ACETAMINOPHEN OVERDOSE

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<A HREF="id33.htm" TARGET="_top" TITLE="OPTIC NERVE GLIOMA"><U><B>OPTIC NERVE GLIOMA</B></U></A></div> <div> <A HREF="id36.htm" TARGET="_top" TITLE="New Born Assessment "><U><B>New Born Assessment </B></U></A></div> <div> <A HREF="id38.htm" TARGET="_top" TITLE="laryngomalacia"><U><B>laryngomalacia</B></U></A></div> <div> <A HREF="id39.htm" TARGET="_top" TITLE="CRANIOSYNOSTOSIS "><U><B>CRANIOSYNOSTOSIS </B></U></A></div> <div> <A HREF="id40.htm" TARGET="_top" TITLE="DANDYWALKER MALFORMATION "><U><B>DANDY-WALKER MALFORMATION </B></U></A></div> <div> <A HREF="id41.htm" TARGET="_top" TITLE="DEJERINESOTTAS DISEASE "><U><B>DEJERINE-SOTTAS DISEASE </B></U></A></div> <div> <A HREF="id42.htm" TARGET="_top" TITLE="DOWN SYNDROME "><U><B>DOWN SYNDROME </B></U></A></div> <div> <A HREF="id43.htm" TARGET="_top" TITLE="Respiratory Syncytial Virus (RSV)"><U><B>Respiratory Syncytial Virus (RSV)</B></U></A></div> <div> <A HREF="id44.htm" TARGET="_top" TITLE="FABRY DISEASE "><U><B>FABRY DISEASE </B></U></A></div> <div> <A HREF="id45.htm" TARGET="_top" TITLE="PRADERWILLI SYNDROME "><U><B>PRADER-WILLI SYNDROME </B></U></A></div> <div> <A HREF="id37.htm" TARGET="_top" TITLE="new born fun"><U><B>new born fun</B></U></A></div> <div> <A HREF="id46.htm" TARGET="_top" TITLE="RETT SYNDROME "><U><B>RETT SYNDROME </B></U></A></div> <div> <A HREF="id47.htm" TARGET="_top" TITLE="Alexander Disease"><U><B>Alexander Disease</B></U></A></div> <div> <A HREF="id49.htm" TARGET="_top" TITLE="leukemia"><U><B>leukemia</B></U></A></div> <div> <A HREF="id17.htm" TARGET="_top" TITLE="Contact Me"><U><B>Contact Me</B></U></A></div> </td> <td valign="top" height=370 BGCOLOR="#FFFFFF" TEXT="#080000"> <div> ACETAMINOPHEN OVERDOSE</div> <div> <IMG BORDER="0" SRC="Symb075c00b700f000000000.gif" HEIGHT="16" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Acetaminophen ingestion is common. A recent study showed a statistically significant difference in hepatotoxicity for patients treated less than 16 hours post ingestion versus patients treated between 16 and 24 hours.</div> <div> <IMG BORDER="0" SRC="Symb075c00b700f000000000.gif" HEIGHT="16" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Acetaminophen is a metabolite of phenacetin. Because of the nonspecific initial features of acute overdose, the lack of coma, the delay in onset of jaundice, and the rapid fall in detectable plasma levels of acetaminophen, the cause and effect relationship may be missed in even a floridly ill or dying patient. Overdose is encountered primarily in children under the age of 6 and in adolescent suicide attempts. Following ingestion of sufficient acetaminophen to produce a potentially toxic blood level, an adolescent is six times more likely to develop evidence of hepatotoxicity than is a child under age 6.</div> <div> <IMG BORDER="0" SRC="Symb075c00b700f000000000.gif" HEIGHT="16" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Acetaminophen is absorbed rapidly after an oral dose producing peak plasma levels between 30 and 60 minutes after ingestion. This absorption may be delayed in overdoses so that peak plasma levels may not occur until as long as 4 hours post ingestion. The drug is distributed beyond total body water so that the volume of distribution is considered to be approximately 1 L/kg. Hepatic metabolism accounts for 98% of acetaminophen elimination. </div> <div> <IMG BORDER="0" SRC="Symb075c00b700f000000000.gif" HEIGHT="16" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">The two major pathways of acetaminophen metabolism involve conjugation with glucuronide or sulfate, accounting for 94% of the metabolites. 4% is metabolized by the cytochrome P- 450 mixed function oxidase system. Glutathione is a necessary part of this smaller pathway. The lower incidence of toxicity in young children may be related to lower amounts of acetaminophen being metabolized by the P- 450 system.</div> <div> <IMG BORDER="0" SRC="Symb075c00b700f000000000.gif" HEIGHT="16" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">After an acetaminophen overdose, normal metabolism is overwhelmed because the sulfate and glucuronide pathways are saturable. As a result, more acetaminophen is metabolized via the P- 450 pathway. When 70% of the available cellular glutathione is depleted, the reactive intermediate metabolites formed by the P- 450 pathway cannot be completely detoxified to mercapturic acid and cysteine. These metabolites than become covalently bound to hepatocellular proteins, causing centrilobular necrosis. This is reflected in increased SGOT, bilirubin, and prothrombin times. </div> <div> <IMG BORDER="0" SRC="Symb075c00b700f000000000.gif" HEIGHT="16" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Alcohol seems to have some degree of hepato- protection when ingested simultaneously with acetaminophen. Simultaneous ingestion of other substances, such as propoxyphene, codeine, antihistamines, and anticholinergic, increases the risk of lethargy and results in a higher elevation of SGOT. The ingestion of 140mg/kg in a child or 7.5gms in an adult may produce hepatotoxicity. These patients, plus all those for whom an exact amount of ingestion cannot be established with certainty, should have a serum acetaminophen level done 4 hours post ingestion. </div> <div> <IMG BORDER="0" SRC="Symb075c00b700f000000000.gif" HEIGHT="16" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">The clinical course after a toxic ingestion follows 4 stages. Stage 1 occurs 12- 24 hours post ingestion. Symptoms present include nausea, vomiting, diaphoresis, and anorexia. Children frequently have episodes of vomiting even without toxic levels. Those patients with plasma levels in the toxic range have a mean onset of symptoms by 6 hours, with 100% showing symptoms by 14 hours. Laboratory studies are typically normal during this time. </div> <div> <IMG BORDER="0" SRC="Symb075c00b700f000000000.gif" HEIGHT="16" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Stage 2 occurs 24- 48 hours post ingestion. By that time, symptoms have decreased but laboratory abnormalities begin to appear with a rise of SGOT, SGPT, bilirubin, and prothrombin time. </div> <div> <IMG BORDER="0" SRC="Symb075c00b700f000000000.gif" HEIGHT="16" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Stage 3 is from 48- 96 hours post ingestion and is when the peak abnormalities are seen. SGOT levels as high as 30,000 may be seen. The definition of hepatotoxicity related to acetaminophen has been accepted as SGOT levels in excess of 1,000. Well under 1% of patients in Stage 3 will develop fulminant hepatotoxicity. </div> <div> <IMG BORDER="0" SRC="Symb075c00b700f000000000.gif" HEIGHT="16" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Stage 4 occurs during the first week after ingestion with hepatic abnormalities returning to near normal by 7 or 8 days.</div> <div> <IMG BORDER="0" SRC="Symb075c00b700f000000000.gif" HEIGHT="16" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Results of acetaminophen levels 4 hours post ingestion should by plotted on the Rumack- Matthew nomogram to determine the probability of toxicity. Activated charcoal and gastric lavage should be initiated in order to prevent further absorption. Patients who present late after a significant ingestion or in whom laboratory results will be delayed more than 10 hours post ingestion should receive a loading dose of N- acetylcysteine while awaiting laboratory results. N- acetylcysteine is approved in the U.S. for oral therapy of acetaminophen overdose. It is available as a 20% or 10% solution and should be diluted to a 5% solution prior to administration. N- acetylcysteine is given as a loading dose of 140mg/k followed by 17 maintenance doses of 70mg/k every 4 hours. A full course lasts for approximately 3 days. If the patient vomits within an hour of administration of a dose, it should be repeated. Administration via nasogastric or duodenal tube as a slow drip may be necessary if vomiting persists. During treatment, the following laboratory tests should be monitored: SGOT, SGPT, bilirubin, prothrombin time, electrolytes, glucose, BUN, creatinine, CBC, and urinalysis. Patients who present 24 or more hours post ingestion will not benefit from treatment with N- acetylcysteine. Intravenous N- acetylcysteine is available in Europe. </div> <div> <IMG BORDER="0" SRC="Symb075c00b700f000000000.gif" HEIGHT="16" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">A recent study showed a statistically significant difference in hepatotoxicity for patients treated less than 16 hours post ingestion versus patients treated between 16 and 24 hours. In those patients treated less than 10 hours post ingestion, 7% developed transient SGOT elevations. 29% of patients treated between 10 and 16 hours post ingestion and 62% of those treated between 16 and 24 hours post ingestion developed hepatotoxicity. The incidence of hepatotoxicity is even lower in children than in adults with similar levels.</div> <bR> </td> </tr></table></body>