What are the possible complications of Haemophilus influenzae type b (Hib) meningitis?

Updated: Jul 09, 2018
  • Author: Prateek Lohia, MD, MHA; Chief Editor: Niranjan N Singh, MBBS, MD, DM, FAHS, FAANEM  more...
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Answer

Acute complications of Hib meningitis are as follows:

  • Persistent fever

  • Recurrence of fever after an afebrile interval (termed secondary fevers)

  • Increased ICP

  • Prolonged obtundation or coma

  • Development of focal neurologic signs

  • Development or recurrence of seizures

Repeat blood cultures or lumbar puncture or other testing may be indicated in patients who develop these complications. However, lumbar puncture may sometimes be contraindicated or must be deferred until after brain imaging is performed.

Prolonged primary fevers are found in about 10-15% of all Hib meningitis cases and necessitate reconsideration of the antibiotic regimen. Additional considerations include the exclusion of pneumonia, urinary tract infection, intravenous line sepsis, or the development of subdural effusions or empyema. [20] The differential diagnosis should also be revisited; for example, the patient may have a brain abscess rather than meningitis.

Subdural effusions may develop in as many as half of all cases of Hib meningitis, but few are clinically significant. They are the putative cause of approximately 25% of all instances of prolonged primary fevers after initiation of appropriate antibiotic therapy in Hib meningitis. Along with nosocomial infections (eg, intravenous line infections), infected subdural effusions are the most commonly identified causes for secondary fevers.

Prolonged coma or progressive deterioration in function raises the possibility of increased ICP. The presence of bulging fontanelle, papilledema, sunsetting or convergence of the eyes, pupillary dilatation, Cushing reflex, or other brainstem signs of herniation suggests potential elevation of ICP, which may be due to brain edema or hydrocephalus.

Brain edema may develop because of hypoxia, ischemia, hypoglycemia, prolonged seizures, inflammatory vasculitis, or other derangements of brain during the initial or subsequent stages of fulminant Hib meningitis. It may also result from brain infarction or from the development of either communicating or noncommunicating hydrocephalus. Management of brain edema entails careful attention to metabolic parameters and avoidance of excessive hypotonic fluids. On the other hand, sufficient fluids must be provided to maintain cerebral perfusion.

Management of this combination of cytotoxic and vasogenic edema by hyperventilation and administration of mannitol is a complex subject, the review of which falls beyond the scope of this article. Suffice it to say that generalizations accepted several years ago concerning the potential efficacy of hyperventilation to achieve carbon dioxide concentrations in the range of 25-30 mm Hg are no longer widely accepted and that evidence suggests such manipulations may be deleterious. Mannitol, in some instances, may prove useful if used over a short term.

Hydrocephalus of either the communicating or the noncommunicating variety responds to interventions much more reliably than brain edema does. Urgent consultation with a neurosurgeon is indicated for the alleviation of pressure. If communicating hydrocephalus develops in Hib meningitis, it is probably because inflammatory exudate across the vertices impaired the resorptive function of arachnoid granulations. Noncommunicating hydrocephalus usually develops because of exudative blockage of the foramina of Magendie and Luschka.

Focal deficits or seizures can be the result of focal processes that should be identified by computed tomography (CT) of the brain. Brain edema or hydrocephalus may produce focal brainstem signs through compression or herniation. Subdural effusions or empyemas may grow large enough to compress the cortex and produce hemiparesis. Other processes that may be identified include cerebral infarctions, cerebritis, or brain abscess. Generally speaking, magnetic resonance imaging (MRI) is far superior to CT scanning in identifying these processes.


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