Diabetes Manual. Hypoglycaemia and hyperglycaemia

Diabetes Manual Hypoglycaemia and hyperglycaemia Diabetes Service, Country Health SA November 2014 Authors/Reviewers Jane Giles, Advanced Clinical...
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Diabetes Manual

Hypoglycaemia and hyperglycaemia

Diabetes Service, Country Health SA November 2014

Authors/Reviewers Jane Giles, Advanced Clinical Practice Consultant, RN CDE Diabetes Service, Country Health SA Collette Hooper, Clinical Practice Consultant, RN CDE Diabetes Service, Country Health SA

Reviewers Dr David Jesudason

Clinical Director, Endocrinology Services, Country Health SA

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Hypoglycaemia and hyperglycaemia Hypoglycaemia and hyperglycaemia occur in both type 1 and type 2 diabetes. The aim of this section is to provide an overview of these acute complications in the context of the home / community setting. Refer to Hospitalisation section to find out more about managing hypoglycaemia and hyperglycaemia in a hospital or health service setting.

Contents Hypoglycaemia Hyperglycaemia References

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Hypoglycaemia Hypoglycaemia occurs when the blood glucose level falls below a particular value and/or low enough to cause signs and symptoms. When the level of glucose falls in the blood, the cells in the periphery, and eventually the brain cells do not get adequate glucose to function. The value at which this occurs is generally defined at below 4mmol/L but can differ according to the age of the person, duration of diabetes and whether there are any associated medical conditions such as liver disease or cerebrovascular disease present. Significant hypoglycaemic symptoms tend not to occur until blood glucose levels fall below 1 4mmol/L. Hypoglycaemia becomes more common with the duration of diabetes due to loss of counter regulatory response over time. Hypoglycaemia can be fatal in both type 1 and type 2 2 diabetes. Health professionals play an important role in educating people so they understand their risks, develop prevention strategies and manage hypoglycaemia events when they do occur.

Impact of hypoglycaemia There is significant physical and psychological morbidity associated with hypoglycaemia. Hypoglycaemia can be very frightening for the person and their family. Furthermore hypoglycaemia can lead to injury such as falling, an accident while driving and sometimes death. There is a growing body of evidence that shows that individuals with type 2 diabetes might be particularly vulnerable to adverse events associated with hypoglycaemia. Three recent trials have shown that an episode of severe hypoglycaemia was associated with an 2 increased risk of subsequent mortality. Elderly people with diabetes and the very young are especially vulnerable to hypoglycaemia.

Clinical features of hypoglycaemia In people who do not have diabetes, a counter-regulatory response is triggered as blood glucose levels drop. When the blood glucose level (BGL) drops to about 4.2mmol/L the secretion of endogenous insulin is suppressed. In type 1 diabetes this does not happen because they have no endogenous insulin and the injected (exogenous) insulin cannot be suppressed. In people with type 2 diabetes the body can suppress some of the insulin 1 because they are still producing their own insulin. At about 3.7mmol/L the secretion of glucagon is increased and this results in the release of stored glucose. Other hormones such as epinephrine, cortisol and growth hormone are also released in order to raise the 1 blood glucose. In people with established type 1 diabetes or those with long standing type 2 diabetes this counter regulatory response is impaired. The symptoms of hypoglycaemia can be classified into two groups: 1. Symptoms in response to adrenaline or the sympathetic nervous system (pale skin, sweating, shakiness, tingling especially around the lips, palpitations and a feeling of anxiety). 2. Symptoms due to decreased glucose in the brain (difficulty concentrating, confusion, inappropriate behavioural and psychological reactions, drowsiness, ultimately seizures and coma). Hypoglycaemia can be defined on the basis of physiology using the terminology mild, moderate or severe (table 1).

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Table 1 Mild

Moderate

Severe

Capable of self-treating

Unable to recognise the hypo but able to self-treat when prompted

Not capable of selftreatment

Tremors, palpitation, sweating, hunger, fatigue

Headache, mood changes, low attentiveness

Conscious or unconscious

Adrenergic

Neuroglycopenic

Neuroglycopenic

Hypoglycaemia at night is often slept through and not noticed. Symptoms of unnoticed nocturnal hypoglycaemia can include:  morning headaches  hangover type feeling on waking  nocturnal sweating.

Primary causes of hypoglycaemia Hypoglycaemia is a risk for people who are taking glucose lowering medicines or insulin. There are a number of possible causes of hypoglycaemia that have been identified:  missing a meal or snack (no carbohydrate)  inadequate carbohydrate intake  delaying a meal (or enteral feeding)  over-administration of insulin or oral hypoglycaemic agents  prolonged physical activity with no carbohydrate or adjustment of insulin  excessive alcohol intake, especially without suitable carbohydrate intake  vomiting eg morning sickness.

Impaired hypoglycaemic awareness Some people with diabetes may have ‘impaired awareness of hypoglycaemia’. In type 1 diabetes it is thought that up to 1/3 of children and adults may experience impaired awareness of hypoglycaemia. It may also be called hypoglycaemia unawareness whereby a person does not detect the warning signs and is at risk of developing severe or unconscious hypoglycaemia. Unawareness or a reduction of hypoglycaemia symptoms occurs more frequently in people who have had diabetes for many years or in people who experience frequent hypoglycaemia, or who maintain lower blood glucose levels. Causes and risks Autonomic neuropathy also leads to hypoglycaemic unawareness. Impaired hypoglycaemia awareness can develop after the occurrence of a single episode of severe 3 hypoglycaemia. This may resolve if the person avoids hypoglycaemia for 2-3 weeks. Inability to recognise the symptoms of hypoglycaemia increases the risk of prolonged and/or unconscious hypoglycaemia because the person is not alerted to symptoms of hypoglycaemia.

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3

People with impaired hypoglycaemic awareness are advised to:  monitor blood glucose levels more frequently  treat any low BGL even when there are no symptoms  consider blood glucose awareness training  ensure meal (CHO intake) patterns and exercise are matched

 discuss blood glucose targets with their specialist/GP and modify as needed.

Education and support for partners/carers and the patient is important in managing hypoglycaemic unawareness.

Management Hypoglycaemia must be treated promptly. People with diabetes should have a hypoglycaemia action plan which clearly steps out their self-management. The following is a suggested action plan for the self-treatment of people with hypoglycaemia in the community. This action plan may be adapted for any hypoglycaemic situation. Refer to Hospitalisation section for information about hypoglycaemia protocols for health services and hospitals. Mild or moderate hypoglycaemia If hypoglycaemia is suspected, the person should check their BGL. Treat if BGL less than 4mmol/L even when there are no symptoms. Step 1  15gm (1 CHO exchange) fast acting carbohydrate (CHO)

eg150mls soft drink (not diet) or 90mls Lucozade original or 15g Glucose tablets or 6 jelly beans (glucose)  Wait 5-10 minutes  Repeat Step 1 if BGL still 7.0mmol/L and 6 post prandial concentration of >11.1mmol/L. However, symptoms are more commonly evident when the blood glucose concentration is >15mmol/L. Hyperglycaemia as a result of uncontrolled diabetes may ultimately lead to two types of metabolic disturbances, conditions known as diabetic ketoacidosis (DKA) and hyperglycaemic hyperosmolar state (HHS). Diabetic ketoacidosis is a serious lifethreatening complication that results from uncontrolled type 1 diabetes. HHS is also a lifethreatening emergency and is usually seen in the elderly or undiagnosed person with type 2 diabetes.

Primary causes  insufficient insulin, omitting the insulin injection  insufficient oral hypoglycaemic agents or omitting to take medications as prescribed  excessive carbohydrate intake  stress – physical stress increases the body’s energy demands, which increase the

production of glucose and counter regulating hormones  infection and illnesses – exacerbation of respiratory conditions, gastroenteritis,

myocardial infarction, urinary tract infection, wound infection, cellulitis surgery  medications - steroids such as prednisolone.

Advanced hyperglycaemia If the symptoms of hyperglycaemia are not recognised and treated early, the hyperglycaemia can become advanced and lead to an emergency situation depending on the type of diabetes.

Diabetic ketoacidosis – type 1 diabetes 7

Diabetic ketoacidosis (DKA) is a medical emergency which has a less than 5% mortality. Infection is the most common cause of DKA and it is present in up to 50% of cases. DKA occurring at diagnosis is most common in the under 5 age group and in children whose families do not have ready access to medical care. The risk of DKA in people with known diabetes ranges from 1-10% per patient year. The risk is increased in people who:  have very poor glycaemic control  history of recurrent of DKA  peri-pubertal and adolescent girls  children with psychiatric disorders (eg eating disorder)  children with unstable family circumstances  are known to frequently and/or inappropriately omit insulin  use an insulin pump (this is because insulin pumps only use rapid acting insulin and so

insulin deficiency can occur very quickly)  are pregnant  have multiple co-morbidities which may include end-stage organ failure  are elderly 9

 live in a remote/isolated area some distance from medical support.

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Given that most cases of DKA occur in people with known diabetes it is believed to be 9 largely preventable by:  frequent monitoring of BG levels  early detection of ketosis and adequate replacement of insulin  patient education and support  health professional awareness and education  access to medical advice (eg 24 hour telephone, home visits, out patients service).

Pathophysiology As previously stated DKA consists of the biochemical triad of hyperglycaemia, ketonaemia 7 and acidaemia. It results from the absence of insulin. Although small amounts of circulating insulin may be present, the presence of large amounts of the counter regulatory hormones such as glucagon, adrenaline and noradrenaline and cortisol, result in the insulin being less effective. The combination of low insulin and high counter-regulatory hormone concentrations causes an accelerated catabolic state, with increased glucose production by the liver and kidneys and impaired peripheral use. If the metabolic disturbances are not appropriately corrected with exogenous insulin and fluid and electrolyte therapy then fatal dehydration and metabolic acidosis will occur. Features of DKA The signs of DKA are hyperglycaemia, glycosuria, ketosis, dehydration and electrolyte imbalance. Glycosuria: occurs as the concentration of glucose in the blood exceeds the renal threshold (ie capacity to reabsorb). Polyuria: glucose in the urine acts as an osmotic diuretic, which can lead to dehydration if left untreated. Polydipsia: thirst will occur as the body attempts to replace the lost fluid. Ketosis: as fats are broken down to supply energy, ketoacids accumulate in the blood stream causing ketosis and acidosis. Due to the lack of insulin, the ketoacids are not able to be cleared. Ketosis can also be recognised by an acetone breath. The accumulation of ketones in the blood and excretion of ketones in the urine (ketonuria) leads to more electrolyte imbalance and dehydration. Gastrointestinal: symptoms are nausea, vomiting, and abdominal pain. Respiratory: symptoms may include hyperpnoea (increased ventilation) and / or deep rapid breathing (Kussmaul’s respirations) which produces a respiratory alkalosis as the body attempts to correct the metabolic acidosis. Polyuria, ketonuria and acidosis cause loss of body potassium. However, acidosis causes potassium to move from the cells to the plasma. Hence, the circulating potassium may be low, normal or high. If acidosis and hyperglycaemia continue, they may lead to coma and death.

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Prevention It is important that the person understands that illnesses particularly those associated with fever and/or inflammation raise BGLs. This occurs because of the higher levels of stress hormones which promote gluconeogenesis (synthesis of glucose from amino acids in the liver) and insulin resistance. Ketone body production increases due to relative or absolute insulin deficiency. If illness causes vomiting and diarrhoea then the person may experience lower BG levels resulting in hypoglycaemia instead of hyperglycaemia. Equipping the person with clear guidance for managing sick days will reduce the risk of developing DKA. Every person no matter what type of diabetes they have or what the treatment is needs to have an individualised sick day action plan. Sick day management principles in type 1 diabetes A comprehensive guide to sick day management in type 1 diabetes has been developed by the Australian Diabetes Educators Association http://www.adea.com.au/about-us/ourpublications These apply when the person with type 1 diabetes:  is feeling unwell or notices signs of an illness  notices ketones in blood (greater than or equal to 0. 6mmol/L) or urine (small)  has blood glucose greater than target.

Ketone testing Ketone monitoring is indicated when the person with type 1 diabetes is unwell or the BGL is greater than 15mmol/L. It is used to avoid DKA by detecting insulin deficiency and guiding insulin replacement. Ketones can be measured in 2 ways: 1. beta-hydroxybutyrate (β-OHB) in capillary blood 2. acetoacetic acid in urine. Evidence shows that measuring blood ketones is a more sensitive test for detecting ketosis as compared with urine ketones. The NHMRC guidelines therefore recommend that blood ketone measurement should be taught as part of a comprehensive sick day management plan. However, if blood ketone strips are not available urine ketone measurement is the alternative test. Supplemental Insulin Supplemental (also known as ‘correctional’) insulin doses of rapid or fast-acting insulin may be administered to manage hyperglycaemia and ketosis. A supplemental insulin dose should be: 1. calculated as a percentage of the usual total daily dose (TDD) 2. given in addition to the usual prescribed insulin doses. Supplemental insulin doses can be given 2-4 hourly, if rapid acting insulin is used. Medical care should be sought if there is no improvement (or indeed if there is deterioration) in 8 blood glucose or ketones after 2 supplemental doses have been given. Insulin Pump Therapy Individuals using Insulin Pump Therapy can develop ketosis and DKA more quickly than those patients using basal bolus insulin as there is no background reservoir of long acting insulin.

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The insulin pump basal rate and/or correctional boluses may need to be increased during the period of illness. If a patient is unwell and the BGL is 15mmol/L or above the following steps should be taken:  check for problems with the pump, line and connections and change the cannula, tubing

and reservoir if required  check for ketones in blood/urine. If ketones are positive OR hyperglycaemia cannot be

corrected, suspect a problem with the pump. The emergency plan should include a subcutaneous insulin regimen and information on calculation of insulin doses should there be an urgent need to switch from insulin pump therapy back to basal bolus insulin. Key points 1. Do not stop basal insulin. 2. Increase frequency of blood glucose monitoring. 3. Ensure person with diabetes has adequate support. 4. Provide advice on maintaining hydration and carbohydrate intake. 5. Pre-meal short/rapid-acting insulin may need to be reduced if dietary carbohydrate intake is poor and blood glucose levels are not elevated. 6. Ketone levels should be measured, even if blood glucose is not high. 7. Consider supplemental insulin or glucose lowering medications to manage hyperglycaemia and ketosis. 8. Manage the underlying illness. 9. Discontinue home management of sick days if condition deteriorates or the person fails to respond to increased insulin.

Hyperglycaemic hyperosmolar state (HHS) Hyperglycaemic hyperosmolar state (HHS) is a medical emergency which must be diagnosed promptly and managed intensively. HHS has a significant mortality rate of 9 approximately 20%. HHS is different to DKA and as such requires a different approach. HHS typically occurs in the older person however, with type 2 diabetes being diagnosed at 10 younger ages it may be seen in young adults or teenagers. Whilst DKA can develop over a few hours to days, HHS often develops over days to weeks. Consequently the 10 dehydration and metabolic disturbances can be more extreme. Definition of HHS In HHS there is usually no significant ketosis/ketonaemia (less than 3mmol/L) though a mild acidosis (pH greater than 7.3, bicarbonate greater than 15mmol/L) may accompany 10 pre renal failure. The basic underlying pathophysiology is similar to that of DKA whereby there is a ‘reduction in the net effective concentration of circulating insulin coupled with a concomitant elevation of counter-regulatory stress hormones’. It is important to be aware that there can be a mixed picture of HHS and DKA. In HHS there is a residual amount of insulin secretion that minimises ketosis but is not enough to control hyperglycaemia. This then leads to severe dehydration and impaired renal function, leading to decreased excretion of glucose. It is the dehydration and renal crisis that causes more severe hyperglycaemia than is seen in DKA.

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The goals of management are to treat the underlying cause and to gradually and safely  normalise the osmolality  replace fluid and electrolyte losses  normalise blood glucose.

Other goals include prevention of  arterial or venous thrombosis  other potential complications eg cerebral oedema/central pontine myelinolysis  foot ulceration.

Features of HHS If the person is unable to replace fluids, dehydration and mental impairment occurs. This is especially likely in the elderly. Hence this acute complication often occurs in the elderly on oral hypoglycaemic agents who may be inadequately monitored or not receiving adequate fluid intake and unable to communicate their needs. The high plasma osmolality and dehydration lead to:  decreased skin turgor  hypotension  elevated body temperature  drowsiness  confusion  convulsions  coma.

Precipitating factors include:  infection  intercurrent illness such as myocardial infarction, acute airway disease  medication, eg high dosage corticosteroids, excessive use of diuretics  pancreatitis  total parental nutrition  renal dialysis  severe burns.

Prevention To prevent hyperglycaemic hyperosmolar state (HHS) from occurring, identify those at high risk and ensure the older person is well hydrated. All people with type 2 diabetes require a sick day action plan. Arrange a referral to a diabetes educator if you identify patients who do not have an action plan specific to their particular risk factors. Teach people with diabetes and family about warning signs and symptoms. Make sure they know about sick day management and when to seek medical advice. All health professionals should be aware of the appropriate management of people who are at risk.

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Sick day management principles in type 2 A comprehensive guide to sick day management in type 2 diabetes has been developed by the Australian Diabetes Educators Association http://www.adea.com.au/about-us/ourpublications These apply when the person with type 2 diabetes  is feeling unwell or notices signs of an illness  has blood glucose greater than 15mmol/L for more than 8-12hours.

Key points 1. Do not stop insulin or diabetes medications unless otherwise advised by their diabetes specialist team. 2. Advice may need to be sought regarding appropriate adjustment of oral and/or injectable diabetes medication (eg continuation of Metformin ® and/or Byetta®). 3. Ask the person to monitor blood glucose more frequently. 4. Ensure person with diabetes has adequate support. 5. Provide advice on maintaining hydration and carbohydrate intake. 6. May need supplemental insulin to manage hyperglycaemia. Medical assistance should be sought if the patient is prescribed basal or pre-mixed insulin and they do not have access to rapid acting insulin for supplemental insulin doses. 7. The presence of co-morbidities and/or end stage organ failure requires medical attention regardless of blood glucose levels. 8. Manage the underlying illness. 9. Discontinue home management of sick days if condition deteriorates or fails to respond to increased insulin.

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References 1. Cryer, P, Davis, S, and Shamoon, H, 2003, Hypoglycemia in diabetes, Diabetes Care, 26(6): p. 1902-1912. 2. Seaquist, E, Anderson, J, Childs, B, Cryer, P, Dagogo-Jack, S, Fish, L, Heller, S, Rodriguez, H, Rosenzweig, J, and Vigersky, R, 2013, Hypoglyceamia and Diabetes: A Report of a Workgroup of the American Diabetes Association and The Endocrine Society, Diabetes Care, (4): p. 1-12. 3. Craig, M, Twigg, S, Donaghue, K, Cheung, N, Cameron, F, Conn, J, Jenkins, A, and Silink, M, 2011, National evidence-based clinical care guidelines for type 1 diabetes in children, adolescents and adults. Australian Government Department of Health and Ageing, Canberra. 4. American Diabetes Association, 2009, Standards of medical care in diabetes - 2009, Diabetes Care, 32(S1): p. S13-S61. 5. Austroads and Australian National Transport Commission, 2012, Assessing fitness to drive for commercial and private vehicle drivers: medical standards for licensing and clinical management guidelines, 4th ed. 2012, Sydney: Austroads Ltd. 6. Harris, P, Mann, L, Marshall, P, Phillips, P, and Webster, C, 2008 / 09, Diabetes management in general practice: Guidelines for type 2 diabetes, Royal Australian College of General Practitioners and Diabetes Australia, Canberra. 7. Kitabachi, A E, Umpierrez, G E, Murphy, M B, Barrett, E J, Kriesberg, R A, Malone, J I, and Wall, B M, 2001, Management of hyperglycemic crisis in patients with diabetes, Diabetes Care, 24(1): p. 131-153. 8. Australian Diabetes Educator Association, 2014, Clinical guiding principles for sick day management of adults with type 1 and type 2 diabetes; Technical document, May, Canberra. 9. Maletkovic, J and Drexler, A, 2013, Diabetic ketoacidosis and hyperglycemic hyperosmolar state, Endocrinology Metabolism Clinics of North America, 42: p. 677-695. 10. Joint British Diabetes Societies, 2012, The management of the hyperosmolar hyperglyacemic state (HHS) in adults with diabetes, NHS, UK.

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