Fatal Cerebral Vasospasm following a <b><i>Haemophilus influenzae</i></b> Meningitis in a Young Child with Ventriculoperitoneal Shunt

Abstract

&lt;b&gt;&lt;i&gt;Introduction:&lt;/i&gt;&lt;/b&gt; Despite the successful implementation of &lt;i&gt;Haemophilus influenzae&lt;/i&gt; vaccination, invasive serotypes still lead to a fatal infection. We recently cared for a patient with a ventriculoperitoneal shunt (VPS) and &lt;i&gt;H. influenzae&lt;/i&gt; meningitis and septicemia complicated by vasospasm. Vasospasm caused by &lt;i&gt;Haemophilus&lt;/i&gt; central nervous system infection has not been previously reported. &lt;b&gt;&lt;i&gt;Case Presentation:&lt;/i&gt;&lt;/b&gt; A 34-month-old patient with a recent VPS presented with &lt;i&gt;H. influenzae&lt;/i&gt; meningitis and sepsis. Despite the explant of hardware, followed by maximum medical management, the patient developed stroke due to severe vasospasm, which led to diffused anoxic brain injury. &lt;b&gt;&lt;i&gt;Conclusions:&lt;/i&gt;&lt;/b&gt; We aim to alert for the possible critical condition caused by &lt;i&gt;H. influenzae.&lt;/i&gt; It is essential to treat the underlying illness, despite the presence of a VPS. Surgical implant tends to be overlooked by other subspecialists. Being vaccinated to &lt;i&gt;H. influenzae&lt;/i&gt; does not protect from different subtypes like non-typeable &lt;i&gt;H. influenzae&lt;/i&gt;. The cause of vasospasm remains unclear.

First use of intraventricular nicardipine in a pediatric patient with vasospasm secondary to meningitis: illustrative case

“… 20–24 Vasospasm is associated with significant morbidity and mortality, and patients are at risk for permanent neurological deficits and death secondary to anoxic brain injury due to hypoperfusion. 22 , 25–27 …”

“…Cerebral vasospasm, defined by a 50% reduction in vessel diameter, secondary to meningitis has been well documented. [20][21][22][23][24] Vasospasm is associated with significant morbidity and mortality, and patients are at risk for permanent neurological deficits and death secondary to anoxic brain injury due to hypoperfusion. 22,[25][26][27] The pathophysiology of cerebral vasospasm has yet to be fully elucidated; multifactorial contributions involve autoregulatory dysfunction, inflammation, cortical spreading depression, and genetics.…”

“…[20][21][22][23][24] Vasospasm is associated with significant morbidity and mortality, and patients are at risk for permanent neurological deficits and death secondary to anoxic brain injury due to hypoperfusion. 22,[25][26][27] The pathophysiology of cerebral vasospasm has yet to be fully elucidated; multifactorial contributions involve autoregulatory dysfunction, inflammation, cortical spreading depression, and genetics. [28][29][30] The inflammation hypothesis primarily centers on the infiltration of macrophages and neutrophils into the subarachnoid space in response to a triggering event, wherein their retention occurs because of the absence of lymphatics and compromised CSF flow.…”

“…Case reports and single-institution reviews have described varied treatments ranging from CCBs (oral, IV, or intraarterial) and milrinone to angioplasties and bypasses. 22,[31][32][33][34] The treatments for vasospasm in the adult population are also variable with a range of reported efficacies (Table 2). 15,[35][36][37] Oral nimodipine has been shown to improve functional outcomes after aSAH in adult patients, though it has not shown a concordant effect on radiographic vasospasm.…”

What Is the Best Surgical Intervention for Patients With Idiopathic Intracranial Hypertension?

“…These risks of venous stenting should be explained to every patient consenting for the procedure but should be placed in context of the myriad risks that are inherent in CSF shunting. These include central nervous system infection and acute or delayed intraparenchymal hemorrhage, all of which can be fatal, 48,49 as well as ectopic migration of the peritoneal tip to sites as disparate as the pulmonary artery (often with secondary thrombosis), 50 mouth, 51 urethra, 52 or rectum. 53 In one single-center series of 95 patients treated with VPS over an 8-year period, 54 there were 5 severe complications, and one fatal, yielding a mortality rate of approximately 1%.…”