Fatal Venous Cerebral Air Embolism Secondary to a Disconnected Central Venous Catheter

212 rather than cytotoxic edema [3] . In contrast, another theory hypothesizes that at elevated blood pressures or from endothelial toxins, the autoregulatory system overcompensates, resulting in decreased blood fl ow, ultimately resulting in ischemia and therefore cytotoxic edema [5] . Though cerebellar and brainstem white matter hyperintensities have been reported, these have been largely asymptomatic features of the disease [6] . A recent review of patients with hypertensive encephalopathy involving the brainstem found that correlated clinical symptoms were present in less than 25% of patients, suggesting a ‘clinical radiologic dissociation’ [7] . Of the reports in which symptoms were detailed, only eight prior cases describe symptomatic brainstem dysfunction from PRES. These cases are summarized in table 1 . Cases of obstructive hydrocephalus and resulting symptoms have also been reported [8] . In our patient, the prominent dysarthria and dysphagia suggesting lower motor neuron involvement could be correlated more directly to the pontine edema. The differential diagnosis of brainstem encephalopathy with associated MRI T 2 -weighted hyperintensities is broad and includes central pontine myelinolysis, autoimmune diseases (systemic lupus erythematosus, Behçet’s disease, polyarteritis nodosa), multiple sclerosis, infectious/postinfectious conditions (acute disseminated encephalomyelitis, Bickerstaff’s encephalitis, Listeria rhombencephalitis, progressive multifocal leukoencephalopathy), neoplastic disorders (lymphoma and glioma), and vascular insults (subacute infarction) [9] . In our case, there was no evidence of metabolic derangements to suggest central pontine myelinolysis, and gadolinium MRI failed to show acute infl ammatory changes or neoplasm. The patient’s clinical history and laboratory values also helped exclude other diagnoses. Initial DWI sequences did not reveal acute infarction, but could not rule out the possibility of subacute infarction. However, the reversible T 2 -weighted hyperintensities on MRI argued against infarction and supported the diagnosis of PRES.