Nursing standard.
Outline
- Summary
- Aims and intended learning outcomes
- Introduction
- Carbohydrate digestion
- Blood glucose homeostasis
- Diabetes
- Type 1 diabetes mellitus
- Case study
- High levels of glucose in the blood
- Low levels of glucose in the cells
- Laboratory testing
- Treatment
- Health promotion
- Conclusion
- REFERENCES
- Multiple-
choice self- assessment - Practice profile assessment
To provide nurses with a greater understanding of the condition, Helen Hand describes the underlying processes responsible for the development of diabetic ketoacidosis and discusses the need for health promotion.
By reading this article and writing a practice profile, you can gain ten continuing education points (CEPs). You have up to a year to send in your practice profile and guidelines on how to write and submit a profile are featured immediately after the continuing professional development article every week.
Most nurses can easily list the presenting signs and symptoms of diabetes mellitus, and the signs indicating the presence of ketoacidosis. Being able to care for a patient with diabetic ketoacidosis (DKA) effectively, however, requires more than the ability to list signs and symptoms. It requires knowledge of how they occurred and the consequences on the patient's health and wellbeing. Such knowledge allows us to understand the rationale for prescribed treatment and to interpret changes in the condition of the patient with insight and confidence. By following a logical structure, this article examines the pathophysiology of ketoacidosis to provide that underpinning rationale. After reading this article and reflecting on your practice, you should be able to:
[black small square] Define homeostasis and illustrate it with reference to the hormones insulin and glucagon.
[black small square] List the signs and symptoms of ketoacidosis and provide a rationale for their occurrence.
[black small square] Explain the effect of ketoacidosis on acid-base balance and electrolyte levels in the blood.
[black small square] Describe the rationale for the treatment of ketoacidosis.
[black small square] Discuss the health promotion that should be offered to help avoid the development of ketoacidosis.
The clinical signs and symptoms of type 1 diabetes that an undiagnosed patient might present with result from the paradox of diabetes, which is that blood rich in glucose surrounds cells that are deficient in glucose. Insulin is required to allow glucose to enter the cell and correct the imbalance. If treatment in the form of insulin is not provided, the body will attempt to compensate for the lack of glucose by increasing the production of counter-regulatory hormones (catecholamines, cortisol, glucagon and growth hormone), thus increasing glucose levels even more. The resulting mobilisation of fats to provide energy leads to the formation of ketones, which accumulate in the blood causing DKA. According to Lewis (2000), DKA is a state of relative or absolute insulin deficiency, aggravated by hyperglycaemia, dehydration and acidosis, producing derangements in the intermediary metabolism. It is most commonly associated with a disruption of insulin treatment, underlying infection and new-onset diabetes. Its presence can be confirmed by a blood glucose greater than 12mmol/l, the presence of ketonuria and arterial blood pH less than 7.35 (Singh et al 1997).
It is impossible to appreciate how the body regulates blood glucose levels unless we have an understanding of where glucose comes from and how it arrives in the blood stream. The basic fuel forms of carbohydrates are starches and sugars which occur naturally in food. Carbohydrates are widely available as they are relatively cheap to produce and easy to grow in plants such as grains, vegetables and fruits. They are also easy to store and, particularly with modern processing and packaging, can be kept for long periods. It is for these reasons that carbohydrates make up a large proportion of dietary intake all over the world.
Most carbohydrate foods, however, cannot be used immediately by the body's cells to make energy; they must first be broken down into glucose by digestion, which involves mechanical and chemical components to reduce food nutrients into smaller usable metabolic products.
Carbohydrates are classified according to the number of saccharide (glucose) units making up their structure. The largest forms in which carbohydrates can exist are polysaccharides made up of many single saccharide units. Carbohydrates are ingested in three forms: starch, by far the most significant polysaccharide; sucrose, a disaccharide (composed of two saccharides) commonly known as table sugar; and lactose, a disaccharide found in milk.
Digestion of carbohydrates begins in the mouth. Although the stomach plays a large role in digestion, the structure of carbohydrates remains unchanged. They pass out of the stomach via the pyloric sphincter into the duodenum and are broken down into single monosaccharides - glucose, fructose and galactose - in the small intestine. These units are now small enough to be absorbed across the walls of the small intestine into the hepatic portal system to be transported to the liver. On arrival at the liver, galactose and fructose are converted into glucose, which is then either released into the bloodstream or stored in the liver in the form of glycogen. Blood-borne glucose not sequestered by the liver enters body cells to be metabolised for energy; any surplus is stored in skeletal muscles as glycogen or in adipose tissue cells as fat (Hansen 1998).
Although many body cells use fat as an energy source, red blood cells and neurones rely almost entirely on glucose to supply their energy needs. Because even a temporary shortage of blood glucose can severely depress brain function and lead to the death of neurones, the body carefully regulates blood glucose levels.
The key hormones in the maintenance of blood glucose homeostasis are insulin and glucagon, both of which are secreted by the pancreas. The pancreas has both an endocrine function, producing hormones, and an exocrine function, producing pancreatic digestive enzymes. It is located behind the stomach, between the spleen and duodenum, and houses the islets of Langerhans, which have three types of hormone-secreting cells: alpha, beta and delta cells.
Insulin is produced and secreted by the beta cells of the pancreas in response to blood glucose levels above 5.5mmol (Marieb 1995). It is also affected by levels of amino acids (lysine, arginine) and gastrointestinal hormones (glucagon, gastrin, cholecystokinin, secretin). It is transported by the blood to its target tissues. Insulin is an anabolic hormone (one that makes complex molecules from simple ones). It promotes glucose uptake and the synthesis of proteins, carbohydrates and lipids, and functions mainly in the liver, muscle and adipose (fat) tissue. In the absence of insulin, muscle and adipose tissue cell membranes are impermeable to glucose, regardless of how much is present in the blood. The binding of insulin to the plasma membrane of the target cell increases the permeability of the cell to glucose, resulting in an increased uptake of glucose. Within seconds to minutes, the rate of glucose entry into cells is increased 15 to 20 times. In other words, insulin quickly gets rid of glucose from the blood.
Insulin acts directly on the liver cells, however, as liver cells are normally permeable to glucose, it does not promote increased transport. Instead, by stimulating the synthesis of specific enzymes, it promotes the utilisation of glucose for the formation of glycogen. As a result of the effects of insulin, blood glucose levels begin to decrease. This is detected by the pancreatic beta cells and results in a diminished production of insulin.
As blood glucose levels and consequently insulin levels fall, such as between meals or during fasting, the alpha cells of the pancreatic islets begin secreting the hormone glucagon. Glucagon is a catabolic hormone (one that breaks down compounds into smaller parts), which binds with specific receptors in the membranes of liver cells. Within seconds, enzymes are mobilised to begin breaking down stored liver glycogen back into glucose for release into the bloodstream, a process called glycogenolysis. Adipose tissue cells respond by mobilising their fatty stores (lipolysis) and release fatty acids and glycerol into the blood. Glucagon also stimulates the formation of new glucose molecules from amino acids in the liver (gluconeogenesis). This action takes much longer and is probably more important in adaptation to starvation and fasting. Secretion of glucagon is halted as the blood sugar level begins to rise. This is known as negative feedback (Huether and McCance 1996).
The sympathetic nervous system plays a crucial role in supplying fuel quickly when blood sugar levels drop suddenly. Adrenaline, supplied by the adrenal medulla in response to sympathetic activation, acts on the liver, skeletal muscle and adipose tissue to mobilise fats and promote glycogenolysis. Although there are several other hormones within the body that control energy metabolism, including adrenaline, growth hormone and the glucocorticoids, only insulin has the effect of lowering the blood glucose level. Alterations in the production of insulin therefore lead to hyperglycemia, which if undiagnosed will have serious widespread consequences.
Define homeostasis. State simply how the body maintains homeostasis in relation to blood glucose levels.
It would appear that the metabolic disease we know as diabetes has been with us for a long time. Williams (1999) suggests that in the 1st century AD, the Greek physician Aretaeus wrote of malady in which the body 'ate its own flesh' and produced large quantities of urine. He gave it the name diabetes from the Greek word meaning to siphon or to pass through. Williams (1999) states that it was not until the 17th century that the word mellitus was added from the Latin word for honey.
As evidence began to point to the pancreas as the primary organ of the disease, Paul Langerhans (1847-1888), a German medical student, discovered clusters of cells, or islets, scattered throughout the pancreas that were different from other pancreatic cells. It was not until 1921 that a team discovered and successfully used the agent from the islet of Langerhans cells: the hormone insulin.
Porth (1998) defines diabetes as: '...a disorder of carbohydrate, fat and protein metabolism resulting from an imbalance between insulin availability and insulin need'. It can represent an absolute insulin deficiency, impaired release of insulin by the pancreatic beta cells, inadequate or defective insulin receptors or the production of inactive insulin or insulin that is destroyed before it is able to carry out its action.
Two types of diabetes are now recognised:
[black small square] Type 1 - insulin-dependent or juvenile-onset diabetes.
[black small square] Type 2 - non-insulin-dependent or maturity-onset diabetes.
Vanderpump et al (1996) found diabetes present in approximately 2 per cent of the population in an English study; Hansen (1998) suggests a figure of 6 per cent for the American population, 90 per cent of whom are type 2.
As already stated, DKA is the result of very low or zero insulin levels and is therefore confined to people with type 1 diabetes. Box 1 lists the signs and symptoms of DKA. People with type 2 diabetes have sufficient insulin reserves to avoid the extreme metabolic disturbances that contribute to ketoacidosis. DKA might be the presenting condition of the undiagnosed patient, or the result of poor control in the diagnosed patient. The following case study illustrates how the signs and symptoms of diabetes develop and, if untreated, lead to DKA.
| [Help with image viewing] [Email Jumpstart To Image] | Box 1. Signs and symptoms of diabetic ketoacidosis |
Before reading the next section, take some time to think about why it might be important to understand why the signs and symptoms of DKA occur. What significance do you think this knowledge will have on the care that you give to patients?
Mrs Smith is 30 years old; she has felt unwell for some weeks and has visited her GP on two occasions with vague symptoms of tiredness and difficulty sleeping. Mrs Smith has also complained of recurrent vaginal Candida albicans, which her GP suggested could have occurred as a result of a recent course of antibiotics prescribed for an infected laceration on her arm. She has been under a lot of pressure recently, bringing up one-year-old twins on her own and having a sick mother to visit. Her GP advised her that she was 'run down', and needed to rest. He suggested that her tiredness resulted from her circumstances. Unbeknown to either of them, changes were taking place within her body that would eventually lead to Mrs Smith being admitted to hospital. Mrs Smith's pancreas has ceased to produce insulin and the level of glucose in her blood is not being controlled. The consequences of this and the way in which her body will attempt to compensate for this will be discussed.
Higgins (1994) suggests that the effects of insulin deficiency can be divided into those that result from high levels of glucose in the blood, and those that result from low levels of glucose in the cells.
As the concentration of glucose in Mrs Smith's blood begins to rise, and insulin is not produced in response, the level of glucose being filtered through the kidney will begin to rise. Glucose is a large water-soluble molecule. Because of this, it uses a type of active transport mechanism known as sodium co-transport to be reabsorbed from the renal tubule and back into the blood. In this mechanism, a carrier molecule in the cell membrane binds to sodium and glucose and transports them both through the proximal tubule into the interstitial fluid and then back to the blood stream. The transport of glucose is, however, dependent on there being a sufficient transport mechanism available.
Previously, Mrs Smith had managed to reabsorb all of the glucose that was filtered by the glomeruli in the kidney. Now, the amount of glucose being filtered has exceeded the amount of transport that is available. The consequence of this is that glucose will now appear in her urine. This is known as glycosuria, which could have been detected during her visit to the GP. The glucose that remains in the renal tubule will exert an osmotic effect and begin drawing water into the tubule. Mrs Smith will notice this as an increase in urination, known as polyuria.
As more water is excreted in the urine, the resulting dehydration stimulates the thirst centres in Mrs Smith's hypothalamus in an attempt to correct the loss by increasing her fluid intake. This leads to another of the common presenting symptoms of diabetes, polydipsia (excessive thirst).
Because of excessive urination, Mrs Smith's blood volume might be reduced and in an attempt to compensate for this, her body will begin to draw water out of the cells into the extracellular fluid. Over a period of time, this action might lead to cellular dehydration. Dehydration of cerebral cells might be seen initially as confusion, and later as coma. Walker et al (1989) imply that while most patients with DKA exhibit signs of clouding of consciousness, only around 10 per cent present with true coma. Without intervention, the consequence for Mrs Smith of uncontrolled fluid loss will be acute circulatory failure, which will manifest as a reduction in her blood pressure, a weak tachycardic pulse and oliguric renal failure. Mrs Smith might also have noticed occasional blurred vision and fatigue as a result of the lowered plasma volume.
High levels of blood sugar known as hyperglycaemia, and glycosuria also favour the growth of yeast organisms, hence pruritis (itching) of the external genitalia might occur as a result of candidal infection. This would explain Mrs Smith's vaginal thrush.
Glucose is important in the metabolism of cells. As the concentration of glucose within Mrs Smith's cells falls, fats will be mobilised from adipose tissue as an alternative energy source. The oxidation of fats in the liver produces the much needed energy-rich compounds, however, it also results in increased levels of compounds collectively known as ketones, in the blood. If the production of ketones continues, to the point where ketone production by the liver exceeds cellular use and renal excretion, ketoacidosis is said to have developed. The smell of acetone (one of the ketones) on Mrs Smith's breath is a classic sign of ketoacidosis. The other two ketones (beta-hydroxybutyric acid and acetoacetic acid) are weak acids, which will accumulate in the blood and overwhelm the bicarbonate buffering system that maintains the blood pH. The characteristic Kussmaul deep sighing respirations that Mrs Smith will now be exhibiting are an attempt by the body to correct the raised pH, by lowering the amount of carbon dioxide in the blood.
Find a patient with type 1 diabetes and with his or her consent, discuss the signs and symptoms of hyperglycaemia. Try to relate the underlying physiological changes with the outward signs and symptoms.
Ketoacidosis can occur at the onset of diabetes mellitus, often before the disease has been diagnosed. It is often preceded by physical or emotional stress such as infection, pregnancy or extreme anxiety. Mrs Smith had two of these factors. In clinical practice DKA can also occur through the omission or inadequate use of insulin. Although clinical signs might be evident, it is important to confirm via laboratory tests. According to Higgins (1994), plasma glucose is normally maintained between 4.5 and 8.0mmol/l. Glucose must be raised for a diagnosis of ketoacidosis to be made and is usually in the range of 25-40mmol/l (Higgins 1994). Since plasma glucose must exceed the renal threshold, glucose is always present in the urine of patients with ketoacidosis, however, it is unwise to rely solely on urine testing as the urine might have been in the bladder for some time, thereby reflecting earlier levels. For a diagnosis of ketoacidosis, there must be evidence of ketones in the urine and blood.
The pH of the blood is important in determining the severity of the condition. Blood normally has a pH of 7.35-7.45, maintained by the buffer systems, the most important of which is the bicarbonate buffer system. When acids accumulate in the blood, they dissociate with an increase in hydrogen ion concentration. Bicarbonate can usually neutralise hydrogen ions by incorporating them into water. If, however, the hydrogen ion concentration continues to rise, the levels of bicarbonate become insufficient to maintain the blood pH. If the acidosis is relatively mild, the compensatory mechanism described above should be sufficient to maintain the pH at the low end of normal. If the acidosis is severe, the pH can fall to as low as 6.9; pCO2 and bicarbonate levels can be measured simply and quickly using a heparinised arterial blood sample.
DKA is also associated with electrolyte imbalances; sodium and potassium levels in particular are affected. Sodium is lost via the urine as a result of osmotic diuresis caused by the high glucose level. In addition, vomiting, a common feature of ketoacidosis, is associated with a loss of sodium from the gastrointestinal tract. This might not always be reflected in the blood results because it is a measure of concentration and, as has already been illustrated, dehydration will be present. Normal plasma sodium levels are maintained between 135 and 145mmol/l, however, despite the actual deficit, patients with DKA might display wide-ranging plasma sodium levels depending on the relative losses of water and sodium (Higgins 1994).
Total body potassium is always depleted in ketoacidosis as potassium is also lost in urine and vomit. The plasma concentration of potassium, however, remains high due to the passage of potassium out of the cells and into the extracellular fluid. One of the mechanisms that normally controls the passage of potassium into and out of cells is the sodium/potassium pump. This pump requires intracellular glucose, which is not available in ketoacidosis, consequently, the pump cannot function and potassium leaks out of the cell and into the plasma. Furthermore, potassium is freely exchangeable with hydrogen across the cell membrane. If the hydrogen concentration is high as in DKA, hydrogen will move into the cell in exchange for potassium. So, despite an overall potassium deficit, plasma levels are usually raised in ketoacidosis, at the expense of the body cells.
Refer back to a patient that you have looked after with diabetic ketoacidosis. Look specifically at the blood tests in relation to pH, sodium, potassium, pO2, pCO2 and bicarbonate levels. See if you can explain the underlying physiology that is producing these levels and how the body is attempting to compensate.
Higgins (1994) suggests that the treatment in relation to DKA is threefold:
[black small square] To correct the fluid and electrolyte disturbances.
[black small square] To correct the low intracellular and raised extracellular levels of glucose.
[black small square] To reduce the blood pH.
According to Hillman (1987), patients with DKA can be estimated to have a fluid deficit of 6-10 litres. Replacement of fluid should take account of the patient's age, degree of dehydration and issues such as history of cardiac disease. Charalambos et al (1999) suggest that 1-2 litres should be given in the first hour, followed by 1 litre per hour until the estimated fluid deficit is replaced. Initially, 0.9 per cent saline should be given, followed by 5 per cent dextrose solution once the blood glucose level decreases below 13mmol/l. Although fluid replacement can significantly lower blood glucose levels, insulin replacement is necessary to allow glucose to enter the body cells and inhibit ketogenesis (ketone formation). This is achieved using a sliding scale insulin regime during which capillary blood is tested at appropriate intervals and the intravenous infusion of insulin adjusted according to blood glucose levels. Even in the context of normal blood glucose levels, the infusion should not be stopped until the urine is free of ketones (Charalambos et al 1999). Once the urine is clear of ketones and blood glucose is maintained within the normal limits, subcutaneous insulin can be commenced. Local hospital protocols usually exist for the treatment of ketoacidosis and it is important to be familiar with such protocols.
Potassium replacement is essential. Insulin administration will shift potassium from the extracellular to the intracellular space as glucose enters the cell and restarts the membrane sodium-potassium pump. This will result in hypokalaemia with the danger of life-threatening arrhythmias if not corrected. Sodium levels are not as problematic and tend to normalise following correction of dehydration and hyperglycemia (Charalambos et al 1999).
Most patients with DKA exhibit metabolic acidosis, partially or fully compensated for by the respiratory system. This is where raised hydrogen ion levels are detected by the peripheral chemoreceptors leading to hyperventilation or Kussmaul's respirations. As a result, carbon dioxide is washed out of the body and the arterial pCO2 falls. Acidosis can have a negative inotropic (weakening) effect on the heart, contribute to coma and confusion, and cause peripheral vasodilatation, however, fluid replacement and insulin should correct acidosis without other specific intervention.
Mrs Smith has now been diagnosed as having insulin-dependent diabetes mellitus. From your experience and with the knowledge of Mrs Smith's circumstances and the symptoms of ketoacidosis, list the specific nursing care that you would provide for Mrs Smith:
The severity of DKA should not be underestimated, according to a study by Edge et al (1999). Of 83 children under 20 years of age recorded as having died from 'diabetes', between 1990 and 1996, 69 deaths were caused by hyperglycaemia/ketoacidosis.
Patient education is, therefore, a vital part of nursing care. Walker et al (1989) state that infection might be the precipitating factor in up to 60 per cent of cases, recognition being difficult, as pyrexia does not always occur in DKA because of acidosis-induced peripheral vasodilation. Other possible causes include withdrawal of insulin, surgery and trauma.
Health promotion is an important aspect of care given by nurses to prevent both hypo- and hyperglycaemia. In Mrs Smith's case, you should stress the importance of regular monitoring of blood sugar levels to avoid further episodes of ketoacidosis. You should also provide information regarding the signs and symptoms of hyperglycaemia and the possible causes. Mrs Smith should be advised to continue taking her insulin even if she feels unwell and is not eating, as failure to do so will contribute to rising blood sugar levels. Regular attendance at clinic and making use of local diabetic services should also be encouraged.
Making use of relevant books, journals or the internet, devise a list of information that you could offer to a patient following a diagnosis of type 1 diabetes. (A useful website is: www.diabetes.org.uk .)
By completing this article you will hopefully have a comprehensive knowledge of how glucose gets into the blood, and of the homeostatic mechanisms that regulate it. You should also appreciate the consequences for the body should those regulatory mechanisms fail. This knowledge should enable you to understand the manifestations of ketoacidosis, its treatment and the importance of health promotion, which will ultimately enhance the quality of patient care
Now that you have completed the article, you might like to think about writing a practice profile. Guidelines to help you write and submit a profile are outlined on page 55.
Charalambos C et al (1999) Acute diabetic emergencies and their management. Care of the Critically III. 15, 4, 132-134. [Context Link]
Edge JA et al (1999) Causes of death in children with insulin-dependent diabetes. Archives of Disease in Childhood. 81, 4, 318-323. Bibliographic Links [Context Link]
Hansen M (1998) Pathophysiology, Foundations of Disease and Clinical Intervention. London, WB Saunders. [Context Link]
Huether SE, McCance KL (1996) Understanding Pathophysiology. St Louis MO, Mosby. [Context Link]
Higgins C (1994) Laboratory backup. Nursing Times. 90, 32, 45-49. Bibliographic Links [Context Link]
Hillman K (1987) Fluid resuscitation in diabetic emergencies: a reappraisal. Intensive Care Medicine. 13, 1, 4-8. Bibliographic Links [Context Link]
Lewis R (2000) Diabetic emergencies part 2. Hyperglycaemia. Accident and Emergency Nursing. 8, 4, 24-30. [Context Link]
Marieb E (1995) Human Anatomy and Physiology. Third edition. California, Benjamin Cummings. [Context Link]
Porth CM (1998) Pathophysiology Concepts of Altered Health. Eighth edition. Philadelphia PA, Lippincott. [Context Link]
Singh R et al (1997) Hospital management of ketoacidosis: are guidelines implemented efficiently? Diabetic Medicine. 14, 7, 482-486. Bibliographic Links [Context Link]
Vanderpump MP et al (1996) The incidence of diabetes mellitus in an English community. A 20-year follow up of the Wickenham study. Diabetic Medicine. 13, 8, 741-747. Bibliographic Links [Context Link]
Walker M et al (1989) Clinical aspects of diabetic ketoacidosis. Diabetes Metabolic Review. 5, 8, 651-663. [Context Link]
Williams SR (1999) Essentials of Nutrition and Diet Therapy. Seventh edition. St Louis MO, Mosby. [Context Link]
This self-assessment questionnaire (SAQ) will help you to test your knowledge. Each week you will find ten multiple-choice questions broadly linked to the continuing professional development (CPD) article. The answers might not be found in the article itself and you may wish to use reference books to assist you. The key words listed at the beginning of the CPD article are used as a basis for the questions.
Note: There is only one correct answer for each question.
There are several ways that you can make use of this assessment.
[black small square] You could test your subject knowledge by attempting the questions before reading the article, and then go back over them to see if you would answer differently.
[black small square] Alternatively, you might like to read the article to update yourself before attempting the questions.
[black small square] The answers will be published in Nursing Standard in two weeks' time.
Each week there is a draw for correct entries. If you wish to enter, send your answers on a postcard to: Nursing Standard, Nursing Standard House, 17-19 Peterborough Road, Harrow, Middlesex HA1 2AX, or via email to: karen.kelly@rcn.org.uk
Ensure you include your name and address and the SAQ number. This is SAQ No 65. Entries must be received by 10am on Tuesday November 21. This week's successful winner will receive £50 in book tokens.
[black small square] When you have completed your self-assessment, cut out this page and add it to your professional portfolio. You can record the amount of time that it has taken you, and don't forget to include any time spent consulting other sources to find answers. Space has also been provided for you to add any comments and additional reading that you might have undertaken.
[black small square] If you wish to further your professional development, you might consider writing a practice profile, see page 26.
| [Help with image viewing] [Email Jumpstart To Image] | Figure 1. No caption available. |
[black small square] Using the information in Box 1 to guide you, write a practice profile of between 750 and 1,000 words - ensuring that you have related it to the article you have studied. See the practice profile on page 26 and the examples in Box 2.
| [Help with image viewing] [Email Jumpstart To Image] | Box 1. Framework for reflection |
| [Help with image viewing] [Email Jumpstart To Image] | Box 2. Examples of possible practice profile entries |
[black small square] Mark the title of the entry as: practice profile and include your name, followed by the title of the article, which is The development of diabetic ketoacidosis, and the article number, which is NS65.
[black small square] Complete all of the requirements of the cut-out form provided and attach it securely to your practice profile. Failure to do so will mean that your practice profile cannot be considered for accreditation.
[black small square] RCN members are entitled to three free entries. Additional entries will be charged at £10. Using an A4 envelope, send for your free RCN assessment or enclose the £10 fee (£15 for non-RCN members) to: RCN CPD articles, Royal College of Nursing, Freepost CF 3790, Cardiff CF23 8ZY by November 8 2001 (cheques payable to RCN). Please do not staple cheques or vouchers to your practice profile and cut-out slip - paper-clips are recommended.
[black small square] You will be informed in writing of your result. Ten continuing education points are awarded for successful completion of this CPD article. You are entitled to one retake if you are unsuccessful.
[black small square] Feedback is not provided: notification of accreditation indicates that you have been successful. If you wish your practice profile to be considered for publication in Nursing Standard (page 26), indicate this in the place provided on the cut-out form.
[black small square] Keep a copy of your practice profile and add this to your professional profile - copies are not returned to you.
[black small square] Study the checklist (Box 3).
| [Help with image viewing] [Email Jumpstart To Image] | Box 3. Portfolio submission |
| [Help with image viewing] [Email Jumpstart To Image] | Figure 2. Continuing professional development |
Key words: Diabetes; Health promotion
No comments:
Post a Comment