The patient reported seven days of fever, upper abdominal pain and bilateral lower-limb pain when he arrived at the medical ward. He also had yellow-red discoloration of the sclera, dark urine, pale stools and generalized itching. His history included a 10-pack-year smoking history and reported consumption of one or two alcoholic drinks per day for five to seven years, although he had been abstinent for five months and could not recall the type of beverage, serving size or alcohol concentration. He reported no biliary colic, known gallstones or use of hepatotoxic medicines. On admission, his blood pressure was 85/50 mmHg, pulse rate 90 beats per minute, respiratory rate 28 breaths per minute, oxygen saturation 95% on room air and temperature 98.8°F. Examination showed marked icterus and conjunctival suffusion without peripheral signs of chronic liver disease. His abdomen was soft and nontender, with no right-upper-quadrant tenderness, guarding or rigidity.

Although fever, jaundice and upper abdominal pain ordinarily prompt evaluation for acute cholangitis, the patient did not meet Charcot’s triad because abdominal tenderness was absent. Initial testing showed predominantly conjugated hyperbilirubinemia: total bilirubin was 10.6 mg/dL and the direct fraction was 9.81 mg/dL. Alkaline phosphatase was elevated at 267 U/L and gamma-glutamyl transferase at 105 U/L, whereas alanine aminotransferase was mildly increased at 58.4 U/L, creating a cholestatic biochemical pattern. The total leukocyte count was 13.8 × 10^3/μL, with 92.4% neutrophils, and the platelet count was markedly reduced to 20 × 10^3/μL. The erythrocyte sedimentation rate was 95 mm/h and C-reactive protein concentration was 223 mg/L, indicating a substantial systemic inflammatory response.

Renal function was severely compromised at presentation. Blood urea was 169 mg/dL, serum creatinine was 4.97 mg/dL and the patient had oliguria, indicating acute kidney injury. Urinalysis showed two-plus protein, pus cells, mild bacteria and granular casts. Prothrombin time was 15.4 seconds, activated partial thromboplastin time 46 seconds and the international normalized ratio 1.28. Screening was negative for hepatitis B surface antigen, anti-hepatitis C virus and HIV. Dengue NS1 antigen was negative, as were malaria immunochromatographic testing and malarial parasite smear. Blood culture was negative, although additional tests for typhoid fever were not performed. A chest radiograph showed clear lung fields without consolidation or pleural effusion.

Abdominal ultrasonography identified no hepatobiliary abnormality, and the common bile duct measured 0.4 cm without evidence of obstruction. This made acute cholangitis substantially less likely because cholangitis commonly arises in association with biliary obstruction, such as a common duct stone or neoplasm. The clinicians consequently considered a wider differential that included acute cholangitis, dengue, malaria, sepsis with multiorgan failure, viral hepatitis, drug-induced liver injury and other tropical febrile illnesses. Negative viral and malaria studies weakened several alternatives, while the lack of a relevant medication history made drug-induced liver injury less likely. The combination of cholestatic jaundice, acute kidney injury, thrombocytopenia and conjunctival suffusion instead favored severe leptospirosis. His work as a farmer, repeated exposure to wet fields and prominent calf muscle pain further supported that possibility.

Leptospirosis is a globally distributed bacterial zoonosis associated particularly with populations affected by socioeconomic vulnerability. Pathogenic Leptospira species infect animal hosts such as rodents, which can shed the organisms in urine. Human infection can follow occupational or recreational contact with contaminated water or soil, with entry through abraded skin or mucous membranes. Its early presentation is often nonspecific, with fever, headache and muscle pain that can resemble dengue, influenza, malaria and other acute febrile illnesses. Approximately 10% of patients develop severe disease. The source article describes a pathogenesis involving direct tissue injury, immune-mediated mechanisms, endothelial dysfunction, disturbed microcirculation and multiorgan damage. Severe manifestations include Weil’s syndrome, classically defined by conjunctival suffusion, jaundice and acute kidney injury, as well as pulmonary, hepatic, renal, cardiac, hematological and gastrointestinal abnormalities.

A serum anti-leptospiral IgM enzyme-linked immunosorbent assay produced an index value of 2.18, above the assay’s positive threshold of 1.1. The result was considered consistent with acute leptospirosis when interpreted alongside the clinical and laboratory pattern. Confirmatory polymerase chain reaction testing for Leptospira DNA and microscopic agglutination testing were unavailable at the treating center. IgM ELISA therefore served as supportive rather than definitive confirmation in this case; the report notes that the method can cross-react and must be interpreted in an appropriate clinical context. Creatine phosphokinase activity was 39 U/L, within the laboratory’s stated reference range of 39–308 U/L.

Because the patient had severe jaundice and renal dysfunction and both leptospirosis and acute cholangitis remained under consideration, the medical team began empirical intravenous ceftriaxone twice daily with intravenous normal saline for hydration. Ceftriaxone was selected because it covers common biliary pathogens and is also an established first-line parenteral agent for severe leptospirosis. Penicillin G and doxycycline are also used for milder disease, whereas third-generation cephalosporins are preferred for severe disease with multiorgan involvement in the case report. Intravenous paracetamol was prescribed as needed for fever and pain, although the patient experienced only one episode of fever during the four-day hospital stay. He received four days of intravenous ceftriaxone in hospital and was advised to complete three additional days at a local outpatient facility, for seven days in total.

Serial laboratory measurements showed changes consistent with improvement after treatment began, although the renal trajectory was not uniformly downward on every measure. By hospital day three, the leukocyte count had fallen to 10.9 × 10^3/μL, the neutrophil percentage to 73% and total bilirubin to 6 mg/dL. Platelet count rose from 20 × 10^3/μL at admission to 22 × 10^3/μL on day one, 31 × 10^3/μL on day two and 55 × 10^3/μL on day three. Alkaline phosphatase declined from 267 U/L at admission to 250, 202 and 202 U/L on successive days. Blood urea initially rose from 169 mg/dL at admission to 196 mg/dL on day one, then fell to 162 mg/dL on day two and 85 mg/dL on day three. Serum creatinine declined across the same interval, from 4.97 to 4.5, 3.6 and 2 mg/dL. The patient remained hemodynamically stable and developed no bleeding despite severe thrombocytopenia, so platelets, fresh frozen plasma and cryoprecipitate were not given; the low platelet count was managed conservatively with close monitoring.

At follow-up one week after the antibiotic course ended, the patient reported complete resolution of fever, jaundice, abdominal pain and calf myalgia. Repeat laboratory testing showed near-normalization of bilirubin, renal parameters, leukocyte count and platelet count. Long-term follow-up was unavailable, so the report cannot establish whether renal recovery was sustained or whether chronic complications later emerged. Severe leptospirosis can produce acute kidney injury through tubulointerstitial damage, often alongside jaundice, thrombocytopenia and abnormal urine findings. Other described severe forms include pulmonary hemorrhagic syndrome, acute respiratory distress syndrome and manifestations that can meet criteria for sepsis because of intense systemic inflammation and multiorgan failure. In this patient, the combination of jaundice, acute kidney injury and hematological abnormalities corresponded to the reported pattern of Weil’s syndrome.

The central diagnostic lesson is that a cholestatic liver profile alone does not establish acute cholangitis. Although the patient had fever, upper abdominal pain, jaundice, leukocytosis and sharply elevated inflammatory markers, imaging showed no biliary obstruction, the abdominal examination did not reproduce the pain and blood cultures were negative. Severe kidney injury, thrombocytopenia, conjunctival suffusion, calf myalgia and exposure to wet agricultural fields instead formed a more coherent pattern of leptospirosis. The report supports considering the infection among the causes of suspected cholangitis when no obstruction is demonstrated, particularly in endemic settings and among people with compatible occupational exposure. As a single case without a comparator group and with limited long-term follow-up, it cannot establish comparative treatment effectiveness or population-level outcomes. Its value instead lies in documenting a severe, non-obstructive presentation and the clinical and laboratory pattern that allowed the diagnosis to be reconsidered.

Subject of Research: Severe leptospirosis presenting as Weil’s syndrome with cholestatic jaundice and multiorgan dysfunction that mimicked acute cholangitis.

Article Title: Weil's Syndrome Masquerading as Acute Cholangitis: A Case Report of a Farmer With Leptospirosis

Article References: Shaikh, A. A., Shaikh, F., Arshad, S., Devrajani, T., Ahmed, H., & Al‐Dhaheri, M. (2026). Weil's Syndrome Masquerading as Acute Cholangitis: A Case Report of a Farmer With Leptospirosis. Clinical Case Reports, 14(10), Article e73751. https://doi.org/10.1002/ccr3.73751

Image Credits: AI Generated

DOI: 10.1002/ccr3.73751

Keywords: leptospirosis, Weil’s syndrome, acute cholangitis, cholestatic jaundice, acute kidney injury, case report, thrombocytopenia, occupational exposure, bacterial zoonosis, conjugate hyperbilirubinemia, Weil's, Syndrome

The patient’s background offered few warnings. He had undergone a laparoscopic cholecystectomy two years earlier, with surgical clips later confirmed to be in their expected position. He carried a diagnosis of poorly controlled type 2 diabetes, with a glycated hemoglobin of 9.7 percent, and took metformin twice daily. He drank no alcohol and had no known liver disease. Four days after his reassuring clinic visit, he underwent an elective ileocolonoscopy for chronic ileocaecal changes, which found three small ulcers in the terminal ileum and a rectal polyp that was removed. Crucially, the procedure involved no biliary instrumentation and no sphincterotomy, so it cannot plausibly explain what followed. On 16 February 2026, he presented acutely with two days of fever, progressive right upper quadrant and epigastric pain, nausea, and jaundice. He was tachycardic at 108 beats per minute but hemodynamically stable, with a blood pressure of 118 over 74 millimeters of mercury and a Glasgow Coma Scale score of 15. Charcot’s triad, the classic combination of fever, jaundice, and right upper quadrant pain, was complete.

The diagnostic machinery of TG18 then clicked into place. The guidelines define acute cholangitis across three domains: systemic inflammation, cholestasis, and imaging evidence of biliary obstruction or an etiology. This patient satisfied all three. He had fever with a white cell count of 14.2 thousand per microliter and C-reactive protein above 100 milligrams per liter. He had jaundice with a total bilirubin of 26 milligrams per deciliter, roughly 445 micromoles per liter, alongside markedly deranged liver enzymes. Triphasic computed tomography showed mild intrahepatic ductal dilatation and hyperattenuating dependent material in the distal common bile duct, three to four filling defects with the largest around four millimeters, suggesting sludge as the culprit. The severity grading, however, is where the case becomes genuinely instructive, because the arithmetic is a common source of clinical error.

TG18 Grade II, or moderate, cholangitis requires any two of five criteria: a white cell count above 12 or below 4 thousand per microliter, temperature of at least 39 degrees Celsius, age of 75 years or more, bilirubin of at least 5 milligrams per deciliter, and hypoalbuminemia defined as albumin below 0.7 times the local lower reference limit. This patient met two: the leukocytosis and the hyperbilirubinemia. He fell short on the other three, with a temperature of 38.9 degrees, an age of 42, and an albumin of 3.4 grams per deciliter. Two criteria are sufficient, so he was Grade II from the moment of diagnosis. Equally important is what he was not. No Grade III organ dysfunction was identified: his mean arterial pressure stayed at 89 millimeters of mercury or above without vasopressors, his creatinine of 1.1 milligrams per deciliter sat well below the 2.0 threshold, his INR of 1.3 was under the 1.5 cutoff, and his platelet count of 228 thousand per microliter exceeded the 100 thousand floor. The report candidly notes that two Grade III components, the respiratory criterion and oliguria, could not be formally assessed because no arterial blood gas was drawn and quantitative urine output was unavailable.

Grade II severity, established at presentation, is itself the indication for early biliary drainage alongside antimicrobial therapy. That is the guideline’s core message, and it is the point the case report hammers home: the drainage indication was created on day zero by the severity grade, not by any later failure to improve. Yet immediate endoscopic retrograde cholangiopancreatography, ERCP, was not feasible because of endoscopy-suite and anesthetic availability. What followed was a transparently documented interval rather than an unexamined one. The team started intravenous piperacillin-tazobactam at 4.5 grams every eight hours immediately after drawing blood cultures, in line with TG18 antimicrobial recommendations, and added fluid resuscitation, fasting, analgesia, and basal-bolus insulin. Severity was formally reassessed at 24 and 48 hours. By the 48-hour mark, fever and jaundice persisted, bilirubin remained at 24 milligrams per deciliter, ALT was still 837 units per liter, and CRP was 86 milligrams per liter. Those persistent abnormalities reinforced the urgency of drainage during the unavoidable delay, but the authors are careful to note they did not constitute a separate TG18 severity criterion and did not create the indication. Magnetic resonance cholangiopancreatography was deliberately skipped: the drainage indication was already established, and further imaging could not have altered it or expedited source control.

ERCP was performed on day three, the earliest available opportunity, and it delivered the definitive answer. The ampulla was edematous. Wire-guided cannulation of the common bile duct and sphincterotomy were carried out, and on aspiration, macroscopic purulent bile was identified at ductal entry, direct intra-procedural evidence of suppurative biliary infection. Fluoroscopy confirmed three to four distal filling defects, and three balloon sweeps extracted copious sludge and purulent material, with repeat imaging confirming clearance. The pancreatic duct was not cannulated and no stent was placed. The microbiology, however, is a lesson in itself. Blood cultures drawn before any antibiotic was given showed no growth at five days, and the bile culture, obtained after roughly 72 hours of piperacillin-tazobactam, was also sterile. The report explains why these two negative results mean different things: bacteraemia is documented in only a proportion of patients with acute cholangitis, so pre-antibiotic blood cultures are often negative, while antimicrobial exposure may have reduced the yield of the bile aspirate. Neither result excludes biliary infection, and neither implies that antibiotics reliably sterilize bile.

The biochemical trajectory raised another teaching point. Admission ALT hit 1020 units per liter, 46 times the patient’s documented baseline of 22 and 18.5 times the upper reference limit. Aminotransferase elevations of that magnitude often steer clinicians toward hepatocellular disease, but the report cites pooled data showing that marked elevations above 1000 units per liter occur in about 7.8 percent of acute choledocholithiasis cases. Two features favored biliary obstruction over ischemic hepatopathy: there was no hypotensive episode, and the enzymes declined in a progressive, stepwise fashion, with ALT falling 81 percent over seven days, rather than showing the massive but transient spike typical of hypoxic hepatitis. Pancreatic enzymes were also dramatically elevated, with amylase at 4830 units per liter, and the authors concede that concurrent mild biliary pancreatitis could not be excluded, since two of three Revised Atlanta criteria were satisfied, though the distinction did not change management. Viral hepatitis was ruled out serologically for hepatitis A, B, and C, with no new drugs or supplements identified, though hepatitis E testing was not performed.

Recovery after drainage was rapid. Fever resolved within 24 hours of ERCP, and by day five bilirubin had fallen to 14 milligrams per deciliter. He was discharged on day six, afebrile and eating normally. At three-month follow-up in mid-May 2026, every hepatobiliary, inflammatory, hematological, and renal parameter had normalized: ALT of 38 units per liter, bilirubin of 0.9 milligrams per deciliter, CRP below 5 milligrams per liter, and a white cell count of 6.8 thousand per microliter. His glycated hemoglobin improved from 9.7 to 8.3 percent, though it remained abnormal. He had suffered no recurrent biliary symptoms. The incidental terminal ileal biopsy was eventually reported as mild, nonspecific active chronic ileitis, with no causal role claimed in the biliary event.

The authors are unusually candid about the imperfections of the pathway they followed. Drainage occurred roughly 72 hours after admission, beyond the 48-hour window suggested by the American Society for Gastrointestinal Endoscopy for biliary decompression in cholangitis. They state plainly that day-three drainage is not a model Grade II pathway, that a fully resourced service would have drained sooner, and that the favorable outcome does not validate the delay. No antibiotics-first observation period, they warn, should be inferred from this recovery. They also list the case’s other limits: no organism was ever identified, the extracted sludge was not analyzed so a passed stone or microlithiasis cannot be excluded, the original ERCP images could not be retrieved from the institutional archive, and as a single case report it supports no causal inference or generalization.

What survives those caveats is the decision-making architecture itself. A documented normal hepatobiliary evaluation seven days earlier, and only mildly impressive CT findings on admission, could each have supplied false reassurance. The TG18 framework instead forced the team to grade severity prospectively, on objective criteria, and to let that grade, not the antecedent normality, drive management. Charcot’s triad, the report reminds readers, is a diagnostic construct that confers no severity grade; a patient can have a complete triad and still be Grade I, while another, like this one, reaches Grade II on leukocytosis and hyperbilirubinemia alone. In an era when cognitive bias quietly shapes clinical judgment, the case is a vivid argument for letting current severity, transparently graded and honestly reassessed, override every reassuring signal that came before.

Subject of Research: TG18-guided severity grading and timing of biliary drainage in ERCP-confirmed purulent cholangitis after a documented normal hepatobiliary evaluation

Article Title: When Current Severity Overrides Reassuring Findings: TG18‐Guided Biliary Drainage in ERCP‐Confirmed Purulent Cholangitis

Article References: Taha, H. M., & Taha, K. H. (2026). When Current Severity Overrides Reassuring Findings: TG18 ‐Guided Biliary Drainage in ERCP ‐Confirmed Purulent Cholangitis. Clinical Case Reports, 14(10), Article e73674. https://doi.org/10.1002/ccr3.73674

Image Credits: AI Generated

DOI: 10.1002/ccr3.73674

Keywords: acute cholangitis, Tokyo Guidelines 2018, biliary drainage, ERCP, biliary sludge, severity grading, Charcot's triad, hyperbilirubinemia, piperacillin-tazobactam, cholecystectomy, case report, clinical decision-making