Acute pediatric exposure to pramipexole dihydrochloride (Mirapex)
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Biomedical subjects
Publications and source records attributed to R S Hoffman.
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Although no major breakthroughs have emerged in the area of lens insertion techniques and technology, small incremental advancements continue to take place for the placement of foldable intraocular lenses through small incisions. Folders have become more innovative in their ability to fold lenses effectively, and inserters have been downsized and enhanced to allow insertion through smaller incisions with more effective purchase of the lens. New cartridge injectors are increasing in popularity because of their ease of use and ability to pass through smaller incisions, especially with modifications. In addition, knowledge regarding techniques and complications of noncapsular supported intraocular lenses continues to increase, adding to our ability to choose the proper technique for secondary lens insertion in these selected patients.
OBJECTIVE: To determine the effects of body temperature, ethanol use, electrolyte status, and acid-base status on the electrocardiograms (ECGs) of hypothermic patients. METHODS: Prospective, two-year, observational study of patients presenting to an urban ED with temperature < or =95 degrees F (< or =35 degrees C). All patients had at least one ECG obtained. Electrocardiograms were interpreted by a cardiologist blinded to the patient's temperature. J-point elevations known as Osborn waves were defined as present if they were at least 1 mm in height in two consecutive complexes. RESULTS: 100 ECGs were obtained in 43 patients. Presenting temperatures ranged between 74 degrees F and 95 degrees F (23.3 degrees C-35 degrees C). Initial rhythms included normal sinus (n = 34), atrial fibrillation (n = 8), and junctional (n = 1). Osborn waves were present in 37 of 43 initial ECGs. Of the six initial ECGs that did not have Osborn waves present, all were obtained in patients whose temperatures were > or =90 degrees F > or =32.2 degrees C). For the entire group, the Osborn wave was significantly larger as temperature decreased (p = 0.0001, r = -0.441). The correlation between temperature and size of the Osborn wave was strongest in six patients with four or more ECGs (range r = -0.644 to r = -0.956, p = 0.001). No correlation could be demonstrated between the height of the Osborn waves and the serum electrolytes, including sodium, chloride, potassium, bicarbonate, BUN, creatinine, glucose, anion gap, and blood ethanol levels. CONCLUSIONS: The presence and size of the Osborn waves in hypothermic patients appear to be a function of temperature. The magnitude of the Osborn waves is inversely correlated with the temperature.
OBJECTIVES: Wyeth polyvalent crotalid antivenin is the only commercial antivenin available in the United States to treat North American crotalid envenomations. Wyeth antivenin is made from the serum of horses hyperimmunized with four crotalid venoms (Crotalus adamanteus, Crotalus atrox, Crotalus durrisus terrificus, and Bothrops atrox). Although Wyeth antivenin is believed to be effective against all North American crotalids, its efficacy against Agkistrodon contortrix (copperhead) has never been tested. The purpose of this experiment was to determine the efficacy of Wyeth antivenin in the treatment of copperhead envenomation. METHODS: Wyeth antivenin was reconstituted in 10 mL of sterile water. In preliminary experiments, 20 mL/kg of Wyeth antivenin administered intraperitoneally prevented death in mice given a lethal subcutaneous injection of Crotalus adamanteus venom. Freeze-dried copperhead venom was reconstituted in sterile water, and a dose-lethality curve for subcutaneous venom was constructed using seven groups of 10 mice each. The endpoint was survival at 24 hours. A dose that is lethal in 90% of the animals receiving it (LD90) was estimated from this curve. Thirty mice were randomly given pretreatment with 20 mL/kg Wyeth antivenin administered intraperitoneally or an equal volume of normal saline as a control. Thirty minutes later, all mice received an LD90 subcutaneous injection of copperhead venom. Lethality was determined at 24 hours. RESULTS: Following the injection of copperhead venom, none of the 15 control mice and 14 of 15 treatment mice survived until 24 hours (p < 0.001). CONCLUSION: Wyeth antivenin is effective in treating copperhead envenomation in mice and may therefore be expected to be effective in humans.
L-Thyroxine (T4) is commonly prescribed medication for hypothyroidism in humans and animals. Overdose has generally resulted in limited symptomatology managed with sedatives and beta-adrenergic receptor antagonists. We describe the largest acute T4 ingestion ever reported, which resulted in a profound thyrotoxicosis, resistant to treatment. A 34-y-old man ingested 900 (0.8 mg) tablets of veterinary T4 (720 mg) and was given 60 g of activated charcoal. He became lethargic on post-ingestion days 2 and 3; had vomiting, diaphoresis and insomnia on day 4; on day 5 he "looked like he had too much coffee", began "using a lot of words" and became agitated, assaultive and stopped speaking intelligibly; and on day 6 returned to the hospital combative and confused. He was diaphoretic, mydriatic, hyperreflexic, tremulous, with clear lungs and active bowel sounds, and received activated charcoal, haloperidol, diazepam, and phenobarbital, and was tracheally intubated. During hospitalization he was rehydrated, treated with propranolol and diazepam, but remained continuously tachycardic. On day 12 he became afebrile and his tachycardia resolved. Free T4 levels ranged from > 13 mcg/dL on day 6 to 1.2 mcg/dL on day 12. By discharge (day 15) he had lost 20 kilograms of body weight, but was clinically euthyroid 2 w later. This case suggests that large intentional T4 ingestions should be managed differently than current T4 overdose protocol.
The pharmacokinetics and adverse effects of an oral loading dose of carbamazepine administered in tablet or suspension form were studied. Patients on a hospital epilepsy unit who were to receive carbamazepine as a discharge medication were randomly assigned to receive either an oral 8-mg/kg loading dose of the tablet formulation or the same dose of the suspension on an empty stomach. Blood samples were drawn before and at intervals up to 12 hours after the loading dose. Adverse effects were evaluated subjectively and objectively. Total and free serum carbamazepine and carbamazepine-10, 11-epoxide (CBZE) concentrations were determined by high-performance liquid chromatography. Six adult patients were enrolled in and completed the study. All the patients achieved therapeutic total carbamazepine levels; the suspension group did so within two hours and the tablet group within five hours. Maximum serum carbamazepine concentrations ranged from 7.10 to 9.92 mg/L, area under the concentration-versus-time curve from 54.85 to 82.23 micrograms.hr/L, and terminal elimination half-life from 14.05 to 15.71 hours. Adverse effects were mild, few, and short-lived; none of the patients developed gastrointestinal toxicity. Adverse effects were not associated with total or free carbamazepine and CBZE concentrations or with total or free CBZE:carbamazepine ratios. An oral loading dose of carbamazepine 8 mg/kg achieved therapeutic levels within two hours when given as a suspension and within five hours when given as tablets and was well tolerated in all patients.
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Trigger-point injection therapy is a common procedure in primary care medicine and emergency medicine and is generally considered safe. A 28-year-old woman experienced respiratory depression and hemiplegia after the injection of a superficial trapezius trigger point. The patient required emergency tracheal intubation for ventilatory support. Computed tomography of her head revealed pneumocephalus. She recovered fully over the course of 24 hours. Intrathecal injection during a trigger-point injection is a previously unreported complication of trigger-point injection therapy.
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Although no major breakthroughs have recently emerged in the area of lens insertion techniques and technology, small incremental advancements continue to take place for the placement of foldable intraocular lenses through small incisions. Folders have become more innovative in their ability to effectively fold lenses, and inserters have been downsized and enhanced to allow insertion through smaller incisions with more effective purchase of the lens. New cartridge injectors are increasing in popularity because of their ease of use and ability to pass through smaller incisions, especially with modifications. In addition, increased knowledge regarding techniques and complications of noncapsular supported intraocular lenses continues to be gained, adding to our ability to choose the proper technique for secondary lens insertion in these selected patients.
BACKGROUND: Inadvertent intrathecal administration of vincristine has been reported and is uniformly fatal except in two of three cases treated with spinal fluid exchange. We report a case of inadvertent direct intraventricular vincristine administration. CASE REPORT: A 59-year-old woman developed acute lymphocytic leukemia with meningeal involvement and was being treated with intraventricular cytarabine (beta-cytosine arabinoside, Ara-C) injected via an Ommaya reservoir, intravenous (i.v.) vincristine, prednisone, and i.v. daunorubicin. The vincristine (2 mg in 10 mL diluent) was inadvertently injected into her Ommaya reservoir. Within 10 minutes, the error was realized. Despite optimal care, nausea and vomiting developed the first night, followed sequentially by coarse tremor, disorientation, horizontal nystagmus, and stupor. Her mental status waxed and waned until day 9, at which time she became responsive only to noxious stimuli. By day 11, she was deeply comatose and on day 40 she died without regaining any neurological function. CONCLUSION: Despite aggressive and immediate therapy, intraventricular vincristine infusion produced neurologic toxicity, with progressive loss of mental function, followed by coma and death. Systems need to be developed to prevent inadvertent central nervous system administrations.
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BACKGROUND: Cocaine is metabolized by a number of enzymes, the activity of one of which, plasma cholinesterase has been associated with dinical manifestations of toxicity. Patients with life-threatening complications of cocaine intoxication have lower plasma cholinesterase activity than less toxic controls. In addition, relatively healthy cocaine users have lower plasma cholinesterase activity than noncocaine using controls. Thus, low plasma cholinesterase activity could be a contributing factor to cocaine toxicity, a consequence of cocaine use, or a confounding variable. The following study was designed to further assess the relationship between cocaine use and plasma cholinesterase activity. METHODS: We studied fluctuations in plasma cholinesterase activity in nine subjects enrolled in an inpatient study of the behavioral pharmacology of smoked cocaine. Subjects used at least 2 g of cocaine weekly for at least 1 year prior to enrollment. The subjects were admitted to the research unit where they remained drug-free for 2 days. They then received smoked cocaine for 4 days (up to 405 mg over 5 hours daily) and were then drug-free again for 2 days. Plasma cholinesterase activity was measured at 9 AM and 4 PM each day. RESULTS: Baseline plasma cholinesterase ranged from 265 to 930 U/L (normal > 450 U/L). The mean plasma cholinesterase increased 112+/-100 U/L from day 1 to day 8 (p = 0.025). There was no daily change in plasma cholinesterase levels from 9 AM to 4 PM (15+/-165 U/L, p > 0.6), and there was no difference in the daily change between high- and low-dose cocaine days (-3+/-137 U/L vs 28+/-165 U/L, p = 0.52). CONCLUSION: These preliminary data suggest that plasma cholinesterase levels do not change over a 7-hour period as a result of cocaine administration, but may increase during a period of inpatient study. Such an increase could potentially influence the pharmacokinetics or effects of cocaine studied in an inpatient setting and may give insight into the etiology of the observed low-plasma cholinesterase activity in cocaine users.