Multiple Gastrointestinal Complications of Crack Cocaine Abuse

Carlin, Neal; Nguyen, Ngoc Lan; DePasquale, Joseph

doi:10.1155/2014/512939

Cited by 16 publications

(19 citation statements)

References 7 publications

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“…Cocaine (benzoylmethylecgonine), a crystalline tropane alkaloid, is extracted from the leaves of the Erythroxylum coca plant [ 8 ]. Cocaine is a drug of abuse and has four main routes of abuse: ingestion, smoking, inhalation, and injecting.…”

Section: Discussionmentioning

confidence: 99%

“…Short-term clinical features include vasoconstriction, high blood pressure, increase heart rate and energy, hypervigilance, pupillary dilation, change in appetite, and temperature surge. Moreover, it also predisposes to thrombus formation secondary to platelets aggregation through direct vasoconstrictive effect on endothelial cells [ 8 ]. The bowel complications of cocaine abuse are a direct consequence of the negative effect of cocaine on neurotransmitter reuptake by presynaptic neurons, which result in the increased local concentration of neurotransmitters at the site of the neurotransmitter receptors causing ischemia, inflammation, and ulcer of the bowel, which result in abdominal pain, nausea, vomiting, diarrhea, and blood in the stool [ 10 ].…”

Section: Discussionmentioning

confidence: 99%

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Cocaine-Induced Acute Pancreatitis: A Rare Etiology

Umar¹,

Noor²,

Ali³

et al. 2020

Cureus

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An 18-year-old male with a medical history of trigeminal neuralgia presented to the emergency department with complaints of severe abdominal pain associated with nausea, projectile vomiting, and watery diarrhea with no fever, rigors, and chills. The abdominal examination was unremarkable. His lab results showed elevated serum lipase and amylase. Gallstones were ruled out by abdominal ultrasonography. His computed tomography (CT) revealed pancreatic enlargement with ill-defined borders. He reported cocaine use but had no history of alcohol abuse. A urine drug screen was positive for cocaine. He was managed conservatively with a possible diagnosis of acute pancreatitis due to cocaine abuse after carefully ruling out other causes. The patient was symptom-free on day 7 and discharged from hospital on day 8 with follow-up with his gastroenterology doctor and drug counseling service. Although cocaine-induced pancreatitis is rare, it should be considered a differential diagnosis in patients with a history of cocaine use.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Cocaine-Induced Acute Pancreatitis: A Rare Etiology

Umar¹,

Noor²,

Ali³

et al. 2020

Cureus

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“…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

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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...

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“…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

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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 ...

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Multiple Gastrointestinal Complications of Crack Cocaine Abuse

Cited by 16 publications

References 7 publications

Cocaine-Induced Acute Pancreatitis: A Rare Etiology

Cocaine-Induced Acute Pancreatitis: A Rare Etiology

Cocaine-induced Fulminant Hepatitis

Cocaine-induced Fulminant Hepatitis

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