Acute Hydrocephalus Associated with Streptococcus anginosus Meningitis

Abstract

Introduction

Meningitis-related acute hydrocephalus is rare, challenging to diagnose, and has a high mortality rate.

Case description

Here we describe the case of a 76-year-old patient diagnosed with bacterial meningitis who developed acute hydrocephalus and subsequently died.

Discussion

Although meningitis-related acute hydrocephalus is usually non-occlusive, occlusive hydrocephalus may also occur. Moreover, worsening hydrocephalus despite cerebrospinal fluid drainage should prompt a diagnosis of obstructive hydrocephalus. In such conditions, potential management strategies include ventriculoperitoneal shunt and endoscopic third ventriculostomy.

Conclusion

In patients with meningitis-related hydrocephalus, worsening despite appropriate antibiotic administration, treatment may be complicated by ventriculitis and obstructive hydrocephalus, which can be fatal. If intracranial pressure is not medically controlled, bilateral decompression craniectomy should be considered as a potential management strategy.

LEARNING POINTS

• The extreme rarity of obstructive hydrocephalus caused by bacterial meningitis can lead to delayed diagnosis and treatment.

• Ventriculoperitoneal shunt and endoscopic third ventriculostomy are the indicated management strategies for early diagnosis of obstructive hydrocephalus.

• Bilateral decompression craniectomy may be an option in such cases.

BACKGROUND

Acute hydrocephalus is a rare complication of meningitis associated with Escherichia coli and Streptococcus pneumoniae ^[1–4]. Meningitis-related acute hydrocephalus has a high mortality rate, ranging between 50% and 60% ^{[4, 5]}. We report a case of hydrocephalus associated with bacterial meningitis caused by Streptococcus anginosus.

CASE DESCRIPTION

A 76-year-old man experienced loss of consciousness at his home and was transported to our emergency medical centre via ambulance. His medical history revealed diabetes, and his family reported seeing him 2 days previously and finding him well.

Investigations

On arrival, the patient’s Glasgow Coma Score was 6 (E1V1M4). Pupils were unequal in size (3.0 and 2.0 mm) and non-reactive to light. The gaze was conjugate and deviated to the right. Heart rate was 90 beats/min, blood pressure was 160/85 mmHg, and SpO₂ was 100% on oxygen delivered at 10 l/min via a mask with a reservoir bag. Respiratory rate was 20 breaths/min, and body temperature was 35.5°C. Laboratory investigations showed a white blood cell count of 26,700/μl, CRP 38.6 mg/l, procalcitonin 19.09 ng/ml, blood urea nitrogen 101.3 mg/dl, creatinine 7.41 mg/dl and potassium 5.6 mEq/l. The results of arterial blood gas analysis indicated pH 7.384, partial pressure of oxygen 178.6 mmHg, partial pressure of carbon dioxide 32.7 mmHg, bicarbonate ion concentration 19.7 mmol/l, base excess −5.50 mmol/l, lactate levels 1.6 mmol/l, and blood glucose concentration 288 mg/dl. Opening pressure during lumbar puncture was 300 mmH₂O. Cerebrospinal fluid examination showed xanthochromia and white turbidity; the cell count and protein concentration were 3,616/mm³ and 300 mg/dl, respectively. Head computed tomography (CT) showed enlargement of the lateral ventricles, including the inferior temporal horns (Fig. 1). The Evans index was 0.384. Extracranial CT findings included abscess formation in the right infratemporal fossa.

Figure 1.

Head computed tomography on patient arrival showing enlargement of the lateral ventricles, including the inferior temporal horns

Differential diagnosis

A diagnosis of non-occlusive hydrocephalus due to bacterial meningitis was suggested by: the loss of consciousness; elevated white blood cell count, CRP and procalcitonin; elevated cell count and protein levels on cerebrospinal fluid examination; and CT findings.

Treatment

The patient was intubated and placed on a mechanical ventilator. Continuous renal replacement therapy was initiated for the acute kidney injury. After blood and cerebrospinal fluid cultures were obtained, meropenem, vancomycin, acyclovir and ampicillin were initiated.

Outcome and follow-up

On the second day of patient illness, his blood pressure dropped and septic shock was suspected. Consequently, vasopressors were initiated. On the third day, S. anginosus was detected in blood and cerebrospinal fluid cultures. Treatment was shifted from meropenem and ampicillin to ceftriaxone, based on antibiotic sensitivity results. The isolated bacterial culture from the blood was positive in BACTEC aerobic and anaerobic bottles (BD, Franklin Lakes, NJ, USA). The isolates were identified by the rapid ID 32 STREP system (bioMérieux Japan Ltd, Tokyo, Japan) with an identification rate of 93.8%. The minimum inhibitory concentration (MIC) of the antibiotics was determined using the MicroScan WalkAwayPlus system (Siemens, Tokyo, Japan) by the broth microdilution method, and the MIC of penicillin G, cefotaxime, meropenem and vancomycin at μg/ml doses of <0.03, <0.12, <0.12 and 1.0, respectively. On Day 3, an incision was made in the area of the right inferior cranial fossa abscess; however, no drainage was performed. On Day 6, fluoroscopy-guided puncture of the right infratemporal fossa abscess was performed, and pus was obtained. Head CT showed worsening hydrocephalus with sediment in the trigone of the lateral ventricles, consistent with ventricular inflammation (Fig. 2). An inadequate treatment response was considered, and so a therapeutic and diagnostic lumbar puncture was performed. Cerebrospinal fluid drainage did not improve the patient’s level of consciousness. However, fluid examination showed a lower cell count and improvement in inflammation. Therefore, we decided that continuous cerebrospinal fluid drainage was unnecessary. A brain MRI scan was scheduled but could not be performed due to lack of an appointment. On Day 10, the patient’s pulse rate and blood pressure decreased, and pupillary light response disappeared. Head CT was repeated and showed aggravation of hydrocephalus (Fig. 3). Consequently, an emergency external ventricular drainage was performed. The lateral ventricular pressure was remarkably high (600 mmH2O). The patient’s neurological status did not improve, and the brainstem reflexes disappeared despite continuous cerebrospinal fluid drainage. On Day 12, repeat head CT showed a properly placed ventricular catheter, narrowed lateral ventricles, and a blurred boundary between the cerebral cortex and white matter (Fig. 4). However, the patient died the following day.

Figure 2.

Day 6 of illness, worsening of acute hydrocephalus

Figure 3.

Day 10 of illness, further worsening of acute hydrocephalus

Figure 4.

Computed tomography on Day 12 of illness showing blurring of the cortical–white matter junction in the cerebral hemispheres

DISCUSSION

The incidence of acute hydrocephalus in bacterial meningitis is approximately 3%. Causative bacteria include E. coli, pneumococci, meningococci and Listeria monocytogenes ^[1–4]. Mortality is high in patients with bacterial meningitis-related hydrocephalus caused by cerebral herniation ^{[4, 5]}. Hydrocephalus in bacterial meningitis is usually non-obstructive and caused by impaired cerebrospinal fluid absorption through the arachnoid villi ^{[1, 4, 6, 7]}. However, obstructive hydrocephalus may occur if the inflammatory exudate obstructs the foramina of Luschka and Magendie; obstruction typically occurs after 2 weeks, when neutrophils begin to degenerate and fibroblasts proliferate in the exudate ^[6].

S. anginosus was detected in the patient’s blood and cerebrospinal fluid cultures. Moreover, there have been reports of invasive pyogenic infections caused by S. anginosus. Furthermore, patients who developed ventriculitis and multiple abscesses subsequent to meningitis caused by S. anginosus later died. However, to our knowledge, there have been no published case reports on bacterial meningitis complicated by hydrocephalus ^[8–10]. Hence, it remains unclear whether bacterial meningitis caused by S. anginosus predisposes to acute hydrocephalus.

In this case, no other infections were found besides the right infratemporal fossa abscess infection. Culture from the abscess detected Bacteroides, which was not thought to be related to the patient’s bacterial meningitis.

Old age is a risk factor for the development of hydrocephalus in the acute phase of bacterial meningitis ^[5]. Persistent intracranial hypertension in patients with bacterial meningitis with acute hydrocephalus may improve after external ventricular drainage ^[5]. On Day 6, the patient underwent a lumbar puncture due to worsening hydrocephalus but was uneventful. In retrospect, based on the patient’s advanced age, ineffectiveness of the multiple lumbar punctures, and presence of deposits in the lateral ventricular triangular pyramids on head CT, occluded hydrocephalus should have been the diagnosis considered, instead of non-occluded hydrocephalus. Decompression craniectomy may be an option when medical intracranial pressure treatment fails to improve intracranial hypertension ^{[11, 12]}.

CONCLUSION

In patients with meningitis-related hydrocephalus, worsening despite appropriate antibiotic administration, treatment may be complicated by ventriculitis and obstructive hydrocephalus, which can be fatal. If intracranial pressure is not medically controlled, bilateral decompression craniectomy should be considered as a potential management strategy.