Blood cocaine and metabolite concentrations, clinical findings, and outcome of patients presenting to an ED

Blaho, Kari; Logan, Barry K.; Winbery, Stephen; Park, Lynda; Schwilke, Eugene W.

doi:10.1053/ajem.2000.9282

Cited by 84 publications

(58 citation statements)

References 38 publications

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“…In the largest series (n=111), serum concentra-tions in emergency department patients averaged approximately 0.9 microM but varied dramatically (standard deviation of = 1.6 microM !). The highest concentration in a surviving patient (who displayed minimal symptoms of toxicity) was 120 micromolar [7]. A second small series (n=29) reported detectable concentrations in only 3 patients (0.05 to 0.4 microM) [8], while a third series (n=19) was unable to detect cocaine in any patient [9].…”

Section: Cocaine Concentrations and Clinical Effectsmentioning

confidence: 90%

Mechanisms of Acute Cocaine Toxicity

Heard¹,

Palmer²,

Zahniser³

2008

TOPHARMJ

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Abstract:Patients with acute cocaine poisoning present with life-threatening symptoms involving several organ systems. While the effects of cocaine are myriad, they are the result of a limited number of cocaine-protein interactions, including monoamine transporter, neurotransmitter receptor and voltage-gated ion channels. These primary interactions trigger a cascade of events that ultimately produce the clinical effects. The purpose of this article is to review the primary interactions of cocaine and the effects that these interactions trigger. We also describe the progression of symptoms observed in cocaine poisoning as they relate to serum cocaine concentrations.

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Section: Cocaine Concentrations and Clinical Effectsmentioning

confidence: 90%

Mechanisms of Acute Cocaine Toxicity

Heard¹,

Palmer²,

Zahniser³

2008

TOPHARMJ

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“…The relationship with its plasma concentrations and its toxic effects has shown a wide variability between patients [1]. Cocaine is well-known for its cardiovascular complications such as stroke and cardiac arrest, and its respiratory problems [2].…”

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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“…The relationship with its plasma concentrations and its toxic effects has shown a wide variability between patients [1].…”

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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Blood cocaine and metabolite concentrations, clinical findings, and outcome of patients presenting to an ED

Cited by 84 publications

References 38 publications

Mechanisms of Acute Cocaine Toxicity

Mechanisms of Acute Cocaine Toxicity

Cocaine-induced Fulminant Hepatitis

Cocaine-induced Fulminant Hepatitis

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