A typical presentation of Diabetic Ketoacidosis, its pathophysiology, management and treatment.
- 1. Case PresentationUzair Ahmed
2. Chief Complaints20 years old female, known case of Type IDiabetes Mellitus, came to OPD on 06-06-14with complaints of Abdominal pain for 1 day Nausea and Vomiting 1 day Productive Cough for 1 week No history of fever 3. History of Presenting Complaints According to attendant, the patient was alright 1 day backwhen she suddenly developed abdominal pain, nausea andvomiting. She also complained of cough with sputum which was yellowin color. Sputum did not contain any blood and it was not foulsmelling. Cough was mild in intensity, no specific time ofoccurrence, no aggravating or relieving factors. It was notassociated with chest pain, shortness of breath or fever. 4. Systemic Review Respiratory System: hx of productive cough with small amount ofyellow sputum. CVS: no breathlessness, palpitation or chest pain. GIT: Nausea and vomiting. Abdominal pain.No heart burn, diarrhea, constipation, hematemesis or melenapresent . CNS: Drowsiness. GENITO-URINARY: Polyuria but no hx of burning micturition orincontinence was present. MUSCULO-SKELETAL: Normal 5. PAST MEDICAL HISTORY: She was diagnosed as Type I DM at age of 9years. Since then she had been on a regimen of Regular and NPH insulin.She had history of multiple hospital admission with very similar complaints.Past Surgical History : Nothing significantDrug History: Insulin R+N8+6 in Morning6+4 in EveningPERSONAL HISTORY: decreased appetite, decreased sleep, normal bowelhabits. No addiction. Increased Micturition.FAMILY HISTORY: Nothing significantSOCIO-ECONOMIC HISTORY: Poor. 6. Examination Young healthy female of average built and height lyingcomfortably on bed, oriented to time place and person. VitalsGCS 15/15B.P. 90/60Pulse 100bpmTemp A/FR/R 24 On Examination there was no evidence of anemia, jaundice ,clubbing or edema. Mild to moderate dehydration was present. No Palpable lymph nodes. 7. Systemic Examination Abdominal Exam :Mild Tenderness at Epigastric and Left Hypochondriacregion. No visceromegaly. CNS Examination : Intact Respiratory System:Chest was clear with NVB.R/R was increased. CVS: S1+S2+0 8. Case Summary 20 years old female, k/c of Type I DM, compliant toinsulin, comes to Emergency with complaints of nausea,vomiting and abdominal pain for 1 day. She hasdecreased appetite, increased thirst and polyuria. Hervitals shows that she has hypotension along withtachycardia and increased Respiratory Rate. O/E she is dehdyrated, and there is tenderness inepigastric and left hypochondriac region. Rest of theexamination is unremarkable. There is also prior hx of hospital admissions withsimilar complaints. 9. Differential Diagnosis? Diabetic Ketoacidosis Acute Pancreatitis Acute Appendicitis Lactic Acidosis Metabolic Acidosis Myocardial Infarction 10. Investigations (06-06-14) RBS: 465 mg/dl Serum Ketones: +++ABGs: pH: 7.2 HCO3: 4 PaCO2: 11 PaO2: 140 SaO2: 99LFTs: SGPT: 31 Al.Phos: 194 BUN: 16 Cre: 1.0 Na:132 K:4.9 Cl: 94Anion gap [Na+K]-[HCo3+Cl] [132+4.9]-[4+94] 38.9CBC: Hb: 13.1 TLC: 13600 MCV: 82.1 HCt: 37.8 Platelets: 270000 11. Investigations(contd.)Urine D/R: Amorphous urates : + Ketone bodies: ++ Pus cells: 4-6 pH: 6.0 Spec. Gravity: 1.010 Glucose: ++ Yeast cells: +++ Urobilin: -ve 12. Investigations(contd.) CXR PA view was done which was found to benormal. ECG was performed, which was also normal. U/S whole abdomen was done which showedhypoechoic liver while the rest of abdomen wasnormal. 13. Requirement toconfirm DKA Our FindingsHyperglycemia(RBS=465 mg/dl)Blood pH=7.2Serum Bicarbonate = 4Serum Ketones +++DKA Confirmed! 14. Treatment given: Inf. N/S to replace the ECF fluid loss. Inf. 5% dextrose to replace ICF fluid loss. Insulin was administered continuously through infusionpump initially @5units/ hour and then at 3units/hour . Potassium was replaced. Injection Ceftriaxone was given to cover up infection ifthere were any. Inj. Gravinate was given to treat nausea and vomiting. RBS , BP & TPR was recorded hourly along with strictI/O charting. Patient clinically improved with the given treatment andwas discharged on her 6th day of admission. 15. Hospital CourseAt time of Admission At time of DischargeABGs pH: 7.2 HCO3: 4 PaCO2: 11 PaO2: 140 SaO2: 99UCE BUN: 16 Cre: 1.0 Na:132 K:4.9 Cl: 94Anion Gap 38.9SerumKetones+++UrinaryKetones+++ABGs pH: 7.44 HCO3: 23.9 PaCO2: 32 PaO2: 171 SaO2: 99.6UCE BUN: 3 Cre: 0.4 Na:137 K:3.9 Cl: 105Anion Gap 12Serum-KetonesUrinayKetones- 16. Topic Discussion 17. Diabetic Ketoacidosis Definition Etiology and Epidemiology Pathogenesis Diagnosis-clinical assessment- lab investigations-Essentials for diagnosis Treatment 18. Definition: Diabetic ketoacidosis (DKA) is an acute, major, life-threateningcomplication of diabetes. DKA mainly occursin patients with type 1 diabetes, but it is also notuncommon in some patients with type 2 diabetes. Also It can be the very initial presentation of thepreviously undiagnosed patients with Type I DM. This condition is a complex disordered metabolic statecharacterized by hyperglycemia, ketoacidosis, andketonuria. 19. Etiology The most common scenarios for diabetic ketoacidosis (DKA) areunderlying or concomitant infection (40%), missed insulintreatments (25%), and newly diagnosed, previously unknowndiabetes (15%). Other associated causes make up roughly 20% in thevarious scenarios. 20. Causes of DKA in type 1 diabetes mellitus In 25% of patients, DKA ispresent at diagnosis of type 1diabetes due to acute insulindeficiency. Poor compliance with insulin Bacterial infection andintercurrent illness (eg,urinary tract infection [UTI],vomiting) Medical, surgical, or emotionalstress Idiopathic In type II diabetes mellitus Intercurrent illness (eg,myocardial infarction,pneumonia, prostatitis, UTI) Medication (eg, corticosteroids,pentamidine, clozapine) 21. Epidemiology DKA accounts for 50% of diabetes-related admissions inyoung persons and 1-2% of all primary diabetes-relatedadmissions. The incidence of DKA is higher in whites because of the higherincidence of type 1 diabetes in this racial group. The incidence of diabetic ketoacidosis (DKA) is slightlygreater in females than in males for reasons that are unclear. Recurrent DKA frequently is seen in young women with type1 diabetes and is caused mostly by the omission of insulintreatment. Among persons with type 1 diabetes, DKA is much morecommon in young children and adolescents than it is inadults. DKA tends to occur in individuals younger than 19years, but it may occur in patients with diabetes at any age. 22. PathophysiologyInsulin is a peptide hormone, produced by beta cells in thepancreas, and is centralto regulating carbohydrate and fat metabolism in the body.Some of its physiological effects are- Decreases blood glucose concentration by1. increasing its uptake in the tissues2. increasing glycogenesis3. inhibiting gluconeogenesis and glycogenolysis- Increases uptake of aminoacid from blood into the cells and increases proteinsyntesis.- Decreases blood fatty acid and ketoacid formation by stimulating fats depositionin adipose tissue and inhibiting lipolysis.- Decreases blood K+ concentration by shifting then from ECF to ICF.Or in a nut shell, Insulin decreases concentration of glucose,FFAs, AAs and K+ levels in blood. 23. Diagnosis: Clinical Assessment:SymptomsPolyuria, thirstWeight lossWeaknessNausea, vomitingLeg crampsBlurred visionAbdominal painSigns DehydrationHypotension (postural or supine)Cold extremities/peripheral cyanosisTachycardiaAir hunger (Kussmaul breathing)Smell of acetoneHypothermiaConfusion, drowsiness, coma (10%) 24. Lab Findings:i. Hyperglycemia-Glucose ranges from 250-1000 mg/dl.ii. Dilutional hyponatremia-Glucose overrides sodium in controlling the osmoticgradient. Water shifts out of the intracellular fluidcompartment into the extracellular fluid compartment anddilutes the serum sodium.iii. Hyperkalemia- Transcellular shift as excess H+ions enter cells inexchange of potassium.iv. Increased anion gap metabolic acidosis.-Due to ketoacidosis and lactic acidosis.v. Prerenal azotemia-Due to volume depletion from osmotic diuresis whichdecreases cardiac output and renal blood flow. 25. Essentials for diagnosis 26. Workup:The following are important but should not delay the institution ofintravenous fluid and insulin replacement: Venous blood: for urea and electrolytes, glucose, bicarbonate. Arterial blood gases to assess the severity of acidosis. Urinalysis for ketones. ECG. Infection screen: full blood count, blood and urine culture, C-reactiveprotein, chest X-ray. Although leucocytosis invariablyoccurs, this represents a stress response and does not necessarilyindicate infection. 27. Management & Treatment:Diabetic ketoacidosis is a medical emergencywhich should be treated in hospital, preferably in ahigh-dependency area.The principal components oftreatment are: fluid replacement the administration of short-acting (soluble) insulin potassium replacement the administration of antibiotics if infection ispresent. 28. Fluid Replacement:0.9% saline (NaCl) i.v.1 L over 30 mins1 L over 1 hr1 L over 2 hrs1 L over next 2-4 hrsWhen blood glucose < 15 mmol/L (270 mg/dL)Switch to 5% dextrose, 1 L 8-hourlyIf still dehydrated, continue 0.9% saline and add 5%dextrose, 1 L per 12 hrsTypical requirement is 6 L in first 24 hrs but fluid overloadin elderly patients should be avoided.Subsequent fluid requirement should be based on clinicalresponse including urine output 29. Insulin: 50 U soluble insulin in 50 mL 0.9% saline i.v. viainfusion pump 6 U/hr initially 3 U/hr when blood glucose < 15 mmol/L (270 mg/dL) 2 U/hr if blood glucose < 10 mmol/L (180 mg/dL) Check blood glucose hourly initially; if no reductionin first hour, rate of insulin infusion should beincreased Aim for fall in blood glucose of 3-6 mmol/L(approximately 55-110 mg/dL) per hour 30. Potassium: None in first L of i.v fluid unles