Therapy-Refractory Ventricular Fibrillation Due to Traumatic Small Bowel Perforation

https://doi.org/10.1007/s00392-025-02625-4

Timm Benjamin Ubben (Hamburg)1, J. Reimers (Hamburg)1, M. Bohné (Hamburg)1, S. Willems (Hamburg)1, E. P. Tigges (Hamburg)1

1Asklepios Klinik St. Georg Kardiologie & internistische Intensivmedizin Hamburg, Deutschland

 

Introduction
Ventricular fibrillation (VF) is a life-threatening arrhythmia that can be triggered by a variety of underlying causes, including traumatic injuries. We report a case of therapy-refractory VF in a patient with a small bowel perforation resulting from blunt abdominal trauma.

Case Presentation
A 65-year-old female presented to the emergency department following a bicycle accident, where she collided with her handlebar, causing diffuse lower abdominal pain. Initial evaluation with focused assessment with sonography for trauma (FAST) and blood tests revealed no acute abnormalities, and she was discharged.

The following day, the patient called for emergency medical services due to worsening abdominal pain. Upon arrival, she collapsed, and cardiopulmonary resuscitation (CPR) was immediately initiated. Initial rhythm analysis revealed VF, which was resistant to multiple defibrillation attempts. The patient was transferred to our cardiac arrest center.

At this stage, a repeat FAST examination revealed small amounts of free fluid in the perisplenic space. The patient was then transferred to the cath lab, where veno-arterial extracorporeal membrane oxygenation (ECMO) was initiated. Coronary angiography ruled out coronary artery disease, and aortography excluded aortic dissection. Despite pharmacological therapy (amiodarone, magnesium, and lidocaine) and multiple defibrillation attempts, VF persisted.The electrolytes were balanced at this point of time.

A subsequent computed tomography (CT) scan revealed significant free fluid, prompting an exploratory laparotomy. Surgical exploration revealed a jejunal perforation with intact mesenteric vessels and no active bleeding, which was repaired. Following the laparotomy and abdominal lavage, the patient was successfully defibrillated into sinus rhythm.

Postoperatively, the patient developed abdominal compartment syndrome and peritonitis, which were managed surgically. Hemodynamics stabilized, and ECMO support was successfully weaned. Transthoracic echocardiography showed intact left and right ventricular function. However, the patient developed an unresponsive wakefulness syndrome in the following days.

Discussion
This case underscores the potential for abdominal trauma, in this case a small bowel perforation, to trigger ventricular fibrillation. The absence of structural heart disease and the successful termination of VF only after surgical intervention suggest that abdominal factors, possibly related to intra-abdominal pressure or release of vasoactive mediators, may have contributed to the arrhythmia. Previous studies in animals have shown that distension of abdominal organs can decrease coronary blood flow and predispose to VF. Additionally, vasoactive intestinal peptide, a mediator released during intestinal trauma, may increase arrhythmia susceptibility and affect myocardial contractility.

Conclusion
VF can occur as a consequence of traumatic abdominal injury, even in the absence of direct cardiac damage.

 

References

1. Gilbert ND, LeRoy GV, Fenn FK. The effect of distention of abdominal viscera on the blood flow in the circumflex branch of the left coronary artery of the dog. Am Heart J. 

2. Henning RJ, Sawmiller DR. Vasoactive intestinal peptide: cardiovascular effects. Cardiovasc Res. 2001;49(1):27-37. 

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