Cerebral hypoxia

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For other uses, see Hypoxia.

Cerebral hypoxia
Critical care medicine

Cerebral hypoxia is a form of

hypoxia (reduced supply of oxygen), specifically involving the brain; when the brain is completely deprived of oxygen, it is called cerebral anoxia. There are four categories of cerebral hypoxia; they are, in order of increasing severity: diffuse cerebral hypoxia (DCH), focal cerebral ischemia, cerebral infarction, and global cerebral ischemia. Prolonged hypoxia induces neuronal cell death via apoptosis, resulting in a hypoxic brain injury.[1][2]

Cases of total

oxygen deprivation are termed "anoxia", which can be hypoxic in origin (reduced oxygen availability) or ischemic in origin (oxygen deprivation due to a disruption in blood flow). Brain injury as a result of oxygen deprivation either due to hypoxic or anoxic mechanisms are generally termed hypoxic/anoxic injuries (HAI). Hypoxic ischemic encephalopathy (HIE) is a condition that occurs when the entire brain is deprived of an adequate oxygen supply, but the deprivation is not total. While HIE is associated in most cases with oxygen deprivation in the neonate due to birth asphyxia, it can occur in all age groups, and is often a complication of cardiac arrest.[3][4][5]

Signs and symptoms

CT in a person after generalized hypoxia.

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.[6]

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

fainting, long-term loss of consciousness, coma, seizures, cessation of brain stem reflexes, and brain death.[7]

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 and 86–90% moderate. Anything below 86% is considered severe.[8]

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.[citation needed]

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 status epilepticus, work in nitrogen-rich environments, ascent from a deep-water dive, flying at high altitudes in an unpressurized cabin without supplemental oxygen
, and intense exercise at high altitudes prior to acclimatization.

Severe cerebral hypoxia and anoxia is usually caused by traumatic events such as

fainting game and in erotic asphyxiation
.

  • contralateral paralysis (opposite side of body from affected brain hemisphere), or sudden weakness or numbness. A TIA may cause sudden dimming or loss of vision, aphasia, slurred speech, and mental confusion. The symptoms of a TIA typically resolve within 24 hours, unlike a stroke. Brain injury may still occur in a TIA lasting only a few minutes. Having a TIA is a risk factor for eventually having a stroke.[10][11]
  • cigarette smoking being predisposing factors.[14][15]

Pre- and postnatal

Further information: Neonatal encephalopathy

Hypoxic-anoxic events may affect the fetus at various stages of

preeclampsia, maternal diabetes with vascular disease, congenital fetal infections, substance/alcohol use, severe fetal anemia, cardiac disease, lung malformations, or problems with blood flow to the placenta
.

Problems during labor and delivery can include

Münchausen syndrome by proxy.[18]

The severity of a neonatal hypoxic-ischaemic brain injury may be assessed using

MRI.[19]
Signs and symptoms of HIE may include:

Mechanism

Main article: Anoxic depolarization in the brain

Details of the mechanism of damage from cerebral hypoxia, along with anoxic depolarization, can be found here: anoxic depolarization in the brain

Diagnosis

Classification

Cerebral hypoxia is typically grouped into four categories depending on the severity and location of the brain's oxygen deprivation:[20]

Aneurysm in a cerebral artery,
one cause of hypoxic anoxic injury (HAI).
  1. Diffuse cerebral hypoxia – A mild to moderate impairment of brain function due to low oxygen levels in the blood.
  2. Focal cerebral ischemia – A stroke occurring in a localized area that can either be acute or transient. This may be due to a variety of medical conditions such as an aneurysm that causes a hemorrhagic stroke, or an occlusion occurring in the affected blood vessels due to a thrombus (thrombotic stroke) or embolus (embolic stroke).[21] Focal cerebral ischemia constitutes a large majority of the clinical cases in stroke pathology with the infarct usually occurring in the middle cerebral artery (MCA).[22]
  3. Global cerebral ischemia – A complete stoppage of blood flow to the brain.
  4. cerebral blood flow
    which affects multiple areas of the brain.

Cerebral hypoxia can also be classified by the cause of the reduced brain oxygen:[23]

Treatment

For newborn infants starved of oxygen during birth there is now evidence that hypothermia therapy for neonatal encephalopathy applied within 6 hours of cerebral hypoxia effectively improves survival and neurological outcome.[25][26] In adults, however, the evidence is less convincing and the first goal of treatment is to restore oxygen to the brain. The method of restoration depends on the cause of the hypoxia. 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 the body's breathing reflexes even after the initial cause of hypoxia has been dealt with;

anti-convulsant
drugs may need to be administered before treatment.

There has long been a debate over whether newborn infants with cerebral hypoxia should be resuscitated with 100% oxygen or normal air.

free radicals, which have a role in reperfusion injury after asphyxia.[28] Research by Ola Didrik Saugstad and others led to new international guidelines on newborn resuscitation in 2010, recommending the use of normal air instead of 100% oxygen.[29][30]

Brain damage can occur both during and after oxygen deprivation. During oxygen deprivation, cells die due to an increasing acidity in the brain tissue (

brain chemistry and cause further damage (this is known as "reperfusion injury
").

Techniques for preventing damage to brain cells are an area of ongoing research.

creatine phosphokinase levels showing a possible reduction in the overall systemic inflammatory process.[32]

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.[31]

Prognosis

Mild and moderate cerebral hypoxia may result in seizures and impaired memory going forward. The outcome of severe cerebral hypoxia will depend on the success of damage control, amount of brain tissue deprived of oxygen, and the speed with which oxygen was restored.

If cerebral hypoxia was localized to a specific part of the brain, brain damage will be localized to that region. A general consequence may be epilepsy. The long-term effects will depend on the purpose of that portion of the brain. Damage to the Broca's area and the Wernicke's area 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

autoimmune response caused by carbon monoxide-induced changes in the myelin sheath surrounding neurons.[33]

If hypoxia results in coma, the length of unconsciousness is often indicative of long-term damage. In some cases coma can give the brain an opportunity to heal and regenerate,[34] but, in general, the longer a coma, the greater the likelihood that the person will remain in a vegetative state until death.[9] Even if the patient wakes up, brain damage is likely to be significant enough to prevent a return to normal functioning.

Long-term comas can have a significant impact on a patient's family.[35] Families of coma patients often have idealized images of the outcome based on Hollywood movie depictions of coma.[36] Adjusting to the realities of ventilators, feeding tubes, bedsores, and muscle wasting may be difficult.[37] Treatment decisions often involve complex ethical choices and can strain family dynamics.[38]

See also

References

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  16. ^ a b "What You Need To Know About Hypoxic Ischemic Encephalopathy (HIE)". Birth Injury Guide. Retrieved 2021-10-05.
  17. ^ "Parent Info". Florida Neonatal Neurologic Network. Retrieved 28 January 2012.
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  19. ^ Gardiner M, Eisen S, Murphy C. Training in paediatrics: the essential curriculum. Oxford University Press, Oxford 2009.[page needed]
  20. ^ "Hypoxia". The Gale Encyclopedia of Neurological Disorders. The Gale Group, Inc. 2005. Retrieved on 2007-04-13 from Answers.com.
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  23. ^ "What is Hypoxia?". Gray Laboratory Cancer Research Trust. 1999-08-01. Archived from the original on 2003-09-21. Retrieved on 2007-04-13 from Archive.org.
  24. ^ Brooks, Kevin E. (May–June 2005). "Are you a hypoxia expert?". Approach. United States Navy Naval Safety Center. Archived from the original on 2007-02-08. Retrieved 2007-04-13. This website provides hypoxia related safety tips for aviators working for the United States Navy aviators.
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  31. ^ a b Richmond, T. S. (May 1997). "Cerebral Resuscitation after Global Brain Ischemia", AACN Clinical Issues 8 (2). Retrieved on 2007-04-13. Free full text Archived September 27, 2007, at the Wayback Machine at the American Association of Critical-Care Nurses website.
  32. PMID 23111939. Archived from the original on September 6, 2013. Retrieved 2013-06-06.{{cite journal}}: CS1 maint: unfit URL (link
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  33. ^ University of Pennsylvania Medical Center (2004-09-06). "Long-Term Effects of Carbon Monoxide Poisoning Are an Autoimmune Reaction". ScienceDaily. Retrieved 2007-04-13.
  34. ^ Phillips, Helen (2006-07-03). "'Rewired brain' revives patient after 19 years". New Scientist. Retrieved 2007-04-13.[permanent dead link]
  35. ^ Mayo Clinic staff (2006-05-17). "Coma: Coping skills". Mayo Clinic. Retrieved 2007-04-13.
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External links
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