Intestinal Infarction after Intravenous Cocaine Administration

Freudenberger, Ronald S; Cappell, Mitchell S.; Hutt, Douglas A.

doi:10.7326/0003-4819-113-9-715

Cited by 58 publications

(18 citation statements)

References 4 publications

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“…Rhabdomyolysis has been reported in other cases of intestinal infarction caused by cocaine [2, 5]. That was to be expected, considering ischaemia is the most frequent cause of rhabdomyolysis.…”

Section: Discussionmentioning

confidence: 70%

“…There were 19 cases to date [2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15], summarized with the current one in table 1. Although a direct causal relationship between cocaine use and bowel ischaemia is difficult to prove, our patient and all the patients described in published reports were relatively young, with no previous history of arteriosclerosis, and had a positive urine toxicology screen for cocaine.…”

Section: Discussionmentioning

confidence: 99%

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Cocaine-Induced Mesenteric Ischaemia

Osorio

Farreras

et al. 2000

Dig Surg

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We report a 33-year-old man with distal ileum infarction after intravenous abuse of cocaine. He underwent resection of a gangrenous bowel segment and survived. We review the literature regarding intestinal ischaemia related to cocaine. To date, 19 cases have been published. Like most previously reported cases, our patient was young and had no previous history of arteriosclerosis. He suffered cocaine-induced rhabdomyolysis and acute renal failure. Mesenteric ischaemia should be considered in the differential diagnosis of acute or chronic abdominal pain in cocaine consumers.

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Section: Discussionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 99%

Cocaine-Induced Mesenteric Ischaemia

Osorio

Farreras

et al. 2000

Dig Surg

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“…The onset of pain will be sudden when ischemia is caused by embolic disease, but may evolve over hours to days with thrombotic, segmen tal, or low flow states. In particular, the young patient with otherwise normal circulation who develops ischemia because of vasculitis (Henoch-Schonlein purpura, systemic lupus erythematosis, or cocaine use) may have se vere pain for days without progressing to irre versible infarction [32,33], The more abrupt and complete the vascular occlusion the more likely that associated symptoms such as nau sea, vomiting, and forceful bowel movements will also be present. In addition, it is impor tant to recognize that pain may be absent if infarction has already occurred, if the patient has been receiving steroids, or if the patient is critically ill and cannot communicate symp toms.…”

Section: Diagnosismentioning

confidence: 99%

“…Therefore, colonic ischemia must be contemplated in all patients with moderate hematochezia, with or without diar rhea, with or without serious underlying dis ease. If ischemia only enters the differential diagnosis in the elderly patient with heart fail ure or recent aortic bypass surgery, it will be missed in the woman who is pregnant [37] or taking birth control medication [38], in the apparently healthy patient with a hypercoagulable state and venous thrombosis [39,40], or in the young adult using cocaine [33] or amphetamines [41].…”

Section: Diagnosismentioning

confidence: 99%

Intestinal Ischemic Disorders

Levine

Jacobson²

1995

Dig Dis

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The physiology of the mesenteric circulation is described emphasizing important aspects of microcirculatory function and the factors which regulate blood flow to the bowel. Next, the pathophysiology of intestinal ischemia is considered with special focus on the disturbed mechanisms involved in ischemic disorders, such as active oxidant formation and inhibition of intrinsic protective systems. The histopathology of small intestinal and colonic ischemia and infarction is described. Finally, clinical issues are addressed including the diagnostic challenge and the management of these life-threatening disorders.

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“…Gastrointestinal complications primarily result from cocaine's vasoconstrictive actions on gastric arteries (Boghdadi and Henning, 1997) and comprise gastroduodenal ulcers (Kram et al, 1992), intestinal tears Freudenberger 1990(Freudenberger et al, 1990, and colitis (Brown et al, 1994).…”

Section: Medical Consequences Of Cocaine Usementioning

confidence: 99%

Metabotropic Glutamate Receptor 5 in the Medial Prefrontal Cortex: Role in Cocaine Sensitization and Addiction

Timmer¹

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AcknowledgementsI would like to thank my advisor, Dr. Jeff Steketee, for his guidance and support throughout this process, as well as my outstanding committee, Drs. Matthew Ennis, Kristin Hamre, Rennolds Ostrom, and Wen Lin Sun for their input, suggestions, and evaluation. I am thankful for my lab buddy, Kyle Summers, for his exceptional conversation and collaboration on the self-administration project, and former post-doc Kun "Luke" Liu for teaching me microdialysis. I would like to thank my husband, Steve, for existing, as I could not have been this happy spending my life with anyone else. Last but absolutely not least, I would like to thank my children, Jack and Cassidy, for motivating me to complete this work.iv AbstractCocaine sensitization is associated with cocaine-induced hyperexcitability of pyramidal projection neurons within the medial prefrontal cortex (mPFC). Such hyperexcitability presumably results in increased glutamatergic input to reward-affiliated brain regions such as the ventral tegemental area (VTA) and nucleus accumbens (NAc), consequently facilitating drug-seeking behavior. Metabotropic glutamate receptor 5 (mGluR5) has been implicated in cocaine addiction and demonstrated to increase neuronal excitability, therefore, the aim of the present study was to investigate the effect of intra-mPFC mGluR5 manipulation on behavioral and neurochemical sensitization and drug-seeking. Bilateral cannulae were implanted into the mPFC of male Sprague-Dawley rats and mGluR5 antagonist MTEP (15 nmol/side) or saline was microinjected into the region five minutes prior to a challenge cocaine injection. Our data showed that intramPFC mGluR5 blockade via MTEP prevented late, but not early, behavioral sensitization. Further, intra-mPFC mGluR5 activation via DHPG (30 uM) increased mPFC and NAc glutamate levels in sensitized animals during early and late withdrawal, respectively. Finally, we observed a nonsignificant trend toward an MTEP-induced reduction in drug-seeking following the presentation of a cocaine-associated cue in animals that had been trained to self-administer cocaine. Taken together, our data suggest mPFC mGluR5 plays a role in cocaine addiction, possibly through the modulation of mPFC pyramidal neuronal excitability.

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Intestinal Infarction after Intravenous Cocaine Administration

Cited by 58 publications

References 4 publications

Cocaine-Induced Mesenteric Ischaemia

Cocaine-Induced Mesenteric Ischaemia

Intestinal Ischemic Disorders

Metabotropic Glutamate Receptor 5 in the Medial Prefrontal Cortex: Role in Cocaine Sensitization and Addiction

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