NRSG265 Endocrine Disorders Complications of DM PDF

Endocrine Disorders NRSG265 Part 1b PRINCIPLES OF NURSING – Week 1 MEDICAL National Lecture Session Objectives At the end of this session and with further reading, you should be able to: Explain the complications that can occur in dia...

Endocrine Disorders NRSG265 Part 1b PRINCIPLES OF NURSING – Week 1 MEDICAL National Lecture Session Objectives At the end of this session and with further reading, you should be able to: Explain the complications that can occur in diabetes, including hypoglycaemia, DKA and HHS Describe the management of the above complications 2 |  Acute Complications of Diabetes Mellitus 3 | Acute Complications of Diabetes Mellitus Acute Complications of DM Hypoglycaemia Hyperglycaemia in very unwell patients Diabetic ketoacidosis Type 1 DM (DKA) Hyperosmolar hyperglycaemic Type 2 DM state/syndrome (HHS) Complications of Type 1 and 2 DM 1. Hypoglycaemia Defined as a BGL < 4mmol/L Can be FATAL In patients who have diabetes, at what time Causes: of day does a Medication overdose (OHA or insulin) hypoglycaemic state commonly occur? Not eating enough carbohydrates or skipping meals Excess alcohol consumption Excessive exercise Malnutrition 5 | Hypoglycaemia – clinical manifestations Early signs and symptoms Later signs and symptoms BGL < 4 mmol/L Difficulty concentrating Trembling Vision changes Sweating Anxiety Pale Seizures Skin – cool, pale & Altered conscious state/ clammy unconscious Hunger Coma Headache Death Dizziness https://www.today.com/health/what-hypoglycemia-diabetes-risk-too-low-blood-sugar-t162055 6 | Hypoglycaemia – management Mild hypoglycaemia 1. Check BGL < 4 mmol/L Fast acting CHO: Slow acting CHO: Glass of orange juice (150mls) 1 slice of Bread 2. Eat 15-20 grams of fast acting carbohydrates ½ can of fizzy soda (non diet Half a bowl of cereal (eg version) cornflakes) 3. Recheck BGL >4 mmol/L 6 -7 jelly beans Glass of milk (150mls) 4. Followed by 20 grams of ½ can of sugar soft drink 1 medium sized piece of fruit slow acting (eg apple, pear) carbohydrates 3 teaspoons of sugar/honey 1 pot of sugar-sweetened yoghurt 7 | Hypoglycemia – management Severe hypoglycaemia If the person is unconscious, drowsy or not able to swallow, do not give them anything to eat or drink Medical emergency! 1. Call for help 2. Position patient on their side, ensuring airway is clear – WHY? 3. IV dextrose bolus 4. If no IV access, administer IM glucagon (can cause vomiting) then IV dextrose as soon as possible 5. Once patient is stabilised and able to eat and drink, follow up with 20 grams of slow acting carbohydrates 8 | Complications of Type 1 and 2 DM 2. Hyperglycaemia Stress Impaired insulin Acutely unwell Hyperglycaemia Mechanism function Inflammatory Cortisol Increased process Glycogen glycogenolysis Noradrenaline 9 |  Complications of Type 1 DM 1. Diabetic Ketoacidosis Very serious medical condition related to hyperglycaemia, which gradually develops over hours – days Due to lack of insulin leading to glucose build up in the blood Risk factors: 1. New diagnosis 2. Acute stress or illness 3. Omission of insulin 4. Lack of access to medical care More common in Type 1 than Type 2 DM – why? 30 | DKA – clinical manifestations Laboratory markers: Later signs and symptoms: Sunken eyes BGL > 11mmol/L Tachycardia Ketones present in blood and urine Dry skin pH 30mmol/L Tachycardia Ketones can be present/absent Hypotension pH > 7.3, HCO3- >15mmol/L Dry skin K+ and Na+ changes Headache High serum osmolality Weakness Cramps Earlier signs and symptoms: Fatigue and lethargy Abdominal pain, N+V Polyuria + Seizures Polydipsia + Altered LOC Coma 15 | HHS – management 1. Correction of dehydration (slowly): Prevention of complications IVF – 24-72 hours NBM 2. Reverse hyperglycaemia (target 10- Strict bed rest 15mmol/L): Strict FBC With IVF Insulin infusion commenced if BGL does not reduce Cardiac monitoring Dextrose infusion with/without KCl Treat underlying cause 3. Acid-base and electrolyte corrections: Regular 1/24 BGLs and 1-4/24 ABGs Reintroduction of fluids and SC insulin once DKA resolved and significant clinical Urine ketones improvement Close monitoring of U&Es (Na+ and K+) 16 | References Brown, D., Edwards, H., Seaton, L., & Buckley, T. (2015). Lewis’s medical-surgical nursing. Assessment and management of clinical problems (4th ed.). Mosby/Elsevier Australia. Bullock, S. & Hales, M. (2019). Principles of Pathophysiology (2nd ed.). Pearson Australia. Cohen, M., Shilo, S., Zuckerman-Levin, N. & Shehadeh, N. (2015). Diabetic Ketoacidosis in the Pediatric Population with Type 1 Diabetes, Major Topics in Type 1 Diabetes. Kenia Pedrosa Nunes: IntechOpen. DOI: 10.5772/60592. Retrieved from https://www.intechopen.com/books/major-topics- in-type-1-diabetes/diabetic-ketoacidosis-in-the-pediatric-population-with-type-1-diabetes Copestead, L.C. & Banasik, J.L. (2018). Pathophysiology (6th ed.). US: Elsevier. EKF Diagnostics. (2019). What is Diabetic Ketoacidosis (DKA)? [Image]. Retrieved from https://www.ekfusa.com/bhb/ Sainsbury, E., Shi, Y., Flack, J. & Colagiuri, S. (2018). Burden of diabetes in Australia: It’s time for more action. Preliminary report. Retrieved from http://www.novonordisk.com.au/content/dam/australia/affiliate/www-novonordisk- au/Home/Documents/180712_Burden%20of%20Diabetes_Its%20Time%20for%20More%20Action %20Report_Digital_%20FINAL....pdf.