ESRD and DKA

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Information about ESRD and DKA

Published on May 25, 2008

Author: ah.alraiyes

Source: slideshare.net

Description

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

Thomas Lanning MD. Abdul Hamid Alraiyes MD.

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

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

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

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

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

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

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

119 – (86 + 12) = 21

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

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

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

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

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

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

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

Uncontrolled blood sugar Ketones accumulation Volume contraction DKA Starvation Sepsis MI

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

•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.

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

•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.)

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

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

+ NADH + NAD

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

DKA + ESRD

INSULIN

INSULIN + ESRD

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.

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.

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.

IVF

IVF

Hemo-dialysis -Indications? -Fluid removal?

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

Hyperkalemia?

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

Central I.V Access

Central I.V Access

NaHCO3?

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

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