A 21‐year‐old healthy woman presented with headache, vomiting, and difficulty following commands. She had no fever, rash, head injury, or recent illness. She has mild seasonal allergies. She worked outdoors as a summer camp counselor. She was afebrile and her other vital signs were normal. She appeared restless and distressed, opened her eyes to voice, followed simple commands, and was oriented to self only. There were no other neurological deficits. She had no photophobia, neck stiffness, or rash. A CT scan of the brain revealed partial obliteration of the basilar cisterns suggestive of blood in the subarachnoid space. Sulci were effaced suggestive of cerebral edema. There was no shift, hydrocephalus, or mass lesion. The patient was transferred to the neurosurgical ICU, and nimodipine was administered. Her sodium was 122 mmol/L, potassium 2.8 mmol/L, and serum osmolality 246 mOsm/kg. Complete blood count, serum glucose, urine toxicology screen, EKG, and chest x‐ray were normal. Further questioning of the patient's parents revealed that she had consumed large amounts of water to stay hydrated while working outdoors. Her urine osmolality was 63 mOsm/kg and urine sodium 19 mmol/L, compatible with hyponatremia secondary to water intoxication, resulting in cerebral edema. Because of worsening mental status, hypertonic saline (23.4%) was administered as emergency therapy for acute symptomatic hyponatremia. Her sodium rose to 127 mmol/L after 4 hours and 136 mmol/L after 9 hours. Her mental status subsequently improved. She underwent 4‐vessel cerebral angiography that showed no aneurysm and no vasospasm or vasculitis. She was discharged on the third hospital day with sodium of 137 mmol/L Repeat 4‐vessel cerebral angiography 1 week later again revealed no source of subarachnoid hemorrhage.
Hyponatremia is a common lab abnormality faced by clinicians, of which acute water intoxication is an important cause. Cerebral edema is a life‐threatening complication of hyponatremia. Hyperosmolar agents such as mannitol or hypertonic saline are often used to reduce intracranial pressure, alongside neurosurgical input in an ICU setting. Confusingly, the appearance of cerebral edema can mimic subarachnoid hemorrhage on a CT brain scan, termed “pseudo‐subarachnoid hemorrhage.” Proposed mechanisms for this appearance include: (1) displacement of low‐attenuated CSF by raised intracranial pressure, (2) filling and engorgement of superficial venous structures appearing as increased blood in the identified areas, and (3) decreased attenuation of brain tissue leading to increased differentiation between CSF and the parenchyma.
Clinicians must recognize cerebral edema as a severe complication of hyponatremia and be aware of the pseudo‐subarachnoid hemorrhage appearance on CT.
To cite this abstract:Arasaratnam R, Dunatov C, Kirsch J. A Bad Impersonation. Abstract published at Hospital Medicine 2013, May 16-19, National Harbor, Md. Abstract 366. Journal of Hospital Medicine. 2013; 8 (suppl 2). https://www.shmabstracts.com/abstract/a-bad-impersonation/. Accessed September 20, 2019.