Hyperglycemic hyperosmolar state due to DM type 2

Diabetes Mellitus complications

1. SEMINAR PRESENTATION BY Dr. A KHABUE S Y L VESTER O SEMUDIAMEN

2. HYPERGLYSEMIC HYPEROSMOLAR SYNDROME

3. INTRODUCTION/DEFINITION ETIOLOGY /RISK FACTORS PATHOPHYSIOLOGY CLINICAL FEATURES DIAGNOSTIC CRITERIA MANAGEMENT COMPLICATION DIFFERENTIAL DIAGNOSIS CONCLUSION

4. HYPERGLYSEMIC HYPEROSMOLAR SYNDROME It is also known as hyperosmolar hyperglycemic non ketotic syndrome It is a life threatening metabolic emergency, a complication of diabetes mellitus in which the high blood glucose results in high osmolarity without significant ketoacidosis. It is characterized by hyperglycemia, hyperosmolarity without ketoacidosis.it is mainly found on type 2 DM patient, unlike DKA which is characterized by hyperglycemia , ketosis and acidosis. These two are not mutually exclusive but rather two conditions that both result from some degree of insulin deficiency. They can and often do occur simultaneously. There are other complications of DM which are usually of chronic types e.g CAD, CVA, retinopathy, glaucoma , cataract, periodontal diseases.

5. AETIOLOGY/RISK FACTORS Relative insulin deficiency and inadequate fluid intake Type 2 DM patient Old age Acute infection (pneumonia ,UTI, Cellulitis, sepsis) CVA MI Undiagnosed DM with/ without access to medical care Drugs ( Thiazide , Steroids, Antiarrhythmics , Antiepileptic Atypical antipsychotic (Clozapine , Risperidone ), Antihypertensive ( CCB,Diuretics ) Comorbid illness such as acute pancreatitis, severe burn, injury, substance abuse,( alcohol or cocaine use)

6. PATHOPHYSIOLOGY In DKA there is relative on absolute insulin deficiency accompanied by counter regulatory hormones excess (glycogen , cortisol, growth hormones and epinephrine which lead to enhanced hepatic gluconeogenesis, glycogenolysis and lipolysis . Hepatic gluconeogenesis and glycogenolysis result in severe hyperglycemia while lipolysis result in increased serum free fatty acid FFA and metabolized into ketones and ketoacid found in blood & urine. However in HHS the insulin deficiency is not severe enough to stimulate hepatic ketogenesis thus ketosis is absent or minimal in HHS Hyperosmolarity result from intravascular volume depletion due to hyperglycemia induced osmotic diuresis, worsened by inadequate fluid intake.

7. DEHYDRATION AND HYPEROSMOLARITY Hyperglysemia Glycosuria Osmotic Diuresis Increased GFR   Dehydration Hypovolemia   Hyperosmolarity Decreased GFR & renal glucose loss &Hyperglycemia

8. CLINICAL FEATURES 3p- polyuria,polydipsia & polyphagia Profound dehydration Weakness Altered metal status (confusion , lethergy , coma) Nausea, vomiting and abdominal pain Weight loss Neurologic signs including blurred vision, headache, focal seizure, myoclonic jerking, reversible paralysis Low blood pressure while standing

9. DIAGNOSTIC CRITERIA Plasma glucose level> 30mmol/L (>600mg/dl) Serum osmolarity > 320mosm/kg serum pH > 7.3 Bicarbonate concentration >15mEq/L Small ketonuria (on dipstick) and absent to low ketonemia (<3mmol/L) Small alteration in consciousness Creatinine >1.5mg/dl Blood urea nitrogen (BUN)>30mg/dl

10. MANAGEMENT History taking physical examination investigation Treatment

11. HISTORY History of previous diabetic status Family history of diabetes Drug use Co- morbidities‘ like hypertension, severe burn Acute infection History of excessive urination, drinking or eating Weight loss, blurred vision Weakness.

12. PHYSICAL EXAMINATION 1. Assessment of vital signs Tachycardia-hypotension – Tachypnoea –hypertension/hypotension 2. Evaluation of DM presence of fingerpricks Ecchymosis on Abdomen, thigh and arm obesity Acanthosis Nigricans Diabetic Dermopathy Tooth Decay Retinopathy

13. 3. Absence of Dehydration Every 1L of body fluid loss, there is 1kg of weight loss Skin Tugor Dryness of Skin Dry Sticky mouth Lethargy

14. INVESTIGATION It involves the diagnostic criteria as listed above

15. TREATMENT The treatment goal Involves 1.Fluid replacement to correct dehydration 2.To correct Hypoglycemia by Insulin 3.Correction of Electrolyte 4. Treat underlying precipipant

16. FLUID REPLACEMENT Rehydrate with 0.9% saline I.V Typical fluid deficit is 110-220ml/Kg. An average regimen would be 1L fast, then 1L in 30mins, then 1L in 1hr, then 1L in 2hrs, then 1L in 4hrs and 1L in 6hrs

17. CORRECTION OF HYPOGLYCEMIA BY INSULIN Insulin should be considered only if blood glucose is not falling by 5mmol/L with rehydration or if there is ketosis. Start slowly 0.15unit/kg/hr(usually 10unit ) then followed by 0.1unit/kg/hr(usually 5-7unit/hr) .If fall is still slow. Target is blood glucose <250mg/dl

18. CORRECTION OF ELECTROLYTE Mild to moderate hyperkalaemia is not uncommon in HHS Insulin therapy and volume expansion decreases the potassium concentration, hence potassium replacement is needed. Once renal function is assured potassium may be given to prevent hyperkalemia.

19. Serum potassium (mmol/L) KCL to add/L of IV fluid >5.5 Nil 3.5-5.5 10-20mmo/L <3.5 20-40mmol/L

20. TREATMENT OF UNDERLYING PRECIPITANT Identify and treating u nderlying precipitant Broad spectrum antibiotics such as amoxicillin(CO-AMOXICLAV),Quinolones e.g Levofloxacin ,Cephalosporin e.g ceftriaxone

21. COMPLICATION Cerebral Oedema Aspiration pneumonia Vascular complication Hypoglycemia Hypokalemia Hypomagnesemia Hypophospatemia Hypotension

22. DIFFERENTIAL DIAGNOSIS Diabetes Insipidus Diabetes ketoacidosis Myocardial infarction Pulmonary Embolism

23. PREVENTION IS BETTER THAN CURE Many cases of HHS can be prevented by better access to medical care, proper education and effective communication with the health care provider during the inter-current illness.

24. THANK YOU