Date post: | 12-Apr-2017 |
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DIABETIC KETOACIDOSIS
DR RAVIKUMAR 1ST YEAR PGPEDIATRICS
MGMCRI
TABLE OF CONTENTS
• DEFINITION
• CLINICAL SIGNS
• RISK FACTORS
• PATHOPHYSIOLOGY
• MANAGEMENT
• COMPLICATIONS OF THERAPY
• DDX
DEFINITION
THE BIOCHEMICAL CRITERIA FOR THE DIAGNOSIS OF DKA ARE • Hyperglycemia [BG >11 mmol/L (≈200 mg/dL)]• Venous Ph<7.3 Or Bicarbonate <15 mmol/L• Ketonemia And Ketonuria.
THE SEVERITY OF DKA IS CATEGORIZED BY THE DEGREE OF ACIDOSIS :• Mild: Venous Ph<7.3 Or Bicarbonate <15 mmol/L• Moderate: Ph<7.2, Bicarbonate <10 mmol/L• Severe: Ph<7.1, Bicarbonate <5 mmol/L.
CLINICAL SIGNS• Dehydration (Which May Be Difficult
To Detect)• Tachycardia• Tachypnea (Which May Be Mistaken
For Pneumonia Or Asthma)• Deep, Sighing (Kussmaul)
Respiration; Breath Has The• Smell Of Acetone (Variously
Described As The Odor Of Nail Polish Remover Or Rotten Fruit)
• Nausea, Vomiting (Which May Be Mistaken For Gastroenteritis)
• Abdominal Pain That May Mimic An Acute Abdominal Condition
• Confusion, Drowsiness, Progressive Reduction In Level Of Consciousness And, Eventually, Loss Of Consciousness.
CLINICAL MANIFESTATION
RISK FACTORS
In Newly Diagnosed Cases :• Children <2 Years Of Age• Delayed Diagnosis• Low Socio-economic Status• Countries With Low Prevalence Of
Type 1 DM
In Patients With Known Diabetes • Insulin Omission • Poor Metabolic Control• Previous Episode Of DKA• Psychiatric Disorders• Failures In Pump Therapy
PATHOPHYSIOLOGY
MANAGEMENTEMERGENCY ASSESSMENT• Immediate Measurement Of BG, Blood Or Urine Ketones, Serum Electrolytes,
Blood Gases And Full Blood Count; • Assessment Of Severity Of Dehydration And Level Of Consciousness• A Second Peripheral IV Catheter Should Be InsertedMETICULOUS MONITORING OF • Hourly Heart Rate, Respiratory Rate, Blood Pressure, Spo2, Fluid Input/Output,
GCS Or AVPU Scale.• Monitor For Warning SignsINVESTIGATION • Hourly CBG (BSL)• VBG, Sr. Electrolytes Q2H for first 12hrs and then as required
MANAGEMENTSTEPS 1. Intravenous Rehydration2. Acidosis & Bicarbonate Therapy3. Potassium Replacement4. Insulin Infusion5. Sodium Replacement6. Treat Precipitating Infection, If Present7. Oral Fluids8. Stop Of Insulin Infusion
MANAGEMENTFLUIDS & SALT REPLACEMENT• Initial Fluid :Severely Volume Depleted But Not In Shock, Volume Expansion (Resuscitation) Should Begin Immediately With 0.9% Saline 10-20 ml/kg over 1 hour To Restore The Peripheral Circulation.
• Subsequent Fluid : IVF 0.9 % NS for Atleast 4-6 hours , Later to 0.45% NS with KCL48 Hrs Maintenance + Deficit – Bolus (Resuscitation Fluid Already Given) Divided By 48• Corrected Sodium levels Rises as BGL fall during Treatment, if not then continue
0.9% NS Measured Na + 2 {(plasma glucose – 100) divided by 100} mg/dL
INSULIN THERAPY• Begin with Regular Insulin 0.05–0.1 U/kg/h 1–2 h after starting fluid
replacement therapy• Preparation : Dilute 50 U of Regular Insulin in 50 ml of NS (1Unit = 1ml)• Titration :Accepted fall in BSL of 100mg/dl/hr Adjust Insulin Infusion rate or Dextrose infusion rate to keep BSL between 100 to 200 mg/dlIf BSL < 100mg/dl - Increase Insulin Infusion rate by 50%If BSL >100mg/dl - Decrease Insulin Infusion rate by 50%• If BSL <300mg/dl change IVF to 0.45% NS or 5% DNS
ISPAD (2014) ALGORITHM
ISPAD (2014) ALGORITHM
COMPLICATIONS OF THERAPY1. CEREBRAL EDEMA• Clinically Significant Cerebral Edema Usually Develops within The First 12 Hr
After Treatment Has Started, But Can Occur Before Treatment Has Begun. Rarely, May Develop As Late As 24–48 Hrs After The Start Of Treatment
SIGNS AND SYMPTOMS INCLUDE:• Headache And Slowing Of Heart Rate• Change In Neurological Status (Restlessness, Irritability, Increased
Drowsiness, And Incontinence)• Specific Neurological Signs (E.G., Cranial Nerve Palsies, Papilledema)• Rising Blood Pressure• Decreased O2 Saturation
COMPLICATIONS OF THERAPYTREATEMENT OF CEREBRAL EDEMA• Reduce The Rate Of Fluid Administration By One-third.• Give Mannitol, 0.5–1 g/Kg IV Over 10–15 Min, And Repeat If There Is No Initial
Response In 30 Min To 2 H• Hypertonic Saline (3%), Suggested Dose 2.5–5 ml/Kg Over 10–15 Min, May Be
Used As An Alternative To Mannitol, Especially If There Is No Initial Response To Mannitol
Other:2. INADEQUATE REHYDRATION3. HYPOGLYCEMIA4. HYPOKALEMIA5. HYPERCHLOREMIC ACIDOSIS
DDXHYPERGLYCAEMIC HYPEROSMOLAR STATE (HHS)
MANAGEMENTGOALS OF THERAPY• Correct Dehydration,• Correct Acidosis And Reverse Ketosis, • Slowly Correct Hyper osmolality And Restore BG To Near Normal,• Monitor For Complications Of DKA And Its Treatment,• Identify And Treat Any Precipitating Event.