Management Of Diabetic Emergencies Flashcards
What are the 3 acute diabetic emergencies
1) DKA
2) HHS (hyperglycemia, hyperosmolar mild ketosis syndrome)
3) hypoglycemia
What is the diagnostic A1c level for diabetes
> 6.5%
Pathophysiology behind DKA
1) Excess glucose causes osmotic diuresis which results in loss of water, potassium and magnesium
- also some mild sodium
2) Excess hypokalmeia produced by excess glucose results in inhibition of insulin releases which results in a vicious snowball effect
3) This eventually leads to dehydration/starvation in cells which leads to:
- cells decreasing AA uptake and accelerates proteolysis
- adipose tissue not clearing circulating lipids which causes excess metabolism into (B-hydroxybuterate and acetoacetate) ketoacids which builds up in blood
- increased ketosis and starvation causes decreased ketone use and more stays in plasma
- uninhibited glycogen and catecholamine releases which further promotes gluconeogenesis and glycogenolysis
4) All of this promotes excessive ketone production from excess FFAs but ALSO decreases total ketone use.
- this results in an even more hyper osmotic state in the blood and excess ketones that just sit around produce acidosis effect
5) All of this hyperosmolarity results in increased acidosis and increased glucose release in the blood
Causes of DKA
Most common = lack of insulin use
Can also be aggregated in diabetic patients by MIs, infections.
this is most common in DM1 but can be seen in DN2
Symptoms of DKA
On top of having the three P’s
- abdominal pain and cramping (in adult diabetics = look for secondary cause in the GI; in children = usually idiopathic and signals DKA as primary cause)
- tachycardia, tachypnea
- AMS
- hypotension
- acetone breath
- significant voiding of bladder
- dry mucous membranes an dehydration symptoms
note DKA almost never produces pyrexia by itself, so if a fever is present = must search underlying infection
Lab values in DKA
80% chance the glucose is >350
- however 20% show normal glucose so this isn’t diagnostic
Hyponatremia/kalemia /magnesia
- note that initially will show hyperkalemia since potassium will leave intracellular to make up for low potassium in blood
Low bicarbonate and low pH
- *ketones in urine and blood elevated as well as elevated blood osmolarity**
- most sensitive
Often shows elevated anion gap metabolic acidosis
- however if the patient is excessively vomiting = may be normal gap
Elevated WBC
Why is ECG important in DKA
The levels of potassium can be measured with this initially as well as be prepared for arrthymias
Initially = hyperkalemia
- peaked T waves with short QT intervals and widened QRS
Later = hypokalemia
- flattening of T waves and inversion of T waves
- also shows visual U wave (really bad)
- eventually leads to Torsades (replace magnesium before potassium otherwise nothing happens)
When do you incubate a patient
GCS is less than 8
Significant AMS is present or coma
No protection fo airway or not able not able to ventilate properly
if patient is in DKA and needs intubation = must continue to hyper ventilate to prevent worsening of acidosis
What should you do in patients who have shock with DKA
Hydrate aggressively and look for causes of shock that is NOT DKA to rule out extrinsic causes
- sepsis
- cardiogenic
- hypovolemic
**usually give greater than 2L per 2hr
Caveats to treatment of DKA
On top of hydrating and intubating as needed:
- must give insulin via a drip with hydration
- DONT hydrate or give insulin too fast (risk increased cerebral edema and worsens acidosis) Usually give 2L 0.45% NS in first two hours and give insulin drip of 0.1g/kg
- NEVER GIVE insulin if potassium is lower than 3.3 mEq/L (must correct this first)**
Once glucose is under 300 mg/dL = give dextrose with normal saline (still 0.45%)
To correct electrolytes
- magnesium = usually give 1-2 g MgSO4- ( increase dose if torsades is present)
- phosphorus = nothing
- sodium = nothing other than NS
- potassium = add 20-40 mEq KCL to each liter of saline if potassium is <5.5. If under 3.3 = give more than 40 mEq/L
- *USUALLY DONT GIVE BICARBONATE**
- makes acidosis worse and worsens electrolyte abnormalties
- only time to give = cardiac arrhythmia present of alcoholic induced DKA
Hyperglycemic hyperosmolar state (HHS)
More common in T2DM but can be in Type 1 also
Characterized By
- mild ketosis or no ketosis
- metabolic acidosis with anion gap
- prominent CNS changes (seizures are more common)
- marked hyperglycemia
- severe dehydration
- can look similar to DKA however*
- is more common in elderly
- longer prodromal than DKA (takes longer than a day)
- 15% may also show GI bleeding, pneumonia, cardiac issues, vascular issues
commonly associated with renal insufficiency, gram (-) sepsis or pneumonia, GI bleeding
Lab values in HHS
Glucose is usually >700
-they are far more dehydrated
Hypotensive
Mild fever
Electrolytes are more wider abnormality than DKA
- also sodium is usually less severely declined
- DONT use potassium equation to overcorrect in this patient since pH is normal
- *pH is usually normal and there are no serum ketones
- also bicarbonate level is >15 usually
**BUN is usually higher than in DKA (>50 compared to 25-50 respectively)
WBC is usually normal unless underlying infection
Management of HHS
Very similar to DKA
Start with insulin at 0.1/kg and 1-2 L 0.45% NS every 1-3 hrs until glucose is <300, then switch to Dextrose in 0.45% NS every 1-3 hrs
Same electrolyte correction measurements
must search for the cause of this and it’s usually lack of insulin but have to rule out infections or acute stress events
*NOTE: cerebral edema is more common in HHS than DKA since glucose is usually even high in HHS
What is the most dangerous complication of diabetes
Hypoglycemia
- is more common in T1DM and is the most common cause of coma in T1DM
- severe hypoglycemia = <50 mg/dL glucose
Caused by excess insulin = most common cause
- also overuse of oral hypoglycemic agents (especially sulfonylureas since it stays in the body forever due to long half life) is the most risky drug in T2DM treatment for this**
- increased energy and output/exercise can be a cause also
- alcohol dependence and malnutrition can make it easier to hit hypoglycemia (give thiamine first for alcoholics)
What is the somogyi effect?
Iatrogenic hypoglycemia inT1DM
- caused by excess insulin dosing which causes hypoglycemia while the patient is sleeping
- *This leads to rebound hyperglycemia when the patient awakens (growth hormone, cortisol and glucagon are released in high quantities in the morning in general, but in a night time hypoglycemic event = release even more)**
- this can lead to misrepresentation of poor control resulting in increased insulin prescription from the doctor and further making this worse and lead to chronic hypoglycemic**
