Cerebral hypoxia

For other uses of the term "hypoxia", see hypoxia.

Cerebral hypoxia refers to deprivation of oxygen supply to brain tissue. Mild or moderate cerebral hypoxia is sometimes known as diffuse cerebral hypoxia. It can cause confusion and fainting, but its effects are reversible. Total deprivation of oxygen to the brain is called cerebral anoxia. Extended periods of cerebral hypoxia can lead to brain death or permanent brain damage.

Most cases of cerebral hypoxia are caused by a sudden change in brain oxygen levels. The body can normally respond to mild gradual changes in blood oxygen with little or no noticeable effect on brain function. The acclimatization process used by high altitude climbers is an example of such adjustment.

The presence of cerebral hypoxia symptoms indicates that the brain has been overwhelmed by a change in its oxygen supply. Consequently, even mild symptoms of cerebral hypoxia require immediate medical attention.

Additional recommended knowledge

Correct Test Weight Handling Guide: 12 Practical Tips

Don't let static charges disrupt your weighing accuracy

Essential Laboratory Skills Guide

Classification

Cerebral hypoxia is typically grouped into four categories depending on the severity and location of the brain’s oxygen deprivation:^[1]

• Diffuse cerebral hypoxia. A mild to moderate impairment of brain function due to low oxygen levels in the blood.
• Focal cerebral ischemia. A small localized reduction in the flow of oxygen from the blood to the brain. Damage to neurons is usually irreversible. Mild strokes.
• Cerebral infarction. A complete stoppage of the flow of oxygen from the blood to a region of the brain. Significant irreversible brain damage occurs in the region around the blockage. Major strokes are an example of cerebral infarction.
• Global cerebral ischemia. A complete stoppage of blood flow to the brain.

Cerebral hypoxia can also be classified by the cause of the reduced brain oxygen:^[2]

• Hypoxic hypoxia. Limited oxygen in the environment causes reduced brain function. Divers, aviators,^[3] mountain climbers and fire fighters are all at risk for this kind of cerebral hypoxia. The term also includes oxygen deprivation due to obstructions in the lungs. Choking, strangulation, the crushing of the windpipe all cause this sort of hypoxia. Severe asthmatics may also experience symptoms of hypoxic hypoxia.
• Hypemic hypoxia. Reduced brain function is caused by inadequate oxygen in the blood despite adequate environmental oxygen. Anemia and carbon monoxide poisoning are common causes of hypemic hypoxia.
• Ischemic hypoxia (a.k.a. stagnant hypoxia). Reduced brain oxygen is caused by inadequate blood flow to the brain. Stroke, shock, and heart attacks are common causes of stagnant hypoxia. Ischemic hypoxia can also be created by pressure on the brain. Cerebral edema, brain hemorrhages and hydrocephalus exert pressure on brain tissue and impede their absorption of oxygen.
• Histotoxic hypoxia. Oxygen is present in brain tissue but cannot be metabolized. Cyanide poisoning is a well known example.

Causes

Cerebral hypoxia can be caused by any event that severely interferes with the brain's ability to receive or process oxygen. This event may be internal or external to the body.

Mild and moderate forms of cerebral hypoxia may be caused by various diseases that interfere with breathing and blood oxygenation. Severe asthma and various sorts of anemia can cause some degree of diffuse cerebral hypoxia. Other causes include work in nitrogen rich environments, ascent from a deep water dive, flying at high altitudes in an un-pressurized cabin, and intense exercise at high altitudes prior to acclimatization.

Severe cerebral hypoxia and anoxia is usually caused by traumatic events. Examples include choking, drowning, strangulation, smoke inhalation, drug overdoses, crushing of the trachea, status asthmaticus, and shock.^[4]

It is also recreationally self-induced in the choking game and in autoerotic asphyxiation.

Signs and symptoms

The brain requires approximately 3.3 ml of oxygen per 100 g of brain tissue per minute. Initially the body responds to lowered blood oxygen by redirecting blood to the brain and increasing cerebral blood flow. Blood flow may increase up to twice the normal flow but no more. If the increased blood flow is sufficient to supply the brain’s oxygen needs then no symptoms will result. ^[5]

However, if blood flow cannot be increased or if doubled blood flow does not correct the problem, symptoms of cerebral hypoxia will begin to appear. Mild symptoms include difficulties with complex learning tasks and reductions in short-term memory. If oxygen deprivation continues, cognitive disturbances and decreased motor control will result.^[5] The skin may also appear bluish (cyanosis) and heart rate increases. Continued oxygen deprivation results in fainting, long term loss of consciousness, coma, seizures, cessation of brain stem reflexes, and brain death.^[6]

Objective measurements of the severity of cerebral hypoxia depend on the cause. Blood oxygen saturation may be used for hypoxic hypoxia, but is generally meaningless in other forms of hypoxia. In hypoxic hypoxia 95-100% saturation is considered normal. 91-94% is considered mild. 86-90% is considered moderate. Anything below 86% is considered severe.^[7]

It should be noted that cerebral hypoxia refers to oxygen levels in brain tissue, not blood. Blood oxygenation will usually appear normal in cases of hypemic, ischemic and hystoxic cerebral hypoxia. Even in hypoxic hypoxia blood measures are only an approximate guide – the oxygen level in the brain tissue will depend on how the body deals with the reduced oxygen content of the blood.

Treatment

The first goal of treatment is to restore oxygen to the brain. The method of restoration depends on the cause of the hypoxia.^[8] For mild to moderate cases of hypoxia, removal of the cause of hypoxia may be sufficient. Inhaled oxygen may also be provided. In severe cases treatment may also involve life support and damage control measures.

A deep coma will interfere with body’s breathing reflexes even after the initial cause of hypoxia has been dealt with. Mechanical ventilation may be required. Additionally severe cerebral hypoxia causes an elevated heart rate. In extreme cases the heart may tire and stop pumping. CPR, defibrilation, epinephrine, and atropine may all be tried in an effort to get the heart to resume pumping.^[7] Severe cerebral hypoxia can also cause seizures. Seizures put the patient at risk of self injury. If convulsions are sufficiently severe medical professionals may not be able to provide medical treatment. Various anti-convulsant drugs may need to be administered before treatment can continue.

Brain damage can occur both during and after oxygen deprivation. During oxygen deprivation, cells die due to an increasing acidity in the brain tissue (acidosis). Additionally, during the period of oxygen deprivation, materials that can easily create free radicals build up. When oxygen enters the tissue these materials interact with oxygen to create high levels of oxidants. Oxidants interfere with the normal brain chemistry and cause further damage. This is called reperfusion injury.

Techniques for preventing damage to brain cells are an area of on-going research. Controlled hypothermia, anti-oxidant drugs, control of blood glucose levels, and hemodilution (thinning of the blood) coupled with drug-induced hypertension are some treatment techniques currently under investigation.^[9]

In severe cases it is extremely important to act quickly. Brain cells are very sensitive to reduced oxygen levels. Once deprived of oxygen they will begin to die off within five minutes.^[9]

Prognosis

Mild and moderate cerebral hypoxia generally has no impact beyond the episode of hypoxia. Severe cerebral hypoxia is another matter. Outcome will depend on the success of damage control measures, the amount of brain tissue deprived of oxygen, and the speed with which oxygen was restored to the brain.

If cerebral hypoxia was localized to a specific part of the brain, brain damage will be localized to that region. The long term effects will depend on the purpose of that portion of the brain. Damage to the Broca and Wernicke’s areas of the brain (left side) typically causes problems with speech and language. Damage to the right side of the brain may interfere with the ability to express emotions or interpret what one sees. Damage on either side can cause paralysis of the opposite side of the body.

The effects of certain kinds of severe generalized hypoxias may take time to develop. For example, the long term effects of serious carbon monoxide poisoning usually may take several weeks to appear. Recent research suggests this may be due to an autoimmune response caused by CO induced changes in the myelin sheath surrounding neurons.^[10]

If hypoxia results in coma, the length of unconsciousness is often used as an indication of long term damage. In some cases coma can give the brain an opportunity to heal and regenerate,^[11] but, in general, the longer a coma continues the greater the likelihood that the person will remain in a vegetative state until death.^[4] Even if the patient wakes up, brain damage is likely to be significant enough to prevent a return to normal functioning.

The effects of long term comas are not limited to the comatose person. Long term coma can have significant impact on their families.^[12] Families of coma victims often have idealized images of the outcome based on Hollywood movie depictions of coma.^[13] Adjusting to the realities of ventilators, feeding tubes, bedsores and muscle wasting may be difficult.^[14] Treatment decision often involve complex ethical choices and can strain family dynamics.^[15]

See also

• Altitude sickness
• Deep water blackout
• Physical trauma
• Hypoxia (medical)
• Choking game

References

1. ^ Hypoxia. The Gale Encyclopedia of Neurological Disorders. The Gale Group, Inc (2005). Retrieved on 2007-04-13 from Answers.com.
2. ^ What is Hypoxia?. Gray Laboratory Cancer Research Trust (August 1, 1999). Retrieved on 2007-04-13 from Archive.org.
3. ^ Brooks, Kevin E. (May–June 2005). Are you a hypoxia expert?. Approach. United States Navy Naval Safety Center. Retrieved on 2007-04-13. This website provides hypoxia related safety tips for aviators working for the United States Navy aviators.
4. ^ ^{a b} National Institute of Neurological Disorders and Stroke (February 8, 2007). Cerebral Hypoxia Information Page. U.S. National Institutes of Health. Retrieved on 2007-04-13.
5. ^ ^{a b} Butterworth, Roger F. (1999). "Hypoxic Encephalopathy". In: Siegel, George J. et al. (eds.) Basic Neurochemistry: Molecular, Cellular and Medical Aspects, 6^th edition, Philadelphia: Lippincott Williams & Wilkins. ISBN 039751820X. Freely available at NCBI Bookshelf. Retrieved on 2007-04-13.
6. ^ Cerebral hypoxia. MedlinePlus Medical Encyclopedia. U.S. National Library of Medicine (2007-04-05). Retrieved on 2007-04-13.
7. ^ ^{a b} The Maryland Medical Protocols for Emergency Medical Services ProvidersPDF (1.00 MiB). Maryland Institute for Emergency Medical Services Systems (2004). Retrieved on 2007-04-13.
8. ^ Cerebral hypoxia. Health-cares.net. Retrieved on 2007-04-13.
9. ^ ^{a b} Richmond TS (May 1997). "Cerebral Resuscitation after Global Brain Ischemia". AACN Clinical Issues 8 (2). Retrieved on 2007-04-13. Free full text at the American Association of Critical-Care Nurses website.
10. ^ University Of Pennsylvania Medical Center. "Long-term Effects Of Carbon Monoxide Poisoning Are An Autoimmune Reaction", ScienceDaily, September 6, 2004. Retrieved on 2007-04-13. 
11. ^ Phillips, Helen. "'Rewired brain' revives patient after 19 years", New Scientist, July 3, 2006. Retrieved on 2007-04-13. 
12. ^ Mayo Clinic staff (May 17, 2006). Coma: Coping skills. Mayo Clinic. Retrieved on 2007-04-13.
13. ^ Wijdicks EFM, Wijdicks CA (2006). "The portrayal of coma in contemporary motion pictures". Neurology 66 (9): 1300–1303. PMID 16682658.
14. ^ Konig P et al (1992). "Psychological counseling of the family of patients with craniocerebral injuries (psychological family counseling of severely ill patients)". Zentralbl Neurochir 53 (2): 78–84. PMID 1636327.
15. ^ Montgomery V et al (2002). "The effect of severe traumatic brain injury on the family". J Trauma 52 (6): 1121–4. PMID 12045640.