Biomedical subjects

R D Fessler

Publications and source records attributed to R D Fessler.

23 records · Page 2Linked to original sources

PubMed1997

The neurovascular complications of cocaine.

BACKGROUND: Cocaine use has been temporally associated with neurovascular complications, including the rupture of intracerebral aneurysms. The purpose of the current study was to determine the type of neurovascular complications associated with cocaine use in our patient population, the temporal relationship between cocaine use and their onset, and whether cocaine users with subarachnoid hemorrhage (SAH) presented with smaller aneurysms at an earlier age than a control group of noncocaine users with SAH. METHODS: Thirty-three patients who presented to the Detroit Medical Center with neurovascular sequelae associated with cocaine use were identified. All patients were chronic cocaine users who related a history of recent use confirmed by a drug screen. Cocaine users with SAH were compared to a control group of 44 patients with SAH who presented without evidence of cocaine use. RESULTS: Sixteen patients presented with SAH. Twelve patients subsequently underwent four-vessel cerebral arteriogram revealing 14 aneurysms; six patients presented with intracerebral hemorrhage (ICH) and seven patients with evidence of ischemic stroke. Eighteen (54.5%) patients noted onset of their symptoms while using cocaine, 87.9% noted onset within 6 hours of use. Delayed presentation occurred predominantly in patients who suffered ischemic strokes. The average age of patients who used cocaine and presented with SAH secondary to a ruptured intracerebral aneurysm was 32.8 years with an average aneurysm diameter of 4.9 mm versus an average age of 52.2 years with an average aneurysm diameter of approximately 11.0 mm in noncocaine users. Population differences were statistically significant at the p < 0.05 level. Mortality was 27.3% for patients who presented with neurovascular sequelae of their cocaine use, with 77.8% of deaths occurring in patients who presented with SAH. CONCLUSIONS: Chronic cocaine use appears to predispose patients who harbor incidental neurovascular anomalies to present at an earlier point in their natural history than similar non-cocaine users.

Adult↗

PubMed1993

The management of cerebral perfusion pressure and intracranial pressure after severe head injury.

Neurosurgical intervention attempts to minimize secondary central nervous system injury after severe head injury through the evacuation of mass lesions with subsequent manipulation of cerebral perfusion pressure and intracranial pressure. The normal brain couples blood flow to metabolic demand through autoregulation of the cerebral vasculature. After severe head trauma and its attendant increase in intracranial pressure, marked alterations in cerebral blood flow and perfusion may occur. Currently, intervention is based on maintenance of coronary perfusion pressure and aggressive management of intracranial pressure. Both may be impacted by manipulation of ventilation, systemic blood pressure and volume status, administration of osmotic diuretics, and head elevation. Such therapy in the patient with severe head injury attempts to maintain coronary perfusion pressure and adequate oxygen delivery in a damaged central nervous system with altered hemodynamics and raised intracranial pressure.

Brain↗

PubMed1988

Anticoagulant effects of protamine sulfate in a canine model.

Protamine sulfate is considered a weak anticoagulant, yet little is known concerning the mechanism of this effect or its relation to prior heparin exposure. This investigation defined the influence of increasing doses of protamine, with and without prior heparin anticoagulation, on the activated clotting time (ACT), thrombin clotting time (TCT), prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen level, platelet count, and platelet aggregation to ADP in dogs (n = 8). Four doses of intravenous protamine sulfate (1.5, 3.0, 6.0, and 15.0 mg/kg) were studied in each animal, with at least 5 days between individual studies. Four dogs received heparin, 150 IU/kg 10 min prior to protamine sulfate administration, and four dogs received protamine sulfate alone. Protamine sulfate caused anticoagulation, both in the presence and absence of heparin, with significant changes occurring in the ACT, PTT, platelet count, and platelet aggregation. Relevant changes did not occur in the TCT, PT, or fibrinogen levels. Platelet effects were capable of causing bleeding with standard or excess use of protamine sulfate, especially if platelet numbers were already decreased, as might occur in surgical procedures where thrombocytopenia commonly accompanies major blood loss and replacement. The ACT, reflecting both the coagulation cascade and platelet function, was the test most profoundly affected by protamine overdosage, and therefore may be misleading as a measure of protamine reversal of heparin. The TCT, which is sensitive to heparin anticoagulation but not protamine-induced anticoagulation, should be more accurate in differentiating inadequate heparin reversal from the effects of excess protamine.

Animals↗

PubMedDate not supplied

Ultrasound abnormalities in term infants on ECMO.

The charts and cranial ultrasounds of 29 infants treated with extracorporeal membrane oxygenation (ECMO) for respiratory insufficiency secondary to meconium aspiration syndrome, primary pulmonary hypertension, congenital diaphragmatic hernia and/or sepsis were examined to identify ultrasound abnormalities. Seventeen (58.6%) developed extra-axial fluid collections, only two of which were progressive. Ten (34.5%) developed evidence of intracranial hemorrhage (ICH): seven caudate, one each in the thalamus, parietal and occipital lobes. Eight (27.65%) of the neonates had seizures while on ECMO, 5 of whom had concurrent ICH.

Adolescent↗

PubMedDate not supplied

Karyotype analysis of cell sex to determine the source of vascular graft luminal linings following autologous and nonautologous endothelial cell seeding.

Endothelial cell-seeded bilateral carotid ePTFE grafts were studied in 11 dogs to determine the source of their eventual luminal linings. One graft was prepared with autologous cells and the other with nonautologous cells. Immunosuppression was accomplished with cyclosporin and prednisolone. At 2 and 3 weeks post implantation, grafts were removed, revealing 9 of 11 autologous and 8 of 11 nonautologous seeded conduits to be patent. Linings were harvested enzymatically and grown in tissue culture, with karyotype analysis limited to cultures that exhibited greater than or equal to 50% endothelium (n5 autologous, n7 nonautologous). Sex type was classified in 20 cells from each graft. All five autologous cell-seeded grafts revealed host cells. Among the seven nonautologous cell-seeded grafts, one harbored only non-autologous cells, three revealed only autologous cells, and three exhibited a predominance of autologous cells with lesser numbers of nonautologous endothelium. All 100 cells from the autologous-seeded grafts were the same sex as seeded cells, while only 28 of the 140 cells from the nonautologous seeded grafts were the same sex as seeded cells (P less than 0.001). Thus, nonautologous endothelial cell seeding with immunosuppression did not uniformly produce nonautologous cell linings, but was more often associated with autologous endothelial cell linings that may have been promoted by the nonautologous cell seeding.

Animals↗