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be based on a fasting blood glucose of more than or equal to 7 mmol/L or a random plasma glucose of more than or equal to 11.1 mmol/L accompanied by symptoms associated with diabetes such as polydipsia, polyuria and weight loss (Blake and Nathan 2004, WHO 2006). These features of diabetes do not appear until 80% of beta cells are lost and so it is possible to reverse type 2 diabetes if it is picked up early enough (Schwab and Porter 2007).

Furthermore, during infection, major surgery or critical illness such as sepsis, pancreatitis or respiratory distress, counterregulatory or stress hormones (adrenaline, noradrenaline, cortisol, growth hormone and glucagon) are released causing significant metabolic alterations. These hormones increase insulin resistance which decreases peripheral intake of glucose and also promotes glucogenesis by stimulating glycogen and fat breakdown, causing hyperglycaemia (Crosser and McDowell 2007). For this reason patients with diabetes may need treatment of insulin or antidiabetic medication during acute illness, in order to replicate this homoeostasis or improve the body’s ability to produce insulin or use it.

Hyperglycaemia

Hyperglycaemia is defined as a random blood glucose of more than 11.1 mmol/L (WHO 2006). When insulin is deficient or absent as in type 1 or 2 diabetes, blood glucose levels will remain high after a meal, in times of illness or stress because it is unable to enter most cells (Wallymahmed 2007). Therefore cells are starved of glucose and the body reacts inappropriately by producing stress hormones that cause glycogenolysis (the breakdown of glycogen to release glucose), lipolysis (the breakdown of stored fat into glycerol and fatty acids) and gluconeogenesis (the conversion of glycerol and amino acids into glucose) (D’Hondt 2008, Marieb and Hoehn 2010) (see Figure 12.25).

Figure 12.25 Consequences of insulin deficiency.

This causes the blood glucose to rise further which results in a number of signs and symptoms. Water reabsorption in the kidneys becomes inhibited, resulting in frequent, large volumes of urine (polyuria). This will cause the person to feel excessive thirst (polydipsia) and may also result in extreme hunger (polyphagia). Polyuria and polydipsia will cause dehydration, a fall in blood pressure and electrolyte imbalance (Marini and Wheeler 2010). Moreover, the subsequent loss of sodium (hyponatraemia) and potassium (hypokalaemia) leads to muscle cramps, nausea, vomiting and diarrhoea, confusion, blurred vision, lethargy, cardiac events, coma and death.

Despite the excessive glucose in the body, the body cannot utilize it, so the body starts to break down its fat and protein stores for energy, which leads to high levels of fatty acids in the blood (lipidaemia) (Marieb and Hoehn 2010). This can also cause sudden and dramatic weight loss. These fatty acids are converted to ketones. They accumulate in the blood more quickly than they can be excreted or used and cause the blood pH to fall, resulting in ketoacidosis. Ketones will also be present in the urine. If ketoacidosis is allowed to continue it can become life threatening, disrupting all physiological processes, including oxygen transportation and heart activity and depression of the nervous system, leading to coma and death (Marieb and Hoehn 2010).

Reasons for hyperglyceamia include:

inadequate doses of insulin

stress

infection/sepsis

surgery

medications, for example steroids

nutritional support, for example parenteral nutrition (PN) or enteral nutrition.

It has been found that enteral and parenteral feeding contributes to hyperglycaemia in both patients with a diagnosis of diabetes and those without (McNight and Carter 2008). This is particularly true of patients receiving PN which bypasses the gut and therefore the incretin hormones that also help to maintain glucose homoeostasis (McNight and Carter 2008). Hyperglycaemia in response to steroids, for example dexamethasone, is another consideration and some researchers believe that their hypermetabolic action decreases glucose uptake, increases