Management of hypertensive emergencies in acute brain disease: evaluation of the treatment effects of intravenous nicardipine on cerebral oxygenation.

OBJECT: Inappropriate sudden blood pressure (BP) reductions may adversely affect cerebral perfusion. This study explores the effect of nicardipine on regional brain tissue O(2) (PbtO(2)) during treatment of acute hypertensive emergencies. METHODS: A prospective case-control study was performed in 30 patients with neurological conditions and clinically elevated BP. All patients had a parenchymal PbtO(2) and intracranial pressure bolt inserted following resuscitation. Using a critical care guide, PbtO(2) was optimized. Intravenous nicardipine (5-15 mg/hour) was titrated to systolic BP < 160 mm Hg, diastolic BP < 90 mm Hg, mean arterial BP (MABP) 90-110 mm Hg, and PbtO(2) > 20 mm Hg. Physiological parameters-intracranial pressure, PbtO(2), central venous pressure, systolic BP, diastolic BP, MABP, fraction of inspired O(2), and cerebral perfusion pressure (CPP)-were compared before infusion, at 4 hours, and at 8 hours using a t-test. RESULTS: Sixty episodes of hypertension were reported in 30 patients (traumatic brain injury in 13 patients; aneurysmal subarachnoid hemorrhage in 11; intracerebral and intraventricular hemorrhage in 3 and 1, respectively; arteriovenous malformation in 1; and hypoxic brain injury in 1). Nicardipine was effective in 87% of the patients (with intravenous beta blockers in 4 patients), with a 19.7% reduction in mean 4-hour MABP (115.3 +/- 13.1 mm Hg preinfusion vs 92.9 +/- 11.40 mm Hg after 4 hours of therapy, p < 0.001). No deleterious effect on mean PbtO(2) was recorded (26.74 +/- 15.42 mm Hg preinfusion vs 27.68 +/- 12.51 mm Hg after 4 hours of therapy, p = 0.883) despite significant reduction in CPP. Less dependence on normobaric hyperoxia was achieved at 8 hours (0.72 +/- 0.289 mm Hg preinfusion vs 0.626 +/- 0.286 mm Hg after 8 hours of therapy, p < 0.01). Subgroup analysis revealed that 12 patients had low pretreatment PbtO(2) (10.30 +/- 6.49 mm Hg), with higher CPP (p < 0.001) requiring hyperoxia (p = 0.02). In this group, intravenous nicardipine resulted in an 83% improvement in 4- and 8-hour PbtO(2) levels (18.1 +/- 11.33 and 19.59 +/- 23.68 mm Hg, respectively; p < 0.01) despite significant reductions in both mean MABP (120.6 +/- 16.65 vs 95.8 +/- 8.3 mm Hg, p < 0.001) and CPP (105.00 +/- 20.7 vs 81.2 +/- 15.4 mm Hg, p < 0.001). CONCLUSIONS: Intravenous nicardipine is effective for the treatment of hypertensive neurological emergencies and has no adverse effect on PbtO(2).

Cerebral oxygenation in major pediatric trauma: its relevance to trauma severity and outcome.

INTRODUCTION: Trauma is the commonest cause of death in the pediatric population, which is prone to diffuse primary brain injury aggravated by secondary insults (eg, hypoxia, hypotension). Standard monitoring involves intracranial pressure (ICP) and cerebral perfusion pressure, which do not reflect true cerebral oxygenation (oxygen delivery [Do(2)]). We explore the merits of a brain tissue oxygen-directed critical care guide. METHODS: Sixteen patients with major trauma (Injury Severity Score, >16/Pediatric Trauma Score [PTS], <7) had partial pressure of brain tissue oxygen (Pbto(2)) monitor (Licox; Integra Neurosciences, Plainsboro, NJ) placed under local anesthesia using twist-drill craniostomy and definitive management of associated injuries. Pbto(2) levels directed therapy intensity level (ventilator management, inotrops, blood transfusion, and others). Patient demographics, short-term physiological parameters, Pbto(2), ICP, Glasgow Coma Score, trauma scores, and outcomes were analyzed to identify the patients at risk for low Do(2). RESULTS: There were 10 males and 6 females (mean age, 14 years) sustaining motor vehicle accident (14), falls (1), and assault (1), with a mean Injury Severity Score of 36 (16-59); PTS, 3 (0-7); and Revised Trauma Score, 5.5 (4-11). Eleven patients (70%) had low Do(2) (Pbto(2), <20 mm Hg) on admission despite undergoing standard resuscitation affected by fraction of inspired oxygen, Pao(2), and cerebral perfusion pressure (P = .001). Eubaric hyperoxia improved cerebral oxygenation in the low-Do(2) group (P = .044). The Revised Trauma Score (r = 0.65) showed moderate correlation with Pbto(2) and was a significant predictor for low Do(2) (P = .001). In patients with Pbto(2) of less than 20 mm Hg, PTS correlated with cerebral oxygenation (r = 0.671, P = .033). The mean 2-hour Pbto(2) and the final Pbto(2) in survivors were significantly higher than deaths (21.6 vs 7.2 mm Hg [P = .009] and 25 vs 11 mm Hg [P = .01]). Although 4 of 6 deaths were from uncontrolled high ICP, PTS and 2-hour low Do(2) were significant for roots for mortality. CONCLUSIONS: Pbto(2) monitoring allows for early recognition of low-Do(2) situations, enabling appropriate therapeutic intervention.

Collagen matrix (DuraGen) in dural repair: analysis of a new modified technique.

STUDY DESIGN: Retrospective review of 110 patients undergoing spinal dural repair and regeneration using an onlay, suture-free, 3-dimensional-collagen matrix graft (DuraGen) over an 8-year period (1995-2003). OBJECTIVES: Technique appraisal of collagen matrix to repair spinal dura following incidental durotomy, spinal tumor surgery, and trauma. SUMMARY OF BACKGROUND DATA: Traditional methods of spinal dural repair following incidental durotomy involve tedious attempts at primary watertight suture with a 5% to 10% failure rate. Dural injury occurs after trauma, or dural excision may be required after tumor resection. Collagen matrix is a newer development in collagen sponge. METHODS: The clinical and demographic data included diagnosis, type and site of surgery, infection risk, size of defect, use of lumbar drains, closed suction subfascial drains, and adverse events. The primary endpoints of graft failure were cerebrospinal fluid leak and pseudomeningocele formation. Neurosurgical wound infection rates were determined. RESULTS: Collagen matrix was used (n = 110) in the following conditions: degenerative (69), pseudomeningocele formation repair (4), tumors (14), trauma (13), and congenital (5). There were 15 cervical (10 anterior), 21 thoracic (3 anterior), and 71 lumbar (all posterior) surgeries. Fibrin glue was used in 7.3%, subfascial drains in 82%, and lumbar drainage in 2.7%. Overall, cerebrospinal fluid leaks occurred in 2.7%. The 2 pseudomeningocele formations (3.2%) resolved at 3 months. There were 2 wound infections. In the subgroup with incidental durotomy (n = 69), failure of cerebrospinal fluid containment occurred in 4.3% [1 cerebrospinal fluid leak (1.4%), 2 pseudomeningocele formations (2.9%)]. CONCLUSIONS: Collagen matrix was successful in cerebrospinal fluid containment in > 95% of patients requiring dural repair following anterior and posterior spinal surgery. Subfascial drains were safe. Routine lumbar drains are not required but are recommended for repair of established pseudomeningocele formations.