Is restrictive fluid resuscitation beneficial not only for hemorrhagic shock but also for septic shock?: A meta-analysis.

BACKGROUND: Whether to use limited fluid resuscitation (LFR) in patients with hemorrhagic shock or septic shock remains controversial. This research was aimed to assess the pros and cons of utilizing LFR in hemorrhagic shock or septic shock patients. METHODS: PubMed, Cochrane Library, Embase, Web of science, CNKI, VIP, and Wan Fang database searches included for articles published before December 15, 2020. Randomized controlled trials of LFR or adequate fluid resuscitation in hemorrhagic shock or septic shock patients were selected. RESULT: This meta-analysis including 28 randomized controlled trials (RCTs) and registered 3288 patients. The 7 of 27 RCTs were the patients with septic shock. Others were traumatic hemorrhagic shock patients. Comparing LFR or adequate fluid resuscitation in hemorrhagic shock or septic shock patients, the summary odds ratio (OR) was 0.50 (95% confidence interval [CI] 0.42-0.60, P < .00001) for mortality, 0.46 (95% CI 0.31-0.70, P = .0002) for multiple organ dysfunction syndrome (MODS), 0.35 (95% CI 0.25-0.47) for acute respiratory distress syndrome (ARDS), and 0.33 (95% CI 0.20-0.56) for disseminated intravascular coagulation (DIC). CONCLUSION: Limited fluid resuscitation is the benefit of both traumatic hemorrhagic shock patients and septic shock patients.

Fresh whole blood from walking blood banks for patients with traumatic hemorrhagic shock: A systematic review and meta-analysis.

BACKGROUND: Whole blood is optimal for resuscitation of traumatic hemorrhage. Walking Blood Banks provide fresh whole blood (FWB) where conventional blood components or stored, tested whole blood are not readily available. There is an increasing interest in this as an emergency resilience measure for isolated communities and during crises including the coronavirus disease 2019 pandemic. We conducted a systematic review and meta-analysis of the available evidence to inform practice. METHODS: Standard systematic review methodology was used to obtain studies that reported the delivery of FWB (PROSPERO registry CRD42019153849). Studies that only reported whole blood from conventional blood banking were excluded. For outcomes, odds ratios (ORs) and 95% confidence interval (CI) were calculated using random-effects modeling because of high risk of heterogeneity. Quality of evidence was assessed using the Grading of Recommendations, Assessment, Development, and Evaluation system. RESULTS: Twenty-seven studies published from 2006 to 2020 reported >10,000 U of FWB for >3,000 patients (precise values not available for all studies). Evidence for studies was "low" or "very low" except for one study, which was "moderate" in quality. Fresh whole blood patients were more severely injured than non-FWB patients. Overall, survival was equivalent between FWB and non-FWB groups for eight studies that compared these (OR, 1.00 [95% CI, 0.65-1.55]; p = 0.61). However, the highest quality study (matched groups for physiological and injury characteristics) reported an adjusted OR of 0.27 (95% CI, 0.13-0.58) for mortality for the FWB group (p < 0.01). CONCLUSION: Thousands of units of FWB from Walking Blood Banks have been transfused in patients following life-threatening hemorrhage. Survival is equivalent for FWB resuscitation when compared with non-FWB, even when patients were more severely injured. Evidence is scarce and of relative low quality and may underestimate potential adverse events. Whereas Walking Blood Banks may be an attractive resilience measure, caution is still advised. Walking Blood Banks should be subject to prospective evaluation to optimize care and inform policy. LEVEL OF EVIDENCE: Systematic/therapeutic, level 3.

The need for red blood cell transfusions in the emergency department as a risk factor for failure of non-operative management of splenic trauma: a multicenter prospective study.

INTRODUCTION: The majority of patients with splenic trauma undergo non-operative management (NOM); around 15% of these cases fail NOM and require surgery. The aim of the current study is to assess whether the hemodynamic status of the patient represents a risk factor for failure of NOM (fNOM) and if this may be considered a relevant factor in the decision-making process, especially in Centers where AE (angioembolization), intensive monitoring and 24-h-operating room are not available. Furthermore, the presence of additional risk factors for fNOM was investigated. MATERIALS AND METHODS: This is a multicentre prospective observational study, including patients presenting with blunt splenic trauma older than 17 years, managed between 2014 and 2016 in two Italian trauma centres (ASST Papa Giovanni XXIII in Bergamo and Sant'Anna University Hospital in Ferrara-Italy). The risk factors for fNOM were analyzed with univariate and multivariate analyses. RESULTS: In total, 124 patients were included in the study. In univariate analysis, the risk factors for fNOM were AAST grade > 3 (fNOM 37.5% vs 9.1%, p = 0.024), and the need of red blood cell (RBC) transfusion in the emergency department (ED) (fNOM 42.9% vs 8.9%, p = 0.011). Multivariate analysis showed that the only significant risk factor for fNOM was the need for RBC transfusion in the ED (p = 0.049). CONCLUSIONS: The current study confirms the contraindication to NOM in case of hemodynamically instability in case of splenic trauma, as indicated by the most recent guidelines; attention should be paid to patients with transient hemodynamic stability, including patients who require transfusion of RBC in the ED. These patients could benefit from AE; in centers where AE, intensive monitoring and an 24-h-operating room are not available, this particular subgroup of patients should probably be treated with operative management.

Impact of high-dose norepinephrine during intra-hospital damage control resuscitation of traumatic haemorrhagic shock: A propensity-score analysis.

INTRODUCTION: The use of norepinephrine (NE) during uncontrolled haemorrhagic shock (HS) has mostly been investigated in experimental studies. Clinical data including norepinephrine dose and its impact on fluid resuscitation and organ function are scarce. We hypothesized that there is great variability in NE use and that high doses of NE could lead to increased organ dysfunction as measured by the sequential organ failure assessment (SOFA). METHOD: We included patients with HS (systolic blood pressure < 90 mmHg in severely injured patients) who required haemostasis surgery and a transfusion of more than 4 packed red blood cells (PRBC) in the first 6 h of admission and the used of norepinephrine infusion to maintain the blood pressure goal, between admission and the end of haemostasis surgery in a prospective trauma database. A ROC curve determined that, using Youden's criterion, a dose of NE ≥ 0.6 µg/kg/min was the optimal threshold associated with intrahospital mortality. Patients were compared according to this threshold in a propensity score (PS) model. In a generalized linear mixed model, we searched for independent factors associated with a SOFA ≥ 9 at 24 h RESULTS: A total of 89 patients were analysed. Fluid infusion rate ranged from 1.43 to 57.9 mL/kg/h and norepinephrine infusion rate from 0.1 to 2.8 µg/kg/min. The HDNE group received significantly less fluid than the LDNE group. This dose is associated with a higher SOFA score at 24h: 9 (7-10) vs. 7 (6-9) (p = 0.003). Factors independently associated with a SOFA score ≥ 9 at 24 h were maximal norepinephrine rate ≥ 0.6 µg/kg/min (OR 6.69, 95% CI 1.82 - 25.54; p = 0.004), non-blood resuscitation volume < 9 mL/kg/h (OR 3.98, 95% CI 1.14 - 13.95; p = 0.031) and lactate at admission ≥ 5 mmol/L (OR 5.27, 95% CI 1.48 - 18.77; p = 0.010) CONCLUSION: High dose of norepinephrine infusion is associated with deleterious effects as attested by a higher SOFA score at 24 h and likely hypovolemia as measured by reduced non-blood resuscitation volume. We did not find any significant difference in mortality over the long term.

Impact of a novel phosphoinositol-3 kinase inhibitor in preventing mitochondrial DNA damage and damage-associated molecular pattern accumulation: Results from the Biochronicity Project.

BACKGROUND: Despite improvements in the management of severely injured patients, development of multiple organ dysfunction syndrome (MODS) remains a morbid complication of traumatic shock. One of the key attributes of MODS is a profound bioenergetics crisis, for which the mediators and mechanisms are poorly understood. We hypothesized that metabolic uncoupling using an experimental phosphoinositol-3 kinase (PI3-K) inhibitor, LY294002 (LY), may prevent mitochondrial abnormalities that lead to the generation of mitochondrial DNA (mtDNA) damage and the release of mtDNA damage-associated molecular patterns (DAMPs). METHODS: Sixteen swine were studied using LY, a nonselective PI3-K inhibitor. Animals were assigned to trauma only (TO, n = 3), LY drug only (LYO, n = 3), and experimental (n = 10), trauma + drug (LY + T) groups. Both trauma groups underwent laparotomy, 35% hemorrhage, severe ischemia-reperfusion injury, and protocolized resuscitation. A battery of hemodynamic, laboratory, histological, and bioenergetics parameters were monitored. Mitochondrial DNA damage was determined in lung, liver, and kidney using Southern blot analyses, whereas plasma mtDNA DAMP analysis used polymerase chain reaction amplification of a 200-bp sequence of the mtDNA D-loop region. RESULTS: Relative to control animals, H + I/R (hemorrhage and ischemia/reperfusion) produced severe, time-dependent decrements in hepatic, renal, cardiovascular, and pulmonary function accompanied by severe acidosis and lactate accumulation indicative of bioenergetics insufficiency. The H-I/R animals displayed prominent oxidative mtDNA damage in all organs studied, with the most prominent damage in the liver. Mitochondrial DNA damage was accompanied by accumulation of mtDNA DAMPs in plasma. Pretreatment of H + I/R animals with LY resulted in profound metabolic suppression, with approximately 50% decreases in O2 consumption and CO2 production. In addition, it prevented organ and bioenergetics dysfunction and was associated with a significant decrease in plasma mtDNA DAMPs to the levels of control animals. CONCLUSIONS: These findings show that H + I/R injury in anesthetized swine is accompanied by MODS and by significant mitochondrial bioenergetics dysfunction, including oxidative mtDNA damage and accumulation in plasma of mtDNA DAMPs. Suppression of these changes with the PI3-K inhibitor LY indicates that pharmacologically induced metabolic uncoupling may comprise a new pharmacologic strategy to prevent mtDNA damage and DAMP release and prevent or treat trauma-related MODS. LEVEL OF EVIDENCE: Therapeutic study, level III.

Effects of Quercetin in a Rat Model of Hemorrhagic Traumatic Shock and Reperfusion.

BACKGROUND: We hypothesized that treatment with quercetin could result in improved hemodynamics, lung inflammatory parameters and mortality in a rat model of hemorrhagic shock. METHODS: Rats were anesthetized (80 mg/kg ketamine plus 8 mg/kg xylazine i.p.). The protocol included laparotomy for 15 min (trauma), hemorrhagic shock (blood withdrawal to reduce the mean arterial pressure to 35 mmHg) for 75 min and resuscitation by re-infusion of all the shed blood plus lactate Ringer for 90 min. Intravenous quercetin (50 mg/kg) or vehicle were administered during resuscitation. RESULTS: There was a trend for increased survival 84.6% (11/13) in the treated group vs. the shock group 68.4% (13/19, p > 0.05 Kaplan-Meier). Quercetin fully prevented the development of lung edema. The activity of aSMase was increased in the shock group compared to the sham group and the quercetin prevented this effect. However, other inflammatory markers such as myeloperoxidase activity, interleukin-6 in plasma or bronchoalveolar fluid were similar in the sham and shock groups. We found no bacterial DNA in plasma in these animals. CONCLUSIONS: Quercetin partially prevented the changes in blood pressure and lung injury in shock associated to hemorrhage and reperfusion.

Modulating the Biologic Activity of Mesenteric Lymph after Traumatic Shock Decreases Systemic Inflammation and End Organ Injury.

INTRODUCTION: Trauma/hemorrhagic shock (T/HS) causes the release of pro-inflammatory mediators into the mesenteric lymph (ML), triggering a systemic inflammatory response and acute lung injury (ALI). Direct and pharmacologic vagal nerve stimulation prevents gut barrier failure and alters the biologic activity of ML after injury. We hypothesize that treatment with a pharmacologic vagal agonist after T/HS would attenuate the biologic activity of ML and prevent ALI. METHODS: ML was collected from male Sprague-Dawley rats after T/HS, trauma-sham shock (T/SS) or T/HS with administration of the pharmacologic vagal agonist CPSI-121. ML samples from each experimental group were injected into naïve mice to assess biologic activity. Blood samples were analyzed for changes in STAT3 phosphorylation (pSTAT3). Lung injury was characterized by histology, permeability and immune cell recruitment. RESULTS: T/HS lymph injected in naïve mice caused a systemic inflammatory response characterized by hypotension and increased circulating monocyte pSTAT3 activity. Injection of T/HS lymph also resulted in ALI, confirmed by histology, lung permeability and increased recruitment of pulmonary macrophages and neutrophils to lung parenchyma. CPSI-121 attenuated T/HS lymph-induced systemic inflammatory response and ALI with stable hemodynamics and similar monocyte pSTAT3 levels, lung histology, lung permeability and lung immune cell recruitment compared to animals injected with lymph from T/SS. CONCLUSION: Treatment with CPSI-121 after T/HS attenuated the biologic activity of the ML and decreased ALI. Given the superior clinical feasibility of utilizing a pharmacologic approach to vagal nerve stimulation, CPSI-121 is a potential treatment strategy to limit end organ dysfunction after injury.

Can venous base excess replace arterial base excess as a marker of early shock and a predictor of survival in trauma?

INTRODUCTION: Arterial base excess is an established marker of shock and predictor of survival in trauma patients. However, venous blood is more quickly and easily obtained. This study aimed to determine if venous base excess could replace arterial base excess as a marker in trauma patients at presentation and if venous base excess is predictive of survival at 24 hours and one week. METHODS: This was a prospective study of 394 trauma patients presenting to the emergency department of a tertiary hospital over a 17-month period. Data on base excess at presentation, vital signs, shock index (SI), injury severity score (ISS), and mortality at 24 hours and one week was collected and analysed. RESULTS: Arterial and venous blood gas tests were performed on 260 and 134 patients, respectively. Patients were stratified into groups based on their SI and ISS for analysis. There was no statistical difference between mean venous blood gas and arterial blood gas levels at presentation when SI > 0.7, regardless of ISS (p > 0.05). The mortality rate was 4.57%. Both venous and arterial base excess was lower in nonsurvivors compared to survivors (p < 0.05). However, at 24 hours and one week, the difference in base excess values at presentation between survivors and nonsurvivors was greater when using venous base excess compared to arterial base excess (11.53 vs. 4.28 and 11.41 vs. 2.66, respectively). CONCLUSION: In conclusion, venous base excess can replace arterial base excess in trauma patients as a means of identifying and prognosticating early shock.

Prevalence, clinical presentation, prognosis, and outcome of 17 dogs with spinal shock and acute thoracolumbar spinal cord disease.

OBJECTIVE: To describe the prevalence, signalment, clinical features, etiology, and outcome in dogs with acute thoracolumbar disease and suspected spinal shock. DESIGN: Retrospective clinical case study (2005-2010). SETTING: Private specialty practice. ANIMALS: Medical records of 263 dogs with thoracolumbar spinal magnetic resonance imaging were reviewed. If decreased or absent withdrawal reflexes were present in 1 or both pelvic limbs, in the absence of a spinal lesion in the lumbosacral intumescence, dogs were diagnosed with spinal shock. Dogs with suspected or confirmed spinal neoplasia, myelomalacia, or meningomyelitis were excluded. Seventeen of 263 dogs (6%) met inclusion criteria. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Thoracic lesions were significantly more likely to result in spinal shock when compared to lumbar lesions (P = 0.03). Fibrocartilaginous embolism was the most commonly diagnosed etiology (7 of 17 dogs), and was more common in the thoracic spine compared to in the lumbar spine (P = 0.10). Six of 17 dogs (35%) were diagnosed with intervertebral disk herniation; 4 of 17 dogs (24%) with suspected acute noncompressive nucleus pulposus extrusion. Two dogs were lost to follow-up. Fourteen of 15 (93%) dogs had improved or normal reflexes by 60 days post injury. CONCLUSIONS: Although the prevalence of spinal shock was low, it should be considered in any dog presenting with an acute history of thoracolumbar spinal injury with reduced or absent reflexes in the pelvic limbs. The presence of spinal shock should not dissuade a veterinarian from pursuing appropriate diagnostic testing and therapy for the underlying etiology.

Research progress of acute coagulopathy of trauma-shock.

Acute coagulopathy of trauma-shock (ACoTS) occurs in 25% of patients with severe trauma in the early phase, and the mortality of those patients is four-fold higher than patients without coagulopathy. The pathophysiology of this complicated phenomenon has been focused on in recent years. Tissue injury and hypoperfusion, activated protein C and Complements play important roles in the early phase after trauma. While the use of blood products, hypothermia, acidosis and inflammation are the main mechanism in late phase. Supplementing coagulation factors and platelets to improve ACoTS are inefficient. Only positive resuscitation from shock and improving tissue hypoperfusion have expected benefits.

Comparison of 3% and 7.5% Hypertonic Saline in Resuscitation After Traumatic Hypovolemic Shock.

Hypertonic saline solutions (HSSs) (7.5%) are useful in the resuscitation of patients with hypovolemic shock because they provide immediate intravascular volume expansion via the delivery of a small volume of fluid, improving cardiac function. However, the effects of using 3% HSS in hypovolemic shock resuscitation are not well known. This study was designed to compare the effects of and complications associated with 3% HSS, 7.5% HSS, and standard fluid in resuscitation. In total, 294 severe trauma patients were enrolled from December 2008 to February 2012 and subjected to a double-blind randomized clinical trial. Individual patients were treated with 3% HSS (250 mL), 7.5% HSS (250 mL), or lactated Ringer's solution (LRS) (250 mL). Mean arterial pressure, blood pressure, and heart rate were monitored and recorded before fluid infusion and at 10, 30, 45, and 60 min after infusion, and the incidence of complications and survival rate were analyzed. The results indicate that 3% and 7.5% HSSs rapidly restored mean arterial pressure and led to the requirement of an approximately 50% lower total fluid volume compared with the LRS group (P < 0.001). However, a single bolus of 7.5% HSS resulted in an increase in heart rate (mean of 127 beats/min) at 10 min after the start of resuscitation. Higher rates of arrhythmia and hypernatremia were noted in the 7.5% HSS group, whereas higher risks of renal failure (P< 0.001), coagulopathy (P < 0.001), and pulmonary edema (P < 0.001) were observed in the LRS group. Neither severe electrolyte disturbance nor anaphylaxis was observed in the HSS groups. It is notable that 3% HSS had similar effects on resuscitation because both the 7.5% HSS and LRS groups but resulted in a lower occurrence of complications. This study demonstrates the efficacy and safety of 3% HSS in the resuscitation of patients with hypovolemic shock.

Noble-Collip Drum Trauma Induces Disseminated Intravascular Coagulation But Not Acute Coagulopathy of Trauma-Shock.

BACKGROUND: There are two opposing possibilities for the main pathogenesis of trauma-induced coagulopathy: an acute coagulopathy of trauma shock and disseminated intravascular coagulation with the fibrinolytic phenotype. OBJECTIVE: The objective of this study was to clarify the main pathogenesis of trauma-induced coagulopathy using a rat model of Noble-Collip drum trauma. METHODS: Eighteen rats were divided into the control, trauma 0, and trauma 30 groups. The trauma 0 and 30 groups were exposed to Noble-Collip drum trauma. Blood samples were drawn without, immediately after, and 30 min after Noble-Collip drum trauma in the control, trauma 0, and trauma 30 groups, respectively. Coagulation and fibrinolysis markers were measured. Thrombin generation was assessed according to a calibrated automated thrombogram. RESULTS: Spontaneous thrombin bursts resulting from circulating procoagulants were observed in the nonstimulated thrombin generation assay immediately after trauma. Soluble fibrin levels (a marker of thrombin generation in the systemic circulation) were 50-fold greater in the trauma groups than in the control group. The resultant coagulation activation consumed platelets, coagulation factors, and antithrombin. Endogenous thrombin potential and factor II ratio were significantly negatively correlated with antithrombin levels, suggesting insufficient control of thrombin generation by antithrombin. High levels of active tissue-type plasminogen activator induced hyperfibrin(ogen)olysis. Soluble thrombomodulin increased significantly. However, activated protein C levels did not change. CONCLUSIONS: The systemic thrombin generation accelerated by insufficient antithrombin control leads to the consumption of platelets and coagulation factors associated with hyperfibrin(ogen)olysis. These changes are collectively termed disseminated intravascular coagulation with the fibrinolytic phenotype.

[PROGNOSIS OF INFECTIVE COMPLICATIONS OF THE GUN-SHOT WOUNDS OF SOFT TISSUES].

The method of prognostication of infectious complications in a gun-shot wound was elaborated, using the methods of logistic regression analysis.

The burden of infection in severely injured trauma patients and the relationship with admission shock severity.

BACKGROUND: Infection following severe injury is common and has a major impact on patient outcomes. The relationship between patient, injury, and physiologic characteristics with subsequent infections is not clearly defined. The objective of this study was to characterize the drivers and burden of all-cause infection in critical care trauma patients. METHODS: A prospective cohort study of severely injured adult patients admitted to critical care was conducted. Data were collected prospectively on patient and injury characteristics, baseline physiology, coagulation profiles, and blood product use. Patients were followed up daily for infectious episodes and other adverse outcomes while in the hospital. RESULTS: Three hundred patients (Injury Severity Score [ISS] >15) were recruited. In 48 hours or less, 29 patients (10%) died, leaving a cohort of 271. One hundred forty-one patients (52%) developed at least one infection. Three hundred four infections were diagnosed overall. Infection and noninfection groups were matched for age, sex, mechanism, and ISS. Infection rates were greater with any degree of admission shock and threefold higher in the most severely shocked cohort (p < 0.01). In multivariate analysis, base deficit (odds ratio [OR], 1.78, 95% confidence interval [CI], 1.48-1.94; p < 0.001) and lactate (OR, 1.36; 95% CI, 1.10-1.69; p = 0.05) were independently associated with the development of infection. Outcomes were significantly worse for the patients with infection. In multivariate logistic regression, infection was the only factor independently associated with multiple-organ failure (p < 0.001; OR, 15.4; 95% CI, 8.2-28.9; r = 0.402), ventilator-free days (p < 0.001; ß, -4.48; 95% CI, -6.7 to -2.1; r = 0.245), critical care length of stay (p < 0.001; ß, 13.2; 95% CI, 10.0-16.4; r = 0.466), and hospital length of stay (p < 0.001; ß, 31.1; 95% CI, 24.0-38.2; r = 0.492). CONCLUSION: Infectious complications are a burden for severely injured patients and occur early in the critical care stay. Severity of admission shock was predictive of infection and represents an opportunity for interventions to improve infectious outcomes. The incidence of infection may also have utility as an end point for clinical trials in trauma hemorrhage given the relationship with patient-experienced outcomes. LEVEL OF EVIDENCE: Prognostic/epidemiologic study, level II.

Venoarterial extracorporeal life support in post-traumatic shock and cardiac arrest: lessons learned.

OBJECTIVES: Venoarterial extracorporeal life support (VA-ECLS) is an effective support of acute hemodynamic collapse caused by miscellaneous diseases. However, using VA-ECLS for post-traumatic shock is controversial and may induce a disastrous hemorrhage. To investigate the feasibility of using VA-ECLS to treat post-traumatic shock or cardiac arrest (CA), a single-center experience of VA-ECLS in traumatology was reported. MATERIALS AND METHODS: This retrospective study included nine patients [median age: 37 years, interquartile range (IQR): 26.5-46] with post-traumatic shock/CA who were treated with VA-ECLS in a single institution between November 2003 and October 2012. The causes of trauma were high-voltage electrocution (n = 1), penetrating chest trauma (n = 1), and blunt chest or poly-trauma (n = 7). Medians of the injury severity score and the maximal chest abbreviated injury scale were 34 (IQR: 15.5-41) and 4 (IQR: 3-4), respectively. All patients received peripheral VA-ECLS without heparin infusion for at least 24 hours. RESULTS: The median time from arrival at our emergency department (ED) to VA-ECLS was 6 h (IQR: 4-47.5). The median duration of VA-ECLS was 91 h (IQR: 43-187) with a duration < 24 h in 2 patients. Among the 9 patients, 5 received VA-ECLS to treat the post-traumatic shock/CA presenting during (n = 2) or following (n = 3) damage-control surgeries for initial trauma, and another 4 patients were supported for non-surgical complications associated with initial trauma. VA-ECLS was terminated in 2 non-survivors owing to uncontrolled hemothorax or retroperitoneal hemorrhage. Three patients survived to hospital discharge. All of them received damage-control surgeries for initial trauma and experienced a complicated hospitalization after weaning off VA-ECLS. CONCLUSION: Using VA-ECLS to treat post-traumatic shock/CA is challenging and requires multidisciplinary expertise.

Anaerobic metabolism associated with traumatic hemorrhagic shock monitored by microdialysis of muscle tissue is dependent on the levels of hemoglobin and central venous oxygen saturation: a prospective, observational study.

BACKGROUND: Traumatic hemorrhagic shock resulting in tissue hypoxia is a significant cause of morbidity and mortality in polytraumatized patients. Early identification of tissue hypoxia is possible with microdialysis. The aim of this study was to determine the correlation between a marker of tissue hypoxia (L/P; lactate to pyruvate ratio) and selected parameters of systemic oxygen delivery (Hb; hemoglobin) and oxygen extraction (ScvO2; central venous oxygen saturation). We also investigated the severity of tissue hypoxia over the course of care. METHODS: Adult patients with traumatic hemorrhagic shock were enrolled in this prospective, observational study. Microdialysis of the peripheral muscle tissue was performed. Demographic data and timeline of care were collected. Tissue lactate, pyruvate, glycerol, glucose levels, hemoglobin, serum lactate and oxygen saturation of the central venous blood (ScvO2) levels were also measured. RESULTS: The L/P ratio trend may react to changes in systemic hemoglobin levels with a delay of 7 to 10 hours, particularly when systemic hemoglobin levels are increased by transfusion. Decrease in tissue L/P ratio may react to increase in ScvO2 with a delay of up to 10 hours, and such a decrease may signify elimination of tissue hypoxia after transfusion. We also observed changes in the L/P trend in the 13 hours preceding a change in the hemoglobin level. Fluid administration, which is routinely used as a first-line treatment of hypovolemic shock, can cause hemodilution and decreased hemoglobin. When ScvO2 decreases, increase in L/P ratio may precede the ScvO2 trend by 10 or 11 hours. An increase in the L/P ratio is an early warning sign of insufficient tissue oxygenation and should lead to intensive observation of hemoglobin levels, ScvO2 and other hemodynamic parameters. Patients who were treated more rapidly had lower maximal L/P values and a lower degree of tissue ischemia. CONCLUSION: The L/P ratio is useful to identify tissue ischemia and can estimate the effectiveness of fluid resuscitation. An increase in the L/P ratio is an early warning sign of inadequate tissue oxygenation and should lead to more detailed hemodynamic and laboratory monitoring. This information cannot usually be obtained from global markers.