Diabetic Ketoacidosis Flashcards
What is the dx criteria for type 1 diabetes, in terms of lab values you would see
- Random BG > 200 mg/dl
- Fasting BG>125 mg/dl
- In glucose tolerance test, BG>200 mg/dl
- HbA1c >6.5 (adults)
What are some clinical features of diabetes type 1
- Polyuria, Polydypsia, polyphagia (eating all the time)
- Noctural enuresis (unintentional night time urination)
- Ketoacidosis: abdominal pain, nausea, vomiting, mental status changes
- Fatigue, weakness
- Blurry vision
- Genital yeast infections
Briefly, what is the pathophysiology of type 1 DM
T-cell mediated autoimmune destruction of the pancreatic beta cells. On histology you see lots of lymphocytes in the Islets of Langerhans
What is the 2-hit hypothesis for DM?
- Genetic susceptibility: HLA DR3/4, DQ2/8 alleles
- Environmental triggers: virus (congenital rubella and others), nutritional factors (early cow’s milk exposure, vitamin D deficiency maybe?)
What is the biochemical criteria for DKA?
- D for diabetes: BG>200 mg/dl
- K for ketones: Ketonemia or ketouria
- A for acid: Venous pH
Which type of diabetic is more likely to get DKA and why?
New onset- Type 1 (25-30%) because they have NO insulin and thus can not counter glucagon, which increases the production of ketones.
In type 2 diabetes it is less common (10%) because there is typically a little bit of insulin circulating still that can counter the effects of glucagon.
Describe the pathophysiology of DKA. YOU CAN DO ITTTT
- Not enough insulin
- Too much glucagon, cortisol, growth hormone, catecholamines, which leads to….
- Lipolysis and proteolysis (helps to fuel gloconeogeneiss as well as ketogenesis). Now you’ve got lots of glucose and ketone bodies leading to…
- Hyperglycemia: leading to osmotic diuresis from too much glucose filtration in the kidneys AND
- Ketoacidosis from too many ketone bodies. This presents with nausea and vomiting (nice and specific).
All of this leads to:
- Dehydration and electrolyte losses (cuz you lose lots of potassium and phosphate as well)
Now you are dehydrated from DKA. How does dehydration serve as a positive feedback mechanism? In other words, how does this become a vicious cycle?
Dehydration leads to poor tissue perfusion. This causes:
- Lactic acidosis (tissues aren’t getting enough O2 for proper energy production, so they’re using anaerobic respiration, leading to increased lactic acid production). This contributes to the ketoacidotic state (more acid=bad)
- Your body thinks its in a stressed state, which causes the further release of cortisol, catecholamines and other hormones that exacerbate DKA
What are the 3 things you must think of when treating DKA?
- Fluids (volume replacement because they’re dehydrated)
- Insulin (duh)
- Electrolytes (especially K+, because they can become hypokalemic with insulin therapy, due to increased activity of Na+/K+ pumps)
If you have DKA, what are you most likely to die from?
Cerebral edema. Usually develops 4-12 hours after tx starts.
What are risk factors for developing cerebral edema secondary to DKA
- Young age
- New-onset diabetes
- Long duration of sx
What should you look for if you suspect your pt is developing cerebral edema? Aka: WARNING SIGNS
- Headache and slowing of HR
- Neurologic changes (restlessness, irritability, increased drowsiness, incontinence)
- Specific neurologic signs (CN palsies)
- Rising BP
- Decreased O2 sats
What is the diagnostic criteria for DKA?
Diagnostic:
◦ Abnormal motor or verbal response to pain
◦ Decorticate or decerebrate posture
◦ Cranial nerve palsy (III, IV, VI esp)
◦ Abnormal neurogenic respiratory pattern
Major Criteria:
◦ Altered MS/fluctuating level of consciousness
◦ Sustained HR deceleration unexplained ◦ Age-inappropriate incontinence
Minor Criteria: ◦ Vomiting ◦ Headache ◦ Lethargy ◦ Diastolic BP >90 mm Hg ◦ Age
How do you treat cerebral edema?
- 3% saline 1mL/kg over 15 min
OR - mannitol 0.5-1g/kg IV over 20 min
Also:
- Elevate head of bed
- Reduce fluid rate by ⅓
- Intubation maybe? Avoid hyperventilation
- Head CT after treatment initiated
