Open reduction and internal fixation of acetabular fractures: heterotopic ossification and other complications of treatment.

Open reduction and internal fixation was performed on 50 displaced acetabular fractures in 49 patients by nine different attending surgeons over a 10-year period. At an average follow-up of 38 months, poor results were noted clinically in 38% and radiographically in 40%. The incidence of short- and long-term complications was greater than in other studies. Particularly distressing was the 58% incidence of heterotopic ossification (HO). Twenty-four percent had grade III or IV; five hips were autofused and the remainder had 40-60% loss of motion. There was no correlation of HO with age, sex, fracture type, degree of comminution, associated femoral head fracture or dislocation, delay to surgery, or operative time. However, 26 of 28 patients who had a trochanteric osteotomy as part of the operative exposure developed HO. Other complications included wound infection (12%), avascular necrosis of the femoral head (10%), nerve palsy (8%), and deep vein thrombosis/pulmonary embolism (8%). The data suggest formulation of specific treatment protocols, an awareness of surgical risks, and that staff specialization may reduce complications and improve outcome. Avoiding a trochanteric osteotomy at surgery and using prophylactic postoperative irradiation or indomethacin are suggested to reduce HO.

Mechanism of immunosuppression following hemorrhage: defective antigen presentation by macrophages.

The mechanism by which simple hemorrhage profoundly impairs the proliferative response of T lymphocytes to mitogen and alloantigen, produces a defect in interleukin-2 generation, and increases the susceptibility to sepsis remains unknown. Since antigen presentation (AP) by the macrophage (M phi) plays a critical role in the antigen-specific activation of T-helper cells and lymphokine production, we investigated whether the function of the M phi as an AP cell is altered following hemorrhage. C3H/HEJ mice were bled to a mean BP of 35 mm Hg, maintained at that level for 1 hr, and then resuscitated. There was no mortality with this model. Control mice were not bled but otherwise treated identically. Immediately after resuscitation the mice were sacrificed and peritoneal M phi (PM phi) as well as splenic adherent cells (SAC) were harvested. AP function was tested by coculturing different numbers of PM phi and SAC with D10.G4.1 cells (2 x 10(4) cells/well) in the presence of conalbumin (300 micrograms/ml). This T-helper cell clone proliferates upon recognition of conalbumin in the context of Iak (a M phi surface membrane glycoprotein), thus directly reflecting M phi AP capability. After 72 hr of incubation, the cultures were pulsed with [3H]thymidine and harvested. D10.G4.1 proliferations induced via AP by PM phi and SAC from hemorrhaged-resuscitated mice were 29 and 24% of control, respectively (P less than 0.05). Thus, we conclude that AP by M phi following hemorrhage is defective despite adequate resuscitation, a mechanism which could explain the state of immunosuppression and enhanced susceptibility to sepsis.

The gut origin septic states in blunt multiple trauma (ISS = 40) in the ICU.

The association between support elements (ventilator days = Vd, enteral protein = EnP, number of antibiotics per day = AB/d) and the magnitude of the septic state (SSS) and its bacteriologic manifestations (bacti. log) in 66 patients with blunt multiple trauma (mean HTI-ISS = 40) over 1649 days have been studied retrospectively. SSS is measured by summing the standard deviation units of change in the septic direction for the 16 measurements taken every day in the intensive care unit. Increasing Vd is tightly associated with an increasing SSS (r = +0.52), after day 10 an increasing bacti. log (r = +0.21 to +0.32), and an increasing AB/d (r = +0.26) (all p less than 0.001, N = 1615 - 1626). The independent variables that best predicted Vd were delayed operations (DORS), day of rising EnP, and total positive blood cultures (TPC) (adj. R sq. = 0.84, F = 104, dF = 3/59). An increasing AB/d was associated with an increasing SSS (r = +0.38), increasing Vd (r = +0.26), and an increased bacti. log (r = +0.14 to +0.18) (all p less than 0.001, N = 1615). Only an increased EnP was consistently associated with a reduced SSS (r = -0.38) and a reduction in bacti. log (r = -0.10 to -0.21) (all p less than 0.001, N = 1626-1636). The independent variables Vd, EnP, AB/d, and TPC best predicted SSS for all surviving patients (adj. R sq. = 0.42, F = 268, dF = 4/1496). The patients who died of sepsis were not different in terms of bacti. log from those with equal Vd but were distinguished by zero EnP, high AB/d, and persistent ventilatory support. In conclusion, DORS is tightly associated with increased Vd, SSS, AB/d, and zero EnP. If Vd exceeds 10, there is an increasing bacti. log and evidence of infection probably from the gut. This responds only to increased EnP and not to AB/d. Death due to sepsis is not associated with increased bacti. log but with zero EnP and high AB/d and their consequences.

Blunt multiple trauma (ISS 36), femur traction, and the pulmonary failure-septic state.

Fifty-six blunt multiple trauma patients (HTI-ISS 22-57) were studied for the effects of immediate versus delayed internal fixation of a femur or acetabular fracture on the pulmonary failure septic state. The pulmonary failure septic state may be defined as an alveolar arterial oxygen tension difference greater than 100, plus fever and leukocytosis. These patients were divided into four groups. Group I (N = 20) had immediate internal fixation, postoperative ventilatory support, and was sitting up at 30 hours. Group II (N = 20) had 10 days of femur traction and postoperative ventilatory support. Group III (N = 9) was immediately extubated after surgery and had 30 days of femur traction. Group IV (N = 7) had special circumstances that should increase the duration of the pulmonary failure septic state. These four groups of patients were statistically identical by 20 different criteria on admission except that Group I had more recognized chest injuries than Group II (12 vs. 9). Group I required 3.4 +/- 2.6 days of ventilator support and 7.5 +/- 3.8 intensive care unit (ICU) days; they had 12 +/- 8.8 elevated white counts, 3.8 +/- 4 febrile days, 0.05 positive blood cultures per patient, four fracture complications out of 93 fractures, 59 injections of narcotics, and 23 +/- 8.6 acute care days. Ten days of femur traction doubled the duration of the pulmonary failure septic state relative to Group I at a statistically significant level for nine out of 10 criteria, while increasing the number of positive blood cultures by a factor of 10, the number of fracture complications by a factor of 3.5, and the use of injectable narcotics by a factor of 2. Thirty days of femur traction increased the duration of the pulmonary failure septic state relative to Group I by a factor of 3 to 5 for all criteria at a statistically significant level, while increasing fracture complications by a factor of 17, positive blood cultures by a factor of 74, and the use of narcotics by a factor of 2. Group IV, which had four out of seven immediate internal fixations, behaved similarly to Group II. Femoral shaft traction should be avoided in the blunt multiple trauma patients because it greatly increases the cost of care and the risk of multiple systems organ failure.(ABSTRACT TRUNCATED AT 400 WORDS)

Multiple systems organ failure: V. Alterations in the plasma protein profile in septic trauma - effects of intravenous amino acids.

The correlations between the acute phase and nutritional plasma proteins and intravenous amino acid dosage have been explored in a group of 25 trauma septic patients of whom 14 survived. The two groups of patients appeared to have equal cardiopulmonary function and exogenous nutritional support. The surviving group showed significant associated changes (p less than or equal to 0.05) between alpha1 acid glycoprotein, alpha2 HS glycoprotein, and ceruloplasmin (acute-phase proteins) and between prealbumin, retinol-binding protein, and transferrin (nutritional proteins). There were no correlations in concentration changes between these two groups of plasma proteins. The surviving group showed significant positive correlations between the nutritional plasma protein and intravenous amino acid dosage (prealbumin, p less than or equal to 0.001; transferrin, p less than or equal to 0.008; retinol-binding protein, p less than or equal to 0.001; and albumin, p less than or equal to 0.004) but no correlations with the acute-phase proteins. The nonsurviving patients showed significant intercorrelations between the acute-phase and nutritional proteins that were not seen in the surviving patients, and showed no relationship between intravenous amino acid dosage and the plasma levels of nutritional proteins. The data are consistent with increased obligatory catabolism of amino acids in the nonsurviving patient which based upon the amino acid behavior documented in the first paper in this series probably involves the branched-chain amino acids.

Multiple systems organ failure: IV. Imbalances in plasma amino acids associated with exogenous albumin in the trauma-septic patient.

In a survey study of septic trauma patients, the response of plasma amino acid concentration to albumin infusion was contrasted in survivors (14 patients) and nonsurvivors (11 patients). Plasma albumin levels were maintained at 3 gm/dl by albumin infusion (0-128 gm/day) because of central venous pressure/adequate circulation considerations. Survivors showed no significant increase in plasma essential amino acid concentration as a function of albumin infusion. In nonsurvivors threonine, valine, leucine, phenylalanine, lysine, and histidine all rose significantly (p less than or equal to 0.025) with albumin infusion. Isoleucine (8 residues/molecule albumin), in contrast to leucine (60 residues/molecule) did not increase. As a result, the ratio of isoleucine to leucine (Ile/Leu) decreased with albumin infusion from 0.47 (no albumin infused) to 0.27 (60 gm albumin/day). Survivors did not exhibit a similar response. The low Ile/Leu increased in most nonsurvivors with amino acid infusion from 0.27 (no amino acids) to 0.59 (150 gm amino acids/day). The data strongly suggest that nonsurvivors had an increased rate of albumin catabolism with subsequent amino acid release. Moreover, hypoalbuminemia treated with albumin infusion without amino acid infusion appears to produce a relative isoleucine deficiency which may detrimentally affect protein synthesis.

Multiple systems organ failure: III Contrasts in plasma amino acid profiles in septic trauma patients who subsequently survive and do not survive-effects of intravenous amino acids.

The response of the plasma substrate and hormone profile of survivor and nonsurvivor septic trauma patients to varying rates of amino acid infusion (IVAA) were contrasted. When IVAA=0 levels of most plasma amino acids (except aspartate, tryptophan, cysteine, and proline) were lower in nonsurvivors. At IVAA=1 to 100, however, 11 of 20 plasma amino acids were significantly (p less than or equal to 0.05) higher in nonsurvivors: only glutamate was significantly lower (p less than or equal to 0.001) and valine, isoleucine, and arginine on average lower. At IVAA less than or equal to 101 to 200, only alanine, methionine, tyrosine, and phenylalanine were significantly (p less than or equal to 0.005) higher in nonsurvivors; isoleucine was significantly (p less than or equal to 0.02) lower. The sharp increase in methionine and decrease in tryptophan in nonsurvivors with IVAA was particularly marked. Polynomial regression analysis showed that urea increased significantly with IVAA in both patient groups, while free fatty acids and cortisol decreased only in nonsurvivors. Insulin increased with IVAA only in survivors, glucagon only in nonsurvivors. Triglycerides, glycerol, acetoacetate, beta OH butyrate, and glucose appeared to show no significant response to IVAA in either patient group. The data are consistent with increased peripheral protein catabolism and branched-chain amino acid oxidation in association with decreased tissue uptake of conventional energetic fuels. These results may be interpreted to be consistent with an impairment of mitochondrial translocase systems.

Multiple systems organ failure: II. The effect of infusion of amino acids and glucose.

Amino acids and dextrose infusion were given for short periods of time to a young man whose basal state is characterized in the previous paper in this series, and their effects were documented in terms of plasma concentrations and splanchnic extraction. The basal state measurements show in the acute trauma state and its subsequent starvation state a largely balanced splanchnic extraction of amino acids but at a decreasing rate. Amino acid (FreAmine) infusion at low rates on this background produced a large increase in extraction of a largely balanced mixture of amino acids but a minimal change in glucose release. The septic state is characterized in both the basal and amino acid infusion state by splanchnic extraction of an unbalanced mixture of amino acids which is deficient in branched-chain amino acids and in relative excess of glucogenic amino acids with increased glucose release and increased utilization of amino acids for gluconeogenesis. In early sepsis this state can largely be repaired by exogenous amino acid infusion but in late sepsis can only be partially repaired. The data suggest that the patient in late sepsis should have a branched-chain rich amino acid mixture and that the hepatic failure of sepsis is strongly associated with peripheral release of an unbalanced mixture of amino acids secondary to enhanced branched-chain catabolism. Infused glucose produces a large increase in the plasma glucose but also improves the balance of the splanchnic amino acids extracted. The statistical validity of the preceding statements are examined in detail in the manuscript.