Anoxic Encephalopathy – StatPearls – NCBI Bookshelf

Bateman RM, Sharpe MD, Jagger JE, Ellis CG, Solé-Violán J, López-Rodríguez M, Herrera-Ramos E, Ruíz-Hernández J, Borderías L, Horcajada J, González-Quevedo N, Rajas O, Briones M, Rodríguez de Castro F, Rodríguez Gallego C, Esen F, Orhun G, Ergin Ozcan P, Senturk E, Ugur Yilmaz C, Orhan N, Arican N, Kaya M, Kucukerden M, Giris M, Akcan U, Bilgic Gazioglu S, Tuzun E, Riff R, Naamani O, Douvdevani A, Takegawa R, Yoshida H, Hirose T, Yamamoto N, Hagiya H, Ojima M, Akeda Y, Tasaki O, Tomono K, Shimazu T, Ono S, Kubo T, Suda S, Ueno T, Ikeda T, Hirose T, Ogura H, Takahashi H, Ojima M, Kang J, Nakamura Y, Kojima T, Shimazu T, Ikeda T, Suda S, Izutani Y, Ueno T, Ono S, Taniguchi T, O M, Dinter C, Lotz J, Eilers B, Wissmann C, Lott R, Meili MM, Schuetz PS, Hawa H, Sharshir M, Aburageila M, Salahuddin N, Chantziara V, Georgiou S, Tsimogianni A, Alexandropoulos P, Vassi A, Lagiou F, Valta M, Micha G, Chinou E, Michaloudis G, Kodaira A, Ikeda T, Ono S, Ueno T, Suda S, Izutani Y, Imaizumi H, De la 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Anoxic Encephalopathy – StatPearls – NCBI Bookshelf

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N, Avard B, Burns R, Patarchi A, Spina T, Tanaka H, Otani N, Ode S, Ishimatsu S, Cho J, Moon JB, Park CW, Ohk TG, Shin MC, Won MH, Dakova S, Ramsheva Z, Ramshev K, Cho J, Moon JB, Park CW, Ohk TG, Shin MC, Cho J, Moon JB, Park CW, Ohk TG, Shin MC, Marudi A, Baroni S, Gaspari A, Bertellini E, Orhun G, Senturk E, Ozcan PE, Sencer S, Ulusoy C, Tuzun E, Esen F, Tincu R, Cobilinschi C, Tomescu D, Ghiorghiu Z, Macovei R, Van Assen M, Admiraal MM, Van Putten MJ, Tjepkema-Cloostermans M, Van Rootselaar AF, Horn J, Fallenius M, Skrifvars MB, Reinikainen M, Bendel S, Raj R, Abu-Habsa M, Hymers C, Borowska A, Sivadhas H, Sahiba S, Perkins S, Rubio J, Rubio JA, Sierra R, English S, Chasse M, Turgeon A, Lauzier F, Griesdale D, Garland A, Fergusson D, Zarychanski R, Tinmouth A, Van Walraven C, Montroy K, Ziegler J, Dupont Chouinard R, Carignan R, Dhaliwal A, Lum C, Sinclair J, Pagliarello G, McIntyre L, English S, Chasse M, Turgeon A, Lauzier F, Griesdale D, Garland A, Fergusson D, Zarychanski R, 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Sharshir M, Khurshid M, Ali Z, Malgapo M, Jamil M, Shafquat A, Shoukri M, Hijazi M, Abe T, Uchino S, Takinami M, Rangel Neto NR, Oliveira S, Reis FQ, Rocha FA, Moralez G, Ebecken K, Rabello LS, Lima MF, Hatum R, De Marco FV, Alves A, Pinto JE, Godoy M, Brasil PE, Bozza FA, Salluh JI, Soares M, Krinsley J, Kang G, Perry J, Hines H, Wilkinson KM, Tordoff C, Sloan B, Bellamy MC, Moreira E, Verga F, Barbato M, Burghi G, Soares M, Silva UV, Azevedo LC, Torelly AP, Kahn JM, Angus DC, Knibel MF, Brasil PE, Bozza FA, Salluh JI, Velasco MB, Dalcomune DM, Marshall R, Gilpin T, Tridente A, Raithatha A, Mota D, Loureiro B, Dias J, Afonso O, Coelho F, Martins A, Faria F, Al-Dorzi H, Al Orainni H, AlEid F, Tlaygeh H, Itani A, Hejazi A, Arabi Y, Gaudry S, Messika J, Ricard JD, Guillo S, Pasquet B, Dubief E, Dreyfuss D, Tubach F, Battle C, James K, Temblett P, Davies L, Battle C, Lynch C, Pereira S, Cavaco S, Fernandes J, Moreira I, Almeida E, Seabra Pereira F, Malheiro M, Cardoso F, Aragão I, Cardoso 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Crit Care. 2016 Apr 20;20(Suppl 2):94. [PMC free article: PMC5493079] [PubMed: 27885969]

Anoxia

This type of brain damage (encephalopathy) is caused by a partial (hypoxia) or complete (anoxia) lack of oxygen supply to the brain tissues for a time longer than the time of maintaining the life of neurons..

Oxygen is very important for normal brain function.

The brain makes up 2% of body weight, while consuming 20% ​​of the oxygen that enters the body.

The brain has an enormous capacity to store nutrients, which requires a constant supply of large amounts of oxygen.

That is why the brain tissue can be without oxygen supply for 4-5 minutes, and only after this time the damage to the brain tissue begins to appear. The longer the anoxia time, the higher the level of tissue damage. So, in 15 minutes of lack of oxygen, about 95% of brain tissues die

Causes

Reduced oxygen supply can be caused by various causes, the most common being heart and respiratory failure. It is also necessary to distinguish between cardio-vascular insufficiency and hypoxia, which coexist together, but provoke the formation of different types of brain damage, the clinical picture of which is different.

ISCHEMIA is associated with a decrease in cerebral blood supply, which reduces the supply of oxygen to the brain (hypoxia). As a result of impaired blood circulation, metabolic products (toxins) that increase brain damage due to ischemia are not removed from the brain

HYPOXIA is a decrease in oxygen supply or use. In the case of isolated hypoxia, a compensatory mechanism of increased blood circulation comes into play, which makes it possible to supply the required amount of glucose to the brain and remove toxins in a limited amount of time.
Depending on the mechanism, the following types of hypoxic brain damage are distinguished.

Anoxic anoxia

due to altitude, the oxygen content in the air is reduced. Other causes include total and incomplete drowning, suffocation, choking, airway obstruction, severe asthma attack, anaphylactic shock, and others.

Anemic anoxia

Caused by lack of oxygen supply to the brain due to low hemoglobin or inability of hemoglobin to bind oxygen

Ischemic anoxia/hypoxia

Caused by low oxygen supply to the brain due to poor circulation or low blood pressure. This mechanism is the main cause of anoxic encephalopathy and includes strokes, cerebral hemorrhages, prolonged acute hypotension, and cardiac arrest.

Cardiac arrest is the main cause of hypoxic brain injury and is usually due to cardiac arrhythmia

The most common causes of problems in newborns are poor blood circulation between mother and unborn child, placental abruption, umbilical cord compression, uterine rupture and others.

TOXIC Anoxia is caused by toxins or substances that bind oxygen, such as carbon monoxide, cyanide, drugs, alcohol, formaldehyde, acetone, toluene, and some anesthetics.

Consequences

The degree of damage caused by the absence of oxygen in the tissues of the brain depends on various factors:

The clinical picture of the disease and symptoms depend on the sensitivity of a certain area of ​​the brain to the concentration of oxygen in the tissues. The most sensitive areas:

• Hippocampus. Zone CA1 and CA4-6, responsible for the assimilation of new information
• Basal ganglia (caudate and lenticular nuclei) responsible for movement.
• Cerebellar Purkinje cells responsible for motor coordination
• Border areas of the vascular system responsible for processing information between different areas of the brain
• Some layers of the cortex (3, 5, 6) of the brain responsible for cognitive functions

Most common symptoms:

• Epileptic crises. Every third patient with anoxia has epileptic crises, the clinical picture of which differs from typical convulsions and takes the form of complex partial crises (with impaired consciousness) or muscle twitches (myoclonus)
• Movement disorder includes rigid akinetic parkinsonism with dystonic postures. Muscle twitches, choreic movements, abnormally slow, uncontrolled movements (athetosis), and tremors also occur.
• Sensorimotor disorders include tetraparesis, paraparesis, and others.
• Visual disturbances – from fixation problem to cortical blindness
• Disorders of consciousness, including vegetative state and state of minimal consciousness
• Cognitive problems manifested in impaired attention and learning

The spectrum of the clinical picture of this disease is very wide, it can manifest itself as minor cognitive impairment up to brain death. In general, about 65% of patients with this disease remain with limited abilities and dependent on other people. This type of brain damage gives the worst prognosis compared to other injuries, especially in the motor and cognitive spheres.

FGBNU NTsPZ. ‹‹Exogenous mental disorders››

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The morphological picture of the brain in various clinical forms of alcoholism can be different – from approaching normal to severe atrophy and acute dystrophic changes. It depends on the stage of the disease, the duration of alcohol consumption, as well as many additional factors.

In those who died in a state of acute alcohol intoxication, which is relatively rare, one can see hyperemia and swelling of the brain, less often pinpoint hemorrhages, which also corresponds to the microscopic picture of the brain tissue. It is dominated by circulatory disorders and more or less pronounced signs of toxic encephalopathy.

With delirium tremens, swelling or pronounced swelling of the brain is macroscopically noteworthy, the hemorrhagic syndrome is unstable. Microscopically, hemorrhages in the brain stem are detected, as well as diffuse phenomena of toxic-anoxic encephalopathy, including pronounced granular decay and vacuolar degeneration of neurocytes. There is a predominant lesion of the stem, in particular the hypothalamic, parts of the brain. This corresponds to changes in the endocrine glands that are characteristic of a state of stress (according to Selye) With delirium tremens, changes in internal organs are possible, dystrophic phenomena in the heart and kidneys, severe fatty degeneration, and sometimes the initial stage of cirrhosis of the liver

The neuroanatomy of chronic alcoholism reflects both the direct toxic effect of alcohol and its indirect effect on the brain caused by alimentary deficiency (especially of B vitamins), as well as metabolic disorders due to alcoholic liver damage.

Histopathological manifestations of chronic alcoholism are characterized by a picture of encephalopathy, while there is a combination of two types of encephalopathy – toxic and alimentary-dystrophic [Snesarev P. E., 1950]. In some, especially in severe cases of chronic alcoholism, atrophy of the brain parenchyma may develop, which is microscopically expressed by the disappearance of nerve cells in the cerebral cortex and cerebellum. Usually there are dystrophic changes in the peripheral nerves, and sometimes the optic nerve. The phenomena of cirrhosis of the liver are also characteristic.

In Gaye-Wernicke disease, microscopically observed dot and spotted hemorrhages and small necrosis in the walls of the third ventricle, the trunk and diencephalic region of the brain and mamillary bodies, less often in the tissue of the corpus callosum and cerebellum. Microscopically, small hemorrhages and their consequences, gliosis reaction, dystrophic changes in nerve cells and their death, signs of cerebral edema are detected. Liver changes are not always found, but in some cases they are very pronounced and reach the degree of cirrhosis (fatty alcoholic cirrhosis). There is an opinion that Gaye-Wernicke encephalopathy is largely due to the development of thiamine deficiency in alcoholism. This encephalopathy is considered one of the most severe forms of alcoholic brain damage.

In Korsakov’s syndrome, vascular disorders of an ischemic nature predominate in the picture of encephalopathy, especially often found in the dorsomedial thalamic nuclei, mamillary bodies, and some other subcortical formations.

In some cases of severe alcoholism, degeneration of the cerebellar tissue (usually its anterior region) is noted. Even rarer findings include lesions of the myelin sheaths of the nerve conductors in the central part of the brain stem and changes corresponding to the picture of Markjafava-Bignyami disease, caused by the processes of demyelination of the medial part of the corpus callosum.

The anatomical basis of fetal alcohol syndrome is brain dysontogenesis, the signs of which are already found in fetuses of 5-15 weeks of development [Kovetsky N. S. et al., 1988]. The most typical changes include disturbances in the formation of the walls of the brain, deviations in the development of the cortical plate with aplasia, developmental delay, and less often in combination with hyperplasia of individual sections of these structures. Quite characteristic of these cases is also the formation of the walls of the brain with excessive folding and fusion of their individual sections with the formation of various variants of porencephaly and cysts; quite typical is the heterotopy of nerve elements and their groups. The described changes were generally designated as “violations of the general structure of the brain” [Konovalov G. V. et al., 1988]. Pronounced changes were established in fetal alcohol syndrome and in the ultrastructural study of the brain of fetuses developing in the body of alcoholic mothers [Solonsky A.V., Kovetsky N.S., 1989].

Many authors believe that the main mechanism of the teratogenic effect of alcohol on the developing brain is a violation of the migration of neurons and glial elements, which leads to their heterotopy in the white matter, meninges, changes in the structure of the layers of the cortex of the cerebral hemispheres, as well as hypoplasia of some of its departments [Clarren S.