The shock bowel sign and the broader CT hypotension complex are frequently triggered by severe systemic hypotension originating from medical conditions other than traumatic haemorrhagic shock. These include cardiac arrest, severe septic shock, neurogenic shock (secondary to critical craniocerebral or spinal cord injuries), bacterial endocarditis, and profound diabetic ketoacidosis (DKA). The classic vascular and solid visceral elements of the hypoperfusion complex-such as the attenuation of the abdominal aorta and inferior vena cava, abnormal pancreatic contrast dynamics with peripancreatic fluid, and marked hypoperfusion of the liver and spleen-are variably paired with the shock bowel sign, regardless of whether the underlying trigger is post-traumatic blood loss or a medical cause of circulatory failure. Recognizing the CT hypotension complex carries critical prognostic weight and immediate therapeutic implications, as it guides clinicians toward aggressive volume resuscitation rather than unnecessary operations. In the majority of clinical presentations, these diffuse hypoperfusion features can be successfully distinguished from localized direct bowel trauma or primary ischemic bowel injury.
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Chandrakar et al. (2026) studied this question.
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