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| == Cerebral hypoxia == | | {{Short description|Condition of reduced oxygen supply to the brain}} |
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| {{Use American English|date = March 2019}}
| | '''Cerebral hypoxia''' is a medical condition characterized by a deficiency of oxygen supply to the brain, despite adequate blood flow. This condition can lead to [[neurological damage]] and, if prolonged, can result in [[brain death]]. |
| {{Short description|Oxygen shortage of the brain}}
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| {{other uses|hypoxia (disambiguation)}}
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| | name = Cerebral hypoxia
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| '''Cerebral hypoxia''' is a form of [[Hypoxia (medical)|hypoxia]] (reduced supply of [[oxygen]]), specifically involving the [[human brain|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 severity: diffuse cerebral hypoxia (DCH), focal cerebral ischemia, [[cerebral infarction]], and global cerebral ischemia. Prolonged hypoxia induces [[neuron]]al cell death via [[apoptosis]], resulting in a hypoxic brain injury.<ref>{{cite journal |vauthors=Malhotra R, etal | date = Nov 2001 | title = Hypoxia induces apoptosis via two independent pathways in Jurkat cells: differential regulation by glucose | url = | journal = [[American Journal of Physiology. Cell Physiology]] | volume = 281 | issue = 5| pages = C1596–603 | pmid = 11600423 | doi=10.1152/ajpcell.2001.281.5.c1596| title-link = Jurkat cells }}</ref><ref>{{cite journal | author = Mattiesen W. R.| date = May 2009 | title = Increased neurogenesis after hypoxic-ischemic encephalopathy in humans is age related | url = | journal = Acta Neuropathol | volume = 117 | issue = 5| pages = 525–34 | pmid = 19277687 | doi=10.1007/s00401-009-0509-0|display-authors=etal| doi-access = free }}</ref> | |
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| [[File:Hypoxic neuronal injury, HE 3.jpg|thumb|Hypoxic neuronal injury, HE 3]] | | ==Pathophysiology== |
| | The brain is highly sensitive to oxygen deprivation. Under normal circumstances, the brain receives about 20% of the body's oxygen supply. [[Neurons]], the primary cells of the brain, are particularly vulnerable to hypoxia. When oxygen levels are insufficient, neuronal metabolism is disrupted, leading to cell injury and death. |
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| Cases of total [[Oxygen saturation in medicine|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 [[Perinatal asphyxia|birth asphyxia]], it can occur in all age groups, and is often a complication of [[cardiac arrest]].<ref>{{cite journal|last1=Robinson|first1=LR|last2=Micklesen|first2=PJ|last3=Tirschwell|first3=DL|last4=Lew|first4=HL|title=Predictive value of somatosensory evoked potentials for awakening from coma.|journal=Critical Care Medicine|date=Mar 2003|volume=31|issue=3|pages=960–7|pmid=12627012|doi=10.1097/01.ccm.0000053643.21751.3b}}</ref><ref>{{cite journal |author1=Geraghty M. C. |author2=Torbey M. T. | year = 2006 | title = Neuroimaging and serologic markers of neurologic injury after cardiac arrest | url = | journal = Neurol Clin | volume = 24 | issue = 1| pages = 107–21 | doi = 10.1016/j.ncl.2005.10.006 | pmid = 16443133 }}</ref><ref>{{cite journal |author1=Busl K. M. |author2=Greer D. M. | date = Jan 2010 | title = Hypoxic-ischemic brain injury: pathophysiology, neuropathology and mechanisms | url = | journal = NeuroRehabilitation | volume = 26 | issue = 1| pages = 5–13 | doi = 10.3233/NRE-2010-0531 | pmid = 20130351 | doi-access = free }}</ref>
| | Cerebral hypoxia can occur due to various reasons, including [[cardiac arrest]], [[stroke]], [[asphyxia]], and [[carbon monoxide poisoning]]. The severity of hypoxia can range from mild, causing temporary confusion, to severe, resulting in coma or death. |
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| == Signs and symptoms ==
| | * '''Cardiac arrest''': Sudden cessation of heart function leads to an immediate stop in blood flow, depriving the brain of oxygen. |
| | * '''Stroke''': An interruption of blood flow to a part of the brain, either due to a blockage or a hemorrhage, can cause localized hypoxia. |
| | * '''Asphyxia''': Conditions such as choking, drowning, or suffocation reduce oxygen intake. |
| | * '''Carbon monoxide poisoning''': Carbon monoxide binds to hemoglobin more effectively than oxygen, reducing the oxygen-carrying capacity of the blood. |
| | * '''Severe asthma or respiratory distress''': Conditions that impair breathing can lead to reduced oxygen levels in the blood. |
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| [[File:CCT Hypoxie-12.jpg|thumb|CT in a person after generalized hypoxia.]]
| | ==Symptoms== |
| | The symptoms of cerebral hypoxia depend on the severity and duration of the oxygen deprivation. They may include: |
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| 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.<ref name="BasicNeurochemistry">Butterworth, Roger F. (1999). "[https://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=bnchm.section.2727 Hypoxic Encephalopathy]". In: Siegel, George J. ''et al.'' (eds.) ''Basic Neurochemistry: Molecular, Cellular and Medical Aspects'', 6th edition, Philadelphia: [[Lippincott Williams & Wilkins]]. {{ISBN|0-397-51820-X}}. [https://www.ncbi.nlm.nih.gov/books/bv.fcgi?call=bv.View..ShowTOC&rid=bnchm.TOC&depth=10 Freely available] at [[National Center for Biotechnology Information|NCBI Bookshelf]]. Retrieved on 2007-04-13.</ref>
| | * Mild hypoxia: Confusion, difficulty concentrating, and impaired judgment. |
| | | * Moderate hypoxia: Dizziness, shortness of breath, and loss of coordination. |
| 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.<ref name="BasicNeurochemistry"/> The skin may also appear bluish ([[cyanosis]]) and heart rate increases. Continued oxygen deprivation results in [[fainting]], long-term loss of consciousness, [[coma]], seizures, [[Brainstem death|cessation of brain stem reflexes]], and [[brain death]].<ref name="MedlinePlus">{{cite web | url = https://www.nlm.nih.gov/medlineplus/ency/article/001435.htm | title = Cerebral hypoxia | date = 2007-04-05 | accessdate = 2007-04-13 | work = [[MedlinePlus|MedlinePlus Medical Encyclopedia]] | publisher = U.S. [[National Library of Medicine]]}}</ref>
| | * Severe hypoxia: Loss of consciousness, seizures, and coma. |
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| 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.<ref name="MIEMSS">{{cite web|url= http://www.miemss.org/Pro2004UpdateSections.pdf |title=The Maryland Medical Protocols for Emergency Medical Services Providers }} {{small|(1.00 [[Mebibyte|MiB]])}}. Maryland Institute for Emergency Medical Services Systems (2004). Retrieved on 2007-04-13.</ref>
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| 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.
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| [[File:Anoxicbraininjury.png|thumb|Anoxicbraininjury]]
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| == Causes ==
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| 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 [[Oxygen saturation in medicine|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 [[Freediving blackout#Ascent blackout|deep-water dive]], flying at [[Effects of high altitude on humans|high altitudes]] in an [[Cabin pressurization|unpressurized]] [[Aircraft cabin|cabin]] without [[Oxygen mask#Oxygen masks for aviators|supplemental oxygen]], and intense exercise at high altitudes prior to acclimatization.
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| Severe cerebral hypoxia and anoxia is usually caused by traumatic events such as [[choking]], [[drowning]], [[strangulation]], [[smoke inhalation]], [[drug overdoses]], crushing of the [[Vertebrate trachea|trachea]], [[status asthmaticus]], and [[Shock (circulatory)|shock]].<ref name="NINDS">{{cite web | url = https://www.ninds.nih.gov/Disorders/All-Disorders/Cerebral-Hypoxia-Information-Page | title = Cerebral Hypoxia Information Page | author = [[National Institute of Neurological Disorders and Stroke]] | date = 2018-03-08 | accessdate = 2007-04-13 | publisher = U.S. [[National Institutes of Health]]}}</ref> It is also recreationally self-induced in the [[fainting game]] and in [[erotic asphyxiation]].
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| * '''[[Transient ischemic attack]]''' (TIA), is often referred to as a "mini-stroke". The [[American Heart Association]] and [[American Stroke Association]] (AHA/ASA) refined the definition of transient ischemic attack. TIA is now defined as a transient episode of neurologic dysfunction caused by [[Focal and diffuse brain injury|focal brain]], [[spinal cord]], or retinal ischemia, without acute [[Cerebral infarction|infarction]]. The symptoms of a TIA can resolve within a few minutes, unlike a stroke. TIAs share the same underlying [[etiology]] as strokes; a disruption of cerebral blood flow. TIAs and strokes present with the same symptoms such as [[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.<ref>{{cite journal | author = Ferro J. M.| date = Dec 1996 | title = Diagnosis of transient ischemic attack by the nonneurologist: A validation study | url = | journal = Stroke| volume = 27 | issue = 12| pages = 2225–9 | doi = 10.1161/01.STR.27.12.2225 | pmid = 8969785 |display-authors=etal}}</ref><ref>{{cite journal |vauthors=Easton JD, etal | date = Jun 2009 | title = Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council | url = | journal = Stroke | volume = 40 | issue = 6| pages = 2276–93 | pmid = 19423857 | doi=10.1161/STROKEAHA.108.192218| doi-access = free }}</ref>
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| * '''[[Silent stroke]]''' is a [[stroke]] which does not have any outward symptoms, and the patient is typically unaware they have suffered a stroke. Despite its lack of identifiable symptoms, a silent stroke still causes [[brain damage]] and places the patient at increased risk for a major stroke in the future. In a broad study in 1998, more than 11 million people were estimated to have experienced a stroke in the United States. Approximately 770,000 of these strokes were symptomatic and 11 million were first-ever silent MRI infarcts or [[hemorrhage]]s. Silent strokes typically cause [[lesion]]s which are detected via the use of [[neuroimaging]] such as [[fMRI]].<ref>{{cite journal |vauthors=Herderscheê D, etal | date = Sep 1992 | title = Silent stroke in patients with transient ischemic attack or minor ischemic stroke. The Dutch TIA Trial Study Group | url = | journal = Stroke | volume = 23 | issue = 9| pages = 1220–4 | pmid = 1519274 | doi=10.1161/01.str.23.9.1220| doi-access = free }}</ref><ref>{{cite journal |author1=Leary M. C. |author2=Saver J. L. | year = 2003 | title = Annual incidence of first silent stroke in the United States: a preliminary estimate | url = | journal = Cerebrovasc Dis | volume = 16 | issue = 3| pages = 280–5 | pmid = 12865617 | doi=10.1159/000071128}}</ref> The risk of silent stroke increases with age but may also affect younger adults. Women appear to be at increased risk for silent stroke, with [[hypertension]] and current [[cigarette smoking]] being predisposing factors.<ref>{{cite journal | author = Vermeer S. E.| date = Jan 2002 | title = Prevalence and risk factors of silent brain infarcts in the population-based Rotterdam Scan Study | url = | journal = Stroke | volume = 33 | issue = 1| pages = 21–5 | pmid = 11779883 | doi=10.1161/hs0102.101629|display-authors=etal| doi-access = free }}</ref><ref>{{cite journal |vauthors=Herderscheê D, etal | date = Sep 1992 | title = "Silent stroke in patients with transient ischemic attack or minor ischemic stroke". The Dutch TIA Trial Study Group | url = | journal = Stroke | volume = 23 | issue = 9| pages = 1220–4 | pmid = 1519274 | doi=10.1161/01.str.23.9.1220| doi-access = free }}</ref> | |
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| ===Pre- and postnatal===
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| {{See|Neonatal encephalopathy}}
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| Hypoxic-anoxic events may affect the fetus at various stages of [[fetal development]], during labor and delivery and in the [[Postnatal|postnatal period]]. Problems during pregnancy may include [[preeclampsia]], [[Gestational diabetes|maternal diabetes]] with [[vascular disease]], congenital fetal infections, drug/alcohol abuse, severe fetal anemia, cardiac disease, lung malformations, or problems with blood flow to the [[placenta]].
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| Problems during labor and delivery can include [[umbilical cord]] occlusion, torsion or [[Umbilical cord prolapse|prolapse]], rupture of the placenta or [[uterus]], excessive bleeding from the placenta, abnormal fetal position such as the [[Breech birth|breech position]], prolonged late stages of labor, or very [[Hypotension|low blood pressure]] in the mother. Problems after delivery can include severe prematurity, severe lung or heart disease, serious infections, trauma to the brain or skull, congenital malformations of the brain or very low blood pressure in the baby<ref>{{cite web|url=http://hopefn3.org/parent-info/|publisher=Florida Neonatal Neurologic Network |title=Parent Info|accessdate=28 January 2012}}</ref> and due to [[suffocation]] in cases of [[Münchausen syndrome by proxy]].<ref>{{cite journal|title=Child abuse by suffocation: A cause of apparent life-threatening events Info|pmc=2528639 | pmid=19030315|volume=11|issue=8|year=2006|journal=Paediatr Child Health|pages=493–5|author=Bellemare S}}</ref>
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| The severity of a neonatal hypoxic-ischaemic brain injury may be assessed using [[Sarnat staging]], which is based on clinical presentation and [[EEG]] findings, and also using [[MRI]].<ref name="Gardiner">Gardiner M, Eisen S, Murphy C. Training in paediatrics: the essential curriculum. Oxford University Press, Oxford 2009.</ref>
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| == Mechanism ==
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| {{Main|Mechanism of anoxic depolarization in the brain}}
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| Details of the mechanism of damage from cerebral hypoxia, along with anoxic depolarization, can be found here: [[Mechanism of anoxic depolarization in the brain]]
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| ==Diagnosis== | | ==Diagnosis== |
| === Classification ===
| | Diagnosis of cerebral hypoxia involves clinical evaluation and diagnostic tests. [[Magnetic resonance imaging]] (MRI) and [[computed tomography]] (CT) scans can help assess brain damage. [[Blood gas analysis]] can measure oxygen levels in the blood. |
| Cerebral hypoxia is typically grouped into four categories depending on the severity and location of the brain's oxygen deprivation:<ref>{{cite web | url = http://www.answers.com/topic/hypoxia | title = Hypoxia | work = The Gale Encyclopedia of Neurological Disorders | publisher = The Gale Group, Inc | year = 2005}} Retrieved on 2007-04-13 from [[Answers.com]].</ref>
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| [[File:Aneurysem.jpg|thumb|Aneurysm in a cerebral artery,<br />one cause of hypoxic anoxic injury (HAI).]]
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| # '''Diffuse cerebral hypoxia''' – A mild to moderate impairment of brain function due to low oxygen levels in the blood.
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| # '''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 [[Vascular occlusion|occlusion]] occurring in the affected blood vessels due to a [[thrombus]] (thrombotic stroke) or [[embolus]] (embolic stroke).<ref>{{cite journal |author1=Pressman B. D. |author2=Tourje E. J. |author3=Thompson J. R. | date = Sep 1987 | title = An early CT sign of ischemic infarction: increased density in a cerebral artery | url = | journal = AJR Am J Roentgenol | volume = 149 | issue = 3| pages = 583–6 | pmid = 3497548 | doi=10.2214/ajr.149.3.583| doi-access = free }}</ref> 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).<ref>Jun Chen, Zao C. Xu, Xiao-Ming Xu, ''Animal Models of Acute Neurological Injuries'', Humana Press; 1 edition, {{ISBN|978-1-60327-184-4}}</ref>
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| # '''Global cerebral ischemia''' – A complete stoppage of blood flow to the brain.
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| # '''[[Cerebral infarction]]''' – A "stroke", caused by complete oxygen deprivation due to an interference in [[cerebral blood flow]] which affects multiple areas of the brain.
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| Cerebral hypoxia can also be classified by the cause of the reduced brain oxygen:<ref>{{cite web | url = http://www.graylab.ac.uk/groups/advtec/hypoxia/hypoxia2.html | title = What is Hypoxia? | date = 1999-08-01 | publisher = Gray Laboratory Cancer Research Trust |archiveurl = https://web.archive.org/web/20030921221421/http://www.graylab.ac.uk/groups/advtec/hypoxia/hypoxia2.html |archivedate = 2003-09-21}} Retrieved on 2007-04-13 from [[Internet Archive|Archive.org]].</ref>
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| * '''[[Hypoxic hypoxia]]''' – Limited oxygen in the environment causes reduced brain function. Divers, aviators,<ref>{{cite web|url=http://www.safetycenter.navy.mil/MEDIA/approach/issues/mayjun05/hypoxiaexpert.htm |title=Are you a hypoxia expert? |last=Brooks |first=Kevin E. |work=Approach |publisher=[[United States Navy]] Naval Safety Center |date=May–June 2005 |accessdate=2007-04-13 |archiveurl=https://web.archive.org/web/20070208102227/http://www.safetycenter.navy.mil/MEDIA/approach/issues/mayjun05/hypoxiaexpert.htm |archivedate=2007-02-08 |url-status=dead }} This website provides hypoxia related safety tips for aviators working for the United States Navy aviators.</ref> 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 [[Vertebrate trachea|windpipe]] all cause this sort of hypoxia. Severe [[asthma]]tics may also experience symptoms of hypoxic hypoxia.
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| * '''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.
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| * '''Ischemic hypoxia''' ( or "stagnant hypoxia") – Reduced brain oxygen is caused by inadequate blood flow to the brain. [[Stroke]], shock, [[cardiac arrest]] and [[heart attack]] may cause stagnant hypoxia. Ischemic hypoxia can also be created by pressure on the brain. [[Cerebral edema]], [[Cerebral hemorrhage|brain hemorrhages]] and [[hydrocephalus]] exert pressure on [[brain tissue]] and impede their absorption of oxygen.
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| * '''[[Histotoxic hypoxia]]''' – Oxygen is present in brain tissue but cannot be metabolized by the brain tissue. [[Cyanide poisoning]] is a well-known example.
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| == Treatment ==
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| 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.<ref>Laurance, Jeremy (October 1, 2009). [https://www.independent.co.uk/life-style/health-and-families/health-news/cooling-cure-averts-infant-brain-damage-1795740.html "Cooling 'cure' averts infant brain damage"], ''[[The Independent]]''.</ref> 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.
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| 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]], and 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.<ref name="MIEMSS"/> Severe cerebral hypoxia can also cause [[seizures]], which put the patient at risk of self-injury, and various [[anti-convulsant]] drugs may need to be administered before treatment.
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| There has long been a debate over whether newborn infants with cerebral hypoxia should be resuscitated with 100% oxygen or normal air.<ref>{{cite journal |last1=Davis |first1=PG |last2= Tan |first2= A |last3= O'Donnell |first3= CPF |last4= Schulze |first4= A | year= 2004|title= Resuscitation of newborn infants with 100% oxygen or air: a systematic review and meta-analysis |journal=[[The Lancet]] |volume= 364 |issue= 9442|pages= 1329–1333 |publisher= |doi= 10.1016/S0140-6736(04)17189-4 |url= |pmid=15474135}}</ref> It has been demonstrated that high concentrations of oxygen lead to generation of oxygen [[free radicals]], which have a role in [[reperfusion injury]] after asphyxia.<ref>{{cite journal |last1=Kutzsche |first1=S |last2= Ilves |first2= P |last3= Kirkeby |first3= OJ |last4= Saugstad |first4= OD | authorlink4 =Ola Didrik Saugstad | year= 2001|title= Hydrogen peroxide production in leukocytes during cerebral hypoxia and reoxygenation with 100% or 21% oxygen in newborn piglets |journal=[[Pediatric Research]] |volume=49 |issue= 6|pages= 834–842 |publisher= |doi= 10.1203/00006450-200106000-00020 |url= |pmid=11385146|doi-access= free }}</ref> 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.<ref>ILCOR Neonatal Resuscitation Guidelines 2010</ref><ref>[http://www.norway.gr/News_and_events/Events/Older-articles/Norwegian-paediatrician-honoured-by-University-of-Athens-/#.VSkP0rtvt2Y Norwegian paediatrician honoured by University of Athens], Norway.gr</ref>
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| 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 known as "[[reperfusion injury]]").
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| Techniques for preventing damage to brain cells are an area of ongoing research. [[Hypothermia therapy for neonatal encephalopathy]] is the only evidence-supported therapy, but antioxidant drugs, control of [[blood glucose]] levels, and hemodilution (thinning of the blood) coupled with drug-induced hypertension are some treatment techniques currently under investigation.<ref name="Richmond">Richmond, T. S. (May 1997). "Cerebral Resuscitation after Global Brain Ischemia", ''AACN Clinical Issues'' 8 (2). Retrieved on 2007-04-13. [http://www.aacn.org/AACN/jrnlci.nsf/0/a522e8311772eca188256576007821ab?OpenDocument Free full text] {{webarchive |url=https://web.archive.org/web/20070927201411/http://www.aacn.org/AACN/jrnlci.nsf/0/a522e8311772eca188256576007821ab?OpenDocument |date=September 27, 2007 }} at the American Association of Critical-Care Nurses website.</ref> [[Hyperbaric oxygen therapy]] is being evaluated with the reduction in total and myocardial [[creatine phosphokinase]] levels showing a possible reduction in the overall systemic inflammatory process.<ref name="pmid23111939">{{cite journal |vauthors=Orozco-Gutierrez A, Rojas-Cerda L, Estrada RM, Gil-Rosales C |title=Hyperbaric oxygen in the treatment of asphyxia in two newborn infants |journal=Diving and Hyperbaric Medicine |volume=40 |issue=4 |pages=218–20 |date=December 2010 |pmid=23111939 |doi= |url=http://archive.rubicon-foundation.org/10239 |accessdate=2013-06-06}}</ref>
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| 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.<ref name="Richmond"/>
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| == Prognosis ==
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| Mild and moderate cerebral hypoxia generally has no impact beyond the episode of hypoxia; on the other hand, 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.
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| 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.
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| 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 carbon monoxide-induced changes in the [[myelin]] sheath surrounding [[neuron]]s.<ref>{{cite news | url = https://www.sciencedaily.com/releases/2004/09/040906083815.htm | title = Long-Term Effects of Carbon Monoxide Poisoning Are an Autoimmune Reaction | author = [[University Of Pennsylvania]] Medical Center | date = 2004-09-06 | accessdate = 2007-04-13 | publisher = ScienceDaily}}</ref>
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| 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,<ref>{{cite news | url = https://www.newscientist.com/article.ns?id=dn9474 | title = 'Rewired brain' revives patient after 19 years | last = Phillips | first = Helen | date = 2006-07-03 | accessdate = 2007-04-13 | publisher = [[New Scientist]]}}</ref> but, in general, the longer a coma, the greater the likelihood that the person will remain in a vegetative state until death.<ref name="NINDS"/> Even if the patient wakes up, brain damage is likely to be significant enough to prevent a return to normal functioning.
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| Long-term comas can have a significant impact on a patient's families.<ref>{{cite web | url = http://www.mayoclinic.com/health/coma/DS00724/DSECTION=10 | title = Coma: Coping skills | author = Mayo Clinic staff | date = 2006-05-17 | accessdate = 2007-04-13 | publisher = [[Mayo Clinic]]}}</ref> Families of coma victims often have idealized images of the outcome based on Hollywood movie depictions of coma.<ref>{{cite journal |author1=Wijdicks E. F. M. |author2=Wijdicks C. A. | year = 2006 | title = The portrayal of coma in contemporary motion pictures | url = | journal = Neurology | volume = 66 | issue = 9| pages = 1300–1303 | doi = 10.1212/01.wnl.0000210497.62202.e9 | pmid = 16682658 }}</ref> Adjusting to the realities of ventilators, feeding tubes, [[Pressure ulcer|bedsores]], and [[Muscle atrophy|muscle wasting]] may be difficult.<ref>{{cite journal |vauthors=Konig P, etal | year = 1992 | title = Psychological counseling of the family of patients with craniocerebral injuries (psychological family counseling of severely ill patients)". | url = | journal = Zentralbl Neurochir | volume = 53 | issue = 2| pages = 78–84 | pmid = 1636327 }}</ref> Treatment decision often involve complex ethical choices and can strain family dynamics.<ref>{{cite journal |vauthors=Montgomery V, etal | year = 2002 | title = The effect of severe traumatic brain injury on the family | url = | journal = Journal of Trauma | volume = 52 | issue = 6| pages = 1121–4 | pmid = 12045640 | doi=10.1097/00005373-200206000-00016}}</ref>
| | ==Treatment== |
| | Immediate treatment is crucial to minimize brain damage. Treatment strategies include: |
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| ==See also==
| | * '''Oxygen therapy''': Administering supplemental oxygen to increase blood oxygen levels. |
| * [[Altitude sickness]]
| | * '''Mechanical ventilation''': Assisting or controlling breathing in patients who cannot breathe adequately on their own. |
| * [[Choking game]] | | * '''Medications''': Drugs to support heart function and blood pressure, and to control seizures. |
| * [[Hypothermia cap]] | | * '''Therapeutic hypothermia''': Cooling the body to reduce metabolic demand and protect the brain. |
| * [[Space exposure]] | |
| * [[Ulegyria]] | |
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| ==References== | | ==Prognosis== |
| {{reflist|colwidth=30em}}
| | The prognosis for cerebral hypoxia depends on the duration and severity of the oxygen deprivation. Rapid intervention can improve outcomes, but prolonged hypoxia often results in significant neurological impairment or death. |
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| == External links == | | ==Prevention== |
| {{Medical resources
| | Preventive measures include managing risk factors for heart disease and stroke, using safety equipment to prevent asphyxia, and ensuring proper ventilation in environments where carbon monoxide exposure is possible. |
| | DiseasesDB =
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| | ICD10 =
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| | ICD9 = {{ICD9|437.9}}
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| | ICDO =
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| | OMIM =
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| | MedlinePlus = 001435
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| | eMedicineSubj =
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| | eMedicineTopic =
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| | MeshID = D002534
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| | SNOMED CT = 389088001
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| }}
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| * [https://www.youtube.com/watch?v=WTNX6mr753w Hypoxia experiment]
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| {{CNS diseases of the nervous system}}
| | ==Related pages== |
| {{Vascular diseases}}
| | * [[Hypoxia (medical)]] |
| | * [[Anoxia]] |
| | * [[Brain ischemia]] |
| | * [[Cardiac arrest]] |
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| {{DEFAULTSORT:Cerebral Hypoxia}}
| | [[Category:Neurology]] |
| [[Category:Brain disorders]] | | [[Category:Medical emergencies]] |
| [[de:Hypoxie (Medizin)#Zerebrale Hypoxie]] | |
| {{dictionary-stub1}}
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Condition of reduced oxygen supply to the brain
Cerebral hypoxia is a medical condition characterized by a deficiency of oxygen supply to the brain, despite adequate blood flow. This condition can lead to neurological damage and, if prolonged, can result in brain death.
Pathophysiology
The brain is highly sensitive to oxygen deprivation. Under normal circumstances, the brain receives about 20% of the body's oxygen supply. Neurons, the primary cells of the brain, are particularly vulnerable to hypoxia. When oxygen levels are insufficient, neuronal metabolism is disrupted, leading to cell injury and death.
Cerebral hypoxia can occur due to various reasons, including cardiac arrest, stroke, asphyxia, and carbon monoxide poisoning. The severity of hypoxia can range from mild, causing temporary confusion, to severe, resulting in coma or death.
Causes
Cerebral hypoxia can be caused by:
- Cardiac arrest: Sudden cessation of heart function leads to an immediate stop in blood flow, depriving the brain of oxygen.
- Stroke: An interruption of blood flow to a part of the brain, either due to a blockage or a hemorrhage, can cause localized hypoxia.
- Asphyxia: Conditions such as choking, drowning, or suffocation reduce oxygen intake.
- Carbon monoxide poisoning: Carbon monoxide binds to hemoglobin more effectively than oxygen, reducing the oxygen-carrying capacity of the blood.
- Severe asthma or respiratory distress: Conditions that impair breathing can lead to reduced oxygen levels in the blood.
Symptoms
The symptoms of cerebral hypoxia depend on the severity and duration of the oxygen deprivation. They may include:
- Mild hypoxia: Confusion, difficulty concentrating, and impaired judgment.
- Moderate hypoxia: Dizziness, shortness of breath, and loss of coordination.
- Severe hypoxia: Loss of consciousness, seizures, and coma.
Diagnosis
Diagnosis of cerebral hypoxia involves clinical evaluation and diagnostic tests. Magnetic resonance imaging (MRI) and computed tomography (CT) scans can help assess brain damage. Blood gas analysis can measure oxygen levels in the blood.
Treatment
Immediate treatment is crucial to minimize brain damage. Treatment strategies include:
- Oxygen therapy: Administering supplemental oxygen to increase blood oxygen levels.
- Mechanical ventilation: Assisting or controlling breathing in patients who cannot breathe adequately on their own.
- Medications: Drugs to support heart function and blood pressure, and to control seizures.
- Therapeutic hypothermia: Cooling the body to reduce metabolic demand and protect the brain.
Prognosis
The prognosis for cerebral hypoxia depends on the duration and severity of the oxygen deprivation. Rapid intervention can improve outcomes, but prolonged hypoxia often results in significant neurological impairment or death.
Prevention
Preventive measures include managing risk factors for heart disease and stroke, using safety equipment to prevent asphyxia, and ensuring proper ventilation in environments where carbon monoxide exposure is possible.
Related pages
