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Cerebral hypoxia occurs when there is not enough oxygen getting to the brain. The brain needs a constant supply of oxygen and nutrients to function.
Cerebral hypoxia refers to the outer part of the brain, an area called the cerebral hemisphere. However, the term is often used to refer to a lack of oxygen supply to the entire brain.
Hypoxic encephalopathy; Anoxic encephalopathy
Causes, incidence, and risk factors
In cerebral hypoxia, sometimes only the oxygen supply is interrupted. This can be caused by:
Breathing in smoke (smoke inhalation), such as during a fire
Pressure on (compression) the windpipe (trachea)
In other cases, both oxygen and nutrient supply are stopped, caused by:
Brain cells are extremely sensitive to a lack of oxygen. Some brain cells start dying less than 5 minutes after their oxygen supply disappears. As a result, brain hypoxia can rapidly cause severe brain damage or death.
Symptoms of mild cerebral hypoxia include:
Symptoms of severe cerebral hypoxia include:
Signs and tests
Cerebral hypoxia can usually be diagnosed based on the person's medical history and a physical exam. Tests are done to determine the cause of the hypoxia, and may include:
If only blood pressure and heart function remain, the brain may be completely dead.
Cerebral hypoxia is an emergency condition that need to be treated right away. The sooner the oxygen supply is restored to the brain, the lower the risk of severe brain damage and death.
Treatment depends on the cause of the hypoxia. Basic life support is most important. Treatment involves:
Breathing assistance (mechanical ventilation) and oxygen
Controlling the heart rate and rhythm
Fluids, blood products, or medications to raise blood pressure if it is low
Medications including phenytoin, phenobarbital, valproic acid, or general anesthetics to calm seizures
Sometimes a person with cerebral hypoxia is cooled to slow down the activity of the brain cells and decrease their need for oxygen. However, the benefit of this treatment has not been firmly established.
The outlook depends on the extent of the brain injury. This is determined by how long the brain lacked oxygen, and whether nutrition to the brain was also affected.
If the brain lacked oxygen for only a very brief period of time, a coma may be reversible and the person may have a full or partial return of function. Some patients recover many functions, but have abnormal movements such as twitching or jerking, called myoclonus. Seizures may sometimes occur, and may be continuous (status epilepticus).
Most people who make a full recovery were only briefly unconscious. The longer a person is unconscious, the higher the risk for death or brain death, and the lower the chances of recovery.
Complications of cerebral hypoxia include a prolonged vegetative state. This means the person may have basic life functions such as breathing, blood pressure, sleep-wake cycle, and eye opening, but the person is not alert and does not respond to his or her surroundings. Such patients usually die within a year, although some may survive longer.
Length of survival depends partly on how much care is taken to prevent other problems. Major complications may include:
Calling your health care provider
Cerebral hypoxia is a medical emergency. Call 911 immediately if someone is losing consciousness or has other symptoms of cerebral hypoxia.
Prevention depends on the specific cause of hypoxia. Unfortunately, hypoxia is usually unexpected. This makes the condition somewhat difficult to prevent.
Cardiopulmonary resuscitation (CPR) can be lifesaving, especially when it is started right away.
Bernat JL. Coma, vegetative state, and brain death. In: Goldman L, Schafer AI, eds. Cecil Medicine. 24th ed. Philadelphia, Pa: Saunders Elsevier; 2011:chap 411.
Wijdicks EFM, Fugate JE. Anoxic-ischemic encephalopathy. In: Daroff RB, Fenichel GM, Jankovic J, Mazziotta JC, eds. Bradley’s Neurology in Clinical Practice. 6th ed. Philadelphia, Pa: Saunders Elsevier; 2012:chap 55.
Zivin JA. Approach to cerebrovascular diseases. In: Goldman L, Schafer AI, eds. Cecil Medicine. 24th ed. Philadelphia, Pa: Saunders Elsevier; 2011:chap 413.
- Last reviewed on 8/29/2012
- David C. Dugdale, III, MD, Professor of Medicine, Division of General Medicine, Department of Medicine, University of Washington School of Medicine; Luc Jasmin, MD, PhD, Department of Neurosurgery at Cedars-Sinai Medical Center, Los Angeles, and Department of Anatomy at UCSF, San Francisco, CA. Review provided by VeriMed Healthcare Network. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M. Health Solutions, Ebix, Inc.
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