Tissue Hypoperfusion Research Articles

Caudal vena cava collapsibility index as a tool to predict fluid responsiveness in dogs.

To evaluate the use of the caudal vena cava collapsibility index (CVCCI) as a predictor of fluid responsiveness in hospitalized, critically ill dogs with hemodynamic or tissue perfusion abnormalities. Retrospective observational study. Private referral center. Twenty-seven critically ill, spontaneously breathing dogs with compromised hemodynamics or tissue hypoperfusion. None. The electronic medical records were searched for dogs admitted for any cause, from August 2016 to December 2017. We included dogs with ultrasound measurements of: CVCCI, performed at baseline; and velocity time integral (VTI) of the subaortic blood flow, carried out before and after a fluid load. CVCCI was estimated as: (maximum diameter-minimum diameter/maximum diameter) × 100. Dogs in which VTI increased ≥15% were considered fluid responders. The CVCCI accurately predicted fluid responsiveness with an area under the receiver operating characteristic curve of 0.96 (95% CI, 0.88 to 1.00). The optimal cut-off of CVCCI that better discriminated between fluid responders and nonresponders was 27%, with 100.0% sensitivity and 83.3% specificity. At baseline, fluid responders had lower VTI (5.48 [4.26 to 7.40] vs 10.61 [7.38 to 13.23] cm, P=0.004) than nonresponders. The basal maximum diameter of the caudal vena cava adjusted to body weight was not different between responders and nonresponders (0.050 [0.030 to 0.100] vs 0.079 [0.067 to 0.140] cm/kg, P=0.339). The increase in VTI was related to basal CVCCI (R=0.60, P=0.001). Bland-Altman analysis showed narrow 95% limits of agreement between measurements of CVCCI and VTI performed by different observers or by the same observer. The results of this small cohort study suggest that CVCCI can accurately predict fluid responsiveness in critically ill dogs with perfusion abnormalities. Further research is necessary to extrapolate these results to larger populations of hospitalized dogs.

Microcirculatory, Endothelial, and Inflammatory Responses in Critically Ill Patients With COVID-19 Are Distinct From Those Seen in Septic Shock: A Case Control Study

Critically ill patients with COVID-19 infection frequently exhibit a hyperinflammatory response and develop organ failures; however, the underlying mechanisms are unclear. We investigated the microcirculatory, endothelial, and inflammatory responses in critically ill COVID-19 patients and compared them to a group of patients with septic shock in a prospective observational case control study. Thirty critically ill patients with COVID-19 were compared to 33 patients with septic shock.Measurements of sublingual microcirculatory flow using Incident Dark Field video-microscopy and serial measurements of IL-6 and Syndecan-1 levels were performed. COVID-19 patients had significantly less vasoactive drug requirement and lower plasma lactate than those with septic shock. Microcirculatory flow was significantly worse in septic patients than those with COVID-19 (MFI 2.6 vs 2.9 p 0.02, PPV 88 vs 97% P < 0.001). IL-6 was higher in patients with septic shock than COVID-19 (1653 vs 253 pg/mL, P 0.03). IL-6 levels in COVID 19 patients were not elevated compared to healthy controls except on the day of ICU admission. Syndecan-1 levels were not different between the two pathological groups. Compared to patients with undifferentiated septic shock an overt shock state with tissue hypoperfusion does not appear typical of COVID-19 infection. There was no evidence of significant sublingual microcirculatory impairment, widespread endothelial injury or marked inflammatory cytokine release in this group of critically ill COVID-19 patients.

Change in strong ion difference and metabolic acidosis after heart surgery

Introduction Metabolic acidosis is a common complication of cardiac surgery involving cardiopulmonary bypass (CPB) which is usually ascribed to tissue hypoperfusion. However, it may be related to the volume and content of the intravascular fluids (IV fluids) administered that cause haemodilution and a decrease in strong ion difference (SID) in the blood, so increasing the concentration of hydrogen ions (δ[H+]). Therefore, we hypothesized that the volume and content of IV fluids administered during cardiac surgery were associated with postoperative metabolic acidosis. The primary aim of this study was to measure the incidence of metabolic acidosis developed on arrival in the intensive care unit (ICU) by patients who had undergone cardiac surgery. Secondary aims were to explore the associations of the change in SID(δSID) and other blood concentrations with δ[H+] and between δSID with the content and volume of IV fluids administered. Methods The study design was a single centre, observational, prospective, cohort study. PlasmaLyte 148 was used to prime the CPB circuit and for intravascular volume replacement. Arterial blood samples were aspirated before induction of anaesthesia and on arrival to ICU and were analysed on a blood gas analyser. Changes in blood electrolytes, lactate concentrations (δlactate), δSID, anion gap, arterial carbon dioxide tension (δPaCO2) and bicarbonate ion concentration (δ[HCO3-]) as well as the total volume of IV fluids administered were then univariately correlated with δ[H+] using Pearson's coefficient. Independent variables that were significantly correlated with δ[H+] (p Results Fifty out of 85 patients (59%) had metabolic acidosis on arrival to ICU. The volume of IV fluids did not significantly correlate with δ[H+] (r= -0.13, p=0.24). A multivariate regression model (adjusted r2 = 0.51, F= 27.89, p Discussion Metabolic acidosis after cardiac surgery was weakly associated with a decrease in SID but not tissue hypoperfusion as estimated by lactate concentration nor effect of haemodilution. Interpretation of metabolic acidosis after cardiac surgery should include assessment of SID. δSID was used to summarize the effects of the change in concentration of individual strong ions on δ[H+] in the regression model. A much larger sample size would be needed to delineate the effects of the administration of specific strong ions contained in IV fluids on δ[H+].

S1893 Black Esophagus (Acute Esophageal Necrosis) and Diabetes Mellitus: Is It Time to Reconsider Their Association?

INTRODUCTION: As awareness for Acute Esophageal Necrosis syndrome increases, so does our ability to understand its associations and causations. It classically presents as a striking necrotic appearance of black mucosa preferentially affecting the distal esophagus and extending proximally to various degrees while stopping at the GEJ. Its etiology is multifactorial and related to tissue hypoperfusion, massive reflux of gastric contents, and compromised local mucosal barriers. Historically, diabetes mellitus was seen in nearly 36% of AEN cases, although its association with hyperglycemia has never been parsed out. We aim to present a case of diabetic ketoacidosis (DKA) and review the literature with a focus on hyperglycemia and acute esophageal necrosis (AEN). CASE DESCRIPTION/METHODS: A 34-year-old female had called emergency services after experiencing coffee-ground emesis, abdominal pain, and pre-syncopal like symptoms for 5 days. She was found hypotensive, tachycardic with a blood sugar over 400 mg/dL. She was an active smoker with a history of diabetes mellitus type 1 with her last hemoglobin A1c at 16.9%. On arrival to the ED, her labs revealed blood glucose greater than 1000 mg/dL, pH of 7.1, bicarbonate <10 mEq/L, anion gap over 30 mEq/L with acute kidney injury and cystitis. She was initiated on an insulin drip and antibiotics, made NPO, and IV esomeprazole was started. Esophagogastroduodenoscopy (EGD) revealed circumferential black appearing mucosa and a necrotic complexion in the middle and distal segments (Figures 1–3). She was managed conservatively with antiacid therapy. Enteral feeds were restarted shortly, and she was discharged home. DISCUSSION: Despite growing literature revealing DKA as a common precipitant for black esophagus, a bonafide association to hyperglycemia has not been shown. A literature review across all reported cases revealed diabetes mellitus as its most common risk factor (39%). Blood glucose over 150 mg/dL was seen in 15% of all black esophagus cases, while 67% of all hyperglycemic patients had blood glucose levels over 350 mg/dL. Average hemoglobin A1c was 11.46%, and approximately 13% that met DKA criteria developed black esophagus. Cases of DKA reported unusually high glucose levels, with the highest recorded at 1294 mg/dL. The mortality amongst patients with black esophagus and hyperglycemia nears 19%, while patients that develop concomitant black esophagus and DKA, mortality is 15%.Figure 1.: Presence of severe inflammation and necrotic appearance of the esophagus.Figure 2.: Presence of severe inflammation and necrosis mainly affecting the middle and distal segments.Figure 3.: Necrotic appearance of the esophagus.

Fluid Resuscitation in Trauma

Introduction: Trauma is a problem faced everyday in the emergency room of the hospital where the researcher works. The degree of trauma from the mildest to life threatening can be found in sufferers. The cause of death in trauma sufferers is hypovolemic shock due to bleeding. The amount of blood loss volume from the patient can be estimated by looking at the clinical signs of the patient. Literature Review: In the condition of tissue hypoperfusion, it will cause a chain process which will eventually lead to cell death. Hypoperfusion causes anaerobic metabolism, lactic acidosis (coagulopathy, enzyme dysfunction), Na-K pump malfunction (cellular swelling and cell death), there is hypothermia (increase of oxygen demand, coagulopathy). Hypoperfusion will cause a vicious circle, in which processes that aggravate one another will occur. With the administration of fluids (crystalloid, colloid, transfusion) will improve the hypoperfusion that occurs in the body. Conclusion: The management of hypovolemic shock due to bleeding requires an understanding of the physiology and pathophysiology that occurs due to bleeding. To get maximum results and improve outcome from sufferers, it needs solid team work. Treatment can be different depending on the conditions, equipment and facilities of the hospital / emergency room as well as the policies of each place.

Paramètres dérivés du CO2 pour évaluer l’état hémodynamique chez le malade de réanimation

Le dioxyde de carbone (CO2) constitue le produit de dégradation final du métabolisme cellulaire. Plusieurs gradients de CO2, obtenus grâce à la mesure de la pression partielle de CO2 (PCO2) dans différents compartiments, sont utilisés afin d’évaluer l’état circulatoire des patients de réanimation. Au cours d’un état de choc, l’augmentation de la PCO2 veineuse et tissulaire est principalement la conséquence d’une hypoperfusion tissulaire et non d’une hypoxémie, reflétant ainsi une anomalie macro et/ou microcirculatoire. Un gradient veino-artériel de PCO2 (Pv-aCO2) ≥ 6 mmHg peut suggérer une inadéquation du débit cardiaque. À l’échelle locale, un gradient tissu-artériel en PCO2 (Pt-aCO2) élevé malgré un Pv-aCO2 normal (&lt; 6 mmHg) peut faire évoquer une atteinte de la microcirculation locale. Enfin, un indice combiné des paramètres dérivés du CO2 et de l’O2, comme le rapport entre le Pv-aCO2 et la différence des contenus artériel et veineux en oxygène (Pv-aCO2 / CaO2 – CvO2), suggère une hypoxie tissulaire lorsqu’il dépasse 1,4. Chez les patients de réanimation en insuffisance circulatoire, les paramètres dérivés du CO2 doivent toutefois s’intégrer dans une approche multiparamétrique (examen clinique, marqueurs biologiques, échocardiographie et autres outils hémodynamiques).

Acute-on-chronic liver failure: Definitions, pathophysiology and principles of treatment.

SummaryThe term acute-on-chronic liver failure (ACLF) defines an abrupt and life-threatening worsening of clinical conditions in patients with cirrhosis or chronic liver disease. In recent years, different definitions and diagnostic criteria for the syndrome have been proposed by the major international scientific societies. The main controversies relate to the type of acute insult (specifically hepatic or also extrahepatic), the stage of underlying liver disease (cirrhosis or chronic hepatitis) and the concomitant extrahepatic organ failure(s) that should be considered in the definition of ACLF. Therefore, different severity criteria and prognostic scores have been proposed and validated. Current evidence shows that the pathophysiology of ACLF is closely associated with an intense systemic inflammation sustained by circulating pathogen-associated molecular patterns and damage-associated molecular patterns. The development of organ failures may be a result of a combination of tissue hypoperfusion, direct immune-mediated damage and mitochondrial dysfunction. Management of ACLF is currently based on the supportive treatment of organ failures, mainly in an intensive care setting. For selected patients, liver transplantation is an effective treatment that offers a good long-term prognosis. Future studies on potential mechanistic treatments that improve patient survival are eagerly awaited.

Early Sequential Microcirculation Assessment In Shocked Patients as a Predictor of Outcome: A Prospective Observational Cohort Study.

A dysfunctional microcirculation is universal in shock and is often dissociated from global hemodynamic parameters. Persistent microcirculatory derangements reflect ongoing tissue hypoperfusion and organ injury. The initial microcirculatory dysfunction and subsequent resolution could potentially guide therapy and predict outcomes. We evaluated the microcirculation early in a heterogenous shocked population. Microcirculatory resolution was correlated with measures of tissue perfusion and global hemodynamics. The relationship between the microcirculation over 24 h and outcome were evaluated. We prospectively recruited patients with all forms of shock, based on global hemodynamics and evidence of organ hypoperfusion. A 30-bed adult intensive care unit (ICU). Eighty-two shocked patients. Following the diagnosis of shock, patients underwent a sublingual microcirculation examination using Sidestream Dark Field Imaging. The median age of patients was 66 years old (interquartile range [IQR] 54-71), with an Acute Physiology and Chronic Health Evaluation II of 27 (IQR 20-32). Microcirculatory parameters included Percentage Perfused Vessels (PPV), De Backer Score, and a heterogeneity index in patients with septic shock, according to the second consensus guidelines Additional parameters collected: temperature, heart rate and arterial pressure, cumulative fluid balance, and vasopressor use. Arterial blood samples were taken at the time of microcirculatory assessments, providing HCO3, lactate concentrations, PaO2, and PaCO2 measurements. A statistically significant improvement in PPV and the heterogeneity index was demonstrated. This improvement was mirrored by biomarkers of perfusion; however, the global hemodynamic parameter changes were not significantly different over the 24-h period. The early microcirculatory improvement was not predictive of an improvement in acute kidney injury, length of stay, ICU, or hospital mortality. Early sequential evaluation of the microcirculation in shocked patients, demonstrated statistically significant improvement in the PPV and microvascular heterogeneity with standard care. These improvements were mirrored by biomarkers of organ perfusion; however, the changes in global hemodynamics were not as pronounced in this early phase. Early improvement in the microcirculation did not predict clinical outcome.

Management of cardiovascular insufficiency in ICU: the BEAT approach.

A large number of patients admitted to ICU display hemodynamic deterioration at some time during their stay. The management of acute hemodynamic derangement of any cause can be difficult and has to be accomplished quickly and correctly as delayed and inappropriate resuscitation treatments carry increased mortality. Cardiovascular insufficiency shows end-organ hypoperfusion-associated dysfunction, thus decreasing level of consciousness, falling urine output, ileus, new onset tachypnea and the presence of skin mottling are important clinical clues to cardiovascular deterioration and should be promptly looked for and if detected alert the bedside clinician that further assessment and potentially treatment is necessary. Although measures of serum lactate are useful to document the presence of tissue hypoperfusion, they are non-specific in defining its etiology. In a patient with acute hemodynamic instability, we propose a step-by-step approach as follows: 1) rapid initial ultrasound assessment of heart function; 2) pathophysiological understanding of heart and circulation interaction; 3) functional hemodynamic monitoring; and 4) treatment. We named such approach BEAT, which stands for: browse the heart, measure the elastances, assess volume status, and treat. Combining bedside echocardiography, including the evaluation of the interaction between the heart and the circulation, with FHM offers the opportunity to personalize the hemodynamic management to the specific requirements.

Microcirculation-guided protection strategy in hemodynamic therapy.

Microcirculatory shock is a condition defined by the presence of tissue hypoperfusion despite the normalization of systemic and regional blood flow. Currently, more evidence shows that intrinsic septic shock is microcirculatory shock, which results in septic shock that is difficult to resuscitate. At present, treatments are aimed at recovering macro-circulation functions and include fluid resuscitation, vasoactive drugs, positive inotropic drugs, de-obstruction, and even mechanical assistance to improve oxygen delivery. However, the application of these treatments to more accurately improve microcirculation or avoid further microcirculatory damage is more important in clinics. In this article, we discuss the need for microcirculation protection and microcirculation-guided protection strategies in hemodynamic therapies.

Microcirculatory, Endothelial and Inflammatory Responses in Critically Ill Patients with COVID-19 Are Distinct from Those Seen in Septic Shock: A Case Control Study

Background: Critically ill patients with COVID-19 infection frequently exhibit a hyperinflammatory response and develop organ failures, however the underlying mechanisms are unclear. We investigated the microcirculatory, endothelial and inflammatory responses in critically ill COVID-19 patients and compared them to a group of patients with septic shock. Methods: Prospective observational case control study. 30 patients with COVID-19 admitted to the ICUs of a tertiary hospital were compared to 33 patients with septic shock. Measurements of sublingual microcirculatory flow were performed using Incident Dark Field (IDF) video-microscopy and serial measurements of IL-6 and Syndecan-1 levels were made. Findings: COVID-19 patients had significantly less vasoactive drug requirement and lower plasma lactate than those with septic shock. Microcirculatory flow was significantly worse in septic patients than those with COVID-19 (MFI 2.6 v 2.9 p 0.02, PPV 88 v 97% p <0.001). IL-6 was higher in patients with septic shock than COVID-19 (1653 v 253 pg/ml, p 0.03) IL-6 levels in COVID 19 patients were not elevated compared to healthy controls except on the day of ICU admission. Syndecan-1 levels were not different between the 2 pathological groups. Interpretation: Compared to patients with bacterial sepsis an overt shock state with tissue hypoperfusion does not appear typical of COVID-19 infection. There was no evidence of significant sublingual microcirculatory impairment, widespread endothelial injury or marked inflammatory cytokine release in this group of critically ill COVID-19 patients. COVID-19 may have a different pathogenesis to bacterial induced septic shock. Funding Statement: Royal Centre for Defence Medicine (UK Ministry of Defence), 2019; European Society of Intensive Care Medicine Point of Care Ultrasound award, 2019. Declaration of Interests: All authors declare that they have no conflicts of interest. Ethics Approval Statement: Yorkshire and Humber (Leeds East) and North West Research Ethics committees (18/YH/0371and 19/NW/0750).

The Relationship Between Initial Hematocrit and Base Excess For Signs Of Hemorrhagic Shock In Patients With Blunt Abdominal Trauma

Introduction: Trauma abdominal and pelvic part of the largest causes of death and, if diagnosed early, the deaths could have been prevented. By increasing the capacity for early detection and prompt and appropriate action, will produce a satisfactory outcome. In patients with bleeding, hemodilution appear within a few minutes to obtain a decrease in hematocrit. BE decline is the result of pyruvic acid metabolism occurring anaerobic tissue hypoperfusion due to bleeding unresolved. There is a strong correlation between the decrease in hematocrit and BE with shock because of intra-abdominal haemorrhage. To analyze the relationship between decreased hematocrit and BE in bleeding patients we investigated the relationship between the initial value of hematocrit and BE against any signs of shock because of intra-abdominal hemorrhage in patients with blunt abdominal trauma.&#x0D; Methods: cross-sectional of the 34 subjects. The research data obtained from history taking, physical examination, investigation, and medical records. Conducted a comparative analysis of Kruskal-Wallis. Test for normality by Kolmogorov-Smirnov test. A p value &lt;0.05 indicates a significant relationship between variables. Data were analyzed using SPSS version 19.&#x0D; Result: It was found an average increase in the pulse (P) frequency with decreasing hematocrit (Ht) is 92.67 ± 6.43x / min for group Ht&gt; 40%, 95.5 ± 16.52x / min for group Ht 37-40%, and 112.89 ± 19.23x / min for group Ht &lt;37%. Obtained an average increase of P frequency with decreasing Base Excess (BE) is 88.0 ± 0x / min for groups BE&gt; 2, 92.33 ± 7.84x / min for BE Group 2 - (- 2), and 112.81 ± 19.22x / min for groups BE &lt; -2. This means that there is a significant relationship between hematocrit decrease with increased of P frequency as one of the signs of hemorrhagic shock with p value = 0.046 and significant correlation between the decrease in BE with increased P frequency as one of the signs of hemorrhagic shock with p value = 0.028.&#x0D; Conclusion: There is a significant correlation between the value of the initial hematocrit and BE with signs of hemorrhagic shock due to intra-abdominal hemorrhage in patients with blunt abdominal trauma.

Inodilators in septic shock: should these be used?

Septic shock involves a complex interaction between abnormal vasodilation, relative and/or absolute hypovolemia, myocardial dysfunction, and altered blood flow distribution to the tissues. Fluid administration, vasopressor support and inotropes, represent fundamental pieces of quantitative resuscitation protocols directed to assist the restoration of impaired tissue perfusion during septic shock. Indeed, current recommendations on sepsis management include the use of inotropes in the case of myocardial dysfunction, as suggested by a low cardiac output, increased filling pressures, or persisting signals of tissue hypoperfusion despite an adequate correction of intravascular volume and mean arterial pressure by fluid administration and vasopressor support. Evidence supporting the use of inotropes in sepsis and septic shock is mainly based on physiological studies. Most of them suggest a beneficial effect of inotropes on macro hemodynamics especially when sepsis coexists with myocardial dysfunction; others, however, have demonstrated variable results on regional splanchnic circulation, while others suggest favorable effects on microvascular distribution independently of its impact on cardiac output. Conversely, impact of inodilators on clinical outcomes in this context has been more controversial. Use of dobutamine has not been consistently related with more favorable clinical results, while systematic administration of levosimendan in sepsis do not prevent the development of multiorgan dysfunction, even in patients with evidence of myocardial dysfunction. Nevertheless, a recent metanalysis of clinical studies suggests that cardiovascular support regimens based on inodilators in sepsis and septic shock could provide some beneficial effect on mortality, while other one corroborated such effect on mortality specially in patients with proved lower cardiac output. Thus, using or not inotropes during sepsis and septic shock remains as controversy matter that deserves more research efforts.

Annexin A1 is a Potential Novel Biomarker of Congestion in Acute Heart Failure

This study sought to identify the role of annexin A1 (AnxA1) as a congestion marker in acute heart failure (AHF) and to identify its putative role in predicting clinical outcomes. AnxA1 is a protein that inhibits inflammation following ischemia-reperfusion injury in cardiorenal tissues. Because AHF is a state of tissue hypoperfusion, we hypothesized that plasma AnxA1 levels are altered in AHF. In the Renal Optimization Strategies Evaluation (ROSE) trial, patients hospitalized for AHF with kidney injury were randomized to receive dopamine, nesiritide, or placebo for 72 hours in addition to diuresis. In a subanalysis, plasma AnxA1 levels were measured at baseline and at 72 hours in 275 patients. Participants were divided into 3 tertiles based on their baseline AnxA1 levels. The prevalence of peripheral edema 2+ increased with increasing AnxA1 levels (P < .007). Cystatin C, blood urea nitrogen, and kidney injury molecule-1 plasma levels were higher among participants in tertile 3 vs tertiles 1 or 2 (P< .05). Patients with a congestion score of 4 had a mean baseline AnxA1 level 8.63 units higher than those with a congestion score of 0 (P = .03). Patients in tertiles 2 and 3 were twice as likely to experience creatinine elevation as patients in tertile 1 (P = .03). Patients in tertiles 2 and 3 were at a higher risk of 60-day all-cause mortality or heart failure hospitalization and 180-day all-cause mortality (P < .05). Among patients hospitalized for AHF with impaired kidney function, elevated AnxA1 levels are associated with worse congestion, higher risk for further creatinine elevation, and higher rates of 60-day morbidity or all-cause mortality and 180-day all-cause mortality. clinicaltrials.gov Identifier: NCT01132846.

Laying Siege to the Castle: The Role of Sepsis Related Cytokines and Inflammation in Bringing Down the Barriers

Abstract The endothelium plays a critical role in the progression from sepsis to organ failure. The endothelium lines all blood vessels and organs in the body. As such, it provides a protective barrier against pathologic micro-organisms. The endothelium is also responsible for dynamically regulating the passage of small molecules, fluid, and cells between the bloodstream and tissues. In sepsis, many factors play a role in compromising the endothelium. Dysfunctional endothelium often results in development of capillary leak, tissue hypoperfusion, hypoxia, edema, and shock. This study evaluates the individual contributions of sepsis-related immunomodulatory cytokines as well as a potential synergistic effect of cytokine combinations on vascular endothelial permeability. The Electric Cell-substrate Impedance Sensor was employed to evaluate the barrier function (Rb) and cell membrane capacitance (CMC) of endothelial cell monolayers treated with an array of cytokines including TNF-α IFN-γ, TGF-β, IL1-β, IL-6, IL-8, IL-10, and IL-12. The ECIS results revealed significant differences in the Rb of cell monolayers exposed to sepsis related cytokines compared to cytokine-free control samples. Components of intercellular tight junctions and associated cell adhesion molecules also revealed differences in the endothelial cell monolayer under immunofluorescence microscopy. Thus, cytokines as individual entities or in combinations that may be produced during episodes of sepsis significantly alter the endothelial morphology and permeability.

Lactic acid level as an outcome predictor in pediatric patients with intussusception in the emergency department

BackgroundIntussusception decreases blood flow to the bowel, and tissue hypoperfusion results in increased lactic acid levels. We aimed to determine whether lactic acid levels are associated with pediatric intussusception outcomes.MethodsThe electronic medical records of our emergency department pediatric patients diagnosed with intussusception, between January 2015 and October 2018, were reviewed. An outcome was considered poor when intussusception recurred within 48 h of reduction or when surgical reduction was required due to air enema failure.ResultsA total of 249 patients were included in the study, including 39 who experienced intussusception recurrence and 11 who required surgical reductions; hence, 50 patients were included in the poor outcome group. The poor and good outcome groups showed significant differences in their respective blood gas analyses for pH (7.39 vs. 7.41, P = .001), lactic acid (1.70 vs. 1.30 mmol/L, P < .001), and bicarbonate (20.70 vs. 21.80 mmol/L, P = .036). Multivariable logistic regression analyses showed that pH and lactic acid levels were the two factors significantly associated with poor outcomes. When the lactic acid level cutoff values were ≥ 1.5, ≥2.0, ≥2.5, and ≥ 3.0 mmol/L, the positive predictive values for poor outcomes were 30.0, 34.6, 50.0, and 88.9%, respectively.ConclusionLactic acid levels affect outcomes in pediatric patients with intussusception; higher lactic acid levels are associated with higher positive predictive values for poor outcomes.

Moderate to severe hyperphosphataemia as an independent prognostic factor for 28-day mortality in adult patients with sepsis

BackgroundIschaemic tissue injury caused by tissue hypoperfusion is one of the major consequences of sepsis. Phosphate concentrations are elevated in ischaemic tissue injury. This study was performed to investigate the...

Bedside prediction of intradialytic hemodynamic instability in critically ill patients: the SOCRATE study

BackgroundDespite improvements in intermittent hemodialysis management, intradialytic hemodynamic instability (IHI) remains a common issue that could account for increased mortality and delayed renal recovery. However, predictive factors of IHI remain poorly explored. The objective of this study was to evaluate the relationship between baseline macrohemodynamic, tissue hypoperfusion parameters and IHI occurrence.MethodsProspective observational study conducted in a 18-bed medical ICU of a tertiary teaching hospital. Cardiovascular SOFA score, index capillary refill time (CRT) and lactate level were measured just before (T0) consecutive intermittent hemodialysis sessions performed for AKI. The occurrence of IHI requiring a therapeutic intervention was recorded.ResultsTwo hundred eleven sessions, corresponding to 72 (34%) first sessions and 139 (66%) later sessions, were included. As IHI mostly occurred during first sessions (43% vs 12%, P < 0.0001), following analyses were performed on the 72 first sessions. At T0, cardiovascular SOFA score ≥1 (87% vs 51%, P = 0.0021) was more frequent before IHI sessions, as well as index CRT ≥ 3 s (55% vs 15%, P = 0.0004), and hyperlactatemia > 2 mmol/L (68% vs 29%, P = 0.0018). Moreover, the occurrence of IHI increased with the number of macrohemodynamic and tissue perfusion impaired parameters, named SOCRATE score (cardiovascular SOFA, index CRT and lactATE): 10% (95% CI [3%, 30%]), 33% (95% CI [15%, 58%]), 55% (95% CI [35%, 73%]) and 80% (95% CI [55%, 93%]) for 0, 1, 2 and 3 parameters, respectively (AUC = 0.79 [0.69–0.89], P < 0.0001). These results were confirmed by analyzing the 139 later sessions included in the study.ConclusionsThe SOCRATE score based on 3 easy-to-use bedside parameters correlates with the risk of IHI. By improving risk stratification of IHI, this score could help clinicians to manage intermittent hemodialysis initiation in critically ill AKI patients.

Thrombectomy from superior mesenteric vein in treatment of small intestine gangrene

The traditional definition of tissue ischemia-a decreased level of oxygen deliverability by bloodstream that results in cell hypoxia. Anatomical and functional hindrance to blood flow is the basis of tissue hypoperfusion. Arterial, venous and functional disturbances in blood circulation lead to acute intestinal ischemia. In 85-90 % of cases acute mesenterial ischemia was caused by arterial reasons: thrombosis or embolism. Venous thrombosis is responsible for 10%-15% of acute mesenterial ischemia cases.

Autosomal dominant transmission of transient neonatal lactic acidosis: a case report

BackgroundLactic acidosis is a common finding in neonates, in whom mitochondrial dysfunction is often secondary to tissue hypoperfusion, respiratory failure, and/or sepsis. Primary (non-physiological) lactic acidosis is comparatively rare, and suggests the presence of an inborn error of mitochondrial energy metabolism. Optimal medical management and accurate prognostication requires the correct determination of the etiology of lactic acidosis in a given patient. Unfortunately, genetic diagnoses are rare and highly variable for neonates presenting with primary lactic acidosis; individual case reports may offer the most promise for treatment considerations.The mitochondrion is a complex molecular machine incorporating the products of > 1000 distinct nuclear genes. Primary lactic acidoses are therefore characterized by high genetic heterogeneity and a specific genetic diagnosis currently remains out of reach in most cases. Most mitochondriopathies with neonatal onset follow autosomal recessive inheritance and carry a poor prognosis. Here we detail the case of a father and daughter with dominantly-inherited, resolving (i.e. transient) neonatal hyperlactatemia due to complex IV deficiency. We found no other published descriptions of benign transient complex IV deficiency with autosomal dominant inheritance.Case presentationBoth individuals presented as neonates with unexplained, marked lactic acidosis suggesting a primary mitochondrial disorder. Within the first weeks of life, elevated blood lactate levels normalized. Their clinical and developmental outcomes were normal. Biochemical studies in the proband showed multiple abnormalities consistent with a complex IV respiratory chain defect. Cultured skin fibroblasts showed an elevated lactate-to-pyruvate ratio, deficient complex IV activity, and normal pyruvate dehydrogenase and pyruvate carboxylase activities. Whole-exome sequencing of the proband and both parents did not identify a causative mutation.ConclusionWe conclude that the proband and her father appear to have a dominant form of transient neonatal hyperlactatemia due to heterozygous changes in an as-yet unidentified gene. This transient neonatal complex IV deficiency should be considered in the differential diagnosis of primary neonatal hyperlactatemia; notable clinical features include autosomal-dominant inheritance and an apparently benign postnatal course. This report exemplifies the growing differential diagnosis for neonatal lactic acidosis and highlights the importance of both physician counselling and the use of family history in communicating with parents.