hecs 2063 care of the critically ill adult diabetes emergencies n.
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HECS 2063 Care of the Critically Ill Adult: Diabetes Emergencies

HECS 2063 Care of the Critically Ill Adult: Diabetes Emergencies

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HECS 2063 Care of the Critically Ill Adult: Diabetes Emergencies

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  1. HECS 2063 Care of the Critically Ill Adult:Diabetes Emergencies Paula Holt Lecturer School of Healthcare University of Leeds

  2. Key Questions • What is the normal pathophysiology of blood glucose control? • What is hypo and hyperglycaemia and what causes them? • What would make us suspect someone is experiencing abnormal blood glucose levels? • How is hypo and hyperglycaemia treated? • What factors would we consider when carrying out a comprehensive assessment of a person having a hypo or hyperglycaemic episode?

  3. The Pancreas

  4. Islets of Langerhans

  5.  cells cells F cells Delta cells

  6. Insulin Insulin release may be triggered by: • increased plasma glucose concentrations • Increased amino acid concentrations • Increased parasympathetic input

  7. Insulin Degradation • Has a plasma half life of 4 - 5 minutes and is mainly cleared from the circulation in 10 – 15 minutes. • Enzyme ‘insulase’ secreted by the liver removes 60% of circulating insulin. • Kidney removes the remaining 35 – 40%. • In insulin treated patients this ratio is reversed with as much as 60% of exogenous insulin being cleared by the kidney.

  8. Hypoglycaemia - Definition • The presence of symptoms associated with subnormal blood glucose levels, but there is no general agreement about which level of glucose defines hypoglycaemia. • It is usually defined as a blood glucose level of <3.0 mmol/l in patients with diabetes treated with insulin or oral hypoglycaemic agents. • However at low blood glucose levels blood glucose strips may be difficult to read accurately therefore Diabetes UK advises that: ‘FOUR IS THE FLOOR’

  9. HYPOGLYCAEMIA • One in three patients (30%) will experience a hypoglycaemic coma during their diabetic lifetime of whom; • One in three (10%) will have experienced a hypoglycaemic coma in the last year of whom; • One in three (2-3%) will have recurrent severe hypoglycaemia which disrupts their lives.

  10. HYPOGLYCAEMIA Hypothalmic glucose sensor Anterior Pituitary Sympathetic nervous system ACTH Islet alpha cells Cortisol Glucagon Growth Hormone Adrenaline Hepatic glucose release • Glucose from amino acids • Glycogen broken down to glucose  Blood glucose concentrations

  11. Causes • Excessive doses of insulin • Delayed or missed meals • Exercise • Alcohol • Injection sites • Skin temperature • Lipohypertrophy • Inadvertent intramuscular injection

  12. Sympathetic -  blood glucose levels: Weakness Trembling Sweating Tachycardia Palpitations Tremor Nervousness Irritability Tingling of mouth and fingers Hunger Neuroglucopenic -  activity of the CNS Headache Hypothermia Visual disturbances Mental dullness Confusion Amnesia Seizures Coma (Nausea and vomiting may occur but are unusual). Signs and Symptoms - Hypoglycaemia

  13. Hyperglycaemia - Definition • Refers to an elevated blood glucose level (>10mmol/l) due to a relative or absolute insulin deficiency. • The symptoms of hyperglycaemia usually occur when the blood glucose is persistently above 15 mmol/l. • Affected by renal threshold

  14. HYPERGLYCAEMIA – Diabetic Ketoacidosis (DKA) • Largest single cause of death in patients with diabetes under the age of 40 years. • Glucose is unable to enter the cells and accumulates in the blood. • Insulin deficiency leads to the metabolism of fats with the formation of free fatty acids and subsequently ketones. • In severe insulin deficiency, glucagon stimulates the liver to produce more glucose which worsens the hyperglycaemia.

  15. CAUSES • Lack of insulin • Lack of oral antidiabetes medication or failure to respond to it • Too much food • Too little exercise • Infection • Emotional stress • Drugs – thiazide diuretics, tricyclic antidepressants • Myocardial infarction

  16. DKA – Signs and Symptoms • Lab results Blood glucose >15mmol/l pH <7.3 {normal 7.35 – 7.45} • Thirst • Polyuria • Fatigue • Weight loss • Leg cramps • Abdominal pain • Nausea and vomiting • Tachycardia • Hyperventilation • Ketosis (acetone on the breath)

  17. As the condition develops: • Warm, dry skin • Circulatory failure due to reduction in blood volume due to polyuria. Leads to: • Hypotension • Decreased renal output • Bradycardia • Decreased respirations as an attempt by the body to correct the raised pH by lowering the amount of carbon dioxide in the blood. (Kussmaul [deep sighing] breathing) • Hypothermia Hypoxia and decreased conscious state • Coma – due to cellular dehydration

  18. Treatment • To correct the fluid and electrolyte disturbances • To correct the low intracellular and reduce extracellular levels of glucose • To reduce the blood pH

  19. Fluid and Electrolyte Disturbances • IV normal saline 0.9% infusion. Change to 5% dextrose when blood glucose <15 mmol/l. • Potassium replacement is vital according to patients serum potassium levels. • Sodium levels not as problematic and tend to normalise following correction of dehydration and hyperglycaemia.

  20. Correct low intracellular and reduce extracellular levels of glucose • If blood glucose > 15mmol/l give 10 – 20u of clear, short-acting insulin IV (actrapid). • Commence IV sliding scale insulin. Usually 6 – 10u/hr (50u actrapid/50mls normal saline). • Continue until eating and drinking.

  21. Reduce the blood pH • Administration of insulin is usually sufficient. • Bicarbonate administration is controversial and is not usually given unless the blood pH is < 7.0 or cardiorespiratory collapse seems imminent.

  22. Patient Assessment • How acutely ill is the patient? • What signs and symptoms does the patient have? • What is the patients past medical history • Does the patient have any significant family history? • What do the patients vital signs and blood results tell us?

  23. Patient Assessment – cont./d • What are the possible causes of this condition? • What is the best way to treat this patient in the initial/immediate phase? • What is the long term aim of care? • Can this condition be prevented from getting worse/happening again? If so, how?

  24. Any Questions? Thank you for listening and good luck with the case study!