Lithium
- PDF / 142,914 Bytes
- 1 Pages / 595.245 x 841.846 pts (A4) Page_size
- 70 Downloads / 191 Views
1
S
Drug toxicity and QTc prolongation: case report A 61-year-old man developed QTc prolongation, and neurological and GI symptoms of lithium toxicity while receiving the drug to treat a depressive personality disorder [not all outcomes stated]. The man was hospitalised with symptomatic lithium toxicity. Lithium sulfate 1320 mg/day [route not stated] and clomipramine had been initiated 11 years earlier; annual renal function tests had been normal until the last check-up 209 days earlier, and lithium concentrations had been therapeutic. Clinic visits due to micturition problems had become more frequent 6 months before admission, and he had consulted his general practitioner (GP) with fever, postural abdominal pain and nausea 38 days before admission. On that occasion, gastroenteritis had been suspected, and he had received symptomatic therapy and lansoprazole. He experienced a fainting spell 4 weeks later, 10 days before admission; at that time, he reported an approximately 4-week history of tremor, vertigo, nausea and occasional vomiting. At an emergency room, he had serum sodium and creatinine levels 131 mmol/L and 141 µmol/L, respectively, and an ECG showed a leftanterior hemiblock, right bundle branch block and ventricular extrasystoles. His QRS, QT and QTc intervals were 160ms, 460ms and 521ms, respectively. He was treated for suggested coprostasis, and appeared well on discharge. Control of his lithium concentration was advised. He returned with worsening of his condition 10 days later and was hospitalised. At this current admission, he exhibited tremor and ataxic gait, and reported nausea and visual impairment. An ECG confirmed left anterior hemiblock, right bundle branch block, ventricular extrasystoles and the following intervals: QRS 162ms, QT 560ms, QTc 613ms. His serum creatinine level was 120 µmol/L, and further investigations revealed prostate hyperplasia and urinary retention. His lithium concentration was 1.82 mmol/L at 22 hours from his last dose (therapeutic range 0.5–1.2 mmol/L 12 hours after intake). Lithium and clomipramine were discontinued, and the man was hydrated; urine was drained. His renal function quickly normalised, and GI and neuronal symptoms settled. On day 12, an ECG showed a persistent bifascicular block, a QT interval of 424ms, a QRS complex of 148ms and a QTc interval of 468ms at a HR of 73/min. His somatic state had markedly improved on day 13, and he was transferred to a psychiatric clinic for re-initiation of drug therapy. He eventually underwent transurethral resection for benign hyperplasia. His personality disorder stabilised, and he was receiving risperidone, valproic acid and escitalopram at last follow-up. Author comment: Retrospectively, it can be suspected, that the described patient had suffered from progressive symptoms of lithium intoxication in the weeks before admission. . . [P]ostrenal, possibly renal and even prerenal factors were likely to have caused continuous worsening of his renal function and elevation of lithium concentrations. Stephan P, et al. Uncommo
Data Loading...
