Fulminant cardiovascular collapse after acute pancreatitis: a case report of non-alcoholic Shoshin beriberi and literature review
Case Report

Fulminant cardiovascular collapse after acute pancreatitis: a case report of non-alcoholic Shoshin beriberi and literature review

Xin Xie1, Liehua Deng2, Jia Zhao1, Xiaocong Sun2, Lizhen Liu2, Xiaoyan Pan2, Yuanli Zhang2

1Emergency Surgery Department, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China; 2Intensive Care Unit, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China

Contributions: (I) Conception and design: Y Zhang; (II) Administrative support: L Deng, Y Zhang; (III) Provision of study materials or patients: J Zhao, X Sun, L Deng; (IV) Collection and assembly of data: X Xie, L Liu; (V) Data analysis and interpretation: X Xie, X Pan; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

Correspondence to: Yuanli Zhang, PhD. Intensive Care Unit, Affiliated Hospital of Guangdong Medical University, No. 57 South Renmin Avenue, Xiashan District, Zhanjiang 524000, China. Email: zhangyuanly@126.com.

Background: Shoshin beriberi—fulminant cardiogenic shock caused by thiamine deficiency—is rare in adults and is rarely reported after acute pancreatitis has been treated with long‑term parenteral nutrition (PN). Timely thiamine administration is curative, but the diagnosis is often delayed, and patients may perish before metabolic therapy takes effect.

Case Description: A previously healthy 25-year-old man developed refractory shock 2 months into PN for necrotizing pancreatitis. His lactate concentration was 17.4 mmol·L−1, and echocardiography revealed global hypokinesis (left ventricular ejection fraction, LVEF, of 15%). Venoarterial extracorporeal membrane oxygenation (VA-ECMO) was started within 90 min. Diplopia plus severe malnutrition raised suspicion of thiamine deficiency, and high-dose intravenous (i.v.) thiamine (200 mg, q8h) was started empirically on day 2. The lactate concentration normalized, and the LVEF increased to 25% within 96 h. ECMO was removed on day 8, and the LVEF fully recovered (to 55%) by day 10. The pretreatment serum thiamine concentration was later confirmed to be low (40 nmol·L−1). Brain magnetic resonance imaging (MRI) demonstrated typical Wernicke’s lesions. The patient was discharged to rehabilitation on day 29 and remained asymptomatic at the 3-month follow-up.

Conclusions: By demonstrating that VA-ECMO can preserve end-organ perfusion until high-dose thiamine reverses fulminant beriberi, this adult case extends the clinical spectrum of thiamine deficiency shock. In practice, diagnosis hinges on a high index of suspicion and simple bedside cues, including prolonged poor intake or PN without vitamin supplementation, otherwise unexplained hyperlactatemia, and subtle neurological signs, such as diplopia, prompting early empirical intravenous thiamine treatment.

Keywords: Thiamine deficiency; Shoshin beriberi; Wernicke’s encephalopathy (WE); cardiogenic shock; case report

Received: 06 December 2025; Accepted: 20 January 2026; Published online: 18 March 2026.

doi: 10.21037/acr-2025-338

Highlight box

Key findings

• A 25-year-old man developed Shoshin beriberi—fulminant thiamine-deficiency shock—after prolonged parenteral nutrition (PN) for pancreatitis.

• Refractory shock was stabilized with venoarterial extracorporeal membrane oxygenation (VA-ECMO), providing a bridge to metabolic rescue until high-dose intravenous thiamine restored cardiac function.

What is known and what is new?

• Shoshin beriberi is an uncommon cardiovascular presentation of thiamine deficiency that can closely mimic septic shock or viral myocarditis, and is therefore frequently overlooked.

• This case illustrates that early VA-ECMO can safeguard end-organ perfusion while thiamine repletion rapidly reverses severe lactic acidosis and myocardial depression in an adult receiving prolonged PN.

What is the implication, and what should change now?

• Thiamine deficiency should be actively considered in otherwise unexplained shock with hyperlactatemia, particularly in malnourished patients and those on prolonged PN without vitamin supplementation.

• Empirical intravenous thiamine should be administered without delay; when profound circulatory collapse persists despite vasopressors, early VA-ECMO may be life-saving.

Introduction

Thiamine (vitamin B1) is an indispensable cofactor for pyruvate dehydrogenase (PDH) and α-ketoglutarate dehydrogenase; its depletion diverts pyruvate to lactate and damages both neuronal and myocardial energetics. While the classical symptoms of Wernicke’s encephalopathy (WE), such as confusion, ophthalmoplegia, and ataxia, remain the archetype (1), nonalcoholic causes, such as prolonged parenteral nutrition (PN), gastrointestinal surgery, and malignant cachexia, are becoming increasingly prevalent (2). Severe acute pancreatitis exemplifies this shift, with catabolism, reduced enteral intake, and often vitamin-free PN creating an unrecognized thiamine deficiency.

At the cardiovascular extreme, thiamine deficiency precipitates Shoshin beriberi, a fulminant low-resistance cardiogenic shock, with a lactate concentration >10 mmol/L and multiorgan hypoperfusion (3,4). This syndrome mimics viral myocarditis, septic shock and acute coronary occlusion, and therefore, definitive therapy with high-dose thiamine is frequently delayed (5). When metabolic rescue cannot outpace hemodynamic collapse, venoarterial extracorporeal membrane oxygenation (VA-ECMO) may provide a bridge to recovery.

We describe the first reported adult case in which pancreatitis-related PN triggered Shoshin beriberi complicated by WE, whereas VA-ECMO preserved end-organ perfusion until high-dose thiamine achieved metabolic reversal. Our experience supports the following bedside protocol in the intensive care unit (ICU) for any patient with unexplained shock and a lactate concentration >10 mmol/L: (I) exclude ST-elevation myocardial infarction (STEMI) and overwhelming sepsis; (II) administer 200 mg of intravenous thiamine immediately as a diagnostic-therapeutic challenge; and (III) initiate mechanical circulatory support if hemodynamics fail to improve within hours. We present this article in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-2025-338/rc).

Case presentation

A 25-year-old previously healthy man developed persistent upper abdominal pain for 2 months after being diagnosed at another hospital (The First Naval Hospital of the PLA Navy, Zhanjiang, China) with acute edematous pancreatitis following binge eating. Despite apparent improvement of the pancreatic episode, he remained markedly weak, lost substantial weight, and developed intermittent acid reflux, belching, hiccups, dysphagia and diplopia, while his daily oral intake was limited to small amounts of rice porridge. During the index hospitalization, he suddenly developed acute dyspnea, profound hypotension and altered consciousness. His blood pressure became unmanageable, despite the use of vasopressor therapy, and laboratory tests revealed severe lactic acidosis (lactate concentration 17.37 mmol/L) and evolving multiorgan dysfunction. Emergency VA-ECMO was initiated at the referring hospital as life-saving circulatory support, and he was transferred to the ICU of the Affiliated Hospital of Guangdong Medical University, Zhanjiang, China, on July 2, 2025. The clinical course is summarized in Table 1. On arrival, his temperature was 36.0 ℃, heart rate was 123 beats/min, and blood pressure was 41/35 mmHg under 1 µg/kg/min norepinephrine treatment and VA-ECMO; liver enzymes and creatinine were markedly elevated, and chest imaging showed bilateral pulmonary infiltrates.

Table 1

Timeline of presentation and clinical course

Date Clinical events
07-02 VA-ECMO was initiated at the referring hospital; the patient was transferred to the intensive care unit on the same day. On arrival, transthoracic echocardiography showed global hypokinesis with LVEF 38%
07-04 Transesophageal echocardiography showed further deterioration (LVEF 15%); high-dose intravenous thiamine (200 mg every 8 h) was started empirically
07-08 Echocardiography showed improvement (LVEF 25%); lactate decreased to 1.51 mmol/L
07-10 VA-ECMO was successfully weaned; LVEF normalized and cardiac biomarkers markedly decreased
07-16 The patient was weaned from mechanical ventilation to high-flow nasal cannula oxygen
07-19 Continuous renal replacement therapy was discontinued
07-31 The patient was discharged in stable condition to a rehabilitation facility
10-31 No recurrence of heart failure or neurological symptoms

LVEF, left ventricular ejection fraction; VA-ECMO, venoarterial extracorporeal membrane oxygenation.

The initial working diagnoses included cardiogenic shock, acute respiratory distress syndrome, severe pneumonia, sepsis and residual acute edematous pancreatitis. Because the electrocardiogram showed sinus tachycardia with ST-T changes and QTc prolongation (Figure 1A) and because the myoglobin concentration was 955.50 ng/mL (reference range, 25–72 ng/mL), the high-sensitivity troponin T concentration was 0.846 ng/mL (reference range, <0.030 ng/mL) and the creatine kinase-MB isoenzyme concentration was 19.8 ng/mL (reference range, 0–5 ng/mL), acute myocardial infarction was initially considered. Coronary angiography on hospital day 2 demonstrated patent coronary arteries without significant stenosis (Figure 1B-1D), effectively ruling out obstructive coronary disease. Broad-spectrum antibiotics (meropenem and vancomycin), continuous renal replacement therapy and mechanical ventilation were continued; however, his hemodynamics remained critically dependent on VA-ECMO. On ICU admission/arrival (July 2), transthoracic echocardiography (TTE) revealed global hypokinesis with a left ventricular ejection fraction (LVEF) of 38%. On July 4, transesophageal echocardiography (TEE) demonstrated global hypokinesis with further deterioration, and the LVEF decreased to 15%, while the lactate concentration was still 5.4 mmol/L, the myoglobin concentration was >3,000.00 ng/mL, the high-sensitivity troponin T concentration was 1.050 ng/mL, and the creatine kinase-MB isoenzyme concentration was 16.1 ng/mL; thus, the levels of cardiac biomarkers remained elevated. Chest radiography did not support massive aspiration pneumonia (Figure 2), and abdominal CT performed 1 month earlier revealed no major progression of pancreatitis (Figure 3). Rapid and profound circulatory collapse was therefore disproportionate to the apparent degree of infection or pancreatic inflammation.

Figure 1 Electrocardiogram and coronary angiography findings. (A) ECG results: sinus tachycardia, ST-T changes, and QT/QTc =328/492 ms; (B-D) normal coronary arteries. ECG, electrocardiogram.
Figure 2 Chest radiograph: multiple scattered exudates in both lungs.
Figure 3 Abdominal CT. (A) 1 month prior to admission; (B) after admission: the pancreatic head and neck appear mildly enlarged (red arrows). CT, computed tomography.

At this stage, two features prompted reconsideration of the diagnosis, namely, the patient’s prolonged malnutrition with more than 1 month of PN and extremely poor oral intake and the presence of diplopia and apathy that could not be explained by sepsis alone. Taken together, these findings raised a strong suspicion of thiamine deficiency with WE and its fulminant cardiac manifestation, Shoshin beriberi. On July 4, high-dose intravenous thiamine (200 mg every 8 hours) was started empirically, without waiting for laboratory confirmation. A blood sample drawn before supplementation later showed a serum thiamine concentration of 40.2 nmol/L (reference range, 70.0–180.0 nmol/L), confirming severe thiamine deficiency and supporting the clinical diagnosis.

After the initiation of thiamine treatment, there were rapid and sustained improvements in both metabolic and cardiac functions. By July 8, echocardiography showed that the LVEF had increased to 25% and that the lactate concentration had decreased to 1.51 mmol/L. VA-ECMO weaning was not feasible earlier because of persistent circulatory dependence with severe myocardial dysfunction. However, VA-ECMO was successfully weaned on July 10, at which time the patient’s LVEF had normalized and cardiac biomarkers had dropped markedly. The repeat thiamine concentration after supplementation was 475.5 nmol/L, which was within the normal range. Cranial MRI demonstrated symmetrical abnormal signals in the mammillary bodies, thalami, periaqueductal gray matter and periventricular regions of the third and fourth ventricles (Figure 4), which was consistent with WE. The patient was subsequently weaned from mechanical ventilation to high-flow nasal cannula oxygen on July 16, and continuous renal replacement therapy was discontinued on July 19. He was discharged in stable condition on July 31 to a rehabilitation facility, with gradual neurological improvement during follow-up and no recurrence of heart failure or neurological symptoms at the 3-month follow-up. All procedures performed in this study comply with the ethical standards of the institution and/or national research committee and follow the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and related images. A copy of the written consent is available for review by the journal’s editorial office.

Figure 4 From left to right are T2 PROPELLER, T1 FLAIR, T2 FLAIR, and sagittal CUBE T1-weighted sequence with contrast enhancement, demonstrating the relevant radiological features of the lesion. (A) Abnormal signal intensities around the floor of the fourth ventricle (red arrows). (B) Symmetrical abnormal signal intensities in the periaqueductal gray matter surrounding the cerebral aqueduct (red arrows). (C) Abnormal signal intensities in the medial thalamus adjacent to the third ventricle (red arrows). (D) A small patchy abnormal signal in the right frontal lobe (red arrows). FLAIR, fluid-attenuated inversion recovery; PROPELLER, periodically rotated overlapping parallel lines with enhanced reconstruction.

Discussion

Thiamine deficiency is a recognized cause of severe neurological and cardiovascular disease and can be fatal. In most cases, chronic alcohol misuse remains the main risk factor (6). WE is an acute neuropsychiatric syndrome caused by marked thiamine depletion and is typically characterized by altered mental status, ocular signs and ataxia (1). In contrast, fulminant cardiogenic shock is the leading presentation of nonalcoholic WE with Shoshin beriberi and is rarely reported.

We searched PubMed by using “Wernicke’s encephalopathy” or “thiamine deficiency” combined with “Shoshin beriberi” or “cardiac beriberi”; the search was restricted to case reports published from 2016 to 2025 and identified 16 reports (Table 2). Infant cases were related mainly to exclusive breastfeeding with inadequate maternal supplementation, whereas adult cases were usually associated with PN or other severe nutritional disorders. Most patients presented with lactic acidosis and circulatory collapse; typical neurological signs of WE were often absent, appeared late or were not detected, which helps explain why the diagnosis is frequently delayed (7-22). In this context, our patient is notable because he was a previously healthy young man who developed abrupt, fulminant cardiac failure after acute pancreatitis was treated with PN for more than 1 month and who had no history of alcohol abuse.

Table 2

Overview of cardiac beriberi-associated thiamine deficiency/Wernicke encephalopathy cases in the literature

Author Year Gender Age Primary risk factor Key clinical presentation Neurological signs on admission Key intervention Outcome†
Salvatori et al. (7) 2016 M 1 W PN for 35 days Metabolic acidosis, hypotension, and hypotonia Unresponsive to stimuli Intravenous thiamine 24 h
F 1 W Postoperative TPN for more than 35 days Metabolic acidosis and hypotonia Hypotonia Intravenous thiamine 5 d
Cottini et al. (8) 2016 F 17 Y Long-term PN for postoperative gastrointestinal malformation Metabolic acidosis and cardiogenic shock None Intravenous thiamine, ECMO, CRRT 12 h
Elias et al. (9) 2019 M 14 Y Post-renal transplantation, ESRD Postoperative metabolic acidosis and reduced myocardial contractility None Intravenous thiamine 12 h
Helali et al. (10) 2019 M 68 Y Chronic malnutrition and a history of alcohol abuse Ischemic cardiomyopathy with acute heart failure Confusion and bilateral abducens nerve palsy Oral thiamine 16 d
M 63 Y Chronic malnutrition and a history of alcohol abuse Severe heart failure, neurological dysfunction, and hyponatremia Confusion and periodic breathing Intravenous thiamine 14 d
Vicinanza et al. (11) 2019 M 6 Y Severe malnutrition and accidental hypothermia (27.2 ℃) Cardiogenic shock and cardiac arrest occurred suddenly after rewarming Coma with fixed and dilated pupils Oral thiamine, ECMO 30 d
Hodgkinson et al. (12) 2020 M 68 Y The presence of dysgeusia led to malnutrition Severe heart failure and metabolic acidosis Dysgeusia Oral thiamine 30 d
Lim et al. (13) 2021 F 57 Y Malnutrition and chronic alcohol abuse Severe metabolic acidosis and sepsis GCS 15, fully conscious Intravenous thiamine 2 d
Samprathi et al. (14) 2021 M 2 M Exclusive breastfeeding, anemia, and nutritional deficiency Metabolic acidosis and PAH GCS 4, coma No thiamine treatment Death
M 2.5M Exclusive breastfeeding, anemia, and nutritional deficiency Respiratory distress and PAH GCS 11, decreased consciousness No thiamine treatment Death
M 2 M Exclusive breastfeeding, malnutrition, and misdiagnosis as pneumonia Metabolic acidosis Somnolence and poor responsiveness Intravenous thiamine 12 h
F 3 M Exclusive breastfeeding, vomiting, seizures, and misdiagnosis as encephalitis Respiratory failure and metabolic acidosis Decline in mental status Intravenous thiamine 12 h
M 3.5 M Exclusive breastfeeding, malnutrition, and misdiagnosis as gastroesophageal reflux Metabolic acidosis and PAH Consciousness preserved Intravenous thiamine 24 h
M 3.5 M Exclusive breastfeeding and malnutrition Respiratory distress, shock, metabolic acidosis, and PAH Severe agitation Intravenous thiamine 12 h
Tanné et al. (15) 2022 F 2 M Exclusive breastfeeding and malnutrition Respiratory distress, metabolic acidosis, and PAH – Intravenous thiamine 4 d
Govind et al. (16) 2023 F 54 Y Malnutrition and alcohol consumption Severe metabolic acidosis, shock, and ST-segment elevation Clouded consciousness Intravenous thiamine 24 h
M 42 Y HIV infection and beer consumption (rich in thiaminase) Shock and metabolic acidosis Clouded consciousness Intravenous thiamine 3 h
Murase et al. (17) 2023 M 24 Y Severe malnutrition due to long-term monotonous diet caused by gambling addiction Dyspnea, chest pain, cardiac arrest, and metabolic acidosis Mental confusion and agitation Intravenous thiamine 48 h
Xavier Alves de Oliveira et al. (18) 2023 M 76 Y A history of chronic alcoholism and malnutrition Dyspnea, right heart failure, severe tricuspid regurgitation, and PAH None Oral thiamine 2 M
Martins Carvalho et al. (19) 2023 M 72 Y Hiatal hernia with malnutrition; 3-week anorexia STEMI-equivalent ECG changes with shock, hypotension and hyperlactataemia Disorientation on admission (later aphasia and nystagmus) Intravenous thiamine Rapid recovery
Böhrer et al. (20) 2024 F 9 Y Short bowel syndrome, long-term PN, and chronic malnutrition Aspiration pneumonia leading to refractory shock, metabolic acidosis, and heart failure Deep coma Intravenous thiamine, ECMO, and CRRT Death
Alamro et al. (21) 2024 M 68 Y Malnutrition (obesity with hypoalbuminemia and vitamin deficiency) Hypotension, pericardial effusion, recurrent pleural effusion, atrial fibrillation, and ST-T abnormalities – Intravenous thiamine 1 h
Huang et al. (22) 2025 F 14 Y Postoperative intestinal malformation, prolonged fasting, PN, and severe malnutrition Metabolic acidosis, refractory hypotension, PSVT, elevated right heart pressure, and seizures Altered consciousness Intravenous thiamine and CRRT 9 M
Our case 2025 M 25 Y Acute pancreatitis and more than 1 month of PN Severe metabolic acidosis and shock Disturbance of consciousness and diplopia Intravenous thiamine, ECMO, and CRRT 4 d

†, in the outcome column: time from initiation of thiamine supplementation to lactate clearance, normalization of cardiac function, and/or improvement in neurological symptoms. “–” indicates not reported; “death” indicates the patient died. CRRT, continuous renal replacement therapy; ECG, electrocardiogram; ECMO, extracorporeal membrane oxygenation; ESRD, end-stage renal disease; GCS, Glasgow Coma Scale; HIV, human immunodeficiency virus; M/F, male/female; PAH, pulmonary arterial hypertension; PN, parenteral nutrition; PSVT, paroxysmal supraventricular tachycardia; STEMI, ST-segment elevation myocardial infarction; TPN, total parenteral nutrition; Y/M/W/d/h, years/months/weeks/days/hours.

At the biochemical level, thiamine is an essential cofactor for PDH and α-ketoglutarate dehydrogenase (α-KGDH) (23). When thiamine is deficient, flux through the tricarboxylic acid cycle decreases, pyruvate is shunted toward lactate, and severe lactic acidosis may develop. Moreover, impaired mitochondrial energy production in cardiomyocytes leads to acute systolic dysfunction, which is known as Shoshin beriberi. The experimental work and clinical reports are consistent with this model (24,25). In the cases that we reviewed, most patients with Shoshin beriberi had marked lactic acidosis and circulatory failure but few or no obvious neurological signs, making thiamine deficiency easy to overlook. Our patient followed the same pattern; he first presented with refractory cardiogenic shock, with a lactate concentration of 17.37 mmol/L and an LVEF of 15%, which was entirely in line with the above mechanism, while diplopia was the only early neurological clue. Subsequent testing confirmed a very low serum thiamine level and MRI changes typical of WE, establishing the diagnosis of WE with Shoshin beriberi.

The main clinical difficulty is that thiamine-deficient cardiogenic shock closely mimics more common conditions, such as myocarditis, acute myocardial infarction and septic shock, and is therefore easily misdiagnosed. Our review confirms that many cases were initially labeled as one of these entities and only later reinterpreted, sometimes too late for reversal (14). Laboratory confirmation is also slow, as assessment of thiamine status relies on whole-blood thiamine diphosphate measurement by high-performance liquid chromatography (HPLC) or liquid chromatography-tandem mass spectrometry (LC-MS/MS), with turnaround times of several days, and magnetic resonance imaging (MRI) is often not feasible in unstable patients (26). In practice, diagnosis depends on a high index of suspicion and on the recognition of simple bedside cues, such as prolonged poor intake, PN without vitamin supplementation and otherwise unexplained hyperlactatemia. In our patient, revisiting his nutritional history and paying attention to diplopia were key steps that redirected the diagnostic process.

Our case also illustrates the therapeutic window and the limits of pharmacological treatment alone. Cardiac function improved markedly within four days of starting high-dose thiamine and in parallel with rapid lactate clearance, as illustrated in (Figure 5). Among the 16 published cases that we reviewed, 13 patients showed comparable hemodynamic and metabolic responses within 12–48 hours of supplementation, which is consistent with the fundamentally reversible nature of thiamine deficiency shock. In contrast, in several infant series reported by Samprathi and colleagues, delayed recognition or failure to give thiamine was followed by death within hours to days, underscoring how short this window can be (14). Most survivors in the literature recovered with thiamine alone, but a small subgroup of patients who presented with fulminant cardiogenic shock (8,11,20), including the cases described by Cottini, Vicinanza and Böhrer, required ECMO as a bridge; without mechanical support, they might not have lived long enough for thiamine to take effect. Our experience fits this pattern: thiamine replacement was the causal therapy, but VA-ECMO provided the time and organ perfusion needed for this therapy to work.

Figure 5 Trends in serum lactate (solid line) and LVEF (dashed line) before and after initiation of IV thiamine on 4 July. LVEF, left ventricular ejection fraction; IV, intravenous.

Taken together, these observations suggest a pragmatic approach for the intensive care setting. In patients with unexplained refractory cardiogenic shock and lactic acidosis, particularly when there is a history of malnutrition, gastrointestinal disease or prolonged PN, clinicians should actively consider thiamine deficiency and start empirical intravenous thiamine administration without waiting for laboratory confirmation, as intravenous thiamine is generally well tolerated and has negligible adverse effects. When circulatory failure is profound or rapidly progresses, mechanical circulatory support, such as VA-ECMO, can be a reasonable adjunct to maintain perfusion until metabolic correction is achieved. Our case therefore extends the clinical spectrum of nonalcoholic WE complicated by Shoshin beriberi and supports a simple bedside strategy that combines careful nutritional assessment, early empirical thiamine administration and, when needed, temporary ECMO as a bridge to full recovery.

Conclusions

This case suggests that thiamine deficiency in nonalcoholic patients may initially present as fulminant cardiogenic shock with a high risk of misdiagnosis. Early recognition and prompt thiamine supplementation are crucial for condition reversal, whereas mechanical circulatory support can provide a critical time window for causal therapy and can significantly improve prognosis.

Acknowledgments

We would like to thank the staff of the Intensive Care Unit of the Affiliated Hospital of Guangdong Medical University for their clinical support. We also thank Editage for English language editing.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-2025-338/rc

Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-2025-338/prf

Funding: This work was supported by the National Natural Science Foundation of China (No. 82172148, to L.D.).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-2025-338/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study comply with the ethical standards of the institution and/or national research committee and follow the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and related images. A copy of the written consent is available for review by the journal’s editorial office.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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doi: 10.21037/acr-2025-338
Cite this article as: Xie X, Deng L, Zhao J, Sun X, Liu L, Pan X, Zhang Y. Fulminant cardiovascular collapse after acute pancreatitis: a case report of non-alcoholic Shoshin beriberi and literature review. AME Case Rep 2026;10:88.

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