QOD 11 25 09

Which of the following statements accurately describes the risk of hepatic failure following acetaminophen overdose?

A. If N-acetylcysteine is started more than 2 hours post-ingestion, the risk of hepatic failure begins to increase.
B. If N-acetylcysteine is started more than 4 hours post-ingestion, the risk of hepatic failure begins to increase.
C. If N-acetylcysteine is started more than 6 hours post-ingestion, the risk of hepatic failure begins to increase.
D. If N-acetylcysteine is started more than 8 hours post-ingestion, the risk of hepatic failure begins to increase.
E. The risk of hepatic failure is dependent on the amount of ingestion, not the time before antidotal therapy is started.

Following ingestion, acetaminophen is rapidly absorbed from the gastrointestinal tract. It has a relatively low volume of distribution (0.8-1.0 L/kg) and is 25% protein-bound. The half-life of acetaminophen is approximately 1.5-2.5 hours, although it can be slightly prolonged at supratherapeutic concentrations.

Following ingestion, approximately 4% of the ingested acetaminophen is excreted unchanged in the urine, while the remainder is metabolized in the liver. In adults, 45-55% of acetaminophen is glucuronidated, while 20-30% is sulfonated. In pediatric patients, however, sulfation is the primary pathway, and glucuronidation is a minor component. The remainder of acetaminophen is metabolized via the cytochrome P450 isoenzyme CYP2E1 to form a substance called N-acetyl-para-benzoquinoneimine (NAPQI). Normally, the body's endogenous glutathione supplies are able to bind to and reduce NAPQI, resulting in renal excretion in the form of cysteine or mercaptopuric acid conjugates. In the setting of overdose, however, the NAPQI production exceeds the body's endogenous glutathione supply, and hepatotoxicity can result.

Acetaminophen's toxicity is due to the metabolism to NAPQI by the cytochrome P450 isoenzyme CYP2E1. Thus, any xenobiotic that induces the P450 isoenzyme CYP2E1 can theoretically increase the risk for acetaminophen-induced hepatotoxicity. Perhaps one of the best-studied agents for inducing CYP2E1 is ethanol. Thus, chronic ethanol consumption leads to increased CYP2E1 activity and, in theory, subsequently increases the risk of hepatotoxicity (see Special Populations below). In contrast, the co-ingestion of ethanol with acetaminophen may result in inhibition of the microsomal oxidation of acetaminophen, thereby providing some degree of protection from acetaminophen-induced hepatotoxicity during acute intoxication. The strongest risk factor for developing hepatotoxicity, however, is the time from a toxic ingestion until the antidote, N-acetylcysteine, is administered. The risk of hepatotoxicity if N-acetylcysteine is started within the first eight hours of the overdose is exceedingly low, while the risk increases substantially with delays longer than eight hours.

Answer: D

Kevin J. Pfeiffer

Kevin J. Pfeifer New YorkFire Department of New York2001
Lt. Kevin J. Pfeifer worked out of Engine 33 on Great Jones Street in Manhattan. He was a Paramedic for NY Hospital and St. Vincent’s Hospital in Manhattan. Kevin loved life! He was an expert sailor and had a private pilot’s license. Kevin always wanted to be like his brother Deputy Chief Joseph, and he adored his sister, Mary Ellen.
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QOD 11 16 09

Which risk factor was found to be associated with a significant increase in mortality from

cocaine overdose by a medical examiner surveillance study?

a. Suicides

b. Age over 50

c. Ambient temperature > 31.1° C (88° F)

d. Concomitant opioid use

e. HIV status

Hyperthermia is the vital sign abnormality that correlates most with

fatality in cocaine users. There are numerous case reports of hyperthermia-related deaths with or

without rhabdomyolysis after cocaine use. Cocaine causes hyperthermia in several ways.

Cocaine increases heat production through psychomotor agitation via its CNS effects. Cocaine also controls

the dopamine-modulated heat-regulatory centers of the hypothalamus.94 Peripherally, cocaine hampers

heat dissipation by vasoconstriction of the vasculature. In addition, high ambient temperatures are

associated with an increase in mortality from cocaine overdose. In a medical examiner surveillance study

in New York City, it was found that significantly more deaths were due to cocaine overdoses on hot days

than on other days. The mean daily mortality began to increase when maximum temperature equaled or

exceeded 31.1° C (88° F). These findings are consistent with data demonstrating that the survival rate of

cocaine-poisoned dogs fell from 100% to 57% when ambient temperature was increased from –5° C to

5° C.

Answer: C

QOD 11 13 09

Which of the following statements is true of heterotopic pregnancies?

A. They have a lower mortality rate than ectopic pregnancies.
B. They have similar risk factors to those of ectopic pregnancies.
C. They occur more commonly in natural cycles than with assisted reproductive treatment.
D. They present with acute rupture very infrequently.

Heterotopic pregnancy (HP) is the coexistence of an intrauterine and an extrauterine pregnancy. The majority of cases of HP are thought to arise from multiple ovulations. Although its incidence was once considered rare (1/30,000 pregnancies), the incidence has increased significantly since the advent of assisted reproductive technology (ART). The true incidence of HP is unknown but has been estimated to be as high as 1.5% in women treated with ART, which is 100 times higher than HP that occurs with natural cycles.

Risk factors for HP are similar to those for ectopic pregnancy and include pre-existing tubal disease, pelvic inflammatory disease, prior ectopic pregnancy, prior tubal surgery, use of intrauterine devices, and ART. Patient presentations vary, and some may even be asymptomatic. Presenting signs and symptoms include lower abdominal pain (30-80%), vaginal bleeding (approximately 30%) and adnexal mass (43%), enlarged uterus, and hemorrhagic shock. Approximately 50% of heterotopic pregnancies present with acute rupture.

Heterotopic pregnancy presents a major diagnostic challenge for the emergency physician as well as the obstetrician. It is common to think that an intrauterine pregnancy on ultrasound rules out an ectopic pregnancy. However, an HP still may exist and, if left undiagnosed or if the diagnosis is delayed, there may be dire maternal consequences. Soriano et al. found that patients with HP were more likely to have hemodynamic instability, to have more free fluid in the pelvis, and to require more blood transfusions than patients with ectopic pregnancy.

Early diagnosis of HP is essential. The majority of heterotopic pregnancies are diagnosed between 5 and 8 weeks (70%), while 20% are diagnosed between 9 and 10 weeks, and the remaining 10% after 11 weeks. The serum beta-hCG levels are not helpful because they are usually high and may in fact appropriately increase in serial examinations.

Because 95% of heterotopic pregnancies are located either in the fallopian tubes or the ovaries, transvaginal ultrasound is superior to transabdominal ultrasound in making the diagnosis of HP. It is important to keep HP in the differential diagnosis for those pregnant patients who present with shock or continue to complain of severe abdominal pain with or without vaginal bleeding. It is crucial that the adnexal structures be visualized. Consider HP if there is an IUP but the adnexa are poorly visualized or abnormal and there is free fluid in the pelvis.

Treatment of the ectopic pregnancy depends on the patient's clinical presentation. The literature states that laparoscopy for salpingectomy or salpingotomy is the standard treatment for these patients. In stable patients, the use of potassium chloride, methotrexate, RU486, or prostaglandins is useful in the treatment of the ectopic pregnancy but raises concern for possible compromise of the intrauterine gestation.

The survival rate for the intrauterine pregnancy has been documented to be approximately 66% in patients who undergo laparoscopic surgery to remove the ectopic pregnancy. Maternal hypovolemia due to hemorrhagic shock increases the likelihood of demise of the intrauterine pregnancy. The maternal mortality rate for HP has been cited as being just under 1% as compared to ectopic pregnancy, which carries a mortality rate of 0.3/1000. This larger mortality rate likely is due to delays in diagnosis.

Answer: B

FW: A Preventing Chronic Disease article referral for you

Preventing Chronic Disease article referral for you

Hello,

You may want to see this recent article from Preventing Chronic Disease, the online e-journal:
http://www.cdc.gov/pcd/issues/2009/oct/08_0246.htm?s_cid=pcd64a118_e

FW: Requested DocAlert: Chocolate Is Associated with Lower Mortality Following First Myocardial Infarction

Chocolate Is Associated with Lower Mortality Following First Myocardial Infarction

Chocolate Is Associated with Lower Mortality Following First MI

Amount of chocolate consumption was related inversely to cardiac-related mortality during an 8-year follow-up

Several studies have suggested that chocolate, perhaps in a process mediated by its antioxidant content, protects the heart (JW Gen Med Jul 10 2007 and JW Gen Med Sep 23 2003). A Swedish team identified 1169 nondiabetic patients who were hospitalized with initial nonfatal myocardial infarctions. Detailed food histories for the preceding 12 months were completed by 86% of patients; participants were followed for an additional 8 years.

Compared with patients who never ate chocolate, those who ate chocolate less than once monthly suffered 27% less cardiac-related mortality (after multivariate adjustments); risk was 44% lower for weekly chocolate eaters and 66% lower for those who ate chocolate two or more times weekly. Nonfatal adverse cardiac events, strokes, and total mortality, however, were not related clearly to chocolate consumption. Consuming other sweets (e.g., cookies, cakes, ice cream) had no relation to cardiac mortality.

Comment: The strengths of this study are its size and long-term follow-up. The main weakness is that chocolate consumption was assessed only once, during hospitalization for initial MIs, and not during follow-up. To me, the most interesting result of the study is that chocolate strongly protected against cardiac mortality but not against adverse cardiac events. The same finding has been reported for ω-3 fatty acid supplements, which suggests that the primary beneficial effect of both chocolate and ω-3 fatty acid supplements is in suppressing arrhythmias.

— Anthony L. Komaroff, MD

Published in Journal Watch General Medicine September 3, 2009

Citation:
Janszky I et al. Chocolate consumption and mortality following a first acute myocardial infarction: The Stockholm Heart Epidemiology Program. J Intern Med 2009 Sep; 266:248. [Medline® Abstract]

Copyright © 2009. Massachusetts Medical Society. All rights reserved.

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