Faculty Bibliography

OBJECTIVE: To report a case in which a crushed extended-release (XL) nifedipine tablet contributed to a patient fatality. CASE SUMMARY: A 38-year-old woman with multiple medical problems presented to the hospital in acute respiratory distress and was diagnosed with acute pulmonary edema and pneumonia. After initial stabilization, her medications were changed to oral hydralazine, labetalol, and nifedipine XL. These medications were crushed and administered through a nasogastric tube. The patient developed worsening bradycardia with hypotension and experienced asystolic cardiac arrest. She was resuscitated; however, the following morning, another dose of labetalol and nifedipine XL was crushed and administered through the nasogastric tube. She again developed worsening bradycardia with hypotension and ultimately died. DISCUSSION: The administration of a crushed nifedipine XL tablet resulted in the patient's severe hypotension. The concurrent administration of labetalol prevented a compensatory heart rate increase. The repeat administration of nifedipine XL in the same manner underscores a fundamental problem in healthcare worker communication and drug delivery system comprehension. Use of the Naranjo probability scale indicated a highly probable relationship between the patient's hypotension and the nifedipine and labetalol therapy. CONCLUSIONS: Simultaneous administration of a beta-blocker and a calcium-channel blocker may produce synergistic effects. The release characteristics of oral controlled-release medications are destroyed when crushed, resulting in the rapid bioavailability of the total drug amount. The importance of education and communication among nurses, physicians, and pharmacists regarding the mechanism of action of controlled-release medications and their administration needs to be emphasized

Children younger than 5 are at greatest risk for unintentional poisonings. Children in low-income situations are particularly vulnerable for exposures to potential poisons. Focus groups were conducted at a Women, Infants, and Children (WIC) program located in a large urban public hospital in New York City to gain information from low-income parents of young children about real and perceived barriers to calling the local poison control center, resources for poison prevention messages, and ideas about public awareness campaigns. All focus group members were low-income parents of young children. Most participants reported that they would call 911 in the event of a poisoning due to child welfare and self-efficacy issues. Health education theory using the social-cognitive theory provides a framework for developing future poison prevention programs to address identified issues with parents of young children

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

Topiramate (Topamax) is an anti-epileptic medication for which acute toxicity is infrequently reported. A 5-yr-old girl, not previously taking topiramate, developed neurological symptoms after acute ingestion of this medication. She was intermittently agitated, complained of 'not being able to feel anything,' demonstrated arching movements of the back, and perseverated upon questioning. Computerized tomography of the head and electroencephalography were both normal, and urine toxicology testing for drugs of abuse was negative. A serum topiramate level was 10.5 mcg/mL, confirming the ingestion. The patient was observed for 24 h, over which time her symptoms completely resolved