for hypoxic ischemic brain injury, than it is for equivalent magnitudes of traumatic brain injury. In other words, in two individuals, one with traumatic brain injury and one with hypoxic ischemic brain injury, who both present with initial Glasgow Coma Scale (GCS) scores of 5, more often than not the person with the traumatic brain injury will fair better in the long run. This is in part due to the fact that hypoxic ischemic injury from a neuro-pathologic standpoint is a "different animal." Specifically, the part of the brain affected by hypoxic anoxic insult are the neurons, whereas brain injury tends to be an axonal phenomena.

Often times, there is a debate about how long the brain can go without oxygen in an absolute fashion before incurring irreversible brain damage. The critical threshold for the minimal oxygen level necessary to result in brain damage is surprisingly unknown. When there is a lack of blood flow to the brain for more than 3-4 minutes, brain damage will be fairly generalized throughout both the cerebral and cerebellar cortex and will also involve, as a rule, subcortical structures such as the basal ganglia. It is important to understand that the types of problems seen from an impairment standpoint after a hypoxic ischemic brain injury are often quite different from those seen after a traumatic brain injury, although there certainly may be some parallels. This disparity in the types of impairments observed is, to a great extent, due to the vulnerability of certain central nervous system structures to hypoxia and/or ischemia.

Areas of the brain that have been shown to be selectively vulnerable to hypoxic ischemic insult include the Purkinje's fibers of the cerebellum and the parieto-occipital cortex, as well as areas of the medial portion of the temporal lobe, specifically the hippocampus which is one of the major structures responsible for memory consolidation. Certain subcortical structures such as the amygdala, globus pallidus, thalamus, caudate nucleus and putamen are also generally considered fairly sensitive to hypoxic ischemic insult. Brain stem structures which may have a greater vulnerability for injury include the reticular zone of the substantia nigra.

When there is significant associated lack of blood flow to the brain, as might be seen with significant peripheral blood loss and/or severe hypotension, the latter which commonly can be seen in cardiac arrest situations, the brain is also subject to ischemic injury. Specifically, this occurs when the perfusion pressure to the brain decreases below the threshold for maintaining adequate cerebral fusion (blood flow). There are certain areas of the brain, termed "watershed areas," which lay between major vascular territories that are particularly sensitive to this type of injury; in fact, when blood flow falls below a critical value, these watershed areas are prone to stroke-like phenomena. These types of strokes have been termed "watershed infarcts." Some of the more common areas affected include the watershed zone between the posterior and middle cerebral artery and, to a lesser extent, the watershed area between the middle cerebral artery and anterior cerebral artery. Often times, one may not see these infarcts on static imaging studies such as CT or MRI, particularly when there are less profound insults involved. Functional imaging, via single photon emission computerized tomography (SPECT), can be particularly helpful in imaging these types of insults as they demonstrate decreased perfusion to the areas that have been affected. SPECT imaging may also be useful in delineating cortical as well as subcortical post hypoxic brain dysfunction, even in the presence of normal static imaging.

Although the types of impairments seen after hypoxic ischemic brain injury are quite heterogeneous, as with traumatic brain injury, there are certain types of problems that are seen more commonly, particularly after more severe hypoxic ischemic insults. In cases of less severe injury, it is fairly typical to see the major problems being in the area of cognitive functioning and, in particular, memory functioning. Individuals may have a constellation of cognitive disorders including, potentially, amnestic disorder which, in its true form, is a relatively rare phenomena following traumatic brain injury when one looks at the entire spectrum and magnitude of impairments following this type of brain insult. With more severe injuries, one can see problems with acute agitation and confusion, as well as protracted vegetative states in the early phases of recovery following hypoxic ischemic brain injury. Generally, there is agreement that once vegetative state has lasted for three months following this type of insult, it can then be determined to be permanent; that is, the individual is not statistically likely to emerge from the vegetative state. This determination can be made in both children and adults following hypoxic ischemic insults. It should be noted that this is very different from traumatic brain injury where the cut-off for permanency generally has been agreed to be at one year post-injury.

Certainly, behavioral problems can be seen in various different presentations. These include problems with behaviors that are commonly seen after traumatic brain injury such as depression; however, at least based on my clinical experience, there is a greater propensity for more severe behavior problems following hypoxic ischemic insult, including psychotic and delusional disorders. One also can see other types of behavioral problems such as organic personality disorders, problems with episodic dyscontrol and, in a milder form, problems with decreased frustration tolerance and irritability.

With bilateral parieto-occipital ischemic damage, one can see a clinical condition, termed Balint's syndrome, which deals with a constellation of problems including difficulty with certain types of voluntary eye movement, problems with optic ataxia and difficulty with overall perspective of complex visual scene. Movement disorders following hypoxic ischemic injury are quite common, particularly when the insult has been severe. These include problems with Parkinsonian types of deficits including rigidity and bradykinesia, as well as other movement disorders such as myoclonus, chorea and athetosis. Due to the sensitivity of the Purkinje's fibers in the cerebellum as previously noted, individuals with more severe insults commonly may be seen to have kinetic and postural tremor in the extremities and trunk, as well as severe ataxia of gait in conjunction with titubation (sort of like the bobbing puppy head that you see in the back of some cars).

With hypoxia induced basal ganglia damage, one can see memory and intellect relatively well preserved, if there has been selective involvement of these subcortical structures. Individuals with these types of injuries tend to be apathetic and/or lack insight. Their behavioral problems tend also to include impulsivity and poor abstraction, as well as problem solving. There are a few "late impairments" that may be seen following hypoxic ischemic insult. These include delayed decline in functioning, which is more commonly seen following carbon monoxide poisoning and has been attributed to extensive demyelination of deep cerebral white matter. This decline is typically seen over the first week to two weeks post-injury and has been reported up to several weeks post injury. Other late complications include movement disorders, action myoclonus and seizures.

When predicting outcome after hypoxic ischemic insult, the factors found to be associated with a worse outcome include: longer duration of coma/vegetative state, older age, anoxia in the presence of significant hypotension (decreased blood pressure), acute neurologic exam abnormalities (with pupillary reflexes probably being the most well studied), premorbid psychiatric illness, premorbid low intellectual status, delayed emergence of motor symptoms, evidence of extensive focal damage on static imaging (CT or MRI) and significant cortical atrophy on static imaging.

As with traumatic brain injury, the approach to rehabilitation of the individual with hypoxic ischemic brain injury should be based on understanding the mechanism of insult, neuropathology, prognosis and current impairments and disability. Many of the types of problems seen in this patient population may be modulated with appropriate neuropsychopharmacologic treatment. Due to the dearth of literature examining specific rehabilitative techniques for this patient population, most physicians and therapists typically will broach care based on their experience in addressing similar types of problems in other types of populations (e.g., strokes and traumatic brain injury in particular). Depending on the magnitude of the insult, it is certainly possible for someone who has incurred a hypoxic ischemic injury to return to independent community living including educational or vocational pursuits. Clearly, in cases where there is more profound insults of a moderate to severe extent, the prognosis for independent community living becomes more guarded.

I am often asked what my experience has been with regard to the recovery course of patients following these types of injuries. My response to this question is one of guarded optimism with the understanding that there is a broad range of time frames in which individuals recover, even after significant injuries where the prognosis is clearly not as bright as with equivalent magnitudes of traumatic brain injury. Based on the literature and my own experience, I feel that most individuals with hypoxic ischemic brain injury, regardless of magnitude, probably make the majority of their recovery within the first six to twelve months post-injury. I certainly have seen individuals, although they are the exception rather than the rule, who continue to make recovery well beyond one year post-injury.

Regarding your last question dealing specifically with the type of outcome you can expect for your child and the things you can do to increase his success when he returns to school, I would have to defer on these questions due to a lack of sufficient information. From an ethical standpoint, I have a consternation about giving specific advice without having seen an individual. I would strongly recommend that if your son is not being followed by a specialist familiar with long-term community based management of persons with acquired brain injury, that you take him to such a clinician. My experience has been that the individuals who receive the most consolidated care, ideally provided in a holistic, interdisciplinary fashion, tend to do the best from a functional standpoint. Therefore, I would recommend that aside from having a good physician involved in your son's care, you also find a team of rehabilitation clinicians to address his current needs. I would assume that, at a minimum, he would need neuropsychological follow-up, preferably by a pediatric neuropsychologist familiar with school re-entry issues. Depending on what other impairments he may have, physical and occupational therapy, as well as speech language pathology and recreational therapy also may be clinically indicated.

I would suggest if you are interested in reading further on the topic of hypoxic ischemic brain injury, you should consider some of the following references. Thanks again for your question.

Sincerely,

Nathan D. Zasler, MD, FAAPM&R, FAADEP, DAAPM, CIME

Medical Director, Pinnacle Rehabilitation and Concussion Care Centre of Virginia

Medical Director, Tree of Life

Suggested Reading List

Bachman D, Katz D: Anoxic-hypotensive brain injury and encephalitis. In: Neurologic Rehabilitation: A Guide to Diagnosis, Prognosis, and Treatment Planning. VM Mills, JW Cassidy & DI Katz (Eds.). Blackwell Science. Pgs. 1145-176, 1997.

Ban E: Review article (IMP). Cardiopulmonary arrest. Pathophysiology and neurologic complications. Annals of Internal Medicine. 103:920-927, 1985.

Bass E: Cardiopulmonary arrest. Annals of Internal Medicine. 103:920927, 1985.

Bates D, Carona JJ: A prospective study of nontraumatic coma. Melhocts and result in 310 pts. Annals of Neurology. 211-220, 1977.

Beretta E, Regli F, de Crousaz G & Steck AJ: Postanoxic Myoclonus Journal Neurology. 225:57-62, 1981.

Bertini G, Margheri M, Giglioli C et al.: Significance of early clinical manifestations in postanoxic coma: A retrospective study of 58 patients resuscitated after prehospital cardiac arrest. Critical Care Medicine. 17(1);627, 1989.

Brierley JB & Graham DI: Hypoxic and vascular disorders of the central nervous system. In: Greenfield's Neuropathology. JH Adams, JAN Corsellis & LW Duchen (Eds.), 4th edition. New York: John Wiley & Sons, 1984. Pgs. 125-156.

Falk RH: Physical and intellectual recovery following prolonged hypoxic coma. Postgrad Med J. 66(775):384-6, 1990.

Grosswasser Z, Cohen M & Costeff H: Rehabilitation outcome after anoxic brain damage. Arch Phys Med Rehab. 70:186-188, 1989.

Hawker K & Lang AE: Hypoxic-ischemic damage of the basal ganglia. Case reports and a review of the literature. Movement Disorders. 5(3):21924, 1990.

Levy DE, Caronna JJ, Singer BH et al.: Predicting outcome from hypoxic-ischemic coma. JAMA. 253(10):14202426, 1985.

Levy DE & Bates D: Prognosis in non-traumatic coma. Annals of Internal Medicine. 94(2) 293-301, 1981.

Longstreth WT, Jr: Neurologic sequelae of cardiac arrest. Western Journal of Medicine. 147:175-180, 1987.

Sazbon L, Zagreba F, Ronen J et al: Course and outcome of patients in vegetative state of non-traumatic etiology. J Neurol Neurosurg Psych. 56:407-409, 1993.

Schneck S: Cerebral anoxia. Joynt (Ed.). Philadelphia: Lippincott, 1991. Pgs. 1-25.

Scollo-Lavizzari G & Bassetti C: Prognostic value of EEG in post-anoxic coma after cardiac arrest. Eur Neurol, 26(3):161-70, 1987.

Snyder BD: Neurologic prognosis after cardiopulmonary arrest. II Level of consciousness. Neurology. 30:52-58, 1980.

Snyder BD: Neurologic prognosis after cardiopulmonary arrest. IV. Brain stem reflexes. Neurology. 31: 1092-1097, 1981.

Somjen G (Ed): Mechanisms of Cerebral Hypoxia and Stroke, Plenum Press, 1988.

Szlabowitz JW: Amitriptyline treatment of agitation associated with anoxic encephalopathy. APMR. Vol. 71, 1990.

White BC, Wiegenstein JG & Winegar CD: Brain ischemic anoxia. JAMA. 251(12):1586-1589, 1984.







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