Medical reconciliation in patients discharged from the emergency department.

BACKGROUND: Medication errors are considered to be a significant cause of morbidity and mortality. For each patient, emergency departments (EDs) are expected to compile a list of medications, reconcile them, and pass them along to the next provider. The electronic medical record provides a method to automatically capture and propagate what may be incorrect information. OBJECTIVES: The aim of this study was to compare the medication information that patients ultimately discharged from the ED provide to the ED staff vs. the medication information the patients provide at follow-up, and to classify and quantify the types of discrepancies between the two. METHODS: We conducted a retrospective descriptive study of a convenience sample of 36 patients who were discharged from the ED and who reported taking five or more medications. Discrepancies were identified by comparing information collected at the time of the index ED visit with that gleaned from follow-up contact within 7 days of discharge. RESULTS: Of the 36 charts analyzed, 286 medications were provided by patients at the time of their ED visit. Subsequent determination of actual medication use on follow-up found 120 discrepancies, for a discrepancy rate of 42.0% (95% confidence interval [CI] 36.4-47.8%). One or more discrepancies were found on 86.1% of charts (95% CI 74.8-97.4%). CONCLUSIONS: Frequent discrepancies are found in the medication information that patients provide in the ED. Requiring the ED to reconcile medication information and to pass it on to the next provider can be a source of treatment errors in the outpatient setting.

Toxin-related seizures.

Toxin-related seizures result from an imbalance in the brain's equilibrium of excitation-inhibition. Fortunately, most toxin-related seizures respond to standard therapy using benzodiazepines. However, a few alterations in the standard approach are recommended to ensure optimal care and expedient termination of seizure activity. If 2 doses of a benzodiazepine do not terminate the seizure activity, a therapeutic dose of pyridoxine (5 g intravenously in an adult and 70 mg/kg intravenously in a child) should be considered. Phenytoin should be avoided because it is ineffective for many toxin-induced seizures and is potentially harmful when used to treat seizures induced by theophylline or cyclic antidepressants.

Spontaneous rupture of an umbilical hernia with evisceration.

Umbilical hernias are a common complication of persistent ascites. Spontaneous rupture of these hernias is a less common complication. We report a case of spontaneous evisceration through an umbilical hernia in a cirrhotic patient with chronic ascites. Definitive surgical repair of the evisceration was not possible secondary to persistent ascites that was refractory to paracentesis and diuresis. Transjugular intrahepatic portocaval shunt (TIPS) placement was ultimately performed in an attempt to eliminate the ascites fluid. This case demonstrates a rare, but life-threatening complication of abdominal ascites that may be prevented by aggressive medical and surgical management.

Cerebrospinal fluid analysis in fatal thallium poisoning: evidence for delayed distribution into the central nervous system.

The neurologic manifestations of thallium poisoning include a severely painful ascending peripheral neuropathy, autonomic dysfunction, cranial nerve abnormalities, and a toxic encephalopathy. Although thallium has a short half-life, these neurologic manifestations commonly progress, even as the blood concentration of thallium decreases. This suggests either that thallium persists in neuronal tissues or that it initiates an injury cascade that takes time to fully manifest. As the latter mechanism is consistent with many toxin exposures, the concept of a central nervous system reservoir for thallium is often discounted. A recent case provided a unique opportunity to evaluate this possibility. A 48-year-old man was acutely and chronically thallium poisoned by his common-law wife. During his initial exposures, only gastrointestinal symptoms manifested. Following an acute ingestion, hospitalization was required. Over 3 days, his symptoms rapidly progressed from a severely painful neuropathy to slurred speech, ptosis, confusion, coma, respiratory insufficiency, and death. Because of considerations of alternative diagnoses, 2 lumbar punctures were performed, one on admission and another on the day of his death. Serum thallium concentrations obtained from stored blood samples were paired with spinal fluid concentrations from the same days. On day 1, serum and spinal fluid concentrations were 8700 mu/L and 1200 mu/L, respectively. On day 3, although the serum concentration had fallen to 7200 mu/L, the spinal fluid concentration had increased to 2100 mu/L. This case provides evidence to support the hypothesis that thallium distributes into the central nervous system more slowly than the blood compartment, and this may in part account for the progression of neurologic findings in the setting of decreasing serum concentrations.

Diphenhydramine-induced wide complex dysrhythmia responds to treatment with sodium bicarbonate.

Diphenhydramine, a common ingredient in over-the-counter medications, is often taken in overdose. Toxicity is usually limited to anticholinergic symptoms. However, because diphenhydramine also exhibits type IA sodium channel blockade, cardiac toxicity is also possible. Although it would be expected that, like other type IA toxicities, diphenhydramine-induced cardiotoxicity could be responsive to hypertonic sodium bicarbonate, this finding is largely unappreciated. We describe 3 cases of diphenhydramine-induced cardiac toxicity that were responsive to bicarbonate.