A 38-year-old male presented to our emergency department after being found unresponsive by his roommate. The patient had been experiencing severe headaches with painful neck stiffness, fatigue, myalgia, loss of appetite, and significant weight loss over 1 month which he had attributed to COVID-19 infection despite a negative testing. The patient was febrile (38.3  C) with a stable blood pressure at the time of admission. On physical examination, weakness of the left upper and lower extremity (MRC grade 3/5) was observed. Cranial nerves and motor function on the right side were intact.
Routine bloodwork demonstrated a leukocytosis of 14.3x103 ul-1 (80 % neutrophils), elevated lactate level of 2.9 mmol l-1, erythrocyte sedimentation rate of 90 mm hr-1, C-reactive protein of 7.84 mg dl-1 and ALT/AST of 219/70 IU l-1. A sepsis protocol was initiated with fluid resuscitation and peripheral blood, urine, and cerebrospinal fluid (CSF) collection for the cultures. Broad spectrum intravenous antibiotics, vancomycin 1.5 g q8h and ceftriaxone 2 g q12h, as well as acyclovir 750 mg q8h were started for the empiric meningitis coverage and the patient was transferred under intensive care unit (ICU) care. Computed tomography (CT) of the head and magnetic resonance imaging (MRI) of the brain revealed a 2.5 cm in size, large cystic lesion located in the right anterior temporal lobe with surrounding oedema involving the anterior and mid temporal region, extending to the external capsule in its entirety and portions of the mid and posterior internal capsule, and a midline shift of 5 mm towards the left side. The cystic lesion demonstrated peripheral enhancement along with restricted diffusion on diffusion weighted imaging (DWI) suggesting a diagnosis of an abscess (Fig. 1a, b). Additional abscesses were also noted in the right temporal lobe, basal ganglia, and the internal capsule. Lumbar puncture and CSF analysis revealed a substantial pleocytosis of 375 ul-1 with 75 % polymorphonuclear leucocytes, low glucose (21 mg dl-1), and high protein levels (65 mg dl-1) suggestive of a pyogenic infective aetiology. However, the cultures from blood, urine, and CSF samples did not grow any organisms. HIV, HSV, acid-fast bacilli, Toxoplasma gondii,   Mycobacterium tuberculosis  , and fungal etiologies were ruled out.
The patient's clinical condition worsened despite broad spectrum antibiotics, and he developed a progressively altered mental status over the next couple days. Repeat CT imaging showed worsening cerebral oedema and the patient was taken for a right temporal craniotomy and abscess drainage. Histopathological examination revealed necrotic cells with inflammation suggesting a fibrinopurulent abscess with no evidence of tumour cells. Antibiotics were subsequently transitioned to intravenous (IV) metronidazole (750 mg q8h), ceftriaxone (2 g q12h) and vancomycin (1.5 mg q8h). The patient was also treated with a routine corticosteroid taper postoperatively (dexamethasone 4 g q12h for 3 days, 3 g q12h for 3 days, 2 g q12h for 3 days, 1 g q12h for 3 days, 1 mg q24h for 3 days).
After the surgical evacuation of the abscess, the patient responded well to the antibiotic treatment with improvement in his clinical examination and normalization of the leucocyte count (10.2x103 ul-1). Post-operative MRI on day 3 demonstrated an evacuation of the right temporal abscess with no foci of contrast enhancement. However, the vasogenic perilesional oedema was persistent. (Fig. 1c). The patient's neurologic examination remained similar, which may be attributed to the involvement of the basal ganglia and persistent right temporal oedema.
On the fourth post-operative day, the patient developed acute hyponatremia (129mEq l-1). Further work-up demonstrated an elevated urinary osmolality (753mOsm kg-1) and urinary sodium suggesting the diagnosis of SIADH. The CT of the head obtained at this time (post-operative day 6) demonstrated a new bony defect at the central skull base involving the anterior wall of the sella with herniation of its contents into the sphenoid sinus (Fig. 2). Next day, MRI to visualize the sella turcica was performed which demonstrated the herniation of an enlarged pituitary mass through a defect in the sellar floor with extension into the sphenoid sinus. The pituitary mass lesion showed heterogeneous signal on T1 and T2 weighted images and contrast enhancement in the gland suggesting infection with no identification of a drainable abscess (Fig. 2). The patient was fluid restricted with gradual improvement in his sodium levels to normonatremia.
Pathogens from the specimen were identified via matrix assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS), and Fusobacterium nucleatum, Corynebacterium striatum, Corynebacterium minutissimum, and Propionibacterium acnes were grown on culture for antibiotic susceptibility testing done on Etest.   Parvimonas micra   and   Prevotella   spp. did not grow on culture for antibiotic susceptibility testing. Antibiotic susceptibility testing guided the transition to a final regimen of IV penicillin G (4 million units q4h), oral metronidazole (750 mg q8h), and intravenous ceftriaxone (2 g q12h) for a 6 week course. Ceftriaxone was empirically prescribed before the pathogens were identified to cover Gram-negative bacteria. Furthermore, it was not discontinued in the final regimen since the infectious disease physicians were uncomfortable with the coverage by metronidazole and penicillin. Metronidazole, which was prescribed to cover   Fusobacterium nucleatum  , was shown to have a minimum inhibitory concentration (MIC) of 0.016. Penicillin, used to cover   Corynebacterium striatum  , Corynebacterium minutissimum, and Propionibacterium acnes, was shown to have a MIC of 0.064, 0.38, and 0.064, respectively. The patient continued to improve and was discharged with 3 months of antibiotics and a steroid taper. MRI at 6 month follow-up showed stable recovery from the procedure. Interestingly, pituitary enlargement seen previously was no longer visualized and the sella appeared grossly unremarkable (Fig. 3). Our patient was watched closely for presence of a potential CSF leak with consultation with the Otolaryngology department and the assessment showed no sign for CSF leak.