Operative stabilization of a flail chest six years after injury.

We report a case of operative stabilization of an incompetent upper chest wall 6 years following flail chest. The indications for stabilization were chronic pain and dyspnea associated with rib malunion and loss of hemithorax volume. At operation, multiple pseudoarthroses were encountered and partial resection of ribs three and four was required. Malleable plates were used to bridge the gaps created by the resection and were secured in place with sternal wire. The patient reported a dramatic relief of symptoms and, at 18 months postoperatively, continues to work full-time on his cattle ranch essentially pain-free.

Hemodynamic effects of S-nitrosocysteine, an intravenous regional vasodilator.

BACKGROUND: S-nitrosocysteine is a carrier form of nitric oxide that can be delivered intravenously. S-nitrosocysteine is rapidly metabolized by plasma (half-life = 2-3 seconds), forming nitric oxide and cysteine. With its short half-life and potent vasodilatory properties, S-nitrosocysteine may be useful as a pulmonary vasodilating agent in cases of postoperative and chronic pulmonary hypertension. OBJECTIVE: Our objective was to determine the hemodynamic properties of S-nitrosocysteine on the pulmonary and systemic circulations to assess its potential utility as a pulmonary vasodilatory agent. METHODS: Eleven adult swine were anesthetized. Thermodilution (Swan-Ganz; Baxter International, Inc, Deerfield, Ill) and arterial catheters were inserted. Flow probes were placed around the coronary, renal, superior mesenteric, and iliac arteries. Incremental infusion doses of S-nitrosocysteine (5-80 nmol. kg(-1). min(-1)) were delivered into the right atrium. Cardiac output, right and left heart pressures, heart rate, Pao(2), and iliac, renal, coronary, and mesenteric blood flow rates were recorded at baseline and at each infusion dose of S-nitrosocysteine. RESULTS: Low-dose S-nitrosocysteine infusion decreased mean pulmonary artery pressure (15%, P =.013) without a significant reduction in mean systemic artery pressure. Higher dose infusions produced further dose-dependent declines in pulmonary vascular resistance and measurable reductions in systemic vascular resistance (P =.01). At an S-nitrosocysteine dosage of 40 nmol. kg(-1). min(-1), there was a significant reduction in renal (P <.001) and mesenteric (P =.003) blood flow but no change in iliac (P >.2) or coronary (P >.2) blood flow. Cardiac output remained constant up to infusion rates of 40 nmol. kg(-1). min(-1) (P >.2). Doses higher than 5 nmol. kg(-1). min(-1) resulted in a substantial dose-dependent reduction in Pao(2) (P <.001), suggesting dilation of atelectatic areas of the lung. CONCLUSION: S-nitrosocysteine is a potent vasodilatory agent capable of overcoming the hypoxic vasoconstrictive response of the lung. Our results suggest it may prove useful as a pulmonary vasodilatory agent at low doses. Higher dose infusions reduce mean systemic pressure and lead to compensatory reductions in renal and mesenteric blood flow without a decrease in cardiac output.

Impact on the new chair.

Since World War II, multiple changes have occurred in medicine that are now affecting academic health centers and department of surgery chairpersons. None of these changes by themselves were intended to adversely affect department of surgery chairpersons, but the sum total effect constitutes a negative external force. In addition, there are internal forces in the schools of medicine and university hospitals that may negatively affect department of surgery chairperson in fulfilling the stated goals of excellent patient care, teaching, and research. Many of the problems brought about by these negative forces cannot be solved by a single department chairperson. However, individual department chairs can contribute to the solution by returning to the values taught to them by the role models of their surgical training.

A comparison of patient characteristics and survival in two trauma centres located in different countries.

INTRODUCTION: The aim of the study was to compare patient characteristics and mortality in severely injured patients in two trauma centres located in different countries, allowing for differences in case-mix. It represents a direct bench-marking exercise between the trauma centres at the North Staffordshire Hospital (NSH), Stoke-on-Trent, UK and the Oregon Health Sciences University (OHSU) Hospital, Portland, Oregon, USA. METHODS: Patients of all ages admitted to the two hospitals during 1995 and 1996 with an Injury Severity Score >15 were included, except for those who died in the emergency departments. Twenty-three factors were studied, including the Injury Severity Score, Glasgow Coma Score, mechanism of injury and anatomical site of injury. Outcome analysis was based on mortality at discharge. RESULTS: The pattern of trauma differed significantly between Stoke and Portland. Patients from Stoke tended to be older, presented with a lower conscious level and a lower systolic blood pressure and were intubated less frequently before arriving at hospital. Mortality depended on similar factors in both centres, especially age, highest AIS score, systolic blood pressure and Glasgow Coma Score.The crude analysis of mortality showed a highly significant odds-ratio of 1.64 in Stoke compared with Portland. Single-factor adjustments were made for the above four factors, which had a similar influence on mortality in both centres. Adjusting for the first three factors individually did not alter the odds-ratio, which stayed in the range 1.53-1.59 and remained highly significant. Adjusting for the Glasgow Coma Score reduced the odds-ratio to 0.82 and rendered it non-significant. In a multi-factor logistic regression model incorporating all of the factors shown to influence mortality in either centre, the odds-ratio was 1.7 but was not significant. CONCLUSION: The analysis illustrates the limitations and pitfalls of making crude outcome comparisons between centres. Highly significant differences in crude mortality were rendered non-significant by case-mix adjustments, supporting the null hypothesis that the two centres were equally effective in terms of this short-term indicator of outcome. To achieve a meaningful comparison between centres, adjustments must be made for the factors which affect mortality.

History and development of trauma care in the United States.

Until recently the development of systems for trauma care in the United States has been inextricably linked to wars. During the Revolutionary War trauma care was based on European trauma principles particularly those espoused by the Hunter brothers. Surgical procedures were limited mostly to soft tissue injuries and amputations. The American Civil War was remarkable because of the contributions that were made to the development of systems for trauma care. The shear magnitude of casualties required extensive infrastructure to support the surgeons at the battlefield and to care for the wounded. For the first time in an armed conflict, anaesthetics were used on a routine basis. Despite these major contributions, hospital gangrene was a terrible problem and was the cause of many mortalities. World War I and World War II were noteworthy because of the contributions made by surgeons in the use of blood. One of the major lessons of World War II was the reemphasis of how frequently lessons have to be relearned regarding the treatment and care of wounds. Between the Korean Conflict and the Vietnam War the discovery was made of the tremendous fluid shifts into the cell after severe hemorrhagic shock. As a consequence, the treatment of patients with shock was altered during the Vietnam Conflict, which resulted in better outcomes and less renal failure. The first trauma centers for civilians were started in the United States in 1966. Since 1988 the number of states with mature trauma systems has expanded from two to 35. During the same period, many studies have documented the efficacy of trauma systems in reducing unnecessary mortality and disability.

Management of the geriatric trauma patient at risk of death: therapy withdrawal decision making.

HYPOTHESIS: The management of geriatric injured patients admitted to a trauma center includes the selective decision to provide comfort care only, including withdrawal of therapy, and a choice to not use full application of standard therapies. The decision makers in this process include multiple individuals in addition to the patient. DESIGN: Retrospective review of documentation by 2 blinded reviewers of the cohort of patients over a recent 5-year period (1993-1997). SETTING: Trauma service of a level I trauma center. PATIENTS: A convenience sample of patients aged 65 years and older who died, and whose medical record was available for review. MAIN OUTCOME MEASURES: Patients were categorized as having withdrawal of therapy, and documentation in the medical record of who made the assessment decisions and recommendations, and to what extent the processes of care were documented. RESULTS: Among 87 geriatric trauma patients who died, 47 had documentation interpreted as indicating a decision was made to withdraw therapy. In only a few circumstances was the patient capable of actively participating in these decisions. The other individuals involved in recommendations for withdrawal of therapy were, in order of prevalence, the treating trauma surgeon, family members (as proxy reporting the patient's preferences), or a second physician. Documentation regarding the end-of-life decisions was often fragmentary, and in some cases ambiguous. Copies of legal advance directives were rarely available in the medical record, and ethics committee participation was used only once. CONCLUSIONS: Withdrawal of therapy is a common event in the terminal care of geriatric injured patients. The process for reaching a decision regarding withdrawal of therapy is complex because in most circumstances patients' injuries preclude their full participation. Standards for documentation of essential information, including patients' preferences and decision-making ability, should be developed to improve the process and assist with recording these complicated decisions that often occur over several days of discussion.

Identification of a functional Ca2+-sensing receptor in normal human gastric mucous epithelial cells.

The purpose of the present study was to determine whether human gastric mucous epithelial cells express a functional Ca2+-sensing receptor (CaR). Human gastric mucous epithelial cells were isolated from surgical tissues and cultured on glass coverslips, plastic dishes, or porous membrane filters. Cell growth was assessed by the MTT assay, CaR localization was detected by immunohistochemistry and confocal microscopy, CaR protein expression was assessed by Western immunoblotting, and intracellular Ca2+ concentration ([Ca2+]i) was determined by fura 2 spectrofluorometry. In paraffin sections of whole stomach, we found strong CaR immunohistochemical staining at the basolateral membrane, with weak CaR-staining at the apical membrane in mucous epithelial cells. Confocal microscopy of human gastric mucous epithelial cell cultures showed abundant CaR immunofluorescence at the basolateral membrane and little to no CaR immunoreactivity at the apical membrane. Western immunoblot detection of CaR protein in cell culture lysates showed two significant immunoreactive bands of 140 and 120 kDa. Addition of extracellular Ca2+ to preconfluent cultures of human gastric mucous epithelial cells produced a significant proliferative response. Changes in [Ca2+]i were also observed in response to graded doses of extracellular Ca2+ and Gd3+. The phospholipase C inhibitor U-73122 specifically inhibited Gd3+-induced changes in [Ca2+]i in the gastric mucous epithelial cell cultures. In conclusion, we have identified the localization of a functional CaR in human gastric mucous epithelial cells.

Surveyed opinion of American trauma surgeons on the prevention of the abdominal compartment syndrome.

OBJECTIVE: To determine the current opinion of American trauma surgeons on the use of the open abdomen to prevent the abdominal compartment syndrome (ACS). METHODS: On a questionnaire survey of expert trauma surgeons regarding 12 clinical factors influencing fascial closure at trauma celiotomy, surgeons graded their willingness to close the fascia in various scenarios on a scale of 1 to 5. The impact of six signs of clinical deterioration on willingness to perform abdominal decompression in a patient with postceliotomy elevated intra-abdominal pressure (IAP) was also queried. Of 292 members of the American Association for the Surgery of Trauma active in abdominal trauma management, 248 members (85%) had experience with ACS one or more times in the previous year. RESULTS: Surgeons' responses to factors found at trauma celiotomy were divided into two distinct categories: factors decreasing willingness to close the fascia, and factors not changing or increasing willingness to close the fascia (p < 0.001). Factors disfavoring fascial closure were pulmonary or hemodynamic deterioration with closure, massive bowel edema, subjectively tight closure, planned reoperation, and packing. Factors not changing or favoring fascial closure were fecal contamination/peritonitis, massive transfusion, hypothermia, multiple abdominal injuries, acidosis, and coagulopathy. Five of the six signs of clinical deterioration increased surgeons' willingness to decompress a patient with elevated IAP (increased O2 requirement, decreased cardiac output, increased acidosis, increased airway pressures, and oliguria). Lowered gastric mucosal pH did not affect willingness. Seventy-one percent of surgeons indicated they would decompress elevated IAP in postceliotomy patient if one or two signs of clinical deterioration were present, but only 14% would decompress a patient for elevated IAP alone. CONCLUSION: A majority of expert American trauma surgeons have experience with ACS and would leave the abdomen open if ACS occurred. A majority would reopen a closed abdomen in cases of elevated IAP with signs of clinical deterioration. A minority would leave the abdomen open when there was only a risk of developing ACS.

Effects of paclitaxel on the growth of normal, polyposis, and cancerous human colonic epithelial cells.

BACKGROUND: The specific paclitaxel dose or time course in the treatment of colon carcinoma without the disruption of normal colonic cell proliferation is currently not known. The aim of this study was to determine the effects of paclitaxel on the growth of human colonic epithelial cells using cultures of normal, polyposis, and cancerous cells. METHODS: Normal, polyposis, and cancerous human colonic cells (Caco-2, T-84, and LoVo cell lines) were cultured, then treated with paclitaxel (10(-9)-10(-5) M) for 0-7 days.[AU: Please verify all dosages throughout.] Cell proliferation was assayed using either a Coulter-Counter or MTT-growth assay. Immunofluorescence and Western immunoblotting measured P-glycoprotein. RESULTS: Low paclitaxel doses (1 x 10(-9)-10(-8) M) were more effective than higher paclitaxel doses (>1 x 10(-8) M) in the growth inhibition of polyposis, Caco-2, and LoVo cancer (but not T-84) cell lines. Low paclitaxel doses had little effect on normal colonic cell growth over 7 days. Higher paclitaxel doses (>1 x 10(-8)-10(-5) M) produced a dose-dependent inhibitory effect on the growth of normal human colonic epithelial cells over 7 days but had no effect on the growth of polyposis, Caco-2, and LoVo cells over 3-7 days of treatment. Immunofluorescence and Western immunoblotting of cultures showed that 1 x 10(-6) M paclitaxel increased P-glycoprotein expression in Caco-2 and LoVo cells. There was no effect of paclitaxel on P-glycoprotein expression in T-84 cancer cells, which were found to have high endogenous basal levels of P-glycoprotein. P-glycoprotein expression in Caco-2 cells was found on plasma membranes and in perinuclear areas. CONCLUSIONS: Lower paclitaxel doses are more effective over time for the growth inhibition of polyposis and cancerous colonic cells, with minimal effects on the growth of normal colonic epithelial cells. Increased P-glycoprotein expression appears to be correlated with paclitaxel resistance in polyposis and cancerous colonic cells.