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To the Editor:—In the ED patients diagnosed with a chronic subdural hematoma (cSDH) are often characterized by old age, alcohol abuse, or coagulation abnormalities. Besides, cSDH might rarely coincide with other not as prominent conditions.
To consider a cSDH early in patients who received a dural puncture and present progressive decline in the level of consciousness or a focal neurologic deficit could prevent serious sequelae of a disease with an otherwise good prognosis.
We report the occurrence of a cSDH in a 31-year-old, healthy nulliparous woman, who received an epidural analgesia for labor pain when delivering twins after an uneventful pregnancy. While attempting epidural catheter positioning, an unintentional dural puncture was made, diagnosed by clear cerebrospinal fluid (CSF) drainage. A second catheter was successfully placed through a 17-g Quincke needle and satisfactory pain control was obtained. The vaginal delivery of both babies had to be assisted by vacuum extraction after insufficient decent during the second stage of labor. The mother reported a bifrontally located headache, which got worse on getting up and improved in the supine position. This headache was interpreted as postdural puncture headache (PDPH) which is seen in up to 74% of obstetric patients after unintentional dural puncture.
On day 17 after delivery, the patient reported a new headache without improvement on lying down. On day 20, she started to feel nauseated, to vomit, and was seen in the ED, where the patient was drowsy but orientated (Glasgow Coma Scale 14). Physical examination did not reveal a focal neurologic deficit. Laboratory tests did not reveal a coagulation disorder.
The computed tomography (CT) scan revealed bilateral cSDHs (Fig 1A) and diminishing of the basal cisterns indicate increased intracranial pressure (Fig 1B). Immediate surgical evacuation was achieved through burr holes on both parietal tubers. Postoperatively, the patient’s condition improved rapidly but she reported an inability to name and recognize objects, whereas her visual acuity and visual field were intact. The visual agnosia resolved completely within 3 days. Regular follow- up investigations did not reveal any focal neurologic deficit.
FIGURE 1Computed tomography scan of the head showing bilateral chronic subdural hematomas at the convexity of both hemispheres (A). The chronic subdural hematoma appears as a mixture of hypo- and hyperdense material corresponding to hemorrhages of different ages. The adjacent cortical sulci are compressed. As a result of bilateral hematoma formation, there is no midline shift. The diminishing of the basal cisterns next to the brain stem (B) indicates increased intracranial pressure and movement of the brain caudally.
cSDHs after dural puncture, spinal or epidural anesthesia are rare. The largest published series on 434 intracranial hemorrhages secondary to regional anesthesia revealed only six cases (1.4%) of cSDHs with a possible link to a primary spinal anesthesia during labor.
cSDHs form when bridging veins rupture and blood accumulates in the space between the arachnoid and the dura. Electron microscopic data on human bridging veins show thin walls of variable thickness, circumferential arrangement of collagen fibers, and a lack of outer reinforcement by arachnoid trabecules, all contributory to the subdural portion of the vein being more fragile than its subarachnoid portion.
This fragility might lead to rupture by traction and tearing in the instant of a head trauma. In the patient we report, the cSDH could have been caused by CSF hypotension. CSF hypotension could be a consequence of CSF outflow into the soft tissue after injury of the lumbar dura.
CSF loss might be accentuated by increased CSF pressure caused by active bearing down during the second stage of labor. In patients receiving spinal anesthesia, larger needles are used, leaving a larger fistula enabling more rapid CSF drainage.
CSF hypotension could have been aggravated by the vacuum extraction assisting the delivery.
The patient we present had no predisposing factors for cSDH. Still the diagnosis of the PDPH had to be doubted because the headache lasted more than 2 weeks. A cranial CT is justified if a suspected PDPH is resistant against conservative therapy, increasing in severity, or recurring after a pain-free interval. Vomiting, somnolence, hemiparesis, hemihypesthesia, aphasia, or signs of personality changes might be present but need not accompany the clinical picture. In bilateral cSDH, unilateral focal deficits could be difficult to recognize. The symptoms could subside after surgical decompression, but permanent neurologic deficits have been reported in old patients and when the hematoma was evacuated only after a long period of time.
In summary, this report highlights the importance of considering a cSDH as differential diagnosis of headache as a rare but serious complication of epidural anesthesia, especially in connection with dural puncture and straining during labor. By the time of hospital presentation, the patient might not link the clinical symptoms to the dural puncture because several days could have passed. Awareness of this diagnosis and treatment are of uttermost importance because in young patients, cSDHs heal without sequelae after evacuation and irrigation through a cranial burr hole.
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