1. DKA/HHS

2. DKA/HHS
Incidence
Physiology
Diagnosis
Predisposing Factors
Treatment

3. Diabetic Ketoacidosis
115,000 hospitalizations in U.S
10-30% of admissions with primary diagnosis of Diabetes
Mortality fallen 22% over the past 20 years

4. Hyperglycemic Hyperosmolar Syndrome
Lower incidence compared to DKA
1% of DM related admissions
Much high mortality rate
~40% compared to <5% for DKA
No significant improvement in recent past

5. Diagnosis
Table with diagnostic parameters

6. DKA Triad
Fig. #2.

8. Pathophysiology Insulin Deficiency
Decreased Glucose utilization
Increased Lipolysis
Increased Ketoacids
Increased Counterregulatory Hormones
Osmotic Diuresis
Dehydration
Electrolyte Loss
Potassium

9. Pathophysiology

10. DKA vs. HHS

11. Ketosis Prone T2DM Mostly minorities Presents with DKA
African Americans and Hispanics
Presents with DKA
Require insulin treatment initially
Can usually be transitioned quickly to Oral hypoglycemics as outpatient
Due to Glucose toxicity or lipotoxicity to the Beta-Cells

12. Presentation Dehydration Weight loss Weakness Abdominal Pain
polyuria, polydipsia
Weight loss
Weakness
Abdominal Pain
Correlates with severity of acidosis
May be confused with Acute Abdomen

13. Presentation Mental Status changes
Related to osmolality more than hyperglycemia or acidosis
More common in HHS
Signs & Symptoms related to underlying cause
Infection, CV disease etc…

14. Which statement is incorrect
Diabetic patients may have silent cardiac ischemia precipitating DKA even without chest pain.
Infection is the most common precipitating factor for DKA.
Cocaine and other illicit drugs are a common factor in DKA.
Prescription drugs only rarely are a precipitating cause of DKA.

15. Predisposing Factors Acute Illness Infection CVA/MI Acute Pancreatitis
Venous Thromboembolism
Acute Abdomen
Renal Failure
Heat Stroke
Burns
Subdural Hematoma
Thyrotoxicosis
Cushing’s Syndrome
Find good table of factors

16. Predisposing Factors Drugs Previously undiagnosed diabetes Pregnancy
Glucocorticoids
Beta-Blockers
Anti-Psychotics
Thiazide Diuretics
Niacin
TPN
Previously undiagnosed diabetes
Pregnancy
Corticosteroids for lung maturity
Terbutiline to prevent pre-term labor

17. Evaluation Metabolic Panel Arterial Blood Gas CBC, Cultures
Glucose, Na, K, CL, BUN, SCr
Anion Gap, Calculate Osm
Arterial Blood Gas
CBC, Cultures
ECG, required in all older patients
Remainder driven by Hx & Px

18. Anion Gap (Na+) - [(Cl-) + (HCO3)] =
12 +/- 2
Increased ketoacids are the cause for acidosis in DKA

19. Calculated Osmolality
2(Na+) + Glu/18 =
>320 usually associated with Mental status change

20. Treatment
Fluids
Potassium
Insulin
Acidosis
Monitoring and Transition

21. Fluids Most Important Initial Treatment
Give Normal Saline, liter in first hr
Can Switch to .45% Saline when patient is Volume replaced and has normal Na+
Add 5% Dextrose when Glucose is <250mg/dl.

22. Which of these therapies for DKA may worsen hypokalemia? And Why?
IV Fluid Hydration
Insulin
Bicarbonate
All of the above

23. Potassium K+ is total body deficient
May be normal to high at presentation
Acidosis, Insulin deficiency
May start supplementation when K+ is <5.0
K+ 4-5meq/L start with 20mEq/L of fluids
K mEq/L - 40mEq/L of fluids

24. Potassium K+ < 3.3mEq/L - Hold Insulin
Insulin will drive K+ into cells acutely
High risk of Hypokalemic arrhythmia
Give 10-20mEq/L per hour until >3.3
Continue to add 40mEq/L to fluids after starting insulin

25. Insulin Fluids and Potassium first! Start with 0.1unit/Kg IV bolus
Insulin in pt that is hypovolemic will produce hypotension secondary to fluid shifts
Insulin drives K+ into the cells causing hypokalemia
Start with 0.1unit/Kg IV bolus

26. Insulin Start Insulin drip Mild cases may be treated with SC insulin
0.1unit/Kg/Hr as continuous infusion
Goal is to lower Glucose 50-70mg/hr
Do Not Forget:
Add 5% Dextrose when glucose <250mg/dl
Goal to keep Glucose with continued insulin infusion
Why?

27. What do you follow to prove the ketoacidosis has resolved?
pH on ABG
Plasma Glucose
Anion Gap
Serum Ketones
Serum Bicarbonate

28. Close the Gap
Insulin necessary to utilize glucose and decrease ketoacids
Recommend continuing insulin infusion until Anion Gap and acidosis resolved
Important to transition to SC insulin and make sure patient is eating before stopping the insulin infusion

29. Acidosis Decrease Ketoacids Bicarbonate
Fluids increase renal clearance
Insulin decreases production
Bicarbonate
Consider bicarb only if pH<7.0 -
Life threatening
Otherwise no indication

30. Phosphate Not an immediate concern
Consider treatment if Phos <1.0mg/dl.
Change KCl replacement to K-Phos
This may help avoid hyperchorlemic acidosis sometimes associated with aggressive NS fluids

31. DKA vs. HHS Differences in treatment: Fluid deficit is larger in HHS
Add 5% Dextrose at 300mg/dl in HHS
No acidosis or AG to follow
HHS resolved when Glucose is <300mg/dl, Osmolality <320mEq/L and mental status is clear

32. Transition to sc Insulin and Ward!

33. Transition Continue Insulin infusion until resolution of ketoacidosis
Start SC insulin at least 1-2 hrs before stopping the infusion
Think Ahead: if planning/hoping to stop infusion - consider starting low dose SC insulin that morning or long acting SC insulin the night before

34. Transition
Make sure the patient is eating before stopping the infusion
Transition is where I see most mistakes made causing either return to ICU or prolonged stay

35. Insulin Dosing Based on underlying cause
If Non-compliance - return to previous dosing that showed good control
Underlying medical disease may cause increased insulin requirements
Several protocols available if patient is newly diagnosed Diabetic
Endocrine team is happy to help!

36. Starting Insulin Weight based insulin regimen 0.4 – 0.8units/Kg/day
How much depends on insulin resistance
Obesity
Fam hx of type II DM
Concomitant illness
40-50% of total as basal and the rest distributed as short acting insulin with meals

37. Questions?