ESRD and DKA

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

Transcript of ESRD and DKA

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

DKA

Uncontrolled blood sugar

Volume contraction

Ketones accumulation

Starvation

Sepsis

MI

Blood Sugar

0

500

1000

1500

Ax

is T

itle

Mon 1

Mon 2

Mon 3

Mon 4

Mon 5

Mon 6

Mon 7

Mon 8

Mon 9

Mon 10

Mon 11

Mon 12

Blood Sugar 671 820 138 266 340 168 393 663 284 736 217 1140

Blood Sugar

•Ansari, A, Thomas, S, Goldsmith, D. Assessing glycemic control in patients with diabetes and end-stage renal failure. Am JKidney Dis 2003; 41:523•Joy, MS, Cefalu, WT, Hogan, SL, Nachman, PH. Long-term glycemic control measurements in diabetic patients receivinghemodialysis. 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 andprogressive in young adults with end-stage renaldisease who are undergoing dialysis. (N Engl JMed 2000;342:1478-83.)

Osmolality

0

200

400

Ax

is T

itle

Mon 1

Mon 2

Mon 3

Mon 4

Mon 5

Mon 6

Mon 7

Mon 8

Mon 9

Mon 10

Mon 11

Mon 12

Osmolality 312 320 248 273 266 243 255 277 244 245 260 348

Osmolality

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 2nd 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 diabetesmellitus 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