CLIPP case 16. DKA Flashcards
7yo girl presents to the ED with two days of vomiting, abdominal pain, and thirst. On physical exam, is afebrile, lethargic, tachypneic, significantly dehydrated, and has mild, diffuse tenderness throughout her abdomen. Labs demonstrate hyperglycemia
and metabolic acidosis.
- DKA
- Immediately give IV fluid bolus
- Other DDx:
- Appendicitis
- Increased intracranial pressure
- Toxic ingestion
- GI obstruction
- Gastroenteritis
- Pyelonephritis
- Bacterial pneumonia
GCS
- Most accepted method of assessing AMS
- Best Eye Response, Best Verbal Response (adjusted for child <5), and Best Motor Response
- GCS ≤8 may need aggressive intervention
T2DM risk factors
-BMI > 95th reference percentile for age
-Native American, African American, Latino,
Asian American, Pacific Islander
-Age: Peak age at diagnosis in youth is between 12 and 16 years (midpuberty)
-Sex (female, 3:1)
-Sedentary lifestyle
T2DM screening
*Fasting BG every 3 years starting at age 10 (or puberty if earlier) for:
-BMI > 85th percentile for age and sex, weight for height > 85th percentile, or weight > 120% of ideal for height
PLUS two risk factors:
-Maternal DM or GDM
-Family history
-Native American, African American, Latino, or Asian American, Pacific Islander
-Signs of insulin resistance (acanthosis nigricans, hypertension, dyslipidemia, polycystic ovary syndrome)
Diagnosis of DM
- Symptoms (polyuria, polydipsia, wt loss) plus random BG ≥ 200 mg/dL
- Fasting BG ≥ 126 mg/dL
- Two-hour glucose ≥ 200 mg/dL in OGTT
- HbA1c > 6.5%
DKA physiology
*Lack of insulin and excess glucagon -> catabolism -> hyperglycemia, ketones, acidosis
*Increased lipolysis -> free fatty acids -> converted to ketones -> metabolic acidosis
*Osmotic diuresis when BG reach 180 mg/dL,
leading to hypovolemia, dehydration, and a loss of sodium, potassium, and phosphate in the urine.
*Hyperosmolarity from osmotic diuresis and hyperglycemia
*Diagnosis: Random BG > 200 mg/dL; Ketonuria or ketonemia; venous pH < 7.3 or serum bicarbonate < 15 mEq/L
Types of dehydration
- Isonatremic: most common type in children, including acute gastroenteritis.
- Hyponatremic < 130: Mild forms can be seen in viral gastroenteritis. More severe forms (< 120) can be seen in free water or diluted formula replacement, or adrenal insufficiency.
- Hypernatremic > 150: Breastfeeding failure, use of inappropriate rehydration solutions, and d iabetes insipidus. Highest mortality.
Admission orders
ADC VANDISMAL
- Admit to (unit, rm, floor, dr)
- Diagnoses
- Condition
- Vitals (q_hr)
- Activity
- Nursing (I&O, wound care, drains)
- IVF
- Studies
- Meds
- Allergies
- Labs
Studies in new onset T1DM
- Anti-pancreas antibodies (insulin, GAD, IA2)
- Celiac disease antibodies (transglutaminase and endomysial)
- Thyroid disease antibodies (TPO)
DKA labs
- Elevated BG and ketones, and urine ketones
- Low venous pH and bicarb
- HypoNatremia (dilutional and renal loss), correct by 1.6 for ever 100 elevation in BG over 100
- Normal/abnormal K (total body low, and drops as correct acidosis)
- Elevated BUN and creatinine
Fluid replacement in hypernatremic hypovolemia and in DKA
Correct evenly over 48 hours to prevent cerebral edema
DKA treatment
- Admit to hospital
- Resuscitate, then insulin gtt + MIVF + replacement over 48hr (to prevent cerebral edema) + K once level known
- Endocrinology consult
- Cardiorespiratory monitoring
- Frequently check VS, BG, ketonuria
- Insulin gtt until no ketones in serum, pH>7.3 or bicarb>15 or anion gap closed
- If ketones or acidosis continues, continue insulin and add D5 when BG <200
Avoiding hypoglycemia in tx of DKA
- Lower BG by 80-100 per hour
- Goal is 120-200 (250 max)
Cerebral edema in DKA epidemiology
0.5-1% of DKA
Leading cause of death in child DM
Can occur at any time in DKA
Cerebral edema in DKA risk factors
- High BUN concentration at presentation
- Profound acidosis with hypocapnia
- Attenuated rise in measured serum sodium with treatment
- Administration of bicarbonate
