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  management of blood glucose

»Acute complications of hyperglycaemia

Why is control of blood glucose levels so important?

Management of blood glucose is essential in avoiding acute and chronic complications that are common to both forms of diabetes.


In a normal adult blood sugar levels are normally between 4 and 7 mmol/l. (Jerreat 1999, Chaisson 2003). In diabetes they can drop much lower. It is a common emergency and can be triggered by missing a meal, strenuous exercise, weight loss and excessive alcohol intake (Konick-McMahan 1999). Symptoms of hypoglycaemia are: sweating; clammy skin; headache; blurred vision; mood change; palpitations and the individual can appear confused or may even lose consciousness (Konick-McMahan 1999).

Hypoglycaemia can usually be treated by a variety of fizzy drinks such as lucozade, or glucose tablets if the patient is conscious. It should then be followed up with some form of carbohydrate and protein. If the patient is not conscious then there are a variety of gels such as Hypo stop gel which can be administered by rubbing on to the gums.

If the patient is in hospital then an I.V. infusion of glucose is usually administered and the patients blood glucose levels are monitored very closely Konick-McMahan 1999, Jerreat 1999).


Hyperglycaemia is a very common problem in poorly controlled diabetic patients. This is where blood glucose levels are raised and the body cannot access the fuel for lack of insulin. Symptoms of hyperglycaemia include excessive urination (Polyuria), excessive thirst (Polydipsia), weight loss and blurred vision. Acute complications of hyperglycaemia are Diabetic Ketoacidosis and Hyperglycaemic hyperosmolar non-ketotic state. These complications and their pathophysiology will be discussed on the complications page.

Chronic hyperglycaemia can also lead to a variety of pathologies. This is because high levels of circulating glucose can damage tissues throughout the body. Long term complications are listed below.

  • Retinopathy with potential loss of vision
  • Nephropathy potentially leading to renal failure
  • Peripheral neuropathy that presents a risk of foot ulcers, amputation and Charcot joints.
  • Autonomic neuropathy leading to gastrointestinal, genitourinary and cardiovascular symptoms.
  • Sexual dysfunction

Patients with diabetes are also at increased risk of: Atherosclerotic cardiovascular disease; peripheral vascular disease; cerebrovascular disease; hypertension and periodontal disease.

(Gavin et al. 2002, Jerreat 1999, Quinn 1998)

It is likely that all nurses will look after a diabetic patient at some point in there careers no matter what area they practice in. A good understanding of how illness can affect the diabetic individual is therefore essential.

How does hospital admission effect management?

Management of diabetes is difficult in a hospital setting for a number of reasons. Disruption to the patients normal routine is a common factor. They may not be as active as usual, losing the hypoglycaemic effects of their usual exercise. The diet provided for them in hospital may not be adequate when compared to what they are used to. Also they may receive any medication they are on at different times than usual, due to the timing of the drug rounds.

In addition, illness or surgery may mean that they have nothing to eat for some time either due to nausea or preoperative starvation. These factors combined with the metabolic disruption that may occur due to illness couldmean that the condition is not as well controlled as one may hope. This can lead to acute complications.


Acute complications of hyperglycaemia

»management of blood glucose

As previously discussed, the management of blood glucose is important for minimising hyperglycaemia for both the long and short term. However, although avoiding the longer-term complications is vital, acute complications of hyperglycaemia are very serious and associated with excess mortality (Chaisson 2003). These are Diabetic Ketoacidosis (DKA) and hyperglycaemic, hyperosmolar non-ketotic state (HHNS).

Precipitating factors

DKA occurs mainly in type 1 diabetes and may be rapid in its onset. There are several reasons why it occurs. The patient may have been non-adherent to insulin regimes or diet. This is particularly the case in younger diabetic individuals and factors that may contribute to this are: fear of the weight gain that occurs with good control of blood glucose; fear of hypoglycaemia and rebellion against authority (Kitabchi et al 2001 Jerreat 1999). Young female type 1 diabetic patients are particularly at risk of recurrent ketoacidosis as they are vulnerable to the psychological problems that precipitate eating disorders (Kitabchi et al. 2001).

It is thought, however, that infection is one of the most important precipitating factors often resulting in the first manifestations of previously undiagnosed diabetes mellitus. Other insults that may result in DKA are myocardial infarction, cerebrovascular accident, acute pancreatitis. Some medications can also cause ketoacidosis. These are, however, more likely to be precipitating factors in HHNS (Chaisson et al. 2003)

HHNS is sometimes known as hyperosmolar non-ketotic coma as this is often how it presents itself primarily. This tends to occur in mainly type 2 diabetic patients whose diabetes is as yet undiagnosed. It can be induced by trauma such as surgery, by medications or infection. (Basset and Makin 2000, Hardman and Young 2001). This condition is slower in its onset than DKA. However, HHNS and DKA do share similar pathogenesis.


If the patient has been suffering from hyperglycaemia then they either have an absolute or relative insulin deficiency. This means that the glucose in the blood stream cannot be utilised in the normal way. The cells of the body are starved of fuel and will try to access the stored fuel in the body. The body will release counter-regulatory hormones in order to try and produce that fuel. These hormones are catecholamines, glucagon, corticosteroids and growth hormone (Quinn 1998, Zaloga 1994) They are insulin antagonists and attempt to raise blood glucose levels. Glucagon first acts on the liver to stimulate the stored glycogen to be converted in to glucose. The liver can store around 500g of glucose as glycogen.

The action of the counter-regulatory hormones further increases hyperglycaemia. They also provide peripheral resistance to the action of insulin. They then act on the liver using a process called gluconeogenisis. This is a process in which fat and protein are converted in to a usable energy source. Fats are broken down and fatty acids are taken up by the liver and are converted into ketone bodies, which are released in to the circulation. These accumulate in the body. The ketoacids which are responsible for the acidosis in DKA are ß-Hydroxybutyric acid and acetoacetic acid. These acids are overproduced in DKA and dissociate to yield hydrogen ions.

These bind to bicarbonate resulting in reduced serum bicarbonate (Chaisson et al 2003). The body tries to compensate for its metabolic acidosis by blowing off carbonic acid. This usually presents as hyperventilation or what is commonly known as Kussmaul-Kien respiration (Basset and Makin 2000 Chaisson et al 2003). Acidosis is extremely dangerous for the patient and if left untreated can result in death.

The production of ketones does not often occur in HHNS but on occasion it does. The fact that there is usually some circulating insulin seems to prevent this.

However in both conditions severe dehydration is a problem. If the hyperglycaemia is sustained then they will be suffering form polyuria and polydypsia. This will lead to an osmotic duresis as the excess glucose will be excreted in the urine, which in turn leads to a loss of fluid and electrolytes. The overall depletion of circulating volume reduces the ability of the kidneys to clear glucose and ketoacids adequately through the urine. In younger patients, they may be able to temporarily compensate by consuming more fluids.

However, in the elderly there is often a reduced thirst mechanism or possibly a debilitating condition which means they are unable to compensate for what they have lost. As these types of patients usually suffer from type 2 diabetes and are often undiagnosed, the onset of HHNS is often insidious creating a more gradual onset and a longer duration of metabolic compensation. Patients with HHNS are usually more severely dehydrated. For this reason, and the fact that this condition often presents with other co morbid complaints, there is a higher mortality rate in HHNS than in DKA (Hardman and Young 2001). Hyperglycaemia in HHNS is usually more pronounced than in DKA

In both conditions fluid and electrolyte replacement is essential. The drop in circulatory volume can be so severe that the patient’s blood pressure can drop dramatically, inducing renal failure and hypovalaemic shock. It is essential to start the patient on intravenous fluids and to monitor their fluid balance ( Konick McMahan 1999, Kitabchi et al. 2001) When the body starts to lose fluid and electrolytes through osmotic duresis, it is likely that there will be serious bodily depletion of potassium. In DKA this may not be immediately apparent, as serum potassium levels may appear normal.

The blood serum levels of sodium may be more concentrated due to dehydration. In HHNS half strength saline is usually used, this is because correction of sodium levels should take place slowly to avoid neurological complaints (Kitabchi et al. 2001 Hardman and Young 2001)

The patient should also be treated for any underlying trauma or infection that precipitated the onset of either DKA or HHNS. Until the underlying cause is treated then counter-regulatory hormones will continue to be produced and insulin resistance will be a problem. Treatment and management will appear in more detail on the clinical presentation and management page. Diagnostic criteria and biochemical abnormalities appear in tables 1 and 2 respectively;

Table 1
Laboratory diagnostic criteria for DKA and HHNS

Parameter Normalal Range DKA HHNS
Plasma glucose levels mmol/L 4.2-6.2 ≥14 ≥34
Arterial pH* 7.35-7.45 ≤7.30 >7.30
Serum Bicarbonate level mmol/L 22-28 ≤15 >15
Effective serum Osmolality, mmol/Kg 275-295 ≤320 >320
Anion gap** mmol/L <12 >12 Variable
Serum ketones Negative Moderate to high None or Trace
Urine ketones Negative Moderate to high None or Trace
(Chaisson et al. 2003)  * If venous pH used correction of 0.03 must be made.
** Calculation Na -(Cl ˉ+HCO3ˉ )

Table 2
Other Biochemichal abnormalities associated with DKA and HHNS

Condition; mean (and Standard deviation)


Normal range



Sodium mmol/L


134 (1.0)

149 (3.2)

Potassium mmol/L


4.5 (0.13)

3.9 (0.2)

Blood urea nitrogen


11.4 (1.1)

21.8 (3.9)

Creatinine µmol/L


97.2 (8.8)

123.8 (8.8)

Free fatty acids mmol/L


1.6 (0.16)

1.5 (0.19)

Β-Hydroxybutyric acid µmol/L

< 300


1000 (200)

Lactate mmol/L




Insulin pmol/L


90 (10)

270 (50)

C-peptide nmol/L



1.75 (0.23)

Glucagon ng/L


580 (147)

689 (215)

Growth hormone µg/L




Cortisol nmol/L


1609 (345)

1539 (490)

Catecholamines ng/ml


1.78 (0.4)

0.28 (0.09)



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