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Irreversible Cranial Nerve Palsies After Resolution of Pneumonia: Clue to Missed Meningitis
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A6872 - Irreversible Cranial Nerve Palsies After Resolution of Pneumonia: Clue to Missed Meningitis
Author Block: L. Yadav1, K. Kailasam2, W. Nichols3; 1Internal Medicine, WMU School of Medicine, Kalamazoo, MI, United States, 2WMU School of Medicine, Kalamazoo, MI, United States, 3Internal Medicine, Bronson Methodist Hospital, Kalamazoo, MI, United States.
Neurologic complications are common in adults with bacterial meningitis. In a review of 493 cases of bacterial meningitis in adults, 28 percent of community-acquired cases resulted in one or more neurologic complications. In a review of 279 cases of community-acquired bacterial meningitis in adults, 4 percent had cranial nerve palsy as the only focal neurologic finding.
A 63 year old previously healthy woman was found to be minimally responsive at home following a week of upper respiratory illness. She was hypoxic and altered but hemodynamically stable when she was brought to the emergency department of an outlying hospital. Endotracheal intubation was performed. CT chest with contrast was negative for pulmonary embolism but showed consolidation in the right upper lobe. CT brain was normal. She was transferred to our ICU and treated with IV Vancomycin and Zosyn followed by Rocephin 1g daily for bacterial pneumonia. MRI brain revealed mild ventriculomegaly. She was successfully extubated on day 4. At that time, she was oriented but found to have left sided facial droop and bilateral hearing loss. MRI brain was repeated which showed normalization of ventricular volume, restricted diffusion within lateral ventricles and edema, and mild enhancement of bilateral VII and VIII cranial nerve complexes. A lumbar puncture was performed and cerebrospinal fluid (CSF) showed glucose 39, protein 104, WBC 57. CSF viral and bacterial serologies, cultures, and autoimmune meningoencephalitis panel were negative. The microbiology lab at the outlying hospital called to report that the first blood culture grew Streptococcus pneumoniae. Cultures drawn at our ICU were all negative. Rocephin dose was increased for CSF penetration. Confusion resolved completely but other deficits remained at the time of discharge.
It is clear that patient had initially presented with pneumococcal meningitis and pneumonia with bacteremia. Inadequate treatment of CNS infection resulted in palsies of cranial nerves VII and VIII. The rate of focal deficits is significantly higher in adults with pneumococcal meningitis than with other pathogens. Early recognition and appropriate treatment of bacterial meningitis is important to prevent debilitating and sometimes irreversible neurological consequences.
Author Block: L. Yadav1, K. Kailasam2, W. Nichols3; 1Internal Medicine, WMU School of Medicine, Kalamazoo, MI, United States, 2WMU School of Medicine, Kalamazoo, MI, United States, 3Internal Medicine, Bronson Methodist Hospital, Kalamazoo, MI, United States.
Neurologic complications are common in adults with bacterial meningitis. In a review of 493 cases of bacterial meningitis in adults, 28 percent of community-acquired cases resulted in one or more neurologic complications. In a review of 279 cases of community-acquired bacterial meningitis in adults, 4 percent had cranial nerve palsy as the only focal neurologic finding.
A 63 year old previously healthy woman was found to be minimally responsive at home following a week of upper respiratory illness. She was hypoxic and altered but hemodynamically stable when she was brought to the emergency department of an outlying hospital. Endotracheal intubation was performed. CT chest with contrast was negative for pulmonary embolism but showed consolidation in the right upper lobe. CT brain was normal. She was transferred to our ICU and treated with IV Vancomycin and Zosyn followed by Rocephin 1g daily for bacterial pneumonia. MRI brain revealed mild ventriculomegaly. She was successfully extubated on day 4. At that time, she was oriented but found to have left sided facial droop and bilateral hearing loss. MRI brain was repeated which showed normalization of ventricular volume, restricted diffusion within lateral ventricles and edema, and mild enhancement of bilateral VII and VIII cranial nerve complexes. A lumbar puncture was performed and cerebrospinal fluid (CSF) showed glucose 39, protein 104, WBC 57. CSF viral and bacterial serologies, cultures, and autoimmune meningoencephalitis panel were negative. The microbiology lab at the outlying hospital called to report that the first blood culture grew Streptococcus pneumoniae. Cultures drawn at our ICU were all negative. Rocephin dose was increased for CSF penetration. Confusion resolved completely but other deficits remained at the time of discharge.
It is clear that patient had initially presented with pneumococcal meningitis and pneumonia with bacteremia. Inadequate treatment of CNS infection resulted in palsies of cranial nerves VII and VIII. The rate of focal deficits is significantly higher in adults with pneumococcal meningitis than with other pathogens. Early recognition and appropriate treatment of bacterial meningitis is important to prevent debilitating and sometimes irreversible neurological consequences.
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