Biomedical subjects
Publications and source records attributed to Y Shapira.
The authors present clinical and radiographic measures for the early detection of potential maxillary canine Impaction. Intercepting the impaction process by timely removal of the primary canines, as demonstrated in several representative cases, allows the permanent canines to erupt normally and, thus, prevents their potential impaction.
OBJECT: The authors sought to determine whether 3,3-bis (3-fluorophenyl) propylamine (NPS 846), a novel noncompetitive N-methyl-D-aspartate receptor antagonist, alters outcome after closed head trauma in rats. METHODS: The experimental variables were: presence or absence of closed head trauma, treatment with NPS 846 or no treatment, and time at which the rats were killed (24 or 48 hours). The NPS 846 (1 mg/kg) was administered intraperitoneally at 1 and 3 hours after closed head trauma or sham operation. Outcome measures were the neurological severity score (NSS), ischemic tissue volume, hemorrhagic necrosis volume, and specific gravity, water content, and concentrations of calcium, sodium, potassium, and magnesium in brain tissue. The following closed head trauma-induced changes in the injured hemisphere (expressed as the mean +/- the standard deviation) were reversed by NPS 846: decreased specific gravity of 1.035 +/- 0.006 at 24 hours was increased to 1.042 +/- 0.004; the decreased potassium level of 0.583 +/- 0.231 mg/L at 48 hours and at 24 hours was increased to 2.442 +/- 0.860 mg/L; the increased water content of 84.7 +/- 2.6% at 24 hours was decreased to 79.8 +/- 2%; the increased calcium level of 0.592 +/- 0.210 mg/L at 24 hours was decreased to 0.048 +/- 0.029 mg/L; and the increased sodium level of 2.035 +/- 0.649 mg/L was decreased to 0.631 +/- 0.102 mg/L. Administration of NPS 846 also lowered the NSS (improved neurological status) at 48 hours (7 +/- 3) and caused no significant changes in ischemic tissue or hemorrhagic necrosis volumes in the injured hemisphere at 24 or 48 hours. CONCLUSIONS: In this model of closed head trauma, NPS 846 improved neurological outcome, delayed the onset of brain edema, and improved brain tissue ion homeostasis.
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The incidence of cloth cover tears in fully covered Starr-Edwards valves, as assessed by autopsy or repeat surgery, is approximately 1% per patient-year. However, no echocardiographic study has explored this phenomenon. This study was designed as a one-time observational study and aimed to explore the ability of two-dimensional transthoracic echocardiography to identify cloth cover tears in 35 late survivors with 38 fully covered Starr-Edwards valves who had been operated on 20 to 24 years earlier. The hemodynamic profile, clinical status, and valve-related complications in this highly selected group of late survivors were also studied. Five patients also underwent transesophageal echocardiography. An elongated echogenic mass attached to the prosthetic valve cage and floating downstream was considered indicative of cloth tear. There were 16 patients with aortic valve prostheses, 16 with mitral valve prostheses, and three with double prosthetic valves. In six (17.1%) patients (four with aortic valve prostheses, two with mitral valve prostheses), an echogenic mass suggestive of cloth cover tear was detected, which was confirmed by transesophageal echocardiography in three patients. In two patients the echocardiographic finding was confirmed at surgery. The initial presentation of these six patients was endocarditis, possible embolism, unexplained dyspnea, and weakness in one patient each. Two patients were asymptomatic. There was no evidence of significant prosthetic valve malfunction in any patient. The transvalvular gradients were similar in patients with and without cloth cover tears. Echocardiographic findings highly suggestive of cloth cover tears are not uncommon and can be detected in the third postoperative decade in patients with fully covered Starr-Edwards valves. A prospective study to evaluate the clinical significance of an incidental echocardiographic finding suggestive of cloth cover tears in asymptomatic patients with these valve models is warranted.
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STUDY OBJECTIVE: To assess the efficacy and safety of hemodilution combined with induced hypotension during surgery. DESIGN: Randomized, nonblinded, controlled study. SETTING: Operating room suite and intensive care unit (ICU) at a university hospital. PATIENTS: 16 ASA physical status I and II patients who underwent general or general plus epidural anesthesia for major orthopedic surgery. INTERVENTIONS: In Group 1 (n = 10), mean arterial blood pressure (MAP) was decreased to 50 mmHg by increasing the inspired concentration of isoflurane and injecting 75 mg of 0.5% bupivacaine into the epidural catheter. Hematocrit was decreased to 20% by phlebotomy and simultaneous infusion of crystalloid and colloid. In Group 2 (n = 6), isoflurane was adjusted to maintain MAP within 20% of baseline values, and no phlebotomy or hemodilution was used. MEASUREMENTS AND MAIN RESULTS: Efficacy of hemodilution combined with induced hypotension (Group 1) was compared to standard management of blood volume and pressure (Group 2) by measuring transfusion volume and length of ICU stay. Safety of hemodilution/hypotension was determined by measuring the electroencephalogram, internal jugular venous oxygen saturation, the electrocardiogram, and central venous oxygen saturation. In Group 1, both the volume of homologous blood (225 +/- 150 ml) and total blood (1440 +/- 286 ml) was significantly less than the volume of homologous blood transfused in Group 2 (2650 +/- 878 ml). No patients in Group 1, but all patients in Group 2 required ICU admission (3.5 +/- 1.6 days) for treatment to prevent sequelae from, or progression of, moderate-severe tissue edema and metabolic acidosis. Cerebral and myocardial measures were not significantly different between groups. CONCLUSIONS: Hemodilution combined with induced hypotension was safe and may reduce the need for transfusion and ICU admission.
We previously reported that in rats with closed head trauma (CHT), intravenous (IV) administration of 0.25 mL/g of 5% dextrose solution (D5W) increased blood glucose (G), decreased blood sodium (Na), caused no change in blood osmolality (Osm), increased brain edema (BE), and worsened neurological severity score (NSS) and mortality rate (MR). D5W in 0.9% saline (D5NS) is isonatremic and hyperosmolar with respect to blood and may avoid the problems reported with D5W. The present study compared the effects of 0.25 mL/g of D5NS or 0.45% saline (0.45 S) after CHT in rats. In 11 groups of rats, the three experimental variables were CHT (yes or no), IV fluid (none, D5NS, or 0.45 S), and time of death (4 or 24 h). D5NS or 0.45 S was given IV at 1 h after surgical preparation with or without CHT, and experimental values were determined at 1, 2, 4, and 24 h. D5NS decreased BE at 4 h compared with the untreated group, increased Osm (380 +/- 2 mOsm/kg) and G (1278 +/- 199 mg/dL), decreased Na (131 +/- 2 mEq/L) in blood, and caused no significant change in hemorrhagic necrosis volume (HNV), NSS, or MR. 0.45 S increased MR (50%) at 24 h, decreased Osm (270 +/- 5 mOsm/kg) and Na (123 +/- 1 mEq/L) in blood, and caused no significant change in G, BE, HNV, or NSS. We conclude that after CHT in rats, D5NS decreased BE without changing NSS or MR. 0.45 S increased MR and significantly altered blood chemistries.
OBJECTIVE: This study examined (1) whether two previously reported, well-established models in rats, one a model of hemorrhagic hypotension and the other a model of closed head trauma, could be combined to evaluate neurologic outcome when hemorrhage occurs subsequent to head injury, and (2) the ability of the traditional, conservative approach to fluid therapy (3 mL of intravenous fluid for 1 mL of blood loss) to reverse the detrimental effects of hemorrhagic hypotension after closed head trauma. In addition, two strategies of fluid therapy (early and delayed) were examined. METHODS: Fifty-six Sprague-Dawley male rats were divided into five groups with head injury at time 0 in groups 3 to 5, hemorrhage at 1 hour in groups 1, 2, 4, and 5, and intravenous fluid at 15 minutes (groups 2 and 5) or 60 minutes (groups 1 and 4) after hemorrhage. Head injury was delivered using a weight-drop impact of 0.5 J onto the closed cranium. Neurologic Severity Score (NSS) was determined at 1 hour (just before hemorrhage) and at 4 hours. RESULTS: NSS at 1 hour did not differ between groups 3 to 5 (15.5 (9-24) to 16 (2-21), median (range)). The amount of bleeding did not differ between groups during the first 15 minutes of hemorrhage (2.8 +/- 0.8 to 3.7 +/- 2.0 mL, mean +/- SD). After 60 minutes, cumulative blood loss in the delayed fluid therapy groups was less (3.1 +/- 1.13 mL in group 1 and 4.25 +/- 2.39 mL in group 4) than in the early fluid therapy groups (7.73 +/- 4.41 mL in group 2 and 6.85 +/- 2.36 mL in group 5) (analysis of variance, p < 0.01). The NSS of group 3 (head injury only) improved at 4 hours after injury (12 (5-20)), whereas the NSS of groups 4 and 5 (head injury followed by hemorrhage) deteriorated (24 (17-25) and 19.5 (9-25), respectively) (Kruskal-Wallis test,p < 0.05). In all the hemorrhage groups, fluid therapy failed to restore blood pressure to prehemorrhage levels. CONCLUSION: It is concluded that the two individual models of hemorrhagic hypotension and closed head trauma in rats can be combined to evaluate outcome when hemorrhage occurs subsequent to head injury. Furthermore, traditional, conservative fluid therapy, whether early or delayed, failed to restore blood pressure or to improve NSS when hemorrhage occurred after head injury. Blood loss was greater with early fluid therapy whether or not head injury was present.
We designed the present study to determine whether the minimum alveolar concentration (MAC) for isoflurane is decreased after closed head trauma (CHT) in rats and, if so, whether the decrease of MAC is related to the severity of neurological impairment following CHT. Isoflurane MAC was determined in 36 Sprague-Dawley rats. Then, at time = 0 h, animals were grouped. Group 1 (n = 8) received no CHT, group 2 (n = 14) received moderate CHT, and group 3 (n = 14) received severe CHT. Neurological severity score (NSS, 0 = no deficit and 25 = maximal impairment) and MAC were determined at 1, 4, 24, and 48 h. In groups 1 and 2, isoflurane MAC at 1, 2, 24, and 48 h (1.0-1.1 +/- 0.8-1.2%, median +/- range) was not significantly different from baseline (1.0-1.1 +/- 1.0-1.1%). In group 3, isoflurane MAC at 1, 2, 24, and 48 h (0.4 +/- 0.2-0.5%) was decreased as compared to baseline (1.1 +/- 1.0-1.1%). In group 2, NSS at 1 h was 18 +/- 11-21 and improved by 48 h to 9 +/- 4-15. In group 3, NSS at 1 h was 24 +/- 22-25 and was not significantly different from NSS at 48 h (24 +/- 24-25). Thus, moderate CHT does not significantly alter isoflurane MAC, whereas severe CHT equivalent to a Glasgow Coma Scale score of 3 to 6 significantly decreases isoflurane MAC.
The aim of this study was to determine the influence of acute and chronic ethanol treatment on neurological outcome following head trauma in rats. Eight-two Sprague-Dawley rats were divided into 10 groups. Four groups received sham head trauma (surgical incision of the scalp but no trauma) and were treated with (A) nothing, (B) chronic ethanol (6% ethanol in drinking water for 40 days), (C) acute ethanol 1.5 g/kg, intraperitoneally (IP) and (D) acute ethanol 3 g/kg IP. Four groups (E-H) received the same treatment; in addition, head trauma was delivered using a weight-drop device to the left cranium (2 h after ethanol treatment in the acute ethanol groups). To assess the influence of acute plus chronic alcohol and whether the glutamate antagonist ketamine can modify the neurologic outcome following head trauma, two additional head trauma groups were studied: group I received both acute and chronic ethanol treatment and group J received acute ethanol (1.5 g/kg) IP plus ketamine (180 mg/kg). Neurologic assessment was performed at 1, 2, 4, 8, 10, and 24 hours after head trauma or sham trauma in all animals who survived the treatment (omitted in group J animals while still under the anesthetic influence of ketamine). At the end of 24 hours, or at the time of death, the animals were decapitated. Specific gravity was determined from brain tissues adjacent to the injury and the contralateral hemispheres and the volume of hemorrhagic necrosis was quantified. None of the rats in the sham trauma groups died or had neurologic deficits. Of the head trauma groups, the mortality in animals that received 3 g/kg of ethanol and the animals that received acute plus chronic ethanol treatment was 100% before the end of 24 hours. Fifty percent of the animals receiving low-dose acute ethanol treatment (1.5 g/kg) died before 24 hours. In contrast, the mortality in the other groups was only 30% (p < 0.05). The neurologic severity score was significantly higher (greater neurological deficit) in the surviving animals that received acute ethanol treatment at 10 and 24 hours than in rats receiving no ethanol or chronic ethanol treatment. Specific gravity was also lower in the acute ethanol-treated groups compared with no ethanol, chronic ethanol, and acute ethanol plus ketamine groups (p < 0.03). Based on these observations, we conclude that in this rat head trauma model acute ethanol treatment increases mortality, neurological deficit, hemorrhagic necrosis volume, and brain edema. On the other hand, chronic ethanol treatment has no apparent effect and ketamine treatment does not counteract the effect of acute ethanol treatment.
The objective of our study was to investigate the influence on central and regional circulation of the application of positive end-expiratory pressure (PEEP=P) in a canine model of low hydrostatic pulmonary edema. Eight mongrel dogs with oleic acid-induced pulmonary edema were artificially ventilated with and without PEEP. Regional blood flow was determined using radioactive microspheres directly injected into the left ventricle. Regional blood flow to the brain was maintained under all experimental conditions, while the blood flow to the gastric fundal mucosa and to the pancreas significantly decreased following PEEP, oleic acid injection (OA) and with PEEP and oleic acid combination (P+OA). The renal blood flow decreased only during the P+OA phase. We conclude that the observed decrease in blood flow to the gastrointestinal mucosa and renal circulation in this acute low hydrostatic pressure pulmonary edema may correlate with the increased incidence of gastrointestinal and renal complications that accompany critically ill patients.
A series of 12 patients with 16 episodes of prosthetic heart-valve thrombosis over 3 years is presented. Most episodes affected mitral or tricuspid bileaflet prostheses. All patients were inadequately anticoagulated at the time of thrombosis. The clinical presentation was acute and severe in 6 patients, and subacute or chronic in the rest. Physical examination was suggestive of stuck valves in most cases. Transthoracic echocardiography revealed increased transvalvular gradients in most. However, clearer evidence of valve thrombosis was obtained from transesophageal echocardiography or fluoroscopy. 9 patients eventually had their valves re-replaced successfully, and the preoperative diagnosis was confirmed in all. 5 patients were operated as soon as the diagnosis was established. and an additional 4 were operated after failure of anticoagulation. In 4 patients the valve leaflets became completely mobile after a course of thrombolysis. Prosthetic valve thrombosis is a severe and potentially fatal complication in patients with mechanical heart valves. Alertness of physicians at all levels- the general practitioner, the internist and the cardiologist- to the possibility of valve thrombosis and to its clinical presentation may lead to prompt and earlier diagnosis and to comprehensive therapy.
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