The patient was admitted on 10 May 2026 after nine days of recurrent fever, altered consciousness and foaming at the mouth during febrile episodes. He had received intravenous levofloxacin at another hospital from 5 to 9 May without clinical improvement. On admission, his temperature was 39.5 °C and he was somnolent but responsive to voice. Blood tests showed normal liver biochemistry, including alanine aminotransferase (ALT) of 39.9 U/L, aspartate aminotransferase (AST) of 45.6 U/L, alkaline phosphatase (ALP) of 61.15 U/L, total bilirubin of 11.9 μmol/L and an international normalized ratio (INR) of 1.16. A chest scan showed partial consolidation in both lower lobes, and clinicians began treating suspected pulmonary and central nervous system infections with intravenous piperacillin-tazobactam at 4.5 g every eight hours.

Four days after treatment began, liver abnormalities appeared, raising the possibility of either infection-associated liver injury or DILI. ALT rose to 151.1 U/L on 14 May, with AST at 176.9 U/L, ALP at 143.31 U/L and gamma-glutamyl transferase (GGT) at 133.54 U/L. The patient also received acyclovir for persistent fever after cerebrospinal fluid culture was negative and brain magnetic resonance imaging showed mild cerebral swelling and leptomeningeal enhancement. His aminotransferases subsequently declined, but ALP and GGT remained elevated. By 31 May, he had developed cutaneous and scleral jaundice, abdominal tenderness, ALT of 410.7 U/L, AST of 502.3 U/L, ALP of 638.21 U/L and total bilirubin of 141.13 μmol/L. Imaging found no biliary obstruction, and testing did not identify viral, autoimmune or parasitic causes.

The treating team stopped piperacillin-tazobactam and acyclovir on 31 May and continued supportive treatment with agents including polyene phosphatidylcholine and magnesium isoglycyrrhizinate. This first withdrawal was followed by a decrease in AST and ALT, although ALP, GGT and total bilirubin continued to rise for several days. The patient was transferred to the gastroenterology department on 2 June with persistent biochemical abnormalities. On 3 June, fever returned to 39 °C, accompanied by cough and sputum production. Although the measured procalcitonin concentration was 0.3 ng/mL, above the cited reference range of 0 to 0.077 ng/mL, clinicians suspected inadequately controlled pulmonary bacterial infection and restarted piperacillin-tazobactam. The drug was the only one of the two suspect agents to be reintroduced.

Following the restart, the patient’s liver profile deteriorated rapidly. By 6 June, ALT had risen to 654.2 U/L and AST to 894.2 U/L, while total bilirubin reached 377.0 μmol/L and marked jaundice persisted. Double plasma molecular adsorption system therapy was initiated, but the patient’s condition worsened further on 7 June. ALT reached 1,263.9 U/L and AST 1,746.1 U/L; the INR rose to 1.95 and then 1.97 on 8 June. The R value, a ratio derived from ALT and ALP relative to their upper limits of normal, was 1.61 on 31 May, consistent with a cholestatic biochemical pattern, and increased to 5.23 by 7 June, indicating a shift toward hepatocellular injury. The case met stated biochemical criteria for acute DILI and was classified as grade 3, or severe, acute DILI.

A clinical pharmacist assessed causality and recommended stopping piperacillin-tazobactam again on 7 June. Its last administration was 8 June, after which it was not used again. Additional double plasma molecular adsorption system sessions were performed on 8, 10, 11 and 13 June alongside continued pharmacological support. AST and ALT subsequently fell markedly, and the INR declined. For example, ALT decreased from 1,310.2 U/L on 8 June to 224.5 U/L on 11 June and 88.4 U/L by 15 June, while AST fell from 1,263.3 to 26.7 U/L over the same period. In contrast, cholestatic measures remained abnormal: on the day of discharge, ALP was 234.6 U/L, GGT 311.1 U/L and total bilirubin 352.9 μmol/L. Thus, the hepatocellular and coagulation abnormalities improved substantially after the second withdrawal, whereas cholestasis had not resolved.

The investigators used the Roussel Uclaf Causality Assessment Method, or RUCAM, to evaluate the suspected adverse reaction and obtained a score of 3, which was interpreted as a possible association between piperacillin-tazobactam and acute liver injury. A Naranjo score of 7 indicated a probable drug-related reaction and supported the RUCAM assessment. These scores were based on the clinical timeline rather than a specific laboratory marker, since no diagnostic biomarker for DILI was available. Other evidence included normal liver tests at admission, onset of abnormalities four days after the antibiotic was started, improvement in aminotransferases after withdrawal and renewed injury after re-exposure. Negative tests reduced support for viral, autoimmune and obstructive alternatives, although infection-associated liver injury could not be excluded completely.

The interpretation carries important limitations. This was a single-patient case report rather than a controlled epidemiological study, and it cannot determine whether piperacillin-tazobactam caused the liver injury with certainty. Other medicines were given during the initial exposure period, including acyclovir, although the fact that only piperacillin-tazobactam was reintroduced during the severe recurrence made acyclovir a less likely explanation for the second episode. Some tests were unavailable, including anti-hepatitis B core IgM, hepatitis B virus DNA, hepatitis C virus RNA, anti-hepatitis E IgM and hepatitis E virus RNA. Cerebrospinal fluid cultures and a sputum culture were negative, and the Sequential Organ Failure Assessment score was below 2. Although sepsis was considered unlikely, infection-associated liver injury could not be completely excluded. No laboratory follow-up was available after discharge on 15 June, leaving the duration and completeness of recovery unknown.

Piperacillin-tazobactam is a widely used antipseudomonal penicillin and beta-lactamase inhibitor combination. The article cites a reported DILI frequency of approximately 0.097% among hospitalized patients receiving it, while previous reports have described predominantly cholestatic or mixed biochemical patterns and a latency of about two weeks. In this patient, the first abnormalities appeared after four days and the second episode produced a different biochemical trajectory: aminotransferases and INR improved after each withdrawal, while ALP, GGT and bilirubin remained elevated or continued to rise. The authors said this contrast may indicate heterogeneity in liver-injury mechanisms between people receiving the same drug, but one case cannot establish a general pattern. The clinical takeaway is observational rather than a controlled efficacy result: suspected DILI warrants a clearly documented exposure timeline, and information about suspected adverse reactions should be transferred explicitly when care changes hands.

Subject of Research: Single-patient case report of possible severe drug-induced liver injury after piperacillin-tazobactam re-exposure

Article Title: Possible severe piperacillin-tazobactam–associated drug-induced liver injury after re-exposure: a case report

Article References: Ren, J., Yu, W., & Dai, Y. (2026). Possible severe piperacillin-tazobactam–associated drug-induced liver injury after re-exposure: a case report. Frontiers in Medicine, 13, Article 1977830. https://doi.org/10.3389/fmed.2026.1977830

Image Credits: AI Generated

DOI: 10.3389/fmed.2026.1977830

Keywords: piperacillin-tazobactam, drug-induced liver injury, antibiotic re-exposure, hepatotoxicity, cholestasis, liver enzymes, adverse drug reaction, case report, clinical pharmacy, Possible, severe, associated

Researchers identified eligible patients through electronic records covering January 2015 through July 2022. Inclusion required pneumonia, a positive respiratory culture for third-generation cephalosporin-resistant Enterobacterales, and definitive treatment with piperacillin/tazobactam, cefepime or a carbapenem. Of the 80 patients, 56% received a carbapenem, 31% received piperacillin/tazobactam and 13% received cefepime. Nanopore sequencing was used for multilocus sequence typing and comprehensive antibiotic-resistance gene detection. Minimum inhibitory concentrations for piperacillin/tazobactam and cefepime were determined by broth microdilution. Clinical factors and outcomes were compared between carbapenem and non-carbapenem groups through univariable analyses.

The isolates were highly diverse. Three-quarters carried an extended-spectrum beta-lactamase, or ESBL, gene, with blaCTX-M-15 the most common among the ESBL genes at 50%. AmpC genes were found in 19 isolates. In vitro susceptibility differed between the two non-carbapenem agents: 88% of isolates were susceptible to piperacillin/tazobactam and 58% to cefepime. Among isolates with AmpC genes, 83% were susceptible to piperacillin/tazobactam, compared with 93% of ESBL-harboring isolates.

Thirty-day mortality was 14% among patients treated with piperacillin/tazobactam or cefepime and 33% among carbapenem recipients, but the difference was not statistically significant in the reported univariable analysis (p = 0.09). In the subgroup of patients infected only with ESBL-producing isolates, mortality was 8% in the non-carbapenem group and 26% in the carbapenem group, also without statistical significance (p = 0.1). These observational comparisons neither establish that non-carbapenem treatment caused better outcomes nor show that the groups were equivalent. The small, selected population and univariable analyses limit interpretation, and the investigators said larger prospective studies are needed to assess non-carbapenem beta-lactams in this patient population.

Subject of Research: Molecular epidemiology and treatment outcomes of cephalosporin-resistant Enterobacterales causing ICU pneumonia

Article Title: Molecular epidemiology and associated treatment outcomes of third generation cephalosporin-resistant enterobacterales causing pneumonia in intensive care unit patients

Article References: DeLaurentis, C., Hokunson, T. W., Jr., Nelson, B., Annavajhala, M. K., Uhlemann, A.-C., & Gomez-Simmonds, A. (2026). Molecular epidemiology and associated treatment outcomes of third generation cephalosporin-resistant enterobacterales causing pneumonia in intensive care unit patients. BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14446-5

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DOI: 10.1186/s12879-026-14446-5

Keywords: Enterobacterales, intensive care units, pneumonia, antibiotic resistance, carbapenems, piperacillin-tazobactam, cefepime, whole-genome sequencing, ESBL, AmpC, Molecular, epidemiology

The numbers behind the study are straightforward but telling. Over a one-year period in 2024, the unit recorded 550 admissions. Twenty-two of those patients, or 4.0 percent, received a diagnosis of pneumonia. That figure may appear modest, but it captures a population whose clinical fragility is extreme: the mean Karnofsky Performance Status, a standard 0-to-100 scale of functional ability, was 44.1, meaning the average patient required substantial assistance with daily activities and spent much of the time resting or in bed. In oncology practice, a KPS in the forties signals a body with limited physiological reserve, where even a localized lung infection can rapidly destabilize multiple organ systems.

What distinguishes this cohort is the diagnostic intensity applied. Every one of the 22 patients underwent computed tomography of the chest to establish the diagnosis. In many palliative settings, imaging beyond a portable chest radiograph is often considered unnecessary or burdensome, particularly when the therapeutic plan would not change. The Palermo team’s decision to obtain CT scans across the board reflects the philosophy of the APCU model: these units are designed to handle acute complications of advanced disease with the same diagnostic rigor as an oncology ward, while keeping the goals of care anchored in symptom relief and rapid stabilization rather than curative pursuit.

Therapeutically, the approach was equally assertive. All patients received antibiotic therapy, and the agents selected were predominantly broad-spectrum intravenous drugs used for hospital-acquired and complicated pneumonias. Piperacillin combined with the beta-lactamase inhibitor tazobactam was the most frequent choice, given to 54.5 percent of the cohort, while the carbapenem meropenem was used in 36.4 percent. These are not marginal drugs; they are workhorses of empirical therapy for serious gram-negative infections, chosen when resistance risk is high or when the clinical picture leaves little room for narrow-spectrum trial and error. The pattern suggests that the treating clinicians regarded these infections as genuine threats requiring potent coverage, not as terminal events to be managed with placebo or minimal intervention.

The outcomes lend weight to that judgment. Among evaluable cases, clinical resolution of the infection was achieved in 80 percent. More striking still, 72.7 percent of the patients were discharged successfully, either to their homes or to community-based palliative care services, and the mortality rate within the APCU itself was 9.1 percent. For a population with a mean KPS of 44 and active pneumonia, those figures challenge the assumption that infection in advanced cancer is an inevitable terminal milestone. Instead, the data support the idea that timely, intensive antimicrobial treatment can buy patients the time and stability needed to return to their preferred care settings, which for most people means being at home.

Symptom trajectories add an important nuance. Dyspnea, the subjective sensation of breathlessness that often accompanies pneumonia, was measured at admission using the Edmonton Symptom Assessment System, a validated patient-reported tool. The mean ESAS dyspnea score was 3.21, with a standard deviation of 2.35, indicating moderate breathlessness on average but with wide variability across patients. Notably, when the researchers compared dyspnea scores at the time of clinical resolution and at discharge against the admission values, they found no statistically significant change, with a p-value of 0.396. In other words, treating the infection did not dramatically worsen or improve the reported breathlessness, a finding that underscores how multifactorial dyspnea is in advanced cancer, where causes such as pleural disease, anemia, muscle weakness, and anxiety frequently coexist with infection.

Oxygen requirements followed a similar pattern of partial stabilization. At admission, 31.8 percent of the patients needed supplemental oxygen. By the time of discharge, that proportion had fallen only slightly, to 27.3 percent. The modest decline suggests that while antimicrobial therapy and supportive care allowed most patients to leave the unit, the underlying respiratory compromise often persisted, consistent with the limited pulmonary reserve typical of this population. For clinicians, the implication is that antibiotic success in this setting should be judged primarily by infection control and functional stabilization rather than by complete normalization of breathing or oxygen needs.

The study sits within a broader and sometimes contentious literature on antimicrobial use at the end of life. Prior research has documented that a large share of hospice and palliative patients receive antibiotics in their final days, raising questions about whether such treatment prolongs suffering, contributes to resistance, or merely delays an inevitable decline. Some studies have found that antibiotics can relieve infection-related symptoms, while others question whether withdrawal of antimicrobials in terminal patients is appropriate or harmful. The Infectious Diseases Society of America and the Society for Healthcare Epidemiology of America have published stewardship guidelines that apply to all clinical settings, yet their implementation in palliative contexts remains uneven and ethically fraught. The Palermo data do not resolve these debates, but they do demonstrate that in a specialized acute unit, high-intensity treatment and palliative goals can coexist without the one negating the other.

The APCU model itself is central to interpreting the findings. Acute palliative care units, often embedded within comprehensive cancer centers, are designed for rapid assessment and short-stay management of severe complications such as uncontrolled pain, delirium, bleeding, and infections. Reviews led by some of the same authors have argued that such units should be considered mandatory infrastructure for cancer centers and tertiary hospitals, precisely because they bridge the gap between the ward, where curative or life-prolonging priorities dominate, and hospice, where the focus shifts entirely to comfort. The present study illustrates that bridge in action: patients arrived acutely ill, received CT-based diagnosis and broad-spectrum antibiotics, and most were stabilized and discharged within the unit’s rapid-cycle framework.

Several caveats temper the conclusions. The study is retrospective and single-center, drawing on 22 patients over one year, so the findings may not generalize to units with different staffing, patient mixes, or antimicrobial policies. The abstract does not report microbiological culture results, which limits insight into whether the chosen broad-spectrum regimens matched the actual pathogens. Nor does it detail long-term survival after discharge, an outcome that matters greatly when weighing the burdens of intensive treatment against its benefits. Nonetheless, the core message is clear and clinically useful: in an acute palliative care unit equipped for high diagnostic and therapeutic intensity, pneumonia in advanced cancer is frequently treatable, and treating it does not conflict with palliative intent. For the four in five patients whose infections resolved and the nearly three in four who went home, the aggressive approach translated into time in the place they most wanted to be.

Subject of Research: Prevalence, management, and outcomes of pneumonia among patients admitted to an acute palliative care unit for advanced cancer

Article Title: Pulmonary infections in an acute palliative care unit

Article References: Mercadante, S., Settepani, S., Grassi, Y., Mancuso, G., & Cascio, A. L. (2026). Pulmonary infections in an acute palliative care unit. Supportive Care in Cancer, 34(10), Article 969. https://doi.org/10.1007/s00520-026-11067-1

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DOI: 10.1007/s00520-026-11067-1

Keywords: pneumonia, palliative care, acute palliative care unit, advanced cancer, antibiotics, piperacillin-tazobactam, meropenem, dyspnea, Karnofsky Performance Status, supportive care, antimicrobial stewardship, cancer center

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

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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