Diabetic Ketoacidosis

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Presentation Transcript



What is Diabetic Ketoacidosis : 

What is Diabetic Ketoacidosis Diabetic ketoacidosis (DKA) is a state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis producing derangements in intermediary metabolism. DKA is a far more characteristic feature of type 1 than of type 2 diabetes but may be seen in persons with type 2 diabetes under conditions of stress.

Diagnostic Criteria : 

Diagnostic Criteria Blood glucose > 250 mg/dl pH < 7.35 HCO3 < 15 mEq/L Anion Gap > 12 Ketonemia

Causes : 

Causes The most common scenarios for diabetic ketoacidosis are- Underlying or concomitant infection (40%) – UTI is the most common. Missed insulin treatments (25%), Newly diagnosed, previously unknown diabetes (15%). Other associated causes (20%) Myocardial Infarction, Cerebrovascular accident, Acromegaly, Complicated pregnancy, Trauma, Stress, Surgery Heavy use of concentrated carbohydrate beverages such as sodas Dental abscess and sports drinks.

Pathophysiology Counter-Regulatory Hormones : 

Insulin Deficiency is the Primary defect. There is excess secretion of primarily glucagon as well as catecholamines, glucocorticoids, and growth hormone Stress hormones accelerate and exaggerate the rate and magnitude of metabolic decompensation Pathophysiology Counter-Regulatory Hormones Pathophysiology Hormone______ Impaired insulin secretion Epi Anti-insulin action Epi, cortisol, GH Promoting catabolism All Dec glucose utilization Epi, cortisol, GH

Pathophysiology : 

Pathophysiology Insulin Glucagon Epinephrine Cortisol Growth Hormone

Pathophysiology : 

Pathophysiology Decreased Glucose Utilization Insulin Glucagon Epinephrine Cortisol Growth Hormone

Pathophysiology : 

Pathophysiology Gluconeogenesis Glycogenolysis Lipolysis Ketogenesis Insulin Glucagon Epinephrine Cortisol Growth Hormone

Slide 9: 

Islets of Langerhans b-cell destruction Insulin Deficiency Adipo - cytes Muscle Liver Decreased Glucose Utilization & Increased Production Glucagon Increased Protein Catabolism Increased Ketogenesis Gluconeogenesis, Glycogenolysis IncreasedLipolysis Hyperglycemia Ketoacidosis HyperTG Polyuria Volume Depletion Ketonuria Amino Acids FattyAcids Stress Epi,Cortisol GH Threshold 180 mg/dl

DKA - Early : 

DKA - Early Relative Insulin Deficiency  Glycogenolysis & gluconeogenesis restrained Peripheral glucose uptake Elevates blood glucose Decreased Utilization  post- prandial and Stress-Induced hyperglycemia

DKA - Late : 

Insulin Deficiency Glycogenolysis Gluconeogenesis Hepatic glucose output Peripheral glucose uptake Elevates blood glucose Lipolysis Release FFA -> liver VLDL & ketones Ketonemia and hyperTG  Acidosis & Diuresis DKA - Late Increased Production & Decreased Utilization  Fasting hyperglycemia

“Typical” Case….. : 

“Typical” Case….. Location : Emergency Room Vital Signs : BP : 90/ 60 mm Hg, HR : 128/ min regular, Temp : 100F, RR: 30/min rapid and shallow C/C : Vomiting and Abdominal Pain HPI : A 20 yr old woman presents to ER with 5 episodes of vomiting, abdominal pain, weakness and increasing drowsiness of 1 day duration. During the last 2 months she has noticed increased thirst and increased urination. The abdominal pain is diffuse, 4-5/10 in severity, constant, non radiating and there are no aggravating or relieving factors. Vomiting is non bloody. She has a family history positive for type 1 diabetes.

“Typical” Case…..continue : 

“Typical” Case…..continue Lab Results – Urine Pregnancy test is negative WBC – 10,000 and normal differential Na – 129, K – 5, Cl – 90, Ca – 8 RBS – 600 Serum Amylase – mildly elevated Serum Lipase – WNL UA showed 4+ sugar, 2+ketones but no evidence of infection ABG showed metabolic acidosis compensated by respiratory alkalosis ( Ph 7.3)

Clinical Features - History : 

Clinical Features - History Classic symptoms of hyperglycemia Thirst Polyuria, polydipsia Nocturia Other symptoms Generalized weakness Malaise/lethargy, fatigue Nausea/vomiting Decreased perspiration Anorexia or increased appetite Confusion

Clinical Features - History : 

Clinical Features - History Symptoms of associated infections and conditions Fever Dysuria Chills Chest pain Abdominal pain Shortness of breath

Clinical Features – Physical Examination : 

Clinical Features – Physical Examination General signs Ill appearance Dry skin Labored respirations Dry mucous membranes Decreased skin turgor Decreased reflexes

Clinical Features – Physical Examination : 

Clinical Features – Physical Examination Vital signs Tachycardia Hypotension Tachypnea Hypothermia Fever, if infection Specific signs Ketotic breath (fruity, with acetone smell) Confusion Coma Abdominal tenderness

Differential Diagnosis : 

Differential Diagnosis Hyperosmolar Hyperglycemic Nonketotic Coma Alcoholic Ketoacidosis Abdominal Pathology like Appendicitis, Gastroenteritis, Pancreatitis, Acute Intestinal Obstruction Pregnancy Drug Intoxication

Work Up – Laboratory Studies : 

Work Up – Laboratory Studies Glucose: Sodium: The osmotic effect of hyperglycemia moves extravascular water to the intravascular space. For each 100 mg/dL of glucose over 100 mg/dL, the serum sodium level is lowered by approximately 1.6 mEq/L. When glucose levels fall, the serum sodium level rises by a corresponding amount. Potassium: This needs to be checked frequently, as values drop very rapidly with treatment. An ECG may be used to assess the cardiac effects of extremes in potassium levels.

Work Up – Laboratory Studies : 

Work Up – Laboratory Studies Bicarbonate: It is used in conjunction with the anion gap to assess degree of acidosis. Complete blood cell (CBC) count: High white blood cell (WBC) counts (>15 X 109/L) or marked left shift may suggest underlying infection. Arterial blood gas (ABG) levels: pH is often <7.3. Venous pH may be used for repeat pH measurement. It has been studied that pH on a venous blood gas level in patients with DKA was 0.03 lower than pH on an ABG. Because this difference is relatively reliable and not of clinical significance, there is almost no reason to perform the more painful ABG. End tidal CO2 has been reported as a way to assess acidosis as well.

Work Up – Laboratory Studies : 

Work Up – Laboratory Studies Ketones: The Acetest and Ketostix products measure blood and urine acetone and acetoacetic acid. They do not measure the more common ketone body, beta-hydroxybutyrate. Beta hydroxybutyrate: Serum or capillary beta hydroxybutyrate can be used to follow response to treatment. Levels greater than 0.5 mmol /L are considered abnormal, and levels of 3 mmol /L correlate with need for diabetic ketoacidosis (DKA) treatment.

Work Up – Laboratory Studies : 

Work Up – Laboratory Studies Urinalysis (UA): Look for glycosuria and urine ketosis. Use this to detect underlying urinary infection. Osmolality: Measured as 2(Na+) (mEq/L) + glucose (mg/dL)/18 + BUN(mg/dL)/2.8. Patients with diabetic ketoacidosis who are in a coma typically have osmolalities >330 mOsm/kg H2 O. If the osmolality is less than this in a patient who is comatose, search for another cause of obtundation. Phosphorous: If the patient is at risk for hypophosphatemia (e.g., poor nutritional status, chronic alcoholism), then the serum phosphorous level should be determined.

Work Up – Laboratory Studies : 

Work Up – Laboratory Studies Hyperamylasemia may be seen, even in the absence of pancreatitis. BUN level is increased. Anion gap is higher than normal.

Monitoring in Diabetic Ketoacidosis : 

Monitoring in Diabetic Ketoacidosis

Work Up – Imaging Studies : 

Work Up – Imaging Studies Chest radiography: To rule out pulmonary infection. CT scanning: The changes of cerebral edema may be seen late on head imaging and should not delay administration of hypertonic saline or mannitol in those pediatric cases where cerebral edema is suspected

Work Up – Other Tests : 

Work Up – Other Tests Electrocardiography (ECG): Diabetic ketoacidosis may be precipitated by a cardiac event, and the physiological disturbances of diabetic ketoacidosis may cause cardiac complications.  An ECG is also a rapid way to assess significant hypokalemia or hyperkalemia Telemetry: Consider telemetry in those with comorbidities (especially cardiac), known significant electrolyte abnormalities, severe dehydration, or profound acidosis

Cardinal Principles of management- : 

Cardinal Principles of management- Replace fluids Replace insulin Correct electrolytes Treat the cause Supportive treatment Prevent complications

Typical Therapy - Fluids : 

Typical Therapy - Fluids The Fluid of choice to correct dehydration is 0.9% NS IV Administer 1 liter over the first 30 minutes. Administer 1 liter over the following 1 hour. Administer 1 liter over the following 2 hours. Administer 1 liter every 4 hours, depending on the degree of dehydration and central venous pressure (CVP) readings.

Typical Therapy - Fluids : 

Typical Therapy - Fluids When the glucose levels begin to approach 270 mg/ dl Switch to 5 % dextrose, 1 litre 8 hourly. If the patient is still dehydrated, continue 0.9 % saline and add 5 % dextrose 1 litre per 12 hours. Typical requirement is 6 litres in first 24 hrs but avoid fluid overload in elderly patients. Subsequent fluid replacement should be based on clinical response including urine output.

Typical Therapy - Insulin : 

Typical Therapy - Insulin Initially an iv bolus of 10- 15 U insulin is administered. This is followed by 50 units soluble insulin in 50 ml 0.9 % saline i.v. via infusion pump. 6 units / hr initially 3 units / hr when the blood glucose is < 270 mg / dl 2 units / hr when the blood glucose is < 180 mg / dl Check Blood glucose hourly initially – if no reduction in first hour, rate of insulin infusion should be increased. The goal should be to decrease blood glucose by 50- 100 mg/dl/hr.

Typical Therapy - Potassium : 

Typical Therapy - Potassium None in first litre of i.v. fluid unless < 3 mmol / L If potassium < 3.5 mmol / L, give 40 mmol added potassium. Give in 1 litre of Fluid Avoid infusion rate of > 20 mmol / hr If potassium is 3.5 – 5 mmol / L, give 20 mmol added potassium. If potassium is > 5 mmol / L, or patient is anuric, give no potassium. Potassium can be given as follows: two thirds as KCl, one third as KPO4.

EKG Changes During DKA : 

EKG Changes During DKA Normal Hi K Lo K

Role of - Bicarbonate : 

Role of - Bicarbonate Administration to acidotic patient generates rapid rise in CO2 CO2 enters CNS rapidly HCO3- is delayed by blood-brain barrier Increased CNS CO2 exacerbates cerebral acidosis CO2 + H2O H2CO3 H+ + HCO3- May also reduce partial pressure of O2 in CSF  vasoconstriction  brain hypoxia/ischemia

Role of - Bicarbonate : 

Role of - Bicarbonate Not routinely necessary. Indicated only in the following cases – Shock or Coma Severe Acidosis ( 6.9- 7.1) Severe depletion of buffer reserve ( HCO3 <5 mEq/l) Acidosis induced cardiac or respiratory dysfunction Severe Hyperkalemia

Procedures : 

Procedures Catheterisation if no urine passed after 3 hrs. Nasogastric tube to keep stomach empty in unconscious or semiconscious patients, or if vomiting is protracted. Central Venous line if CVS is compromised to allow fluid replacement to be adjusted accurately. Airway management and Intubation in any patient with a significantly depressed mental status or with respiratory distress.

Complications : 

Complications Cerebral Edema - The leading cause of diabetic ketoacidosis (DKA) mortality in children. The child presents with abnormal response to pain, decorticate and decerebrate posturing, cranial nerve palsies, abnormal CNS respiratory patterns, fluctuating level of consciousness, sustained heart rate deceleration, incontinence, as well as more nonspecific criteria such as vomiting, headache, lethargy, and elevated diastolic blood pressure. Mannitol or hypertonic saline should be available if cerebral edema is suspected.

Complications : 

Complications Hypokalemia  is a complication that is precipitated by failing to rapidly address the total body potassium deficit brought out by rehydration and insulin treatment, which not only reduces acidosis but directly facilitates potassium reentry into the cell. Hypoglycemia may result from inadequate monitoring of glucose levels during insulin therapy. Acute pulmonary edema is potentially related to aggressive or excessive fluid therapy. Although initial aggressive fluid replacement is necessary in all patients, particular care must be taken in those with comorbidities such as renal failure or congestive heart failure.

During Discharge : 

During Discharge Discontinue IV Insulin, IVF Regular Insulin NPH Insulin Diabetic Diet Patient Education, Diabetes Home Glucose Monitoring

Thank You for your attention : 

Thank You for your attention Thank you for saving me from DKA

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