High altitude cerebral edema ( HACE ) is a medical condition in which the brain swells with fluid due to the physiological effects of traveling to high altitudes. It usually appears in patients who have acute mountain disease and involves disorientation, lethargy, and nausea among other symptoms. This happens when the body fails to adjust when it rises to high altitude.
It appears to be vasogenic edema (penetration of the blood-brain barrier fluid), although cytotoxic edema (cellular fluid retention) may play a role as well. Individuals with conditions should immediately descend to lower altitudes or coma and death may occur. Patients are usually given supplemental oxygen and dexamethasone as well.
HACE can be prevented by rising to altitude slowly to allow the body more time to adjust. Acetazolamide also helps prevent the condition. Untreated patients usually die within 48 hours. Those receiving treatment may take weeks to fully recover. This is a rare condition, occurring in less than one percent of people who climb to 4,000 meters (13,000 feet). First described in 1913, little is known about the cause of the condition until MRI research was conducted in the 1990s.
Video High-altitude cerebral edema
Signs and symptoms
The initial symptoms of high altitude cerebral edema (HACE) are commonly associated with moderate or severe acute mountain disease (AMS). The initial symptoms of HACE generally include confusion, loss of consciousness, fever, ataxia, photophobia, rapid heartbeat, lethargy, and changing mental state. Patients generally try to stop physical activity, regardless of their need to survive. Severe headaches develop and the person loses the ability to sit down. Retinal vein widening occurs in 59% of people with HACE. Rougher symptoms include deep tendon reflexes, retinal hemorrhage, blurred vision, extrane plantar reflexes, and ocular paralysis. Cervical nerve palsies occur in some unusual cases.
In the 1996 book of bestselling non-fiction Into Thin Air: Personal Account of Mt. Everest Disaster , Jon Krakauer describes the effect of HACE on Dale Kruse, a forty-four year old dentist and one of the team members of Scott Fischer:
'Kruse is having a very difficult time just trying to dress himself. He mounted his climbing harness on the inside out, twisted it through his flies, and failed to tie the buckle; Fortunately, Fisher and Neal Beidleman noticed the chaos before Kruse began to descend. "If he tries to drop a rope like that," said Beidleman, "he'll get out of his harness and fall to the bottom of Lhotse Face." '"Looks like I'm very drunk," Kruse recalled. "I can not walk without stumbling, and completely lose the ability to think or speak.That is a really strange feeling.I have a few words in my mind, but I do not know how to bring it to my lips So Scott and Neal have to make me dressed up and made sure my armor was properly installed, then Scott lowered my rope. "When Kruse arrived at the Base Camp he said," it's still three or four days before I can walk from my tent to a mess tent without stumbling everywhere. everywhere. "
Patients with HACE have an increased number of white blood cells, but otherwise their blood and biochemical counts are normal. If a lumbar puncture is performed, it will show normal cerebral spinal fluid and cell count but increased pressure. In one study, CT scans of patients with HACE demonstrated ventricular compression and low density in the cerebellum. Only a few autopsies have been performed in the case of a fatal HACE; they showed swollen gyri, spongiosis of white matter, and compressed sulci. There are several variations between individuals, and the results may not be typical of HACE death.
Maps High-altitude cerebral edema
Causes and mechanisms
Most people who travel to altitude adjust themselves. Acclimatization precludes the development of HACE by maintaining adequate levels of cerebral oxygen. The main cause of HACE is hypoxia (oxygen deprivation). This occurs after the body is exposed to low oxygen environments and before acclimatization. The rate of change from the normal oxygen environment and how little oxygen in the new environment can be used to predict the likelihood of developing HACE. Prolonged deployment in low oxygen also causes serious hypocapnia, lowering carbon dioxide in the bloodstream, which may play a role in HACE. These factors cause the brain to swell with fluid, which causes severe damage. If the swelling is not treated, it causes death by brain herniation.
Brain swelling is probably caused by vasogenic edema, penetration of blood-brain barrier by fluid. This process has been observed in the MRI study. Hypoxia increases extracellular fluid, which passes through the vasogenic endothelium in the brain. Leakage can be caused by increased pressure, or may be caused by inflammation that makes the endothelium susceptible to leakage. An MRI study found microhemorrhages in the corpus callosum of HACE patients, and hypoxia may also cause microvascular permeability. It has been hypothesized that vascular endothelial growth factors can lead to permeability of blood vessels in HACE roots. MRI scans of patients with HACE showed an increase in T2 in the corpus callosum, although the gray matter did not change. This suggests that the blood-brain barrier is damaged by the blood vessels of the brain, thus disrupting the metabolism of white matter. Another study looked at the brains of HACE sufferers several months after their recovery; it shows the deposition of hemosiderin in the corpus callosum, evidence of blood vessel permeability.
Despite strong evidence that vasogenic edema plays a major role in HACE, cytotoxic edema, cellular cellular retention, may contribute as well. Cytotoxic edema may be caused by cellular ion pump failure, which results from hypoxia. Then intracellular sodium and osmolarity increase, and there is an influx of water that causes cellular swelling. After the failure of the ATPase pump, free radicals are formed and cause damage that complicates edema. Evidence of cytotoxic edema includes high levels of hypoxemia (low blood oxygen flow) required to cause it.
It is not known why some are more susceptible to HACE than others. One theory is that variations in brain size play a role, but an increase in brain volume from edema is unlikely to cause cranial collisions. The presence of a large sulci indicates that the condition may be affected by a strong brain. Increased intracranial pressure is generally accepted as a late HACE effect. High central venous pressure may also occur late in the development of this condition.
One study showed that normal autorelation of cerebral blood flow did not cause HACE. What role does the sympathetic nervous system play in determining who gets HACE is unclear, but may have an effect.
Another theory about the cause of HACE is that hypoxia can induce nitrous oxide synthase. Vasodilation is caused by the release of nitric oxide and adenosine. This in turn can increase the permeability of the blood vessels and cause edema. It can combine with low cytokine levels to cause HACE.
Diagnosis and prevention
Generally, high altitude pulmonary edema (HAPE) or AMS precede HACE. In patients with AMS, HACE onset is usually characterized by vomiting, a headache that does not respond to non-steroidal anti-inflammatory drugs, hallucinations, and fainting. In some situations, however, AMS develops into HACE without these symptoms. HACE should be distinguished from conditions with similar symptoms, including stroke, intoxication, psychosis, diabetes symptoms, meningitis, or toxic substance consumption. This should be the first diagnosis to be ruled out when the disease occurs as it rises to high altitude.
HACE can generally be prevented by rising gradually with frequent rest days when climbing or trekking. Not rising more than 1,000 meters (3,300 feet) each day and not sleeping at altitudes greater than 300 meters (980 feet) more than the previous night suggested. The risk of developing HACE decreases if acetazolamide or dexamethasone is given. Generally, the use of acetazolamide is preferred, but dexamethasone may be used for prevention if there are side effects or contraindications. Some individuals are more susceptible to HACE than others, and physical fitness is not preventative. Age and gender do not themselves influence susceptibility to HACE.
Treatment and prognosis
Patients with HACE should be brought to a lower place and provide additional oxygen, and a rapid decline is sometimes necessary to prevent death. Early recognition is important because along with the development of the condition, the patient can not go down unaided. Dexamethasone should also be administered, although it fails to correct some of the symptoms that can be cured by descending to a lower altitude. It can also mask the symptoms, and sometimes continue after termination. Prevention of angiogenesis Dexamethasone may explain why it treats HACE well. Three studies that examined how rat rats and brains react to hypoxia confidence in this idea.
If available, supplemental oxygen may be used as adjunctive therapy, or when it is not possible to descend. FiO2 should be titrated to maintain arterial oxygen saturation of more than 90%, given that oxygen supply is often limited to high altitude clinics/environments.
In addition to oxygen therapy, the portable hyperbaric chamber (Gamow bag) can be used as a temporary measure in the treatment of HACE. This device simulates a height decrease of up to 7000 ft, but they are resource intensive and symptoms will often return after discontinuation of the device. The portable hyperbaric space should not be used as a descent or evacuation to a definitive treatment.
Diuretics may be helpful, but they pose risks outside the hospital setting. Sildenafil and tadalafil may help HACE, but there is little evidence of their efficacy. Theophylline also theorized to help this condition.
Although AMS is not life-threatening, HACE is usually fatal within 24 hours if left untreated. Without treatment, the patient will go into a coma and then die. In some cases, the patient has died within a few hours, and some persist for two days. The fatal case description often involves climbers who continue to rise while suffering from symptoms of the condition.
Recovery varies between days and weeks, but mostly recovers within a few days. Once the condition is successfully treated, it is possible for the climber to return. Dexamethesone should be discontinued, but acetazolamide is constantly recommended. In one study, patients took between one week and one month to show normal CT scans after HACE.
Epidemiology
HACE occurs in 0.5% to 1% of people who climb or travel between 4,000 meters (13,000 feet) and 5,000 meters (16,000 feet). In some unusual cases, up to 30% of expedition members suffer from this condition. This condition is rarely seen below 3,000 meters (9,800 feet), but in some rare cases it has grown as low as 2,500 meters (8,200 feet). This condition generally does not occur until someone spends 48 hours at an altitude of 4,000 meters (13,000 feet).
History
HACE was first described by a medical officer stationed in Chile in 1913, but few paid any attention to it. Then, access to air travel makes the condition more general as it allows more people accessing high mountains, such as in the Himalayas. An early description of HACE may have been published in 1969 after a group of Indian soldiers made a rapid climb up to nearly 6,000 meters (20,000 feet). It is unclear whether they suffer from HACE or an acute decompression disease. MRI has been used to study the effects of high altitude in the brain, providing the best evidence of the condition. A 1998 MRI study of nine climbers with HACE clearly demonstrated vasogenic edema.
Data on HACE is lacking because it is common in remote areas, away from hospitals and generally rare. It is not uncommon for physicians to be able to study the victim within six days of the development of the condition. HACE animal models have not been developed yet. Some genes are being examined for roles they can play in the development of conditions.
Source of the article : Wikipedia
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