The Angiographic Demonstration of Arterial Vascular Disease in Purulent Meningitis

Arterial and arteriolar stenoses have been observed in such disease processes as subarachnoid hemorrhage, atherosclerosis, cerebral emboli, tumors, periarteritis nodosa, endangiitis obliterans, and lues. Similar changes have also been seen after head trauma (5). The angiographic demonstration of arterial stenosis or occlusion has been rarely observed in patients with infectious disease (3). The case presented demonstrates unusual angiographic changes in a patient with purulent meningitis which included arterial stenosis, occlusion, and collateral blood supply. A 6-month-old Negro male was admitted to the Children's Hospital of Philadelphia with a seventeen-day history of fever, listlessness, and intermittent vomiting. The examination revealed nuchal rigidity, opisthotonus, and left spastic hemiplegia. The pertinent laboratory findings included an anemia (hemoglobin 7.0 g per 100 cc), leukocytosis (31,000 white blood cells with a shift to the left) and cloudy spinal fluid with 9,870 white blood cells/mm3; all of these were polymorphonuclear cells. Gram stain and culture revealed H. influenzae. Blood culture was also positive for H. influenzae. The third hospital day one to two drops of purulent fluid was obtained by subdural puncture from both subdural spaces. Carotid angiography was performed to evaluate the degree of subdural effusion because of the clinical deterioration on the tenth hospital day. Thirteen days after admission, the child died. In H. influenzae meningitis, purulent material may surround the arteries at the base of the brain and spread over the convexity along the vessels, invading the blood vessel walls (1, 2). Pathologists observe vasculitis as a frequent complication of meningitis with resultant vascular thrombosis and formation of cerebral infarcts (1–3). A striking feature of nearly all types of subacute and chronic meningeal infections, especially tuberculous meningitis, is the subintimal cellular infiltration of arteries (2). In inflammatory processes in other organs, this is found infrequently. Its unusually frequent occurrence in meningitis suggests a possible relationship to anatomical peculiarities of the meningeal arteries (1). A marked decrease in caliber of the supraclinoid portion of the internal carotid arteries was demonstrated bilaterally at angiography (Figs. 1, 4, 5). Greitz (3) considered the etiology of the local vasoconstriction at the base of the brain in his patients with tuberculous meningitis to be due to generally increased intracranial pressure, locally increased pressure within the basal cisterns, spastic contractions of the arteries, and tuberculous vasculitis. He commented on the effects of each at the base and concluded that the most probable cause was the local involvement by the tuberculous process and the vasculitis, but he did not completely exclude spasm. An important factor not mentioned, however, is the effect of the contrast material used during angiography.