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Biomedical subjects

S R Cohen

Publications and source records attributed to S R Cohen.

At least 145 records · Page 8Linked to original sources

Retropharyngeal abscess in children: a retrospective and historical analysis.

The charts of 65 pediatric patients with the diagnosis of retropharyngeal abscess were reviewed. These represented a 36-year experience with the disease. The findings were compared with those documented at the turn of the century and were also compared with findings over the last four decades. The data suggests that retropharyngeal abscess may be occurring later in childhood and may not always be preceded by a major detectable infection. Classic diagnostic findings of retropharyngeal bulge and neck stiffness were present in less than half of the patients. Gram-negative and anaerobic organisms are being documented on culture more frequently than in the past. We theorize that liberal use of oral antibiotics prior to admission may have brought about these changes.

Abscess↗

Sources of information for occupational dermatology.

It is a virtual certainty that the dermatologist will be called upon routinely to evaluate illness caused by occupational factors. Unfortunately, few are prepared adequately during formal training to care for the worker-patient. Reliance on crisis-oriented treatment(s) is frequently insufficient to manage this type of skin disease. One remedy for this problem is simply to read the literature; even limited acquaintance with the occupational health literature should begin to clarify the unique aspects of diagnosis and treatment. Consulting a single occupational dermatology reference will often lead to critical insights about an industrial setting, extracutaneous disease manifestations, toxicology, and preventive methods. Perhaps less obvious, this knowledge is essential to recognize and effectively support claims for workers' compensation, claims that may be the only means of redress for the tragic socioeconomic difficulties befalling those who are occupationally impaired. Bibliographic citations in this paper offer a stepwise approach to the literature and identify the important sources applicable to dermatology.

Dermatology↗

Hemodynamic correlates of left ventricular versus right ventricular radionuclide volumetric responses to vasodilator therapy in congestive heart failure secondary to ischemic or dilated cardiomyopathy.

Previous studies have failed to demonstrate the clinical relevance of radionuclide functional measurements during treatment of congestive heart failure (CHF). In the present study, data derived before and during nitroprusside infusion were analyzed in 16 patients with CHF to compare correlations of changes in left (LV) and right ventricular (RV) radionuclide measurements with simultaneous changes in 8 hemodynamic variables. Nitroprusside infusion decreased systemic artery pressure, pulmonary arterial wedge pressure, pulmonary artery pressure, right atrial pressure, and pulmonary and systemic vascular resistance, and increased cardiac output. Nitroprusside decreased LV and RV end-diastolic and end-systolic volumes and increased LV and RV ejection fraction and stroke volume. Changes in RV volumes exceeded changes in LV volumes. LV radionuclide measurements did not correlate significantly with any hemodynamic measurement except for a weak correlation between changes in LV end-systolic volume and right atrial pressure (r = 0.51). In contrast, the combination of changes in RV end-systolic volume and stroke volume predicted changes in pulmonary artery peak systolic (r = 0.90) and mean (r = 0.89) pressures. Changes in pulmonary arterial wedge pressure correlated with changes in RV end-diastolic (r = 0.78) and end-systolic (r = 0.71) volumes. In conclusion, LV radionuclide measurements are of limited value in predicting hemodynamic responses to vasodilator therapy in CHF, whereas RV volumes are strongly influenced by load changes. Their responses to nitroprusside correlate well with changes in pulmonary artery and pulmonary arterial wedge pressures.

Adult↗

Animal model of acute pericarditis and its progression to pericardial fibrosis and adhesions: ultrastructural studies.

To study the evolution of pericardial inflammation, we have developed a model of pericarditis in sheep by surgically injecting heat-killed staphylococci and Freund's adjuvant into the pericardial cavity under sterile conditions. The pericarditis evolved through the following phases: 1) inflammatory response, 2) mesothelial cell injury and desquamation, and 3) fibrotic phase. At 3-24 hr there was increased microvascular permeability, which resulted in the exudation of fluid, neutrophils, macrophages, and fibrin into the pericardial cavity and the pericardial interstitium. By 72 hr, large numbers of inflammatory cells were aggregated on the mesothelial surfaces and dispersed throughout the pericardial cavity, either as free-floating cells or located between strands of fibrin. At 6 days, fibrinolysis was apparent along the mesothelial surfaces; and newly formed collagen fibrils were deposited throughout the interstitial spaces and among the aggregated cells. These fibrils provided a matrix for the growth of new blood and lymphatic vessels into new connective tissue on both parietal and visceral pericardial surfaces. At 2 weeks, intrapericardial fibrosis had produced focal adhesions between the pericardial surfaces. At 1 month, extensive areas of the pericardial cavity were obliterated. By 9 months, there was a marked reduction in the numbers of cells and blood vessels and increased deposition of collagen and elastic fibers. The intrapericardial injection of heat-killed staphylococci and adjuvant provides a reproducible animal model to study the time course of pericardial inflammation.

Acute Disease↗

Mammographic changes following reduction mammaplasty.

Mammographic findings after reduction mammaplasty may be similar to those seen with carcinoma. A knowledge of the expected mammographic alterations would be helpful in differentiating postoperative changes from those seen with carcinoma of the breast. Accordingly, the clinical records and mammograms of patients who underwent reduction mammaplasty at the Dartmouth-Hitchcock Medical Center between March of 1977 and July of 1985 were analyzed. Forty-two patients had at least one mammographic examination following reduction mammaplasty. Periareolar soft-tissue changes and inferior pole alterations were present in almost all examinations of patients during the first 6 months after operation, but they decreased during the next few years. Asymmetrical densities were present in approximately half the patients throughout the follow-up period but decreased in degree. Parenchymal calcifications occurred later; few x-rays showed these calcifications during the first year, but 50 percent were apparent after 2 years. Evidence of fat necrosis occurred in approximately 10 percent. Four patients had biopsies for suspicious densities. Chronic inflammation and inclusion cyst were reported. We believe that changes after reduction mammaplasty are predictable and can usually be differentiated from those associated with cancer.

Adipose Tissue↗

Tricuspid regurgitation in patients with acquired, chronic, pure mitral regurgitation. I. Prevalence, diagnosis, and comparison of preoperative clinical and hemodynamic features in patients with and without tricuspid regurgitation.

Most reports of clinical experiences with palliation of acquired tricuspid regurgitation have failed to address the issue of coexisting disease of the mitral or aortic valve, or both. To accurately determine the natural history and the effect of operative interventions, we studied patients with chronic, pure mitral regurgitation who had surgical treatment at the National Heart, Lung, and Blood Institute from 1968 to 1984. Forty-seven patients fulfilled the criteria of a documented history of mitral regurgitation for more than 1.5 years, minimal mitral diastolic gradient, severe mitral regurgitation by angiography, and no prior mitral or tricuspid operative procedure. Twenty-five of the 47 patients (53%) had evidence of tricuspid regurgitation. No statistical differences in age, sex, mean duration of symptoms of congestive heart failure, or functional class were found between those patients with and those without tricuspid regurgitation. However, patients with symptoms of congestive heart failure for more than 6 years were more likely to have tricuspid regurgitation. This increased prevalence also correlated with higher elevations of left ventricular end-diastolic, systolic pulmonary artery, and mean right atrial pressures. The severity of tricuspid regurgitation estimated preoperatively did not correlate statistically with that determined by digital palpation, although the presence of tricuspid regurgitation was reliably confirmed. These data demonstrate that tricuspid regurgitation is frequently present in patients with chronic, pure mitral regurgitation and is associated with prolonged symptoms of congestive heart failure and significant alterations in right heart dynamics.

Blood Pressure↗

Tricuspid regurgitation in patients with acquired, chronic, pure mitral regurgitation. II. Nonoperative management, tricuspid valve annuloplasty, and tricuspid valve replacement.

The incidence, preoperative and intraoperative diagnosis, methods, and the clinical and hemodynamic features of patients with and without tricuspid regurgitation associated with chronic mitral regurgitation were presented in Part I. This study (Part II) compares the early and late results in patients with chronic, pure mitral regurgitation undergoing isolated mitral valve replacement, mitral replacement and tricuspid valve annuloplasty, and mitral and tricuspid valve replacement. The mean follow-up interval was 6 years. Those with the longest duration of symptoms (18 years) required tricuspid and mitral valve replacement (11 patients), whereas those with the shortest duration (8.1 years) had only mitral replacement (22 patients). Eight patients had minimal tricuspid regurgitation by digital palpitation, with no procedure performed, and six had tricuspid valve annuloplasty, only one of whom received a ring support. Operative mortality rate was similar in all groups (13% to 18%). All but two of the surviving patients improved by at least one New York Heart Association functional class, and no statistically significant differences were found between preoperative and postoperative hemodynamic data. There were no statistically significant differences in survival at 1, 5, or 8 years (85%, 70%, and 60%, respectively) for patients with or without TR. Only two of the surviving five patients who underwent tricuspid valve annuloplasty were alive 3 years after operation, whereas 70% to 80% of those with mitral replacement or mitral and tricuspid replacement were alive after the same time interval. It is not clear whether or not the pathogenesis of tricuspid regurgitation resulting from mitral regurgitation is different from that of tricuspid regurgitation resulting from mitral stenosis. It is our contention that whether tricuspid regurgitation arises because of anatomic destruction of the tricuspid valve or because of right ventricular dilatation with tricuspid annular enlargement, the underlying mitral valve lesion may determine the preoperative and postoperative courses of these patients. Therefore, when tricuspid valve disease is being evaluated, we urge that patients be categorized by the nature of their underlying mitral or aortic valve lesions.

Adult↗

Contribution of reduced mitral regurgitant volume to vasodilator effect in severe left ventricular failure secondary to coronary artery disease or idiopathic dilated cardiomyopathy.

Although vasodilators improve cardiac output in severe left ventricular (LV) failure, the degree to which reduction in mitral regurgitation (MR) contributes to this response is unknown. In the present study, nitroprusside-induced changes in forward cardiac output were compared with simultaneous radionuclide LV output in 14 patients with severe LV systolic dysfunction in the absence of known primary valvular disease. Regurgitant output was estimated as LV output minus forward output and regurgitant fraction was calculated as regurgitant output/LV output. At rest, LV ejection fraction averaged 0.16 +/- 0.04 (mean +/- standard deviation). Patients were classified into 2 groups based on regurgitant fraction at rest. Group I (n = 5) had little or no detectable valvular regurgitation, with regurgitant fraction less than 0.10; group II (n = 9) had evidence of MR with regurgitant fraction greater than 0.30. Nitroprusside increased forward cardiac output in all patients in both groups, but this effect was significantly greater in group II (64 +/- 34%) than in group I (31 +/- 17%) (p less than 0.01). Nitroprusside decreased regurgitant fraction in all group II patients, with mean regurgitant fraction decreasing from 0.44 +/- 0.12 to 0.26 +/- 0.15 (p less than 0.005). Thus, a large percentage of patients with severe LV systolic dysfunction have clinically relevant MR, defined as a regurgitant fraction greater than 0.30. Nitroprusside has a greater effect on forward cardiac output in patients with LV failure and MR than in patients with comparable ventricular dysfunction in the absence of detectable MR.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Habenular stimulation produces analgesia in the formalin test.

Electrical stimulation of the habenula produces a striking reduction of continuous, formalin-induced pain in the rat. The analgesia occurs at current levels which do not appear aversive and persists for variable durations, ranging from 1 to 21 min in this experimental situation. The effect is not blocked by subcutaneous administration of a large dose of naloxone prior to the stimulation, indicating that it is not dependent on an opiate-sensitive system. Stimulation of the adjacent paraventricular nucleus of the thalamus was either aversive or had no effect on the pain scores. The anatomical connections of the habenula suggest that it may mediate the interaction of limbic forebrain structures with midbrain structures known to play a role in pain and analgesia.

Animals↗

Relative contribution of inotropic and vasodilator effects to amrinone-induced hemodynamic improvement in congestive heart failure.

The relative contribution of inotropic and vasodilator effect to amrinone-induced hemodynamic improvement in congestive heart failure (CHF) is unknown. In 9 patients with CHF, the effects of amrinone and nitroprusside on hemodynamic and radionuclide measurements were compared to determine whether reduced afterload accounts for the amrinone-induced decrease in left ventricular end-systolic volume. In each patient, the end-systolic pressure-volume relation was derived using nitroprusside. After terminating nitroprusside treatment, intravenous amrinone (3 mg/kg) caused end-systolic volume to decrease from 148 +/- 32 ml/m2 (mean +/- standard deviation) to 133 +/- 32 ml/m2 (p less than 0.05), causing an increase in cardiac index from 1.9 +/- 0.8 to 2.7 +/- 0.8 liters/min/m2 (p less than 0.001). Arterial end-systolic pressure decreased in all patients during amrinone administration, from 96 +/- 22 to 84 +/- 19 mm Hg (p less than 0.005), as did systemic vascular resistance. Nitroprusside doses needed to match the decrease in LV end-systolic volume induced by amrinone caused significantly greater decreases in arterial end-systolic pressure than did amrinone (p less than 0.01). The amrinone-induced decrease in end-systolic volume exceeded that predicted for a pure vasodilator based on arterial end-systolic pressure and the nitroprusside-derived pressure-volume relation in 6 patients. In 3 patients, the decrease in end-systolic volume did not exceed that expected for a pure vasodilator. In conclusion, after amrinone treatment, afterload reduction occurs in all patients with severe CHF and is the sole effect in some.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Effect of amrinone on right ventricular function: predominance of afterload reduction.

Although the bipyridine agent amrinone is reported to have a positive inotropic effect on the left ventricle, the effect of this drug on right ventricular contractility in the clinical setting is unknown. We studied the effect of short-term intravenous administration of amrinone on right ventricular systolic function in nine patients with severe congestive heart failure and, using radionuclide ventriculography, examined the right ventricular end-systolic pressure-volume relationship to determine whether reduced right ventricular afterload or increased contractility predominantly accounted for the observed improvement in right ventricular systolic function. In each patient the right ventricular end-systolic pressure-volume relationship was derived with use of varying doses of nitroprusside. After nitroprusside was stopped, intravenous amrinone (3 mg/kg) caused decreases from baseline in pulmonary arterial end-systolic pressure in eight of nine patients (23 +/- 11% [overall mean +/- SE], p less than .05), and in pulmonary vascular resistance in all patients (38 +/- 6%, p less than .001). Right ventricular end-systolic volume decreased (23 +/- 8%, p less than .01) and right ventricular ejection fraction increased (31 +/- 10%, p = .01). The amrinone-induced decrease in right ventricular end-systolic volume was compared with that predicted for right ventricular afterload reduction alone based on the effect of amrinone on pulmonary arterial end-systolic pressure and the pressure-volume relationship observed during infusion of nitroprusside.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Morphine injected into the habenula and dorsal posteromedial thalamus produces analgesia in the formalin test.

Microinjection of morphine into the area of the habenula and dorsal posteromedial thalamus (H-PMT) produces analgesia for tonic pain as measured by the formalin test in the rat. Control injections of morphine into sites near the H-PMT result in less or no reduction in pain, indicating that the analgesia observed is probably due to a site of action within the H-PMT rather than at surrounding neural structures. The analgesia is fully developed by the first time of testing, 10-16 min following the microinjection, and is completely reversible by naloxone, an opiate antagonist. The analgesia recorded is most likely due to morphine's action on the habenula, parafascicular or paraventricular nucleus of the thalamus, or a combination of these structures.

Animals↗