Does Insulin Requirement Post Cardiac Surgery Predicts The Risk Of Developing Diabetes

Critically ill patients frequently suffer from acute hyperglycemia, (a blood glucose level of more than 6.1 mmol/L (110 mg/dL)) and is observed in around 90 percent of ICU patients. Additionally, insulin resistance is expected in more than 80 percent of the critically ill which contributes to the problem. The hypothalamic-pituitary axis, sympathetic adrenergic system, and circulating pro-inflammatory cytokines including tumor necrosis factor alpha (TNF-α) and interleukins modulate hyperglycemia during stress. The seriousness of illness as expressed by the acute physiology and chronic health evaluation score (APACHE II), injury severity, surgery type and the Glasgow Coma Scale correlate with catecholamine and cortisol levels. Catecholamines are released mainly from the adrenal medulla. Multiple effects are assumed to be due to the surge of stress hormones (cardiovascular, immune and metabolic) targeting restoration of homeostasis during stress. Excessive glycogenolysis, gluconeogenesis, and insulin resistance characterize the neuroendocrine stress response. Increased hepatic output of glucose is predominantly the reason of stress hyperglycemia. Mediated through the liver adrenaline and noradrenaline excite gluconeogenesis and glycogenolysis; the latter has additional effects of enhancing glycerol provisions through lipolysis in the liver.

Additionally, the emergence of insulin resistance could be due to the release of adipokines from adipose tissue during critical illness. Downgrading of insulin signal transduction is associated with increased TNF-α due to phosphorylation of different molecules straight over the path of insulin-signaling. Glucose redistribution from peripheral tissues towards immune cells during infection could be mediated by variable regulation of glucose transporter-1 and glucose transporter-4.

Contributing factors for acute hyperglycemia during critical illness includes the concomitant secretion of additional stress hormones and the use of medications (steroids, lithium, vasopressors, inotropes and β-blockers). Intravenous glucose solutions, overfeeding, parenteral nutrition, and antibiotic and dialysis solutions, also precipitate hyperglycemia. Insulin deficiency or hypovolemia may also lead to hyperglycemia. Peripheral insulin resistance could be promoted with bed rest even without an obvious disease. Bed rest causes reduced skeletal muscle glucose uptake. Hyperglycemia in critically ill diabetics is an integration of pancreatic β-cell secretory disorders and insulin resistance.

Consequences of hyperglycemia in the Critically ill patients: in different ICU populations Short-term drawbacks of hyperglycemia include effects on fluid balance through glycosuria and subsequently dehydration. Hyperglycemia associated with white blood cell abnormalities which could impair the complement pathway. Mitochondrial protein could be damaged with hyperglycemia, amplification of inflammatory pathways, altered innate immune system, and downgrading of endothelial functions. The peripheral blood flow could be compromised due to the reduction in endothelial nitric oxide and vascular reactivity with hyperglycemia. Acute hyperglycemia boosts proteolysis and is accompanied by a high risk of cardiac complications, electro-myocardial alteration, hemodynamic compromise, acute kidney injury, and death. Therefore poor clinical outcome and complications are associated with hyperglycemia. The persistence of hyperglycemia for a longer time distinctly associated with pediatric population outcome as expressed by morbidity and mortality.

In Individual ICU populations, the risk of hyperglycemia and hypoglycemia increased in patients with sepsis. The Surviving Sepsis Campaign Guidelines recommend keeping the blood sugar below 10mmol/L. In neuro-critical care improved neurological outcome was observed with glucose control in patients, with a less strict glycemic target (7.7-10mmol/L). The impact of hyperglycemia was quantified in a meta-analysis for patients who had acute myocardial infarction. Postoperatively, intensive glucose control was associated with reduced acute heart failure, myocardial infarction, and death in vascular surgeries. Reduced death, infections and post-operative atrial fibrillation were observed after cardiac surgery with moderate blood sugar control. Interestingly, in a recent systemic review and meta-analysis stress hyperglycemia was associated with increased risk of subsequent diabetes in the critically ill. No previous studies went through future development of diabetes or impaired glucose tolerance after cardiac surgeries.