Biomedical subjects

Grant P Sinson

Publications and source records attributed to Grant P Sinson.

6 recordsLinked to original sources

PubMed2006

Biomechanical characterization of internal layer subfailure in blunt arterial injury.

Blunt carotid artery injuries occur in 0.3% of blunt injured patients and may lead to devastating neurological consequences. However, arterial mechanics leading to internal layer subfailure have not been quantified. Twenty-two human carotid artery segments and 18 porcine thoracic aorta segments were opened to expose the intimal side and longitudinally distracted to failure. Porcine aortas were a geometrically accurate model of human carotid arteries. Internal layer subfailures were identified using videography and correlated with mechanical data. Ninety-three percent (93%) of vessels demonstrated subfailure prior to catastrophic failure. All subfailures occurred on the intimal surface. Initial subfailure occurred at 79% of the stress and 85% of the strain to catastrophic failure in younger porcine specimens, compared to 44% and 60%, respectively, in older human specimens. In most cases, multiple subfailures occurred prior to catastrophic failure. Due to limitations in human specimen quality (age, prior storage), young and fresh porcine aorta specimens are likely a more accurate model of clinical blunt carotid artery injuries. Present results indicate that vessels are acutely capable of maintaining physiologic function following initial subfailure. Delayed symptomatology commonly associated with blunt arterial injuries is explained by this mechanics-based and experimentally quantified onset of subcatastrophic failure.

Animals↗

PubMed2002

Perioperative assessment of coagulability in neurosurgical patients using thromboelastography.

BACKGROUND: Thrombelastography is a useful technique for evaluating coagulability. We hypothesized that it could be used to determine postoperative hematologic complications during and after neurologic surgery. METHODS: Forty-six neurosurgical patients were stratified by diagnosis: subarachnoid hemorrhage from ruptured intracranially aneurysms, intracranial-axial lesions, intracranial-extra-axial lesions, and degenerative spine disease. Thromboelastograms were performed before, during, and after surgery. Hematologic data were collected preoperatively and postoperatively; computed tomography scans and lower extremity Doppler sonography were performed postoperatively. A thrombosis index (TI) was used to assess coagulability. RESULTS: Coagulability increased over the course of surgery for all patients (p < 0.0001). In craniotomy patients, coagulability increased over the course of surgery (p < 0.05) with the most dramatic increase from intubation to skin incision (p < 0.05), and then after tumor removal or aneurysm clipping (p < 0.10). Univariate analysis among craniotomy patients showed that female gender (p < 0.0004) and smoking (p < 0.06) were associated with hypercoagulability. Among craniotomy patients, younger age was associated with hypercoagulability in the preoperative period (p < 0.01). There was no significant association between coagulability and aspirin or NSAID use, or intraoperative fluid volume. No patient developed a postoperative hematoma and one patient (2.2%) developed a lower extremity deep vein thrombosis. CONCLUSIONS: Increased coagulability begins between induction of anesthesia and skin incision, and continues to increase throughout surgery. These changes are more pronounced in patients undergoing craniotomy compared to patients undergoing spine procedures.

Adolescent↗

PubMed2002

Alternative management considerations for ethmoidal dural arteriovenous fistulas.

BACKGROUND: Ethmoidal dural arteriovenous fistulas (EDAFs) are an unusual type of intracranial vascular lesion that commonly present with acute hemorrhage. They are often best treated surgically; however, recent endovascular advances raise questions concerning the best therapeutic approach. METHODS: We present 7 cases of EDAFs managed at this institution over a 6-year period, which demonstrate the broad spectrum of clinical behavior associated with the lesions. Four patients presented with intracranial hemorrhage, 1 patient with rapidly progressive dementia, 1 patient with a proptotic, red eye, and 1 with a retro-orbital headache. RESULTS: One patient underwent no treatment, 1 underwent embolization alone, 2 underwent embolization and resection, and 3 patients underwent resection alone. There was complete obliteration of the EDAF in all of the patients who underwent surgical resection. Embolization was performed through the external carotid circulation and not the ophthalmic artery. There were no treatment-related neurologic deficits. CONCLUSIONS: Treatment is best managed with a multidisciplinary approach, which emphasizes complete resection of the lesions with assistance from interventional neuroradiology techniques. However, each patient must be evaluated independently as treatment may vary depending on the angioarchitecture of the lesion.

Aged↗

PubMed2002

Intravascular coagulation: a major secondary insult in nonfatal traumatic brain injury.

OBJECT: The goal of this study was to determine the frequency with which cerebral intravascular coagulation (IC) complicates traumatic brain injury (TBI). The authors also investigated the incidence of IC in relation to varying mechanisms, time courses, and severities of TBI and in different species. METHODS: Tissue was sampled from surgical specimens of human cerebral contusions, from rats with lateral fluid-percussion injuries, and from pigs with head rotational acceleration injuries. Immunohistochemical fluorescent staining for antithrombin III was performed to detect cerebral intravascular microthrombi. Abundant IC was found in all specimens, and microthrombi had formed in arterioles and venules of all sizes, ranging from 10 to 600 microm. Although it was more pronounced in focal lesions and more severe injuries, considerable IC was also observed in mild and diffuse injuries. The authors found a strong association between the severity of coagulopathy and the density of IC. CONCLUSIONS: These results strongly support the contention that IC is a universal response to TBI and an important secondary cerebral insult.

Animals↗

PubMed2002

Propofol.

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Adolescent↗

PubMed2002

Brain atrophy in mild or moderate traumatic brain injury: a longitudinal quantitative analysis.

BACKGROUND AND PURPOSE: Although mild or moderate traumatic brain injury (TBI) is known to cause persistent neurologic sequelae, the underlying structural changes remain elusive. Our purpose was to assess decreases in the volume of brain parenchyma (VBP) in patients with TBI and to determine if clinical parameters are predictors of the extent of atrophy. METHODS: We retrospectively assessed the total VBP in 14 patients with mild or moderate TBI at more than 3 months after injury and in seven patients at two time points more than 3 months apart. VBP was calculated from whole-brain MR images and then normalized by calculating the percent VBP (%VBP) to correct for intraindividual variations in cranial size. Clinical parameters at the time of trauma were evaluated for potential predictors of atrophy. Findings were compared with those of control subjects of similar ages. RESULTS: In the single time-point analysis, brain volumes, CSF volumes, and %VBP were not significantly different between patients and control subjects. In the longitudinal analysis, the rate of decline in %VBP (0.02 versus 0.0064 U/day, P =.05) and the change in %VBP between the first and second time points (-4.16 +/- 1.68 versus -1.49 +/- 1.7, P =.022 [mean +/-SD]) were significantly greater in patients. Change in %VBP was significantly greater in patients with loss of consciousness (LOC) than in those without LOC (P =.023). CONCLUSION: Whole-brain atrophy occurs after mild or moderate TBI and is evident at an average of 11 months after trauma. Injury that produces LOC leads to more atrophy. These findings may help elucidate an etiology for the persistent or new neurologic deficits that occur months after injury.

Adult↗