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Diabetic ketoacidosis

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DKA

Text of Diabetic ketoacidosis

  • 1. Dr Summera Amir FCPS II UNIT II NICH

2. 12 years old male Ayaz weighing 32 kg resident of Thatta presented in E.R with complain of Fever 15 days abdominal pain 1 week Shortness of breath 1 day 3. Past History : Unremarkable Birth history :SVD at home no History of birth asphyxia or jaundice Vaccination : only polio drops taken Developmental Hx : Development appropriate to age achieved all mile stone acc to age Nutirional history : satisfactory Family Hx : 1st issue of consangious marriage 2sister and one brother All are alright and healthy Socio-Economic Hx : belong to poor class family father is labourar 4. Sick looking irritable child having VITALS: H/R : 98b/m R/R : 48b/m Temp :A/ f B.P 105/70mm 50th centile My patient is mildly anemic while there is no evidence of jaundice clubbing cyanosis There is no lymphadenopathy 5. Height = 134cm below 3rd centile SDS (-1.997) Weight = 32Kg below 3rd centile SDS (-1.067) 6. Systemic examination RESPIRATORY Chest :normal vesicular breathing with no added sounds. CVS : S1 + S2 Audible No added sound present Abdominal Examination Abdomen soft non tender . distended no visible vein No viseromegaly 7. CNS Examination : irritable child with Tone .Normal in All limbs Power : 5/5 in four limbs Reflex's : normal in all four Planter: down going Cranial nerve. Intact Back examination: normal Sensory system :intact 8. Diabetic ketoacidosis sec to IDDM Chronic kideny disease 9. CBC : Hb : 8.1 TLC : 10000 N : 60 E : 04 M :03 L : 40 Plt : 376000 10. Na 152meq/l K 5.3meq/l Cl 108meq/l Serum Calcium 9.3mmol/l Serum creatinine 1.1mg/dl 11. PH 7.2 Pco2 20 Po2 124 Hco3 10mmol/l 12. Urinary ketones 150mg/dl Hb A1c waiting 13. DKA(diabetic ketoacidosis) sec to IDDM (insulin dependent diabetes mellitus) 14. Diabetic ketoacidosis 15. DKA is a serious acute complications of Diabetes Mellitus. It carries significant risk of death and/or morbidity especially with delayed treatment. The prognosis of DKA is worse in the extremes of age, with a mortality rates of 5-10%. With the new advances of therapy, DKA mortality decreases to > 2%. Before discovery and use of Insulin (1922) the mortality was 100%. 16. You should suspect DKA if a diabetic patient presents with: Dehydration. Acidotic (Kussmauls) breathing, with a fruity smell (acetone). Abdominal pain &or distension. Vomiting. An altered mental status ranging from disorientation to coma. 17. To diagnose DKA, the following criteria must be fulfilled : 1. Hyperglycemia: of > 250 mg/dl & glucosuria 2. Ketonemia and ketonuria 3. Metabolic acidosis: pH < 7.25, serum bicarbonate < 15 mmol/l This is usually accompanied with severe dehydration and electrolyte imbalance. 18. The management steps of DKA includes: Assessment of causes & sequele of DKA by taking a short history & performing a scan examination. Quick diagnosis of DKA at the ER. Baseline investigations. Treatment, Monitoring & avoiding complications. Transition to outpatient management. 19. History: Symptoms of hyperglycemia, precipitating factors , diet and insulin dose. Examination: Look for signs of dehydration, acidosis, and electrolytes imbalance, including shock, hypotension, acidotic breathing, CNS statusetc. Look for signs of hidden infections (Fever strongly suggests infection) and If possible, obtain accurate weight before starting treatment. 20. The initial Lab evaluation includes: Plasma & urine levels of glucose & ketones. ABG, U&E (including Na, K, Ca, Mg, Cl, PO4, HCO3), & arterial pH Venous pH is as accurate as arterial (an error of 0.025 less than arterial pH) Complete Blood Count with differential. Further tests e.g., cultures, X-raysetc , are done when needed. 21. High WCC: may be seen in the absence of infections. BUN: may be elevated with prerenal azotemia secondary to dehydration. Creatinine: some assays may cross-react with ketone bodies, so it may not reflect true renal function. Serum Amylase: is often raised, & when there is abdominal pain, a diagnosis of pancreatitis may mistakenly be made. 22. Principles of Treatment: Careful replacement of fluid deficits. Correction of acidosis & hyperglycemia via Insulin administration. Correction of electrolytes imbalance. Treatment of underlying cause. Monitoring for complications of treatment. Manage DKA in the PICU. If not available it can be managed in the special care room of the pediatric inpatient ward. 23. Determine hydration status: Hypovolemic shock: administer 0.9% saline, Ringers lactate or a plasma expander as a bolus dose of 20-30 ml/kg. This can be repeated if the state of shock persists. Once the patient is out of shock, you go to the 2nd step of management. 24. B- Dehydration without shock: Administer 0.9% Saline 10 ml/kg/hour for an initial hour, to restore blood volume and renal perfusion. The remaining deficit should be added to the maintenance, & the total being replaced over 36-48 hours. To avoid rapid shifts in serum osmolality 0.9% Saline can be used for the initial 4-6 hours, followed by 0.45% saline. 25. When serum glucose reaches 250mg/dl change fluid to 5% dextrose with 0.45 saline, at a rate that allow complete restoration in 48 hours, & to maintain glucose at 150-250mg/dl. Pediatric saline 0.18% Na Cl should not be used even in young children. 26. Continue the Insulin infusion until acidosis is cleared: pH > 7.3. Bicarbonate > 15 mmol/l Serum sodium 135-145 27. If no adequate settings (i.e. no infusion or syringe pumps & no ICU care which is the usual situation in many developing countries) Give regular Insulin 0.1 U/kg/hour IM till acidosis disappears and blood glucose drops to 2.5 and monitor K conc. hourly. If serum potassium is 6 or more, do not give potassium till you check renal function and patients passes adequate urine. 30. A flow chart must be used to monitor fluid balance & Lab measures. serum glucose must be measured hourly. electrolytes also 2-3 hourly. Ca, Mg, & phosphate must be measured initially & at least once during therapy. Neurological & mental state must examined frequently, & any complaints of headache or deterioration of mental status should prompt rapid evaluation for possible cerebral edema. 31. Cerebral Edema Intracranial thrombosis or infarction. Acute tubular necrosis. peripheral edema.