Micronutrient Status of Critically Ill Patients with COVID-19 Pneumonia

Micronutrient deficiencies can develop in critically ill patients, arising from factors such as decreased intake, increased losses, drug interactions, and hypermetabolism. These deficiencies may compromise important immune functions, with potential implications for patient outcomes. Alternatively, micronutrient blood levels may become low due to inflammation-driven redistribution rather than consumption. This explorative pilot study investigates blood micronutrient concentrations during the first three weeks of ICU stay in critically ill COVID-19 patients and evaluates the impact of additional micronutrient administration. Moreover, associations between inflammation, disease severity, and micronutrient status were explored. We measured weekly concentrations of vitamins A, B6, D, and E; iron; zinc; copper; selenium; and CRP as a marker of inflammation state and the SOFA score indicating disease severity in 20 critically ill COVID-19 patients during three weeks of ICU stay. Half of the patients received additional (intravenous) micronutrient administration. Data were analyzed with linear mixed models and Pearson’s correlation coefficient. High deficiency rates of vitamins A, B6, and D; zinc; and selenium (50–100%) were found at ICU admission, along with low iron status. After three weeks, vitamins B6 and D deficiencies persisted, and iron status remained low. Plasma levels of vitamins A and E, zinc, and selenium improved. No significant differences in micronutrient levels were found between patient groups. Negative correlations were identified between the CRP level and levels of vitamins A and E, iron, transferrin, zinc, and selenium. SOFA scores negatively correlated with vitamin D and selenium levels. Our findings reveal high micronutrient deficiency rates at ICU admission. Additional micronutrient administration did not enhance levels or expedite their increase. Spontaneous increases in vitamins A and E, zinc, and selenium levels were associated with inflammation resolution, suggesting that observed low levels may be attributed, at least in part, to redistribution rather than true deficiencies.</p

Micronutrient Status of Critically Ill Patients with COVID-19 Pneumonia

Micronutrient deficiencies can develop in critically ill patients, arising from factors such as decreased intake, increased losses, drug interactions, and hypermetabolism. These deficiencies may compromise important immune functions, with potential implications for patient outcomes. Alternatively, micronutrient blood levels may become low due to inflammation-driven redistribution rather than consumption. This explorative pilot study investigates blood micronutrient concentrations during the first three weeks of ICU stay in critically ill COVID-19 patients and evaluates the impact of additional micronutrient administration. Moreover, associations between inflammation, disease severity, and micronutrient status were explored. We measured weekly concentrations of vitamins A, B6, D, and E; iron; zinc; copper; selenium; and CRP as a marker of inflammation state and the SOFA score indicating disease severity in 20 critically ill COVID-19 patients during three weeks of ICU stay. Half of the patients received additional (intravenous) micronutrient administration. Data were analyzed with linear mixed models and Pearson’s correlation coefficient. High deficiency rates of vitamins A, B6, and D; zinc; and selenium (50–100%) were found at ICU admission, along with low iron status. After three weeks, vitamins B6 and D deficiencies persisted, and iron status remained low. Plasma levels of vitamins A and E, zinc, and selenium improved. No significant differences in micronutrient levels were found between patient groups. Negative correlations were identified between the CRP level and levels of vitamins A and E, iron, transferrin, zinc, and selenium. SOFA scores negatively correlated with vitamin D and selenium levels. Our findings reveal high micronutrient deficiency rates at ICU admission. Additional micronutrient administration did not enhance levels or expedite their increase. Spontaneous increases in vitamins A and E, zinc, and selenium levels were associated with inflammation resolution, suggesting that observed low levels may be attributed, at least in part, to redistribution rather than true deficiencies.</p

Hemostasis

Inflammation and coagulation are tightly connected, whereby an inflammatory host response will activate coagulation, resulting in a spectrum of coagulopathies that range from a mildly decreased platelet count to disseminated intravascular coagulation (DIC). Since also mild forms of coagulopathies are clinically relevant, this phenomenon is referred to as inflammation-induced coagulopathy. A variety of conditions causing critical illness are associated with inflammation-induced coagulopathy, the most important of which is sepsis. Inflammation-induced coagulopathy is characterized by a depletion of coagulation factors and platelets, as well as a decrease in anticoagulant proteins and inhibition of fibrinolysis. The result is that patients across the whole range of inflammation-induced coagulopathy have an increased risk of bleeding as well as thrombosis, rendering management complex. Treatment of the underlying cause remains key. Pharmacological thromboprophylaxis should be started. There are data suggesting possible benefit of anticoagulant interventions for DIC, although not robust enough to warrant any recommendations. Prophylactic platelet transfusion is recommended in case of a platelet count beneath 10 × 109/L, whereas administration of prophylactic plasma is not advised. Antifibrinolytics should generally be withheld but are advised early in case of severe bleeding due to trauma, childbirth, or cardiac surgery.</p

Hemostasis

Inflammation and coagulation are tightly connected, whereby an inflammatory host response will activate coagulation, resulting in a spectrum of coagulopathies that range from a mildly decreased platelet count to disseminated intravascular coagulation (DIC). Since also mild forms of coagulopathies are clinically relevant, this phenomenon is referred to as inflammation-induced coagulopathy. A variety of conditions causing critical illness are associated with inflammation-induced coagulopathy, the most important of which is sepsis. Inflammation-induced coagulopathy is characterized by a depletion of coagulation factors and platelets, as well as a decrease in anticoagulant proteins and inhibition of fibrinolysis. The result is that patients across the whole range of inflammation-induced coagulopathy have an increased risk of bleeding as well as thrombosis, rendering management complex. Treatment of the underlying cause remains key. Pharmacological thromboprophylaxis should be started. There are data suggesting possible benefit of anticoagulant interventions for DIC, although not robust enough to warrant any recommendations. Prophylactic platelet transfusion is recommended in case of a platelet count beneath 10 × 109/L, whereas administration of prophylactic plasma is not advised. Antifibrinolytics should generally be withheld but are advised early in case of severe bleeding due to trauma, childbirth, or cardiac surgery.</p

Older females have increased mortality after trauma as compared with younger females and males, associated with increased fibrinolysis

INTRODUCTION:Female sex may provide a survival benefit after trauma, possibly attributable to protective effects of estrogen. This study aimed to compare markers of coagulation between male and female trauma patients across different ages. METHODS:Secondary analysis of a prospective cohort study that was conducted at six trauma centers. Trauma patients presenting with full trauma team activation were eligible for inclusion. Patients with a penetrating trauma or traumatic brain injury were excluded. Upon hospital arrival, blood was drawn for measurement of endothelial and coagulation markers and for rotational thromboelastometry measurement. Trauma patients were divided into four categories: males younger than 45 years, males 45 years or older, females younger than 45 years, and females 45 years or older. In a sensitivity analysis, patients between 45 and 55 years old were excluded to control for menopausal transitioning. Groups were compared with a Kruskal-Wallis test with Bonferroni correction. A logistic regression was performed to assess whether the independent effect of sex and age on mortality. RESULTS: A total of 1,345 patients were available for analysis. Compared with the other groups, mortality was highest in females 45 years or older, albeit not independent from injury severity and shock. In the group of females 45 years or older, there was increased fibrinolysis, demonstrated by increased levels of plasmin-antiplasmin complexes with a concomitant decrease in α2-antiplasmin. Also, a modest decrease in coagulation factors II and X was observed. Fibrinogen levels were comparable between groups. The sensitivity analysis in 1,104 patients demonstrated an independent relationship between female sex, age 55 years or older, and mortality. Rotational thromboelastometry profiles did not reflect the changes in coagulation tests. CONCLUSION:Female trauma patients past their reproductive age have an increased risk of mortality compared with younger females and males, associated with augmented fibrinolysis and clotting factor consumption. Rotational thromboelastometry parameters did not reflect coagulation differences between groups. LEVEL OF EVIDENCE Prognostic and Epidemiological; Level III.</p

Older females have increased mortality after trauma as compared with younger females and males, associated with increased fibrinolysis

INTRODUCTION:Female sex may provide a survival benefit after trauma, possibly attributable to protective effects of estrogen. This study aimed to compare markers of coagulation between male and female trauma patients across different ages. METHODS:Secondary analysis of a prospective cohort study that was conducted at six trauma centers. Trauma patients presenting with full trauma team activation were eligible for inclusion. Patients with a penetrating trauma or traumatic brain injury were excluded. Upon hospital arrival, blood was drawn for measurement of endothelial and coagulation markers and for rotational thromboelastometry measurement. Trauma patients were divided into four categories: males younger than 45 years, males 45 years or older, females younger than 45 years, and females 45 years or older. In a sensitivity analysis, patients between 45 and 55 years old were excluded to control for menopausal transitioning. Groups were compared with a Kruskal-Wallis test with Bonferroni correction. A logistic regression was performed to assess whether the independent effect of sex and age on mortality. RESULTS: A total of 1,345 patients were available for analysis. Compared with the other groups, mortality was highest in females 45 years or older, albeit not independent from injury severity and shock. In the group of females 45 years or older, there was increased fibrinolysis, demonstrated by increased levels of plasmin-antiplasmin complexes with a concomitant decrease in α2-antiplasmin. Also, a modest decrease in coagulation factors II and X was observed. Fibrinogen levels were comparable between groups. The sensitivity analysis in 1,104 patients demonstrated an independent relationship between female sex, age 55 years or older, and mortality. Rotational thromboelastometry profiles did not reflect the changes in coagulation tests. CONCLUSION:Female trauma patients past their reproductive age have an increased risk of mortality compared with younger females and males, associated with augmented fibrinolysis and clotting factor consumption. Rotational thromboelastometry parameters did not reflect coagulation differences between groups. LEVEL OF EVIDENCE Prognostic and Epidemiological; Level III.</p