Dural repair using acellular human dermis: experience with 200 cases: technique assessment.

OBJECTIVE: Many craniotomies require a watertight dural closure. When primary dural repair is not possible, a graft is necessary. Autograft material is not always easily accessible or available, necessitating the use of other material. We performed 200 craniotomies using an acellular human dermal graft (AlloDerm; LifeCell Corp., The Woodlands, TX) to determine its suitability as a dural substitute. METHODS: From June 1996 through March 1998, all patients at Allegheny General Hospital who required a dural substitute graft and in whom autograft harvest was impractical or impossible received the acellular dermal autograft. The running suture technique was used to form a watertight seal. RESULTS: After follow-up for a minimum of 1 year, seven patients have required subsequent surgery. Three patients developed cerebrospinal fluid leaks that were repaired without removing the dermal graft. Four patients developed wound infections that required debridement. In each patient, the graft seemed to be uninvolved in the infectious process and was left in place. The patients were administered antibiotics postoperatively, and there have been no recurrent infections. No adhesion formation or scarring was noted around or underneath the graft in any patient. CONCLUSION: AlloDerm is a reasonable alternative to the available dural graft materials. Its handling characteristics are similar to those of dura, it is biologically inert, and it does not produce adhesion formation.

Prolonged survival in a patient with sinonasal teratocarcinosarcoma with cranial extension. Case report.

Sinonasal teratocarcinosarcoma is a rare malignant neoplasm characterized by the combined histological features of carcinosarcoma and teratoma. The primary symptoms of this tumor are usually nasal obstruction and epistaxis, and a nasal cavity mass is the most common clinical finding. The authors describe an exceptionally rare case in which the patient presented with massive intracranial extension and exhibited confusion as an initial symptom. He subsequently underwent combined radical surgery and radiation therapy and has remained free of disease for 31 months. The surgical approach to the lesion, histological features, and clinical course are detailed.

Early white blood cell dynamics after traumatic brain injury: effects on the cerebral microcirculation.

Increasing clinical and experimental evidence suggests that traumatic brain injury (TBI) elicits an acute inflammatory response. In the present study we investigated whether white blood cells (WBC) are activated in the cerebral microcirculation early after TBI and whether WBC accumulation affects the posttraumatic cerebrovascular response. Twenty-four anesthetized rabbits had chronic cranial windows implanted 3 weeks before experimentation. Animals were divided into four experimental groups and were studied for 7 hours (groups I, IIa, and III) or 2 hours (group IIb). Intravital fluorescence videomicroscopy was used to visualize WBC (rhodamine 6G, intravenously), pial vessel diameters, and blood-brain barrier (BBB) integrity (Na+-fluorescein) at 6 hours (groups I, IIa, and III) or 1 hour (group IIb) after TBI. Group I (n = 5) consisted of sham-operated animals. Groups IIa (n = 7) and IIb (n = 5) received fluid-percussion injury at 1 hour. Group III (n = 7) received fluid-percussion injury and 1 mg/kg anti-adhesion monoclonal antibody (MoAb) "IB4" 5 minutes before injury. Venular WBC sticking, intracranial pressure (ICP), and arterial vessel diameters increased significantly for 6 hours after trauma. IB4 reduced WBC margination and prevented vasodilation. Intracranial pressure was not reduced by treatment with IB4. Blood-brain barrier damage occurred at 1 hour but not at 6 hours after TBI and was independent of WBC activation. This first report using intravital videomicroscopy to study the inflammatory response after TBI reveals upregulated interaction between WBC and cerebral endothelium that can be manipulated pharmacologically. White blood cell activation is associated with pial arteriolar vasodilation. White blood cells do not induce BBB breakdown less than 6 hours after TBI and do not contribute to posttraumatic ICP elevation. The role of WBC more than 6 hours after TBI should be investigated further.

Hypertonic/hyperoncotic saline attenuates microcirculatory disturbances after traumatic brain injury.

BACKGROUND: Traumatic brain injury (TBI) induces an acute inflammatory response characterized by early recruitment of inflammatory cells (white blood cells). Rapid resuscitation of TBI with hypertonic saline/dextran (HS/DEX) yields promising results in clinical and experimental studies. The purpose of this paper was to test the hypothesis that HS/DEX exerts its effects in part through a modulation of the acute inflammatory response to TBI. METHODS: Rabbits equipped with chronic cranial windows underwent fluid-percussion injury and were followed up for 6 hours. Intravital fluorescence videomicroscopy technique was used to visualize white blood cell trafficking and to measure pia vessel diameters and venular shear rates. Three groups were studied: sham (group I, n = 5), trauma (group II, n = 7), and trauma and 4 mL/kg 7.2% NaCl/10% dextran 60 IV over 5 minutes at 10 minutes after TBI (group III, n = 7). RESULTS: TBI in groups II and III led to significant increases of intracranial pressure. Arteriolar diameters after trauma increased by 17 +/- 8% at 6 hours in group II. Infusion of HS/DEX completely prevented this secondary diameters increase. At 6 hours, the increase of "sticking" white blood cells in group III was reduced by approximately 90% compared with group II. CONCLUSIONS: Whether the anti-inflammatory effect of HS/DEX plays a role in reducing delayed brain damage (> 6 hours after TBI) or other systemic complications of TBI arises as an important question and should be investigated further.