An 86-year-old man was admitted to our hospital on Feb. 13, 2020 with the chief complaint of chills and fever during the past 13 h. His body temperature had been at the peak of 39.0°C. Apart from fatigue and weakness, he vomited bile-stained fluid. Medical history included well-controlled essential hypertension, stable coronary artery disease, and asymptomatic cholelithiasis. On admission, physical examination did not reveal any remarkable signs. His body temperature was 35.0°C, pulse rate 87 beats per minute, respiratory rate 21 breaths per minute, blood pressure 102/62 mmHg, and oxygen saturation 96%. Electrocardiogram showed sinus rhythm and normal ST segments. Laboratory tests demonstrated that the serum amylase, lipase, and urinary amylase were all within the reference ranges, but the inflammatory parameters increased and the platelet count decreased (102×103/μL). In addition, mild transaminitis and acute kidney injury were present (). Conventional chest CT, which covered part of the epigastrium, reported not only chronic inflammation in both lungs, but intrahepatic gas and cholecystolithiasis. The gas was perplexing, because it was hard to tell whether it was in the intrahepatic bile ducts or in the portal venous system. Anyway, all the rapid changes indicated a severe infection. The patient was managed empirically with intravenous moxifloxacin, a fluoroquinolone antibiotic, but his condition deteriorated 8 h after admission. Fever recurred with chills. The temperature increased to 38.8°C. Venous blood was drawn immediately for germiculture and antibiotic susceptibility test. Then, he started to show unbearable headache and abdominal distension, neck stiffness, and Kernig's and Brudzinski's sign. No tenderness was detected in the abdomen. The platelets dropped abruptly to 46×103/μL in 24 h and to 27×103/μL in 48 h. D-dimer was >20 mg/L. Blood culture for 12 h was astonishingly positive for Gram-negative bacilli, and then E. coli was identified. Contrast-enhanced abdomen CT (, ) was conducted on hospital day 2. The image of thrombosis with diffuse gas was demonstrated in the superior mesenteric and portal veins, which suggested a hypercoagulable state of DIC caused by E. coli bacteremia. Abdominal ultrasonography revealed a normal gallbladder wall and common bile duct, but a mural thrombus in the main portal vein. A trace-back inquiry revealed that the patient had eaten cooked oysters and spat out debris of the shells prior to becoming ill. It was speculated that the debris from oyster shell might have injured his intestinal mucosa and resulted in systemic inflammation and bacterial embolus. However, the most worrying point was what actually caused the neurological anomaly: purulent meningitis or cerebral hemorrhage? For the time being, the patient was in the hypercoagulable state of DIC, which was manifested as diffuse venous thrombosis. Meanwhile, he got caught in a consumed hypocoagulable stage with an apparent drop of platelets. Hence, intracranial hemorrhage was strongly suspected. Unfractionated heparin was intended to be attempted but was abandoned because of the uncertainty of cerebral condition. Nevertheless, antibiotic regimen was switched to cefoperazone/sulbactam and then imipenem/cilastatin upon results of pathogenic culture and susceptibility test, which showed that the strains of E. coli were most susceptible to these antibiotic agents. Levornidazole was added later to reinforce the antimicrobial therapy. Human immunoglobulin, fresh plasma, recombinant human thrombopoietin, and platelets were administered as well. However, the headache was getting even worse. It was urgent to identify the cause of the encephalopathy. On hospital day 5, a stratification of cerebrospinal fluid (CSF) in the lateral ventricles was suspected on brain magnetic resonance imaging. The substratum had the feature of high signal on T1WI, which implied SAH. Lumbar puncture yielded bloody CSF with an opening pressure of 200 mmH2O. Hemophagocytosis was observed, but CSF culture was negative for any bacteria. These results ruled out purulent meningitis and confirmed the presence of SAH. Corticosteroids, diuretics, and mannitol were used to lower the elevated intracranial pressure and prevent cerebral edema. On the very night, the patient experienced a grand mal epilepsy lasting for about 10 min. Phenobarbital sodium was injected intramuscularly, and valproate sodium and levetiracetam were taken orally. The temperature began to drop since the adjustment of antibiotics based on culture result, and the inflammatory parameters declined as well. Although persistent, the headache did not aggravate. Neither chills nor epileptic seizure happened again. It looked like the patient was on the mend, but 10 days after admission, his abdominal discomfort became the dominant symptom. He was anorexic, and complained of abdominal distension. He defecated only once on hospital day 3, and passed less flatus since then. Therefore, adynamic ileus was considered. Meanwhile, the laboratory parameters got worse again. WBC was 14.08×103/μL with 88.6% neutrophilia. Among the hepatic biomarkers, bilirubins were moderately compromised, and gamma-glutamyl transferase (GGT) increased to 398 U/L. Abdominal ultrasonography discovered extension of thrombus from the main portal vein to its branches. Contrast-enhanced abdomen CT was repeated. It showed that the thrombosis in superior mesenteric and portal veins enlarged distinctly, and the left branch of portal vein was completely obstructed, which was speculated to be responsible for above symptoms and aberrant laboratory findings (, ). Brain CT demonstrated SAH in the right and left parietal and occipital lobes (). The patient was caught between Scylla and Charybdis. If the thrombosis had not been treated, liver failure and intestinal necrosis would have been resulted from persistent ischemia. But if anticoagulants had been delivered, SAH might have been exacerbated and threatened his life. We weighted the dilemma carefully. Because the SAH was thought to be diffuse oozing of blood resulting from thrombocytopenia, and the platelet count had recovered to 321×103/μL by now, we decided to try low molecular weight heparin (LMWH) under close monitoring. Enoxaparin was started subcutaneously from a daily small dose of 2000 u. To our surprise, the symptoms and signs of adynamic ileus began to subside on the next day. Enoxaparin was supposed to bring about the improvement. Then it was up-titrated gradually to 3000 u on the 4th day and to 6,000 u on the 6th day. Abdominal ultrasonography detected blood flow in main portal vein, but not in the sagittal part of left portal vein. CT was repeated after 10 days of anticoagulation. In comparison with previous findings, not only thrombosis in the superior mesenteric and portal veins diminished (, ), but SAH in both sides was absorbed (). Enoxaparin had been kept in use for 18 days, and then was replaced by oral rivaroxaban. It seemed that the patient's condition was getting better, however, the adventure was not over yet. When he woke up in the morning of hospital day 19, he felt pain in both wrists, and then fell into a sudden onset of chills with the temperature rising to 38.7°C. Physical examination detected symmetrical redness, swelling, and heat on his wrists. It was considered as reactive arthritis, although his human leukocyte antigen (HLA)-B27 allele was negative. Methylprednisolone and celecoxib were prescribed. This syndrome took a favorable turn on the next day. After 33-day hospitalization, the patient's condition was greatly improved. Most laboratory abnormalities were normalized (). He was discharged on March 16, 2020. shows the timeline for events and interventions during hospital stay. During the hospitalization, the patient's body weight reduced from 65 to 57 kg. He did not experience a septic shock or fluid depletion. His lowest mean arterial pressure was 72 mmHg, 24-h fluid input was 3,000–4,000 ml, and the urine output was 0.91–3.11 ml/kg/h. Renal function was assessed by estimated glomerular filtration rate (eGFR), which was calculated according to Creatinine-Cystatin C Equation (CKD-EPI 2012) (). It was improved from 44 ml/min/1.73 m2 at admission to 70 ml/min/1.73 m2 at discharge.