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Fam Med: Diabetes > DKA > Flashcards

DKA Flashcards

1
Q

What % of patients with T1DM will experience DKA?

A

5%

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2
Q

What is the pathophysiology of DKA?

A

Catabolic condition that results from severe insulin deficiency, often associated with stress and activation of counterregulatory hormones (eg catecholamines, glucagon)

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3
Q

What are precipitating factors of DKA?

A
  • Inadvertent or deliberate interruption of insulin therapy
  • Sepsis
  • Trauma
  • MI
  • Pregnancy
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4
Q

What type of patient education should you provide for T1DM regarding prevention of DKA?

A
  • Reinforced at every opportunity, with special emphasis on:
    • Self-management skills during sick days
    • The body’s need for more, rather than less, insulin during illness
    • Testing of blood or urine for ketones
    • Procedures for obtaining timely preventive medical advice
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5
Q

What are sx of DKA?

A
  • Polyuria
  • Polydipsia
  • Weight loss
  • N/V
  • Vaguely localized abdominal pain
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6
Q

What do you find on PE in a patient with DKA?

A
  • Tachycardia
  • decrease in cap filling
  • rapid, deep, and labored breathing (Kussmaul respiration)
  • fruity breath odor
  • Prominent GI sx and abdominal tenderness
  • Dehydration is invariable and resp. distress, shock, and coma
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7
Q

What is the lab workup for someone with DKA and what do you expect to see reflected in those labs?

A
  • Labs: anion gap metabolic acidosis and positive serum B-hydroxybutyrate or ketones
  • Plasma glucose level elevated but may be moderate (<300mg/dL) in 10-15%
  • Urine ketones
  • Hyponatremia, hyperkalemia, azotemia, hyper osmolality
  • Serum amylase, transaminase, and/or triglycerides may be elevated
  • Focused search for precipitating infection if clinically indicated
  • ECG for electrolyte abnormalities and unsuspected MI
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8
Q

What are the three main focuses of DKA management?

A
  • Fluid replacement
  • Adequate insulin administration
  • Potassium repletion
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9
Q

What are the two main interventions/goals of fluid resuscitation?

A

Restoration of circulating volume

Replenish total body water deficits

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10
Q

Which type of fluid should be used to restore circulating volume?

A
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11
Q

At what rate is the fluid restoring circulating volume infused?

A

Rapidly (if cardiac function is normal) and should be followed by additional fluids at a rate of 0.5-1.0L/hr until vital signs have stabilized and UO has been established

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12
Q

What type of fluid should be used to replenish total body water deficits?

A
  1. 45% saline if the corrected serum sodium level is normal or elevatd
  2. 9%NaCl if corrected serum sodium level is low
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13
Q

At what rate is the fluid to replenish total body water deficits infused?

A

Infusion at 150-500 mL/hr: rate depends on degree of dehydration, cardiac and renal status

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14
Q

What are end targets for replenishing total body water deficits?

A
  • Not exceeding a change in osmolality >3 mOsm/kg/hr
  • Success is judged by improvement of BP, UO, and clinical examination
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15
Q

How long does it typically take for fluid replacement to occur in the typical DKA patient?

A

12-24 hours

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16
Q

Which type of insulin is used in DKA?

A

Regular Insulin

17
Q

How is insulin for DKA dosed?

A

IV bolus 10-15 U administered immediately followed by a continuous infusion of regular insulin at an initial rate of 5-10 U/hr

18
Q

What is the target rate of decrease in blood sugar levels in DKA?

A

50-75mg/dL/hr

19
Q

If dropping quicker than the above answer, what do you need to be concerned about?

A

If corrected at rates >100mg/dL, can increase risk of osmotic encephalopathy

20
Q

How long do you continue maintenance infusion rates in DKA?

A

Maintenance insulin infusion rates of 1-2 U/hr can be continued until the patient is clinically improved, the serum bicarb levels rise >15meq/L, and the anion gap has closed

21
Q

How do you manage insulin and fluid therapy once glucose reaches 250 in DKA?

A

Dextrose (5%) in 0.45% saline should be infused and the insulin infusion rate should be decreased to 0.05U/kg/hr to prevent dangerous hypoglycemia

22
Q

Why are we concerned about potassium levels in DKA and its management?

A
  • Insulin admin results in rapid shift of potassium into the intracellular compartment
  • Goal is to maintain plasma potassium level in the normal range to prevent the potentially fatal cardiac effects of hypokalemia
23
Q

Discuss management of potassium levels in DKA

A

K should be added routinely to the IV fluids (starting with 2nd or 3rd L of fluid replacement) at a rate of 10-20 meq/hr except in patients with hyperkalemia, renal failure, or oliguria

24
Q

How often do you monitor glucose levels in DKA? How often do you monitor other labs?

A
  • BG: hourly
  • Serum electrolytes: 1-2 hours
  • Arterial blood gas: as often as necessary for a severely acidotic or hypoxic patient
25
Q

Why is it pertinent to monitor sodium levels in the treatment of DKA?

A

Serum sodium tends to rise as hyperglycemia is corrected and failure to observe this trend suggests that the patient is being overhydrated with free water

26
Q

How often do you monitor ketone levels in DKA?

A

Not necessary

ketonemia may persist after clinical recovery and because the most commonly used assays measure all ketones and not just B-hydroxybutyrate

27
Q

When is bicarb therapy indicated in DKA?

A
  • Not routinely necessary and may be deleterious in certain situations
  • May be considered for DKA patients who develop
    • Shock or coma
    • Severe acidosis (pH<6.9)
    • Severe depletion of buffering reserve (plasma bicarb <5meq/L)
    • Acidosis-induced cardiac or resp. dysfunction
    • Severe hyperkalemia
28
Q

Name complications of DKA and their clinical presentations

A
  • Lactic acidosis: results from prolonged dehydration, shock, infection, and tissue hypoxia
    • Suspected with refractory metabolic acidosis and a persistent anion gap despite therapy for DKA
    • Management: adequate volume replacement, co troll of sepsis, judicious use of bicarb constitutes the approach to management
  • Arterial thrombosis: manifests as stroke, MI, or ischemic limb
  • Cerebral edema: observed more frequently in children
    • Sx: increased intracranial pressure (HA, altered mental status, papilledema) or sudden deterioration in mental status after initial improvement
    • Risk factors: over hydration with free water and excessively rapid correction
    • CT scan can establish dx
    • Tx: recognition and IV mannitol
  • Rebound ketoacidosis from premature cessation of IV insulin infusion or inadequate doses of SC insulin after infusion d/c.

Fam Med: Diabetes (4 decks)

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