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Bacterial Meningitis and Neurological Complications in Adults

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Bacterial Meningitis and Neurological Complications in Adults OCUSED EVIEW Parunyou J. et al. Bacterial meningitis F R Bacterial meningitis and neurological complications in adults Parunyou Julayanont MD, Doungporn Ruthirago MD, John C. DeToledo MD ABSTRACT Bacterial meningitis is a leading cause of death from infectious disease worldwide. The neurological complications secondary to bacterial meningitis contribute to the high mortality rate and to disability among the survivors. Cerebrovascular complications, including infarc- tion and hemorrhage, are common. Inflammation and increased pressure in the subarach- noid space result in cranial neuropathy. Seizures occur in either the acute or delayed phase after the infection and require early detection and treatment. Spreading of infection to other intracranial structures, including the subdural space, brain parenchyma, and ventricles, in- creases morbidity and mortality in survivors. Infection can also spread to the spinal canal causing spinal cord abscess, epidural abscess, polyradiculitis, and spinal cord infarction secondary to vasculitis of the spinal artery. Hypothalamic-pituitary dysfunction is also an un- common complication after bacterial meningitis. Damage to cerebral structures contributes to cognitive and neuropsychiatric problems. Being aware of these complications leads to early detection and treatment and improves mortality and outcomes in patients with bacte- rial meningitis. Key words: meningitis; meningitis, bacterial; central nervous system bacterial infection; nervous system diseases INTRODUCTION prove recovery and outcomes. Bacterial meningitis is a leading cause of death In this article, we present a case of bacterial men- from infectious disease worldwide. Despite the avail- ingitis complicated by an unusual number of neuro- ability of increasingly effective antibiotics and inten- logical complications that occurred in spite of a timely sive neurological care, the overall mortality remains diagnosis, adequate treatment, and intensive neuro- high, with 17-34% of the survivors having unfavorable logical monitoring. We also review various neurologi- outcomes.1,2,3 Neurological complications associated cal complications of bacterial meningitis in adults with with bacterial meningitis are major contributing fac- emphasis on the incidence, clinical characteristics, tors to this high disability and mortality among survi- pathophysiology, and treatment. vors. Being aware of these potential complications leads to early detection and treatment and may im- CASE A 45-year-old man with rheumatoid arthritis and Corresponding author: Parunyou Julayanont, MD chronic hepatitis C infection presented with a two day Contact Information: [email protected] history of low grade fever and confusion and required DOI: 10.12746/swrccc 2016.0414.182 intubation. He had been recently treated for sinusitis The Southwest Respiratory and Critical Care Chronicles 2016;4(14) 5 Parunyou J. et al. Bacterial meningitis with five days of amoxicillin-clavulanate. Head com- diffuse irregularity of the intracranial arteries consis- puted tomography (CT) without contrast on admis- tent with a diffuse intracranial vasculitis. sion showed the subarachnoid hemorrhage (SAH) in the fronto-parieto-temporal convexities and Sylvi- Over the next six weeks his condition improved an fissures bilaterally. He also had opacification of significantly, and he was discharged to an inpatient the maxillary and sphenoid sinuses. Computed to- rehabilitation facility with a modified Rankin Scale of mography angiography showed no aneurysm or any 4. He could not remember events during his hospi- other explanation for the subarachnoid hemorrhage. talization. Three months later, he had some recovery A lumbar puncture showed yellowish cerebrospinal with a modified Rankin Scale of 3 and a Barthel index fluid (CSF) with 4,352 WBCs (neutrophils 87%, lym- of 55/100. phocytes 2%, and monocytes 11%) and 1,707 RBCs with positive xanthochromia. The opening pressure DISCUSSION was 58 cmH2O, protein was 442 mg/dL, and glucose was 3 mg/dL. Cerebral spinal fluid gram stain and cul- EREBROVASCULAR COMPLICATIONS ture, S. pneumoniae, H. influenzae, N. meningitides C antigen panel, cryptococcal antigen, beta D-glucan, Ischemic and hemorrhagic strokes are common fungal and mycobacterial cultures, and herpes sim- complications of bacterial meningitis. These compli- plex virus-1,2 DNA were all negative. The patient was cations are reported in 14-37% of patients and are empirically started on high dose ceftriaxone and van- associated with poor neurological outcomes and in- comycin. Pus cultured from the left maxillary and eth- creased mortality.4,5,6,7,8 Cerebrovascular complica- moid sinuses showed skin flora. Magnetic resonance tions can occur at the onset of the infection, during imaging (MRI) of the head with gadolinium showed hospitalization, or weeks after successful treat- scattered leptomeningeal enhancement with residual ment.4,7,9 SAH. His level of consciousness markedly improved, and he was extubated after seven days of antibiotics. Arterial infarction One week after extubation, the patient had an Arterial infarction (Figure 1) occurs in 8-25% of acute change in mental status. A repeat MRI showed bacterial meningitis cases and accounts for 70-85% hydrocephalus, obstruction of the cerebral aqueduct, of all cerebrovascular events.4,5,6,7,10 Even though and intraventricular empyema of the occipital horns of ischemic events tend to occur early in the course of the lateral ventricles. It also showed a subdural em- disease (1-2 weeks), ischemic stroke or vasculopa- pyema in the posterior fossa. He underwent posterior thy may develop months after successful treatment or craniotomy with right occipital ventriculostomy. Intra- recovery.9,11,12 In 1,032 meningitis episodes, delayed operatively, large amounts of pus were drained from cerebral thrombosis defined as initial recovery with the posterior fossa. No organisms grew from this cul- sudden deterioration after the first week of admission ture. He had an MRI of the whole spine performed caused by cerebral infarction occurred in 11 patients due to persistent leukocytosis and back pain. The (1.1%).13 The outcome of patients with delayed cere- MRI showed an epidural abscess extending from T9 bral thrombosis is very poor.13,14 to the thecal sac. Three milliliters of pus was aspirat- ed from the epidural space between L1 and L2 level. A reduced level of consciousness at admission, the No organism was found in the epidural pus. presence of seizures, low CSF white cell counts, and high ESR are predictors of infarction or cerebral arteri- A follow up head MRI showed new areas of isch- al narrowing.5,7,15 The posterior circulation is less com- emic infarction at right medial pons, left capsulotha- monly affected than anterior circulation, and strokes lamic area, right-sided splenium of corpus callosum, in this region are better tolerated clinically than in the and mesial temporal areas bilaterally. A magnetic anterior circulation.16,17 The middle cerebral artery is resonance angiogram of the head and neck showed the most commonly affected artery in bacterial men- 6 The Southwest Respiratory and Critical Care Chronicles 2016;4(14) Parunyou J. et al. Bacterial meningitis ingitis-induced cerebral infarction.4 cranial stenosis of the middle and anterior cerebral arteries was detected by transcranial Doppler sono- Cerebral angiography typically shows vascular grams (TCD) in 50 % of patients within day 3-5 of changes in various segments of the arteries. Small onset of the disease.17 Some studies have demon- vessel involvement may result in loss of arterial au- strated an association between the arterial narrowing toregulation demonstrated angiographically by focal detected by the bedside TCD and increased risk of abnormal parenchymal blush associated with hyper- stroke.8,18 perfusion.6 In a series of 35 patients, transient intra- Figure 1. New infarction at the right medial pons (a1, a2), the left capsu- lothalamic area (b1, b2), the right-sided splenium of corpus callosum (c1, c2) and the bilateral me- sial temporal areas (d1, d2) shown by FLAIR (top row) and DWI (middle row) (day 30 after admis- sion); The MRI on the day of admission showed no infarction at these ar- eas (a3,b3,c3,d3; bottom row) The inflammatory process in the subarachnoid eventually cause vascular stenosis.19 The activation space may have a primary role in causing vasculitis, of coagulation and attenuation of fibrinolysis in the vasospasm, and localized or diffuse thrombosis of the CSF may also contribute to the cerebral infarction.21 vessels (Figure 2).7,19,20 Three phases of meningitis-in- Post-infectious processes may trigger autoimmunity duced cerebral angiopathy are recognized. The ini- to the cerebral vessels and cause late onset vascu- tial phase is the presence of vasospasm triggered by lopathy. the surrounding purulent material in the subarachnoid space and Virchow Robin spaces. This is followed The role of antithrombotic or thrombolysis in the by myonecrosis of the vessel wall that subsequently treatment of arterial ischemia associated with bacteri- results in vasodilatation. In the final phase, suben- al meningitis is unclear. Delayed vasculopathy is rare, dothelial edema and proliferation of smooth muscle and there are no systematic studies on how to best The Southwest Respiratory and Critical Care Chronicles 2016;4(14) 7 Parunyou J. et al. Bacterial meningitis treat this complication. Immunosuppressive therapy Based on limited information, heparin should be start- was
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