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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)
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• 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?