This case presentation will help you managing the patients with DKA and ESRD regarding the fluid managment

1. Thomas Lanning MD.
Abdul Hamid Alraiyes MD.

2. 47 years old AAM
Chief Complaints
Nausea
Vomiting
Abdominal Pain
CP

6. Past surgical Hx:
Lt AKA (1 year ago)
Rt AVF (radial artery)
Rt Big toe amputation
Lt IJ Dialysis catheter (3/10/2007)

7. Allergies:
Penicillin “rash”
Social History:
Resident at Cleveland Rehab
Denies any Hx of:
 ETOH
 Drug abuse
 Ex- SMOKER
Family History:
DM
HTN

8. Medications:
Insulin aspart 5 units S.Q. Q AC
Lantus 20 units S.Q. QHS
Hydralazine 100mg P.O. Q8hr
Lisinopril 20mg P.O. QD
Lopressor 50mg P.O. BID
Norvasc 10mg P.O. QD
Renagel 800mg P.O. TID
Nephrocap 1 tab P.O. QD
Neurontin 300mg P.O. Q 8hr
Fluoxetine 20mg P.O. QD
Vancomycin 600mg I.V. with HD

10. Physical Exam:
 V/S : 36- 120/56 - 62 – 17 - SPO2= 86% on RA
 Pt is drowsy, dehydrated, not in distress
 Skin: dry
 Chest: Bil crackles, no wheezing + decreased air entry.
 CVS: S1 + S2 + no M
 ABD: soft, distended epigastric, tenderness, no rebound, BS+.
 EXT: no edema , Lt AKA, Rt Big toe amputation, AVF on the Lt
arm

11. Labs:
 WBC = 10.9 , Hb= 12.6, Ht= 39.2, Plt= 184
 Na= 119, K= 8, Cl= 86, CO2= 12
BUN= 103, Cr= 9.9 , Glucose=1140

12. Labs:
 AG= 21
Serum Osmolality= 348 (275-290)
 ABG= 7.048 / 41.8 / 75.1 / 11 A-a= 32 SAT= 86
FiO2 = 21%

14. 119 – (86 + 12) = 21

16. Expected AG = 21 + [ 2.5 X (4.5 – 3.8] = 22.75

18. PCO2 = (1.5 X 12 ) + 8 +/_ 2 = 28 - 24

19. PCO2 = (1.5 X 12 ) + 8 +/_ 2 = 28 – 24
ABG= 7.048 / 41.8 / 75.1 / 11
Metabolic Acidosis + Respiratory Acidosis

21. AG Excess / HCO3 deficit = 22 – 12 / 24 – 12 =~ 1

22. Labs:
 Amylase= 102 Lipase=1082
LFT WNL ALP=242
CPP = 94 / 3 / 0.14
UA not done “Pt is anuric”
EKG: LVH

24.  Cardiomegaly Bil pleural effusion
 Small amount of ascites
 Wall thickening of proximal Small bowel in
Lt upper abdomen
 Mild renal atrophy

25. 10 units R insulin x 2 I.V.
No I.V.F
naHCO3 tow Apm
Kayexalate 30 gram PO
CaCl 1 Amp

28. Uncontrolled
blood sugar
Ketones
accumulation
Volume
contraction
DKA Starvation
Sepsis
MI

29. Blood Sugar
1500
Axis Title
1000
500
0
Blood Sugar
Mon Mon Mon Mon Mon Mon Mon Mon Mon Mon Mon Mon
1 2 3 4 5 6 7 8 9 10 11 12
Blood Sugar 671 820 138 266 340 168 393 663 284 736 217 1140

30. •Ansari, A, Thomas, S, Goldsmith, D. Assessing glycemic control in patients with diabetes and end-stage renal failure. Am J
Kidney Dis 2003; 41:523
•Joy, MS, Cefalu, WT, Hogan, SL, Nachman, PH. Long-term glycemic control measurements in diabetic patients receiving
hemodialysis. Am J Kidney Dis 2002; 39:297.

31. •K/DOQI clinical practice guidelines for cardiovascular disease in dialysis patients. Am J Kidney Dis 2005; 4(Suppl 3):S1.

32. •Coronary-artery calcification is common and
progressive in young adults with end-stage renal
disease who are undergoing dialysis. (N Engl J
Med 2000;342:1478-83.)

33. Osmolality
400
Axis Title
200
0
Osmolality
Mon Mon Mon Mon Mon Mon Mon Mon Mon Mon Mon Mon
1 2 3 4 5 6 7 8 9 10 11 12
Osmolality 312 320 248 273 266 243 255 277 244 245 260 348

34. Hyperglycemia > 250
Anion Gap
Serum HCO3 < 20
Urine or Blood Ketones

35. + NADH + NAD

36.  NPO
 INSULIN ( Bolus + Infusion)
 IVF
 Hyperkalemia / Hypokalemia
 ? NaHCO3

37. DKA + ESRD

38. INSULIN

39. INSULIN + ESRD

40. INSULIN resistance 2 nd to uremia
1) Increased hepatic gluconeogenesis.
2) Reduced hepatic and/or skeletal muscle glucose uptake.
3) Impaired intracellular glucose metabolism.
4) abnormalities in phosphate and vitamin D metabolism
5) Anemia
•Mak, RH, DeFronzo, RA. Glucose and insulin metabolism in uremia. Nephron 1992; 61:377.
•McCaleb, ML, Izzo, MS, Lockwood, DH. Characterization and partial purification of a factor from
uremic human serum that induces insulin resistance. J Clin Invest 1985; 75:391.

41. Decreased insulin degradation
 Decreased until GFR of 15-20 ml/min.
 Uremia will be higher and this will lead to an increase in
resistance to insulin when GFR 10 ml/min.

42. INSULIN
 No dose adjustment is required if the GFR is above 50 mL/min.
 The insulin dose should be reduced to approximately 75% of baseline when the
GFR is between 10-50 mL/min.
 The dose should be reduced by as much as 50% when the GFR is less than 10
mL/min.
 in pt HD patients the insulin requirement in any given patient will depend upon
the net balance between improving tissue sensitivity and restoring normal
hepatic insulin metabolism.
•Snyder, RW, Berns, JS. Use of insulin and oral hypoglycemic medications in patients with diabetes
mellitus and advanced kidney disease. Semin Dial 2004; 17:365.

43. IVF

44. IVF

46. Hemo-dialysis
-Indications?
-Fluid removal?

47.  Indications?
• Metabolic Acidosis
• Hyperkalemia
• Uremia
• Decrease the Insulin resistance
• Low S O2 ? Pulmonary edema

48. Hyperkalemia?

49.  Usually no potassium replacement
 Check within 2 Hr after HD
 If AVF avoid the site of HD
 ESRD no osmotic diuretic effect.

50. Central I.V Access

51. Central I.V Access

52. NaHCO3?

60. DKA + ESRD + Questions
1. Metabolic Acidosis could be from multiple sources.
2. Insulin doses
3. Importance of HD
4. Role of IVF
5. Role central venous pressure and (risk / benefit)
6. Treatment of Hyperkalemia / Hypokalemia
7. Role of HCO3