Hyperglycemia due to stress: What you need to know

Article by Specialist Doctor I Tran Ngoc Thuy Hang - Resuscitation - Emergency Doctor - Emergency Resuscitation Department - Vinmec Central Park International General Hospital

The neuroendocrine response to stress is characterized by excessive glucose synthesis (gluconeogenesis), glycogenolysis (glycogenolysis) and insulin resistance. However, stress-induced hyperglycemia is primarily due to increased hepatic glucose production (gluconeogenesis) rather than to impaired tissue breakdown of glucose. Cortisol increases blood glucose levels through the activation of important enzymes involved in glucose production in the liver and inhibition of glucose absorption in peripheral tissues such as skeletal muscle. Both epinephrine and norepinephrine stimulate hepatic glucose production and glycogenolysis; norepinephrine has the added effect of increasing glycerol supply to the liver through lipolysis. Stress-induced hyperglycemia and insulin resistance are evolutionary conserved responses that allow the host to survive periods of severe stress [14]. Insects, worms, and all carnivores including fish have hyperglycemic responses to stress.
Glucose is largely used by non-insulin-dependent tissues and these include the central and peripheral nervous systems, bone marrow, white blood cells and red blood cells, and the reticuloendothelial system. Cellular glucose uptake is mediated by plasma membrane glucose transporters (GLUTs), which facilitate the movement of glucose along a concentration gradient across the undifferentiated lipid cell membrane. pole. Insulin increases GLUT4-mediated glucose transport in adipose and skeletal muscle by increasing GLUT4 translocation from intracellular stores to the cell membrane. Stress and inflammation reduce translocation of GLUT-4 to cell membranes. It is likely that proinflammatory mediators, particularly TNF-α and IL-1, are responsible for the interactions on the surface expression of these glucose transporters. During infection, GLUT1 upregulation and GLUT-4 downregulation may play a role in the redistribution of glucose from peripheral tissues to immune cells and the nervous system.
In order for glucose to reach cells with reduced blood flow (in the case of ischemia, sepsis), glucose must diffuse along a concentration gradient from the blood stream, across the interstitial space, and into the cell. Glucose migration is completely dependent on this concentration gradient, and for distribution to be assured when blood flow is reduced, blood glucose levels must be higher. Stress-induced hyperglycemia leads to a new glucose balance, allowing a higher 'glucose diffusion gradient' in the blood, which maximizes cellular uptake of glucose in the face of reduced tissue blood flow. In patients with infection and tissue damage, the increased energy requirements of activated macrophages and neutrophils are modulated by enhanced cellular glucose uptake associated with increased diffusion gradients. glucose and increase the activity of glucose transporters.
In addition, acute hyperglycemia may counteract post-ischemic cell death by promoting angiogenesis and counteracting the natural cell death pathway. These mechanisms ensure adequate glucose uptake by immune cells and neuronal tissue in the face of reduced microvascular outflow. Indeed, two groups of independent investigators using microdialysis and the brain pyruvate/lactate ratio demonstrated that efforts to normalize blood glucose in patients with severe brain injury are associated to the risk of severe hypoglycemia in the brain and brain energy crisis. Similarly, Duning et al demonstrated that hypoglycemia exacerbates critical conditions causing neurocognitive dysfunction. Many studies have demonstrated that even moderate hypoglycemia is harmful and increases mortality in critically ill patients.
Normalization of blood glucose can impair immune function and brain function at times of critical condition. In summary, these data suggest that stress-induced hyperglycemia provides fuel for the immune system, the brain at times of stress, and that attempting to interfere with this conservative adaptive response may be harmful. .
The relationship between hyperglycemia and clinical outcomes is complex if diabetes is pre-existing. Observational data demonstrated that the association between hyperglycemia and mortality in non-diabetic subjects was much stronger than in patients with diabetes. Egi et al demonstrated that in patients with high HbA1c (>7%) there was an inverse relationship between ICU glycemic control and mortality - higher blood glucose levels during ICU stay. associated with lower mortality [28]. Biological regulation of pre-existing hyperglycemia may explain this phenomenon. These observations support the hypothesis that non-diabetic target glycemic targets differ from those in diabetic patients with chronic hyperglycemia. In patients with poorly controlled diabetes prior to ICU admission, rapid and significant lowering of blood glucose levels during their acute illness/surgery may worsen outcomes.
Chronic hyperglycemia in patients with diabetes is associated with a multitude of harmful complications. Complications include proinflammatory factor activation, prothrombotic events, and hyperoxidation.... The duration and extent of hyperglycemia appear to be important in determining whether hyperglycemia is protective or protective. harmful. Acute hyperglycemia limits myocardial damage following hypoxia and ischemia. However, in experimental models, chronic hyperglycemia is associated with increased cell death rates and increased infarct size. These data suggest that acute hyperglycemia may be protective and may lead to higher cellular plasticity and resistance to ischemic and hypoxic lesions. Severe stress-induced hyperglycemia (BG > 220 mg/dL) may be harmful; However, this has yet to be proven.

Multiple studies in both hospitalized ICU and non-ICU patients have demonstrated a strong association between hyperglycemia and poor clinical outcomes, including mortality, morbidity, and length of stay. hospital, infection, and overall complications. These studies included post-traumatic, burn, and surgical patients as well as patients with cerebrovascular accident and acute coronary syndromes.
Hyperglycemia is thought to increase infarct size and worsen outcomes in patients with ischemic stroke. Therefore, tight glycemic control has been recommended in patients with ischemic stroke. However, the INSULINFARCT trial demonstrated that aggressive intravenous insulin infusion versus subcutaneous injection in patients with fulminant stroke significantly increased infarct size.
Recently De Mulder et al randomly selected 294 hospitalized ACS patients with blood glucose levels between 140 and 288 mg/dL for tight glycemic control (85–100 mg/dL). ) or routine blood glucose management. In this study, tight glycemic control did not reduce infarct size, but was associated with an increased risk of death and second myocardial infarction. Guidelines from the American College of Physicians, currently recommend a target blood glucose level of 140–200 mg/dL in surgical/medical ICU patients with hyperglycemia. They do not recommend intensive insulin therapy because of the high potential for hypoglycemia and no benefit. It should be noted that “tight blood glucose control” is laborious, with nurses spending hours each day on this task, limiting the amount of time they actually spend taking care of their patients.

Don't be too obsessive about blood sugar control. Check HbA1C on admission in all diabetic patients Non-diabetic and diabetic patients with HbA1C <7%. Target BG 140 to 200 mg/dL Diabetics have HbA1C >7%. BG goal 160 to 220 mg/dL So how to achieve goal:
Avoid IV glucose and never use IV bag altogether Use enteral formula with ratio Fat ratio (omega-3) is higher than cholesterol and not overfed. Limit corticosteroid dose, consider continuous intravenous infusion if used. Consider taking insulin supplements. Discontinuation of oral hypoglycemic agents in diabetic patients Intermittent rapid insulin regimen every 6 hours/24 hours (patients are fed through a continuous nasogastric tube). Consider long-acting basal insulin in diabetics. Consider using long-acting basal (low-dose) + insulin bolus in patients who are being fed bolus via a nasogastric tube from time to time. Infuse insulin if the above measures are unsuccessful or in patients with severe hyperglycemia (blood sugar > 300 mg/dL). In the case of an ICU with a nurse who closely monitors the patient (1 nurse takes care of one patient) it may be better to choose an insulin infusion in a patient with blood glucose > 200 mg than to attempt glycemic control with injectable insulin. subcutaneous.
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