lapkas GH.docx

8/14/2019 lapkas GH.docx

1/9

1

Contrast Nephropathy Prevention Measures Coronary Angiography

Riyandy Pratama, Abdullah, Maimun SyukriDivision of Nephrologi and Hipertension

Department of Internal MedicineRSUZA/ Medical Faculty of UNSYIAH Banda Aceh

Abstract

Contrast nephropathy is a kidney function decline within 48-72 hours after

administration of contrast media.These events often occur after coronary angiography using

kontras.Media action containing ionic contrast nephrotoxic.

Reported one case of a man, 44 years old will be taken Coronary - angiography,

patients diagnosed coronary arterial with AKI stage injury, with acomplaint history of chest

pain radiating to the left shoulder and left with difficult breathe.ECG results deduced old

myocardial infarction inferior + ischemic lateral, vital signs encountered awareness compos

mentis, blood pressure, pulse, respiration and temperature in normal urine 2000cc/24 hours.

In the laboratory Hb: 16 g / dl, leukocytes 8,700 / ul, erythrocyte 5.730.000/ul, platelets284.000/ul LED 13 mm / h Ht: 48%, urea 52 mg / dl, creatinine: 2.2 mg / dl , HBsAg:

negative,In the management of patients with infusion of Ringer's lactate administration 20 gtt

/ I, at the time of NaCl 0.9% flush action as much as 2 liters, After action recheck urea: 37

mg / dl and creatinine 1.0 mg / dl urine 700 cc/4 hours. Patients currently undergoing

refurbishment and control poly regularly.

Keywords: contrast nephropathy, acute kidney injury

1stCase Report

Div.Nephrology and

Hypertension

Agreement of supervisor

Dr.Maimun Syukri SpPD, K-GH


2/9

2

I.INTRODUCTION

Radiocontrast use led to increased cases of acute renal failure (ARF) nephrotoxic, an

estimated 10% of cases occur during treatment pasien.Variasi contrast nephropathy incidents

were reported from several studies is influenced by differences in definition, the observation

period after the use of contrast and the prevalence of risk factors in a population study 1.

Mitchell et al (2010) in his research found radiocontrast nephropathy occurs more than 10%

in patients who underwent computed tomography scanning (CT scan) with contrast at the

emergensi2.

Radiocontrast nephropathy was defined as an increase in serum creatinine 0.5-1.0 mg / dl

or 25% -50% of the initial value that occurs the first 24 hours after administration of contrast

media and reached the top 5 days later. European Society of Urogenital Radiology define

radiocontrast nephropathy is a disorder of renal function (serum kretinin increase> 0.5 mg / dl

or> 25%) within 3 days after contrast exposure, without alternative etiology els.according to

acut kidney injury network (AKIN ) radiocontrast nephropathy is an increase in serum

creatinine> 0.3 mg / dl with oliguria3. absolute increase in serum creatinine> 0.3 mg / dl as

sensitive and more specific for severe kidney trouble and complications death.2

The following will be in the report of a coronary heart disease patients who experience

acute kidney injury will do the coronary angiography

II Cases

Reported a case of a male, 44 years of Consult patients in the cardiology section for

the action-coronary angiography, patients diagnosed coronary arterial with AKI stage injury,

with acomplaint history of chest pain radiating to the left shoulder and left with difficult

breathe.ECG results deduced old myocardial infarction inferior + ischemic lateral, vital signs

encountered awareness compos mentis, BP : 11o/70mmHG, pulse: 88x/i, respiration: 20x/i

and temperature : 36,7 C urine 2000cc/24 hours. In the laboratory Hb: 16 g / dl, leukocytes

8,700 / ul, erythrocyte 5.730.000/ul, platelets 284.000/ul LED 13 mm / h Ht: 48%, urea 52

mg / dl, creatinine: 2.2 mg / dl , HBsAg: negative, In the management of patients with

infusion of Ringer's lactate administration 20 gtt / I, at the time of NaCl 0.9% flush action as

much as 2 liters, After action recheck urea: 37 mg / dl and creatinine 1.0 mg / dl urine 700

cc/4 hours. Patients currently undergoing refurbishment and control poly regularly,


3/9

3

From investigation; reports angiography left anterior descending: Total osteal stenosis,

antegrade from the proximal and of left-lateral circumflex got CO from RCA,,

Left circumflex: total block on the proximal after antegrade gets old myocardial

infarction from distal to proximal,

Old myocardial infarction: 60% stenosis in the mid segment osteal and 70%, RCA:

total stenosis in the mid segment, antegrade from the proximal and distal RCA gets co-Left

anterior lateral desending. Conclusion: three vessel desease..

III Discussion

Acute kidney injury is a rapid decrease (within hours to weeks) glomerular filtration rate

which generally lasts reversible, followed by failure of the kidneys to excrete residual

nitrogen metabolism, with / without fluid and electrolyte balance disorders 4. Causes of Acute

Kidney Injury divided into 3 major sections5,6:

1. Prerenal: hypovolemia, decreased cardiac output, renal vascular resistance ratiochange systemic, renal hypoperfusion with impaired renal autoregulation,

hyperviscosity syndrome

2. Renal: renovascular obstruction, glomerular disease, acute tubular necrosis, interstitialnephritis, and deposition intratubular obstruction, renal allograft rejection

3. Post renal: obstruction ureter, bladder neck obstruction, urethral obstructionClassificationRIFLE5,6

RIFLE category Serum creatinine criteria Kriteria urine output

Risk The increase in serum creatinine> 1.5 x baseline

value or decreased glomerular filtration rate>

25%

2x baseline or

decreased glomerular filtration rate> 50%

< 0,5 ml/kg/hour for 12 hours

Failure The increase in serum creatinine> 3x baseline or

decreased glomerular filtration rate> 75%


4/9

4

ESRD

function> 4 week

Terminal renal failure

Some parameters of the diagnosis of acute kidney injury assessment5,6

1. Serum creatinine levels2. Urine volume3. Serum cystatin c level4. Biological markers (NGAL, interleukin 18)

In patients, the result of lab urea: 52 mg / dl, creatinine: 2.2 mg / dl,

2000cc/24 hour urine production in patients diagnosed coronary heart disease

and coronary angiography will be performed the patient is examined serum levels

of cystatin C because of funding limitations patients, and no examination NGAL

and interleukin 18 as no reagents for examination in the laboratory.

Contrast nephropathy is a decline in renal function is occurring abruptly

within 48-72 hours after patients received the injection of contrast media with an

increase in serum creatinine> 25% of the value baseline4.Patients with impaired

renal function who receive radiocontrast usually will have a second phase of

oliguria after up to five days radiocontrast administration and an improvement of

serum creatinine and urine volume on the seventh day.

7,8,9

Contrast nephropathy risk factors involving age, male - female, preexisting

renal dysfunction, diabetes mellitus, dehydration, congestive heart failure, multiple

myeloma and given the volume of radiocontrast.10,11

Risk factors for contrast-induced nephropathy8

A. Factors related to patient: CKD, CHF, diabetes mellitus, age> 75 years, dehydration,

systemic hypotension, nephrotoxic drugs, anemia related to blood loss during PCI, renal

transplant, hypoalbuminemia (


5/9

5

Risk factors Skor

hypotension 5

Intra-aortic balloon counter pulsation 5

CHF 5Diabetes 3

Age > 75 tahun 4

Anemia 3

The volume of contrast medium 1 for each 100 ml

Serum kreatinin > 1,5 mg/dl or estimated

glomerular filtration rate < 60 ml/min/1,73

m2

eLFG (ml/min/1,73m2)= 186,3x( kreatinin)-

1,154x(age)-0,203x0,742 if woman)x1,210 if

man

eLFG 40-60

eLFG 20-40

eLFG < 20

4

2

4

6

Risk scores Risk of contrast nephropathy Risk of dialysis

16 57,3% 12,6%

Radiocontrast use with low osmolarity (ratio of iodine atoms to osmotic active

particles) is useful for reducing the incidence of nephropathy. Meta-analysis of studies

comparing high and low osmolality radiocontrast, obtained with low osmolarity radiocontrast

nephropathy radiokontras slight lead.7,9,11

Contrast media should be considered in some instances before given such as high

osmolarity, ionic contrast, Visikositas contrast media and contrast volume was sendiri.Suatu

randomized study states contrasts with high osmolarity (> 1400 mOsm) at greater risk of the

occurrence of contrast nephropathy. Iohexol significantly related to increased risk of contrast

nephropathy compared Iopamidol or iodixanol.2,3


6/9

6

In this case a man - 44 years old at diagnosis of coronary artery disease encountered in

awareness of the vital signs that compost mentis, blood pressure, pulse, respiration and

temperature within normal limits. Urea: 52 mg / dl, creatinine: 2.2 mg / dl, using the contrast

agent iopamiro 370 50 ml mild risk factor for radiocontrast nephropathy

Recommendation and selection of patients for the prevention of contrast nephropathy10,12,13

1. Patients who received angiography scheduled to be checked serum creatinine2. Kliren examination creatinine3. Patients with moderate to severe risk :

a. Selection of imaging examinations (gadolinium angiography)b. Cessation of NSAIDs, dipiridamol, metformin 48 hours before the procedurec. Stop diuretics and ACE inhibitors 24 hours before the procedured. Hydration

- Moderate risk: 0.45% saline (1.0-1.5 ml / kg / h) 4 hours before the procedures / d 24 hours after the procedure.

- Risk weight: 0.45% saline (1.0 to 1.5 ml / kg / hour) 12 hours before theprocedure s / d 24 hours after the procedure.

e. The use of low molecular radiocontrastf. Radiocontrast volume limitedg. Monitor urine output, BUN and serum creatinine examination 24 hours after the

procedure.

Bartoreli et al (2008) found in some studies of hydration with isotonic saline is superior than

isotonic saline as isotonic fluid capacity building extends to the intravascular volume8 ..

Fluid administration aims to reduce vasoconstriction stimulation in patients with

dehydration, compensate for fluid loss due to the use of osmotic diuresis, lowering the

concentration of radiocontrast in intraluminal urinary tubules and reduce the viscosity and

reduce the toxicity of the tissue fluid ginjal.pemberian inpatients performed with saline 0.45

% 1 ml / kg / hour for 24 hours and 6-12 hours before tindakan.Pemilihan saline 0.45% is

now replaced by saline 0.9%.7,8,12


7/9

7

The guide recommendation of the UK Health care is as follows16:

Hydration with saline

IVFD 1ml/kg/hr (max 100 ml / hour) 12 hours before and 12 hours post-contrast (total

infusion time 24 hours) CHF or left ventricular ejection fraction (LVEF)


8/9

8

VI Prognosis

Contrast nephropathy is usually a process while the renal function returned to normal

7-14 day delivery kontras.kurang of one third of patients had residual renal damage, patients

with diabetes mellitus, hypovolemia, heart failure, liver cirrhosis, hypertension and

proteinuria are at high risk for the occurrence of nephropathy this contrasts with patients

given contrast nephropathy have a poor prognosis.

In this case the patient's prognosis good

VII Summary

Reported one case of a man - 44 year old be taken Cast - ndiagnosa angiography in CAD with

urea: 52 mg / dl, creatinine: 2.2 mg / dl ditatalaksanaan patient with ringer lactate infusion

administration GTT 20 / I at the time the action flush Nacl 0 , 9% post actions 2 liter urea: 37

mg / dl and creatinine 1.0 mg / dl and the patient can go home and control back to the

cardiology and GH


9/9

9

REFERENCES

1. Coffman T, Kidney function impairment caused by therapeutic agents.In : GreenbergA.Editor. Primer on Kidney disease,5thed.Philadelphia, Elseveir. 2009.P.288-9

2. Mitchell AM, Jones AE. Incidence of contrast induced nephropaty after contrastenhanced computed tomography in the outpatient setting. Clin J Am Soc Nephrol

2010;5:49.

3. McCullough PA,Contras induced acut kidney injury.J. Am. Coll. Cardiol2008;51:1419-28.

4. Abuelo JG. Normotensive ischemic acute renal failure. N Engl J Med. 2007;357:797-805

5. Adhiutami,R, 2008 Kasus AKI pada Dehidrasi Akut. http//fkumycase.net6. Baratawidjaja KG, Iris R 2009. Imunologi dasar edition VIII FK Universitas

Indonesia.

7. Heyman S, Mayer B, Robert EC. Radiocontrast media induced acut renal failure.In :Robert WS, editor. Dissease of the kidney & urinary tractus,8 th ed.Philadelphia:

Churchill Livingstone 2007;45 : 110217.

8. Bartorelli AL,Marenzi G. Contrast induced nephropathy. Journal of IntervensionalCardiology 2008;21:74-85

9. Kawashima A, LeRoy AS. Plain radiography, excretion radiography,and contrastradiography. In: Davison AM editor. Oxforord Text Book of Clinical Nephrology, 3rd

Ed.Oxford University Press 2005:97-9.

10.Weisbord s,Palevsky P. Contrast induced acute kidney injury:Short and long termimplications.semin Neprol 2011;31(3):300-9.

11.Magee C.Guidelines for the prevention of contrast induce nephropathy. BeaumontHospita 2009:3-5.

12.Barrett BJ,Partrey PS.Preventing nepropathy induced by contrast medium. NEJM2006.354:379-86.

13.Schweiger M,Chambers C,Davidson C et al.Prevention of contrast inducednephropaty:recommendations for the high risk patient undergoing cardiovascular

procedures. Catherization and cardiovascular Interventions 2007;69:135-40.

14.Adhiutami,R, 2008 Kasus AKI pada Dehidrasi Akut. http//fkumycase.net15.Baratawidjaja KG, Iris R 2009. Imunologi dasar edition VIII FK Universitas

Indonesia.

16.Andrew B, Margaret FH, Peter M, et al. Guidelines for the prevention of contrastinduced nefropaty. Canadian Association of Radiologist. Approved : june 17.2011:12.

17.Rihal CS, Textor SC, Grill DE,et al. Incidence and prognostic importance of acuterenal failure after percutaneous coronary intervention.Circulation 2002;105:2259-

2264

Documents

lapkas GH.docx