Hyperglycaemia shouldn't be confused with hypoglycaemia , which is when a person's blood sugar level drops too low. The aim of diabetes treatment is to keep blood sugar levels as near to normal as possible.
But if you have diabetes, no matter how careful you are, you're likely to experience hyperglycaemia at some point. It's important to be able to recognise and treat hyperglycaemia, as it can lead to serious health problems if left untreated.
Occasional mild episodes aren't usually a cause for concern and can be treated quite easily or may return to normal on their own.
However, hyperglycaemia can be potentially dangerous if blood sugar levels become very high or stay high for long periods.
Regularly having high blood sugar levels for long periods of time over months or years can result in permanent damage to parts of the body such as the eyes, nerves, kidneys and blood vessels. If you experience hyperglycaemia regularly, speak to your doctor or diabetes care team. You may need to change your treatment or lifestyle to keep your blood sugar levels within a healthy range. Symptoms of hyperglycaemia in people with diabetes tend to develop slowly over a few days or weeks.
In some cases, there may be no symptoms until the blood sugar level is very high. Symptoms of hyperglycaemia can also be due to undiagnosed diabetes, so see your GP if this applies to you. You can have a test to check for the condition. When you're first diagnosed with diabetes, your diabetes care team will usually tell you what your blood sugar level is and what you should aim to get it down to. You may be advised to use a testing device to monitor your blood sugar level regularly at home, or you may have an appointment with a nurse or doctor every few months to see what your level is.
A variety of things can trigger an increase in blood sugar level in people with diabetes, including:. Occasional episodes of hyperglycaemia can also occur in children and young adults during growth spurts. If you've been diagnosed with diabetes and you have symptoms of hyperglycaemia, follow the advice your care team has given you to reduce your blood sugar level. However, a critical appraisal of the literature has demonstrated that attempts at tight glycemic control in both ICU and non-ICU patients do not improve health care outcomes.
We suggest that hyperglycemia and insulin resistance in the setting of acute illness is an evolutionarily preserved adaptive responsive that increases the host's chances of survival. Furthermore, attempts to interfere with this exceedingly complex multi-system adaptive response may be harmful.
This paper reviews the pathophysiology of stress hyperglycemia and insulin resistance and the protective role of stress hyperglycemia during acute illness. In , Claude Bernard described hyperglycemia during hemorrhagic shock [ 1 ]; and it is now well known that acute illness or injury may result in hyperglycemia, insulin resistance and glucose intolerance, collectively termed stress hyperglycemia.
Numerous studies in both ICU and hospitalized non-ICU patients have demonstrated a strong association between stress hyperglycemia and poor clinical outcomes, including mortality, morbidity, length of stay, infections and overall complications [ 2 — 5 ].
This association is well documented for both the admission as well as the mean glucose level during the hospital stay. Based on these data clinicians, researchers and policy makers have assumed this association to be causal with the widespread adoption of protocols and programs for tight or intensive in-hospital glycemic control.
However, a critical appraisal of the data has consistently demonstrated that attempts at intensive glycemic control in both ICU and non-ICU patients do not improve health care outcomes [ 6 — 8 ]. This information suggests that the degree of hyperglycemia is related to the severity of the disease and is an important prognostic marker.
This is, however, not a cause and effect relationship. Indeed, Green and colleagues [ 10 ] demonstrated that hyperglycemia was not predictive of mortality in non-diabetic adults with sepsis after correcting for blood lactate levels, another marker of physiological stress.
Tiruvoipati and colleagues [ 11 ] demonstrated that those patients with septic shock who had stress hyperglycemia had a significantly lower mortality than those with normal blood glucose levels. We suggest that hyperglycemia in the setting of acute illness is an evolutionarily preserved adaptive response that increases the host's chances of survival. Furthermore, iatrogenic attempts to interfere with this exceedingly complex multi-system adaptive response may be harmful.
The stress response is mediated largely by the hypothalamic-pituitary-adrenal HPA axis and the sympathoadrenal system. In general, there is a graded response to the degree of stress. Adrenal cortisol output increases up to ten-fold with severe stress approximately mg hydrocortisone per day [ 12 ].
In patients with shock, plasma concentrations of epinephrine increase fold and norepinephrine levels increase fold [ 13 ]. The adrenal medulla is the major source of these released catecholamines [ 13 ].
Adrenalectomy eliminates the epinephrine response and blunts the norepinephrine response to hemorrhagic shock [ 13 ]. The increased release of stress hormones results in multiple effects metabolic, cardiovascular and immune aimed at restoring homeostasis during stress. The neuroendocrine response to stress is characterized by excessive gluconeogenesis, glycogenolysis and insulin resistance Figure 1 [ 5 ]. Stress hyperglycemia, however, appears to be caused predominantly by increased hepatic output of glucose rather than impaired tissue glucose extraction.
The metabolic effects of cortisol include an increase in blood glucose concentration through the activation of key enzymes involved in hepatic gluconeogenesis and inhibition of glucose uptake in peripheral tissues such as the skeletal muscles [ 5 ].
Both epinephrine and norepinephrine stimulate hepatic gluconeogenesis and glycogenolysis; norepinephrine has the added effect of increasing the supply of glycerol to the liver via lipolysis.
In addition, the altered release of adipokines increased zinc-alpha2 glycoprotein and decreased adiponectin from adipose tissue during acute illness is thought to play a key role in the development of insulin resistance [ 14 ]. The degree of activation of the stress response and the severity of hyperglycemia are related to the intensity of the stressor and the species involved. Hart and colleagues [ 15 ] demonstrated that hemorrhage, hypoxia and sepsis were amongst those stressors that resulted in the highest epinephrine and norepinephrine levels.
In reviewing the literature, we have demonstrated large interspecies differences in the degree of activation of the HPA axis with stress, with humans having the greatest increase in serum cortisol level Figure 3 [ 16 ].
The neuroendocrine response to stress is characterized by gluconeogenesis and glycogenolysis resulting in stress hyperglycemia providing the immune system and brain with a ready source of fuel.
Postulated interaction between the insulin signaling pathway and activation of the pro-inflammatory cascade in the pathogenesis of insulin resistance in sepsis. Variability of the basal and stress cortisol level amongst various animal species [ 16 ]. Stress hyperglycemia and insulin resistance are evolutionarily preserved responses that allow the host to survive during periods of severe stress [ 17 ]. Insects, worms and all verterbrates, including fish, develop stress hyperglycemia when exposed to stress [ 17 , 18 ].
In animal models of hemorrhagic shock the administration of a hypertonic glucose solution increased cardiac output, blood pressure and improved survival [ 19 ]. In these experiments, similar osmolar doses of saline or mannitol, with greater accompanying fluid volumes, failed to produce the sustained blood pressure changes or to improve the survival. Glucose is largely utilized by tissues that are non-insulin dependent, and these include the central and peripheral nervous system, bone marrow, white and red blood cells and the reticuloendothelial system [ 20 ].
Glucose is the primary source of metabolic energy for the brain. Cellular glucose uptake is mediated by plasma membrane glucose transporters GLUTs , which facilitate the movement of glucose down a concentration gradient across the non-polar lipid cell membrane [ 20 ].
These transporters are members of a family of structurally related facilitative glucose transporters that have distinct but overlapping tissue distribution. Thermal injury and sepsis have been demonstrated to increase expression of GLUT-1 mRNA and protein levels in the brain and macrophages [ 21 , 22 ]. Concomitantly, stress and the inflammatory response result in decreased translocation of GLUT-4 to the cell membrane. During infection, the upregulation of GLUT-1 and downregulation of GLUT-4 may play a role in redistributing glucose away from peripheral tissues towards immune cells and the nervous system.
For glucose to reach a cell with reduced blood flow ischemia, sepsis , it must diffuse down a concentration gradient from the bloodstream, across the interstitial space and into the cell. Glucose movement is dependent entirely on this concentration gradient, and for adequate delivery to occur across an increased distance, the concentration at the origin blood must be greater.
Stress hyperglycemia results in a new glucose balance, allowing a higher blood 'glucose diffusion gradient' that maximizes cellular glucose uptake in the face of maldistributed microvascular flow [ 23 ]. Furthermore, acute hyperglycemia may protect against cell death following ischemia by promoting anti-apoptotic pathways and favoring angiogenesis. In this study, hyperglycemia resulted in increased capillary density and a reduction in fibrosis. In vitro and in vivo studies have demonstrated that cardiomyocytes exposed to an insulin-free medium supplemented with high glucose concentrations are resistant to pathological insults such as ischemia, hypoxia and calcium overload [ 25 ].
Macrophages play a central role in the host response to injury, infection and sepsis. Macrophage activities include antigen presentation, chemotaxis, phagocytosis, bactericidal activity, cytokine secretion and wound repair.
Glucose is the primary metabolic substrate for the macrophage and efficient glucose influx is essential for optimal macrophage function. Macrophages and neutrophils require NADPH for the formation of the reactive oxygen species, nitric oxide and superoxide as well as many biosynthetic pathways.
Metabolism of glucose via the pentose pathway provides the metabolic intermediates required for the generation of NADPH. Foot infections are common in people who have high blood sugar from diabetes. Nerve damage neuropathy combined with poor blood supply to the feet puts people who have high blood sugar from diabetes at high risk for infected foot ulcers. Other infections for which people with high blood sugar from diabetes are at increased risk include:.
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