A 68-year-old man with a past medical history of type 2 diabetes mellitus and deep vein thrombosis, who had refused medical treatment for personal reasons for one year, presented at the emergency department after two weeks of general weakness. The patient had been in his usual state of health until the day before the current evaluation. He is a smoker but rarely drinks alcohol and does not use illicit drugs. On presentation, his initial vital signs included a body temperature of 39.4°C, heart rate of 118 beats per minute, respiratory rate of 22 breaths per minute, blood pressure of 88/53 mmHg, and oxygen saturation of 96% on ambient air. On physical examination, he appeared to be normal waking, uncomfortable, and diaphoretic, with dry mucous membranes, warm extremities, and mild tenderness on palpation of his upper abdomen.
Septic shock was first suspected. The complete blood count demonstrated leukocytosis with a white blood cell count(WBC) of 12.95 × 103/uL, neutrophil predominance of 77.4% segments and 10.4% bands, and thrombocytopenia indicated by a platelet count of 26 × 103/uL without evidence of anemia. Laboratory analysis also revealed an alanine transaminase level of 103 IU/L, creatinine of 1.60 mg/dL, glucose of 496 mg/dL, and C-reactive protein of 24.016 mg/dL. Venous blood gas results were as follows: pH of 7.363, PaCO2 of 26.4 mmHg, PaO2 of 30.8 mmHg, HCO3 of 14.7 mmol/L, and ketone of 5.6 mmol/L. Blood osmolality was 288 mOsm/kg. The coagulation profile showed a prothrombin time of 12.6 s, an international normalized ratio of 1.13, and an activated partial thromboplastin time of 31.3 s. Urinalysis showed 6–10 red blood cells and 6–10 white blood cells per high-powered field with positive leukocyte esterase and ketone body. Peripheral blood cultures were collected twice from separate sites. Suspecting septic shock and diabetic ketoacidosis, we prescribed broad-spectrum empiric antibiotics with Flomoxef and continuous intravenous insulin infusion.
A contrast-enhanced abdominal computerized tomography (CT) scan showed a lobulated hypodense mass (93 × 53 × 48 mm) with hypoenhancement and some internal eccentric liquefied areas at S7, S8, and S5 of the liver, where thrombosis of the anterior superior branch of the intrahepatic portal vein was noted, which suggested a possible liver abscess (Fig. 1). After the patient received medical care for about six hours at our emergency department, sudden disturbed consciousness was noticed by the family with presentation of conjugate eye deviation to the left and severe left-sided hemiparesis (muscle strength grading of 1/5). The patient could withdraw his right arm and right leg in response to pain, and a jerking motion of the head was noted. The pupils were 2.5 mm, symmetrical, and reactive to light. The score on the Glasgow Coma Scale was 6 (E1M4V1, with lower scores indicating greater alteration of consciousness).
A differential diagnosis of septic cerebral emboli resulting in ischemic stroke was first considered. CT angiography of the cerebral arteries showed cerebrovascular atherosclerosis without obvious vessel occlusion or thrombosis. The patient underwent a lumbar puncture to rule out meningitis. The cerebrospinal fluid (CSF) appeared yellow and turbid. CSF analysis revealed a WBC count of 4141 cells/µL, with 87% neutrophils and 3% lymphocytes, protein level of 414 mg/dL, and glucose level of 59 mg/dL. Puncture examination showed that the opening pressure was 50 cm H2O. The lumbar puncture result was consistent with bacterial meningitis. CSF was submitted for Gram staining and bacterial culture. The patient was preliminarily diagnosed with a primary liver abscess and meningitis. Owing to his severely impaired consciousness and critical illness, he received endotracheal intubation and was admitted to the intensive care unit for further medical treatment. Antibiotic therapy was escalated to Doripenem 1000 mg intravenously every 12 hours on the recommendation of the infectious disease specialist. Two sets of blood culture were reported as K. pneumoniae. Urine cultures also revealed K. pneumoniae. Culture from CSF was negative. Nucleic acid amplification testing for herpes simplex virus type 1 and type 2 DNA was negative, and Gram staining revealed no organisms. No acid-fast bacilli were observed on a mycobacterial smear, and no fungi were seen on examination of a fungal wet preparation. Tests of CSF for cryptococcal antigen, Streptococcus pneumoniae antigen, and meningococcal antigen were negative.
The patient’s condition gradually stabilized under intensive treatment. On the sixth hospital day, he fully recovered consciousness. He was successfully extubated and transferred to a general ward on the 10th day. A brain magnetic resonance imaging scan with contrast was performed after extubation. The report showed one 0.4-cm nodular enhancement in the left higher frontal lobe, without an increase in the diffusion-weighted image; microabscess was thus suspected (Fig. 2). Despite no visual complaint by the patient, we consulted an ophthalmologist to detect intraocular diseases and exclude endophthalmitis, which was confirmed by funduscopic examination. Cardiac sonography revealed normal contractility without vegetation. The patient unexpectedly became infected with SARS-CoV-2 virus on day 25. He was then transferred to a negative pressure isolation ward for further antibiotic treatment. After six weeks of antibiotic treatment, he was successfully discharged directly from the isolation ward. No focal neurological deficit was observed.