INTRACRANIAL hypotension is an important cause of new daily persistent postural headaches.1Among the causes of intracranial hypotension, many cases are due to spontaneous cerebrospinal fluid (CSF) leak, often associated with an underlying generalized connective tissue disorder.2Intracranial hypotension may also be due to dural puncture after epidural catheter positioning.
Most cases of intracranial hypotension are believed to be self-limiting, and initial treatment is based on antiinflammatory drugs, bed rest, and hydration. In some patients, persistent symptoms are present; for them, available treatment options include epidural blood patching,3percutaneous fibrin sealant placement,4and surgical repair of the underlying CSF leak.5
We report a case of intracranial hypotension due to spontaneous arachnoid rupture in a parturient woman during the effort of delivery.
A 36-yr-old primiparous woman started spontaneous term labor after a physiologic pregnancy. Her only clinical record was recurrent tensive cephalea and a sense of tightness in her shoulders and neck few days before delivery.
At 3 cm of dilatation, with the baby’s head at level 0 in the correct position, epidural catheter positioning was performed by a skilled anesthesiologist. Aspiration was performed, and a test dose of 40 mg lidocaine was administered to rule out intravascular or intrathecal placement of the catheter. Fentanyl, 100 μg, was then administered, followed by boluses of 8 mg ropivacaine, 0.2%, up to 32 mg local anesthetic solution. After approximately 20 min, good analgesia was achieved, and continuous infusion of 8–12 mg/h ropivacaine, 0.15%, was started. When complete dilatation was reached, the continuous infusion of local anesthetic solution was stopped.
During the expulsive phase of delivery, the patient was kept in the squatting position. This phase lasted 20 min. The newborn was female, weighed 3,200 mg, had an Apgar score of 10/10, and had a cord pH of 7.37. During labor and delivery, no motor blockade was observed.
One hour after delivery, the patient began to report frontal headache, radiating to the whole head and exacerbated by movement. No laboratory blood abnormality was present, nor was any blood pressure alteration. Ketorolac, 30 mg, was administered without any benefit.
On the seventh postdelivery day, the headache became worse: The symptoms were continuous even in the recumbent position, worsening when the patient was upright. Vertigo, obtundation, and nausea were also present.
The patient was treated as if she had a dural break due to the epidural catheter positioning: She received hydration with 2,000 ml/day intravenous saline, 90 mg/day ketorolac, and 3 g/day paracetamol with no benefit.
Ten days after delivery, the patient underwent cranial magnetic resonance imaging scanning. The scanning was performed without contrast because the patient was breastfeeding. Neuroimaging showed diffuse bilateral subdural collections in both hemispheres and in the posterior cranial fossa extending to the craniospinal junction, with a modest downward displacement of the cerebellar tonsilla. A C5–C6 herniation was also present. No extradural CSF collection was present (fig. 1).
The diagnosis was spontaneous effort-related rupture of the arachnoid membrane. It is possible that the cervical hernia may have caused the presence of an easier point of break and that the position kept by the patient during expulsive phase of delivery may have played a role. The symptoms were due both to the intracranial hypotension and to the compression on the brain by the CSF sequestered between the arachnoid membrane and dura madre. Bed rest proved to be the appropriate therapy, with relief of the symptoms within 1 month.
The syndrome of low-pressure headache is usually due to a leak of CSF through the dura, either because of a spontaneous tear or as a complication of a dural puncture. In this case, the dura was intact, and the leak involved only the arachnoid, so that CSF collection was subdural. In spontaneous intracranial hypotension syndrome, the occurrence of subdural collections is secondary to the rupture of bridging veins when the brain pulls away from the dura as the CSF decreases.6
The main controversial question of this report can be considered the potential of unrecognized dural puncture. However, the anesthesiologist excluded a wet tap defined as an inadvertent dural puncture by the epidural needle or catheter with CSF return or clinical evidence of motor blockade.7Moreover, the start of symptoms in addiction to the evidence of C5-C6 herniation suggested a different etiology.
The different forms of low-pressure headache must be distinguished to start a correct treatment. Treatment of spontaneous intracranial hypotension syndrome begins with noninvasive therapeutic modalities, including bed rest, use of an abdominal binder, oral caffeine, and steroids. If the patient continues to be symptomatic, available treatment options include epidural blood patching, percutaneous fibrin sealant placement, and surgical repair of the underlying CSF leak. Treatment options for postdural puncture headache include bed rest, intravenous saline infusion, steroids, and antiinflammatory drugs. Our patient was successfully treated with bed rest, while antiinflammatory drugs and intravenous saline infusion proved to be inefficient.