Cerebral hypoxia

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Cerebral hypoxia is a form of hypoxia (reduced oxygen supply), especially involving the brain; when the brain is completely deprived of oxygen, it's called cerebral anoxia . There are four categories of cerebral hypoxia; they, in order of severity: diffuse brain hypoxia (DCH), focal cerebral ischemia, cerebral infarction, and global cerebral ischemia. Prolonged hypoxia induces neuronal cell death through apoptosis, resulting in hypoxia brain injury.

The cases of total oxygen deprivation are called "anoxia", which can be derived from hypoxia (reduced availability of oxygen) or ischemic origin (oxygen deficiency due to impaired blood flow). Brain injury as a result of oxygen deprivation either due to hypoxic or anoxic mechanism is commonly called hypoxic/anoxic injury ( HAI ). Hypoxic ischemic encephalopathy ( HIE ) is a condition that occurs when the entire brain lacks sufficient oxygen supply, but the deficiency is not total. While HIE is associated in many cases with oxygen deprivation in neonates because of birth asphyxia, it can occur in all age groups, and is often a complication of a heart attack.

Video Cerebral hypoxia

Signs and symptoms

The brain requires about 3.3 ml of oxygen per 100 g of brain tissue per minute. Initially the body responds to lower blood oxygen by directing blood to the brain and increasing cerebral blood flow. Blood flow may increase up to twice that of normal flow but no more. If an increase in blood flow is sufficient to supply the brain's oxygen requirements then no symptoms will arise.

However, if blood flow can not be increased or if blood flow twice does not fix the problem, symptoms of cerebral hypoxia will begin to appear. Mild symptoms include difficulty with complex learning tasks and reduction in short-term memory. If oxygen deficiency persists, cognitive impairment, and motor control decline will occur. The skin may also appear bluish (cyanosis) and heart rate increases. Further reductions in oxygen result in fainting, loss of long-term consciousness, coma, seizures, cessation of brainstem reflex, and brain death.

The objective measurements of cerebral hypoxia severity depend on the cause. Blood oxygen saturation may be used for hypoxic hypoxia, but is generally meaningless in other forms of hypoxia. In hypoxia hypoxia 95-100% saturation is considered normal; 91-94% are considered mild and 86-90% moderate. Anything under 86% is considered heavy.

It should be noted that cerebral hypoxia refers to oxygen levels in brain tissue, not blood. Blood oxygenation usually appears normal in hypoxic hypoxia, ischemic, and hypoxic histoxic cases. Even in the hypoxic hypoxia blood measurement is only an approximate guide; the level of oxygen in the brain tissue will depend on how the body handles the reduced oxygen content of the blood.

Maps Cerebral hypoxia

Cause

Cerebral hypoxia can be caused by any event that greatly interferes with the brain's ability to receive or process oxygen. This event may be internal or external to the body. Form of mild and moderate cerebral hypoxia can be caused by various diseases that interfere with breathing and blood oxygenation. Severe asthma and various anemia can cause some degree of diffuse cerebral hypoxia. Other causes include the status of epilepticus, working in a nitrogen-rich environment, climbing from deep water diving, flying at high altitudes in the cabin without pressure without additional oxygen, and intense exercise at high altitudes before acclimatization.

Severe cerebral hypoxia and anoxia are usually caused by traumatic events such as choking, drowning, strangulation, inhalation of smoke, drug overdose, tracheal destruction, asthmatic status, and shock. It is also a recreation itself caused by fainting games and erotic asphyxia.

• Transient ischemic attack (TIA), often referred to as "mini-stroke". The American Heart Association and American Stroke Association (AHA/ASA) refine the definition of transient ischemic attacks. TIA is now defined as a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction. The symptoms of a TIA can resolve within minutes, unlike a stroke. TIA has the same basic etiology as stroke; disruption of cerebral blood flow. TIA and stroke present with the same symptoms as contralateral paralysis (the opposite side of the body of the affected hemisphere), or sudden weakness or numbness. TIA can cause sudden dimming or loss of vision, aphasia, slurred speech, and mental confusion. The symptoms of TIA usually disappear within 24 hours, unlike a stroke. Brain injury may still occur in TIA that lasts only a few minutes. Having a TIA is a risk factor for ultimately having a stroke.
• Silent stroke is a stroke that has no outward symptoms, and patients usually do not realize they have a stroke. Although there are no identifiable symptoms, a silent stroke still causes brain damage and puts the patient at increased risk for major strokes in the future. In extensive research in 1998, more than 11 million people were estimated to have suffered a stroke in the United States. Approximately 770,000 of these strokes are symptomatic and 11 million are the first silent MRI infarction or bleeding. A silent stroke usually causes lesions detected through the use of neuroimaging such as fMRI. The risk of a silent stroke increases with age but can also affect young adults. Women appear to be at high risk for a silent stroke, with hypertension and current smoking being a predisposing factor.

Pre and post

Anoxic-anoxic events can affect the fetus at various stages of fetal development, during labor and delivery and in the postnatal period. Problems during pregnancy may include preeclampsia, maternal diabetes with vascular disease, congenital fetal infection, drug/alcohol abuse, severe fetal anemia, heart disease, lung malformation, or problems with blood flow to the placenta.

Problems during labor and delivery may include cord occlusion, torsion or prolapse, rupture of the placenta or uterus, excessive bleeding from the placenta, abnormal fetal positions such as the positions of the buttocks, prolonged working stages, or very low blood pressure in the mother. Postnatal problems may include severe prematurity, lung or severe heart disease, serious infections, brain or skull trauma, congenital brain malformations or very low blood pressure in infants and from suffocation in the case of MÃÆ'¼nchausen syndrome proxies.

The severity of neonatal hypoxia-ischemic brain injury can be assessed using Sarnat staging, based on clinical presentation and EEG findings, and also using MRI.

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Mechanism

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

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Diagnosis

Classification

Cerebral hypoxia is usually grouped into four categories depending on the severity and location of the oxygen deprivation in the brain:

1. Diffuse cerebral hypoxia - Decreased mild to moderate brain function due to low oxygen levels in the blood.
2. Focal cerebral ischemia - Strokes occurring in local areas that may be acute or temporary. This may be due to various medical conditions such as aneurysms that cause hemorrhagic strokes, or occlusion occurring in the affected blood vessels due to thrombotic (strombotic stroke) or embolus (embolic stroke). Focal cerebral ischaemia is the majority of clinical cases in stroke pathology with infarction that usually occurs in the middle cerebral artery (MCA).
3. Global cerebral ischemia - The total cessation of blood flow to the brain.
4. Cerebral infarction - "Stroke", caused by complete oxygen deprivation due to impaired cerebral blood flow that affects several areas of the brain.

Cerebral hypoxia can also be classified by the causes of brain oxygen depletion:

• Hypoxic hypoxia - Limited oxygen in the environment causes less brain function. Divers, aviators, mountaineers, and firefighters are all at risk of such cerebral hypoxia. This term also includes oxygen deprivation due to obstructions in the lungs. Choking, choking, crushing the throat that causes this kind of hypoxia. Severe asthma can also develop hypoxic hypoxic symptoms.
• Hypoxic hypoxia - Reduces brain function caused by inadequate oxygen in the blood despite adequate environmental oxygen. Anemia and carbon monoxide poisoning are the most common causes of hypoxic hypoxia.
• Ischemic hypoxia (or "stagnant hypoxia") - Reduces brain oxygen caused by inadequate blood flow to the brain. Stroke, shock, cardiac arrest and heart attack can cause stagnant hypoxia. Ischemic hypoxia can also be caused by pressure on the brain. Brain edema, cerebral hemorrhage and hydrocephalus put pressure on brain tissue and inhibit oxygen uptake.
• Histotoxic hypoxia - Oxygen is present in brain tissue but can not be metabolized by brain tissue. Cyanide poisoning is a well-known example.

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Treatment

For newborns oxygen starvation during birth now there is evidence that hypothermia therapy for neonatal encephalopathy is applied in 6 hrs of cerebral hypoxia effectively improves survival and neurological outcomes. In adults, however, the evidence is less convincing and the first goal of treatment is to return oxygen to the brain. The method of restoration depends on the cause of hypoxia. For mild to moderate hypoxic cases, removal of the hypoxic causes may be sufficient. Inhaled oxygen may also be administered. In severe cases, treatment may also involve life support and damage control measures.

Deep coma will disrupt the respiratory reflex even after the initial cause of hypoxia has been treated; mechanical ventilation may be required. In addition, severe cerebral hypoxia causes an elevated heart rate, and in extreme cases the heart can be tired and stop pumping. CPR, defibrillation, epinephrine, and atropine can all be tried in an attempt to make the heart pump again. Severe cerebral hypoxia can also cause seizures, which put the patient at risk for self-injury, and various anti-convulsant medications may need to be given before treatment.

There is a debate about whether newborns with cerebral hypoxia should be resuscitated with 100% oxygen or normal air. It has been shown that high oxygen concentrations lead to the formation of oxygen-free radicals, which have a role in reperfusion injury after asphyxia. Research by Ola Didrik Saugstad and others lead to new international guidelines on resuscitation of newborns in 2010, recommending the use of normal air as a replacement for 100% oxygen.

Brain damage can occur both during and after oxygen deprivation. During oxygen deprivation, cells die from increasing acidity in brain tissue (acidosis). In addition, during periods of lack of oxygen, materials that can easily create free radicals accumulate. When oxygen enters the tissue, these materials interact with oxygen to produce high levels of oxidants. Oxidants interfere with normal brain chemistry and cause further damage (this is known as "reperfusion injury").

Techniques to prevent damage to brain cells are an ongoing area of ​​research. Hypothermia therapy for neonatal encephalopathy is the only evidence-supported therapy, but antioxidant drugs, blood glucose control, and hemodilution (blood thinning) coupled with drug-induced hypertension are some of the treatment techniques under study. Hyperbaric oxygen therapy is being evaluated with a decrease in total creatin phosokinase and myocardial levels suggest a possible reduction in overall systemic inflammatory processes.

In severe cases it is very important to act quickly. Brain cells are very sensitive to decreased oxygen levels. Once lack of oxygen, they will start to die within five minutes.

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Prognosis

Mild and moderate cerebral hypoxia generally have no impact beyond the episode of hypoxia; on the other hand, the result of severe cerebral hypoxia will depend on the success of damage control, the amount of brain tissue lacking oxygen, and the rate at which oxygen is restored.

If cerebral hypoxia is localized to a specific part of the brain, brain damage will be localized to the region. The general consequence may be epilepsy. Long-term effects will depend on the purpose of that part of the brain. Damage to Broca's area and Wernicke's brain area (left side) usually causes problems with speech and language. Damage to the right side of the brain can interfere with the ability to express emotions or interpret what one sees. Damage to both sides can cause paralysis on the opposite side of the body.

The effects of some types of severe general hypoxia may take time to develop. For example, the long-term effects of serious carbon monoxide poisoning typically take several weeks to appear. Recent research suggests this may be caused by an autoimmune response caused by changes caused by carbon monoxide in the myelin sheath around the neurons.

If hypoxia causes coma, long unconsciousness often shows long-term damage. In some cases coma can give the brain a chance to heal and regenerate, but, in general, the longer the coma, the more likely that the person will remain in a vegetative state to death. Even if the patient wakes up, brain damage may be significant enough to prevent a return to normal function.

Long-term coma can have a significant impact on the patient's family. The families of the coma victims often have an idealized picture of the results based on the portrayal of coma films in Hollywood. Adjusting to the reality of ventilators, food hoses, bedsores, and muscle wasting may be difficult. Treatment decisions often involve complex ethical choices and can burden family dynamics.

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See also

• Higher disease
• Choking game
• Hypothermia cap
• Room lighting
• Ulegyria

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References

src: www.jneurosci.org

External links

• The hypoxia experiment

Source of the article : Wikipedia