Triage vital signs do not correlate with serum lactate or base deficit, and are less predictive of operative intervention in penetrating trauma patients: a prospective cohort study.

BACKGROUND: Triage vital signs are often used to help determine a trauma patient's haemodynamic status. Recent studies have demonstrated that these may not be very specific in determining major injury. The purpose of this study was to determine if there is any correlation between triage vital signs, base deficit (BD) and lactate, and to determine the odds of operative intervention in penetrating trauma patients. METHODS: A prospective observational cohort study was undertaken. Baseline vital signs, BD and lactate were recorded in all patients for whom the trauma team was activated. Pearson correlation and coefficient (ρ) were calculated. ORs were calculated. RESULTS: 75 patients were enrolled. Pearson correlations and coefficients calculated for lactate to systolic blood pressure were: -0.052 (ρ=0.0011, 95% CI -0.225 to 0.228); lactate and HR: 0.23 (ρ=0.0166, 95% CI -0.211 to 0.242); lactate and RR: 0.23 (ρ=0.054, 95% CI -0.174 to 0.277). BD to systolic blood pressure were: 0.003 (ρ=0.00001, 95% CI -0.229 to 0.224); BD and HR: -0.19 (ρ=0.038, 95% CI -0.399 to 0.038); BD and RR: -0.019 (ρ=0.0004, 95% CI -0.244 to 0.208). Odds of operative intervention were greater in patients with abnormally high lactate, OR 4.17 (95% CI 1.57 to 11), but not for BD, OR 2.53 (95% CI 0.99 to 6.45), or any of the vital signs. CONCLUSIONS: Triage vital signs have no correlation to lactate or BD levels in penetrating trauma patients. Odds of operative intervention are greater in patients with abnormally high serum lactate levels, but not in those with abnormal triage vital signs or BD.

Nasal cannula end-tidal CO2 correlates with serum lactate levels and odds of operative intervention in penetrating trauma patients: a prospective cohort study.

BACKGROUND: Penetrating trauma patients in shock often require urgent operative intervention. Studies have demonstrated that variables obtained in the emergency department, such as lactate levels, can help the physician determine the presence of hemorrhagic shock, leading to more rapid intervention and improve prognosis in trauma patients. The purpose of the study is to determine if end-tidal (ET) CO2 correlates with serum lactate levels, a measure of tissue hypoxia and subsequently shock, in penetrating trauma patients. Secondarily, we sought to determine whether ET CO2 could be used to determine the patient's odds of requiring operative intervention. METHODS: A prospective observational cohort study was undertaken at an urban Level 1 trauma center. Baseline ET CO2 from nasal cannula and serum lactate level were recorded in all patients in whom the trauma team was activated. Outcomes defined were whether operative intervention was needed. Pearson correlation (R), correlation coefficient (r(2)), and odds ratio were calculated. RESULTS: One hundred five patients were enrolled. Pearson correlations and coefficients calculated for serum lactate level to ET CO2 were R = -0.86 (r(2) = 0.74, p < 0.0001). Of patients requiring operative intervention, 81.97% had abnormally low ET CO2 and 54.1% had abnormally high serum lactate levels. Odds ratios of patients needing an emergent operation with abnormally low ET CO2 was 20.4 (95% confidence interval, 7.47-55.96) and with abnormally high serum lactate levels was 4 (95% confidence interval, 1.68-5.93). CONCLUSION: ET CO2 has a strong inverse correlation to serum lactate levels. Abnormally low ET CO2 values were associated with greater increased odds compared with serum lactate levels of penetrating trauma patients requiring operative intervention. LEVEL OF EVIDENCE: Prognostic/diagnostic study, level I.

p38 mitogen-activated protein kinase (MAPK) first regulates filamentous actin at the 8-16-cell stage during preimplantation development.

BACKGROUND INFORMATION: The MAPK (mitogen-activated protein kinase) superfamily of proteins consists of four separate signalling cascades: the c-Jun N-terminal kinase or stress-activated protein kinases (JNK/SAPK); the ERKs (extracellular-signal-regulated kinases); the ERK5 or big MAPK1; and the p38 MAPK group of protein kinases, all of which are highly conserved. To date, our studies have focused on defining the role of the p38 MAPK pathway during preimplantation development. p38 MAPK regulates actin filament formation through the downstream kinases MAPKAPK2/3 (MAPK-activated protein kinase 2/3) or MAPKAPK5 [PRAK (p38 regulated/activated kinase)] and subsequently through HSP25/27 (heat-shock protein 25/27). We recently reported that 2-cell-stage murine embryos treated with cytokine-suppressive anti-inflammatory drugs (CSAIDtrade mark; SB203580 and SB220025) display a reversible blockade of development at the 8-16-cell stage, indicating that p38 (MAPK) activity is required to complete murine preimplantation development. In the present study, we have investigated the stage-specific action and role of p38 MAPK in regulating filamentous actin during murine preimplantation development. RESULTS: Treatment of 8-cell-stage embryos with SB203580 and SB220025 (CSAIDtrade mark) resulted in a blockade of preimplantation development, loss of rhodamine phalloidin fluorescence, MK-p (phosphorylated MAPKAPK2/3), HSP-p (phosphorylated HSP25/27) and a redistribution of alpha-catenin immunofluorescence by 12 h of treatment. In contrast, treatment of 2- and 4-cell-stage embryos with CSAIDtrade mark drugs resulted in a loss of MK-p and HSP-p, but did not result in a loss of rhodamine phalloidin fluorescence. All these effects of p38 MAPK inhibition were reversed upon removal of the inhibitor, and development resumed in a delayed but normal manner to the blastocyst stage. Treatment of 8-cell embryos with PD098059 (ERK pathway inhibitor) did not affect development or fluorescence of MK-p, HSP-p or rhodamine phalloidin. CONCLUSION: Murine preimplantation development becomes dependent on p38 MAPK at the 8-16-cell stage, which corresponds to the stage when p38 MAPK first regulates filamentous actin during early development.

p38 MAPK signaling during murine preimplantation development.

Mitogen-activated protein kinase (MAPK) pathways mediate some important cellular processes and are likely to also regulate preimplantation development. The role of p38 MAP kinase signaling during murine preimplantation development was investigated in the present study. p38 MAPK, p38-regulated or -activated kinase (PRAK; MK5), map kinase-activated protein kinase 2 (MK2), and heat shock protein 25 (hsp25) mRNAs and proteins were detected throughout preimplantation development. Two-cell stage embryos cultured in the presence of SB220025 and SB203580 (specific inhibitors of p38 MAPK alpha/beta), progressed to the eight-cell stage with the same frequency as controls; however, treated embryos halted their development at the 8- to 16-cell stage. In addition, embryos treated with p38 MAPK inhibitors displayed a complete loss of MK2 and hsp25 phosphorylation and also a complete loss of filamentous actin as indicated by the absence of rhodamine-phalloidin staining. In these inhibitor-treated groups, the embryos were composed of a mixture of compacting and noncompacting cells, and the embryos were one to two cell divisions behind controls. Treated embryos remained viable as the developmental blockade was rescued by removing embryos from the drug treatment and placing them in drug-free medium until they progressed to the blastocyst stage. This study demonstrates that p38 MAPK activity is required to support development through the murine preimplantation interval.