Related Experiment Video
Updated: May 3, 2026
Investigating Alterations in Caecum Microbiota After Traumatic Brain Injury in Mice
Published on: September 19, 2019
Gastrointestinal bleeding following traumatic brain injury: A clinical study on predisposing factors and outcomes
Mehdi Mahmoodkhani1, Arvin Naeimi2, Amirhosein Zohrehvand3
1Department of Neurosurgery, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Background:
Traumatic brain injury (TBI) is one of the most common causes of death and disability worldwide. Stress ulcers are common in critically ill patients and can lead to life-threatening gastrointestinal bleeding (GIB). This study investigates the impact of predisposing factors on GIB and outcomes of TBI patients.
Methods:
This retrospective cohort study included TBI patients admitted between February 2019 and November 2021. Patients' demographic information and clinical characteristics were collected and divided into Post-TBI GIB and No-GIB groups. During clinical follow-up, the Glasgow Outcome Score (GOS) and mortality were assessed. The correlation between predisposing factors and GIB was investigated.
Results:
Out of 164 eligible patients, 66.5% were males, and the mean age was 31.38 ± 13.44 years. There was a higher rate of severe TBIs (p<0.001), intra-axial lesions (P=0.014), hypotension at admission (p<0.001), and concurrent coagulopathies (p<0.001) in the Post-TBI GIB group compared to the No-GIB group. In contrast, the Glasgow Coma Scale (GCS) level upon admission and discharge (p<0.001) and serum hemoglobin level at admission (p<0.001) were lower in the Post-TBI GIB group than in the other group. Moreover, primary GCS (P=0.017) and hypotension at admission (P=0.009), spinal injury (P=0.028), and intra-axial brain injury (P=0.018) were independently associated with GIB in TBI patients.
Conclusion:
Primary GCS and hypotension at admission, spinal injury, and intra-axial brain injury are independent predictors for GIB in TBI patients. The presence of GIB in TBI patients is associated with worse neurological outcomes as assessed by GOS at approximately 18 months.
Related Concept Videos
01:22Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
01:28Esophageal Varices-II: Clinical Features and Management
In the initial assessment, a thorough review of the patient's medical history is vital to identify risk factors such as liver disease, alcohol...
01:23Gastritis III: Clinical Manifestations and Management
Clinical manifestations of acute gastritis
The patient with acute gastritis may have a rapid onset of symptoms, such as epigastric pain or discomfort, dyspepsia, anorexia, hiccups, or nausea and vomiting, which can last from a few hours to a few days. Erosive or hemorrhagic gastritis may cause bleeding, which may manifest as blood in vomit or as...
01:30Peptic Ulcer Disease I: Introduction
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
01:28Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
01:25Peptic Ulcer Disease I: Introduction