Assessment of Tissue Perfusion Using the Peripheral Perfusion Index and Lactate Clearance in Shock in Pediatric Patients.

BACKGROUND: Pediatric shock has a high mortality rate because many of the early clinical signs are subtle and have poor sensitivity and specificity. Pediatric shock was categorized either: compensated with normal blood pressure, poor skin perfusion (CRT >2 s, mottled, cool peripheries, peripheral cyanosis), weak peripheral pulse, age specific tachycardia, tachypnoea, and oliguria or decompensated with hypotension (SBP < 70 + (2× age in years) mm Hg and decreased mental status. The perfusion index is a non-invasive method for assessing peripheral perfusion and may be a useful marker for identifying shock early in pediatric patients. OBJECTIVE: This prospective cohort study (November 2019 to August 2020) evaluated whether the perfusion index, lactate, and/or lactate clearance could predict mortality among pediatric shock patients. METHODS: Fifty children (68% male) with shock underwent assessments at presentation to the emergency room to evaluate their heart rate, blood pressure, capillary refill time, central venous pressure, perfusion index, cardiac index, systemic vascular resistance, central venous oxygen saturation, and lactate clearance. RESULTS: The perfusion index range was 0.03 to 2.2 and ≤0.18 as the cut-off for mortality prediction providing 74% sensitivity and 78% specificity. The serum lactate concentration range was 0 to 16 mmol/L and >5.7 mmol/L as the cut-off for mortality prediction provided 70% sensitivity and 96% specificity at presentation to the emergency room. The lactate clearance range was 3% to 75% and >10% as the cut-off for survival prediction after resuscitation and at 6 h later. CONCLUSION: Perfusion index (PI), lactate, and lactate clearance provided comparable sensitivity and specificity for predicting outcomes among pediatric patients with shock Therefore, we suggest that the PI is an inexpensive, rapid, and non-invasive tool that can be used to predict illness severity and mortality in busy pediatric intensive care units and emergency departments. This tool may guide better patient triage and an earlier diagnosis of shock in this setting.

Cardio-renal syndrome: an entity cardiologists and nephrologists should be dealing with collegially.

Heart failure may lead to acute kidney injury and vice versa. Chronic kidney disease may affect the clinical outcome in terms of cardiovascular morbidity and mortality while chronic heart failure may cause CKD. All these disorders contribute to the composite definition of cardio-renal syndromes. Renal impairment in HF patients has been increasingly recognized as an independent risk factor for morbidity and mortality; however, the most important clinical trials in HF tend to exclude patients with significant renal dysfunction. The mechanisms whereby renal insufficiency worsens the outcome in HF are not known, and several pathways could contribute to the "vicious heart/kidney circle." Traditionally, renal impairment has been attributed to the renal hypoperfusion due to reduced cardiac output and decreased systemic pressure. The hypovolemia leads to sympathetic activity, increased renin-angiotensin-aldosterone pathways and arginine-vasopressin release. All these mechanisms cause fluid and sodium retention, peripheral vasoconstriction and an increased congestion as well as cardiac workload. Therapy addressed to improve renal dysfunction, reduce neurohormonal activation and ameliorate renal blood flow could lead to a reduction in mortality and hospitalization in patients with cardio-renal syndrome.

Assessment of adipose tissue metabolism by means of subcutaneous microdialysis in patients with sepsis or circulatory failure.

To evaluate the role of adipose tissue in the metabolic stress response of critically ill patients, the release of glycerol and lactate by subcutaneous adipose tissue was assessed by means of microdialysis in patients with sepsis or circulatory failure and in healthy subjects. Patients with sepsis had lower plasma free fatty acid concentrations and non-significant elevations of plasma glycerol concentrations, but higher adipose-systemic glycerol concentrations gradients than healthy subjects or patients with circulatory failure, indicating a stimulation of subcutaneous adipose lipolysis. They also had a higher lipid oxidation. Lipid metabolism (adipose-systemic glycerol gradients, lipid oxidation) was not altered in patients with circulatory failure. These observations highlight major differences in lipolysis and lipid utilization between patients with sepsis and circulatory failure. Hyperlactataemia was present in both groups of patients, but the adipose-systemic lactate concentration gradient was not increased, indicating that lactate production by adipose tissue was not involved. This speaks against a role of adipose tissue in the development of hyperlactataemia in critically ill patients.

Start with a subjective assessment of skin temperature to identify hypoperfusion in intensive care unit patients.

OBJECTIVE: To determine whether physical examination alone or in combination with biochemical markers can accurately diagnose hypoperfusion. METHODS: Data from 264 consecutive surgical intensive care unit patients were collected by two intensivists and included extremity temperature, vital signs, arterial lactate, arterial blood gases, hemoglobin, and pulmonary artery catheter values with derived indices. Days of data were divided into data collected from patients with cool extremities (cool skin temperature [CST] group) versus warm extremities (warm skin temperature [WST] group). Values are means +/- SD. Comparisons between groups were made by two-tailed unpaired t test; significance was assumed for p < or = 0.05. RESULTS: There were 328 days of observations in the CST group versus 439 in the WST group. There were no differences (p > 0.05) between CST and WST data with regard to heart rate (107 +/- 14 vs. 99 +/- 19 beats/min), systolic blood pressure (118 +/- 24 vs. 127 +/- 28 mm Hg), diastolic blood pressure (57 +/- 14 vs. 62 +/- 15 mm Hg), pulmonary artery occlusion pressure (14 +/- 6 vs. 16 +/- 5 mm Hg), Fio2 (0.48 +/- 0.7 vs. 0.45 +/- 0.2), hemoglobin (8.8 +/- 1.6 vs. 9.3 +/- 1.3 g/dL), Pco2 (44.3 +/- 11.8 vs. 40.7 +/- 9.2 mm Hg), or Po2 (96.4 +/- 12.6 vs. 103.8 +/- 22.2 mm Hg). However, cardiac output (5.3 +/- 2.2 vs. 8.2 +/- 2.6 L/min), cardiac index (2.9 +/- 1.2 vs. 4.3 +/- 1.2 L/min/m2), pH (7.32 +/- 0.2 vs. 7.39 +/- 0.07), TCO2 (19.5 +/- 3.1 vs. 25.1 +/- 4.8 mEq/L), and Svo2 (60.2 +/- 4.4% vs. 68.2 +/- 7.8%) were all significantly lower (p < 0.05) in CST patients compared with WST patients. By comparison, lactate (4.7 +/- 1.5 vs. 2.2 +/- 1.6 mmol/L, p < 0.05) was significantly elevated in patients with cool extremities. CONCLUSION: Combining physical examination with serum bicarbonate and arterial lactate identifies patients with hypoperfusion as defined by low Svo2 and cardiac index. Hypoperfusion may occur despite supranormal cardiac indices. Patients with cool extremities and elevated lactate levels may benefit from a pulmonary artery catheter to guide but not initiate therapy.

Production of PEG-modified bovine hemoglobin: economics and feasibility.

Bovine hemoglobin has many advantages as a blood substitute: a) it's ready availability; b) it's low cost; c) it's oxygen carrying capacity; and d) the ease with which it can be modified with polyethylene glycol (PEG) to improve its pharmacokinetic profile. This study investigates the potential of PEG-modified bovine hemoglobin as a cost-effective blood substitute.

Early detection of shock in critically ill patients by skeletal muscle PO2 assessment.

The usefulness of skeletal muscle PO2 assessment in monitoring patients at risk of shock was evaluated in 20 critically ill patients. A shock score, inotropic score, and combined inotropic-shock score were calculated. If the median skeletal muscle PO2 assessment was more than 31.5 mm Hg, no shock occurred in the period from 4 hours before to 6 hours after the measurement. The risk of shock occurring during the first 2 hours after the skeletal muscle PO2 assessment was 2.2 times higher if median skeletal muscle PO2 assessment was below 22.5 mm Hg. If inotropes were administered, no significant difference was found in the incidence of shock if skeletal muscle PO2 was below or above 22.5 mm Hg. Skeletal muscle PO2 assessment enables the determination of the severity of shock and determination of risk of shock in critically ill patients, provided no treatment with inotropes has been instituted.

Assessment of intestinal and renal perfusion using surface oximetry.

Using a miniaturized polarographic oxygen sensor, we studied the sequential effects of graded hypoxia and standardized hemorrhagic shock on organ surface oxygen tension (PsO2) measurements obtained from the canine small intestine and kidney. During hypoxia, intestinal and renal PsO2 values decreased along with PaO2. The weighted mean correlation coefficients for intestinal and renal PsO2 vs. PaO2 were 0.94 and 0.98, respectively. During severe hypoxia, intestinal and renal PsO2 values fell by 55 +/- 8% and 55 +/- 7% (SEM), respectively, while oxygen delivery fell by 58 +/- 10% (SEM). During active hemorrhage, intestinal and renal PsO2 values decreased along with cardiac output, while PaO2 remained relatively constant. Intestinal and renal PsO2 values correlated with cardiac output during hemorrhage and reinfusion of the shed blood. Initially, intestinal PsO2 values fell more quickly than did renal PsO2; the latter decreased by approximately half as much as intestinal PsO2 after 15 and 30 ml/kg of blood loss. After a 45-ml/kg blood loss, however, the decreases in intestinal and renal PsO2 values were not significantly different from each other. During the terminal stage, cardiac output declined progressively, as did intestinal and renal PsO2 values, despite a relatively high PaO2. Overall, intestinal and renal PsO2 values tracked PaO2 during hypoxia, cardiac output during hemorrhage and reinfusion, and oxygen delivery during both conditions. Clinical and experimental experience indicates that organ PsO2 monitoring is potentially valuable for the intraoperative assessment of tissue perfusion and viability.