DKA Flashcards
definition of diabetic ketoacidosis
-Clinically is an acute state of severe uncontrolled diabetes that requires emergency treatment with insulin and intravenous fluids (dilute it)
-Biochemically - DKA is defined as an
-Increase in the serum concentration of ketones > 5 mEq/L
-Blood glucose level of > 250 mg/dL (although it is usually much higher)
-Blood pH of < 7.2
-Bicarbonate level of 18 mEq/L or less
-pure lack of insulin causes this
-non-ketotic failure for type 2
-not common for type 2
-understand the underlying cause of DKA
DKA main symptoms
-dehydration
-hyperglycemia
-acidosis
-ketonuria
pathophysiology
-Insulin deficiency and glucagon excess are necessary for DKA
-Body metabolizes triglycerides and muscle instead of glucose for energy
-Serum levels of glycerol and free fatty acids (FFAs) rise -> Unrestrained lipolysis, muscle catabolism
-These provide substrate for hepatic gluconeogenesis
-Also stimulated by excess of glucagon
-Glucagon also stimulates FFAs into ketones
-Insulin normally blocks ketogenesis by inhibiting the transport of FFA derivatives into the mitochondrial matrix
-in absence of insulin – ketogenesis proceeds
-TWO MAJOR TYPES OF KETONES: acetoacetic acid and β-hydroxybutyric acid!*- strong organic acids that create metabolic acidosis
-Acetone derived from the metabolism of acetoacetic acid accumulates in serum and is slowly disposed of by respiration – ‘fruity breath’.
-Hyperglycemia - produces an osmotic diuresis
-Urinary excretion of ketones obligates additional losses of Na and K
-Serum Na may fall from natriuresis or rise due to excretion of large volumes of free water
potassium
-K is also lost in large quantities, sometimes > 300 mEq/24 h
-insulin shifts K into the cell
-if K is 5 -> good to give insulin
-if pt has 4.5 in DKA -> give insulin slowly and carefully
-3.3 or less DO NOT GIVE INSULIN -> causes severe hypokalemia
-correct K before you give insulin
-Significant total body deficit of K
-BUT initial serum K is typically normal or elevated because of the extracellular migration of K
-K levels generally fall further during treatment as insulin therapy drives K into cells
-If serum K is not monitored and replaced as needed, life-threatening hypokalemia may develop
precipitating events
-Inadequate insulin administration
-Infection: pneumonia/UTI/gastroenteritis/sepsis
-Infarction- cerebral, coronary, mesenteric, peripheral
-Drugs (cocaine)
-Pregnancy
symptoms and signs
-Nausea/vomiting
-Thirst/polyuria
-Abdominal pain
-Shortness of breath
-Tachycardia
-Dry mucous membranes/reduced skin turgor
-Dehydration / hypotension/tachycardia
-Tachypnea / Kussmaul respirations (slow deep labored breathing) /respiratory distress (fruity breath)
-Abdominal tenderness (may resemble acute pancreatitis or surgical abdomen)
-Lethargy /obtundation / cerebral edema / possibly coma
-Abdominal pain- particularly in children
-Lethargy and somnolence - of more severe decompensation
-Fever is not a sign of DKA itself and, if present, signifies underlying infection
-In the absence of timely treatment, DKA progresses to hyperglycemic coma and death
-Acute cerebral edema- Primarily in children (weaker BBB) -> monitor how much fluid your giving bc of this!
-Headache and fluctuating level of consciousness
-Respiratory arrest - initial manifestation in others
-Cause –??? may be related to too-rapid reductions in serum osmolality or to brain ischemia
-It is most likely to occur in children < 5 yr when DKA is the initial presentation of DM
-*Children with the highest BUN and lowest PaCo2 at presentation appear to be at greatest risk
-Additional risk factors
-Delays in correction of hyponatremia
-Use of HCO3 during DKA treatment
essential for dx
-hyperglycemia > 250
-acidosis with blood pH < 7.2
-serum bicarbonate < 15
-serum positive for ketones
-urine can have trace of ketones
dx
-Serum electrolytes, BUN and creatinine, glucose, ketones, and osmolarity
-Urine - tested for ketones
-ABG measurement
-DKA is diagnosed by an arterial pH < 7.20 with an anion gap > 12 *****
-Serum ketones in the presence of hyperglycemia!!!
-Presumptive diagnosis - urine glucose and ketones are strongly positive
-Urine test strips and some assays for serum ketones may underestimate the degree of ketosis because they detect acetoacetic and not β-hydroxybutyric acid, which is usually the predominant ketoacid
lab results
-Hyponatremia , elevated serum creatinine, and elevated serum osmolarity
-Hyperglycemia may cause dilutional hyponatremia, so measured serum Na is corrected by adding 1.6 mEq/L for each 100 mg/dL elevation of serum glucose over 100 mg/dL
-To illustrate, for a patient with serum Na of 124 mEq/L and glucose of 600 mg/dL, add 1.6 ([600-100]/100) = 8 mEq/L to 124 for a corrected serum Na of 132 mEq/L
-dont need to calculate anything
Harrisons: DKA and Hyperosmolar hyperglycemic syndrome (HHS) picture
-trace ketones? - > unsure about the point shes making with that
lab results: postassium
-As acidosis is corrected, serum K drops
-An initial K level < 4.5 mEq/L indicates marked K depletion and requires immediate K supplementation
-Serum amylase and lipase are often elevated, even in the absence of pancreatitis (which may be present in alcoholic DKA patients and in those with coexisting hypertriglyceridemia
treatment
-MOST URGENT GOALS:
-rapid IV volume repletion correction and hyperglycemia and acidosis, and prevention of hypokalemia
-identify precipitating facotrs
-ICU- clinical an lab assessment are needed every hour or every other hour with appropriate adjustments in tx
management
-confirm dx- plasma glucose, + serum ketones, metabolic acidosis
-admit to hospital: frequent monitoring or if pH <7 or unconscious
-assess- serum electrolytes (K, Na, Mg, Cl, bicarbonate phosphate), acid-base status (pH, HCO3-, PCO2, hydroxybutyrate), renal function (creatinine, urine output)
-replace fluids- 2-3 L of 0.9% saline over first 1-3 h (5-10 ml/kg per hour)
-subsequently 0.45% saline at 150-300ml/h
-change to 5% glucose and 0.45% saline at 100-200 ml/h when plasma glucose reaches 250 mg/dL (14mmol/L)
fluid replacement
-IV volume should be restored rapidly
-remaining total body water deficits are corrected more slowly, typically over about 24 h
-initial volume repletion in adults is typically acheived with rapid IV infusion to raise BP, correct hyperglycemia, and keep urine flow adequate
-adults with DKA typically need a min of 3L of saline over the first 5 h
-when BP is stable and urine flow adequate, normal saline is replaced by 0.45% saline
-when plasma glucose falls to <250, IV fluid should be changed to 5% dextrose in 0.45% saline
management of hyperglycemia
-administer regular insulin:
-continuous IV infusion
-increase 2- to 10-fold if no response by 2-4 h
-if initial serum K is < 3.3 do not administer insulin until K is corrected to > 3.3
-When plasma glucose becomes 250 to 300 mg/dL (13.88 to 16.65 mmol/L)
-5% dextrose added to IV fluids to reduce the risk of hypoglycemia
-Insulin dosage can then be reduced (minimum 1 to 2 units/h)
-But the continuous IV infusion of regular insulin should be maintained until the anion gap has narrowed and blood and urine are consistently negative for ketones
