DKA Vignette Flashcards
Vital signs of DKA
No fever
Elevated HR (case - 135bpm)
Elevated Respiratory Rate (case - 40)
Normal Blood Pressure
Common patient complaints, possibly Diabetic Ketoacidosis
"Breathing deep and fast" "Stomach ache" Intermittent vomiting Poor appetite No diarrhea Fatigue for past week
Five common symptoms in patients with DKA
Thirsty Fluids cause nausea and vomiting - worsening in last 12 hours Frequent urine output Dizzy/weak when standing Appears thinner
Physical examination findings DKA
General: rapid & deep respirations, sunken eyes & cheeks, dry mucous membranes and lips Fruity breath Inc HR and RR Diffuse abdominal tenderness Cool hands and feet, slow cap refill A+O x 4, but sleepy (somnolent)
Diagnostic criteria for diabetes
Elevated blood sugar
>200 mg/dL at anytime is diagnostic
>126 mg/dL fasting is diagnostic
Hemoglobin A1c >6.5% correlates to ~140 mg/dL
Abnormal hemoglobin negates this test (ie Sickle Cell)
Pancreatic function in Type 1 diabetes
Exocrine pancrease function is OK
Endocrine pancrease function is OK except for cells producing insulin
Islet of Langerhans(hormone producing cells) - many different cells; only beta cells (insulin producers) are defective
Definition of DKA
D - diabetes: Blood sugar >200 K - Ketonemia/ketonuria: Body using fats for energy A - Acidosis: Venous pH < 7.3 or HCO3 < 15mmol/L
Process by which insulin release is triggered by glucose (five steps)
Glucose enters beta cell through Glu2 transporter
Glycolysis produces ATP
ATP shuts potassium channel (leaky channel), charge builds up
Membrane depolarizes, calcium influx (voltage gated gate)
Calcium triggers secretory vesicles to release insulin
Insulin actions
Insulin makes you store energy Glucose uptake by liver: Glycogen synthesis, lipogenesis muscle: Glycogen synthesis, protein synthesis adipose tissue: Lipogenesis
Results of insulin deficiency
Glucose not taken into cells - hyperglycemia
Body still needs energy -
lipolysis
fatty acid oxidation (liver)
Ketoacidosis (acetoacetate, betahydroxybutyrate)
How does the body compensate for acidosis?
H+ + HCO3 H2CO3 H2O + CO2 Kussmaul respirations (rapid, deep) expel excess CO2
How does DKA lead to dehydration?
Glucose re uptake proteins in the kidneys are overwhelmed, excess glucose leaks out in the urine. More glucose = higher osmolarity in urine = less H2O reabsorbed in distal tubules
Consequences of dehydration
Electrolyte imbalances
Na+ is preferentially retained b/c it helps hold water (aldosterone)
K+ is lost to urine
Plasma K+is maintained through depletion of cellular K+
How do you treat hyperglycemia in DKA?
IV fluids (dilution) Insulin
How do you treat dehydration in DKA patients?
Isotonic IV fluids
How do you treat acidosis in DKA patients?
Insulin (stop ketone formation)
Fluids (urinary excretion of acid and ketones)
How do you treat potassium imbalance in DKA?
Careful K+ supplementation
5-7 times normal supplementation levels
One major complication resulting from DKA and it’s potential outcomes.
Cerebral edema (rare ~0.5-0.9% of childhood DKA)
Leading cause of death associated with DKA
24% case fatality
20% mild to severe neurologic outcomes
What causes cerebral edema?
Anything that causes an abrupt lowering of the serum osmolarity can lead to cerebral edema. Brain tissues are in equilibrium with hyperosmolar serum, so diluting the serum causes H2O to cross into brain tissue causing swelling.
Early and late signs of cerebral edema
Early signs are often subtle: Newly combative, new headache Later signs: Hypertension, bradycardia, agonal respirations (Cushing's Triad) Fixed, dilated pupils Think "Compression of the brainstem"
Treatment for cerebral edema in DKA patient
Isotonic solutions, watch serum Na+ Monitor glucose level, must not drop too quickly Also: Hypertonic saline possible Mannitol (nonmetabolized sugar osmals)
Brief presentation of DKA
Ill appearing
Breathing rapidly
Nausea, vomiting, diffuse belly pain (no diarrhea)
Dehydrated
Labs: hyperglycemia, metabolic acidosis (low pH, low HCO3)
