Clinical Presentation

SCU

Dr. Shoeb Bin Islam

Senior Clinical fellow

Icddr,b

Case HistoryName : x

Age : 18 years

Sex : Female

D/A : 20/04/09

D/D : 02/05/09

Admission problems :

(Partial History at the beganing)

1) Diarrhoea - 1 days

2) Vomiting - 1days

3) Fever - 1days

4) Drowsy – 1 hour

(Actually patient had no real attendant, we collected information from a person who did not give proper history and after than he left away )

On Examination

Patient was Drowsy followed by Unconciousness and febrile

Pulse : 100 / min, regular, moderate volume

R/R : 22 / min, no chest in drawing.

Temperature : 39`C

Blood Pressure : 100/65mmHg

Pallor, cyanosis, jaundice, oedema - Nil

Dehydration :Some DH

ON EXAMINATION

Nervous sytem Examination-

patient unconcious

Kernig`s Sign - Negative

Pupil – normal in size and reacting to light

After 10-12 hours patient developed repeated convulsion

Urination- Urine Passed ?7-8 hour prior to admission (scanty)

Other systems(CVS,RESPIRATORY,GIT) revealed nothing abnormalities

*� Actually patient had no real attendant, we collected information from a person who did not give proper history and after than he left away .

PROBLEM LIST

*ACUTE WATERY DIARRHOEA

*SOME D/H

*FEVER

*UNCONCIOUSNESS (? MENINGITIES )

*?RENAL FAILURE( Uremic Encephalopathy)

*SEPTECEMIA

* LACK OF PROPER HISTORY

LABORATORY INVESTIGATIONS

CBC:- Hemoglobin-10.9gm/dlHct – 33.6%,

TC- 12.97 / 10^u, Poly – 83.8%, Lymp – 12.7%, Band – 00%, Monocytes – 3.4%, Eosinophil – 00%Basophil- 0.1%ESR - 48 mm/1st hour

R/S for Cholera:- Vibrio Cholera01 E1 Tor Ogawa

CXR- Normal study

Blood C/S No GrowthUSG and Urine R/M/E WBC cast and Epithelial cell-7-8 Protein-+

21/04/09 24/04/09 25/04/09 01/05/09

S.Na+ 126.7mmol/l 128.6mmol/L 130.7mmol/L 141.2

S.K+ 2.4 mmol/L 2.73 mmol/L 2.45 mmol/L 3.02

S.Cl- 90.1mmol/l 93 mmol/L 95.8mmol/L 106

TCO2 16.8mmol/L 13.5mmol/L 14.8mmol/L 23.9

ANION GAP

22.2mmol/L 24.83mmol/L 22.5 mmol/L 14.32

OTHERS BUN- 138.94mg/dlUREA- 49.26 mmol/L

BUN- 133.94mg/dlUREA- 47.83mmol/L

BUN- 60.76mg/dlUREA- 21.7mmol/L

URINARY ELECTROLYTEU.Sodium- 44.7mmol/LU.Potassium- 12.77mmol/LU.Cl- - 33mmol/LTCO2- 5mmol/LU.Creatinine (Random)-7211 umol/L

SERUM ELECTROLYTE REPORTS

21/04/09 23/04/09 24/04/09 25/04/09 29/04/09 1/5/20090

100

200

300

400

500

600

700

800

900

1000DATE SERUM

CREATININE (UMOL/L)

SERUMCREATININE(mg/dl)

21/04/09 582.6 6.5

23/04/09 773.3 8.7

24/04/09 882.3 9.9

25/04/09 915.6 10.3

29/04/09 459.2 5.1

01/05/09 126.4 1.4

*TOTAL DAYS - 11 DAYS

SERUM CREATININE

1 mg/dl = 88.4 umol/L

MANAGEMENT

Tab.Azythromycin for Cholera

Some D/H - I/V Acetate

Septicemia – Inj. Ceftriaxone

Convulsion - Inj. Diazepam + Inj. Phenoberbitone

For Hypokalamia – Syp Kcl through NG Tube

For Fluid over load - Inj Frusemide

Changing position Frequently

Proper Nursing care

Maintain urine input &output chart and fluid Intake accordingly

We had a plan to Refer the patient to Kidney hospital but we could not manage any attendant .

RENAL FAILURE

DIAGNOSIS & MANAGEMENT OF

AN UNCONCIOUS & UNATTENDENT PATIENT

Anatomy: The Renal System

• Kidneys• Ureters

– Enter at oblique angle– Peristalsis

• Both prevent reflux• Bladder

– Capacity 300–500 ml

• Urethra– Excretion; outside of body.– In Males surrounded by

prostate

Reduce Urine output/Anuria /urine abnormality

?Renal failure

?Acute or Chronic Renal Failure

Prerenal Renal Postrenal

If Acute renal Failure

ATN cause by Ischemia ATN caused by Nephrotoxic Drugs

Fig: Algorithm for diagnosis and causes of renal failure of a unconscious patient where proper history cannot elicited .

ATN Develop or Not

How Do We Proceed?

Classification system for AKI

HighSpecificity

Risk

Injury

Failure

Loss

EKSD

GFR Criteria Urine Output criteria

HighSensitivity

Classification system for AKI

Increase in SCr Urine output

Risk of renal injury

Injury to the kidney

Failure of kidney function

0.3 mg/dl increase

2 X baseline

3 X baseline OR> 0.5 mg/dl increase if SCr >=4 mg/dl

< 0.5 ml/kg/hr for > 6 h

< 0.5 ml/kg/hr for >12h

Anuria for >12 h

Loss of kidney functionEnd-stage disease

Persistent renal failure for > 4 weeksPersistent renal failure for > 3 months

RIFLE criteria for diagnosis of AKI

Definition:Means an abrupt deterioration of renal function within hours, leading to retention of water, crystalloids and nitrogenous products.

DEFINATION

Rapid decline in the GFR over days to weeks-

Cr increases by >0.5 mg/dL

GFR <10mL/min, or <25% of normal

Acute Renal Insufficiency-

Deterioration over days-wks

GFR 10-20 mL/min

Documented oliguria of <0.5 ml/kg/hr for 12 hrs

Definition  •Acute renal failure is sudden loss of the ability of the kidneys to excrete wastes, concentrate urine, and conserve electrolytes. ("Acute" means sudden, "renal" refers to the kidneys.)

– Rapid decline in GFR (Over Hours To Days)

– Usually Reversible

 • Chronic renal failure

is a gradual and progressive loss of the ability of the kidneys to excrete wastes, concentrate urine, and conserve electrolytes.– Kidney Damage for > 3

months– Irreversible– 75-60% of function can be

lost before its noticeable

1) History

2) Oliguria = ARF; acute CRF decompensation

3) Renal ultrasound• Normal or large = acute• CRF – small (unless PKD, diabetes, amyloid)

4) ARF =Unstable azotemia (↑ or ↓ over days)

5) Anemia – unreliable for ARF vs. CRF

6) ↑PO4, ↑K+, metabolic acidosis, ↑uric acid –little diagnostic value

7) Urinalysis – no value unless normalsuggesting pre-renal azotemia .

Differentiating ARF vs. Chronic Renal Failure (CRF)

CLASSIFICATION OF RENAL FILURE

Classification GFR (mls/min/1.73m2) Serum Creatinine (mol/L)

Mild 20 to 50 150 to 300

Moderate 10 to 20 300 to 700

Severe < 10 > 700

Appendix 3 : BNF

Types of Acute Renal Failure

JASN 1998;9(4):710-718

Onset – 1-3 days with ^ BUN and creatinine and possible decreased UOP

Oliguric – UOP < 400/d, ^BUN,Crest, Phos, K, may last up to 14 d

Diuretic – UOP ^ to as much as 4000 mL/d but no waste products, at end of this stage may begin to see improvement

Recovery – things go back to normal or may remain insufficient and become chronic

STAGES

Anuria: No UOP or urine output less than 50cc/24hr.

Oliguria: UOP<400-500 mL/d

Azotemia: Incr Cr, BUN• May be prerenal, renal, postrenal• Does not require any clinical findings

Ureamia : Azotemia + Clinical Menifastation

Definitions

• It occurs when renal blood flow is decreased before reaching the kidney, causing ischemia of nephrons.– ↓ Renal Perfusion = ↓ GFR leading to Oliguria

– Most common type of ARF

– Common Causes:

• Hypotension (severe and abrupt)

• Hypovolemia

• Low Cardiac Output States

– Treatment to correct cause, if not corrected it may lead to permanent renal damage.

Prerenal ARF

THE KIDNEYS ARE NORMAL

26

Prerenal Disease

*True volume depletion *Advanced liver disease*Congestive heart failure*Renal arterial disease*Perinatal or Neonatal hemorrhage*Perinatal asphyxia and hyaline membrane disease*Gastroenteritis*Congenital and acquired heart diseases

Prerenal Disease

27

Intrinsic Renal Failure

Intrinsic Renal FailureI. Renovascular obstruction (bilateral, or unilateral in the setting of one kidney)-

  A. Renal artery obstruction: atherosclerotic plaque, thrombosis, embolism, dissection aneurysm, large vessel vasculitis .

   B. Renal vein obstruction: thrombosis or compressionII. Diseases of the glomeruli or vasculature -

  A. Glomerulonephritis or vasculitis  B. Other: thrombotic microangiopathy, malignant hypertension, collagen vascular diseases (SLE)

III. Acute tubular necrosis -

  A. Ischemia: causes are the same as for prerenal ARF, but generally the insult is more severe and/or more prolonged

  B. Infection, with or without sepsis syndrome

  C. Toxins:    1. Exogenous: radiocontrast, calcineurin inhibitors, antibiotics (e.g., aminoglycosides),

    2. Endogenous: rhabdomyolysis, hemolysis

IV. Interstitial nephritis –

  A. Allergic: antibiotics ( -lactams, sulfonamides, quinolones, rifampin), nonsteroidal anti-inflammatory drugs, diuretics, other drugs

  B. Infection: pyelonephritis (if bilateral)

  C. Infiltration: lymphoma, leukemia, sarcoidosis

  D. Inflammatory, nonvascular: Sjögren's syndrome, tubulointerstitial nephritis with uveitis

V. Intratubular obstruction –

  A. Endogenous: myeloma proteins, uric acid (tumor lysis syndrome), systemic oxalalosis

  B. Exogenous: acyclovir, gancyclovir, methotrexate, indinavir

Prerenal azotemia - Intact Tubular Function

ATN - Renal Tubule Epithelium ( also Basement Membrane) Destruction.

There are two major histiologic changes that take place in ATN: -

(1) tubular necrosis with sloughing of the epithelial cells

(2) occlusion of the tubular lumina by casts and by cellular debris.

Prerenal Azotemia is the main factor that predisposes patients to ischemia- induced acute tubular necrosis (ATN)Most cases of ischemic ARF are reversible if the underlying cause is corrected.

Prerenal Azotemia and Ischemic tubular necrosis

In addition of the tubular obstruction, two other factors appear to contributeto the development of renal failure in ATN:-

across the damaged tubular epithelia backleak of filtrate and

a primary reduction in glomerular filtration.

The decrease in glomerular filtration results both from arteriolar vasoconstriction and from mesangial contraction.

The decline in renal function beginsabruptly following a hypotensive

episode, rhabdomyolysis, or the administration of a radiocontrast media.

When aminoglycosides are the cause, the onset is more insidious, with the first rise in creatinine being at seven or more days.

Renal damage is NOT dose-dependentMay take wks after initial exposure to drug• Up to 18 mos to get AIN from NSAIDS!

But only 3-5 d to develop AIN after second exposure to drug

• Fever (27%)• Serum Eosinophilia (23%)• Maculopapular rash (15%)

• Bland sediment or WBCs, RBCs, non-nephrotic proteinuria• WBC Casts are pathognomonic!• Urine eosinophils on Wright’s or Hansel’s Stain

– Also see urine eos in RPGN, renal atheroemboli...

AIN From Drugs

Ischaemic ATN (Due to Hypovolumia)

Nephrotoxic ATN

Background History Diarrhoea,Vomitting,heart failure,Shock Drugs,Toxin

Kidney Invilvement 3rd Segment of proximal tubule (proximal tubule – Reabsorb 65% of Sodium) and Assending Loop of henlee (Reabsorb 25% of Sodium)

Mostly proximal convoluted tubule

FeNa Usually >3% Usually >1% ( 2-3%)Clinical Triat Fever ,Rash ,Eosinophilia nit associated Mostly Present

UNa Usually Greater >40 (Gradually Increasing from >20)

Comperatively low(>20)

Urinary Protein Absent/+ +/++WBC Cast Absent pathognomicEosinophiluria on Wrights or Hansels Strain

Absent Mostly present

Treatment Restore renal function Usually Fluid And Stop Offending drugs and sometimes Steroid

Difference Between Ischemic and Nephrotoxic ATN

Reabsorb 65% of Sodium

Reabsorb 25% of Sodium

Reduce Urine output/Anuria /urine abnormality

?Renal failure

?Acute or Chronic Renal Failure

Prerenal Renal Postrenal

If Acute renal Failure

ATN cause by Ischemia ATN caused by Nephrotoxic Drugs

Fig: Algorithm for diagnosis and causes of renal failure of a unconscious patient where proper history cannot elicited .

ATN Develop or Not

How Do We Proceed

MINIMUM STEPS FOR DIAGNOSIS

History Taking

General and Systemic Examination

Laboratory investigation

Serum ElectrolyteSerum CreatinineBUN

Urine R/M/EUrinary ElectrolyteUrinary CreatinineUrinary Urea

USG OF ABDOMAN

Urea - Is the By-product of Protein metabolismCreatinine- Is the By-product of Muscle metabolism

FeNa = (urine Na x plasma Cr) x100 (plasma Na x urine Cr)

GFR = F (140 – age [yrs]) Ideal Body Wt (kg)Serum creatinine (mol/L)

Where:F = 1.23 for males and 1.04 for females

BUN: Cr = blood urea nitrogen:creatinine ratio

UNa = urinary concentration of sodium;

Pre-renal=Creatinine cannot be reabsorbed, thus leading to a BUN/Cr ratio of > 20

Some Important Formula

Predicting GFR using serum and urine creatinine concentrations.

Cockcroft and Gault Equation

GFR = F (140 – age [yrs]) Ideal Body Wt (kg)Serum creatinine (mol/L)

Where:F = 1.23 for males and 1.04 for females

IBW = 50 kg + 2.23 kg for every 1” > 5 feet in height (male)IBW = 45.5 kg + 2.3 kg for every 1” > 5 feet in height (female)

Assessing the patient with acute renal failure – Laboratory analysis

• Fractional excretion of sodium:

(UrineNa+ x PlasmaCreatinine) FENa= ______________________ x 100

(PlasmaNa+ x UrineCreatinine)

It is the Simple measurement of Tubular Excretory function

– FENa < 1% → Prerenal

– FENa > 2% → Epithelial tubular injury (acute tubular necrosis), obstructive uropathy

– If patient receiving diuretics, can check FE of urea.

FeNa = (urine Na x plasma Cr) (plasma Na x urine Cr)

FeNa <1% 1. PRERENAL• Urine Na < 20. Functioning tubules reabsorb lots of filtered Na 2. ATN (unusual)• Postischemic dz: most of UOP comes from few normal

nephrons, which handle Na appropriately• ATN + chronic prerenal dz (cirrhosis, CHF)3. Glomerular or vascular injury• Despite glomerular or vascular injury, pt may still have well-

preserved tubular function and be able to concentrate Na

More FeNaFeNa 1%-2% 1. Prerenal-sometimes (eg-Related with Sepsis)2. ATN-sometimes3. AIN-higher FeNa due to tubular damage

FeNa >2%-3%4. ATN Damaged tubules can't reabsorb Na.usually

nephrotoxic ,Sepsis

FeNa >3%Goes in Favour of Ischaemic ATN

Guide To The Differential Diagnosis of intrinsic ARF

Muddy Brown Granular Casts

Eosinophiluria Present:Acute Interstitial nephritis likely

Eosinophiluria Absent:Acute interstial nephritis possible

Assessing patient with acute renal failure – Urinary Casts

Red cell casts GlomerulonephritisVasculitis

White Cell casts Acute Interstitial nephritis

Fatty casts Nephrotic syndrome, Minimal change disease

Muddy Brown casts Acute tubular necrosis

RBC cast

Hyaline cast Granular cast

Granular castGranular cast

WBC cast

WBC castOval fat body and Hyaline cast

Intrinsic Renal Disease

Prerenal Azotemia Postrenal Azotemia Acute Tubular Necrosis (Oliguric or Polyuric)

Acute Glomerulonephritis

Acute Interstitial Nephritis

Etiology Poor renal perfusion

Obstruction of the urinary tract

Ischemia, nephrotoxins

Poststreptococcal; collagen-vascular disease

Allergic reaction; drug reaction

Serum BUN:Cr ratio > 20:1 > 20:1 < 20:1 > 20:1 < 20:1 Urinary indices UNa (mEq/L)

< 20 Variable > 20 < 20 Variable

FENa (%)

< 1 Variable > 1 < 1 < 1; > 1

Urine osmolality (mosm/kg)

> 500 < 400 250–300 Variable Variable

Urinary sediment Benign or

hyaline castsNormal or red cells, white cells, or crystals

Granular (muddy brown) casts, renal tubular casts

Dysmorphic red cells and red cell casts

White cells, white cell casts, with or without eosinophils

BUN: Cr = blood urea nitrogen:creatinine ratio; UNa = urinary concentration of sodium; FENa = fractional excretion of sodium

Classification and differential diagnosis of acute renal failure

ATN PrerenalCr increases at

0.3-0.5 /dayincreases slower than 0.3 /day

U Na, FeNa

UNa>40FeNa >2%

UNa<20FeNa<1%

UA epi cells, granular casts

Normal

Response to volume

Cr won’t improve much

Cr improves with IVF

BUN/Cr 10-15:1 >20:1

The FENa tends to be high in ischemic ATN but is often low in patients with sepsis-induced, pigment-induced, and some forms of nephrotoxic ATN (e.g., contrast-associated).

Patients with acute interstitial nephritis may present with triad of fever, rash, and eosinophilia)UA (1 - 2+ protein, renal tubular epithelial cells, wbc’s - eosinophils, wbc casts)

1st 2nd 3rd 4th 5th 6th Total Duration

Pt-1 6.9 9.45 6.09 2.7 2.0 1.4 6 DaysPt-2 4.6 3.4 6.0 4.8 3.3 2.3 (day 6)

1.3(day 7)7 days

Pt-3 6.5 8.7 Day -3

9.9day-4

10.3Day-5

5.1Day-9

1.4 day-11

11 Days

Cholera patient-1 Cholera patient-2 Septicemia patient

FeNa 4.24% 3% 1.13%

GFR 7 ( Severe) 8 (Severe) 18.6 ( Moderate)

BUN/Cr 13.92 5.06 20

Urinary Na 44.7 17.9 34.6

Renal Index 5.46 3.7 1.5

USG Noraml Normal Suggestive of bilateral parenchymal Diseases

Intervention by Inj.Frusemide and its outcome of an ARF ( Develop ATN)

Patient develop ATN Due to Prerenal cause

Acute Renal FailureUrinary Indices

UOsm

(mOsm/L)(U/P)Cr UNa

(mEq/L)

RFI FENa

ATN ATN

ATNATN ATN

PR PR

PRPR PR

1.01.0

350

500 40

20

40

20

Pathoetiology Medication Clinical findings Treatment

ACE, angiotensin-converting enzyme; ATN, acute tubular necrosis; CPK, creatinine phosphokinase; FENa, fractional excretion of sodium; LDH, lactate dehydrogenase; NSAIDs, nonsteroidal anti-inflammatory drugs; UOsm, urine osmolality.

Prerenal injury

Diuretics, NSAIDs, ACE inhibitors, ciclosporin, tacrolimus, radiocontrast media, interleukin-2, vasodilators (hydralazine, calcium-channel blockers, minoxidil, diazoxide)

Benign urine sediment, FENa <1%, UOsm >500

Suspend or discontinue medication, volume replacement as clinically indicated

Intrinsic renal injury (vascular effects: thrombotic microangiopathy)

Ciclosporin, tacrolimus, mitomycin C, conjugated estrogens, quinine, 5-fluorouracil, ticlopidine, clopidogrel, interferon, valaciclovir, gemcitabine, bleomycin

Fever, microangiopathic, hemolytic anemia, thrombocytopenia

Discontinue medication, supportive care, plasmapheresis if indicated

Intrinsic renal injury (vascular effects: cholesterol emboli) Heparin, warfarin, streptokinase

Fever, microangiopathic, hemolytic anemia, thrombocytopenia

Discontinue medication, supportive care, plasmapheresis if indicated

Intrinsic renal injury (tubular toxicity)

Aminoglycosides, radiocontrast media, cisplatin, nedaplatin, methoxyflurane, outdated tetracycline, amphotericin B, cephaloridine, streptozocin, tacrolimus, carbamazepine, mithramycin, quinolones, foscarnet, pentamidine, intravenous gammaglobulin, fosfamide, zoledronate, cidofovir, adefovir, tenofovir, mannitol, dextran, hydroxyethylstarch

FENa >2%, UOsm <350, urinary sediment with granular casts, tubular epithelial cells

Drug discontinuation, supportive care

Intrinsic renal injury (rhabdomyolysis)

Lovastatin, ethanol, codeine, barbiturates, diazepam

Elevated CPK, ATN urine sediment

Drug discontinuation, supportive care

Intrinsic renal injury (severe hemolysis)

Quinine, quinidine, sulfonamides, hydralazine, triamterene, nitrofurantoin, mephenytoin

High LDH, decreased hemoglobin

Drug discontinuation, supportive care

Intrinsic renal injury (immune-mediated interstitial inflammation)

Penicillin, methicillin ampicillin, rifampin, sulfonamides, thiazides, cimetidine, phenytoin, allopurinol, cephalosporins, cytosine arabinoside, furosemide, interferon, NSAIDs, ciprofloxacin, clarithromycin, telithromycin, rofecoxib, pantoprazole, omeprazole, atazanavir

Fever, rash, eosinophilia, urine sediment showing pyuria, white cell casts, eosinophiluria

Discontinue medication, supportive care

Intrinsic renal injury (glomerulopathy)

Gold, penicillamine, captopril, NSAIDs, lithium, mefenamate, fenoprofen, mercury, interferon-, pamidronate, fenclofenac, tolmetin, foscarnet

Edema, moderate to severe proteinuria, red blood cells, red blood cell casts possible

Discontinue medication, supportive care

Obstruction (intratubular: crystalluria and/or renal lithiasis)

Aciclovir, methotrexate, sulfanilamide, triamterene, indinavir, foscarnet, ganciclovir

Sediment can be benign with severe obstruction, ATN might be observed

Discontinue medication, supportive care

Obstruction (ureteral; secondary to retroperitoneal fibrosis)

Methysergide, ergotamine, dihydroergotamine, methyldopa, pindolol, hydralazine, atenolol

Benign urine sediment, hydronephrosis on ultrasound

Discontinue medication, decompress ureteral obstruction by intrarenal stenting or percutaneous nephrostomy

24/04/09

S.Na + -128.6mmol/L

S.K+ - 2.73 mmol/L

S.Cl - 93 mmol/L

TCO2 - 13.5mmol/L

Anion gap -24.83mmol/L

BUN - 138.94mg/dlUREA - 49.26 mmol/L

Serum Creatinine – 882.3u mol/L

URINARY ELECTROLYTEU.Sodium - 44.7mmol/L

U.Potassium - 12.77mmol/L

U.Cl- - 33mmol/L

TCO2 - 5mmol/L

U.Creatinine (Random)-7211 umol/L

24/04/09

GFR -6.5 ml/min(SEVERE RENAL FAILURE)

FeNa -4% ( >2%) (ATN)

FENa - 35% ( Pre Renal )

Urinary Na+ - 44.7 mmol/L ( <20mmol/L ATN)

Oliguria - Urine out put less than 500 cc

Urinary Creatinine = 8.17% (<20% ATN)Serum Creatinine

BUN/Creatinine = 14.03 ( <20% Renal)

Urine R/M/E - No Eosinophilurea, WBC cast and Epithelial cell-7-8 Protein-+

BUN: Cr = blood urea nitrogen:creatinine ratio; UNa = urinary concentration of sodium; FENa = fractional excretion of sodium

Result Interpretations

FeNa = (urine Na x plasmaCr) 100 (plasma Na x urineCr)

SO,PATIENT DEVELOPED-

-SEVERE RENAL FAILURE

- PRERENAL CAUSE AND

- DEVELOPED ACUTE TUBULAR NECROSIS (ATN)

Etiology of ARF among Inpatients

ATN (45%)

Prerenal (21%)

ARF on CKD (13%)

Obstruction (10%)

GN/vasc (4%)

AIN (2%)

Atheroemboli (1%)

KI 50:811-818, 1996

Etiology of ARF among Outpatients

Prerenal (70%)

Intrarenal (11%)

Obstruction(17%)

idiopathic(2%)

AJKD 17:191-198, 1991

• Nausea? Vomiting? Diarrhea?• Hx of heart disease, liver disease, previous renal disease,

kidney stones, BPH?• Any recent illnesses?• Any edema, change in urination?• Any new medications? • Any recent radiology studies?• Rashes?

Acute renal failure: Focused History

• azotemia

• hypervolemia

• electrolytes abnormalities:

K+ phosphate

Na+ calcium

• metabolic acidosis

• hypertension

• oliguria - anuria

acute renal failure: common clinical features

• Vital Signs:• Elevated BP: Concern for malignant hypertension• Low BP: Concern for hypotension/hypoperfusion (acute tubular

necrosis)• Neuro:

• Confusion: hypercalcemia, uremia, malignant hypertension, infection, malignancy

• HEENT: • Dry mucus membranes: Concern for dehydration (pre-renal)

• Abd: • Ascites: Concern for liver disease (hepatorenal syndrome), or

nephrotic syndrome• Ext:

• Edema: Concern for nephrotic syndrome• Skin:

• Tight skin, sclerodactyly – Sclerodermal renal crisis• Malar rash - Lupus

Assessing the patient with acute renal failure – Physical exam

Treatment of ARF

• Eliminate the toxic insult• Hemodynamic support• Respiratory support• Fluid management• Electrolyte management• Medication dose adjustment• Dialysis

If patient is fluid overloaded• fluid restriction (insensible losses)• attempt furosemide 1-2 mg/kg• Renal replacement therapy (see later)

If patient is dehydrated: • restore intravascular volume first• then treat as euvolemic (below)

If patient is euvolemic:• restrict to insensible losses (30-35 ml/100kcal/24 hours) +

other losses (urine, chest tubes, etc) or

Acute Renal Failure: Fluid Therapy

Management of ARF - Volume status

• Water balance – "Maintenance" is IRRELEVANT in ARF!!!– If euvolemic, give insensibles + losses + UOP– If volume overloaded, they don't need anything

(except the minimum for meds and glucose)• concentrate all meds; limit oral intake

– Need frequent weights and BP, accurate I/O– Insensibles = 30 cc/100 kcal or 400cc/M2/day– If has any UOP, Frusemide may help with fluid

overload

• With ARF, K+ will increase and will be worsened by infection, hemolysis, acidosis

• DON'T IGNORE A HIGH K+ just because the specimen is hemolyzed especially in a patient who could easily be hyperkalemic

• How can you tell if it is “real”? -check EKG for peaked T waves, widened QRS

• It’s real. What’s the first thing to do?- Restriction of dietary K+ intake

- Eliminate K+ supplements and K+-sparing diuretics

-Emergently stabilize membranes with calcium to prevent arrhythmia

HYPERKALAMIA

Hyperkalemia• What’s next?

– Shift K+ intracellularly with:• insulin + hypertonic dextrose: 1 unit of insulin/4 g

glucose • bicarbonate infusion ((1-2 mEq/kg)• Inhaled –B2 agonist therapy to promote intracellular

mobilization.– Check IV fluids to ensure no intake

• What happens to ionized calcium level as you correct the acidosis?• Increases albumin binding so ionized calcium decreases

• What’s the third step?– Remove from body with Lasix, dialysis

• total caloric intake– 35~ 50 kcal/kg/day to avoid catabolism Salt restriction– 2~4 g/day Potassium intake– 40 meq/day• Phosphorus intake– 800 mg/day• Uremia-nutrition

– Restriction protein is not necessary in ARF, maintain caloric intake– Carbohydrate ≥ 100gm/day to minimize ketosis and protein catabolism

• Drug– Review all medication, Stop magnesium-containing medication– Adjusted dosage for renal failure, Readjust with improvement of GFR

DIETARY MODIFICATION

Management Issue Therapy Reversal of Renal Insult Ischemic ATN Restore systemic hemodynamics and renal perfusion through volume resuscitation

and use of vasopressors

Nephrotoxic ATN Eliminate nephrotoxic agents  Consider toxin-specific measures: e.g., forced alkaline diuresis for rhabdomyolysis,

allopurinol/rasburicase for tumor lysis syndrome

Prevention and Treatment of ComplicationsIntravascular volume overload Salt and water restriction

Diuretics  UltrafiltrationHyponatremia Restriction of enteral free water intake  Avoidance of hypotonic intravenous solutions, including dextrose-containing

solutions

Hyperkalemia Restriction of dietary K+ intake 

  Eliminate K+ supplements and K+-sparing diuretics 

  Loop diuretics to promote K+ excretion 

  Potassium binding ion-exchange resins (e.g., sodium polystyrene sulfonate or Kayexelate)

  Insulin (10 units regular) and glucose (50 mL of 50% dextrose) to promote intracellular mobilization

  Inhaled –B2 agonist therapy to promote intracellular mobilization  Calcium gluconate or calcium chloride (1 g) to stabilize the myocardium

  Dialysis

Management of Ischemic and Nephrotoxic Acute Renal Failurea

Metabolic acidosis Sodium bicarbonate (maintain serum bicarbonate >15 mmol/L or arterial pH >7.2)

  Administration of other bases, e.g., THAM

  Dialysis

Hyperphosphatemia Restriction of dietary phosphate intake

  Phosphate binding agents (calcium carbonate, calcium acetate, sevelamer hydrochloride, aluminum hydroxide)

Hypocalcemia Calcium carbonate or gluconate (if symptomatic)

Hypermagnesemia Discontinue Mg++ containing antacids 

Hyperuricemia Treatment usually not necessary if <890 mol/L or <15mg/dL

  Allopurinol, forced alkaline diuresis, rasburicase

Nutrition Protein and calorie intake to avoid net negative nitrogen balance

Dialysis To prevent complications of acute renal failure

Choice of agents Avoid other nephrotoxins: ACE inhibitors/ARBs, aminoglycosides, NSAIDs, radiocontrast unless absolutely necessary and no alternative

Drug dosing Adjust doses and frequency of administration for degree of renal impairment

• Maintain serum bicarbonate >15 mmol/L or arterial pH >7.2

• Acidosis makes the kids feel terrible• BUT...

– watch sodium and fluid overload– watch lowering ionized calcium levels (by

increasing binding of calcium to albumin)

Acidosis

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• Dialysis may not be necessary for all people, but is frequently lifesaving, particularly if serum potassium is dangerously high.

• Common symptoms that require the use of dialysis include-

Uremia - Obtundation, asterxis, seizures,decreased mental status,pericarditis increased potassium levels,

Urine Output-total lack of urine production,

Metabolic Acidosis – PH< 7.2mmol/L despite Sodium Bicarbonate Therapy

Sodium Bicarbonate therapy not tolerate due to fluid over load

INDICATION FOR DIALYSIS

Indications for renal replacement therapy• Volume overload - - Resistance to Diuretics ,Specially pulmonary oedema

– Pulmonary edema, CHF, refractory HTN– NOT for peripheral edema, esp. with cap. leak

• Hyperkalemia - (S.Potassium >6.5mmol/L S.Potassium>5.5 mmol/L with ECG change)

.waste products- uncontrolled accumulation of nitrogen waste products (serum creatinine > 10 mg/dl and BUN > 120 mg/dl).

• Nutrition- Need to maximize nutrition

• Sodium imbalance - Severe dysnatremias (sodium concentration greater than 155 meq/L or less than 120 meq/L)

• Hyperthermia

• Drug overdose-Overdose with a dialyzable drug/toxin

Mnemonic “AEIOU”

• Acid-base Imbalances

• Electrolyte Disturbances

• Intoxication

• Overload, Fluid

• Uremic Symptoms

Modes of renal replacement therapy

• Peritoneal dialysis - also gentle and don't need heparinization but slow and catheter may leak or not work.

• Hemodialysis - very fast, but need big lines and systemic heparinization; causes hemodynamic instability and uremic dysequilibrium symptoms

Hyperkalemia.

Acute pulmonary edema.

Cardiac arrhythmia.

Convulsions.

Infections e.g. Pneumonia.

Deep venous thrombosis and pulmonary embolism.

Gastrointestinal bleeding.

Complications of acute renal failure

ARF: Risk factors for mortality

• Multi-organ failure• Bacterial Sepsis• Fungal sepsis• Hypotension/vasopressors• Ventilatory support • Initiation of dialysis late in hospital course• Oliguria/anuria: with oliguric ARF, mortality is >

50% compared to < 20% with non-oliguric ARF

• Infection e.g.pneumonia• Hyperkalemia.• Pulmonary edema.• Cardiac arrhythmia.• Deep venous thrombosis and pulmonary embolism.• Acute pericarditis.• Convulsions and coma.

Causes of death in acute renal failure

Oliguria, renal failure.

Renal failure Obstruction

-Rehydrate.-Fluid and diuretic challenge-Mannitol

Dehydration:•U.Na<20mmol/l.•U.Osmol.>500

Chronic

-Correct Reversible Factors.-Dialysis.

-U.catheter-Percutaneous nephrostomy.-Ureteric catheter.

Acute-AGN, RPGN and, vasculitis

Acute tubular necrosis

•C3,ANCA,,ANA,AdsDNA… etc•Consider steroid,immunosuppressive and plasma exchange.

-CVP, fluid balance, electrolyte balance,acid base balance, diet,dopamine infusion, high dose diuretic dose, monitoring, treatment of complications, and consideration of dialysis

Management of acute renal failure

Best cure is to prevent

• Have a high index of suspicion for reversible factors - volume depletion, decreasing cardiac function, sepsis, urinary tract obstruction

• Be sure patient is well-hydrated when exposing patient to nephrotoxic drugs

• Avoid worsening the ARF– Adjust medicines for renal insufficiency– Avoid nephrotoxins if possible– Think about to avoid less potent drug prescribtion– Close observation of toxic effect of drugs. – Early detection of toxic effect of drug.– Avoid intravascular volume depletion (especially in

third-spacing or edematous patients)

Anticipate Problems

•Monitor I/O, including all body fluids

• Monitor lab results

• Watch hyperkalemia symptoms: malaise, anorexia, paresthesia, or muscle weakness, EKG changes

• watch for hyperglycemia or hypoglycemia if receiving TPN or insulin infusions

Nursing Interventions

• Maintain nutrition

• Safety measures-Mouth careDaily weights

• Assess for signs of heart failure

• GCS

• Skin integrity problems

Complications (ARF)

87

• Increased risk of infections • Gastrointestinal loss of blood • Chronic renal failure • End-stage renal disease • Damage to the heart or nervous

system • Hypertension

Patient / Family Education

88

• Call your health care provider if decreased urine output or other symptoms indicate the possibility of acute renal failure.

• Call your health care provider if nausea or vomiting persists for more than 2 weeks.

• Call your health care provider if decreased urine output or other symptoms of chronic renal failure occur.

.

Thanks for your attention

PROBLEM-1

X- 80 years old male presented with Cough for 7, Fever for 6 days , diarrhoea and vomiting for 1 day. Patient was previously diagnosed as a case of COPD. On Examination Patient was drowsy, some D/H present,Pulse-101/min BP- 75/35 mmHg , SPO2 without O2-90% R/R-30/min RBS-6.8 mmol/L..Patient last pass urine 6 hour back (scanty).S.Electrolyte- S.Na - 133.2mmol/L S.K - 4.36 mmol/L S.Cl – 98.5 Tco2-19.9 mmol/L Anion Gap- 19.9mmol/L S.Creatinine-223.4 umol/L ( 2.5 mg/dl) BUN- 50.34mg/dl U.Creatinine- 5103 umol/L (57.7mg/dl) U.Specific Grvity – 1.003 U.Na – 34.6mmol/LUrine R/M/E – R.B.C- 1-2

Puss cell - 6-8 Epithelial Cell – 4-6Cast - granular (1-2)

USG of Whole Abdoman- Sugestive of bilateral paranchymal diseases.Kidney size is normal.

Bilateral Pleural Effusion (mild?) Dilated portal vein But no spleenomegaly.

QUESTIONSQ-1 In which stage patient is in RIFLE CRITERIA?Q-2 Is patient acute or chronic renal failure?Q-3 Is it Prerenal Renal or Post renal?Q-4 ATN developed or not?Q-5 What is the -daily raising of Creatinine?

FeNa - ? U Na - ? Important findings related with diagnosis?

Q-6 What is the final Diagnosis and Differential Diagnosis?Q-7 Treatment Option for the patient ?Q-8 Dialysis Needs or not?

PROBLEM-2

Y- 65years old male presented with diarrhoea and vomiting for 1 and half day.He Non Diabetic But Hypertensive. On Examination Patient was Alart but feeling restless his pulse-92/min ,BP-105/70mmHg Some D/H was present , RBS-6.1mmol/L..Patient last pass urine 5-6 hour back (scanty)1st Day – S.Cretinine- 610umol/L (6.9mg/dl)S.Electrolyte- S.Na - 128.2mmol/L S.K - 3.6 mmol/L S.Cl – 90.5 Tco2-19 mmol/L Anion Gap- 22.4mmol/L S.Creatinine-836 umol/L ( 9.45 mg/dl) BUN- 50.34mg/dl U.Creatinine- 3940.1 umol/L U.Specific Grvity – 1.018 U.Na – 19.8mmol/LUrine R/M/E – R.B.C- 4-6

Puss cell - 15-20 Epithelial Cell – 4-6Cast - granular (0-1)

USG of Whole Abdoman-Normal Study QUESTIONSQ-1 In which stage patient is in RIFLE CRITERIA?Q-2 Is patient acute or chronic renal failure?Q-3 Is it Prerenal Renal or Post renal?Q-4 ATN developed or not?Q-5 What is the -daily raising of Creatinine?

FeNa - ? U Na - ? Important findings related with diagnosis?

Q-6 What is the final Diagnosis and Differential Diagnosis?Q-7 Treatment Option for the patient ?Q-8 Dialysis Needs or not?

PROBLEM-3

Z- 18 years old Female presented with diarrhoea and vomiting for 1and half day, Fever since morning , For Diarrhoea she took I/V Fluid and Some Medication from outside. On Examination Patient was drowsy follwed by unconciousness, some D/H present,Pulse-98/min BP- 95/60 mmHg , SPO2 without O2-90% R/R-30/min RBS-6.8 mmol/L..Patient last pass urine 5-6 hour back (scanty) Temp-39`C.No Pupil Dilated,No Neck rigidity, After 10-12 hour patient develop repeated convulsion.1st S.creatinine – 582.6 umol/L ( 6.5 mg/dl)S.Electrolyte- S.Na - 132.6mmol/L S.K - 3.2 mmol/L S.Cl – 98.5 Tco2-14.9 mmol/L Anion Gap- 19.9mmol/L S.Creatinine-882.3 umol/L ( 9.9mg/dl) BUN- 138.94mg/dl U.Creatinine- 7481 umol/L , U.Na – 26.7mmol/LUrine R/M/E – R.B.C- 7-8 CBC – Hb%- 10 , TWBC -14700Puss cell - 12-14 Nutrophil- 81.4% Poly-10% Epithelial Cell – 4-6 monocyte- 0.2% ,Eosinophil-7.4%Protien- ++Cast - granular (2-4) Eosinophil-+USG of Whole Abdoman- Normal Study.QUESTIONSQ-1 In which stage patient is in RIFLE CRITERIA?Q-2 Is patient acute or chronic renal failure?Q-3 Is it Prerenal Renal or Post renal?Q-4 ATN developed or not?Q-5 What is the -daily raising of Creatinine?

FeNa - ? U Na - ? Important findings related with diagnosis?

Q-6 What is the final Diagnosis and Differential Diagnosis?Q-7 Treatment Option for the patient ?Q-8 Dialysis Needs or not?