A reappraisal of appendicitis in the elderly

Historically, appendicitis in the elderly is associated with higher morbidity and mortality. Ninety-six patients over 60 years of age with appendicitis treated over a 10-year period were reviewed. Only 20% presented classically with anorexia, fever, right lower quadrant pain, and an elevated white blood cell count. One third of the patients had greater than 48 hours delay to admission. Objective diagnostic testing was often confusing and unreliable. At the time of admission, only 51% were diagnosed as having possible appendicitis. Eighty-three percent of our patients underwent surgery within 24 hours, and 72% had frank perforation. Thirty-two percent of those surviving developed complications, and 83% of these patients had perforated appendicitis. Complications were twice as likely in patients with perforation. Despite the relatively high morbidity, there were only four deaths in patients with coexistent carcinoma. Because of the later and atypical presentation of appendicitis in this age group, a high index of suspicion and early operation are important in avoiding perforation and subsequent morbidity.     

Management of postoperative mediastinitis in infants and children by muscle flap rotation

Between July 1, 1976, and June 30, 1986, at the Henrietta Egleston Hospital for Children, 2,242 infants and children underwent palliation or repair of a congenital heart defect. Twenty-one (0.94%) of these patients developed mediastinitis following a median sternotomy. Nineteen of these twenty-one patients had required cardiopulmonary bypass. All patients had positive mediastinal cultures. The first 8 patients were managed traditionally by debridement and irrigation. Three of these patients suffered serious metabolic complications related to the povidone-iodine irrigant, which resulted in 1 death. Another patient died from persistent sepsis following debridement. Subsequently, 13 patients were managed by early debridement and rotation of the pectoralis major or rectus abdominis muscle flaps, or both. Following muscle flap rotation and early wound closure, 2 patients had subsequent incisional complications. One patient had incisional dehiscence and 1 had a superficial skin separation. Two deaths in this group, 28 and 51 days, respectively, following muscle flap rotation, resulted from nonincisional problems in patients with healed median sternotomies. The group having muscle flap rotation required a significantly shorter duration of postoperative ventilatory support (3.2 versus 24 days, p less than 0.05) and a significantly shorter confinement in the intensive care unit (6.2 versus 33 days, p less than 0.01). Also, the physiological and physical trauma of continued wound care in the awake child was minimized in the group with muscle flap rotation.     

New vitamin D3 derivatives with unexpected antiproliferative activity: 1-(hydroxymethyl)-25-hydroxyvitamin D3 homologs.

Surprisingly, both of the synthetic 1-(hydroxymethyl)-25-hydroxyvitamin D3 diastereomers (-)-2 and (+)-3 retained the antiproliferative activity of natural calcitriol in murine keratinocytes. Preliminary studies indicated, however, that both of these synthetic diastereomers were less than 0.1% as effective as calcitriol for binding to the 1,25-(OH)2-D3 receptor and that they were less than 0.1% as potent as calcitriol for calbindin-D28K induction in organ-cultured embryonic chick duodenum. 1-(Hydroxymethyl)-25-hydroxyvitamin D3 homologs (-)-2 and (+)-3 were synthesized in a convergent manner by combining enantiomerically pure C,D-ring ketone 12 with highly enantiomerically enriched A-ring phosphine oxides (-)-11a and (+)-11b. These A-ring chirons were prepared starting from thermal [2 + 4] cycloaddition of 3-bromo-2-pyrone and acrolein.     

Leukocyte Depletion of Blood Cardioplegia Attenuates Reperfusion Injury

Background. Leukocytes are associated with myocardial injury during reperfusion after ischemia. Short periods of leukocyte depletion during reperfusion result in persistent attenuation of postischemic myocardial dysfunction.

Methods. Leukocyte depletion was examined in a canine model of regional myocardial ischemia and reperfusion. The extracorporeal circuit and cardioplegia circuits underwent leukocyte depletion by mechanical filtration. Animals were instrumented for baseline global function before 90-minute occlusion of the left anterior descending coronary artery. Global function during ischemia and at 5, 30, 60, and 90 minutes after a 60-minute cardioplegic arrest using continuous blood cardioplegia was assessed in leukocyte-depleted (n = 9) and control (n = 10) groups.

Results. No significant difference between groups was seen for systemic leukocyte counts, global function, or water content. Endothelial function was significantly protected as assessed by response to both calcium ionophore (endothelial-dependent, receptor-independent relaxation: leukocyte-depleted, 72% ± 19% of endothelin-induced constriction versus control, 46% ± 14%; p < 0.05) and acetylcholine (endothelial-dependent, receptor-dependent relaxation: leukocyte-depleted, 83% ± 11% versus control, 44% ± 15%; p < 0.05).

Conclusions. Leukocyte-mediated endothelial reperfusion injury can be attenuated by leukocyte depletion during reperfusion.     

Aphakic reading adds. An error in traditional teaching

It is traditionally taught in ophthalmic optics that the "effective" bifocal add is greater than the prescribed add in aphakic spectacles. Because the reading segment is fabricated on the front surface of the lens, the added back vertex power is significantly greater than the prescribed add. It is taught that the effective power should be measured at the back surface. The authors explain informally why the effective add is, in truth, exactly equal to the prescribed add and not equal to the difference in back vertex power between the top and bottom segments. Practitioners who prescribe spectacles by the traditional teaching may leave their aphakic patients with suboptimal reading vision.     

Magnitude of the inflammatory response to cardiopulmonary bypass and its relation to adverse clinical outcomes

INTRODUCTION: Cardiopulmonary bypass (CPB) induces an inflammatory response believed to contribute to postoperative morbidity. We hypothesized that the magnitude of the inflammatory response following CPB would be associated with adverse clinical outcomes. METHODS: Twenty-nine patients had plasma TNF, IL-6, IL-8, elastase, histamine, complement C5a, and complement C3a measured by ELISA before, during, and after cardiac operations employing CPB. Inflammatory mediator levels were analyzed with respect to outcomes. RESULTS: Mediator levels peaked at 4 h post-CPB and either returned to baseline or substantially decreased by 24 h. Patients with peak mediator levels above the median for the group as a whole were classified as 'hyper-responders'; those with levels below the median were classified as 'normal responders'. While IL-8, C3a, and IL-6 levels were independently associated with adverse outcomes, TNF, histamine, and C5a levels were not. Elastase levels trended towards adverse outcomes. IL-8 'hyper-responders' experienced significantly greater postoperative weight gain and had higher IL-8 levels at 24 h (p<0.05), with trends towards renal impairment and protracted supplemental oxygen requirements. C3a 'hyper-responders' strongly trended towards increased bleeding, delayed extubation, greater postoperative weight gain, and decreased levels of independent functioning at discharge (p < or = 0.10). IL-6 'hyper-responders' experienced significantly more postoperative bleeding, delayed extubation, and higher IL-6 levels at 24 h compared to 'normal responders' (p < 0.05). They strongly trended towards greater postoperative weight gain and decreased levels of independent functioning at discharge (p < or = 0.10). CONCLUSIONS: Patients who have an exaggerated inflammatory response to CPB tend to bleed more, require more respiratory support, demonstrate greater capillary leak via weight gain, and display a decline in independent functioning relative to normal responders. Thus, it appears that the magnitude of the inflammatory response to CPB adversely influences clinical outcomes.     

Human immunodeficiency virus infection of the developing human nervous system

Human immunodeficiency virus (HIV), the etiologic agent of acquired immune deficiency syndrome (AIDS) and AIDS-related complex, has recently been implicated as a factor in the development of AIDS-related neurologic dysfunction and may be responsible for an increasing number of neonatal immunologic and neurologic disorders. However, as yet there is no model system available to investigate the interaction of HIV with the developing human nervous system in vitro. To approximate the intracellular events associated with HIV infection of the human fetus nervous system we infected cells obtained by enzymatic dissociation of aborted human fetus dorsal root ganglia and their attached spinal roots and nerves. The expression of the HIV gag gene protein products (p17 and p24) was detected in a subpopulation of cells with a nonneuronal morphology, reaching a maximum within 3 days. Although 70% of the nonneuronal cells were p17- and p24-positive 3 days after infection, a majority of the cell population survived acute HIV infection, with the expression of p17 and p24 decreasing below the limit of detection by 12 days postinfection. This system may prove useful for examining the neuropathology and neurobiology of acute, persistent, or latent HIV infection of the developing human nervous system.