Subdural hematoma associated with high altitude.

Altitude illness is common in people ascending to more than 2500 m, especially when the ascent is rapid. In most cases, it may manifest as a mild and self-limited illness, but in a few cases it can develop into more severe forms, such as subdural hematoma (SDH). Here we report a rare case of SDH evidenced by the neuro-imaging method before and after ascension to a high altitude.

The patient is a 60-year-old right-handed female, self-referred, with a history of recurrent headache for 4 weeks. The patient scheduled a plateau tour and had not been exposed to an altitude higher than 2000 m before. Since she had a history of hypertension for 10 years, she underwent a cranial magnetic resonance imaging (MRI) scan just before the trip on June 1, 2012 which is a standard protocol to ensure tourists’ safety. The result of MRI was normal [Figure 1a]. After the elevation of 4400 m to 4900 m within 12 hours, she experienced a severe frontal headache with breathlessness, dizziness, nausea and vomiting. Her blood pressure was 130/80 mmHg at that time. She was suspected as acute mountain sickness (AMS) and was descended to 1000 m within an hour. But the symptoms were exacerbated obviously. In the next few days, she experienced recurrent frontal headache which could be partially relieved by ibuprofen or lying down. Fifteen days later, the patient underwent computed tomography (CT) and MRI scans of the brain at a local hospital which revealed bilateral fronto-parietal subdural low-density effusion [Figure 1b and 1c] on June 28, 2012. She was treated with dexamethasone and mannitol, but her symptoms had not been relieved. She denied any history of head trauma, drug abuse or intoxication. Other than hypertension, she had a 10-year history of type 2 diabetes and took aspirin 100 mg daily.

Figure 1

Brain scans before and after elevation. Panel a shows a normal T2-weighted magnetic resonance imaging (MRI) scan before ascent. Panels b and c show subdural effusion 15 days after ascent in computed tomography (CT) and T2-weighted MRI scans respectively. Panels d and e show subdural hematoma 1-month after ascent in CT and T2-weighted MRI scans respectively. Panel f shows no subdural effusion or hematoma in a CT scan at a 4 months follow-up. Arrows indicate the locations of subdural effusion or hematoma.

The patient's physical and neurologic examinations were otherwise normal. Signs of meningeal irritation were absent. CT and MRI scans of the brain revealed subdural high-density hematoma [Figure 1d and 1e] on July 23, 2012. The opening pressure of cerebrospinal fluids was 140 mmH2O, with 6 cells/mm3 and 0.80 g/L protein (normal 0.15–0.45 g/L). Ophthalmoscopy was normal. The following radiographic and laboratory studies were normal: CT angiography of the brain, electroencephalogram, paraneoplastic antibodies, screening for coagulation disorders including platelet count, fibrinogen, prothrombin time, activated partial thromboplastin time, international normalized ratio, platelet aggregation and anticardiolipin antibodies. A diagnosis of SDH accompanying AMS was made. Her headache gradually improved, so no specific treatments were applied. At a 4-month follow-up, no severe headache was noted, and another cranial CT revealed no SDH or effusion [Figure 1f].

Rapid ascent to altitude over 2500 m can result in AMS. High altitude cerebral edema is the most common neurological complications of AMS. Other severe neurological conditions of AMS include cerebral infarction, subarachnoid hemorrhage and retinal hemorrhage.

Subdural hematoma, also known as subdural hemorrhage, is a type of hematoma between the brain and the duramater, usually associated with traumatic brain injury, usually resulting from tears in bridging leptomeningeal veins which cross the subdural space. The clinical manifestations include headache, loss of consciousness, seizure, and irritability. The incidence of spontaneous SDH that is defined as a situation without a traumatic history ranges from 2.0% to 6.7%. Conditions associated with the development of spontaneous SDH include coagulopathies related to coagulation factor deficiencies and immune thrombocytopenic purpura, aneurysms, arterio-venous malformations, hypertension, cocaine usage, and pharmacologic therapy with aspirin, heparin, or warfarin. Acute SDH is readily visualized on head CT as a high-density crescentic collection across the hemispheric convexity. Subacute and chronic SDH appear as isodense or hypodense crescent-shaped lesions. The MRI signal appearance of SDH evolves over time: The acute clot is hypointense on T2-weighted images due to the presence of deoxyhemoglobin, over subsequent weeks, deoxyhemoglobin degrades to methemoglobin which appears bright on both T1 and T2-weighted images, at several months, only hemosiderin remains, and the clot again becomes hypointense on the T1-weighted images.

In this patient, Figure 1b was taken 15 days after the ascent. The subdural low-density effusion is probably the manifestation of subacute SDH. And the high-density hematoma presented in Figure 1d and 1e on July 23, 2012 was recurrence of hemorrhage.

Subdural hematoma induced by high altitude was only previously reported in a young male, who developed headache and confusion after a high-altitude (>2700 m) disco party.[1] But he didn’t have a MRI scan before the ascension to ensure that he was normal, so there is no comparison of brain conditions before and after the onset. Our case represents the first report of SDH with neuroimaging evidence before and after the ascent.

Two factors may contribute to the risk of SDH at high altitude. Firstly, hypoxia results in markedly increased cerebral blood flow to maintain oxygen. Therefore, a greater venous pressure is required to increase the venous drainage to match the increased arterial delivery. This theory can be proved by marked dilation of retinal veins without high intracranial pressure at altitude. Also, a susceptibility-weighted MRI study of venous changes with hypoxia demonstrated marked cerebral venous distension.[2] Increased cerebral venous pressure may lead to retinal hemorrhage that is common at altitude. Perhaps as the same manner, the veins between the surface of the brain and the dura are more liable to bleed at high altitude, which causes subdural hemorrhage. Our conjecture was supported by a study on alterations in the intracranial venous sinuses in spontaneous nontraumatic chronic SDH, which concluded increased intravenous pressure to be a pathogenic factor that causes nontraumatic SDH.[3] Secondly, the patient had been taking aspirin preventively, possibly affecting her outcome. Aspirin inhibits platelet function and results in an increased risk of bleeding. A retrospective analysis was performed of patients who received operative intervention for SDH. The reoperation rate in the group on aspirin and anticoagulants was twice that in the nonaspirin/nonanticoagulant group.[4] But this theory is not supported by a recent meta-analysis on the relationship between aspirin therapy and risk of SDH, the result of which showed no statistical correlation between the two elements.[5]