Palacios Argueta Pedro José, Sánchez Rosenberg Guillermo Francisco, Pineda Alvaro
Facultad de Medicina, Universidad Francisco Marroquín, 6 Avenida 7-55, zona 10, 01010, Guatemala City, Guatemala.
J Med Case Rep. 2018 Jul 11;12(1):202. doi: 10.1186/s13256-018-1744-6.
Severe hyponatremia is rare when carbamazepine is used as monotherapy. It is common to encounter this imbalance in the hospital setting, but rare in the ambulatory one. Here, we present a case of hyponatremia secondary to carbamazepine use in an otherwise asymptomatic patient.
A 44-year-old Guatemalan woman presented to our outpatient clinic with a chief complaint of left knee pain. One month prior, our patient had previously consulted with an outside physician, who prescribed her with 300 mg of carbamazepine, 5 mg of prednisone every 24 hours, and ibuprofen every 8 hours as needed. The symptoms did not resolve and our patient had increased the dose to 600 mg of carbamazepine and 20 mg of prednisone 7 days prior. Our patient complained of left knee pain, fatigue, and bilateral lower limb cramps. No pertinent medical history was recorded and her vital signs were within normal limits. A physical examination was non-contributory, only multiple port-wine stains in the upper and lower extremities associated with mild hypertrophy of the calves, more prominent on the right side. Laboratory studies revealed: a serum sodium level of 119 mmol/L, potassium level of 2.9 mmol/L, thyroid-secreting hormone of 1.76 mIU/m, thyroxine of 14.5 ng/dL, and serum osmolality at 247 mmol/kg. No neurologic or physical disabilities were recorded. In the emergency department, her electrolyte imbalance was corrected and other diagnostic studies revealed: a urinary sodium level of 164 mmol/L and osmolality at 328 mmol/kg. Our patient was diagnosed with syndrome of inappropriate antidiuretic hormone secretion secondary to carbamazepine use, hypokalemia secondary to corticosteroid therapy, and Klippel-Trénaunay-Weber syndrome. Carbamazepine was discontinued, fluid restriction ordered, and hypokalemia was corrected. One week after discharge, our patient no longer felt fatigued, the cramps were not present, and her left knee pain had mildly improved with acetaminophen use and local nonsteroidal anti-inflammatory cream. Electrolyte studies revealed a sodium level of 138 mmol/L, potassium level of 4.6 mmol/L, and serum osmolality at 276 mmol/L.
Hyponatremia can be misdiagnosed if not recognized promptly; suspicion should be high when risk factors are present and the patient has been prescribed antiepileptic drugs. Presence of mild symptoms such as fatigue or dizziness should lead to suspicion and subsequent laboratory testing. Patients can suffer from neurologic complications if the imbalance is not corrected.
卡马西平单药治疗时严重低钠血症罕见。在医院环境中遇到这种失衡很常见,但在门诊环境中罕见。在此,我们报告一例在其他方面无症状的患者因使用卡马西平继发低钠血症的病例。
一名44岁危地马拉女性因左膝疼痛为主诉前来我们门诊就诊。1个月前,该患者曾咨询过一名外部医生,医生给她开了300毫克卡马西平、每24小时5毫克泼尼松以及按需每8小时服用布洛芬。症状未缓解,患者在7天前将卡马西平剂量增加到600毫克,泼尼松剂量增加到20毫克。患者主诉左膝疼痛、疲劳和双侧下肢痉挛。未记录到相关病史,其生命体征在正常范围内。体格检查无异常发现,仅上下肢有多处葡萄酒色斑,伴有小腿轻度肥大,右侧更明显。实验室检查结果显示:血清钠水平为119毫摩尔/升,钾水平为2.9毫摩尔/升,甲状腺分泌激素为1.76毫国际单位/毫升,甲状腺素为14.5纳克/分升,血清渗透压为247毫摩尔/千克。未记录到神经或身体残疾情况。在急诊科,她的电解质失衡得到纠正,其他诊断检查显示:尿钠水平为164毫摩尔/升,渗透压为328毫摩尔/千克。该患者被诊断为因使用卡马西平继发抗利尿激素分泌不当综合征、因皮质类固醇治疗继发低钾血症以及Klippel-Trénaunay-Weber综合征。停用卡马西平,下令限制液体摄入,并纠正低钾血症。出院1周后,患者不再感到疲劳,痉挛消失,使用对乙酰氨基酚和局部非甾体抗炎乳膏后左膝疼痛稍有改善。电解质检查显示钠水平为138毫摩尔/升,钾水平为4.6毫摩尔/升,血清渗透压为276毫摩尔/千克。
如果不及时识别,低钠血症可能会被误诊;当存在危险因素且患者已被开具抗癫痫药物时,应高度怀疑。出现疲劳或头晕等轻微症状应引起怀疑并随后进行实验室检查。如果失衡未得到纠正,患者可能会出现神经并发症。