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Diabetic keto acidosis in children ... Dr.Padmesh

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Diabetic Keto acidosis in Children

Diabetic Keto acidosis in Children


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  • 1. DIABETIC KETOACIDOSIS Dr.Padmesh. V Dept of Pediatrics Dr.SMCSI Medical College, Karakonam, Trivandrum
  • 2. DKA
    • Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes.
    • DKA mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes.
    • DKA is clinically defined as an acute state of severe uncontrolled diabetes that requires emergency treatment with insulin and intravenous fluids.
  • 3. DKA :definition
    • A state of absolute or relative insulin deficiency resulting in hyperglycemia and an accumulation of ketoacids in the blood with subsequent metabolic acidosis
    • Hyperglycemia
      • Blood glucose >250mg%
    • Acidosis
      • pH < 7.30
      • Bicarb < 20 mmol/L
    • Ketosis
      • Elevated serum or urine ketones
      • Serum ketones >5mEq/L
  • 4. Physiology of carbohydrate metabolism
    • Glucose and lipid metabolism are regulated by the pancreatic hormone Insulin ,
    • and its C ounter-regulatory hormones :
      • G lucagon
      • G rowth hormone
      • C atecholamines
      • C ortisol
  • 5. To develop DKA there must be both a relative lack of insulin and a relative overactivity of counter-regulatory hormones
    • Insulin (anabolic)
      • Glucose used for energy substrate or stored as glycogen
      • Protein formation
      • Fats stored as triglycerides
    • C ounterregulatory hormones ( c atabolic)
      • Glycogenolysis
      • Proteolysis-gluconeogenesis
      • Lypolysis-FFA & ketone bodies
    Physiology
  • 6. Physiology of DKA
    • Diabetic ketoacidosis is a superfasted state in which the body’s tissues are robbed of their normal energy substrate Glucose,
    • And the body resorts to catabolism of glycogen, protein and fat for energy.
  • 7. Physiology of carbohydrate metabolism
      • Glycogen is broken down to form glucose ( glycogenolysis )
      • P rotein is catabolized to a mino acids which are converted to g lucose ( gluconeogenesis )
      • Fats are broken down to free fatty acids, which
      • are converted in the liver to glucose or ketoacids ( ketogenesis )
    To develop DKA there must be both a relative lack of insulin and a relative overactivity of counter-regulatory hormones
  • 8.
    • Thus,this type of hormonal imbalance enhances Hepatic Gluconeogenesis, Glycogenolysis,
    • &
    • Lipolysis.
  • 9.
    • Hepatic Gluconeogenesis,
    • Glycogenolysis secondary to insulin deficiency, and counter-regulatory hormone excess result in severe hyperglycemia.
    • Lipolysis increases serum free fatty acids .
    • Hepatic metabolism of free fatty acids as an alternative energy source (ie, ketogenesis) results in accumulation of acidic metabolites (ie, ketones, ketoacids).
    • ( Ketones include acetone, acetoacetate & beta hydroxybutyrate)
  • 10. Pathophysiology of DKA
    • Severe insulinopenia or lack of effective insulin action results in a physiological cascade of events in
    • 3 PATHWAYS
  • 11.
    • 1. Excessive glucose production
    • + Reduced glucose utilization
    • Increased serum glucose
    • Osmotic diuresis,with loss of fluids,electrolytes
    • Dehydration
    • Activation of Renin-Angiotensin-Aldosterone axis
    • Accelerated Potassium loss
  • 12.
    • 2. Increased Catabolic processes
    • Cellular losses of sodium,potassium,phosphate
    • 3. Increased release of free fatty acids from
    • peripheral fat stores
    • Substrate for hepatic ketoacid production
    • Ketoacids accumulate
    • Buffer systems are depleted
    • METABOLIC ACIDOSIS occurs
  • 13.
    • Progressive rise of blood concentration of these acidic organic substances initially leads to a state of ketonemia.
    • Natural body buffers can buffer ketonemia in its early stages.
    • When the accumulated ketones exceed the body's capacity of buffering them, they overflow into urine (ie, ketonuria ).
    • If the situation is not treated promptly, more accumulation of organic acids leads to frank clinical metabolic acidosis (ie, ketoacidosis ), with a drop in pH and bicarbonate serum levels.
    • Respiratory compensation of this acidotic condition results in rapid shallow breathing ( Kussmaul respirations ).
  • 14.
    • Ketones, in particular beta hydroxybutyrate , induce nausea and vomiting that consequently aggravate fluid and electrolyte loss already existing in DKA.
    • Acetone produces the characteristic fruity breath odour of ketotic patients.
    • Hyperglycemia usually exceeds the renal threshold of glucose absorption  Significant glycosuria  Osmotic diuresis  Water is lost in urine resulting in Severe dehydration, thirst, tissue hypoperfusion, and, possibly,lactic acidosis.
  • 15.
    • Hyperglycemia, osmotic diuresis, serum hyperosmolarity, and metabolic acidosis result in severe electrolyte disturbances.
    • The most characteristic disturbance is total body potassium loss.
    • This loss is not mirrored in serum potassium levels, which may be low, within the normal range, or even high.
  • 16. Potassium
    • K + is largely an intracellular ion.
    • Both lack of insulin (catabolic predominance) and acidosis cause a shift of K + extracellularly.
    • High urinary losses of K + occur due to this compartmental shift ,due to osmotic diuresis & due to kaliuretic effect of hyperaldosteronism.
    • Serum K + levels are usually normal, even when total body K + is depleted, because:
      • The compartmental shift of K + inside to outside the cell
      • Only extracellular K + is measured
  • 17. Pathophysiology of Potassium loss
    • Acidosis
    • Extracellular accumulation of Hydrogen ions
    • Shift of Potassium from the intracellular to the extracellular space in exchange with hydrogen ions
    • A large part of this shifted extracellular potassium is lost in urine because of osmotic diuresis
    • HYPOKALEMIA
  • 18. Sodium
    • Initial serum sodium may be ‘low’ for several reasons:
      • Depletion secondary to urinary losses / vomiting
      • Hyperlipidemia displaces sodium in the most frequently used laboratory assay, factitiously lowering sodium values.
      • Hyperglycemia  High serum osmolarilty 
      • Water driven from Intra to Extracellular space 
      • Dilutional hyponatremia
  • 19.
    • For each 100mg% increase of serum glucose above 100mg%, there is an expected decrease of about 1.6mEq/L in measured sodium.
    • The ‘true’ serum sodium level can be calculated as:
    • [Na] + Glucose-100 x 1.6
    • 100
    • The sodium should increase by about 1.6 mmol/L for each 100mg/dL decline in glucose.
    • If the corrected value is >150 mmol/L, severe hypernatremic dehydration may be present and may require slower fluid replacement.
    • Declining sodium may indicate excessive water accumulation & risk of cerebral edema.
  • 20.
    • With prolonged illness & severe DKA, total body losses can approach:
    • - 10-13 mEq/kg of Sodium
    • - 5-6 mEq/kg of Potassium
    • - 4-5 mEq/kg of Phosphate
    • These losses continue for several hours during therapy until catabolic state is reversed & diuresis is controlled.
    • Even though Sodium deficit may be repaired within
    • 24 hours, intracellular Potassium & Phosphate may not be completely restored for several days.
  • 21.
    • The combined effects of
    • Serum hyperosmolarity,
    • Dehydration, and
    • Acidosis
    • Result in increased osmolarity in brain cells
    • Clinically manifests as an altered
    • consciousness.
  • 22. CLINICAL FEATURES
    • Precipitated by intercurrent illness, trauma,
    • infections.
    • Symptoms:
    • -Nausea / Vomiting
    • -Polydipsia / Polyuria / Nocturia
    • -Abdominal pain
    • -Shortness of breath
    • -Weakness
  • 23.
    • Signs:
    • - Dehydration
    • - Hypotension
    • - Tachycardia
    • - Tachypnea / Kussmaul respirations
    • - Acetone odour of breath
    • - Abdominal tenderness
    • - Lethargy / altered level of
    • consciousness / possibly coma
  • 24. Lab Abnormalities and Diagnosis
    • Serum glucose is elevated >250mg/dL
    • Serum bicarbonate <20 mmol/L
    • Arterial pH <7.3 , depending on the severity of the acidosis.
    • Anion gap [ (Na+K) – (Cl+HCO3) ] >12-16 mEq/L
    • Urine analysis: Glucosuria + Ketones
  • 25. Laboratory Abnormalities and Diagnosis
    • Serum amylase - may be due to pancreatitis.
    • (but if S.lipase is not ,this is likely to be non-specific/salivary)
    • Serum Creatinine may be falsely elevated due to interference by ketones in the autoanalyzer methodology.
    • Blood Urea Nitrogen (BUN) may be elevated.
    • Complete Blood Counts: may reveal possible
    • infectious etiology.
    • CSF study, CXR to rule out other causes
    • for the clinical condition.
    Should be re-checked after rehydration
  • 26.
    • Despite a total-body potassium deficit , the serum potassium at presentation may be mildly elevated, secondary to the acidosis.
    • Total-body stores of sodium, chloride, phosphorous, and magnesium are also reduced in DKA but are not accurately reflected by their levels in the serum because of dehydration and hyperglycemia.
    • Elevated blood urea nitrogen (BUN) and serum creatinine levels reflect intravascular volume depletion.
  • 27. To summarize..
  • 28. In short…
  • 29.
    • MANAGEMENT
    • OF DKA
  • 30. Aims of management:
    • Restore normal hemodynamic status.
    • Restore normal acid-base balance.
    • Correct blood glucose level.
    • Restore perfusion by giving fluids , which will increase glucose use in the periphery, restore GFR, and reverse the progressive acidosis.
    • Stop ketogenesis by giving insulin , which will reverse proteolysis and lipolysis, and stimulate glucose uptake and processing, normalize blood glucose, and reverse acidosis.
    • Correct electrolyte losses by electrolyte supplementation.
    • Avoid the complications of treatment, including
    • intracerebral complications, hypoglycemia, and
    • hypokalemia.
  • 31. TREATMENT OF DKA (Milwaukee DKA PROTOCOL)
    • Time Therapy Comments
    • 1 st hour 10-20 ml/kg IV bolus NS or RL NPO.
    • Insulin drip at 0.05-0.1 U /kg/ hr Can be repeated.
    • 2 nd hour until 0.45% NS + Continue insulin drip . If K<3mEq/L, give 0.5-1mEq/Kg
    • DKA resolution 20 mEq/L Kphos & 20 mEq/L KAc. as oral K soln or increase IV K
    • 5% glucose if bl.sugar <250mg/dL to 80 mEq/L
    • Variable Oral intake + S/C insulin No emesis.Normal electrolytes.
    • CO2 >16mEq/L. pH>7.30
    • IV rate = 85ml/kg + maintenance – bolus
    • 23 hr
    * *
  • 32.
    • This protocol corrects a deficit of 85ml/kg (8.5% dehydration) for all patients in the first 24 hours.
    • Children with mild DKA rehydrate earlier & can be switched to oral intake, whereas those with severe DKA and a greater volume deficit require 30-36 hours with this protocol.
    • The initial BOLUS given is a sugar free ISOTONIC solution. The patient is invariably hypertonic,keeping most of the initial infusion in the intravascular space . This ensures quick volume expansion.
    • Subsequent fluid is HYPOTONIC t o repair the free water deficit,to allow intracellular rehydration and to allow a more appropriate replacement of on-going hypotonic urine losses.
    IV rate = 85ml/kg + maintenance – bolus 23 hr
  • 33.
    • Insulin should be given at the beginning to
    • -accelerate the movement of glucose into cells
    • -to subdue hepatic glucose production
    • -to halt movement of fatty acids from periphery to liver
    • However,an initial insulin BOLUS does NOT speed recovery,and may increase the risk of hypoglycemia and hypokalemia. Therefore,insulin INFUSION is started (WITHOUT A BOLUS) at the rate of 0.1 U/kg/hour.
    • Rehydration also lowers glucose levels by
    • -improving renal perfusion  enhancing renal excretion
    • Once glucose level goes below 180 mg/dL, osmotic diuresis stops and therefore rehydration becomes faster without further increase in fluid infusion rate.
  • 34.
    • Hyperglycemia is corrected well before the correction of acidosis.
    • Therefore,even after normal glucose levels are reached, insulin is
    • still required to control fatty acid release.
    • Thus insulin infusion can be lowered but NOT STOPPED once
    • hyperglycemia has resolved.
    • However ,to continue insulin infusion without causing
    • hypoglycemia, GLUCOSE should be added to the solution-
    • usually as a 5% solution.
    • This glucose is added when serum glucose has decreased to 250
    • mg/dL, so that there is sufficient time to infusion before serum
    • glucose falls further.
  • 35. Cautious rehydration :
    • Important to approach any child with hyperosmotic state with cautious rehydration.
    • Effective Serum Osmolality =
    • { 2 x [Na uncorrected] + [Glucose] }
    • (This is an accurate index of tonicity of body fluids reflecting the intracellular & extracellular hydration better than measured plasma osmolality.)
    • This value is usually elevated in the beginning,and should gradually normalize.
    • A rapid decline or a slow decline to a sub-normal range may indicate an excess of free water entering the vascular space,and therefore an increasing risk of developing CEREBRAL EDEMA.
  • 36. Complications of DKA
    • Dehydration/shock/ hypotension
    • Hypokalemia – hyperkalemia
    • Hypoglycemia
    • Aspiration pneumonia
    • Sepsis
    • Acute tubular necrosis
    • Myocardial infarction
    • Stroke
    • Cerebral edema
  • 37. Cerebral edema
    • Clinically apparent cerebral edema occurs in approximately 1% of childhood DKA and is associated with high mortality and neurological morbidity.
    • The pathogenesis of the cerebral edema is not understood; Some studies have attributed it to cellular swelling as a result of rapid osmolar changes occurring during intravenous infusions.
    • Several studies, however, have shown no relationship to the volume or sodium content of the infusion nor any association with the rate of change in serum glucose concentration. This suggests that other factors may be important in the pathophysiology of DKA-related cerebral edema.
    • Clinical signs are variable
      • Gradual deterioration and worsening of conscious level, or
      • More commonly a gradual general improvement followed by sudden neurological deterioration
    • Requires a high index of suspicion.
  • 38. Cerebral Edema – Clinical Features:
    • Decreased sensorium
    • Sudden and severe headache
    • Incontinence
    • Persistent vomiting
    • Disorientation; agitation
    • Ophthalmoplegia
    • Pupillary changes
    • Papilledema
    • Posturing; Seizure
  • 39. Cerebral edema –Treatment :
    • Urgent recognition and treatment are essential.
    • Mannitol
    • Reduce IV fluid rate to 70% maintenance
    • Elevate head end of bed to 45 o
    • Consider intubation & Controlled hyperventilation ( vasoconstrictor effect of hypocarbia)
  • 40.
    • PREVENTION IS
    • BETTER THAN CURE!!!
  • 41.