Subcutaneous gas tensions closely track ileal mucosal gas tensions in a model of endotoxaemia without anaerobism

Objective Few comparative data exist on the responses of the subcutaneous and splanchnic circulations to evolving endotoxic shock. We therefore compared continuous subcutaneous pO₂ (pO_2sc) and pCO₂ (pCO_2sc) with simultaneous continuous gut luminal pCO₂ (pCO_2gi) in an animal model of endotoxaemia and examined whether changes in gas tensions track tissue energy charge (EC).Design Prospective observational study.Subjects Fourteen anaesthetized rats, 7 controls and 7 experimental.Interventions Controls were injected with saline, the experimental group with 20 mg/kg Klebsiella endotoxin. pCO_2sc, pO_2sc, and pCO_2gi were measured continuously. Plasma lactate concentrations were measured at defined periods during the study. After 2 h ileal segments were snap frozen and assayed for tissue EC.Measurements and results Endotoxaemia resulted in a significant decrease in mean arterial blood pressure (132±9 to 71±20 mmHg) and pO_2sc (71±23 to 33±22 torr) and a significant increase in pCO_2gi (58±10 to 90±20 torr) and pCO_2sc (56±6 to 81±25 torr). During endotoxaemia pCO_2gi was directly correlated with pCO_2sc (R ²=0.5) and inversely correlated with pO_2sc (R ²=0.63). Plasma lactate concentrations were significantly elevated from baseline in the endotoxin limb. The mean EC was not significantly different in the two groups.Conclusions Both subcutaneous tissue gas tensions and intestinal luminal carbon dioxide tensions are rapidly responsive during evolving hypodynamic endotoxic shock. Alterations in tissue gas tensions were not associated with dysoxia.Electronic Supplementary Material Electronic supplementary material to this paper can be obtained by using the Springer Link server located at .This work was made possible by a generous grant from the Australia and New Zealand Intensive Care Society and from institutional funds from the Royal Brisbane Hospital. The Paratrend 7 sensors used in the study were supplied by Diametrics Medical Inc, UK. The work was performed in the Intensive Care Laboratory, Division of Anesthesiology and Critical Care, University of Queensland.     

Connection between genetically determined blood coagulation factors and haemorheology

BACKGROUND: The phenotype caracteristic of blood clotting factors are well known, however few data has been documented about effects on haemorheology. The connection among genetic polymorphisms, haemorheological factors and vascular mortality is also studied poorly. PURPOSE: Our aim was: to study six genetic polymorphisms of blood clotting factors, which presents the role of platelet-plasmaprotein-endothel system in thrombotic course in controls and ischaemic stroke cohort. Second, to study the connection of genotypes and haemorheologic factors and both with five years vascular mortality in patients. PATIENTS AND METHODS: It was studied the genetic polymorhisms of GP IIb/IIIa Leu33Pro, prothrombin gene G20210A, ACE I/D, fibrinogen gene-455 G/A, Leiden mutation and MTHFR C677T alleles or genotypes in blood samples of 433 ischaemic stroke patients and 173 controls by PCR. Haematocrit values, plasma fibrinogen (FIB) concentration, whole blood viscosity (WBV) at 90 s(-1) and also the plasma viscosity (PV) were measured. Vascular mortality of patients were followed during five years and studied by curves Kaplan-Meier. RESULTS: A higher plasma FIB concentration in non smoker patients, carrying A alleles of FIB gene could be observed as compared to wild types (p<0.05). Also a moderate WBV increasing in smoker patients with A alleles was found against wild types (p=0.11), at the same time we observed a significant WBV increasing in non smoker patients (p<0.05).The highest quartile of PV showed a connection with Leiden mutation in whole group of patients (p=0.01), in subgroup of young patients (<50 years) (p=0.03) and also in non smoker groups (p<0.05) as compared to patients having wild types. No association could be detected between different genetic polymorphisms and vascular mortality, however it was observed significant mortality increasing in patients having PV above 1.51 mPa s (p=0.03). CONCLUSION: Certain genetic polymorphisms of coagulation system could result unfavorable haemorheological changes, however non of them increases the mortality. The connection between higher mortality and PV focuses the attention for the necessity of PV measuring and correction in stroke patients.     

Brain injury biomarkers may improve the predictive power of the IMPACT outcome calculator

Outcome prediction following severe traumatic brain injury (sTBI) is a widely investigated field of research. A major breakthrough is represented by the IMPACT prognostic calculator based on admission data of more than 8500 patients. A growing body of scientific evidence has shown that clinically meaningful biomarkers, including glial fibrillary acidic protein (GFAP), ubiquitin C-terminal hydrolase-L1 (UCH-L1), and αII-spectrin breakdown product (SBDP145), could also contribute to outcome prediction. The present study was initiated to assess whether the addition of biomarkers to the IMPACT prognostic calculator could improve its predictive power. Forty-five sTBI patients (GCS score≤8) from four different sites were investigated. We utilized the core model of the IMPACT calculator (age, GCS motor score, and reaction of pupils), and measured the level of GFAP, UCH-L1, and SBDP145 in serum and cerebrospinal fluid (CSF). The forecast and actual 6-month outcomes were compared by logistic regression analysis. The results of the core model itself, as well as serum values of GFAP and CSF levels of SBDP145, showed a significant correlation with the 6-month mortality using a univariate analysis. In the core model, the Nagelkerke R(2) value was 0.214. With multivariate analysis we were able to increase this predictive power with one additional biomarker (GFAP in CSF) to R(2)=0.476, while the application of three biomarker levels (GFAP in CSF, GFAP in serum, and SBDP145 in CSF) increased the Nagelkerke R(2) to 0.700. Our preliminary results underline the importance of biomarkers in outcome prediction, and encourage further investigation to expand the predictive power of contemporary outcome calculators and prognostic models in TBI.     

Reduced health-related quality of life in former North Sea divers is associated with decompression sickness

BACKGROUND: Diving is associated with long-term effects on several organ systems. AIM: The objective was to investigate the impact of decompression sickness (DCS) and diving exposure on health-related quality of life (HRQL) in former Norwegian North Sea divers. METHODS: HRQL was recorded by a questionnaire in the cohort of 375 Norwegian North Sea divers registered before 1990. Demographic data, relevant health data and data on diving education, history of DCS and SF-36 were recorded in 230 divers. RESULTS: All SF-36 sub-scores were significantly reduced compared with Norwegian norms. Reduced scores were seen for all scales among divers who reported previous DCS compared to those without DCS. A decreasing trend in scores was seen when comparing no DCS, skin or joint DCS and neurological DCS. There was a decreasing trend in scores related to number of days in saturation and maximal depth. Stratification on DCS showed that the impact of saturation diving was present only in divers with DCS. CONCLUSIONS: HRQL was reduced in this study sample of divers. Having had DCS during the diving career contributed significantly to the reduction in all SF-36 scales, and apparently neurological DCS has the most pronounced impact. Cumulative diving exposure including days in saturation and maximal depth contributed to a reduced HRQL.