LAUSR

Dear Editor, In case of malignant cerebral infarction and progressive neurological worsening, randomized controlled trials have demonstrated improved survival and functional outcome after decompressive craniectomy and dural expansion. The occurrence of an intracerebral hemorrhage after cranioplasty is extremely rare. To date, only four cases have been reported [1–4]. A 54-year-old man with an extensive left middle cerebral artery territory infarction and progressive neurological impairment (from NIHSS 18 to NIHSS 22) underwent decompressive craniectomy with removal of a large fronto-temporo-parietal bone flap. The patient regained consciousness after the procedure; however, motor right-sided hemiparesis and aphasia were unchanged (NIHSS 15). After 7 days, the patient was transferred to the rehabilitation unit. Ninety-three days later, because of good wound healing and the patient’s desire, he was newly admitted to the hospital for autologous bone flap repositioning. Preoperative control computed tomography (CT) did not show any abnormality except for a large left post-ischemic area in the frontotemporal region. Routine screenings were in the normal range, and low-dose heparin 4000 IU and anti-epileptic drugs were in use. The cranioplasty was performed in 90 min, without complications. Immediately after awakening, the patient experienced a generalized epileptic seizure. Control CT disclosed a hemorrhage in the left cerebellar hemisphere, with mild perilesional edema but no significant abnormalities in the post-ischemic area under the repositioned bone flap (Fig. 1a, b). Blood analysis showed hemoglobin was 12.6 g/dL (13.3 g/dL preoperative), the white cell count was 13,370 (6560 WC preoperative), C-reactive protein was 39,900 μg/L (normal value 100–6000 μg/L), and D-dimer was 1321 μg/L (normal value 0–550 μg/L). Serological protein was slightly reduced from 7.4 to 6.9 g/dL. During the subsequent 12 h, the patient’s level of consciousness deteriorated (GCS 8) and CT displayed an increase of the perilesional edema; therefore, a left suboccipital craniotomy was performed with removal of the cerebellar hemorrhage. The patient did not improve, and CT revealed the occurrence of left cerebellar, mesencephalic, and intraventricular hemorrhages (Fig. 2). Control blood examinations showed acute reduction of the white cell count to 6050, hemoglobin to 8.2 g/dL, and serum protein to 4.7 g/dL. Systemic inflammatory response syndrome (SIRS) was suspected, and the patient died 72 h after cranioplasty. The four cases reported thus far in the literature [1–4] were adults (mean age 66.75 years), with ischemic or hemorrhagic infarction in the brain tissue. As in our case, early or late closure of the bone defect did not appear to be related to the occurrence of the hemorrhage: two patients underwent bone flap repositioning 2 months after decompressive craniectomy, while others underwent repositioning at 9 and 12 months after the procedure. Indeed, this complication appears to be more characteristic of patients with previous ischemic brain stroke (5/5: 100%). The hemorrhagic event after cranioplasty appears to be characterized by diffuse atypical distribution, which varies to * Paolo Missori [email protected]