Case of the Month Discussion
While in the ED the patient became febrile to 102.7 and received decadron 10mg IV followed by empiric IV antibiotics: ceftriaxone 2 grams and vancomycin 1 gram for presumed bacterial meningitis. He became prgoressively confused, disoriented and agitated. He began to desaturate and was emergently intubated with etomidate 20 mg iv followed by succinylcholine 100mg Iv. .
A lumbar puncture was performed which showed the following:
LP:
Opening Pressure 35.
Tube 1:
rbc-1420, wbc-250
Tube 4:
rbc-200, wbc-1280 (59%segs, 30% lymphs, 3%eos, 3%monos)
Tot protein-137,
glucose-133
India Ink neg
Gram Stain:
gram pos cocci pairs/chains, few polys, rare wbc’s.
Final
Culture: Streptococcus pneumoniae sensitive to ceftriaxone,penicillin,rifampin.
The patient was admitted to the ICU.
Upon arrival to the ICU he had a generalized seizure which was succesfully treated with Ativan IV. He had a repeat brain CT at 8 hours which showed the following:
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CT reading: Acute hydrocephalus. Note the relative increase in size of the lateral ventricles from the previous brain CT as well as the loss of sulci.
Hospital Course: Neurosurgery was consulted and placed a ventriculostomy tube. ENT was consulted and performed a miringotomy to drain pus from the middle ear. Ear cultures were negative. The patient went into septic shock with hypotension and required pressors for blood pressure support . Antibiotics were changed to Amikacin, Vancomycin, and Merepenem. Dexamethasone was continued every 6 hours for 4 days. The ventriculostomy was removed on HD#4 and the patient self extubated himself on HD#5. The patient was transferred to the floor on HD#6 and continued on Merepenem for strep pneumonia meningitis and neurontin for seizure prophylaxis. His WBC count rose to 40.0 and he developed C difficile diarrhea and was subsequently started on flagyl. Within a week the patient was discharged from the hospital with no neurological sequela.
Discussion
Complications from otitis
media can be broken down into intra- and extracranial manifestations.
Extracranial complications are typically due to direct extension from the middle
ear and usually manifest as mastoiditis, postauricular abscess or chronic
supparative otitis media. Intracranial complications usually occur by
hematogenous spread and manifest as meningitis, brain abscess or sinus
thrombosis. The overall incidence of all complications of otitis media is
rare and has decreased significantly since the advent antibiotics.
In the preantibiotic era, complications from otitis media were as high as 50%.
In 1995,
Kangsanarak et al conducted a review of more than 24,000 patients with
otitis media and found an intracranial complication rate of 0.36%. In
another series by Gower, looking at over 300,000 patients admitted, only 100
suffered CNS complications of middle ear disease. Most complications
occurred in children and young adults less than 20 years old. Mortality
from intracranial complications was greater than 10% despite treatment.
Presentation: Meningitis can be broken down into acute (<24 hours duration), subacute (1-7days) and chronic (>7days). While subacute and chronic meningitis can have a myriad of diagnoses, acute meningitis is almost always bacterial in origin. The converse, however, is not always the case. About 75% of cases of bacterial meningitis present subacutely. Bacterial meningitis can present with fever, headache, neck stiffness, confusion, lethargy, and irritability . 25% of cases can begin with fulminant disease with high morbidity. As many as 40% of patients with meningitis were previously treated with antibiotics in which case a high index of suspicion has to be maintained despite a paucity of symptoms.
Incidence: 2-3 per 100,000.
Likely bacterial
pathogens differ amongst different age groups:
Neonates - Group B or D streptococci, nongroup B streptococci, Escherichia coli, and L monocytogenes
Infants and children - , S pneumoniae, N meningitidis and H influenzae
Adults - S pneumoniae, (30-50%), N meningitidis (10-35%), H influenzae (1-3%), gram-negative bacilli (1-10%), staphylococci (5-15%), streptococci (5%), and Listeria species (5%)
Findings: The classic
findings described for meningitis were Kernig's sign and Brudzinski's sign.
Kernig first described his sign in 1882. During Kernig’s examination, the
patient was seated upright with hips and knees flexed. Kernig would then attempt
to extend the patient’s knee. He noted that, in patients with meningitis, he was
unable to extend the knee beyond 135 degrees without causing pain.
Brudzinski was a polish physician of the early 20th century. The
Brudzinski sign is conducted as follows: With the patient supine, the
physician places one hand behind the patient’s head and places the other hand on
the patient’s chest. The physician then raises the patient’s head (with the hand
behind the head) while the hand on the chest restrains the patient and prevents
the patient from rising. Flexion of the patient’s lower extremities (hips and
knees) constitutes
a positive sign.
Thomas, et al. examined the diagnostic
accuracy of Kernig's and Brudzinski's signs in patients with documented
meningitis. Kernig's sign and Brudzinski's sign had very low sensitivity
for detection of the documented meningitis cases (5 percent each).
Treatment: Given the high prevalence of penicillin-resistant S.pneumoniae, treatment in adults consists of a third generation cephalosporin. There are now cephalosporin resistant strains of Pneumococcus developing and Vancomycin should be considered first line treatment as well. Treatment with antibiotics sterilizes the CSF within 24-48 hrs of treatment and as such, antibiotics should not be held in suspected cases for fear of sterilizing CSF cultures.
Prognosis: 20-30% mortality. Deafness occurs in 6-10% of survivors. 1-18% of people have other serious neurologic sequela.