RESUMEN
We report an uncommon case of a 38-years-old pregnant woman affected by HHT (Hereditary haemorrhagic telangiectasia; Osler-Weber-Rendu syndrome) who underwent to a caesarean section (CS) without any complication. The patient at 36th weeks+1 day pregnancy referred to the Emergency Obstetric Unit due to a intercostals pain on left side. On third day after admission the woman started travailing and physicians decided to perform the CS. Considering that no AVMs was found at MRI, a continuous spinal anaesthesia was planned. On postpartum day 4 the patient was discharged. This represents the only case published in the literature. Women with HHT, especially those with arteriovenous malformations (AVM), are at high risk in pregnancy due to physiological haemodynamic changes pregnancy associated. Early screening of patients with HHT for the presence of spinal cord or cerebral AVMs is recommended to optimise perioperative anaesthetic management and to avoid severe complications.
Asunto(s)
Cesárea , Complicaciones del Embarazo/prevención & control , Telangiectasia Hemorrágica Hereditaria/complicaciones , Adulto , Anestesia Obstétrica/efectos adversos , Anestesia Raquidea/efectos adversos , Cesárea/efectos adversos , Femenino , Edad Gestacional , Humanos , Embarazo , Complicaciones del Embarazo/etiología , Medición de Riesgo , Factores de Riesgo , Telangiectasia Hemorrágica Hereditaria/diagnósticoRESUMEN
We report a case of a woman presenting, 7 days after epidural analgesia for a caesarean section, to the emergency room for a worsening of the headache and tonico-clonic seizures. MRI showed alterations suggestive of the presence of intracranial hypotension (IH) as well as evidence of posterior reversible encephalopathy syndrome (PRES). She was treated with a blood patch which leads to the prompt regression of the clinical symptoms and follow-up MRI, after 15 days, showed complete resolution of radiological alterations. The possible pathogenetic relationship between IH, secondary to the inadvertent dural puncture, and PRES is discussed. We suggest that venous stagnation and hydrostatic edema, secondary to intracranial hypotension, probably played a crucial role in the pathogenesis of PRES.