ARF pdf - D. Dhyiaa - Muhadharaty

Fifth Stage

Internal Medicine

Dr. Dhyiaa – Lecture 5

ACUTE RENAL FAILURE

DEFINITION:

It is abrupt decrease in renal function which developed over a period of days or weeks
and usually accompanied by reduction in urine volume and retention of nitrogenous
waste (( eg. Blood urea and createnin ))

CAUSES:

1. Pre renal:

a. Absolute decrease in effective blood volume eg. Hemorrhage, burns, diarrhea,

vomiting.

b. Relative decrease in effective blood volume eg. Congestive heart failure, sepsis,

anaphylaxis

c. Arterial occlusion

2. Renal:

a. Acute tubular necrosis (( ATN ))
1.

Ischemic insult

( prolonged hypotension )

Nephrotoxic insult

which is either:

▪

Exogenous nephrotoxins

eg. Aminoglycosides, amphotericin B, contrast

agents.

▪

Endogenous substances

: Haemoglobuline, myoglobulin, uric acid,

bacterial toxins.

b. Acute interstitial nephritis
c. Acute glomerulonephritis

3. Post renal

a. Obstructive uropathy
b. Bladder neck obstruction.

Clinical presentations & evaluation

Reversible pre renal ARF:

•

Marked hypotension and signs of poor peripheral perfusion

•

Postural hypotension

(fall > 20/10 mmHg )

•

Evidence of the underlying cause but some time concealed blood loss can occur
eg GI-bleeding, pelvic fracture

•

Metabolic acidosis and hyperkalaemia are often present

•

Significant oliguria with concentrated urine

•

Elevated blood urea level with no or minimal increase in serum creatinine.
(B.urea/S.creatinine ratio

> 40

•

Low urine sodium

< 20 meq/L.

Management:

1. Establish and correct the underlying cause of ARF.
2. If the patient is hypovolaemic, restore the blood volume as rapidly as possible with

blood, plasma or normal saline.

3. Vital signs monitoring and central venous pressure monitoring.
4. Correct metabolic acidosis by:

a. Restoration of blood volume.

b. Isotonic Sodium bicarbonate may be used.

* If the treatment given sufficiently early, renal function will improve rapidly but
in some cases the treatment is ineffective and renal failure become established.

Established ARF:

CLINICAL FEATURES:

1. Features of the

underlying

cause

eg. Trauma, sepsis

Alteration in urine volume

usually started as oliguric phase followed by polyuric

phase which carry better prognosis and may indicate regeneration and recovery

from ATN.

3. GIT symptoms

((early uremic symptoms)) include: anorexia, nausea, vomiting and

hiccoughs.

4. Neurological manifestations:

drowsiness,apathy,confusion, fit, muscle twitching and

comma.

5.Cardiovascular features:

: pericarditis and arrhythmias which may be due to uremia

itself or as a resut of electrolyte disturbances.

6. Electrolytes and metabolic abnormalities:

a. Hyperkalemia:

particularly with massive tissue break down or haemolysis, ECG

changes ((tinted T-wave, absence of P-wave, wide QRS complex and Sine wave)),
elevated serum potassium.

b. Metabolic acidosis.

c. Dilutional hyponatermia.

d.Hypocalcaemia& Hyperphosphatemia.

7.Increased

respiratory rate

due to acidosis, pulmonary oedema or respiratory

infection.

Anaemia

may be present due to excessive blood loss or it may indicate acute

exacerbation on CRF.

9.Severe infection

may complicate ARF due to decreased immunity.

10. Volume overload:

bilateral leg oedema,

Pulmonary oedema,

Pericardial effusion.

Clinical approach to the diagnosis of ARF:

The clinical evaluation of ARF is achieved by answering the following

five questions

Is it ARF or an

acute on chronic

renal failure?

Is there renal tract

obstruction

Is there

reduction in effective ECF

volume?

Has there been a major

vascular occlusion

Is there

parenchymal renal disease

other than ATN?

A complete history, physical examination and chart review, as well as a careful

urinalysis, a renal ultrasound, and a few routine blood tests should be performed in all

patients with ARF .

This approach will reveal the likely cause of ARF in most patients. In a few carefully

selected patient ,additional ,selected special investigations-imaging, serology, renal

biopsy-may be necessary to establish the cause of renal dysfunction.

History

The diagnosis of prerenal failure is often facilitated by careful evaluation of the patient

fluid balance during the few days preceding the onset of ARF.

H/O vomiting or diarrhea

provides useful clues to the source of loss of ECF volume.

Symptoms of dry

cough,orthopnea, or ankle swelling

may indicate the possibility of

early volume overload.

Frequency, urgency, and hesitancy

are important symptoms in patient with bladder

dysfunction or bladder neck obstruction.

H/O ingestion of a nephrotoxic drugs

Systemic symptoms

such as fever, malaise or fatigue, and joint pain or skin rash raise

the possibility of ARF caused by acute GN associated with SBE, vasculitis or connective

tissue disease like SLE

H/O previous renal disease or hypertension

may point to pre-existing chronic renal

insufficiency .

Chart review

Since most ARF occurs in patients in hospital,the hospital record represent an

extremely an important source of information regarding the possible cause. A

chart review should be considered as an extension of the

history

, daily record of

vital signs

, changes in body

weight

and records of

fluid intake and out put.

The

record of all

drugs taken by the patient

must be examined for potentially

nephrotoxic drugs.

PHYSICAL EXAMINATION

Loss of skin turgor and postural hypotension when fluid loss exceed

5-10% of ECF volume.

Supine hypotension when the fluid loss exceed 20% of ECF volume.

Raised JVP ,pedal edema and pulmonary crackles indicate cardiac failure.

Skin:

* Jaundice

and other evidence of acute or chronic liver disease

*Maculopapular

skin rash may indicate drug induced AIN or acute GN.

*Malar rash

or photosensitivity in SLE

*Livedo reticularis

associated with cryoglobulinemia or atheroembolic disease

*Palpable purpura

commonly caused by cutaneous vasculitis or atheroembolic disease

*Nonpalpable purpura

may suggests the presence of thrombocytopenia associated with

SLE or thrombotic microangiopathy.,

Eye examination

*Jaundice, hypertensive retinopathy, Roth spots (endocarditis)or cholesterol emboli

(atheroembolic disease)

Abdominal examination:

*Ascites

may indicate chronic liver disease or congestive cardiac failure

*Bruits

over the anterior abdomen or confirmed to the renal angles

Any evidence of bladder neck obstruction

Rectal or pelvic examination

The presence of large postvoid residual (more than 200-300 ml) is strongly suggestive

of functionally significant urinary retention.

Urine volume

Patient with prerenal azotemia almost always have oliguria, but non oligureic ARF

seen in :

1. diabetes insipidus

2. sodium wasting disease such as adrenal insufficiency

3. hyperglycemia

4. malnutrition

5. chroniclly ill patient

6. urinary tract obstruction ( unilateral or partial )

7. contrast induced ARF

8. aminoglycosid induced ARF

*Anuria is unusual in patient with ATN but it is more common with rapidly progressive
GN, acute interstitial nephritis or vascular catastrophes such as renal artery embolism

or renal vein thrombosis .

If patient thought to have ATN have persistent anuria lasting more than

24 -48

hours,

the other causes of ARF must be reconsidered.

SERUM CHEMISTRY

Blood urea nitrogen

The clearance of urea is always less than the GFR. This is because of the back

diffusion of urea which is inversely related to the rate of urine flow and is

enhanced by vasopressin.

BUN rises more rapidly than the creatinine in patient with Prerenal failure

The ratio BUN : Cr is normally

15:1

(mg:mg) (

60:1

mmol:mmol)

High ratio > 20:1 caused by:

1. Prerenal failure

2. GI bleeding

3. increased protein intake

4. catabolic state

5. infusion of amino acids

6. corticosteroid therapy

7. tetracycllines

Low ratio < 5-10 :1 caused by:

1. severe liver disease

2. malnutrition

3. rhabdomyolysis

4. cimetidine

5. trimethoprim

6. cephalosporins

SERUM CREATININE

*As renal function deteriorates ,the Cr becomes progressively less reliable as an index

of GFR..

*BUN rarely exceeds 30mg/dl.and serum Cr > 2 mg/dl.unless there is concurrent
underlying chronic renal insufficiency.

OTHER SERUM CHEMISTRY:

*They are usually unhelpful in the diagnostic process.

Hyperkalemia, hyperuricemia,

hypocalcemia and hyperphosphatemia

are all common in ARF of any cause also

they are

not

useful in distinguishing ARF from CRF

URINALYSIS:

Microscopy

Hematuria

protienuria

condition

normal

Prerenal
azotemia

normal

Vascular
occlusion

Dysmorphic RBC
RBC cast
Granular cast

+++

Pyuria,WBC cast
eosinophiluria

AIN

Normal

HUS/TTP

Muddy brown granular
cast,epithelial cast,
sometime NONE in
nonoliguric ATN

ِATN

GUE may shows evidence of underlying renal pathology eg. GN, Interstitial nephritis or
evidence of underlying cause eg DM, Multiple myeloma

URINE CHEMISTRY

ATN

Prerenal

Index

>40

<20

Urine sodium

<20

>40

U. cr / P.cr. (mg/dl)

<300-350

>500

U.osm

<1.1

>1.5

U./ P. osmolality

<1.015

>1.018

Specific gravity

U. / P. urea

.>2

FeNa=U.Na/Ucr×Pcr/PNa×100

RFI=U.Na/ (U.cr/P.cr)

Hematological indices

-the

hematocrit is not useful

discriminate between ARF and CRF.

High WBC

count may point to systemic infection, lymphoma and leukemia

Eosinophelia

may suggest a drug induced ATN or atheroembolic disease

Thrombocytopenia

suggest HUS,TTP, SLE, myeloma, sepsis, and DIC.

RENAL ULTRASOUND

- It is a

key investigation

for the diagnosis of obstruction or CRF.

- It is

not a reliable method

for identifying the anatomical site of obstruction

Even

if the kidneys are reduced in size , the possibility of Prerenal ARF or ATN

superimposed on CRF must always be considered.

SEROLOGY

- ANA, ANCA, anti GBM, RF, C3 & complement levels

- They are useful for vascullitic or glomerular process

- Hepatitis and HIV serology (especially if dialysis is indicated)

: may shows Pulmonary oedema, pericardial effusion

CXR

: evidence of pericarditis, arrhythmia, Hyperkalemia

ECG

CT scan

It can delineate the level of obstruction and define retroperitoneal inflammation or

retroperitoneal malignant mass

RENAL ANGIOGRAPHY:

*It is

indicated

when renal artery occlusion is suspected

as a useful investigation in

diagnosing classical PAN

Renal venography

may be indicated to confirm the diagnosis of renal vein

thrombosis.

RENAL BIOPSY

It is unnecessary in ARF but can be useful in patient in whom parenchymal renal

disease other than ATN is suspected.( AIN or RPGN)

Renal biopsy also indicated in presence of systemic illness manifestations or for

unexplained ARF. or for unexpected cause for ARF.

After 4-6 weeks , a renal biopsy may be considered In patient with ATN who do not
recover renal function, renal biopsy indicated to determine the cause of ARF and clarify

the prognosis.

Treatment of ARF

1. Fluid balance

(input and output chart) with central venous pressure monitoring,

daily body weight and treatment of fluid over load with diuretics.

Emergency

treatment of Hyperkalemia

with ca-gluconate

Correction of acidosis

by giving Sodium bicarbonate.

Bolus dose of

loops diuretics

to initiate dieresis but if it fail, No farther diuretics

5. Restriction of salt intake &

protein intake into

40-60 gm/day

6. vigorous treatment of infection

. should be given.

7. Drugs

that are nephrotoxic should be omitted or dose adjustment.

8. Dialysis

( When ever indicated should not be delayed ) Which is

indicated

in:

a. Severe Hyperkalemia

b. Severe acidosis

not corrected by sodium bicarbonate.

c. Fluid overload

not corrected by diuretics.

d. Blood urea > 200mg/dL

. Or rapidly rising blood urea

more than 40mg/dL

. over 24hr.

e. Uremic encephalopathy

f. uremic pericarditis

g. severe uremic symptoms

not controlled by medical treatment.

Outcome & Prognosis

-The oliguric phase last 1-2 weeks.

- Those with oliguria more than 3 weeks carry poor prognosis.

- Uncomplicated ARF due to simple hemorrhage or drug carry better prognosis and low
mortality.

*ARF associated with serious infection and multiple organ failure carry poor prognosis

with 50-70% mortality

* Outcome is usually determined by the severity of the underlying disorder other

complication rather than by renal failure itself..

Thank you,,,