Contributed by Suzanne Bakdash, MD, MPH, Marta Couce, MD, PhD, Larry Nichols,
MD & William Pasculle, ScD Published on line in May, 2003
Contributed by Suzanne Bakdash, MD, MPH, Marta Couce, MD, PhD, Larry Nichols,
MD & William Pasculle, ScD Published on line in May, 2003
PATIENT HISTORY:
The patient was a male in his 40s with a history of asthma, smoking and possible ethanol abuse, who was otherwise in good health and not on any medication. The patient suffered a traumatic injury to his head after falling down a flight of stairs, while under the influence of alcohol, on the evening of Day 1. It is unclear whether or not the patient suffered a loss of consciousness at that time; he went to bed and complained of a severe headache when awakened around noon the next day
CLINICAL COURSE:
The patient presented to the hospital on Day 2 with a chief complaint of headache. He denied having any nausea, vomiting, visual disturbance, neck or back pain, weakness, numbness, or paresthesias in his arms or legs, chest pain or shortness of breath. On examination, the patient was in no obvious distress, his vital signs were within normal limits and he did not have any obvious external signs of trauma to the head. The patient's pupils were equal and reactive; his cervical spine was non-tender to palpation. His lungs had a few scattered crackles at the bases.
An initial CT scan of the patient's head showed a small right-sided temporoparietal intraparenchymal hemorrhage. His glucose, hemoglobin, hematocrit, platelets, PT, PTT and INR were all within normal limits. The patient remained neurologically stable and was admitted with a diagnosis of intracranial hemorrhage.
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A CT scan of the head performed on Day 3 (Figures 1 & 2), showed a right temporal contusion, subarachnoid hemorrhage and an old left frontal traumatic injury. It also showed possible bilateral mastoiditis with fluid in both middle ears and scattered mastoid air cells, suggesting a possible temporal bone fracture. The patient remained alert and oriented with no focal neurological deficits. He was placed on phenytoin prophylaxis against seizures, and discharged home.
Two days later, on Day 5, the patient presented to an outside hospital with a headache. He described his pain as constant since his discharge two days earlier, worsening to the point of interfering with concentration, physical activity and sleep. The patient also reported feeling nauseated and weak. On exam, he was alert and oriented, but lethargic at times; his pupils were normally reactive. He had a nonproductive cough, with rhonchi in the right posterior lung base and scattered rales. The patient's temperature was 36.3°C, pulse 80 beats per minute, blood pressure (BP) 175/102 mmHg and respirations 20 per minute. The patient's temperature rose to 37.4°C and his skin became pale, moist and clammy; he was then transferred to our medical center for further evaluation.
Upon arrival at the emergency room, the patient was alert and oriented, complaining of headache but able to follow commands. He had no focal neurologic deficits; his pupils were equal and reactive and he was moving all extremities with 2+ reflexes. His neck was supple and tympanic membranes were clear bilaterally. The patient was afebrile, with a pulse of 72 bpm, BP of 150/94 mmHg and respiratory rate of 20. The lungs were clear to auscultation and a chest x-ray showed no abnormalities.
Laboratory results from Day 5 (Table 1) showed an elevated white blood cell count of 13,800 per cu mm (87% polymorphonuclear cells).
The patient was admitted at 7:30 PM on Day 5, after he started moaning and became agitated and uncooperative. He was given Ativan, phenytoin, folate and thiamine (due to concerns of possible ETOH withdrawal), but remained non-verbal and did not follow commands.
By 3:45 AM on Day 6, the patient had ceased to move his lower left extremity spontaneously and in response to stimuli; the movement of his right extremity was minimal. His pupils were fixed and non-reactive. A CT scan showed stable cortical hemorrhage in the right temporal lobe with no hydrocephalus or new areas of hemorrhage.
The patient's temperature rose to 40.5°C at around 5:30 AM on Day 6. His laboratory findings at that time (Table 2) included a white blood cell count of 10,900 per cu mm (60% polys, 28% bands with toxic granulations and Dohle bodies).
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An extraventricular drain was placed with drainage of 50 ml of purulent cerebrospinal fluid (CSF). Analysis of the CSF showed 2,680 leukocytes per cu mm (100% neutrophils), 1,900 erythrocytes/cu mm, a protein level of 761 mg/dL and a glucose level of < 20 mg/dL (see Discussion for comparison to normal CSF findings). A Gram stain of the CSF (Figures 3 & 4) showed red blood cells, many neutrophils and gram-positive cocci in pairs. The patient was diagnosed with acute bacterial meningitis and placed on vancomycin and cefepime. A stat electroencephalogram (EEG) showed no meaningful brain function on the right and hyperactive brain function on the left, with no evidence of seizure activity.
The patient did not show any improvement and soon lost his corneal reflexes. His blood pressure dropped shortly thereafter and his EEG became flat. His examination showed no evidence of meaningful neurologic activity and he was judged to have suffered brain death. The patient was pronounced dead at 10:30 AM on Day 6 after his initial fall.
CSF cultures later yielded heavy Streptococcus pneumoniae. Peripheral blood cultures taken on Day 6, postmortem blood and lung-tissue cultures were all subsequently reported positive for S. pneumoniae.
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