The effect of surgery clerkship timing on fourth-year students' surgery knowledge.
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Biomedical subjects
Publications and source records attributed to F A Baciewicz.
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Marfan syndrome is a hereditable disorder of connective tissue that causes several distinct cardiovascular abnormalities, including aortic regurgitation, dissection, and aneurysm. These cardiac manifestations can be identified with echocardiography, computer tomography, and angiography. Standard treatment of an acute hypertensive crisis in Marfan syndrome uses propranolol and sodium nitroprusside. This patient with Marfan syndrome whose case is reported herein presented with chest pain, hypertensive crisis, and aortic insufficiency; labetalol was used successfully to treat the acute hypertensive crisis and magnetic resonance imaging (MRI) was used to differentiate between aortic dissection and an expanding aortic aneurysm. This report is unique in that labetalol was used to control the hypertensive crisis in Marfan syndrome and MRI was used as the initial diagnostic modality in an emergency setting.
The study proposed to determine if a preclinical basic science index comprised of anatomy, behavioral medicine, biochemistry, microbiology, pathology, pharmacology, and physiology courses or any one of these basic science courses would predict student performance during surgical clerkship. The basic science index demonstrated a correlation of 0.55 and 0.35 with the individual student's written and oral clerkship scores, respectively. A stepwise multiple regression using a backward stepping algorithm was applied; the dependent variables were oral and written clerkship scores, and the independent variables were the basic science courses. Microbiology, pathology, and physiology course scores were predictors of written score (R = 0.60). Pathology course scores were the sole predictor of oral score (R = 0.43). Medical student basic science performance was not a strong forecaster of performance on the surgical clerkship. The pathology basic science score was the only consistent predictor of performance on the written and oral evaluations given at the end of the clerkship.
A compilation of drug interactions between H2 antagonists and cardiovascular drugs is found in Table I. Cimetidine's potency, lipophilicity, and affinity for binding to the P-450 cytochrome system can probably be attributed to the drug interactions that have been identified with the H2 antagonists. The mechanism for most cimetidine drug interactions is inhibition of hepatic metabolism. There is conflicting evidence regarding significance of altered liver blood flow for both cimetidine and ranitidine and their influence on other agents. Cimetidine may increase propranolol's blood concentrations and potentiate beta blocking effects through inhibition of hepatic microsomal enzymes and possibly through reduction of hepatic blood flow. Ranitidine has no effect on propranolol. Cimetidine, when administered concurrently with metoprolol, could possibly cause an increase in plasma metoprolol concentrations or bioavailability through inhibition of hepatic P-450 metabolizing enzymes. No effect of cimetidine on metoprolol pharmacodynamics was evident. Ranitidine has no effect on metoprolol pharmacokinetics or pharmacodynamics. Neither H2 antagonist altered the kinetics or physiologic effects of atenolol. Atenolol is the drug of choice in patients receiving H2 antagonists, since no interaction has been observed. Metoprolol could probably be used safely in most patients, as no change in pharmacodynamics has been evident. Concurrent administration of cimetidine and nifedipine may result in alterations in heart rate and blood pressure. The mechanism is inhibition of oxidative liver metabolism. Ranitidine has no effect on nifedipine. Studies are needed to investigate the interaction between the H2 antagonists and diltiazem or verapamil. Cimetidine, given concomitantly with lidocaine, may increase lidocaine concentrations and clinical symptoms of lidocaine toxicity. The mechanism involved is probably a reduction in oxidative drug metabolism or liver blood flow. Ranitidine has no significant effects on lidocaine pharmacokinetics. Cimetidine may increase quinidine levels and symptoms of quinidine toxicity. Additionally, enhanced arrhythmic effects may be observed. The interaction probably caused by an inhibition of hepatic drug metabolism of quinidine by cimetidine would be most significant in patients with liver disease and in the elderly. Ranitidine may enhance quinidine's arrhythmic effect. Cimetidine can possibly increase procainamide and NAPA serum concentrations, especially in the elderly and in patients with renal dysfunction, predisposing them to adverse side effects. The interaction is mediated by a reduction of tubular secretion of procainamide and NAPA.
Cyclosporine (CyA) is commonly prescribed as an immunosuppressive to prevent rejection of organ transplants. Numerous pharmacokinetic drug interactions of potential clinical significance exist because other drugs may induce or inhibit the metabolism of CyA. Case reports and studies demonstrate that rifampin, phenytoin, phenobarbital, and carbamazepine may induce the hepatic metabolism of CyA, causing decreased CyA concentrations. Graft rejection through inadequate immunosuppression may be associated with subtherapeutic or decreased CyA levels. Erythromycin, ketoconazole, calcium channel blockers, and sex hormones appear to inhibit CyA metabolism, causing increased CyA concentrations. Signs and symptoms of renal, hepatic, or neurotoxicity may be evident with increased or toxic CyA levels. Mutual inhibition of metabolism occurs between CyA and corticosteroids. Intravenous sulphadimidine and trimethoprim may cause decreased CyA concentrations by an unknown mechanism.
Patients with Down's syndrome represent a significant subset of patients with congenital heart disease. Fifty-five patients with Down's syndrome have undergone surgical treatment for congenital heart disease at our institution in the past decade. Twenty-six had atrioventricular canal, 11 had ventricular septal defect, 7 had secundum atrial septal defect, 7 had tetralogy of Fallot, 3 had primum atrial septal defect and 1 patient had double outlet right ventricle. The thirty day mortality following operative intervention was 16.4%. Mortality was highest for tetralogy of Fallot followed by atrioventricular canal and ventricular septal defect. Long term mortality for all lesions was 27.3% over our follow-up period which averaged 33 months. Thirty day mortality compared similarly to previous reports of surgically treated Down's syndrome patients. When compared to our patients without Down's syndrome, the Down's population did not exhibit an increased risk for surgical treatment of congenital heart disease.
A series of 106 consecutive ductal closures in premature infants was reviewed to assess the incidence of left vocal cord paralysis. To our knowledge, this syndrome is described for the first time in premature infants. In our experience, it is a relatively benign complication that completely resolves clinically in several weeks. This complication occurred in 5.2% of patients closed by suture ligature and in none of those closed by a surgical clip. Although the series is too small for this difference to be statistically significant, we believe it strongly favors the use of the clip, with less dissection.
Placement of a Swan-Ganz catheter can cause many complications. This case report presents a new complication of Swan-Ganz catheter insertion--placement of the Swan-Ganz catheter tip in the coronary sinus.
Rapid atrial pacing by means of temporary atrial pacing wires was used to effect a regular sinus rhythm in a patient with 2:1 atrioventricular block and frequent premature atrial contractions. The change in rhythm allowed effective intra-aortic balloon counterpulsation and markedly improved the hemodynamic situation.
Recent data indicate that the gastrointestinal bleeding due to angiodysplasia associated with aortic stenosis (Heyde's syndrome) can be alleviated by aortic valve replacement with a bioprosthesis. This report details a situation in which valve replacement with a mechanical prosthesis and the subsequent anticoagulation promoted gastrointestinal bleeding from angiodysplastic lesions. Only when the mechanical prosthesis was replaced with a porcine prosthesis and the anticoagulation discontinued did the gastrointestinal bleeding stop.
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An intraaortic balloon pump (IABP) was inserted through the ascending aorta during a coronary artery bypass operation. Five days later, after removal of the IABP and ligation of the end-to-side Dacron graft, the patient became acutely anuric. Abdominal aortography demonstrated a large "trapeze-shaped" thrombus which occluded both renal arteries. Following thrombectomy the patient recovered, with eventual return of renal function to the preoperative state.
Current noninvasive methods of imaging esophageal lymph nodes have an accuracy, specificity, and sensitivity of 70%. Using a flexible esophagoscope, technetium-99m antimony sulfide colloid was injected in the esophageal submucosa of six dogs who then underwent nuclear scans to identify lymph-node location. The euthanized animals underwent dissection of cervical, thoracic, and abdominal lymph nodes. Student's t-test showed no statistical difference in the number of lymph nodes visualized in the neck (3.5 +/- 0.6), parietal thorax (1.2 +/- 0.4), visceral thorax (2.2 +/- 0.7), and abdomen (1.0 +/- 0.0) on premorbid nuclear scans and in the number of radiolabeled lymph nodes found in the neck (3.2 +/- 0.9), parietal thorax (1.2 +/- 0.2), visceral thorax (1.8 +/- 1.0), and abdomen (1.2 +/- 0.2) on dissection of the carcass. The positions of the lymph nodes based on the premorbid nuclear scans matched the locations of the radiolabeled lymph nodes at dissection. Dissected tissue was pathologically confirmed as lymph node. The position and number of lymph nodes in the cervical, intrathoracic, and abdominal regions on nuclear scan correlated with the position and number of lymph nodes found on anatomic dissection. This technique may have a higher sensitivity and specificity than current noninvasive techniques in the staging of esophageal lymphatic metastasis.
Hyperthermia has shown promise as an anticancer therapy, but its application to lung neoplasms has been limited by whole body hyperthermia complications and the intrathoracic location of lung neoplasms. Previous studies have shown that interstitial hyperthermia could be performed through a thoracotomy approach and that animals tolerated the procedure without biochemical or hematologic abnormalities. The normal lung's local blood flow pattern and parenchymal changes due to hyperthermia of various temperatures and durations were studied. The experimental protocol applied hyperthermia through interstitial electrodes at temperatures of 39 degrees, 41 degrees, 43 degrees, and 45 degrees C. Tissue blood flow was measured with radioactive microspheres at 20, 40, and 60 minutes of hyperthermia. Histologic examination was performed of biopsy specimens taken from the heated area, from 2 and 5 cm from the heated area, and from distant parenchyma. These initial studies demonstrate that interstitial hyperthermia in the normal lung does not cause a decrease in pulmonary vascular resistance, that interstitial hyperthermia in the normal lung at temperatures of 43 degrees or 45 degrees C for durations of longer than 20 minutes decreases local pulmonary blood flow, that interstitial hyperthermia causes mild vascular disruption at temperatures of 39 degrees C or greater in the heated area but does not affect adjacent or distant lung parenchyma, and that lung hyperthermia causes generalized vascular disruption with severe widening of the pulmonary interstitium and severe hemorrhage in the heated areas when temperatures of 43 degrees or 45 degrees C are applied. Because interstitial hyperthermia affected only local lung damage, it may be applicable in the treatment of localized lung tumors.