2. Case History
Name : 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 )
3. ON EXAMINATION
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
4. 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 .
5. PROBLEM LIST
*ACUTE WATERY DIARRHOEA
*SOME D/H
*FEVER
*UNCONCIOUSNESS (? MENINGITIES )
*?RENAL FAILURE( Uremic Encephalopathy)
*SEPTECEMIA
* LACK OF PROPER HISTORY
6. LABORATORY INVESTIGATIONS
CBC:-
Hemoglobin-10.9gm/dl
Hct – 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 Growth
USG and Urine R/M/E WBC cast and Epithelial cell-7-8 Protein-+
9. 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 .
10. RENAL FAILURE
DIAGNOSIS & MANAGEMENT
OF
AN UNCONCIOUS & UNATTENDENT
PATIENT
11. 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
12. How Do We Proceed?
Reduce Urine output/Anuria /urine abnormality
?Renal failure
?Acute or Chronic Renal Failure
If Acute renal Failure
Prerenal Renal Postrenal
ATN Develop or Not
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 .
13. Classification system for AKI
Classification system for AKI
GFR Criteria Urine Output criteria
Risk
High
Sensitivity
Injury
Failure
High
Specificity
Loss
EKSD
14. RIFLE criteria for diagnosis of AKI
Increase in SCr Urine output
Risk of renal injury 0.3 mg/dl increase < 0.5 ml/kg/hr for > 6 h
Injury to the kidney 2 X baseline < 0.5 ml/kg/hr for >12h
Failure of kidney 3 X baseline OR Anuria for >12 h
function > 0.5 mg/dl increase if
SCr >=4 mg/dl
Loss of kidney Persistent renal failure
function for > 4 weeks
End-stage disease Persistent renal failure
for > 3 months
15. DEFINATION
Definition:
Means an abrupt deterioration of renal function within hours, leading to
retention of water, crystalloids and nitrogenous products.
Rapid decline in the GFR over days to weeks-
Cr increases by >0.5 mg/dL
GFR <10mL/min, or <25% of normal
Documented oliguria of <0.5 ml/kg/hr for 12 hrs
Acute Renal Insufficiency-
Deterioration over days-wks
GFR 10-20 mL/min
16. Definition
•Acute renal failure is • Chronic renal failure
sudden loss of the is a gradual and
ability of the kidneys to progressive loss of
excrete the ability of the
wastes, concentrate kidneys to excrete
urine, and conserve wastes, concentrate
electrolytes. ("Acute" urine, and conserve
means sudden, "renal" electrolytes.
refers to the kidneys.) – Kidney Damage for > 3
– Rapid decline in GFR months
(Over Hours To Days) – Irreversible
– Usually Reversible – 75-60% of function can
be lost before its
noticeable
17. Differentiating ARF vs. Chronic Renal Failure (CRF)
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 normal
suggesting pre-renal azotemia .
18. 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
20. STAGES
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
21. Definitions
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
22. Prerenal ARF
• 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.
THE KIDNEYS ARE NORMAL
24. Intrinsic Renal Failure
Intrinsic Renal Failure
I. 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 compression
II. 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 27
25. 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
26. Prerenal Azotemia and Ischemic tubular necrosis
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.
27. In addition of the tubular obstruction, two other factors appear to contribute
to 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 begins
abruptly 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.
28. AIN From Drugs
Renal damage is NOT dose-dependent
May 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...
29. Difference Between Ischemic and Nephrotoxic ATN
Ischaemic ATN Nephrotoxic ATN
(Due to Hypovolumia)
Background History Diarrhoea,Vomitting,heart failure,Shock Drugs,Toxin
Kidney Invilvement 3rd Segment of proximal tubule Mostly proximal convoluted
(proximal tubule – Reabsorb 65% of tubule
Sodium) and Assending Loop of henlee
(Reabsorb 25% of Sodium)
FeNa Usually >3% Usually >1% ( 2-3%)
Clinical Triat Fever ,Rash ,Eosinophilia nit associated Mostly Present
UNa Usually Greater >40 Comperatively low(>20)
(Gradually Increasing from >20)
Urinary Protein Absent/+ +/++
WBC Cast Absent pathognomic
Eosinophiluria on Wrights Absent Mostly present
or Hansels Strain
Treatment Restore renal function Usually Fluid And Stop Offending
drugs and sometimes Steroid
31. How Do We Proceed
Reduce Urine output/Anuria /urine abnormality
?Renal failure
?Acute or Chronic Renal Failure
If Acute renal Failure
Prerenal Renal Postrenal
ATN Develop or Not
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 .
32. MINIMUM STEPS FOR DIAGNOSIS
History Taking
General and Systemic Examination
Laboratory investigation
Serum Electrolyte Urine R/M/E USG OF ABDOMAN
Serum Creatinine Urinary Electrolyte
BUN Urinary Creatinine
Urinary Urea
Urea - Is the By-product of Protein metabolism
Creatinine- Is the By-product of Muscle metabolism
33. Some Important Formula
GFR = F (140 – age [yrs]) Ideal Body Wt (kg)
Serum creatinine (mol/L)
Where:
F = 1.23 for males and 1.04 for females
FeNa = (urine Na x plasma Cr) x100
(plasma Na x urine Cr)
BUN: Cr = blood urea nitrogen:creatinine ratio
Pre-renal=Creatinine cannot be reabsorbed, thus leading to a BUN/Cr ratio of > 20
UNa = urinary concentration of sodium;
34. 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)
35. 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.
36. 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
37. More FeNa
FeNa 1%-2%
1. Prerenal-sometimes (eg-Related with Sepsis)
2. ATN-sometimes
3. AIN-higher FeNa due to tubular damage
FeNa >2%-3%
1. ATN Damaged tubules can't reabsorb Na.usually
nephrotoxic ,Sepsis
FeNa >3%
Goes in Favour of Ischaemic ATN
38. Guide To The Differential Diagnosis of intrinsic ARF
Eosinophiluria Present:
Acute Interstitial
nephritis likely
Eosinophiluria Absent:
Acute interstial
nephritis possible
Muddy Brown Granular Casts
39. Assessing patient with acute renal failure –
Urinary Casts
Red cell casts Glomerulonephritis
Vasculitis
White Cell casts Acute Interstitial
nephritis
Fatty casts Nephrotic
syndrome, Minimal
change disease
Muddy Brown casts Acute tubular
necrosis
41. Classification and differential diagnosis of acute renal failure
Intrinsic Renal Disease
Prerenal Azotemia Postrenal Azotemia Acute Tubular Acute Acute
Necrosis Glomerulonephritis Interstitial
(Oliguric or Polyuric) Nephritis
Etiology Poor renal Obstruction of the Ischemia, Poststreptococcal; Allergic
perfusion urinary tract nephrotoxins collagen-vascular reaction; drug
disease 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 > 500 < 400 250–300 Variable Variable
(mosm/kg)
Urinary sediment Benign or Normal or red cells, Granular Dysmorphic red cells White cells,
hyaline casts white cells, or crystals (muddy brown) and red cell casts white cell
casts, renal tubular casts, with or
casts without
eosinophils
BUN: Cr = blood urea nitrogen:creatinine ratio;
UNa = urinary concentration of sodium;
FENa = fractional excretion of sodium
42. ATN Prerenal
Cr increases at increases
0.3-0.5 /day slower than
0.3 /day
U Na, UNa>40 UNa<20
FeNa FeNa >2% FeNa<1%
UA epi cells, Normal
granular casts
Response to Cr won’t Cr improves
volume improve much 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)
43. Intervention by Inj.Frusemide and its outcome of an ARF ( Develop ATN)
1st 2nd 3rd 4th 5th 6th Total
Duratio
n
Pt-1 6.9 9.45 6.09 2.7 2.0 1.4 6 Days
Pt-2 4.6 3.4 6.0 4.8 3.3 2.3 (day 6) 7 days
1.3(day 7)
Pt-3 6.5 8.7 9.9 10.3 5.1 1.4 11 Days
-Day -3 day-4 Day-5 Day-9 day-11
Patient develop ATN Due to Prerenal cause
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
46. Intrinsic renal injury Lovastatin, ethanol, codeine, Elevated CPK, ATN urine Drug discontinuation,
(rhabdomyolysis) barbiturates, diazepam sediment supportive care
Quinine, quinidine,
Intrinsic renal injury sulfonamides, hydralazine, High LDH, decreased Drug discontinuation,
(severe hemolysis) triamterene, nitrofurantoin, hemoglobin supportive care
mephenytoin
Penicillin, methicillin ampicillin,
rifampin, sulfonamides,
thiazides, cimetidine,
phenytoin, allopurinol,
Intrinsic renal injury Fever, rash, eosinophilia,
cephalosporins, cytosine
(immune-mediated urine sediment showing Discontinue medication,
arabinoside, furosemide,
interstitial pyuria, white cell casts, supportive care
interferon, NSAIDs,
inflammation) eosinophiluria
ciprofloxacin, clarithromycin,
telithromycin, rofecoxib,
pantoprazole, omeprazole,
atazanavir
Gold, penicillamine, captopril,
NSAIDs, lithium, mefenamate, Edema, moderate to severe
Intrinsic renal injury Discontinue medication,
fenoprofen, mercury, interferon- proteinuria, red blood cells,
(glomerulopathy) supportive care
, pamidronate, fenclofenac, red blood cell casts possible
tolmetin, foscarnet
Obstruction Aciclovir, methotrexate, Sediment can be benign
Discontinue medication,
(intratubular: crystalluria sulfanilamide, triamterene, with severe obstruction,
supportive care
and/or renal lithiasis) indinavir, foscarnet, ganciclovir ATN might be observed
Discontinue medication,
Methysergide, ergotamine,
Obstruction (ureteral; Benign urine sediment, decompress ureteral
dihydroergotamine,
secondary to hydronephrosis on obstruction by intrarenal
methyldopa, pindolol,
retroperitoneal fibrosis) ultrasound stenting or percutaneous
hydralazine, atenolol
47.
48. Result Interpretations
24/04/09 24/04/09
S.Na + -128.6mmol/L GFR -6.5 ml/min(SEVERE RENAL FAILURE)
S.K+ - 2.73 mmol/L FeNa -4% ( >2%) (ATN)
S.Cl - 93 mmol/L FENa - 35% ( Pre Renal )
TCO2 - 13.5mmol/L Urinary Na+ - 44.7 mmol/L ( <20mmol/L ATN)
Anion gap -24.83mmol/L Oliguria - Urine out put less than 500 cc
BUN - 138.94mg/dl Urinary Creatinine = 8.17% (<20% ATN)
UREA - 49.26 mmol/L Serum Creatinine
Serum Creatinine – 882.3u mol/L BUN/Creatinine = 14.03 ( <20% Renal)
URINARY ELECTROLYTE
Urine R/M/E - No Eosinophilurea, WBC cast and
U.Sodium - 44.7mmol/L
Epithelial cell-7-8 Protein-+
U.Potassium - 12.77mmol/L BUN: Cr = blood urea nitrogen:creatinine ratio;
UNa = urinary concentration of sodium;
U.Cl- - 33mmol/L FENa = fractional excretion of sodium
FeNa = (urine Na x plasmaCr) 100
TCO2 - 5mmol/L
(plasma Na x urineCr)
U.Creatinine (Random)-7211 umol/L
49. SO,PATIENT DEVELOPED-
-SEVERE RENAL FAILURE
- PRERENAL CAUSE AND
- DEVELOPED ACUTE TUBULAR NECROSIS (ATN)
50. 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
51. Etiology of ARF among Outpatients
P rerenal (70% )
Intrarenal (11% )
O bs truc tion(17% )
idiopathic (2% )
AJKD 17:191-198, 1991
52. Acute renal failure: Focused History
• 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?
55. Treatment of ARF
• Eliminate the toxic insult
• Hemodynamic support
• Respiratory support
• Fluid management
• Electrolyte management
• Medication dose adjustment
• Dialysis
56. Acute Renal Failure: Fluid Therapy
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
57. 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
58. HYPERKALAMIA
• 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
59. 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
60. DIETARY MODIFICATION
• 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
61. Management of Ischemic and Nephrotoxic Acute Renal Failurea
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 Complications
Intravascular volume overload Salt and water restriction
Diuretics
Ultrafiltration
Hyponatremia 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
62. 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
63. Acidosis
• 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)
64. INDICATION FOR DIALYSIS
• 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
65. 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
67. 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
68. Complications of acute renal failure
Hyperkalemia.
Acute pulmonary edema.
Cardiac arrhythmia.
Convulsions.
Infections e.g. Pneumonia.
Deep venous thrombosis and pulmonary embolism.
Gastrointestinal bleeding.
69. 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
70. Causes of death in acute renal failure
• Infection e.g.pneumonia
• Hyperkalemia.
• Pulmonary edema.
• Cardiac arrhythmia.
• Deep venous thrombosis and pulmonary embolism.
• Acute pericarditis.
• Convulsions and coma.
71. Oliguria, renal failure.
Dehydration: Obstruction
•U.Na<20mmol/l. Renal failure
•U.Osmol.>500
Chronic -U.catheter
-Percutaneous nephrostomy.
-Rehydrate. -Ureteric catheter.
-Fluid and diuretic
challenge -Correct Reversible Factors.
-Mannitol -Dialysis.
-AGN, RPGN and, Acute Acute tubular necrosis
vasculitis
•C3,ANCA,,ANA,Ad -CVP, fluid balance, electrolyte balance,acid
sDNA… etc base balance, diet,dopamine infusion, high
•Consider dose diuretic dose, monitoring, treatment of
steroid,immunosuppr complications, and consideration of dialysis
essive and plasma
exchange.
Management of acute renal failure
72. 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
73. Anticipate Problems
• 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)
74. Nursing Interventions
•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
75. • Maintain nutrition
• Safety measures-
Mouth care
Daily weights
• Assess for signs of heart failure
• GCS
• Skin integrity problems
76. Complications (ARF)
• Increased risk of infections
• Gastrointestinal loss of blood
• Chronic renal failure
• End-stage renal disease
• Damage to the heart or nervous system
• Hypertension
77. Patient / Family Education
• 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.
79. 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/L
Urine R/M/E – R.B.C- 1-2
Puss cell - 6-8
Epithelial Cell – 4-6
Cast - 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.
QUESTIONS
Q-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?
80. 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/L
Urine R/M/E – R.B.C- 4-6
Puss cell - 15-20
Epithelial Cell – 4-6
Cast - granular (0-1)
USG of Whole Abdoman-Normal Study
QUESTIONS
Q-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?
81. 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/L
Urine R/M/E – R.B.C- 7-8 CBC – Hb%- 10 , TWBC -14700
Puss 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.
QUESTIONS
Q-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?
