Clinical Reasoning: An Older Woman With Headaches and Lethargy After a Fall
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Abstract
In this case, a 77-year-old woman presented with generalized weakness, difficulty ambulating, lethargy, loss of appetite, and headaches after a mechanical fall. This case discusses the management of acute neurologic emergencies such as subdural hematoma, status epilepticus, and bacterial meningitis. Potential etiologies for stroke and CNS infection are highlighted. Readers are led through the diagnostic approach to a patient presenting with a complex array of neurologic symptoms causing rapid clinical decompensation.
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.
(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).
Questions for Consideration:
How would you manage the patient after the CT findings?
Should surgical evacuation be considered?
All patients with SDH should have a prompt evaluation of their airway, breathing, and circulation. In addition, any anticoagulation and antiplatelet agents should be reversed given the risk of hematoma expansion.1 Common surgical indications for SDH evacuation include clot thickness >10 mm, midline shift >5 mm, and intracranial pressure (ICP) exceeding 20 mm Hg.2 All patients with acute intracranial hemorrhage should be placed on basic measures to protect against elevated ICP and hematoma expansion, such as elevating the head of the bed to 30°, minimizing pain, maintaining normothermia, and decreasing the systolic blood pressure below 160 mm Hg. Furthermore, patients initially managed conservatively should have a repeat CT scan within 6 hours to assess for expansion.3
AP was admitted to the medicine service for evaluation of acute kidney injury and electrolyte abnormalities. The next day, she was febrile to 38.8°C and had multiple seizures described as left head tilt and left arm shaking followed by rigidity of the entire body. The convulsions lasted 10 minutes without return to baseline. She was intubated for airway protection in the setting of status epilepticus (SE).
Questions for Consideration:
How would you manage a patient in SE?
What other tests would you order once the patient is stabilized?
GO TO SECTION 2
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.
Questions for Consideration:
What etiologies would you consider to explain the new found stroke and vasospasm?
What empiric therapy if any should be considered?
What additional testing and information would you want?
GO TO SECTION 3
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.
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).
Questions for Consideration:
What are the possible etiologies for subdural empyema?
What other questions might you have about her history?
GO TO SECTION 4
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.
Discussion
Common etiologies for subdural empyema include head trauma with depressed skull fractures, cranial surgery, infected SDH, and improperly treated ear and sinus infections.6 Of these, sinonasal and otomastoid infections are the leading causes.7 For cases of subdural empyema secondary to paranasal sinusitis, the most common organism is Streptococcus milleri.6,7
S. intermedius is a member of the S. milleri group. While S. milleri are a part of the normal microbiota in many mucosal sites, they are also found in suppurative infections that include periodontal abscesses, intracranial abscesses, and infective endocarditis.8 S. intermedius bacteremia has been found in patients after dental work because it is part of the normal oral flora and may spread hematogenously with manipulation.9 Issa et al.10 showed that 18.8% of patients with S. intermedius infections experienced a recent dental manipulation. Of note, 98% of these infections were associated with abscess development, which were most commonly in the brain at 41.6%.10 Whiley et al.11 also showed a strong association between S. intermedius with infections involving the CNS. In May 2022, the Centers for Disease Control and Prevention identified 81 cases of pediatric brain abscess, epidural empyema, or subdural empyema with 41.6% of them identified as S. intermedius.12
It is probable that our patient with S. intermedius bacteremia after recent dental manipulation had bacterial hematogenous spread resulting in subdural empyema. Surgical evacuation and antibiotics are recommended for treatment, with the commonest agents being cefotaxime and metronidazole.13
In an older woman with a recent fall and subsequent subdural collection, SDH might be assumed. However, AP's fever and seizures prompted us to get further imaging and history. Clinicians must remain vigilant when managing a patient with a seemingly classic presentation and consider S. intermedius subdural empyema in patients with unexplained CNS collections after dental work.
Study Funding
No targeted funding reported.
Disclosure
The authors report no relevant disclosures. Go to Neurology.org/N for full disclosures.
Appendix Authors

Footnotes
Go to Neurology.org/N for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article.
Submitted and externally peer reviewed. The handling editor was Resident & Fellow Section Editor Whitley Aamodt, MD, MPH.
- Received April 4, 2023.
- Accepted in final form July 19, 2023.
- © 2023 American Academy of Neurology
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