DKA Vignette

Question 0

Vital signs of DKA

Answer 0

No fever
Elevated HR (case - 135bpm)
Elevated Respiratory Rate (case - 40)
Normal Blood Pressure

Question 1

Common patient complaints, possibly Diabetic Ketoacidosis

Answer 1

"Breathing deep and fast"
"Stomach ache"
Intermittent vomiting
Poor appetite 
No diarrhea
Fatigue for past week

Question 2

Five common symptoms in patients with DKA

Answer 2

Thirsty
Fluids cause nausea and vomiting
-  worsening in last 12 hours
Frequent urine output
Dizzy/weak when standing
Appears thinner

Question 3

Physical examination findings DKA

Answer 3

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)

Question 4

Diagnostic criteria for diabetes

Answer 4

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)

Question 5

Pancreatic function in Type 1 diabetes

Answer 5

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

Question 6

Definition of DKA

Answer 6

D - diabetes:
Blood sugar >200 
K - Ketonemia/ketonuria:
Body using fats for energy
A - Acidosis:
Venous pH < 7.3 or HCO3 < 15mmol/L

Question 7

Process by which insulin release is triggered by glucose (five steps)

Answer 7

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

Question 8

Insulin actions

Answer 8

Insulin makes you store energy 
Glucose uptake by liver:
Glycogen synthesis, lipogenesis
muscle:
Glycogen synthesis, protein synthesis
adipose tissue:
Lipogenesis

Question 9

Results of insulin deficiency

Answer 9

Glucose not taken into cells - hyperglycemia
Body still needs energy -
lipolysis
fatty acid oxidation (liver)
Ketoacidosis (acetoacetate, betahydroxybutyrate)

Question 10

How does the body compensate for acidosis?

Answer 10

H+ + HCO3    H2CO3    H2O + CO2
Kussmaul respirations (rapid, deep) expel excess CO2

Question 11

How does DKA lead to dehydration?

Answer 11

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

Question 12

Consequences of dehydration

Answer 12

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+

Question 13

How do you treat hyperglycemia in DKA?

Answer 13

IV fluids (dilution)
Insulin

Question 14

How do you treat dehydration in DKA patients?

Answer 14

Isotonic IV fluids

Question 15

How do you treat acidosis in DKA patients?

Answer 15

Insulin (stop ketone formation)

Fluids (urinary excretion of acid and ketones)

Question 16

How do you treat potassium imbalance in DKA?

Answer 16

Careful K+ supplementation

5-7 times normal supplementation levels

Question 17

One major complication resulting from DKA and it’s potential outcomes.

Answer 17

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

Question 18

What causes cerebral edema?

Answer 18

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.

Question 19

Early and late signs of cerebral edema

Answer 19

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"

Question 20

Treatment for cerebral edema in DKA patient

Answer 20

Isotonic solutions, watch serum Na+
Monitor glucose level, must not drop too quickly
Also:
Hypertonic saline possible
Mannitol (nonmetabolized sugar osmals)

Question 21

Brief presentation of DKA

Answer 21

Ill appearing
Breathing rapidly
Nausea, vomiting, diffuse belly pain (no diarrhea)
Dehydrated
Labs: hyperglycemia, metabolic acidosis (low pH, low HCO3)