Impact of presenting physiology and associated injuries on outcome following traumatic rupture of the thoracic aorta.

We hypothesized that the predominant factor influencing outcome of traumatic rupture of the thoracic aorta (TRA) was the degree of shock on presentation and associated injuries. We reviewed our experience with TRA over a 15-year period. Patients were classified as "unstable" if presenting systolic blood pressure was <90 mm Hg or if it decreased to <90 mm Hg after admission. We determined the presence of closed head injury, cardiac risk factors, a preoperative acute lung injury (ALI). The influence of these factors on mortality, postoperative adult respiratory distress syndrome (ARDS), and paralysis was analyzed. One hundred thirty-six patients were admitted with TRA. One hundred twenty underwent operative repair with a mortality of 31 per cent. Operative mortality was significantly higher in unstable patients (62%) versus stable patients (17%, P = 0.001), in patients with cardiac risk factors (71%) versus those without (24%, P = 0.001), and in patients with preoperative free rupture (83%) with versus those without (19%, P = 0.001). Free rupture was the cause of hypotension in only 10 of 42 unstable patients, with the remainder being due to other causes. Preoperative ALI was associated with a marked increase in postoperative ARDS (47% with vs 9% without, P = 0.001) but not operative mortality. Mechanical circulatory support (MCS) was used in 59 cases, none of whom experienced paralysis, whereas eight of 61 operated on without MCS developed paralysis (P = 0.001). When logistic regression was applied the use of MCS was not determined to be statistically significant. However, preoperative instability was found to be a significant predictor of postoperative paralysis with the risk being increased 5.5 times (confidence interval 3.3-10). The predominant factor influencing mortality, postoperative ARDS, and paralysis was preoperative instability and associated injuries. In patients who are hypotensive, other injuries should take precedence over repair of TRA. Patients who are stable but who have cardiac or pulmonary risk factors may be better managed by a period of nonoperative management until their condition improves.

Improvement of rejection-induced diastolic abnormalities in rat cardiac allografts with inducible nitric oxide synthase inhibition.

OBJECTIVE: Inhibition of inducible nitric oxide synthase (nitric oxide II) activity has been proposed as a method to attenuate capillary leak and edema during rejection of heterotopically transplanted rat hearts. Myocardial edema has previously been implicated in diastolic dysfunction during allograft rejection. Accordingly, we tested the hypothesis that inducible nitric oxide synthase inhibition with aminoguanidine would alleviate left ventricular stiffening and myocardial edema formation in 4-day heterotopic rat heart allografts. METHODS: Passive left ventricular filling was studied in American Cancer Institute Lewis rats receiving heterotopic heart transplants receiving either aminoguanidine, a selective nitric oxide synthase inhibitor (n = 6); dexamethasone (1 mg. kg(-1). d(-1) administered subcutaneously) for 4 days after transplantation (n = 6); or intravenous saline solution (n = 6). American Cancer Institute-to-American Cancer Institute isografts (n = 6) were used as controls. RESULTS: Serum nitrite/nitrate levels in the aminoguanidine group (18 +/- 3 mmol/L) and dexamethasone group (22 +/- 4 mmol/L) were reduced versus the intravenous saline group (144 +/- 36 mmol/L [SEM]) to levels seen in controls (25 +/- 9 mmol/L). Left ventricular volume at 15 mm Hg for the aminoguanidine group was increased versus that for the intravenous saline solution group, similar to that for controls, and reduced versus dexamethasone-treated animals. Myocardial water content for the aminoguanidine-treated animals (78.3% +/- 0.4%) was similar to those of intravenous saline-treated animals (78.0% +/- 0. 3%) but greater than those of controls (77.1% +/- 0.2%) and dexamethasone-treated animals (76.7% +/- 0.3%). CONCLUSIONS: Nitric oxide II inhibition with aminoguanidine minimizes the reduction in left ventricular filling that is seen with allograft rejection through a mechanism that is not associated with attenuation of myocardial edema.

Incidence of the concrete scalp deformity associated with deep scalp donor sites and management with the Unna cap.

The scalp has become a popular donor site for split-thickness skin grafts. This donor site does, however, have complications, including the concrete scalp deformity, which consists of hairs embedded in a thick, desiccated, exudative crust. This article presents our burn unit's experience with this complication. Fifty-six patients underwent scalp skin graft harvesting between 1984 and 1996. All grafts were quite thick and were used for resurfacing facial burns. Thirty-eight donor sites were treated with medicated gauze, and 18 were treated with the Unna cap, which is an Unna dressing applied over Aquaphor gauze (Beiersdorf, Norwalk, Conn). Eighteen of the 38 patients (32%) treated with medicated gauze developed the concrete scalp deformity. None of the patients treated with the Unna cap developed the deformity. Although useful, the deep scalp donor site has complications, including the concrete scalp deformity. However, with use of the Unna cap dressing, we have had no occurrences of this problem.

Effect of improved myocardial protection on edema and diastolic properties of the rat left ventricle during acute allograft rejection.

BACKGROUND: Studies of myocardial edema and diastolic dysfunction in rat heart transplantation have been flawed by ischemic injury. This study uses improved methods to prevent ischemic contracture. METHODS: Hearts of 30 ACI rats were transplanted into the abdomen of Lewis rats by use of cold University of Wisconsin solution for improved preservation. Left ventricular diastolic properties were expressed as volume at standardized pressure intervals. RESULTS: On posttransplantation day 3, mean left ventricular volume at 15 mm Hg in allografts (290 +/- 9 microl, SEM) was not significantly different vs isografts (299 +/- 32 microl), allografts on day 0 (337 +/- 28 ml) or day 1 (324 +/- 20 microl), or native hearts (334 +/- 19 microl). However, volume was reduced to 173 +/- 17 microl on day 4 and to 70 +/- 23 microl on day 5 (p < 0.05). Similar findings were obtained for volume at 5 and 10 mm Hg. Allograft myocardial water content on day 3, 76.3% +/- 5%, similar to allografts on day 0 and 1 and to isografts on day 3, increased to 77.6% +/- 8% on day 4 (NS) and 79.4% +/- 6% on day 5 (p < 0.05 vs day 0). Histologically, rejection in allografts was mild on day 3, moderate on day 4, and severe on day 5. CONCLUSIONS: Reduced left ventricular filling volume during rejection is only partially explained by edema. Abnormalities of diastolic properties previously attributed to the unloaded state of nonworking heart models may actually reflect inadequate peritransplantation myocardial protection.

Diastolic properties, myocardial water content, and histologic condition of the rat left ventricle: effect of varied osmolarity of a coronary perfusate.

BACKGROUND: Although myocardial edema is known to impair diastolic filling of the left ventricle, the interrelation of edema, histologic condition, and function has not been quantitated sufficiently for extrapolation to studies of multifactorial influences on diastolic properties. METHODS: Accordingly, ACI rat hearts arrested at 4 degrees C underwent coronary artery perfusion with a cardioplegia solution that was either unaltered (288 mOsm/L, P288 group, n = 6), diluted (144 mOsm/L, P144 group, n = 6), or concentrated (380 mOsm/L, P380 group, n = 6). Postmortem left ventricular pressure-volume curves and myocardial water content were measured. Myocardial samples were fixed in varying dilutions of glutaraldehyde. After dehydration and paraffin embedding, edema was graded subjectively (0 to 5), and myocardial interstitial spaces were determined by use of a semiquantitative method. RESULTS: Mean normalized left ventricular filling volume at 20 mm Hg filling pressure in the P144 group, 189 +/- 16 microliters (SEM), was reduced versus both the P288 (278 +/- 26 microliters) and the P380 (332 +/- 18 microliters) groups (p < 0.05, ANOVA). Mean myocardial water content in the P144 group, 80.7% +/- 1%, was increased versus the P380 (76.7% +/- 0.4%, p < 0.05) but not versus the P288 group (78.4% +/- 0.8%). In hearts preserved with 2.5% glutaraldehyde, mean edema grade and interstitial space in the P144 group (4.0 +/- 0.3) were increased versus the P380 (1.8 +/- 0.3, p < 0.05) but not the P288 group (2.7 +/- 0.5). Derived linear regressions relate water content to filling volume and histologic condition. CONCLUSIONS: Coronary perfusate osmolarity is thus associated with predictable changes in myocardial water content, left ventricular filling volume, and edema. These correlations allow definition of new hypotheses for the study of cardiac allograft rejection in patients and experimental animals.