What is cerebral hypoxia

Cerebral hypoxia or brain hypoxia refers to a condition in which there is a decrease of oxygen supply to the brain even though there is adequate blood flow ¹⁾. Cerebral hypoxia affects the largest parts of the brain, called the cerebral hemispheres. However, the term is often used to refer to a lack of oxygen supply to the entire brain. Anoxic brain injury represents a complete lack of oxygen delivery to the brain ²⁾. Drowning, strangling, choking, suffocation, cardiac arrest, head trauma, carbon monoxide poisoning, and complications of general anesthesia can create conditions that can lead to cerebral hypoxia.

Cognitive symptoms secondary to cardiac arrest affect up to 50–83% of survivors after discharge from the hospital. The incidence rates are approximately 50 per 100,000 population and survival-to-discharge rates of roughly 8% which represents over 10,000 patients per year in the United States alone ³⁾.

The literature describes MRI findings in anoxic brain injury in four phases: an acute phase which lasts 24 hours after anoxia or hypoxia; an early subacute phase lasting from one to thirteen days, a late subacute phase lasting from fourteen to twenty days; and a chronic phase, starting at day twenty-one. MRI will show swelling, a hyper signal of basal ganglia, delayed white matter degeneration, cortical laminar necrosis, and atrophy occurring in succession ⁴⁾.

Somatosensory evoked potentials are of use in the setting of anoxic brain injury and are helpful in predicting the prognosis ⁵⁾.

Treatment depends on the cause of the cerebral 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 medicines to raise blood pressure if it is low
• Medicines 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 brief period, a coma may be reversible and the person may have a full or partial return of function. Some people 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.

Cerebral hypoxia causes

Anoxic and hypoxic brain injury is most often the result of cardiac arrest, vascular injury, near drowning, strangulation, smoke inhalation, shock, poisoning from a drug overdose such as opiates, intoxication from carbon monoxide intoxication or head trauma. Cardiac arrest is the most common cause of anoxic brain injury.

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
• Carbon monoxide poisoning
• Choking
• Diseases that prevent movement (paralysis) of the breathing muscles, such as amyotrophic lateral sclerosis (ALS)
• High altitudes
• Pressure on (compression) the windpipe (trachea)
• Strangulation

In other cases, both oxygen and nutrient supply are stopped, caused by:

• Cardiac arrest (when the heart stops pumping)
• Cardiac arrhythmia (heart rhythm problems)
• Complications of general anesthesia
• Drowning
• Drug overdose
• Injuries to a newborn that occurred before, during, or soon after birth such as cerebral palsy
• Stroke
• Very low blood pressure

Brain cells are very 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.

Effects of hypoxia on the brain

Your brain depends on a constant energy supply provided by glucose and oxygen but is unable to store energy. Anaerobic glycolysis may generate lactate and provide neurons with lactate that the mitochondria can use. However, this is not sufficient to meet the needs of your brain. Your brain cannot use fatty acids as a direct source of energy, but it can use ketone bodies that derive from fat. In the ketogenic diet used for the treatment of drug-resistant epilepsy, ketone bodies become the primary energy source. Decreased oxygen will decrease the energy that can be produced by the cell and in turn, lead to cell death.

The mechanisms that lead to delayed cell death following hypoxic-ischemic brain injury in the developing brain remain unclear ⁶⁾. What is, however, more clear is that ischemic cell death occurs via two different modes: necrosis and apoptosis. During hypoxia-ischemia of the brain, acute energy failure leads to loss of ion homeostasis where intracellular sodium and calcium accumulates creating osmotic swelling which, can lead to cell lysis ⁷⁾. This process releases glutamate and free radicals which are cytotoxic and exacerbate the injury. A secondary phase of neuronal death can occur hours later.

Moderate global ischemia leads to infarcts in watershed areas (e.g., the area lying between regions fed by the anterior and middle cerebral artery). These infarcts can damage the highly vulnerable areas such as pyramidal neurons of the hippocampus, pyramidal neurons of the cerebral cortex (layers 3, 5, and 6) which leads to laminar necrosis, the death of neurons in the basal ganglia (caudate nucleus and putamen), and the Purkinje cell layer of the cerebellum ⁸⁾.

The cells of these areas are high in metabolic demand and contain a high concentration of excitatory neurotransmitter receptors. Other histologic findings include a shrunken eosinophilic neuron (anoxic neuron) and a red neuron which represents neuronal cells that die because of hypoxia.

Cerebral hypoxia symptoms

Symptoms of mild cerebral hypoxia include:

• Change in attention (inattentiveness)
• Poor judgment
• Uncoordinated movement

Symptoms of severe cerebral hypoxia include:

• Complete unawareness and unresponsiveness (coma)
• No breathing
• No response of the pupils of the eye to light

Symptoms of mild brain hypoxia include inattentiveness, poor judgment, memory loss, and a decrease in motor coordination. Brain cells are extremely sensitive to oxygen deprivation and can begin to die within five minutes after oxygen supply has been cut off. When hypoxia lasts for longer periods of time, it can cause coma, seizures, and even brain death. In brain death, there is no measurable activity in the brain, although cardiovascular function is preserved. Life support is required for respiration.

Brain hypoxia complications

Complications of cerebral hypoxia include a prolonged vegetative state or prolonged coma, but the pattern of recovery ranges from recovery to mild cognitive deficits to coma and possibly death. 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 their surroundings. Such people 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:

• Bed sores
• Clots in the veins (deep vein thrombosis)
• Lung infections (pneumonia)
• Malnutrition

Trials show that 27% of patients with post-hypoxic coma regained consciousness within 28 days, Nearly 9% remained comatose or in a vegetative state, and unfortunately, 64% died. Common complications can occur after sustaining an anoxic brain injury and may vary from persistent vegetative states, seizures, myoclonus, movement disorder, cognitive dysfunction, and other neurological abnormalities ⁹⁾.

Cerebral hypoxia diagnosis

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:

• Angiogram of the brain
• Blood tests, including arterial blood gases and blood chemical levels
• CT scan of the head
• Echocardiogram which uses ultrasound to view the heart
• Electrocardiogram (ECG), a measurement of the heart’s electrical activity
• Electroencephalogram (EEG), a test of brain waves that can identify seizures and show how well brain cells work
• Evoked potentials, a test that determines whether certain sensations, such as vision and touch, reach the brain
• Magnetic resonance imaging (MRI) of the head

If only blood pressure and heart function remain, the brain may be completely dead.

Cerebral hypoxia treatment

Cerebral hypoxia is an emergency condition that needs to be treated right away. The sooner the oxygen supply is restored to the brain, the lower the risk for severe brain damage and death.

Treatment depends on the underlying cause of the brain hypoxia, but basic life-support systems have to be put in place: mechanical ventilation to secure the airway; fluids, blood products, or medications to support blood pressure and heart rate; and medications to suppress seizures. There is evidence that artificially lowering body and brain temperature can significantly improve the outcomes in anoxia or hypoxia to the brain ¹⁰⁾. Hypoxic-ischemic brain injury and traumatic brain injury both trigger a series of biochemical and molecular events that cause additional brain insult. Suspicions are that induction of therapeutic hypothermia may dampen the molecular cascade that results in neuronal damage, and that hypothermia may attenuate the toxicity produced by the initial injury that typically produces reactive oxygen species, apoptosis, neurotransmitters such as glutamate, and inflammatory mediators ¹¹⁾. In some animal studies, melatonin has also been shown to be protective against hypoxic as it attenuates the damage in different areas of the brain.

Cerebral hypoxia prognosis

Recovery depends on how long the brain has been deprived of oxygen and how much brain damage has occurred, although carbon monoxide poisoning can cause brain damage days to weeks after the event. Furthermore, it is often challenging to predict the prognosis based on clinical findings ¹²⁾. Evaluation with somatosensory evoked potentials, an absent bilateral cortical response and status epilepticus during active cooling period represent a poor prognosis ¹³⁾. A Glasgow Coma Scale (GCS) of 4 or less within the first 48 hours correlates with poor outcomes ¹⁴⁾. Poor neurological outcomes are the rule in patients who sustained a cardiac arrest and those who have an absent pupillary light response or corneal reflexes, absent motor response, or myoclonus status epilepticus ¹⁵⁾.

Most people who make a full recovery have only been briefly unconscious. The longer someone is unconscious, the higher the chances of death or brain death and the lower the chances of a meaningful recovery. During recovery, psychological and neurological abnormalities such as amnesia, personality regression, hallucinations, memory loss, and muscle spasms and twitches may appear, persist, and then resolve.