Cocaine-Associated Ischemic Colitis

Linder, Jeffrey D.; Mönkemüller, Klaus; Raijman, Isaac; Johnson, Lorin K.; Lazenby, Audrey J.; Wilcox, C. Mel

doi:10.1097/00007611-200093090-00015

Cited by 47 publications

(27 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In general, it is common in the elderly [3] , and its prevalence increases with age, although it is seen in younger patients as well [4][5][6] . Its causes include vascular factors such as ischemia and embolus [7][8][9] , intestinal factors such as constipation [5,10] , irritable bowel syndrome [11,12] and history of intestinal surgery [13,14] as well as administration of drugs such as alosetron [11] , cocaine [15] , non-steroidal anti-inflammatory drugs [16] , oral contraceptives [17] and oral laxatives [18] . While surgery is indicated for the gangrenous form of this disease, transient and stricturing forms are often ameliorated by bowel rest, fasting, and parenteral fluid administration alone.…”

Section: Introductionmentioning

confidence: 99%

Clinical investigation of 41 patients with ischemic colitis accompanied by ulcer

Matsumoto¹,

Tsuji²,

Shirahama³

2007

WJG

View full text Add to dashboard Cite

AIM: To investigate the relationship among the presence of ulcer lesions, underlying disease, and clinical course in patients with ischemic colitis. METHODS:The subjects were 41 patients (10 male and 31 female; mean age 70 years) with ischemic colitis who were admitted to and received treatment in our hospital from 2000 to 2006. We compared their characteristics and analyzed the mean lengths of admission and fasting for 9 patients with ulcer lesions (ulcer group) and 32 without (non-ulcer group). RESULTS:The groups with presence and absence of ulcer differed significantly only in white blood cell (WBC) count. Lengths of fasting and admission were 7.9 d and 17.9 d for the ulcer group and 4.4 d and 10.7 d for the non-ulcer group, respectively, and significantly longer in the ulcer group (P = 0.0057 and 0.0001). There was no correlation between presence of ulcer and presence of underlying diseases. CONCLUSION:Lengths of fasting and admission were significantly longer in patients with ischemic colitis with ulcer than for those without ulcer.

show abstract

Section: Introductionmentioning

confidence: 99%

Clinical investigation of 41 patients with ischemic colitis accompanied by ulcer

Matsumoto¹,

Tsuji²,

Shirahama³

2007

WJG

View full text Add to dashboard Cite

show abstract

“…Gastrointestinal complications are uncommon and little documented. They include vasoconstriction and ischemia as the most common, which may result in gastrointestinal ulceration (most of times juxtapyloric, or within the first part of the duodenum [3]), infarction, perforation with intraperitoneal hemorrhage, pancreatitis, and rarer, retroperitoneal fibrosis and ischemic colitis [4][5][6][7][8][9]. As far as we know, this is the first case of acute liver failure and fulminant hepatitis caused by cocaine.…”

Section: Discussionmentioning

confidence: 99%

Cocaine-induced Fulminant Hepatitis

Roque¹,

Soy²,

Retto³

et al. 2017

J Gastrointest Dig Syst

View full text Add to dashboard Cite

Cocaine abuse and intoxication is a global problem leading to many medical complications that can result in significant morbidity and mortality. We present the clinical case of a young man who presented with a fulminant hepatic failure, renal failure and a duodenal ulcer related to cocaine consumption. Keywords: Fulminant hepatitis; Cocaine; Clinical case Case PresentationA 28-year-old man was admitted to our hospital on November 14, 2016 because of psychomotor agitation with fear delusions after ingesting 0.5 g of cocaine. He had no medical history of interest. As a toxic consumption history, he referred being an excigarette smoker of a pack a day, referred an ex-consumption of 10-12 alcohol units per day, and an ex-consumption of cannabis. Cocaine consumption started at 16 years old but at that time it had become sporadic. On examination in the emergency department, the patient presented a Glasgow Coma Score (GCS) of 12 with bilateral mydriasis, skin and mucous dryness, tachycardia and self-limiting temperature peak of 39.5°C. First blood test analysis showed a 51% hematocrit (43-49), 219 K/mcl platelets (150-450), 13.98 K/mcl leukocytosis (4.4-11.3), a prothrombin time (PT) of 86% (65-100), a 2.67 mg/dl creatinine (0.7-1.2), a 63 mg/dl urea (16.6-48.5), a 0.42 mg/dl total bilirubin (0.1-1.2), a 93 U/L aspartate aminotransferase (AST) (0-40), a 28 U/L alanine transaminase (ALT) (0-41), a 23 U/L gamma-glutamyltransferase (GGT) (0-60), a 97 U/L alkaline phosphatase (ALP) (40-129), a 863 U/L creatine kinase (CK) (0-190) and a high anion gap metabolic acidosis: pH 7.18, 38 mmHg pCO 2 , 39 mmHg pO 2 and 14.2 mmol/L bicarbonate. Troponin curve realized at 3 hours was flat. Toxics in urine were tested, being only positive for cocaine. Ethyleneglycol and methanol serum levels were normal and hepatitis A, B and C viruses were negative. Blood test control at 3 hours showed increasing levels of CK to 5.529 U/L and at 6 hours CK levels had arisen to 16.242 U/L, creatinine levels to 3.31 mg/dl and PT had decreased to 52%. At 24 hours, CK levels were 49.162 U/L, creatinine levels had increased to 4.79 mg/dl, platelets had fallen to 39 K/mcl and International Normalized Ratio (INR) had increased to 5.54. Brain computerized tomography (CT) scan was normal. Initial supportive treatment (such as serum therapy and bicarbonate) was initiated in the emergency room.First diagnostic approach was an acute renal failure AKIN III probably due to microangiopathy and rhabdomyolysis because of cocaine consumption. In the following hours, the patient began with a decreased level of consciousness and oligoanuria. In blood test controls, platelet levels dropped to 18 K/mcl, INR increased to 5.54, total bilirubin increased to 2.03 mg/dl, AST increased to 3.610 U/L, ALT increased to 3.287 U/L, CK levels were about 33.327 U/L and creatinine levels were still increasing to 6.44 mg/dl. A fulminant hepatic failure was diagnosed in addition to an acute renal failure, since previous abdominal ultrasound found in his clinical history showed n...

show abstract

“…Gastrointestinal complications are uncommon and little documented. They include vasoconstriction and ischemia as the most common, which may result in gastrointestinal ulceration (most of times juxtapyloric, or within the first part of the duodenum [3]), infarction, perforation with intra-peritoneal hemorrhage, pancreatitis, and rarer, retroperitoneal fibrosis and ischemic colitis [4][5][6][7][8][9].…”

Section: Discussionmentioning

confidence: 99%

Cocaine-induced Fulminant Hepatitis

Roque¹

2017

GHOA

View full text Add to dashboard Cite

Gastroenterol Hepatol Open Access 2017, 7(2): 00234 presented a Glasgow Coma Score (GCS) of 12 with bilateral mydriasis, skin and mucous dryness, tachycardia and selflimiting temperature peak of 39.5ºC. First blood test analysis showed a 51% hematocrit [43][44][45][46][47][48][49] and a high anion gap metabolic acidosis: pH 7.18, 38 mmHg pCO2, 39 mmHg pO2 and 14.2 mmol/L bicarbonate. Troponin curve realized at 3 hours was flat. Toxics in urine were tested, being only positive for cocaine. Ethyleneglycol and methanol serum levels were normal and hepatitis A, B and C viruses were negative.Blood test control at 3 hours showed increasing levels of CK to 5.529 U/L and at 6 hours CK levels had arisen to 16.242 U/L, creatinine levels to 3.31 mg/dL and PT had decreased to 52%. At 24 hours, CK levels were 49.162 U/L, creatinine levels had increased to 4.79 mg/dL, platelets had fallen to 39 K/mcL and International Normalized Ratio (INR) had increased to 5.54. Brain computerized tomography (CT) scan was normal. Initial supportive treatment (such as serum therapy and bicarbonate) was initiated in the emergency room.First diagnostic approach was an acute renal failure AKIN III probably due to microangiopathy and rhabdomyolysis because of cocaine consumption. In the following hours, the patient began with a decreased level of consciousness and oligoanuria. In blood test controls, platelet levels dropped to 18 K/mcL, INR increased to 5.54, total bilirubin increased to 2.03 mg/dL, AST increased to 3.610 U/L, ALT increased to 3.287 U/L, CK levels were about 33.327 U/L and creatinine levels were still increasing to 6.44 mg/ dL. A fulminant hepatic failure was diagnosed in addition to an acute renal failure, since previous abdominal ultrasound found in his clinical history showed no abnormalities.Liver transplant was rejected by our transplant referent center because of active cocaine consumption. The patient was then admitted to Intensive Care Unit (ICU) and progressively developed a complete anuria with top creatinine levels of 10.1 mg/dL accompanied by anasarca. Regarding the hepatic failure, the patient presented jaundice, a top of grade II hepatic encephalopathy, an episode of severe hypoglycemia and, analytically, the lower PT was 8%, top bilirubin total level was 16.95 mg/dL, AST top level of 5.788 U/L, ALT top level of 5.875 U/L and the lower platelet level was 18 K/mcL. The patient started renal replacement therapy with continuous venovenous hemodiafiltration that was changed to standard hemodyalisis when clinical status allowed it, besides vitamin K and plasma transfusions when needed. Low oxygen therapy was also required due to pleural effusion caused by accumulated hypervolemia. The patient was hemodynamically stable and conscious at all times without presenting signs of hepatic insufficiency (except for a short period of encephalopathy grade II presented at the first day). Furthermore, an ultrasound guided evacuator paracentesis was required because of the development of tension ascites that conditioned respiratory ...

show abstract

Cocaine-Associated Ischemic Colitis

Cited by 47 publications

References 0 publications

Clinical investigation of 41 patients with ischemic colitis accompanied by ulcer

Clinical investigation of 41 patients with ischemic colitis accompanied by ulcer

Cocaine-induced Fulminant Hepatitis

Cocaine-induced Fulminant Hepatitis

Contact Info

Product

Resources

About