Management of colonic obstruction: a review.

Large bowel obstruction is a common problem with many different causes, the most common being colorectal adenocarcinoma, extracolonic adenocarcinoma, diverticular disease, volvulus, and inflammatory bowel disease. The nature of the obstruction can influence the best management. Historically, treatment of obstruction consisted of surgical removal of the obstruction if possible and decompression of the bowel with an ostomy. Other strategies for managing obstruction have evolved as alternatives to stomas, including primary resection with anastomosis and endoscopic stent placement. The choice of treatment can therefore be tailored to the individual patient with good success.

Resuscitation of haemorrhagic shock with normal saline vs. lactated Ringer's: effects on oxygenation, extravascular lung water and haemodynamics.

INTRODUCTION: Pulmonary oedema and impairment of oxygenation are reported as common consequences of haemorrhagic shock and resuscitation (HSR). Surprisingly, there is little information in the literature examining differences in crystalloid type during the early phase of HSR regarding the development of pulmonary oedema, the impact on oxygenation and the haemodynamic response. These experiments were designed to determine if differences exist because of crystalloid fluid type in the development of oedema, the impact on oxygenation and the haemodynamic response to fluid administration in early HSR. METHODS: Twenty anaesthetised swine underwent a grade V liver injury and bled without resuscitation for 30 minutes. The animals were randomised to receive, in a blinded fashion, either normal saline (NS; n = 10) or lactated Ringer's solution (LR; n = 10). They were then resuscitated with study fluid to, and maintained at, the preinjury mean arterial pressure (MAP) for 90 minutes. RESULTS: Extravascular lung water index (EVLWI) began to increase immediately with resuscitation with both fluid types, increasing earlier and to a greater degree with NS. A 1 ml/kg increase in EVLWI from baseline occurred after administartion of (mean +/- standard error of the mean) 68.6 +/- 5.2 ml/kg of normal saline and 81.3 +/- 8.7 ml/kg of LR (P = 0.027). After 150 ml/kg of fluid, EVLWI increased from 9.5 +/- 0.3 ml/kg to 11.4 +/- 0.3 ml/kg NS and from 9.3 +/- 0.2 ml/kg to 10.8 +/- 0.3 ml/kg LR (P = 0.035). Despite this, oxygenation was not significantly impacted (Delta partial pressure of arterial oxygen (PaO2)/fraction of inspired oxygen (FiO2)

Ketamine-based total intravenous anesthesia versus isoflurane anesthesia in a swine model of hemorrhagic shock.

BACKGROUND: Inhalational anesthetics can cause profound hemodynamic effects including decreases in systemic vascular resistance and cardiac inotropy. Although widely used in uncontrolled hemorrhagic shock (UHS), their consequences compared with other anesthetic regimens are not well-studied. Ketamine-based total intravenous anesthesia (TIVA) may produce less profound cardiovascular depression, and has been used during elective surgery but rarely during traumatic shock. The purpose of this study was to compare the effects of isoflurane (ISO) and TIVA regimens in a swine grade V liver injury model. We hypothesized that TIVA would result in less hypotension and dysfunctional inflammation than ISO. METHODS: Twenty swine were randomized blindly to receive either 1% to 3% ISO, or intravenous ketamine, midazolam, and buprenorphine for maintenance anesthesia. Six animals acted as controls. After sedation and intubation, randomized anesthesia was initiated and monitored by an independent animal technician. Invasive lines were placed followed by celiotomy and splenectomy. Baseline mean arterial pressure (MAP) was documented and a grade V liver injury created. After 30 minutes of UHS, animals were resuscitated with 8 mL of Ringer's lactate per milliliter blood loss at 165 mL/min. MAP and tissue oxygen saturation (StO2) were continuously recorded. The animals were sacrificed 120 minutes after injury and lung tissue was harvested. Serum cytokines (interleukin-6 [IL-6], IL-8, and tumor necrosis factor-alpha [TNF-alpha]) were quantified with enzyme-linked immunosorbent assay. Lung cytokine mRNA levels were quantified with real time reverse transcriptase polymerase chain reaction. RESULTS: Animal weight, liver injury pattern, and blood loss were similar (p > 0.1). The ISO group had a lower MAP at baseline (p = 0.02), at injury (p = 0.004), and study completion (p = 0.001). After resuscitation, MAP decreased in the ISO group but remained stable in the TIVA group. StO2 was significantly higher in the TIVA group immediately after injury (p = 0.004), but similar between groups throughout the remainder of the study. Animals who received TIVA trended toward higher levels of lactate and lower pH throughout the study, reaching significance at 30 minutes postinjury (p = 0.037 and 0.043). Inflammatory cytokine (IL-6, IL-8, and TNF-alpha) production did not differ between groups, however TNF-alpha mRNA production was significantly lower in the TIVA group (p = 0.04). CONCLUSION: Although a TIVA regimen produced less pronounced hypotension in a swine model of UHS than did ISO, end-organ perfusion with TIVA appeared to be equivalent or inferior to ISO. In circumstances of limited resources, such as those experienced by forward Army surgical teams, a ketamine-based TIVA regimen may be an option for use in UHS.

The influence of sex hormones on coagulation and inflammation in the trauma patient.

Recent clinical studies have shown a sex dimorphism of morbidity and mortality due to shock, trauma, and sepsis, with females tolerating these insults better than males. Experimental animal studies have suggested that sex hormones have a pivotal role in this dimorphism. In the present investigation, a prospective cohort study at a university level-1 trauma center was conducted to evaluate the association between sex hormones and alterations in coagulation and inflammation. Patients with an admission to the intensive care unit, injury severity score (ISS) greater than 4, and obtainable consent were included in the study. In addition to routine clinical laboratories and patient outcomes, plasma TNF-[alpha], IL-6, IL-8, estradiol, progesterone, and testosterone were measured. Sixty-two patients (71% men, 29% women) met criteria for entry. Mean age was 42 +/- 17 years, and mean ISS was 23 +/- 13, with no statistical difference in age or ISS between sexes. Estradiol levels were positively correlated with ISS (P < 0.05) and negatively correlated with TNF-[alpha] (P < 0.01). Initial estradiol levels were higher in patients who developed an infection (P < 0.05). Testosterone was negatively correlated with age (P < 0.01) and was higher in patients who developed acute respiratory distress syndrome (P < 0.05) and in patients who did not survive (P < 0.05). The estradiol-to-progesterone ratio (E2-Pr) was higher in the survivors (P < 0.05). The E2-Pr had positive correlations with fibrinogen levels, rate of fibrin deposition and cross-linking, and overall clot strength (P < 0.05). Estradiol-to-progesterone ratio was negatively correlated with partial thromboplastin times (P < 0.01). In men, the E2-Pr was also negatively correlated with the time to onset of clot formation (P = 0.03). Sex hormone levels (or their ratios) were not correlated to platelet count or international normalized ratios. These findings provide evidence that sex hormone levels in the early posttraumatic period are significantly associated with alterations in the hemostatic and inflammatory response to trauma.

Resuscitation with normal saline (NS) vs. lactated ringers (LR) modulates hypercoagulability and leads to increased blood loss in an uncontrolled hemorrhagic shock swine model.

BACKGROUND: Lactated ringers (LR) and normal saline (NS) are used interchangeably in many trauma centers. The purpose of this study was to compare the effects of LR and NS on coagulation in an uncontrolled hemorrhagic swine model. We hypothesized resuscitation with LR would produce hypercoagulability. METHODS: There were 20 anesthetized swine (35 +/- 3 kg) that underwent central venous and arterial catheterization, celiotomy, and splenectomy. After splenectomy blinded study fluid equal to 3 mL per gram of splenic weight was administered. A grade V liver injury was made and animals bled without resuscitation for 30 minutes. Animals were resuscitated with the respective study fluid to, and maintained, at the preinjury MAP until study end. Prothrombin Time (PT), Partial Thromboplastin Time (PTT), and fibrinogen were collected at baseline (0') and study end (120'). Thrombelastography was performed at 0'and postinjury at 30', 60', 90', and 120'. RESULTS: There were no significant baseline group differences in R value, PT, PTT, and fibrinogen. There was no significant difference between baseline and 30 minutes R value with NS (p = 0.17). There was a significant R value reduction from baseline to 30 minutes with LR (p = 0.02). At 60 minutes, R value (p = 0.002) was shorter while alpha angle, maximum amplitude, and clotting index were higher (p < 0.05) in the LR versus the NS group. R value, PT, and PTT were significantly decreased at study end in the LR group compared with the NS group (p < 0.05). Overall blood loss was significantly higher in the NS versus LR group (p = 0.009). CONCLUSIONS: This data indicates that resuscitation with LR leads to greater hypercoagulability and less blood loss than resuscitation with NS in uncontrolled hemorrhagic shock.

Pulsatile flow-induced angiogenesis: role of G(i) subunits.

OBJECTIVE: Angiogenesis plays a key role in the growth and function of normal and pathological tissues. We investigated the effect of pulsatile flow on endothelial cell (EC) in vitro angiogenic activity. METHODS AND RESULTS: Bovine aortic ECs were exposed to "static" or "flow" (1.2 to 67.0 mL/min, shear stress 1.4 to 19.2 dyne/cm2) conditions for 2 to 24 hours. After exposure, angiogenesis was measured as tubule formation on Matrigel, and EC migration was assessed by filter migration assay. Pulsatile flow increased angiogenesis and EC migration in a temporal and force-dependent manner, with a maximal effect at 16 hours (13.2 dyne/cm2). Pertussis toxin completely inhibited the effect of pulsatile flow on angiogenesis and migration. Transfection of ECs with inhibitory mutants of the alpha subunit of G(i)1 or G(i)3, but not G(i)2, inhibited the flow-induced angiogenic response by 61+/-2% and 32+/-6%, respectively, whereas transfection with constitutively activated mutants of the alpha subunit of G(i)1 or G(i)3, but not G(i)2, increased the flow-induced response by 202+/-23% and 70+/-4%, respectively. In contrast, inhibition of Gbetagamma by the carboxy terminal fragment of beta-adrenergic receptor kinase overexpression increased the flow-induced response by 82+/-8%. CONCLUSIONS: These results suggest that pulsatile flow stimulates angiogenesis and that this effect is mediated by activation of G(ialpha)1 or G(ialpha)3, but not Gbetagamma, subunits.