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Diabetes Emergencies Diabetes Emergencies Diabetic Ketoacidosis, Hyperosmolar Hyperglycaemic State, Hypoglycaemia and Feet! Dr Kath Higgins Clinical Lead Inpatient Diabetes, UHL Overview DKA, HHS, Hypo’s and Feet Background Management Challenges / controversies Case histories Key messages Diabetic Ketoacidosis Acidosis – acute metabolic decompensation Case History 1 24yr female – abdo pain, vomiting – 24hrs Temp 36.4 RR 40 BP 115/50 Pulse 117 Looks dehydrated, smells of ketones Generally tender abdo Na 134 K 6.1 Ur 13.7 Cr 159 pH 6.9 Bic 5.6 pO2 20.16 pCO2 1.19 DKA - introduction DKA is a serious and life threatening complication of Type 1 diabetes Mortality from DKA has decreased in past 20 yrs from 10% to 2% Diabetes NSF Standard 7 (2001) – The NHS will develop, implement and monitor agreed protocols for rapid and effective treatment of diabetic emergencies NICE Quality Standard (2011) - Quality Statement 14 - People admitted to hospital with diabetic ketoacidosis receive educational and psychological support prior to discharge and are followed up by a specialist diabetes team JBDS – The Management of Diabetic Ketoacidosis (DKA) in Adults – Sept 2013 DKA • Predominantly in patients with autoimmune type 1 diabetes • BUT may also occur in those with: • “ketosis-prone type 2 diabetes” • Latent autoimmune diabetes of adults (LADA) What is the physiology? • absolute (or relative) insulin deficiency which leads to……. • reduced peripheral uptake of glucose which leads to hyperglycaemia and…. • lipolysis and increased mobilisation of FFA from adipose tissue to liver – switch to free fatty acid metabolism • production and accumulation of acidic ketone bodies • 3Bhydroxybutyric acid (Optium plus) and acetoacetic acid (Ketostix) • Early stages ketone production buffered but when capacity to buffer / extract ketones is exceeded overt ketosis develops and urine becomes positive. •Hypergycaemia/osmotic diuresis/serum hyperosmolality and metabolic acidosis cause severe electrolyte imbalance. •Total body potassium loss – normal potassium poorly reflects total body potassium stores. •Ketones induce nausea and vomiting – worsens fluid depletion What are the precipitating factors in DKA? •Poor compliance – commonest •New presentation of Type 1 diabetes •Errors in insulin prescription / management •Infection •MI What are the signs and symptoms? • osmotic symptoms • weight loss • SOB – kussmaul breathing • abdo pain (especially children) • cramps • nausea and vomiting • confusion, drowsiness, coma • DKA can develop in <24hrs • need to make a rapid diagnosis and initiate treatment without delay DKA What are the 3 key features to make the diagnosis? The triad of uncontrolled hyperglycemia, metabolic acidosis, and increased total body ketone concentration characterizes DKA significant ketonuria >++ or blood ketone >3mmol/l known diabetes or blood glucose >11mmol/l bicarbonate <15mmol/l or venous pH <7.3 Diabetes Medicine 2005 (22) 221 – 50 patients admitted to ED with high CBG. Assessed using blood ketone meter. 9 had DKA, 8 compensated metabolic acidosis, 33 not DKA. Ketones >3.0mmol/l 100% sensitive for DKA, 86% specific Consider other causes of acidosis or ketosis? Ketosis •Ketotic hypoglycaemia •Alcoholic ketosis •Starvation ketosis – pH rarely <7.3 ketones rarely >2.0mmol/l Acidosis •Lactic acidosis •Hyperchloraemic acidosis •Salycilate poisoning •Uraemic acidosis Which 2 feature correlate closely with poor prognosis? • age and conscious level What is the typical fluid deficit in DKA? • 6 litres • Electrolyte deficits – Na 500 – 1000mmol, K 300 – 1000mmol, Cl 350mmol, Ca 50-100 mmol, PO4 50-100mmol, Mg 25-50mmol Commonest causes of death? • Precipitating illnes, hypokalaemia, aspiration and cerebral oedema Core principles in managing DKA • restore circulating volume – caution in elderly, young and pregnant • monitor and replace potassium • commence iv insulin • aiming to switch off ketone production and correct metabolic disturbance • avoid complications of treatment Principles of Management JBDS Inpatient Care Group : The Management of Diabetic Ketoacidosis in Adults. March 2010 Revised Sept 2013 •Diagnostic requirement - is this DKA? •Investigation •Assessment of severity – do I need to involve ITU? •Immediate management – first 60mins •Recommended area of care – right place and right team •Management guideline for insulin / fluid / potassium •Guidance on clinical and laboratory monitoring – rigorous monitoring •Confirmation of resolution – ketones <0.6mmol/l, pH >7.3 •Involvement of the diabetes team - early •Prevention of future episodes – education, ketone meter, sick day rules Joint British Diabetes Societies – DKA guidelines Controversial areas / Modifications in 2013 • arterial v venous blood gas – difference between venous and arterial pH is 0.02-0.15 pH units and difference between venous and arterial bicarb is 1.88 mmol/l. • use of blood ketone measurement – best practice in monitoring response to treatment • continuation of long-acting insulin analogues (and basal insulin) • fixed rate v variable rate iv insulin infusion – max infusion rate 15units/hr • bolus dose of insulin at presentation • use of iv bicarbonate • 5% or 10% dextrose when BM <14mmol/l • resolution when blood ketone <0.6mmol/l (previously <0.3mmol/l) • consider if newly diagnosed type 1 diabetes background insulin analogue at 0.25units/kg sc daily Regular assessment of clinical and biochemical parameters Avoid complications of treatment How well do we do? National DKA Survey – 2014 N=281 Time to N Saline – 41mins Time to iv insulin – 60mins Resolution at 18hr LOS 2.6 days Hypoglycaemia – 27% Hypokalaemia – 55% 95% seen by specialist team Dhatariya KK et al. Diabet Med 2015. Education and prevention Discuss precipitating cause and early warning symptoms of DKA •Sick day rules •Review of insulin regime •Provision of blood ketone meter and education on use Diabetes Medicine 2006 (23) 278 – In 123 young adults and children with Type 1 diabetes, 62 were taught how to use a blood ketone meter, 61 used urine testing. 50% reduction in days spent in hospital in group using blood ketone meter •Education of staff, patient and family Special circumstances FDA Drug Safety Communication: FDA warns that SGLT2 inhibitors for diabetes may result in a serious condition of too much acid in the blood – May 2015 •Type 2 diabetes, UTI, unwell, poor oral intake, picture of DKA with only slightly increased glucose levels – euglycaemic DKA Pregnancy •Use pregnant weight for FRII, discuss with obstetric team most appropriate place to care for pt, Cons – Cons discussion. Adolescents •16-18yr olds – Paed v Adult DKA protocol. Regional variation depending on age cut off for adult services. Demonstration of the cascade of clinical events and metabolic changes that contribute sequentially to progressive clinical deterioration and development of full-blown episodes of euDKA. Julio Rosenstock, and Ele Ferrannini Dia Care 2015;38:1638-1642 ©2015 by American Diabetes Association DKA but what type of diabetes? Does it matter on AMU? Case History 2 • A 42 year old south East Asian man presented to A&E dept with reduced conscious level. • The family reported that he had had diarrhoea and vomiting for a week. • He was not known to have diabetes. • No family history of diabetes. Arterial pH 7.2 Na 148 mmol/l K 4.4 mmol/l Urea 39.4 mmol/l Creatinine 764 micromoles/l Bicarbonate 11.7 mmol/l Base excess -15 Urine ketones +++ Venous plasma glucose 93.3 mmol/l Serum osmolality 435 mosmol/kg 2 HbA 1c 13.8% BMI was 27 kg/m How are you going to treat this patient? What is the diagnosis? Diagnosis – Type 1.5 / Type 1B / Atypical DM / Flatbush diabetes Ketosis Prone Diabetes Heterogenous group of patients presenting in DKA that do not fit the traditional autoimmune classification of diabetes More common in African, African-American and Hispanic people and young “type 2” phenotype pts Hyperglycaemia _> glucose toxicity which results in acute impairment of B- cell function which resolves when glucose levels return to normal. Negative autoantibodies Improve significantly with return to normoglycaemia and have a temporary insulin requirement P Chellmutha et al. Practical Diabetes International 2010; 27(3): 118-119. Case History 3 • 76-year-old caucasian lady referred with uncontrolled diabetes. • Diagnosed with type 2 diabetes in 2006. • Had been controlled on diet alone. • Over the previous two weeks she had become more and more lethargic with polyuria, polydipsia, loss of appetite and nausea. • Had lost 1.5 stones over the previous 10 months. • O/E - Thin lady, weight 45 kg, BMI 17 kg/m 2 • Smelled of ketones • Urinalysis showed 3+ glucose and 3+ ketones. • Arterial pH 7.241 • Bicarbonate 12 mmol/l • Sodium 129 mmol/l • Potassium 4.9 mmol/l • Urea 29.3 mmo/l • Creatinine 213 micromol/l • Blood glucose 59.3 mmol/l • Treated for diabetic ketoacidosis. • Made an uneventful recovery. • Discharged home 5 days later on 16 U of insulin/day. • Reviewed in the outpatient clinic 2 months later • Had gained 14 kg. HbA1c was 6.8%. • Anti-GAD antibody checked - strongly positive. •What is the diagnosis? • Diagnosis of latent autoimmune diabetes in adults (LADA) was made. • Of note is that she had a nephew with type 1 diabetes and her grandfather also had diabetes but she could not ascertain whether it was Type 1 or Type 2. • Form of Type 1 diabetes which occurs in adults often with slower onset. Despite presence of islet cell antibodies at diagnosis of diabetes, the progression of autoimmune B-cell failure is slow • It
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