Clinical Reasoning: An Older Woman With Headaches and Lethargy After a Fall

Section 1

A 77-year-old woman, named AP, with a history of hypertension and hyperlipidemia presented with generalized weakness, difficulty ambulating, lethargy, loss of appetite, and headaches. She was in her usual state of health until 4 days before admission when she fell in her bathroom while attempting to sit. Her family brought her to the emergency department (ED) because of her evolving symptoms.

On arrival, AP was alert, oriented, and able to follow commands. Her neurologic examination showed intact cranial nerves, including a brisk and symmetric pupillary reflex, and intact motor strength and sensation in her extremities. She was hypertensive to 158/81 with all other vital signs stable and within normal limits. Her laboratory tests were significant for elevated white blood cell count of 17.9, a blood urea nitrogen of 40, and a creatinine of 1.84. As seen in Figure 1A, a CT head demonstrated a 9-mm subacute right isodense subdural collection with 4 mm of midline shift. Neurosurgery was consulted for subdural hematoma (SDH), and they recommended no acute neurosurgical intervention given the hematoma size and AP's intact neurologic examination.

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Figure 1 Axial CT Scans of the Head Without Contrast

(A) Initial CT head on presentation to the emergency department showing a 9-mm subacute right subdural collection (blue arrow) with 4 mm of midline shift. (B) Repeat CT head 24 hours later, fever and status epilepticus, showing enlargement of the right subdural collection to 11 mm (blue arrow) and increased midline shift and mass effect on the adjacent parenchyma. There is also increased hypoattenuation within the right parieto-occipital lobe suggesting an acute infarct (black arrow).

Section 2

The goals of managing SE include rapid cessation of the seizure and establishment of adequate airway, breathing, and circulation. First-line therapy is high-dose benzodiazepines; diazepam, lorazepam, or midazolam are most commonly used.⁴ Neurocritical Care Society guidelines recommend 4 mg of IV lorazepam or 10 mg of intramuscular midazolam (maximum benzodiazepine dose 0.1 mg/kg) as first-line therapy. If patients do not respond after 5–10 minutes, a second round of high-dose benzodiazepines is indicated in addition to a long-acting antiseizure medication.⁴ A recent randomized control trial showed no significant difference in efficacy of IV fosphenytoin, valproate, or levetiracetam in the treatment of convulsive SE.⁵ If the seizures continue, the patient should be intubated and started on an IV anesthetic such as midazolam, propofol, or pentobarbital.⁴

AP was given 2 mg of IV midazolam without clinical improvement. She was then was given 4 mg more of midazolam and intubated. After intubation, AP was loaded with brivaracetam 400 mg and sedated with propofol, after which time her seizures aborted, and she was transferred to the Neuro-ICU.

Blood glucose fingerstick was unremarkable, and a full set of laboratories including blood cultures and urine cultures were sent. After the airway was secured, the patient was sent for stat CT head and CT angiogram (CTA) of the head and neck. The CT head showed an enlarging subdural collection, now measuring 11 mm with increased midline shift and mass effect (Figure 1B). There was also an increased hypoattenuation within the right parieto-occipital lobe suggestive of an acute infarct. The CTA showed vasospasm of the middle cerebral arteries. After emergency head imaging, she was connected to continuous video EEG because of persistently poor neurologic examination. The EEG showed diffuse slowing and right hemisphere–lateralized periodic discharges without seizures.

Section 3

After reviewing the CT, one could consider the patient's clinical decompensation to be secondary to an expanding SDH in the setting of new ischemic strokes. However, the presence of an enlarging subdural collection in the absence of acute blood on imaging makes this less likely. Given the patient's decompensation, recent fever, and expanding collection on CT imaging, there was a greater concern for subdural empyema and bacterial endocarditis. Of note, vasospasm, though traditionally seen in the context of an aneurysmal subarachnoid hemorrhage, can also occur in the setting of bacterial meningitis, thus further suggesting that AP was suffering from a CNS infection.

AP was started on vancomycin and ceftriaxone to cover for gram-positive skin and mouth flora such as streptococcus and methicillin-resistant staphylococcus aureus, in addition to common gram-negative organisms. Blood cultures came back positive for Streptococcus intermedius in 2 bottles. Off sedation, AP opened her eyes to noxious stimulation, did not follow commands nor track, had intact cranial nerves, withdrew to noxious in her right arm and leg, and had minimal movement on the left side of her body.

After EEG confirmed no seizures, AP underwent an emergent MRI brain to better delineate the etiology of her CNS lesions. The MRI brain, as seen in Figure 2, showed an extensive right hemispheric multiloculated subdural empyema extending over the right hemisphere. The collection tracked along the inferior temporal lobe and into the subdural space causing mass effect on the right dorsal midbrain. Diffuse leptomeningeal enhancement and cerebral edema with diffusion restriction in the right parietal-occipital lobe was suggestive of meningitis and cerebritis. Thus, the patient's hypodensity on CTH, believed to be an infarct, was likely secondary to infectious embolic particulate. Neurosurgery performed a right craniotomy and subdural evacuation which improved the mass effect and midline shift. Intraoperative cultures grew S. intermedius.

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Figure 2 Initial MRI Brain

MRI brain shows an extensive right hemispheric, multiloculated restricting and enhancing subdural fluid collection tracking along the right frontal and inferior temporal lobe and extending into the subdural space (red arrows). There is increased intensity in the subarachnoid space consistent with meningitis and cortical edema in the right posterior parieto-occipital lobe suggesting cerebritis (green arrowheads).

Section 4

AP's bacteremia in the setting of stroke or intracranial hemorrhage was concerning for infective endocarditis. Infectious disease was consulted to assist with antibiotic recommendations and workup of her bacteremia. The blood cultures rapidly cleared with initiation of antibiotics, making an endovascular infection unlikely. Transthoracic and transesophageal echocardiograms showed no cardiac valve vegetations.

On further discussion with the patient's family, they revealed that 10 days before her presentation, AP had right facial swelling after placement of prosthetic teeth. Oral and maxillofacial surgery was consulted and described purulence over the right mandible, although a maxillofacial CT with contrast did not reveal an odontogenic abscess.

AP's neurologic examination remained at a Glasgow Coma Scale of 6 in the weeks after her surgery; thus, she required a tracheostomy and percutaneous endoscopic gastrostomy tube placement. She was continued on ceftriaxone for 8 weeks postoperatively and discharged to a long-term acute care hospital where she died 1 month later.