Splenectomy is associated with altered leukocyte kinetics after severe trauma.

BACKGROUND: Inadequate activation of the innate immune system after trauma can lead to severe complications such as Acute Respiratory Distress Syndrome and Multiple Organ Dysfunction Syndrome. The spleen is thought to modulate the cellular immune system. Furthermore, splenectomy is associated with improved outcome in severely injured trauma patients. We hypothesized that a splenectomy alters the cellular immune response in polytrauma. METHODS: All adult patients with an ISS ≥ 16 and suffering from splenic or hepatic injuries were selected from our prospective trauma database. Absolute leukocyte numbers in peripheral blood were measured. White blood cell kinetics during the first 14 days were compared between splenectomized patients, patients treated surgically for liver trauma and nonoperatively treated individuals. RESULTS: A total of 129 patients with a mean ISS of 29 were included. Admission characteristics and leukocyte numbers were similar in all groups, except for slightly impaired hemodynamic status in patients with operatively treated liver injuries. On admission, leukocytosis occurred in all groups. During the first 24 h, leukopenia developed gradually, although significantly faster in the operatively treated patients. Thereafter, leukocyte levels normalized in all nonoperatively treated cases whereas leukocytosis persisted in operatively treated patients. This effect was significantly more prominent in splenectomized patients than all other conditions. CONCLUSIONS: This study demonstrates that surgery for intra-abdominal injuries is associated with an early drop in leucocyte numbers in peripheral blood. Moreover, splenectomy in severely injured patients is associated with an altered cellular immune response reflected by a persistent state of prominent leukocytosis after trauma.

Trauma results in immune cell-induced intestinal epithelial damage with subsequently increased sepsis rate.

BACKGROUND: The detrimental effect of trauma on the immune system has been a subject of interest for decades. The gut-associated lymphoid tissue (GALT) of the bowel that encompasses different lymphocyte subpopulations may be an important pillar of human immunity in the context of trauma. Neither the short-term histological trauma-induced changes in the GALT nor its impact on the outcome after trauma surgery has been investigated. METHODS: This prospective, longitudinal proof-of-concept study included patients who required damage-control surgery after abdominal gunshot wounds with small bowel involvement. Bowel specimens were obtained during the index and relook operations, and the T-lymphocytic quantity therein was analyzed via immunohistochemistry. We scrutinized how the lymphocyte structure and numbers of the GALT altered, and whether the extent and nature of these changes had an impact on the postoperative outcome with regard to septic and surgical complications. RESULTS: A total of 31 damage-control patients were recruited for the study. The main histological changes between the index and relook specimen was a shift of CD8+ T cells from the lamina propria (LP) into the epithelium and a decrease of T lymphocytes in the LP. The significant increase of the intraepithelial CD8+ T cells was associated with a more extensive enterocyte apoptosis, and correlated significantly, positively with the number of postoperative septic complications. CONCLUSION: Our data support that trauma induces an immune cell-driven impairment of the intestinal epithelium, as well as an increased apoptosis of lymphocytes in the LP, which is associated with a worse clinical outcome. The underlying mechanism suggests that a therapeutic approach to minimize apoptosis in the intestine may impact the outcome of severely injured trauma patients. LEVEL OF EVIDENCE: Therapeutic/care/management, level lV.

Clinical Evaluation of "Shock Bowel" Using Intestinal Fatty Acid Binding Protein.

"Shock bowel" is one of the computed tomographic (CT) signs of hypotension, yet its clinical implications remain poorly understood. We evaluated how shock bowel affects clinical outcomes and the extent of intestinal epithelial damage in trauma patients by measuring the level of intestinal fatty acid binding protein (I-FABP). We reviewed the initial CT scans, taken in the emergency room, of 92 patients with severe blunt torso trauma who were consecutively admitted during a 24-month period. The data collected included CT signs of hypotension, I-FABP, feeding intolerance, and other clinical outcomes. Demographic and clinical outcomes were compared in patients with and without hemodynamic shock and shock bowel. Shock bowel was found in 16 patients (17.4%); of them 7 patients (43.8%) did not have hemodynamic shock. Certain CT signs of hypotension, namely free peritoneal fluid, contrast extravasation, small-caliber aorta, and shock bowel, were significantly more common in patients with hemodynamic shock than in patients without (P < 0.05). Injury severity score and the rate of consciousness disturbance were significantly higher in patients with shock bowel than in patients without (P < 0.05). The rate of feeding intolerance and median plasma I-FABP levels were significantly higher in patients with shock bowel than in patients without (75.0% vs. 22.4%, P < 0.001 and 17.0 ng/mL vs. 3.7 ng/mL, P < 0.001, respectively). There was no difference in mortality. In conclusion, shock bowel is not always due to hemodynamic shock. It does, however, indicate severe intestinal mucosal damages and may predict feeding intolerance.

Thorax injury lowers resistance to infection in Drosophila melanogaster.

The route of infection can profoundly affect both the progression and outcome of disease. We investigated differences in Drosophila melanogaster defense against infection after bacterial inoculation into two sites--the abdomen and the thorax. Thorax inoculation results in increased bacterial proliferation and causes high mortality within the first few days of infection. In contrast, abdomen inoculation results in minimal mortality and lower bacterial loads than thorax inoculation. Inoculation into either site causes systemic infection. Differences in mortality and bacterial load are due to injury of the thorax and can be recapitulated by abdominal inoculation coupled with aseptic wounding of the thorax. This altered resistance appears to be independent of classical immune pathways and opens new avenues of research on the role of injury during defense against infection.

Mitochondrial damage-associated molecular patterns released by abdominal trauma suppress pulmonary immune responses.

BACKGROUND: Historically, fever, pneumonia, and sepsis after trauma are ascribed to pain and poor pulmonary toilet. No evidence supports that assertion however, and no known biologic mechanisms link injury to infection. Our studies show that injured tissues release mitochondria (MT). Mitochondrial damage-associated molecular patterns (mtDAMPs) however can mimic bacterial pathogen-associated danger molecules and attract neutrophils (PMN). We hypothesized that mtDAMPs from traumatized tissue divert neutrophils from the lung, causing susceptibility to infection. METHODS: Anesthetized rats (6-10 per group) underwent pulmonary contusion (PC) by chest percussion. When modeling traumatic MT release, some rats had MT isolated from the liver (equal to 5% liver necrosis) injected intraperitoneally (IPMT). Negative controls had PC plus buffer intraperitoneally. Positive controls underwent PC plus cecal ligation and puncture. At 16 hours, bronchoalveolar and peritoneal lavages were performed. Bronchoalveolar lavage fluid (BALF) and peritoneal lavage fluid were assayed for PMN count, albumin, interleukin ß, (IL-ß), and CINC-1. Assays were normalized to blood urea nitrogen to calculate absolute concentrations. RESULTS: PC caused alveolar IL-1ß and CINC production and a 34-fold increase in BALF neutrophils. As expected, IPMT increased peritoneal IL-1ß and CINC and attracted PMN to the abdomen. However, remarkably, IPMT after PC attenuated BALF cytokine accumulation and decreased BALF PMN. Cecal ligation and puncture had no direct effect on BALF PMNs but, like IPMT, blunted BALF leukocytosis after PC. CONCLUSION: Rather than acting as a "second hit" to enhance PMN-mediated lung injury, mtDAMPs from trauma and pathogen-associated danger molecules from peritoneal infection diminish PMN accumulation in a contused lung. This may make the lung susceptible to pneumonia. This paradigm provides a novel mechanistic model of the relationship among blunt tissue trauma, systemic inflammation, and pneumonia that can be studied to improve trauma outcomes.

[Vacuum sealing drainage promotes experimental pig explosive abdomen wound healing].

OBJECTIVE: To explore the roles of vacuum sealing drainage (VSD) in controlling infection and promoting healing on the experimental pigs with blast injury in the abdomen and exposed internal organs. METHODS: All animals with full-thickness abdominal wall defect were randomly divided into experimental group (VSD group) and control group (saline gauze group). Debridement was performed 6 hours after wounding. VSD devices (-125 mmHg) were imbedded on animals in the experimental group, while in the control group gauzes with saline solution were used to cover the wound and conventional treatment of dressing change was done. Specimens of muscle tissue in the wound were collected respectively from the two groups to make bacteria quantification 6 hours before the treatment and on the 1st, 3rd, 5th, and 7th day of treatment. Specimens of abdominal drainage fluid were collected respectively on the 1st, 3rd, 5th, and 7th day of treatment to detect inflammatory cytokines (TNF-α, IL-1, IL-6) using ELISA kit. Specimens of the skin and muscle tissues were collected respectively from the two groups on the 7th day to detect target genes (VEGF, bFGF, EGF, and MMP-9) using qRT-PCR. RESULTS: The bacteria counts (CFU/g) in the VSD group on the 1st, 3rd, 5th, and 7th day of treatment were significantly less than those in the control group at the corresponding time points, and the differences between the two groups were statistically significant (P<0.01). There were no distinct differences between the two groups in the expressions of TNF-α, IL-1 and IL-6 in the abdominal drainage fluid of pig on the 1st day of treatment. The expressions of TNF-α, IL-1 and IL-6 on the 3rd, 5th, and 7th day of treatment in the VSD group were significantly lower than those in the control group at the corresponding time points (P<0.01). The expressions of VEGF, EGF and bFGF in the skin and soft tissues in the VSD group on the 7th day was higher than those in the control group (P<0.01), while the expression of MMP-9 showed no statistical significant difference between the two groups (P>0.05). CONCLUSION: VSD can effectively control the amount of bacteria in the wound, and reduce the expressions of pro-inflammatory factors such as TNF-α, IL-1 and IL-6 in drainage fluid. VSD also promotes the expressions of growth factors in the wound.

An in vivo model system for evaluation of the host response to biomaterials.

We describe an in vivo model system designed to evaluate the host response to implanted biomaterials: The partial thickness rat abdominal wall defect model. The model allows for determination of the temporal and spatial distribution of the cellular and vascular response, the remodeling of the implanted material and surrounding host soft tissue, and the function of the remodeled tissue over time.

Efficacy and safety of active negative pressure peritoneal therapy for reducing the systemic inflammatory response after damage control laparotomy (the Intra-peritoneal Vacuum Trial): study protocol for a randomized controlled trial.

BACKGROUND: Damage control laparotomy, or abbreviated initial laparotomy followed by temporary abdominal closure (TAC), intensive care unit resuscitation, and planned re-laparotomy, is frequently used to manage intra-abdominal bleeding and contamination among critically ill or injured adults. Animal data suggest that TAC techniques that employ negative pressure to the peritoneal cavity may reduce the systemic inflammatory response and associated organ injury. The primary objective of this study is to determine if use of a TAC dressing that affords active negative pressure peritoneal therapy, the ABThera Open Abdomen Negative Pressure Therapy System, reduces the extent of the systemic inflammatory response after damage control laparotomy for intra-abdominal sepsis or injury as compared to a commonly used TAC method that provides potentially less efficient peritoneal negative pressure, the Barker's vacuum pack. METHODS/DESIGN: The Intra-peritoneal Vacuum Trial will be a single-center, randomized controlled trial. Adults will be intraoperatively allocated to TAC with either the ABThera or Barker's vacuum pack after the decision has been made by the attending surgeon to perform a damage control laparotomy. The study will use variable block size randomization. On study days 1, 2, 3, 7, and 28, blood will be collected. Whenever possible, peritoneal fluid will also be collected at these time points from the patient's abdomen or TAC device. Luminex technology will be used to quantify the concentrations of 65 mediators relevant to the inflammatory response in peritoneal fluid and plasma. The primary endpoint is the difference in the plasma concentration of the pro-inflammatory cytokine IL-6 at 24 and 48 h after TAC dressing application. Secondary endpoints include the differential effects of these dressings on the systemic concentration of other pro-inflammatory cytokines, collective peritoneal and systemic inflammatory mediator profiles, postoperative fluid balance, intra-abdominal pressure, and several patient-important outcomes, including organ dysfunction measures and mortality. DISCUSSION: Results from this study will improve understanding of the effect of active negative pressure peritoneal therapy after damage control laparotomy on the inflammatory response. It will also gather necessary pilot information needed to inform design of a multicenter trial comparing clinical outcomes among patients randomized to TAC with the ABThera versus Barker's vacuum pack. TRIAL REGISTRATION: ClinicalTrials.gov identifier http://www.clicaltrials.gov/ct2/show/NCT01355094.

Trauma-hemorrhage inhibits splenic dendritic cell proinflammatory cytokine production via a mitogen-activated protein kinase process.

Although splenic dendritic cell (DC) functions are markedly altered following trauma-hemorrhage, the mechanism(s) responsible for the altered DC functions remains unknown. We hypothesized that trauma-hemorrhage inhibits DC function via suppressing toll-like receptor 4 (TLR4) expression and mitogen-activated protein kinases (MAPKs). To examine this, male C3H/HeN (6-8 wk) mice were randomly assigned to sham operation or trauma-hemorrhage. Trauma-hemorrhage was induced by midline laparotomy and approximately 90 min of hypotension [blood pressure (BP) 35 mmHg], followed by fluid resuscitation (4x the shed blood volume in the form of Ringer lactate). Two hours later, mice were euthanized, splenic DCs were isolated, and the changes in their MAPK activation, TLR4-MD-2 expression, and ability to produce cytokines were measured. The results indicate that trauma-hemorrhage downregulated the lipopolysaccharide (LPS)-induced MAPK activation in splenic DCs. In addition to the decrease in MAPK activation, surface expression of TLR4-MD-2 was suppressed following trauma-hemorrhage. Furthermore, LPS-induced cytokine production from splenic DCs was also suppressed following trauma-hemorrhage. These findings thus suggest that the decrease in TLR4-MD-2 and MAPK activation may contribute to the LPS hyporesponsiveness of splenic DCs following trauma-hemorrhage. Hyporesponsiveness of splenic DCs was also found after stimulation with the TLR2 agonist zymosan. Our results may thus explain the profound immunosuppression that is known to occur under those conditions.

Proximal splenic artery embolization for blunt splenic injury: clinical, immunologic, and ultrasound-Doppler follow-up.

BACKGROUND: To evaluate the clinical, US (ultrasound)-Doppler and hematologic findings after proximal splenic artery embolization (PSAE) for blunt injury. METHODS: From August 1998 to February 2003, 37 patients (28 men and 9 women; 20-89 years old, mean 40 years) underwent PSAE for blunt injuries. One patient required secondary splenectomy after PSAE. Early complications were investigated during the hospital stay. Delayed follow-up included review of the outpatient records, telephone interview, consultation, US-Doppler splenic study, Howell-Jolly body search, and serum antibody titer determinations (pneumococcus and Haemophilus influenzae B). RESULTS: No early postprocedural complications were depicted. Ten patients were lost on follow-up. Two patients had a telephone interview that revealed no complication. Twenty-four patients were examined 6 to 63 (mean 26) months after the embolization. No late complication was reported. Splenic measurements were in the normal range: length (53-110 mm; mean, 73), width (49-110 mm; 76), thickness (26-56 mm; 38), volume (61-508 mL; 226), standard ellipsoid formula volume (32-265 mL; 118), corrected volume (29-238 mL; 106), and splenic volumetric index (2.3-18.8; 8.4). The spleen was homogeneous in 23 patients (96%). Intrasplenic vascularization was present and splenic vein was patent in all patients. Howell-Jolly bodies were found in two patients. All patients (24 of 24) evaluated for exposure-driven immunity against Haemophilus Influenza b had sufficient immunity. Seventeen of the 18 patients (94%) evaluated for exposure-driven immunity against pneumococcus had sufficient immunity. Five of the six patients (83%) evaluated for pneumococcus vaccine response had a sufficient response. CONCLUSIONS: Proximal splenic artery embolization in blunt splenic injuries is a well-tolerated technique without major long-term impact on the splenic anatomy and immune function.

[Immune status late after surgery for spleen injuries].

Immune status was studied in patients who had undergone surgery for spleen injuries (splenectomy, autolientransplantation and organ-saving surgeries). It is demonstrated that splenectomy leads to immunosuppression in long-term postoperative period. For prevention of these complications the organ-saving surgeries or autolientransplantation in addition to splenectomy are recommended.

[Effect of early enteral nutrition on immune function of the patients after operation for severe abdominal trauma].

OBJECTIVE: To determine the effect of early enteral nutrition (EN) on immune function of the patients after operation for severe abdominal trauma. METHODS: Fourty patients who underwent operation for severe abdominal trauma were randomly divided into two groups, and received an early enteral nutrition (EN group, n=20) through jejunal nutritional tube from postoperative day 1, or parental nutrition (PN group, n=20) for 7 days. C3, IgA, IgM, IgG and CD3+, CD4+, CD8+, CD4+/CD8+ of the two groups patients were detected on the day before operation and the postoperative day 1 and 8. The infection complications were compared. RESULTS: After 7 days, the levels of C3+, IgA, IgG, CD3+, CD4+, CD8+, and CD4+/CD8+ in EN group increased significantly compared with those in PN group (P< 0.05). The incidence of infection was 10% in EN group, while 30% in PN group (P< 0.05). CONCLUSION: Early enteral nutrition can improve immune function and decrease postoperative infection after operation for severe abdominal trauma.

Effect of astragalus injection on serious abdominal traumatic patients' cellular immunity.

OBJECTIVE: To explore the change of serious abdominal traumatic patients' cellular immunity and the effect of Astragalus Injection (AI) on it. METHODS: Sixty-three serious abdominal traumatic patients were randomly assigned into two groups, the conventional group and the treated group, patients in the conventional group were given conventional treatment, while others in the treated group were given conventional treatment as the basis, with AI 20 ml was added into 250 ml of 5% glucose solution given through intravenous dripping, and then on the first day and 14th day, their T cell activated antigens as well as that of 10 healthy subjects were monitored. RESULTS: On the first day, in the conventional group and treated group, the levels of CD(3)(+), CD(4)(+), CD(4)(+)/CD(8)(+), CD(16)(+), CD(69)(+) and CD(3)(+)/homologous leucocytic antigen-DR (HLA-DR(+)) were apparently lower than those in the healthy group (P < 0.05), while the CD(8)(+) was significantly higher than that in the healthy group (P < 0.05), and there was no significant difference between the conventional group and the treated group (P > 0.05); on the 14th days, the levels of CD(3)(+), CD(4)(+), CD(4)(+)/CD(8)(+), CD(16)(+), CD(69)(+) and CD(3)(+)/HLA-DR(+) of the treated group got closed to healthy subject value, and got even higher than those of conventional group (P < 0.05); CD(8)(+) got close to that of healthy subjects, while obviously lower than that of conventional group (P < 0.05). CONCLUSION: After serious abdominal trauma, cellular immunity lowered, auxiliary use of AI was beneficial to the restoration of cellular immunity.

Differential effect of imipenem treatment on wild-type and NK cell-deficient CD8 knockout mice during acute intra-abdominal injury.

CD8 knockout mice depleted of natural killer (NK) cells by treatment with anti-asialoGM1 (CD8KO/alphaAsGM1 mice) are resistant to injury caused by cecal ligation and puncture (CLP). However, CLP-induced injury is complex. Potential sources of injury include bacterial dissemination, cecal ischemia, and translocation of bacterial toxins. We treated wild-type and CD8KO/alphaAsGM1 mice with imipenem after CLP to decrease bacterial dissemination. Additional mice were subjected to cecal ligation without puncture of the cecal wall or cecal ligation and removal of cecal contents. Imipenem treatment decreased bacterial counts by at least two orders of magnitude. However, all wild-type mice, whether treated with saline or imipenem, died by 42 h after CLP and exhibited significant hypothermia, metabolic acidosis, and high plasma cytokine concentrations. Wild-type mice subjected to cecal ligation without puncture also died, despite very low bacterial counts in blood, but wild-type mice subjected to cecal ligation and washout of cecal contents survived. In CD8KO/alphaAsGM1 mice subjected to CLP, imipenem treatment increased survival from 50% to 100%. After cecal ligation without puncture, long-term survival was 80-90% in CD8KO/alphaAsGM1 mice. Hypothermia, metabolic acidosis, and cytokine production were attenuated in CD8KO/alphaAsGM1 mice compared with wild-type controls. These results indicate that bacterial dissemination is not a major source of injury in wild-type mice after CLP, but the presence of gut flora in the cecal lumen is required for induction of systemic inflammation after cecal injury. CD8KO/alphaAsGM1 mice are resistant to the systemic manifestations of cecal injury.

[Immune correction in patients with colostomas and fistulas].

Symptoms of secondary immune deficiency were revealed in 37 out of 84 wounded with colonic fistulas and colostomas. During the preparation of the patients to restorative operations for the improvement of the immune system functions the patients were given transfusions of donor leuko-suspension taken from subjects with high titer of antibody in blood serum to colon bacillus and intravenous infusions of immunoglobulin. Such immunocorrection allowed restoration of immune potential of organism during a short time and improvement of the operation results.

Response of circulating immune cells to major gunshot injury, haemorrhage, and acute surgery.

PURPOSE: The purpose of this study was to use an established porcine model to investigate the effects on immune function of severe gunshot injury. METHODS: Twelve pigs sustained two standardised rounds, one through right femur and one through left upper abdomen. First aid treatment and acute surgery was started immediately. Blood samples were drawn before shooting and after 75 min. Circulating neutrophils were isolated and reactive oxygen species (ROS) measured. Serum levels of tumour necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), IL-6, and IL-10 were determined at 0, 75 min, as well as 2h after incubation with 1 microg/ml endotoxin in an ex vivo whole blood model. RESULTS: TNF-alpha, IL-1beta, and IL-6 significantly increased at 75 min. ROS in circulating granulocytes tended to increase (NS). Incubation with endotoxin led to a more than 100-fold increase of TNF-alpha pre-trauma, compared to a three-fold increase post-trauma (p<0.0001 between groups). A similar pattern was obtained for IL-1beta, and IL-6. IL-10 was below detection in all samples. The granulocytes maintained their ability to react to the protein kinase C activator phorbol myristate acetate (PMA) after trauma. CONCLUSION: Severe gunshot injury and peritraumatic stress rapidly activate circulating immune cells, but reduce their capacity to react to a subsequent challenge to endotoxin.

Amplified cytokine response and lung injury by sequential hemorrhagic shock and abdominal compartment syndrome in a laboratory model of ischemia-reperfusion.

BACKGROUND: Increased intra-abdominal pressure has been shown to result in a myriad of physiologic aberrations that result in the abdominal compartment syndrome (ACS). The clinically relevant combination of hemorrhagic shock and resuscitation and subsequent ACS, however, has not been studied in detail. We hypothesized that sequential hemorrhagic shock (HS) and ACS would result in greater cytokine activation and polymorphonuclear neutrophil (PMN)-mediated lung injury than with either insult alone. METHODS: Twenty Yorkshire swine (20-30 kg) were studied. Group 1 (n = 5) was hemorrhaged to a mean arterial pressure of 25 to 30 mm Hg for 60 minutes and resuscitated to baseline mean arterial pressure. Intra-abdominal pressure was then increased to 30 mm Hg above baseline and maintained for 60 minutes. Group 2 (n = 5) was subjected to HS alone and Group 3 (n = 5) to ACS alone. Group 4 (n = 5) had sham experiment without HS or ACS. Central and portal venous interleukin-1beta, interleukin-8, and tumor necrosis factor-alpha levels were serially measured. Bronchoalveolar lavage (BAL) for protein and PMNs was performed at baseline and 24 hours after resuscitation. Lung myeloperoxidase was evaluated at 24 hours after resuscitation. RESULTS: Portal and central vein cytokine levels were equivalent but were significantly higher in Group 1 than in other groups. BAL PMNs were higher (p < 0.05) in Group 1 (4.1 +/- 2.0 x 106) than in the other groups (0.6 +/- 0.5, 1.4 +/- 1.3, and 0.1 +/- 0.0 x 106, respectively) and lung myeloperoxidase activity was higher (p < 0.05) in Group 1 (134.6 +/- 57.6 x 106/g) than in the other groups (40.3 +/- 14.7, 46.1 +/- 22.4, and 7.73 +/- 4.4 x 106/g, respectively). BAL protein was higher (p < 0.01) in Group 1 (0.92 +/- 0.32 mg/mL) compared with the other groups (0.22 +/- 0.08, 0.29 +/- 0.11, and 0.08 +/- 0.06 mg/mL, respectively). CONCLUSION: In this clinically relevant model, sequential insults of ischemia-reperfusion (HS and resuscitation) and ACS were associated with significantly increased portal and central venous cytokine levels and more severe lung injury than HS or ACS alone.

[State of the immune system in patients with penetrating thoracic and abdominal injuries complicated by massive hemorrhage]. / Sostoianie immunnoi sistemy postradavshikh s pronikaiushchimi raneniiami grudi i zhivota, oslozhnennymi massivnoi krovopoterei.

Results of immune status examination on day 1-2 and 4-8 after operation in 217 patients with penetrating gunshot and stab-incised wounds of thorax and abdomen were analyzed. Correlation between immunogram and volume of acute hemorrhage was studied. Types of immunograms characteristic of good and complicated postoperative period were determined, their frequency was estimated, that permits to perform substantiated and timely special correction for acceleration of immunorehabilitation and prevention of infectious complications.

[Prognostic significance of immune reactions in multiple injuries involving thoracic and abdominal cavities]. / Prognosticheskoe znachenie immunnykh reaktsii pri politravme s povrezhdeniem organov grudnoi i briushnoi polostei.

Prognostic informativity some indexes of immune response in severe shockogenic combined thoracoabdominal trauma was studied. In 92 patients aged from 17 to 85 years (68 men and 24 women) in acute period of traumatic disease (TD) quantity of T-, B-, 0-lymphocytes, immunoregulating subpopulations, the main immunoglobulins classes concentration, circulating immune complex were determined. Significant disorders of the organism immune system of injured persons were revealed, but prognostic significance of the data obtained in determination of the TD course severity was not large.