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The high frequency of cocaine abuse has been well documented. In a university population in the US 6% of adolescents were cocaine users as documented by hair analysis , in Switzerland about 3% of adolescents had taken heroin or cocaine at least once in their life. Apart from having mood elevating properties, cocaine is capable of causing myocardial infarction, arrythmia, sudden death, stroke, seizures, bowel necrosis, and numerous other complications. The acute and chronic effects of cocaine use on other vasculatures than the kidney have been reasonably well known, the full extent of the effects of cocaine on the kidney, however, has become apparent more recently.In the following, I discuss renal pathology induced by or associated with cocaine use. Cocaine and rhabdomyolysisThe first reports on the association between cocaine abuse and acute renal failure were on cases with rhabdomyolysis.
This is still the most common form of cocaine-induced renal pathology. Cocaine-related rhabdomyolysis has a high mortality. The mechanism of cocaine-associated rhabdomyolysis is unclear, but potentially includes ischaemia due to vasoconstriction, direct toxicity, hyperpyrexia, and increased muscle activity from agitation or seizure. Cocaine-associated rhabdomyolysis shares many features with excited delirium. Compared with victims of fatal acute cocaine toxicity, both victims of rhabdomyolysis and fatal delirium are more likely to be black, male and younger; to have administered cocaine by smoking or injection; and to have experienced excitement, delirium, and hyperthermia; they are also less likely to have had seizures. Elegance jc 5428 manual lawn. It is thought that this syndrome is caused by changes in dopamine processing induced by chronic and intense use of cocaine rather than by the acute toxic effects of the drug.
Histology shows necrosis of skeletal muscle without specific lesions. Cocaine and end-stage renal disease without rhabdomyolysisSeveral patients with accelerated or malignant hypertension have been described in whom the habitual use of cocaine appears to have hastened the development of renal failure, often requiring dialysis ,.
The patients had smoked cocaine for several years, often continuously, and presented with severe hypertension and renal insufficiency. Blood pressure was extremely elevated, often quite out of proportion to the degree of end organ damage and frequently quite refractory to treatment. It has also been described that scleroderma renal crisis, characterized by accelerated hypertension, rapidly progressive renal failure and hyperreninaemia can be precipitated by heavy cocaine abuse. Surprisingly, hypertension may be absent on presentation and severe renal arterio-arteriolosclerosis without hypertension has been reported after cocaine use ,. Apart from rare cases with renal infarction , antiglomerular basement membrane antibody-mediated glomerulonephritis or acute interstitial nephritis , the mechanisms leading to renal insufficiency after cocaine abuse are at present not clear.Hypertension was thought to be a major factor , especially in black patients. It was speculated that the habitual use of cocaine might worsen hypertension, make it more difficult to control, thus precipitating hypertensive crises culminating in uraemia.
The association of acute hypertension with cocaine use has been well documented ,. The acute effects are thought to be at least partially caused by vasoconstriction, such as has been described with ergotamine, epinephrine, and amphetamine derivatives. Recently it was shown, however, that there are no differences of blood pressure in black cocaine users as compared to an appropriate age matched control group (NHANES III study). It was concluded that chronic cocaine use is associated with acute but not chronic hypertension in middle-aged black males.
Cocaine did not cause microalbuminuria. Thus, the discussion about the relationship between cocaine abuse and chronic hypertension is not easy. In an autopsy study of cocaine-induced cerebral haemorrhage, 88.5% of cases had hypertensive cardiovascular disease as shown by increased heart weight, left ventricular hypertrophy, and nephrosclerosis. Cardiac hypertrophy can be associated with cocaine in the absence of hypertension, however.
Since it is known that cocaine may accelerate atherosclerosis in the aorta and coronary arteries, it has been speculated that a similar phenomenon may occur in the renal vasculature. Few papers have systemically addressed the question whether chronic cocaine use directly leads to nephropathy. Barroso-Moguel et al.
treated male Wistar rats with an aqueous solution of cocaine hydrochloride by daily intraperitoneal injection. Renal histology showed early changes on day 15, with damage to glomerular capillary walls and swelling of tubular epithelium. After 90 days lesions had progressed to glomerular atrophy and sclerosis. The tubular epithelial cells were necrotic and sloughed, and the lumen of papillary ducts contained destroyed red blood cell casts. The interstitium had numerous foci of necrosis and haemorrhage.
Most unfortunately, data on the acute and chronic effects of cocaine on blood pressure, renal function or proteinuria were not given in the paper. DiPaolo et al.
investigated kidneys at autopsy obtained from 40 cocaine users and made a histological comparison with kidneys from victims of automobile accidents, that were not known to have used cocaine and were race and age matched. Semi-quantitative analysis showed that the ratio of hyaline glomeruli to normal glomeruli was increased in the users as compared to the non-users (0.09, SD 0.13 and 0.005, SD 0.001 respectively). The difference was highly significant ( P.
BackgroundCocaine (koe kane') is a potent local anesthetic that appears to act by inhibition of voltage-gated sodium channels, increasing the threshold for electric excitability of nerve axons and thus decreasing neuroconduction. In the central nervous system, cocaine appears to block both norepinephrine and serotonin reuptake.
High doses produce euphoria followed by withdrawal symptoms, leading to a repeated desire to restart it and great abuse potential. Chronic use is associated with irritability, paranoia, violence and drug seeking behavior. Cocaine is one of the most addictive medications known. For this reason, cocaine is listed as a Schedule I drug, indicating that it has high abuse potential and no current medical usefulness.
Cocaine abuse is relatively common; an estimated 600,000 Americans regularly abuse cocaine. HepatotoxicityCocaine has many serious medical consequences including cardiac arrhythmias, coronary artery spasm and myocardial infarction, cerebrovascular accidents, subarachnoid hemorrhage, seizures, hallucinations, intestinal ischemia, renal infarction, rhabdomyolysis and acute liver injury. Cocaine is a not infrequent cause of sudden “unexplained” death in young adults.
Usually arises hours to a few days after an acute overdose, generally following or accompanying other major organ involvement. The clinical phenotype of cocaine hepatototoxicity is usually acute hepatic necrosis. Initially, serum aminotransferase and LDH levels are markedly elevated with minimal increase in alkaline phosphatase.
The prothrombin time becomes abnormal rapidly and may also reflect disseminated intravascular coagulation (DIC). The serum bilirubin begins to rise after 2 to 3 days. Immunoallergic features and autoantibodies are usually absent. Usually shows centrolobular (zone 3) necrosis and fatty change, features that resemble ischemic hepatitis or liver injury due to hyperthermia, factors that may partially mediate the hepatotoxic effects of cocaine.
In self-limited cases, recovery is rapid and serum aminotransferase levels usually return to normal within 1 to 2 weeks.Likelihood score: AHD (well known cause of acute liver injury, but only when taken as an overdose). Outcome and ManagementThe liver injury due to the cocaine is usually self-limited and resolves rapidity. However, fatal instances have been reported often due to the other major systemic effects of cocaine overdose (myocardial infarction, stroke, multiorgan failure). There is no specific therapy or antidote for acute cocaine toxicity. Infusions of N-acetylcysteine are often given because of the similarity of the injury to acetaminophen hepatotoxicity.Drug Class:, Agents of AbuseOther CNS Stimulants:,. Acute hepatic necrosis and rhabdomyolysis after cocaine use.Modified from: Kanel GC, Cassidy W, Shuster L, Reynolds TB.
Cocaine-induced liver cell injury: comparison of morphological features in man and in experimental models. Hepatology 1990; 11: 646-51. A 24 year old man with bizarre behavior after cocaine use was admitted for observation in a jail ward with tachycardia (100/min), fever (100 oF) and tachypnea (30/min). Examination showed small pupils, but was otherwise normal.
He had a history of snorting and “free-basing” cocaine and a previous history of injection drug use. Laboratory results showed elevations in CPK,. He was given intravenous hydration, but developed progressive renal failure and was started on dialysis. His liver tests progressively worsened (Table). After three days he became confused, hypoglycemic, and had signs of progressive hepatic failure. The following day he developed respiratory failure followed by hypotension and cardiac arrest not responding to resuscitative measures.
On autopsy, the liver showed midzonal and central (zones 2 and 3) coagulative necrosis, with prominent fatty change in surviving periportal hepatocytes and minimal inflammatory change with no cholestasis, fibrosis or bile duct injury. CommentCocaine is one of the most addictive and dangerous drugs of abuse. This case demonstrates the range of its medical complications, including initial bizarre and combative behavior followed by rhabdomyolysis, hepatic and renal failure, respiratory arrest and cardiovascular collapse.
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The pattern of liver injury was acute hepatic necrosis with rapid rise and fall of serum aminotransferase levels, little change in alkaline phosphatase and delayed rise in serum bilirubin. Typically, the prothrombin time becomes abnormal early and signs of hepatic encephalopathy can arise at the time that serum bilirubin levels are minimally elevated. Rhabdomyolysis and renal failure are also frequent and the cause of death is usually multiorgan failure rather than acute liver failure per se. Resembles that of acute ischemic hepatitis and acetaminophen poisoning.