An Overview of Diabetic Ketoacidosis

Summary

This article provides an overview of diabetic ketoacidosis, a life-threatening complication of diabetes mellitus. It highlights the signs, symptoms and acute management of this condition.

Key words

* Diabetes

* Diabetes: health promotion

* Diabetes: nursing

* Metabolic system and disorders

These key words are based on the subject headings from the British Nursing Index. This article has been subject to double- blind review.

DIABETIC KETOACIDOSIS (DKA) is a life-threatening complication of diabetes mellitus. It is predominantly associated with type 1 diabetes, but people with type 2 diabetes can experience ketoacidosis during severe infections and other illnesses (Williams and Pickup 2004). DKA accounts for 14 per cent of all diabetic- related hospital admissions and has a mortality rate of 5-10 per cent (Pickup and Williams 2003). It is classed as a medical emergency. Rapid identification is necessary to improve patient outcome. Gillespie and Campbell (2002) suggest patient outcomes are affected by the nurse’s ability to recognise the clinical features of DKA. It is important, therefore, for nurses to understand the signs, symptoms and treatment of the condition.

National Service Framework for Diabetes

The National Service Framework for Diabetes (DoH 2003) aims to address inequalities in health care by setting minimum standards for diabetes care. Standard 7 is relevant to DKA. It states that the NHS will develop, implement and monitor protocols for rapid and effective treatment of diabetic emergencies by appropriately trained healthcare professionals. Protocols will include the management of acute complications and procedures to minimise the risk of recurrence. The risk and severity of DKA can be reduced by giving advice and guidance to people with diabetes on how to manage blood glucose control during other illnesses (the sick-day rules discussed later). It Is important not to lose sight of the person who lives with diabetes and to whom these targets relate (MacKinnon 2003).

Diabetic ketoacidosis

DKA is a metabolic complication of diabetes mellitus. It consists of three concurrent abnormalities: hyperglycaemia, hyperketonaemia and metabolic acidosis (Miller 1999). It can be confirmed by blood glucose greater than 12mmol/l (216mg/dl) and the presence of ketonuna, and an arterial blood pH of less than 7.35 (Singh et al 1997).

Fourteen per cent of all diabetic-related hospital admissions are due to DKA (McIntyre 1996). Any age group can be affected. However, younger people with type 1 diabetes are typically affected (Williams and Pickup 2004). Potentially avoidable episodes occur in patients with established diabetes because of dosing errors or discontinuation of insulin therapy. In a study of 3,000 people with type 1 diabetes, 9 per cent were admitted with DKA one or more times in a 12-month period (EURODIAB IDDM Complications Study Group 1994).

DKA is a life-threatening medical emergency and without medical treatment it can lead to coma and death (Pickup and Williams 2003). Before the discovery of insulin, DKA was invariably fatal, the most common cause of death being ketoacidotic coma. After the introduction of insulin in 1922, mortality fell to approximately 30 per cent (Page and Hall 1999). Mortality declined further in the 1960s and 1970s due to earlier recognition, enhanced patient care and improved patient management (Pickup and Williams 2003). There is currently a 5-10 per cent mortality rate in Western societies (Pickup and Williams 2003). DKA remains the highest cause of death for patients with diabetes aged under 20 (Marinac and Mesa 2000). Mortality can be as high as 50 per cent in older people (Pickup and Williams 2003). Delays in presentation and treatment increase mortality.

Ketoacidosis occurs as a result of insulin deficiency and counter- regulatory hormone excess (Pickup and Williams 2003). Lack of insulin leads to decreased uptake of glucose by the tissues, increased hepatic glucose production from glycogen (glycogenolysis) and increased glucose synthesis from amino acids (gluconeogenesis), resulting in hyperglycaemia. Hyperglycaemia leads to an increased urine output, due to osmotic diuresis. Counter-regulatory hormones (such as glucagon) enhance fat breakdown into fatty acids. Oxidation of fatty acids leads to the formation of ketones, which deplete the body’s acid buffers (Lewis 2000).

Complications include (Page and Hall 1999):

* Cerebral oedema – this is often fatal, accounting for 50 per cent of deaths in newly presenting cases of DKA.

* Adult respiratory distress syndrome (ARDS).

* Thromboembolism.

* Gastric stasis.

* Mediastinal surgical emphysema.

Causes

The common precipitating causes of DKA are (Williams and Pickup 2004):

* Infection (30-40 per cent). Even minor infections, such as urinary tract infections, can be enough to upset diabetic control.

* Treatment errors (15-30 per cent). These might include giving the wrong dose of insulin, omitting dose(s) or failing to increase the dose during episodes of illness.

* Newly presenting type 1 diabetes (10-20 per cent).

* Myocardial infarction (1 per cent).

* Miscellaneous (5 per cent). This could include drugs and alcohol misuse.

* There is no obvious cause in approximately 40 per cent of cases.

* Diarrhoea and vomiting can also cause DKA.

* Recurrent DKA affects a small subgroup of patients, most of whom are women under 20. Deliberate omission of insulin is likely to be common among such patients (Williams and Pickup 2004). Page and Hall (1999) suggest deliberate omission of insulin among adolescent girls is a way to seek attention. This group often have an eating disorder. Pickup and Williams (2003) suggest that adolescent girls with an eating disorder and diabetes are associated with non- concordance, omission or underdosing of insulin, to induce weight loss. A study by Biggs et al (1994) found that up to 80 per cent of adolescent girls with diabetes admitted to binge eating. One-third of these regularly omitted or decreased their insulin dose in an attempt to control weight and compensate for binge eating.

Signs and symptoms

Signs include dehydration, hypotension, tachycardia, hyperventilation and hyperthermia (Williams and Pickup 2004). Symptoms include (Williams and Pickup 2004):

* Polyuria and polydipsia due to osmotic diuresis.

* Kussmaul respiration (deep, rapid breathing) due to metabolic acidosis.

* Ketotic breath. As well as being excreted in the urine, ketones are also excreted via the lungs, leading to ketotic or ‘pear drop’ breath (Lewis 2000).

* Nausea and vomiting due to hyperketonaemia.

* Weight loss as a a result of tissue catabolism and dehydration.

* Generalised weakness.

* Abdominal pain.

* Drowsiness.

* Coma (10 per cent of cases).

Treatment

Because DKA is a life-threatening condition, prompt, skilled management is crucial. Insulin deficiency is the principal cause of DKA, and insulin needs to be replaced with an intravenous (IV) infusion (Goldberg et al 2004). The aims of treatment are to rehydrate the patient, correct hypotension, decrease blood glucose levels to 10mmol/l (180mg/dl) or less within 24 hours, correct electrolyte imbalances and correct acidosis (Jerreat 2003).

It may be useful to remember the first seven letters of the alphabet in relation to treatment:

* Airway support: depending on the degree of coma or level of consciousness.

* Breathing: administer high-flow oxygen and monitor respiratory rate and rhythm.

* Circulation: monitor blood pressure and pulse – patients with DKA are usually hypotensive and tachycardic. Assess for signs of hypokalaemia, which may present as small T waves on an electrocardiogram (Houghton and Gray 2001).

* Drug therapy: insulin replacement is an essential part of treatment. This is achieved by commencing an IV sliding-scale insulin regimen. This will help to lower serum glucose, inhibit ketone production and reverse metabolic acidosis (Page and Hall 1999).

* Electrolyte replacement: sodium and potassium are lost through osmotic diuresis and vomiting. They need to be replaced using a slow IV infusion.

* Fluid resuscitation: replace intra- and extracellular fluid, dilute glucose levels in the blood and correct dehydration.

* Gases (arterial blood gases): pH can fall as low as 6.9 with severe acidosis, because the bicarbonate buffer system is unable to neutralise increasing hydrogen ions.

Sick-day rules Intercurrent illness causes hyperglycaemia and deterioration of diabetic control. This usually requires an increased insulin dose even if the patient is not eating. A common cause of severe DKA is misplaced advice given by healthcare professionals to stop insulin during intercurrent illness, when the patient is vomiting or not eating (Diabetes UK 2004). All patients requiring insulin need to be aware of sick-day rules (Box 1) – the most important of which is ‘never stop taking insulin’ (Page and Hall 1999).

Nursing care

On admission, there are several immediate nursing priorities (Gillespie and Campbell 2002). If the patient is comatose, an artificial airway will need to be inserted to prevent asphyxia. To prevent aspiration of vomitus, a nasogastric tube should be inserted, aspirated and left on free drainage. Breathing must be supported. High-flow oxygen should be administered to correct hypoxia. Regular blood pressure and pulse measurements are necessary. A cardiac monitor should be connected to the patient to \detect the effects of potassium replacement (hypokalaemia can lead to heart block, hyperkalaemia can cause ventricular fibrillation). Assessment of neurological function must also be made. The Glasgow Coma Score should be used to assess for responsiveness. Rapid acting insulin should be administered via an IV sliding scale to correct hyperglycaemia and ketonaemia.

Box 1. Sick-day rules

Blood glucose should be monitored hourly to evaluate response to insulin therapy. Sodium and potassium need to be replaced due to losses caused by vomiting and diuresis. Potassium is mainly an intracellular ion and there is always depletion of total body potassium. Once insulin is commenced, levels in the blood will fall further. IV fluids are prescribed to rehydrate the patient and correct hypovolaemia. Monitoring central venous pressure, blood pressure and hourly urine volumes will give an indication of the effects of rehydration. A urinary catheter will need to be inserted if the patient is unconscious or oliguric. A thorough nursing assessment is essential in the management of DKA to help identify precipitating factors. This can be obtained from relatives if the patient is unable to provide it. Once identified, these factors may help to avoid recurrence of DKA.

Patient education

In line with standard 3 of the National Service Framework for Diabetes (DoH 2003), the emphasis of patient education is empowerment and self-care. Self-care is also explored in the NHS Plan (DoH 2000), where the aim is for patients to be active participants and decision-makers in health care. It is essential that patients have a good understanding of diabetes to effectively self-manage their condition. Diabetes UK (2004) advocates that all people with diabetes should receive education and support to enable self-management. The education provided must be ongoing, consistent, up-to-date and individualised. Most cases of DKA can be prevented by effective self-management, thus reducing incidence, morbidity and mortality. Jervell (1996) claims that education can prevent 70 per cent of DKA episodes. Patients, therefore, need to be well informed about diabetes management to prevent further episodes of DKA. On discharge from hospital, it is imperative that patient education is reinforced by primary care follow-up. Gillespie and Campbell (2002) suggest that knowing the correct management during concurrent illness and regularly monitoring blood glucose levels enable patients to prevent further admissions with DKA.

Conclusion

Diabetic ketoacidosis is a medical emergency that without treatment can lead to coma and death. Prompt, skilled management is crucial. The nurse’s ability to recognise the clinical features of DKA can have a positive effect on patient outcomes. It is therefore important for nurses to understand the signs, symptoms and treatment of this condition

Acknowledgement

The author would like to acknowledge the advice and support provided by Cassie Dean, staff nurse and Niki Robinson, practice development nurse for diabetes.

Palmer R (2004) An overview of diabetic ketoacidosis. Nursing Standard. 19, 10, 42-44. Date of acceptance: September 16 2004.

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REFERENCES

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Department of Health (2000) The NHS Plan: A Plan for Investment, A Plan for Reform. London, The Stationery Office.

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Richard Palmer RN, Dip HE is staff nurse, St Richard’s Hospital, Chichester, West Sussex.

Copyright RCN Publishing Company Ltd. Nov 17-Nov 23, 2004