Early symptoms of high-altitude cerebral edema (HACE) generally correspond with those of moderate to severe acute mountain sickness (AMS). Initial symptoms of HACE commonly include confusion, loss of consciousness, fever, ataxia, photophobia, rapid heart beat, lassitude, and an altered mental state. Sufferers generally attempt to cease physical activities, regardless of their necessity for survival. Severe headaches develop and sufferers lose the ability to sit up. Retinal venous dilation occurs in 59% of people with HACE. Rarer symptoms include brisk deep tendon reflexes, retinal hemorrhages, blurred vision, extension plantar reflexes, and ocular paralysis. Cranial nerve palsies occur in some unusual cases.

In the bestselling 1996 non-fiction book "Into Thin Air: A Personal Account of the Mt. Everest Disaster", Jon Krakauer describes the effects of HACE upon Dale Kruse, a forty-four-year-old dentist and one of the members of Scott Fischer's team:

‘Kruse was having an incredibly difficult time simply trying to dress himself. He put his climbing harness on inside out, threaded it through the fly of his wind suit, and failed to fasten the buckle; fortunately, Fisher and Neal Beidleman noticed the screwup before Kruse started to descend. "If he'd tried to rappel down the ropes like that," says Beidleman, "he would have immediately popped out of his harness and fallen to the bottom of the Lhotse Face."

‘"It was like I was very drunk," Kruse recollects. "I couldn't walk without stumbling, and completely lost the ability to think or speak. It was a really strange feeling. I'd have some word in my mind, but I couldn't figure out how to bring it to my lips. So Scott and Neal had to get me dressed and make sure my harness was on correctly, then Scott lowered me down the fixed ropes." By the time Kruse arrived in Base Camp, he says, "it was still another three or four days before I could walk from my tent to the mess tent without stumbling all over the place."’

Patients with HACE have an elevated white blood cell count, but otherwise their blood count and biochemistry are normal. If a lumbar puncture is performed, it will show normal cerebral spinal fluid and cell counts but an increase in pressure. In one study, CT scans of patients with HACE exhibited ventricle compression and low density in the cerebellum. Only a few autopsies have been performed on fatal cases of HACE; they showed swollen gyri, spongiosis of white matter, and compressed sulci. There was some variation between individuals, and the results may not be typical of HACE deaths.

High-altitude cerebral edema (HACE) is a medical condition in which the brain swells with fluid because of the physiological effects of traveling to a high altitude. It generally appears in patients who have acute mountain sickness and involves disorientation, lethargy, and nausea among other symptoms. It occurs when the body fails to acclimatize while ascending to a high altitude.

It appears to be a vasogenic edema (fluid penetration of the blood–brain barrier), although cytotoxic edema (cellular retention of fluids) may play a role as well. Individuals with the condition must immediately descend to a lower altitude or coma and death can occur. Patients are usually given supplemental oxygen and dexamethasone as well.

HACE can be prevented by ascending to heights slowly to allow the body more time to acclimatize. Acetazolamide also helps prevent the condition. Untreated patients usually die within 48 hours. Those who receive treatment may take weeks to fully recover. It is a rare condition, occurring in less than one percent of people who ascend to . First described in 1913, little was known about the cause of the condition until MRI studies were performed in the 1990s.

Embolized fat travels through the venous system to the lungs and can occlude pulmonary capillaries, fat emboli may cause cor pulmonale if adequate compensatory pulmonary vasodilation does not occur.Circulating free fatty acids are directly toxic to pneumocytes and capillary endothelium in the lung, causing interstitial hemorrhage, edema and chemical pneumonitis.Complications from a fat embolism can be serious such as:

1. "Pulmonary fat embolism": Obstruction causes sudden death.

2. "Systemic fat embolism": These may get lodged in capillaries of organs like the brain, kidneys, or skin, causing minute hemorrhage and microinfarcts.

In terms of signs and symptoms the severe form of this condition presents as acute pulmonary heart disease this may lead to death.Clinical fat embolism syndrome presents with tachypnea, elevated temperature, anuria, drowsiness, and occasionally mild neurological symptoms.A petechial rash appears on the upper anterior portion of the body, including the chest, neck, upper arm, oral mucosa and conjunctivae; it appears late and often disappears within hours.

Central nervous system signs in an affected individual include acute confusion, stupor, coma, rigidity (neurology), or convulsions; cerebral edema contributes to the neurologic deterioration.

High-altitude pulmonary edema (HAPE) ("HAPO" spelled oedema in British English) is a life-threatening form of non-cardiogenic pulmonary edema (fluid accumulation in the lungs) that occurs in otherwise healthy mountaineers at altitudes typically above . However, cases have also been reported at lower altitudes (between in highly vulnerable subjects), though what makes some people susceptible to HAPE is currently unknown. HAPE remains the major cause of death related to high-altitude exposure, with a high mortality rate in the absence of adequate emergency treatment.

Physiological and symptomatic changes often vary according to the altitude involved.

The Lake Louise Consensus Definition for High-Altitude Pulmonary Edema has set widely used criteria for defining HAPE symptoms:

Symptoms: at least two of:

- Difficulty in breathing (dyspnea) at rest

- Cough

- Weakness or decreased exercise performance

- Chest tightness or congestion

Signs: at least two of:

- Crackles or wheezing (while breathing) in at least one lung field

- Central cyanosis (blue skin color)

- Tachypnea (rapid shallow breathing)

- Tachycardia (rapid heart rate)

The initial cause of HAPE is a shortage of oxygen caused by the lower air pressure at high altitudes.

The mechanisms by which this oxygen shortage causes HAPE are poorly understood, but two processes are believed to be important:

1. Increased pulmonary arterial and capillary pressures (pulmonary hypertension) secondary to hypoxic pulmonary vasoconstriction.

2. An idiopathic non-inflammatory increase in the permeability of the vascular endothelium.

Although higher pulmonary arterial pressures are associated with the development of HAPE, the presence of pulmonary hypertension may not in itself be sufficient to explain the development of edema: severe pulmonary hypertension can exist in the absence of clinical HAPE in subjects at high altitude.

Certain changes in morphology are associated with cerebral edema: the brain becomes soft and smooth and overfills the cranial vault, gyri (ridges) become flattened, sulci (grooves) become narrowed, and ventricular cavities become compressed.

Symptoms include nausea, vomiting, blurred vision, faintness, and in severe cases, seizures and coma. If brain herniation occurs, respiratory symptoms or respiratory arrest can also occur due to compression of the respiratory centers in the pons and medulla oblongata.

Dysbarism refers to medical conditions resulting from changes in ambient pressure. Various activities are associated with pressure changes. underwater diving is the most frequently cited example, but pressure changes also affect people who work in other pressurized environments (for example, caisson workers), and people who move between different altitudes.

Decompression sickness, also called caisson workers' disease and the bends, is the most well-known complication of scuba diving. It occurs as divers ascend, and often from ascending too fast or without doing decompression stops. Bubbles are large enough and numerous enough to cause physical injury. It is quite possible that all divers have microbubbles in their blood to some extent, but that most of the time these bubbles are so few and so small that they cause no harm. When DCS occurs, bubbles disrupt tissues in the joints, brain, spinal cord, lungs, and other organs. Symptoms vary enormously. DCS may be as subtle as unusual tiredness after a dive, or an aching elbow, or a mottled skin rash. Or, it may present dramatically, with unconsciousness, seizures, paralysis, shortness of breath, or death. Paraplegia is not uncommon.

Cerebral edema is excess accumulation of fluid in the intracellular or extracellular spaces of the brain.

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.

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. The skin may also appear bluish (cyanosis) and heart rate increases. Continued oxygen deprivation results in fainting, long-term loss of consciousness, coma, seizures, cessation of brain stem reflexes, and brain death.

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.

It should be noted that 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.

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 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 deep-water dive, flying at high altitudes in an unpressurized cabin without supplemental oxygen, and intense exercise at high altitudes prior to acclimatization.

Severe cerebral hypoxia and anoxia is usually caused by traumatic events such as choking, drowning, strangulation, smoke inhalation, drug overdoses, crushing of the trachea, status asthmaticus, and shock. It is also recreationally self-induced in the fainting game and in erotic asphyxiation.

- 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 brain, spinal cord, or retinal ischemia, without acute 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.

- 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 hemorrhages. Silent strokes typically cause lesions which are detected via the use of neuroimaging such as fMRI. 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.

All symptoms normally resolve within three weeks, and may only last days. Permanent deficits are seen in a minority of patients, ranging from under 10% to 20% in various studies. Less than 5% of patients experience progressive vasoconstriction, which can lead to stroke, progressive cerebral edema, or even death. Severe complications appear to be more common in postpartum mothers.

The key symptom of RCVS is recurrent thunderclap headaches, which over 95% of patients experience. In two-thirds of cases, it is the only symptom. These headaches are typically bilateral, very severe and peak in intensity within a minute. They may last from minutes to days, and may be accompanied by nausea, photophobia, phonophobia or vomiting. Some patients experience only one headache, but on average there are four attacks over a period of one to four weeks. A milder, residual headache persists between severe attacks for half of patients.

1–17% of patients experience seizures. 8–43% of patients show neurologic problems, especially visual disturbances, but also hemiplegia, ataxia, dysarthria, aphasia, and numbness. These neurologic issues typically disappear within minutes or a few hours; more persistent symptoms may indicate a stroke. Posterior reversible encephalopathy syndrome is present in a small minority of patients.

This condition features the unique property that the patient's cerebral arteries can spontaneously constrict and relax back and forth over a period of time without intervention and without clinical findings. Vasospasm is common post subarachnoid hemorrhage and cerebral aneurysm, but in RCVS only 25% of patients have symptoms post subarachnoid hemorrhage.

The symptoms of generalized hypoxia depend on its severity and acceleration of onset.

In the case of altitude sickness, where hypoxia develops gradually, the symptoms include fatigue, numbness / tingling of extremities, nausea, and anoxia. In severe hypoxia, or hypoxia of very rapid onset, ataxia, confusion / disorientation / hallucinations / behavioral change, severe headaches / reduced level of consciousness, papilloedema, breathlessness, pallor, tachycardia, and pulmonary hypertension eventually leading to the late signs cyanosis, slow heart rate / cor pulmonale, and low blood pressure followed by death.

Because hemoglobin is a darker red when it is not bound to oxygen (deoxyhemoglobin), as opposed to the rich red color that it has when bound to oxygen (oxyhemoglobin), when seen through the skin it has an increased tendency to reflect blue light back to the eye. In cases where the oxygen is displaced by another molecule, such as carbon monoxide, the skin may appear 'cherry red' instead of cyanotic. Hypoxia can cause premature birth, and injure the liver, among other deleterious effects.

If tissue is not being perfused properly, it may feel cold and appear pale; if severe, hypoxia can result in cyanosis, a blue discoloration of the skin. If hypoxia is very severe, a tissue may eventually become gangrenous.

Extreme pain may also be felt at or around the site.

In an acute context, hypoxemia can cause symptoms such as those in respiratory distress. These include breathlessness, an increased rate of breathing, use of the chest and abdominal muscles to breathe, and lip pursing.

Chronic hypoxemia may be compensated or uncompensated. The compensation may cause symptoms to be overlooked initially, however, further disease or a stress such as any increase in oxygen demand may finally unmask the existing hypoxemia. In a compensated state, blood vessels supplying less-ventilated areas of the lung may selectively contract, to redirect the blood to areas of the lungs which are better ventilated. However, in a chronic context, and if the lungs are not well ventilated generally, this mechanism can result in pulmonary hypertension, overloading the right ventricle of the heart and causing cor pulmonale and right sided heart failure. Polycythemia can also occur. In children, chronic hypoxemia may manifest as delayed growth, neurological development and motor development and decreased sleep quality with frequent sleep arousals.

Other symptoms of hypoxemia may include cyanosis, digital clubbing, and symptoms that may relate to the cause of the hypoxemia, including cough and hemoptysis.

Serious hypoxemia occurs (1) when the partial pressure of oxygen in blood is less than 60 mm Hg, (the beginning of the steep portion of the oxygen–haemoglobin dissociation curve, where a small decrease in the partial pressure of oxygen results in a large decrease in the oxygen content of the blood); or (2) when hemoglobin oxygen saturation is less than 90%. Severe hypoxia can lead to respiratory failure

Clinical manifestations of intraparenchymal hemorrhage are determined by the size and location of hemorrhage, but may include the following:

- Hypertension, fever, or cardiac arrhythmias

- Nuchal rigidity

- Subhyaloid retinal hemorrhages

- Altered level of consciousness

- Anisocoria, Nystagmus

- Focal neurological deficits

- Putamen - Contralateral hemiparesis, contralateral sensory loss, contralateral conjugate gaze paresis, homonymous hemianopsia, aphasia, neglect, or apraxia

- Thalamus - Contralateral sensory loss, contralateral hemiparesis, gaze paresis, homonymous hemianopia, miosis, aphasia, or confusion

- Lobar - Contralateral hemiparesis or sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, abulia, aphasia, neglect, or apraxia

- Caudate nucleus - Contralateral hemiparesis, contralateral conjugate gaze paresis, or confusion

- Brain stem - Tetraparesis, facial weakness, decreased level of consciousness, gaze paresis, ocular bobbing, miosis, or autonomic instability

- Cerebellum - Ataxia, usually beginning in the trunk, ipsilateral facial weakness, ipsilateral sensory loss, gaze paresis, skew deviation, miosis, or decreased level of consciousness

The symptoms of a cerebral contusion (bruising on the brain) depend on the severity of the injury, ranging from minor to severe. Individuals may experience a headache; confusion; sleepiness; dizziness; loss of consciousness; nausea and vomiting; seizures; and difficulty with coordination and movement. They may also have difficulty with memory, vision, speech, hearing, managing emotions, and thinking. Signs depend on the contusion's location in the brain.

Hypoxic hypoxia is a result of insufficient oxygen available to the lungs. A blocked airway, a drowning or a reduction in partial pressure (high altitude above 10,000 feet) are examples of how lungs can be deprived of oxygen. Some medical examples are abnormal pulmonary function or respiratory obstruction. Hypoxic hypoxia is seen in patients suffering from chronic obstructive pulmonary diseases (COPD), neuromuscular diseases or interstitial lung disease.

The most common symptom of pulmonary edema is difficulty breathing, but may include other symptoms such as coughing up blood (classically seen as pink, frothy sputum), excessive sweating, anxiety, and pale skin. Shortness of breath can manifest as orthopnea (inability to lie down flat due to breathlessness) and/or paroxysmal nocturnal dyspnea (episodes of severe sudden breathlessness at night). These are common presenting symptoms of chronic pulmonary edema due to left ventricular failure. The development of pulmonary edema may be associated with symptoms and signs of "fluid overload"; this is a non-specific term to describe the manifestations of left ventricular failure on the rest of the body and includes peripheral edema (swelling of the legs, in general, of the "pitting" variety, wherein the skin is slow to return to normal when pressed upon), raised jugular venous pressure and hepatomegaly, where the liver is enlarged and may be tender or even pulsatile. Other signs include end-inspiratory crackles (sounds heard at the end of a deep breath) on auscultation and the presence of a third heart sound.

People have different susceptibilities to altitude sickness; for some otherwise healthy people, acute altitude sickness can begin to appear at around above sea level, such as at many mountain ski resorts, equivalent to a pressure of . This is the most frequent type of altitude sickness encountered. Symptoms often manifest themselves six to ten hours after ascent and generally subside in one to two days, but they occasionally develop into the more serious conditions. Symptoms include headache, fatigue, stomach illness, dizziness, and sleep disturbance. Exertion aggravates the symptoms.

Those individuals with the lowest initial partial pressure of end-tidal pCO (the lowest concentration of carbon dioxide at the end of the respiratory cycle, a measure of a higher alveolar ventilation) and corresponding high oxygen saturation levels tend to have a lower incidence of acute mountain sickness than those with high end-tidal pCO and low oxygen saturation levels.

Headaches are the primary symptom used to diagnose altitude sickness, although a headache is also a symptom of dehydration. A headache occurring at an altitude above a pressure of combined with any one or more of the following symptoms, may indicate altitude sickness:

"Hypoxemia" refers to low oxygen in the blood, and the more general term "hypoxia" is an abnormally low oxygen content in any tissue or organ, or the body as a whole. Hypoxemia can cause hypoxia (hypoxemic hypoxia), but hypoxia can also occur via other mechanisms, such as anemia.

Hypoxemia is usually defined in terms of reduced partial pressure of oxygen (mm Hg) in arterial blood, but also in terms of reduced content of oxygen (ml oxygen per dl blood) or percentage saturation of hemoglobin (the oxygen binding protein within red blood cells) with oxygen, which is either found singly or in combination.

While there is general agreement that an arterial blood gas measurement which shows that the partial pressure of oxygen is lower than normal constitutes hypoxemia, there is less agreement concerning whether the oxygen content of blood is relevant in determining hypoxemia. This definition would include oxygen carried by hemoglobin. The oxygen content of blood is thus sometimes viewed as a measure of tissue delivery rather than hypoxemia.

Just as extreme hypoxia can be called anoxia, extreme hypoxemia can be called anoxemia.

Shortness of breath is the most common symptom, followed by face or arm swelling.

Following are frequent symptoms:

- Difficulty breathing

- Headache

- Facial swelling

- Venous distention in the neck and distended veins in the upper chest and arms

- Upper limb edema

- Lightheadedness

- Cough

- Edema (swelling) of the neck, called the "collar of Stokes"

- Pemberton's sign

Superior vena cava syndrome usually presents more gradually with an increase in symptoms over time as malignancies increase in size or invasiveness.