Hyperglycaemic Emergencies GRI EDUCATION

Transcription

1 Hyperglycaemic Emergencies GRI EDUCATION

2 LEARNING OUTCOMES Develop and describe your system of blood gas interpretation and recognise common patterns of acid-base abnormality. Describe the pathophysiology of diabetic ketoacidosis and hyperosmolar hyperglycaemic state. Implement initial management of DKA and HHS, noting the key differences in management.

3 ARTERIAL BLOOD GAS Normal Reference Range Hydrogen Ions (H + ) Carbon Dioxide (PCO 2 ) Oxygen (PO 2 ) Bicarbonate (HCO 3- ) CO 2 + H 2 O H 2 CO 3 H + + HCO 3 -

4 ARTERIAL BLOOD GAS ANALYSIS First assess oxygenation?hypoxic Next assess hydrogen?high (overall acidotic)?low (overall alkalotic) Next assess CO 2?high (respiratory acidosis)?low (respiratory alkalosis) Last assess HCO 3?high (metabolic alkalosis)?low (metabolic acidosis)

5 PATTERNS OF ABNORMALITY Respiratory Acidosis: High H +, High CO 2 Respiratory Alkalosis: Low H +, Low CO 2 Metabolic acidosis: High H +, Low HCO 3 - Metabolic Alkalosis: Low H +, High HCO 3 - Compensation may occur eg elevated bicarbonate in respiratory acidosis, low CO 2 in metabolic acidosis.

6 EXAMPLE Measurement Reference Range Hydrogen Ions (H + ) Carbon Dioxide (PCO 2 ) Oxygen (PO 2 ) Bicarbonate (HCO 3- ) What is the abnormality?

7 EXAMPLE Measurement Reference Range Hydrogen Ions (H + ) Carbon Dioxide (PCO 2 ) Oxygen (PO 2 ) Bicarbonate (HCO 3- ) What is the abnormality?

8 EXAMPLE Measurement Reference Range Hydrogen Ions (H + ) Carbon Dioxide (PCO 2 ) Oxygen (PO 2 ) Bicarbonate (HCO 3- ) What is the abnormality?

9 EXAMPLE Measurement Reference Range Hydrogen Ions (H + ) Carbon Dioxide (PCO 2 ) Oxygen (PO 2 ) Bicarbonate (HCO 3- ) What is the abnormality?

10 EXAMPLE Measurement Reference Range Hydrogen Ions (H + ) Carbon Dioxide (PCO 2 ) Oxygen (PO 2 ) Bicarbonate (HCO 3- ) What is the abnormality?

11

12

13 PATHOPHYSIOLOGY OF DKA Insulin deficiency Hyperglycaemia & electrolyte loss Lipolysis unopposed catabolism: free fatty acids Hepatocyte fatty acid metabolism Raised ketones exceed buffer system profound diuresis with dehydration, hypovolaemic shock acidic ketones metabolic acidosis and coma Catecholamines and cortisol released during illness/stress oppose actions of insulin and accelerate the process.

14 DEFINITION OF DKA Severe, uncontrolled diabetes with ketonaemia/ketonuria, metabolic acidosis and (usually) hyperglycaemia H + > 45 (PH < 7.3) or HCO 3 < 18 with ketonuria/ketonaemia Severe DKA: H + > 80 (PH < 7.1) HCO 3 < 5 Note that glucose is not always markedly elevated and therefore not in definition

15 PRECIPITANTS OF DKA New onset type 1 diabetes Changes in insulin dose Missed insulin dose Infection MI Stroke Pancreatitis Glucocorticoids Sympathomimetics

16 CLINICAL FEATURES OF DKA Rapid progression of symptoms Polydipsia, polyuria N&V, abdominal pain (delayed gastric emptying and ileus in severe acidosis and electrolyte abnormalities) Ketotic breath - exhaled acetone (smells like nail polish remover) Kussmaul breathing (compensatory hyperventilation in acidosis) Dehydration and shock Altered mental state

17 MANAGEMENT OF DKA ABCDE IV fluids Insulin infusion (ensure IV fluids given first as intracellular glucose and electrolyte shift will cause fluid to follow, depleting fluid in the intravascular space and worsening hypovolaemia) Treat the underlying cause Correct potassium levels (total potassium levels are usually low due to osmotic diuresis and excretion of ketone-potassium salts. Serum potassium may be normal or elevated as in the absence of insulin potassium leaves the intracellular space. Hyperosmolarity due to hyperglycaemia also draws fluid and electrolytes out of cells)

18 THE 1 ST HOUR ABCDE Get venous access (try for 2 x green cannulas) Confirm diagnosis with ketones, BM and VBG 1L 0.9% NaCL over 1 hour Make up 50 units of actrapid in a 50 ml syringe with 0.9% NaCl Commence IV insulin 6 units/hour as soon after IVF as possible Ensure bloods (esp U&E) are sent

19 OTHER INTERVENTIONS ECG -?arrhythmia, signs electrolyte abnormalities Sepsis screen with MSSU, blood culture, CXR (note WCC is often elevated in the absence of infection due to elevated cortisol and catecholamine levels) Record GCS Insert catheter if oliguric Consider central line, especially if peripheral IV access difficult DVT prophylaxis

20 HOURS 1-4 Continue IV 0.9% NaCl Replace potassium: No KCl if anuric or initial K + > 5 10 mmol KCl in 500 ml NaCl if K mmol KCl in 500 ml NaCl if K + < 3.5 Repeat VBG, U&E and bicarbonate at 2 hours, check BM hourly

21 ONCE GLUCOSE FALLS BELOW14 Commence 10% glucose 100ml/hour Reduce IV insulin to 3 units/hour Aim to maintain BM between 9 and 14 by altering insulin rate as necessary Rapid falls in glucose may be associated with cerebral oedema so try to avoid fall > 5 mmol per hour

22 DISPOSITION Different depending on hospital. In GRI non-severe DKA may be managed on the ward as long as showing signs improvement with initial management. However, DKA patients are often managed in HDU as they have potential to deteriorate and are a big drain on nursing resources. Discuss DKA patients with the medical registrar on-call to determine the best setting - do not admit to the receiving wards without alerting the medical registrar!

23 COMPLICATIONS OF DKA Cerebral oedema Shock with multiorgan failure Potassium derangements Pulmonary oedema (aggressive fluid therapy) Thromboembolic events

24 CEREBRAL OEDEMA

25 CEREBRAL OEDEMA Incompletely understood?due to fluid shifts during treatment. As fluids and insulin are given serum glucose falls and glucose and electrolytes are uptaken by cells. Extracellular osmolality falls compared with intracellular osmolality. Fluid is drawn osmotically into the brain - if this occurs rapidly it may exceed ability to regulate intracranial pressure. Ischaemic, vasogenic and cytotoxic hypotheses have been proposed.

26 CEREBRAL OEDEMA Headache Lethargy Reduced GCS Seizures Hypertension, bradycardia Herniation syndromes Most common in children and young adults Get a CT head if headache, altered GCS or signs elevated ICP - will show loss of sulci and small ventricles.

27 CEREBRAL OEDEMA - TREATMENT Raise the head of the bed Slow the rate of insulin and fluid infusion IV mannitol 100 ml 20% over 20 mins Dexamethasone 8 mg IV as alternative Perform CT head Consider admission to ICU As a last resort decompressive craniectomy can be considered.

28 HYPEROSMOLAR HYPERGLYCAEMIC STATE (HHS) Similar mechanisms to DKA but without the ketoacidosis. Lipolysis and ketogenesis are more sensitive to insulin than gluconeogenesis. In T2DM there is resistance to insulin but not complete absence. Insulin activity is able to prevent lipid catabolism and ketone generation but unable to prevent carbohydrate catabolism. The result is profound hyperglycaemia with severe dehydration and electrolyte abnormalities due to osmotic diuresis. Slower onset than DKA - onset over several days.

29 HHS DEFINITION Severe hyperglycaemia > 30 mmol/l Total Osmolality > 340 mosmol/kg Serum Bicarbonate > 15 mmol/l Absent or 1 + urinary ketones Serum osmolality = [2 x (Na + + K + ) + urea + glucose]

30 HHS CLINICAL FEATURES Insidious onset Polydipsia, polyuria Severe dehydration Impaired level of consciousness or focal neurology (correlates with plasma osmolality, dehydration and shock) Often presents with concurrent illness eg infection, stroke, MI More common in the elderly and in those with T2DM Signs of acidosis not present eg SOB, abdo pain, N&V, ketotic breath

31 HHS APPROACH Similar approach to DKA, but need to avoid sudden drop in osmolality which may precipitate cerebral oedema. ABCDE Establish diagnosis Give IV fluids according to fluid status and comorbidity Commence 6 unit/hour Insulin infusion

32 HHS APPROACH CONTINUED Aim for 2-3 mmol/hour drop in glucose - titrate the insulin Keep glucose level 9-14, add 10% dextrose 100 ml/hour when BM <14 Monitor potassium levels frequently to guide replacement at 0, 2 and 4 hours Treat the underlying cause Give thromboprophylaxis

33 TROUBLE SHOOTING Glucose not falling? Check IV lines, pumps and cannulas to ensure infusion is running and at the correct rate.

34 FURTHER READING

35 SUMMARY Developed and described a system for blood gas interpretation and recognised common patterns of acid-base abnormality. Described the pathophysiology of diabetic ketoacidosis and hyperosmolar hyperglycaemic state. Learned how to implement initial management of DKA and HHS, noting the key differences in management.

36 QUESTIONS