Related Experiment Video
Updated: May 13, 2026

07:56
Transient Middle Cerebral Artery Occlusion Model of Neonatal Stroke in P10 Rats
Published on: April 21, 2017
10.5K
Non-occlusive Mesenteric Ischemia Following Severe Traumatic Brain Injury: A Case Report
Kazuki Fujii1, Kiyoshi Takemoto1, Shiho Yoshida1
1Emergency and Critical Care Medicine, Nara Prefecture General Medical Center, Nara, JPN.
Cureus
|March 20, 2025
Summary
Severe traumatic brain injury (sTBI) may be a risk factor for non-occlusive mesenteric ischemia (NOMI). This case report highlights a potential link between sTBI and NOMI development, suggesting further investigation into this association.
Area of Science:
- Neuroscience
- Gastroenterology
- Critical Care Medicine
Background:
- Non-occlusive mesenteric ischemia (NOMI) is a serious condition with several known risk factors.
- The association between severe traumatic brain injury (sTBI) and NOMI has not been previously reported.
Observation:
- A young woman with no prior risk factors developed NOMI following sTBI.
- The patient experienced sudden cardiac arrest on postoperative day 14, attributed to aspiration.
- Aspiration was linked to abdominal distension and vomiting secondary to NOMI.
Findings:
- This case presents the first reported instance of NOMI in a patient with sTBI as the sole apparent risk factor.
- The clinical course suggests a potential causal relationship between sTBI and the subsequent development of NOMI.
Implications:
- Severe traumatic brain injury may represent a novel risk factor for non-occlusive mesenteric ischemia.
- Clinicians should consider NOMI in patients with sTBI, particularly those presenting with gastrointestinal complications.
- Further research is warranted to elucidate the pathophysiological mechanisms linking sTBI and NOMI.
Related Concept Videos
Ischemic Stroke ll: Pathophysiology
An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Transient Ischemic Attack l: Introduction
A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.Mechanisms of Transient Cerebral IschemiaTransient cerebral ischemia may arise through several mechanisms. One...
Traumatic Brain Injury l: Introduction
DefinitionTraumatic brain injury, or TBI, is a disturbance of normal brain function induced by an external mechanical force, such as a direct blow to the head or a penetrating injury. It can affect both brain structure and function, producing a wide range of clinical outcomes. TBI is a heterogeneous condition, meaning its effects may differ based on the type, location, and severity of the injury.Basis of ClassificationTBI is classified based on severity, injury mechanism, or pathophysiology. In...
Secondary Spinal Cord Injury llI: Pathophysiology
Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...

