Carbamazepine
1
Carbamazepine Multisystem toxicity Docusate sodium 200 mg/day , pentazocine 100-200 mg/day and carbamazeplne 200 mgjday were added to the drug regimen of a 73-year-old man with severe chronic obstructive lung disease aggravated by intercostal postherpetic neuralgia. Other medication being taken daily included theophylline 400mg, prednisone 15mg, salbutamol 1.5ml, sucralfate 39 and frusemide [furosemide] 80mg. The carbamazepine dose was increased to 600 mg/day on day 5 and, following this increase, the neuralgia almost completely disappeared. However, carbamazepine was wi1hdrawn after the patient presented with confusion on day 7 and slurred speech, drowsiness, ataxia and urinary incontinence on day 10. The confusion and drowsiness then became less evident but occasional premature supraventricular beats, nausea, vomiting and diarrhoea were noted. Haematological investigations found the lotal leucocyte count was 0.7 x 10 9 jL with 1 % neutrophils and the serum electrolyte concentrations were: sodium 126 mmol/L, potassium 3.4 mmolfL; and chloride 82 mmol/L. Frusemide was discontinued. Ampicillin SOOmg qid plus gentamiCin 40mg tid were administered parenterally and reverse isolation precautions taken. However, severe monilial pharyngitis and transient fever (38.4°C) developed. Frusemide was restarted on day 14 and therapy with IV saline plus hydrocortisone 200mg qid begun. By day 16 the leucocyte count was 2.0 x 109/L (35% neutrophils, 20% bands, 6% metamyelocytes and 3% myelocytes), serum sodium concentration 122 mmol/L. plasma osmolality 255 mmol/kg and urine osmolality 368 mmol/kg (suggesting dilutional hyponatraemia resulting from inappropriate ADH secretion). The patient's mental state improved but increased dyspnoea, CO 2 retention and respiratory acidosis developed The man died following respiratory and cardiac arrest. 'The onset of the severe, rapidly progressive hematologic. neurologic and metabolic changes after therapy with carbamazepine was begun leaves little doubt that this drug was responsible.' Further, 'the reaction and its sequlae undoubtedly precipitated the patient's death by aggravating his already serious respiratory and cardiac problems'. MIniCh. PJ and Younq. WA. Canadian Medical ASSOCiation Journal 132. 1040 (1 May 1985)
Transcript of Carbamazepine
Carbamazepine Multisystem toxicity
Docusate sodium 200 mg/day, pentazocine 100-200 mg/day and carbamazeplne 200 mgjday were added to the drug regimen of a 73-year-old man with severe chronic obstructive lung disease aggravated by intercostal postherpetic neuralgia. Other medication being taken daily included theophylline 400mg, prednisone 15mg, salbutamol [albu~erol) 1.5ml, sucralfate 39 and frusemide [furosemide] 80mg. The carbamazepine dose was increased to 600 mg/day on day 5 and, following this increase, the neuralgia almost completely disappeared. However, carbamazepine was wi1hdrawn after the patient presented with confusion on day 7 and slurred speech, drowsiness, ataxia and urinary incontinence on day 10. The confusion and drowsiness then became less evident but occasional premature supraventricular beats, nausea, vomiting and diarrhoea were noted. Haematological investigations found the lotal leucocyte count was 0.7 x 109jL with 1 % neutrophils and the serum electrolyte concentrations were: sodium 126 mmol/L, potassium 3.4 mmolfL; and chloride 82 mmol/L. Frusemide was discontinued. Ampicillin SOOmg qid plus gentamiCin 40mg tid were administered parenterally and reverse isolation precautions taken. However, severe monilial pharyngitis and transient fever (38.4°C) developed.
Frusemide was restarted on day 14 and therapy with IV saline plus hydrocortisone 200mg qid begun. By day 16 the leucocyte count was 2.0 x 109/L (35% neutrophils, 20% bands, 6% metamyelocytes and 3% myelocytes), serum sodium concentration 122 mmol/L. plasma osmolality 255 mmol/kg and urine osmolality 368 mmol/kg (suggesting dilutional hyponatraemia resulting from inappropriate ADH secretion). The patient's mental state improved but increased dyspnoea, CO2 retention and respiratory acidosis developed The man died following respiratory and cardiac arrest.
'The onset of the severe, rapidly progressive hematologic. neurologic and metabolic changes after therapy with carbamazepine was begun leaves little doubt that this drug was responsible.' Further, 'the reaction and its sequlae undoubtedly precipitated the patient's death by aggravating his already serious respiratory and cardiac problems'. MIniCh. PJ and Younq. WA. Canadian Medical ASSOCiation Journal 132. 1040 (1 May 1985)
