Stress ulcers in neurosurgery [Neurosurgery Wiki]

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====== Stress ulcers in neurosurgery ======

The [[risk]] of developing [[stress ulcer]]s (SU) AKA [[Cushing’s ulcer]]s is high in critically ill patients with [[CNS]] [[pathology]]. These [[lesion]]s are AKA Cushing’s ulcers due to Cushing’s classic treatise
((Cushing H. Peptic Ulcers and the Interbrain. Surg Gynecol Obstet. 1932; 55:1–34)).

17% of SUs produce clinically significant hemorrhage. CNS risk factors include intracranial pathology: 

[[brain injury]] (especially Glasgow Coma scale score < 9), [[brain tumor]]s, [[intracerebral hemorrhage]], SIADH, CNS [[infection]], [[ischemic stroke]], as well as [[spinal cord injury]]. The odds are increased with the coexistence of extra-CNS risk factors including long-term use of steroids (usually>3 weeks), burns>25% of body surface area, hypotension, respiratory failure, coagulopathies, renal or hepatic failure, and sepsis.

The pathogenesis of SUs is incompletely understood but probably results from an imbalance of destructive factors (acid, pepsin & bile) relative to protective factors (mucosal blood flow, mucus- bicarbonate layer, endothelial cell replenishment & prostaglandins).

CNS pathology, especially that involving the diencephalon or brainstem, can lead to a reduction of vagal output which leads to hypersecretion of gastric acid and pepsin. There is a peak in acid and pepsin production 3–5 days after CNS injury
((Lu WY, Rhoney DH, Boling WB, et al. A Review of Stress Ulcer Prophylaxis in the Neurosurgical Intensive Care Unit. Neurosurgery. 1997; 41:416– 426)).