Crack-Related Perforated Gastropyloric Ulcer

Abramson, David L.; Gertler, Jonathan P.; Lewis, Theophilus; Kral, John G.

doi:10.1097/00004836-199102000-00006

Cited by 39 publications

(13 citation statements)

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“…[1,2] In these case series and other retrospective reviews, cocaine-associated gastrointestinal injury involved the colon, the juxtapyloric region of the stomach, and proximal duodenum of the small intestine. [3][4][5] …”

Section: Discussionmentioning

confidence: 99%

Massive pan-gastrointestinal bleeding following cocaine use

2009

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Section: Discussionmentioning

confidence: 99%

Massive pan-gastrointestinal bleeding following cocaine use

2009

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“…Since 1959 Szakacs observed that prolonged NE infusion induced endothelial proliferation, occasionally sufficient to cause complete obstruction of small arteries of the gastrointestinal tract [354]. Gastric mucosal cells and duodenal villi rapidly become ischaemic in response to reductions in mesenteric blood flow, leading to gastritis and ulceration, this may theoretically be potentiated by cocaine-mediated gastric hypomotility and delayed gastric emptying (which prolongs mucosal exposure to gastric acid) [251,[355][356][357]. Some investigators have suggested that cocaine has a direct toxic effect on the gut mucosa [358].…”

Section: Gastrointestinal Toxicity and Cocainementioning

confidence: 99%

Side Effects of Cocaine Abuse: Multiorgan Toxicity and Pathological Consequences

Riezzo

Fiore²,

Carlo³

et al. 2012

CMC

168

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Cocaine is a powerful stimulant of the sympathetic nervous system by inhibiting catecholamine reuptake, stimulating central sympathetic outflow, and increasing the sensitivity of adrenergic nerve endings to norepinephrine (NE). It is known, from numerous studies, that cocaine causes irreversible structural changes on the brain, heart, lung and other organs such as liver and kidney and there are many mechanisms involved in the genesis of these damages. Some effects are determined by the overstimulation of the adrenergic system. Most of the direct toxic effects are mediated by oxidative stress and by mitochondrial dysfunction produced during the metabolism of noradrenaline or during the metabolism of norcocaina, as in cocaine-induced hepathotoxicity. Cocaine is responsible for the coronary arteries vasoconstriction, atherosclerotic phenomena and thrombus formation. In this way, cocaine favors the myocardial infarction. While the arrhythmogenic effect of cocaine is mediated by the action on potassium channel (blocking), calcium channels (enhances the function) and inhibiting the flow of sodium during depolarization. Moreover chronic cocaine use is associated with myocarditis, ventricular hypertrophy, dilated cardiomyopathy and heart failure. A variety of respiratory problems temporally associated with crack inhalation have been reported. Cocaine may cause changes in the respiratory tract as a result of its pharmacologic effects exerted either locally or systemically, its method of administration (smoking, sniffing, injecting), or its alteration of central nervous system neuroregulation of pulmonary function. Renal failure resulting from cocaine abuse has been also well documented. A lot of studies demonstrated a high incidence of congenital cardiovascular and brain malformations in offspring born to mothers with a history of cocaine abuse.

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“…Multiple authors have reported on their experience treating this group of patients. [11][12][13][14][15] A wide range of theories have been proposed by these authors and others, including focal ischemia, 11,14 in-situ mesenteric thrombi, 14,21-23 elevated ACTH, 14,15,24 delayed gastric emptying, 12,15 and increased aerophagia resulting in increased intra-abdominal pressure. 13,15 H. pylori infection has also been proposed as a contributing factor.…”

Section: Discussionmentioning

confidence: 99%

“…10 Since that time, several other reports have appeared documenting this phenomenon. [11][12][13][14][15] No long-term follow-up of these patients is reported. Although the etiology remains unclear, the pathogenesis is most commonly attributed to local ischemia caused by crack cocaine-induced profound vasoconstriction.…”

Section: Introductionmentioning

confidence: 99%

Outcomes of Cocaine-Induced Gastric Perforations Repaired With an Omental Patch

Schuster

Feuer

Barquist

2007

Journal of Gastrointestinal Surgery

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Crack cocaine has been associated with acute gastric perforation. The appropriate surgical treatment and long-term outcomes remain unclear. A retrospective chart review of all gastroduodenal perforations associated with crack cocaine use was performed. Data abstracted included details of short- and long-term outcomes. Kaplan-Meier methods were used to evaluate surgical outcomes. Over the 14-year period ending December 2005, 16 cases of crack-induced gastric perforations were identified. Most (75%) were treated with an omental patch. The other patients underwent a formal antiulcer operation, including one vagotomy and pyloroplasty (V&P), one vagotomy and antrectomy, one subtotal gastrectomy, and one ulcer excision and V&P. All patients after antiulcer procedures were followed for a median of 63 months (range 27-120) with no recurrences. Follow-up data were available in 75% of the omental patch patients. Recurrence of disease was observed in 56% of these omental patch patients at a median of 20 months (range 11-39). Those without recurrence were followed for a median of 67 months (range 12-96). The recurrence rate was borderline lower in the antiulcer group (P = 0.072). Omental patch closure results in a recurrence rate over 50% compared with no recurrence for formal antiulcer procedures.

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Crack-Related Perforated Gastropyloric Ulcer

Cited by 39 publications

References 0 publications

Massive pan-gastrointestinal bleeding following cocaine use

Massive pan-gastrointestinal bleeding following cocaine use

Side Effects of Cocaine Abuse: Multiorgan Toxicity and Pathological Consequences

Outcomes of Cocaine-Induced Gastric Perforations Repaired With an Omental Patch

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