Christian Hariman Christian.hariman@uhcw.nhs.uk Diabetes Emergencies Christian Hariman Christian.hariman@uhcw.nhs.uk

Today’s talk Diabetes Ketoacidosis (DKA) Hyperosmolar Non Ketotic (HONK) Hypoglycaemia

Objectives Recognise and participate in the management of diabetic ketoacidosis. Recognise Hyperosmolar Non ketotic state Recognise and manage hypoglycaemia.

Case – Rose Smith 18 year old girl, known diabetic type 1 Brought in by her parents as she had been sick Recently split from her boyfriend 2 days ago Has been vomiting all night She had been drinking alcohol with her mates yesterday to “cheer her up”

How would you proceed? (1)

How would you proceed? ABC of resuscitation History + examination Pregnancy check? Blood tests – FBC, U+E, LFTs, CRP, amylase Blood glucose Arterial blood gas Urinary ketones

A - patent B - 29 breaths per minute, rapid shallow breaths, 100% on air C – BP 102/68. Pulse 107. Cap refill 7 sec History – as above Examination – slightly tender abdomen Pregnancy check –ve Bloods taken Peripheral blood glucose 9.0

ABG Urinary ketones +ve pH 7.20 pO2 16.0 pCO2 2.70 HCO3- 13.8 Na 140

What is your differentials + why? (2)

What is your differentials + why? Diabetes Ketoacidosis pH, blood glucose (serum), ketones Metabolic acidosis – other causes Sepsis, poisoning Pregnancy Pancreatitis Gastroenteritis

Diabetes Ketoacidosis

Who gets DKA? Hallmark of type 1 diabetes (insulin insufficiency) Previously undiagnosed DM (about 25 – 30%) Interruption to normal insulin regime Intercurrent illness - usually infection

Loss of Beta cell function in pancreas Loss of beta cell function is gradual over time “Honeymoon period” alpha-cell beta-cell

Symptoms and signs Nausea Vomiting Abdominal pain Often preceding polyuria, polydipsia, weight loss Drowsiness/confusion/coma (severe) Kussmaul respiration - hyperventilation ‘Pear drops’ breath Sign of associated systemic illness (MI, infection, etc)

Diabetic Ketoacidosis:Pathophysiology Normal – glucose in blood B L O O D MUSCLE

Diabetic Ketoacidosis:Pathophysiology Normal Mechanism B L O O D MUSCLE Insulin

Diabetic Ketoacidosis:Pathophysiology Liver Glucagon Insulin deficiency *lack of glucose in muscle glucagon excess *increase in gluconeogenesis B L O O D MUSCLE Insulin

Diabetic Ketoacidosis:Pathophysiology 3. Rapid lipolysis into free fatty acids and ketone bodies release of Beta-hydroxybutyrate ketones makes you sick B L O O D ketones ketones MUSCLE ketones ketones

Diabetic Ketoacidosis:Pathophysiology 4. Hypovolaemia – vomitting + osmotic diuresis Increases concentration of ketones + glucose ketones B L O O D MUSCLE ketones

How do I diagnose DKA? Diagnosis requires all 3 of the following: High blood sugar (i.e diabetes) Glucose > 11 mmol *Finger-prick blood glucose can be normal* Ketones (blood or urine ≥ +++) Acidosis (pH<7.30 or HCO3<15mmol)

How do I Manage DKA? ABC – if impaired – consider early ITU input / central venous access Replace fluids Resolution of ketonaemia / insulin Replace electrolytes Look for cause Close monitoring Consider Low molecular weight heparin

Replacing fluids Initial management 1L 0.9% NaCl 30 mins* 1hr 2hr 4 hr Then continue NaCl 0.9% as dictated by fluid status *beware of elderly patients Later Once blood glucose <14 mmol/L – give 10% dextrose alongside 0.9% Normal Saline at 125ml / hour Colloid initially if hypotensive Don’t switch NaCl to 5% dextrose alone - results in swinging results

Resolution of ketonaemia Insulin infusion 50units actrapid made to 50ml with NaCl 0.9% Rate: 0.1 units/kg/hour 70kg = 7 units/hour Aim for fall in serum ketone of 0.5 mmol/L per hour OR rise in serum HCO3- by 3 mmol/hr or reduction of Blood glucose by 3 mmol/hr Increase rate of insulin by 1 unit per hour if above not achieved Continue infusion until blood ketones <0.3, venous pH >7.3 and/or HCO3- >18

Replace electrolytes K+ is most important Insulin shifts K+ into cells therefore K+ will fall as rehydrate Serum K+ ≥ 5.5 No potassium supplement Serum K+ 3.5 - 5.4 Add 20mmol per litre Serum K+ <3.5 Add 40mmol per litre Hyponatraemia may occur due to osmotic effect of glucose - it will correct with treatment of DKA

Monitoring Monitor urine output and vital signs closely catheterize Repeat U&E, glucose, VENOUS bicarbonate – ABG PAINFUL 2 – 4 hours, 6 - 8 hours, 12 hours, 24 hours Repeat ABG at 2 hours if not improving ? Alternative cause for acidosis e.g. lactate

Pitfalls Does a high wcc mean infection? No, not necessarily! Give antibiotics as guided by findings Absence of fever doesn’t mean absence of infection Consider alternative cause for acidosis if glucose and acidosis markedly out of proportion Non specific abdo pain and raised amylase doesn’t always mean pancreatitis Do not stop insulin even if the blood glucose is normal or below 4

Discharge, Prognosis and Prevention How do you stop a sliding scale? Overlap with normal insulin (breakfast) and keep in for an other 24 hours to monitor BMs Prevention Diabetic nurse + docs can use opportunity for patient education about insulin regime etc. Mortality is < 5% Patients with frequent episodes are at increased risk of dying and diabetic complications

Hyperosmolar Non-Ketotic Hyperglycaemic State (HONK/HHS)

HONK: Hyperosmolar hyperglycaemic state (HHS) Hallmark of type 2 DM May occur in: New diagnosis Poor compliance with treatment Intercurrent illness – especially MI, Infection, CVA Drugs- Steroids Sugary drinks

HONK:Pathophysiology Insulin production markedly reduced but NOT absent. No switch to fat metabolism and therefore no ketones or acidosis Gluconeogenesis Loss of intravascular volume B L O O D MUSCLE Insulin

Importance Mortality markedly higher compared to DKA Co-morbidities, longer time to diagnosis, electrolyte disturbances Cerebral oedema and Pulmonary Embolism more common

Clinical Presentation Possibly osmotic symptoms Dehydration around 10L deficit Decreased level of conciousness Signs of underlying infection in up to 50% +/- thrombo-embolism in up to 30% 2/3 cases previously undiagnosed As high as 50% mortality

How do I recognise it? Diagnosis requires ALL of the following: Raised blood glucose (usually >30mmol) Absence of ketones (or + or ++ only) Serum osmolality >350mmol

How do you calculate osmolality? 2(Na+K) + urea + glucose Or Ask for a serum osmolality level (U and E bottle, biochemistry)

Is the treatment the same as DKA? 1L 0.9% NaCl 1 hr* 2 hr 4 hr 8 hr Then continue NaCl 0.9% as dictated by fluid status *half the rate of DKA Fluid replacement – SLOWER (may be a marker of population not pathology) Electrolyte replacement (pseudohyponatraemia) Insulin – ‘slower’ scale – normally very responsive to IV insulin Search for cause ANTICOAGULATION Monitor

Insulin 50units actrapid made to 50ml with NaCl 0.9% Rate: 0.1 units/kg/hour 70kg = 7 units/hour More insulin sensitive Reduce rate if Blood glucose falls >10 mmol / hour Consider halving the rate within the first 1-2 hours Stop when patient is recovered

Hypoglycaemia

Hypoglycaemia In diabetes: blood sugar < 4 mmol/l Symptoms may not present at the same level of blood glucose Autonomic: sweating, palpitations, tremor, hunger Neuroglycopenic confusion, clumsiness, behavioural changes, seizures Non-specific nausea, headache, tiredness

Causes Drug Induced insulin sulphonylureas Alcohol Reactive Hypoglycaemia Post prandial gastric surgery

Treatment of hypoglycaemia If able to eat glucose: e.g 3 dextrosol tabs / 200mls of orange juice/ coca cola followed by long acting carbohydrate eg toast/ sandwich In the community: 1mg glucagon im and long acting carbohydrate on recovery Hospital options- I.M. glucagon 1mg I.V. 20ml of 50% dextrose* Other: hypostop *Extravasation of 50% dextrose can cause severe tissue loss; 20% preferable

Any questions about diabetic emergencies?

Summary You should be able to: Recognise diabetic ketoacidosis. Participate in the management of diabetic ketoacidosis. Recognise Hyperosmolar Non ketotic state Recognise and manage hypoglycaemia. Christian.Hariman@uhcw.nhs.uk