|Year : 2023 | Volume
| Issue : 1 | Page : 1-2
Quantification of microcirculatory failure: Is it far from reality?
Surjeet Kumar Thapa1, Suresh Kumar Angurana2
1 UKL Medical Center, Lajwanti Trust Hospital, Jammu, Jammu and Kashmir, India
2 Division of Pediatric Critical Care, Department of Pediatrics, Advanced Pediatric Centre, Postgraduate Institute of Medical Education and Research, Chandigarh, India
|Date of Submission||30-Nov-2022|
|Date of Acceptance||12-Dec-2022|
|Date of Web Publication||20-Jan-2023|
Dr. Suresh Kumar Angurana
Division of Pediatric Critical Care, Department of Pediatrics, Advanced Pediatric Centre, Postgraduate Institute of Medical Education and Research, Chandigarh
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Thapa SK, Angurana SK. Quantification of microcirculatory failure: Is it far from reality?. J Pediatr Crit Care 2023;10:1-2
The microcirculation consists of very small blood vessels of diameter <100 μm. It is the major site of gas exchange between blood and interstitial fluid and cells. It works as an integrated system that ensures tissue oxygen delivery adequate to meet oxygen demand. In sepsis, every cellular component of microcirculation is affected including endothelial cells, smooth muscle cells, platelets, leukocytes, and red blood cells (RBCs), leading to microcirculatory failure and impaired tissue perfusion. The changes that occur in microcirculation during sepsis include glycocalyx shedding, rolling and adhesion of leukocytes, impaired RBCs deformability, endothelial swelling, microthrombosis, and capillary leak syndrome. These changes cause heterogeneity in blood flow to the tissues, hemodilution resulting in decreased oxygen carrying capacity of blood, vasoconstriction, and decreased oxygen diffusion to tissues due to edema. After resuscitation, an improvement in macrocirculatory parameters or systemic hemodynamic variables does not imply improvement in microcirculatory flow and microcirculatory parameters, a phenomenon which has been termed as 'hemodynamic incoherence'. In patients in whom microcirculatory flow fails to improve, there is increased risk of mortality. Therefore, it is imperative that microcirculation should be evaluated in addition to macrohemodynamic parameters.
There are several indirect and direct methods for the assessment of microcirculation. Various indirect methods include transcutaneous tissue PO2, capillary refill time, lactate, ScVO2, delta pCO2, and near-infrared spectroscopy. Direct methods include laser Doppler, video microscopic techniques (orthogonal polarization spectral imaging, side stream dark-field imaging, and incident dark-field imaging-CytoCam), and dynamic methods like vascular occlusion tests., Among the indirect methods, lactate, ScVO2, and Delta pCO2 are easy to measure and do not require sophisticated equipment. Delta pCO2 is a surrogate marker of cardiac output and significantly correlates with microcirculatory dysfunction. In septic children, the delta pCO2 value above 6 mmHg indicates inadequate tissue perfusion. A prospective observational study by El-Nawawy et al. concluded that delta pCO2 of <6 mmHg after 6 h of resuscitation indicates normalization of tissue perfusion during pediatric septic shock management.
Among critically ill children with circulatory insufficiency, there are limited studies that compared the levels of lactate (arterial and central venous), ScVO2, and delta pCO2 among survivors and nonsurvivors. In the current issue of Journal of Pediatric Critical Care, Aygüler et al. presented a prospective observational study that aimed to evaluate the utility of lactate, ScvO2, and delta pCO2 levels and their relationship with the prognosis among critically ill children with circulatory failure in pediatric intensive care unit. The authors enrolled 30 children (1 month to 18 years) with circulatory failure and analyzed lactate (arterial and venous), ScvO2, and delta pCO2 levels at admission (T0), and at 4 hours (T4), 12 hours (T12) and 24 hours (T24) of admission. Most of the children had sepsis (n = 24, 80%), followed by postsurgical and cardiogenic shock. The mortality was 30% (n = 9). Authors noted that the arterial and venous lactate levels were highly correlated and the median arterial and venous lactate levels were similar at T0, T4, T12, and T24. Nonsurvivors had significantly higher PRISM-III score, PELOD-2, pSOFA, vasoactive inotrope score, and number of organ failures. Nonsurvivors had higher arterial and central venous lactate levels at all 4 time points when compared with survivors. Lactate levels ≥2 mmol/L at T0 were noted in 88.9% of nonsurvivors and 52.5% of survivors (P = 0.057). Nonsurvivors had similar ScvO2 values at 4 time points. The ScvO2 level <65% was not found to be associated with mortality at T0, T4, and T12, while it was found to be associated with mortality at T24 (P = 0.035). Delta pCO2 at T0 was significantly higher among nonsurvivors as compared to survivors but similar at T4, T12, and T24. Receiver operating characteristic analysis showed that T24 arterial lactate (AUC 0.918), T0 arterial lactate (AUC 0.775), and T0 delta pCO2 levels (AUC 0.741) were predictive of mortality.
The study by Aygüler et al. is an important addition to the limited literature on the microcirculatory parameters and their relationship with the outcome among children with circulatory insufficiency. The study highlighted that the arterial or venous lactate is an important marker of microcirculatory dysfunction and predictor of poor outcome. The predictive ability of ScVO2 for mortality was poor. Delta PCO2 is also an important marker of microcirculation. Several studies demonstrate its correlation with mortality and other clinical outcomes.,,,, Small sample size and single-center study are important limitations. The lack of utilization of direct methods for assessment of microcirculation is another limitation, though these may require sophisticated equipments.
In absence of an ideal parameter to assess the microcirculation, management of critically ill children with circulatory insufficiency should be based on the underlying disease characteristics, macrocirculatory parameters, and easily available microcirculatory parameters (lactate, delta PCO2 and ScVO2).
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