Faculty Bibliography

PURPOSE: Two cases of penile angioedema associated with the use of angiotensin-converting-enzyme inhibitors and angio-tensin II receptor blockers are reported. SUMMARY: The first case of penile angioe-dema involved a 68-year-old man who arrived at the emergency department (ED) with a 2-12-hour history of penile swelling occurring three days after initiation of irbesartan in addition to longstanding lisinopril therapy. All parts of the physical examination were normal, except for the genital examination. The patient's penis was edematous at midshaft only and was nontender with normal skin coloring. The edema was nonpitting and limited to the skin. The patient was instructed to stop taking both lisinopril and irbesartan, and symptoms resolved within 48 hours with supportive care alone. In the second case, a 48-year-old man arrived at the ED complaining of penile swelling over the previous two days. Enalapril had been initiated one month before his arrival at the ED. The patient's penis was nontender and edematous at midshaft. The edema was nonpitting and limited to the skin. The patient was instructed to stop taking enalapril, given oral prednisone 60 mg, and asked to continue his prednisone for five days after discharge. The swelling resolved within two days of stopping enalapril, and he had no further episodes of penile swelling. Neither patient was rechallenged with the offending medications. CONCLUSION: Penile angioedema was reported in two patients. The first case involved a patient receiving both lisinopril and irbesartan. The second patient was receiving enalapril only.

BACKGROUND: Intravenous fat emulsion (IFE) decreases cardiotoxicity from several lipid-soluble drugs, including verapamil. OBJECTIVES: To verify if the addition of IFE to the standard treatment of severe verapamil toxicity would improve hemodynamics and survival. METHODS: Fourteen dogs were instrumented to measure systolic blood pressure, diastolic blood pressure, mean arterial pressure (MAP), heart rate, cardiac output, central venous pressures, left ventricular pressure changes over time, mixed venous oxygen saturation, pH, and base excess. Verapamil toxicity, defined as a 50% decrease in MAP, was induced with verapamil at 6 mg/kg/hr and maintained for 30 minutes by titrating the verapamil infusion rate. Following verapamil toxicity, the verapamil infusion rate was changed to 2 mg/kg/hr and continued for 90 minutes. All dogs were resuscitated with atropine (0.04 mg/kg intravenously) and calcium chloride (15 mg/kg intravenously every 5 minutes for three doses) and then randomized to receive either IFE (7 mg/kg of 20%) intravenously or equivalent volumes of 0.9% normal saline over 30 minutes. Measurements were recorded for 120 minutes by investigators blinded to the treatment. Data were analyzed using analysis of variance, survival analysis, and log-rank test. RESULTS: Before the 30-minute IFE or normal saline infusion, there were no differences in hemodynamic parameters. After IFE or normal saline infusion, the IFE-treated group had higher MAP at 30 minutes (95% confidence interval [CI] = 5.6 to 44.7 mm Hg), 45 minutes (95% CI = 10.8 to 50.0 mm Hg), and 60 minutes (95% CI = 10.2 to 53.1 mm Hg). Kaplan-Meier 120-minute survival rate was 14% (95% CI = 0.5% to 53%) for the saline group as compared with 100% (95% CI = 59% to 100%) for the IFE group (p = 0.01). CONCLUSIONS: Standard resuscitation and IFE increase MAP and survival in an animal model of severe verapamil toxicity compared with standard resuscitation alone.

Poisoning by hydrofluoric acid or fluoride salts results in hypocalcemia, hypomagnesemia, and hyperkalemia with subsequent cardiac dysrhythmias. In previous studies, quinidine attenuated fluoride-induced hyperkalemia in vitro, and enhanced survival in animals. Like quinidine, amiodarone is a potassium channel blocker, although amiodarone is more familiar to clinicians due to its recent inclusion in advanced cardiac life support (ACLS) protocols. OBJECTIVES: This in-vitro study of human erythrocytes was designed to determine whether amiodarone could attenuate fluoride-induced hyperkalemia. METHODS: Six healthy volunteers each donated 60 mL of blood on three occasions. Each specimen was divided into 12 tubes, incubated at 37 degrees C, and oxygenated with room air. An aqueous sodium fluoride (F(-)) solution was added to tubes 1-9. Incremental amounts of quinidine were added to tubes 1-4 (Q(1)-Q(4)) to attain calculated concentrations of 0.73 microg/mL, 1.45 microg/mL, 2.9 microg/mL, and 5.8 microg/mL, respectively. Incremental amounts of amiodarone were added to tubes 5-8 (A(1)-A(4)) to attain calculated concentrations of 0.38 microg/mL, 0.75 microg/mL, 1.5 microg/mL, and 3.0 microg/mL, respectively. Tubes 9-12 were controls for each of F(-), amiodarone, quinidine alone, and no additive, respectively. Extracellular potassium concentration ([K(+)]) was followed, and an objective endpoint was defined as the rise in potassium concentration at 6 hours. RESULTS: Fluoride produced a significant change in [K(+)] by 6 hours in all samples. Quinidine produced a J-shaped curve in its ability to attenuate the rise in [K(+)], with only one concentration, Q(3), demonstrating significance versus tube 9 (control). Amiodarone also demonstrated a J-shaped dose-response effect, with statistical significance at A(1), A(2), and A(3) versus tube 9 (control). There was no significant difference among the effective concentrations (Q(3), A(1), A(2), and A(3)) of both drugs. CONCLUSIONS: In this in-vitro model using human blood, amiodarone and quinidine both attenuated F(-)-induced hyperkalemia. Further study is indicated to determine whether amiodarone enhances survival in F(-)-poisoned animals

Although lead poisoning (plumbism) has been recognized for centuries, lead exposures still occur frequently today because of its varied uses and persistence in the environment. Despite the awareness of the adverse effects of lead on adults, childhood plumbism was first reported only about a century ago. Young children are one of the most vulnerable groups to the adverse effects of lead because of their rapidly developing central nervous systems. Federal regulations in the 1970s have been successfully implemented to decrease the amount of environmental lead by decreasing the content of lead in gasoline and indoor paint. However, almost 30 years after these laws were passed, inner-city housing with leaded paint still exists. We describe three children living in New York City who developed plumbism from the ingestion of leaded paint chips