INTRACRANIAL subdural hematoma is a rare but potentially fatal complication of dural puncture after spinal anesthesia or accidental puncture with a Tuohy needle. The leakage of cerebrospinal fluid may lower intracranial pressure, and caudal movement of the spinal cord and brain stretches and tears dural veins, resulting in subdural bleeding. Cerebrospinal fluid leakage more often causes postdural puncture headache (PDPH), of which the incidence and severity correlate well with the needle size and tip design. Using the smallest possible spinal pencil-point needles is recommended to minimize these complications. The purpose of this article is to report a case of fatal subdural hematoma after spinal anesthesia with a 27-gauge Whitacre needle.

A 42-yr-old man, who was healthy except for long-standing asthma treated with inhaled salbutamol, underwent uneventful anesthesia using a 27-gauge needle for surgical management of an Achilles tendon rupture. He had no history of trauma, headache, or coagulation abnormalities. Preoperative laboratory blood tests, including platelet count, prothrombin time, and activated prothromboplastin time, yielded normal results. Because of the asthma, a regional anesthetic technique was chosen. Spinal anesthesia, performed at the L3–L4 interspace using a 27-gauge Whitacre needle, was successful on the first attempt. The intraoperative course was uneventful except for a moderate decrease in blood pressure (from 140 mmHg to 110 mmHg for systolic blood pressure), which necessitated no treatment. The leg was placed in a plaster cast at the end of surgery.

Postoperative medication consisted of proacetamol (2 g three times a day) and enoxaparin (40 mg subcutaneously daily). The patient experienced a generalized headache 2 h later, which was particularly severe in the occipital area. It was interpreted as a PDPH because it was more intense while seated. The patient declined autologous epidural blood patch, proposed by the anesthesiologist. Treatment for the next 3 days consisted of an increase in fluid intake (2,500 ml/day) and bed rest in the supine position. The headache improved and the patient was discharged on day 4. Thromboprophylaxis was continued.

On the ninth postoperative day, the patient contacted the anesthesiologist because of a severe headache, both in the upright and in the recumbent position. The physician advised hospital admission, but this was declined by the patient. The next day, the headache decreased in severity and was localized to the frontotemporal region. The patient became sleepy and vomited, as his family reported later. He became comatose on the afternoon of the same day. An endotracheal tube was inserted, and he was transported to our hospital.

At admission, the patient was comatose, with the left pupil dilated and minimally reactive, presenting with right hemiparesis. Both plantar responses were in extension. Transcranial Doppler ultrasonography indicated increased intracranial pressure, with very low diastolic velocity in the middle cerebral artery because blood pressure was increased. A computed tomographic scan showed a 2-cm–thick acute left subdural hematoma. Left temporal craniotomy was performed immediately (52 min after admission) to remove this recent and homogenous hematoma. No bleeding point was identified. Postoperatively, the patient remained comatose and decerebrate. Angiography ruled out the presence of a vascular malformation, and magnetic nuclear resonance imaging showed important mesencephalic and thalamic lesions. The patient died 2 days later (on the twelfth postoperative day).

Acute intracranial subdural hematoma is a rare but potentially lethal complication that can occur after spinal anesthesia, epidural anesthesia, or myelography. 1–3The needles used ranged in size from 16 to 25 gauge. Five deaths have been recorded. The same pathogenic mechanism has been postulated for PDPH and subdural hematoma. 4Cerebrospinal fluid leakage from the dural hole reduces cerebrospinal fluid volume. The reduced intracranial pressure allows the brain to move caudally with stretching of the dural veins. This produces pain. Vasodilatation of intracranial vessels also may contribute to pain. The needle hole in the dura can remain open for many weeks. PDPH is a relatively common complication, whereas subdural hematoma is rare. In these more serious cases, cortical veins are stretched and torn, which results in subdural bleeding. In some cases, the source of bleeding is identified by the neurosurgeon (small artery in subarachnoid tissue or cortical veins). Small-size needles with a pencil-point tip are known to produce the lowest incidence and severity of postspinal headache. 5One does not expect an easy dural puncture with use of a 27-gauge Whitacre needle to produce a tear sufficiently large to create cerebrospinal fluid loss and subdural hematoma. One important clinical feature of PDPH is its relation with position. Headache becomes more severe when the patient is in the upright position, and it is relieved by lying down. Very few other diseases can display posturodependent headache (cerebral thrombophlebitis, 6incipient eclampsia, 7meningitis, 8and others), and, thus, position-related headache is almost synonymous with PDPH. Diagnosis of PDPH probably should be excluded when the relation with position is not found. When a posturodependent headache after a dural tap becomes permanent and loses its relation with position, a subdural hematoma should be sought urgently with computed tomography. In the case presented herein, on the ninth postoperative day, the nature of the headache changed and became unrelated to position. The patient declined hospital admission, which might have avoided a fatal outcome.

The development of cerebral subdural hematoma might have been a spontaneous event related to the administration of low-molecular-weight heparin (LMWH), used to prevent deep vein thrombosis in a patient with a plaster cast. 9Although spontaneous hematoma may occur in patients treated with anticoagulants, recent literature has emphasized the deleterious role of LMWH in producing spinal or epidural subdural hematoma. In the current case, the patient was administered a prophylactic dose of LMWH, which is considered adequate. 10Platelet count and coagulation profile (prothrombin time and activated prothromboplastin time) were normal at admission to the intensive care unit, as expected with LMWH. This indicates either that anticoagulant administration should be discontinued when PDPH occurs or that assessment of headache characteristics (its relation with position particularly) should be performed with increased frequency in anticoagulated patients.

To avoid a potential negative outcome, regular follow-up of patients with headache after neuraxial block helps delineate between a typical PDPH and a nonpostural headache, the latter necessitating more aggressive attention, particularly in a patient with another risk factor of bleeding, such as LMWH treatment.

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