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Acute renal failure in icu .....
1. Rapid loss of renal function leading to
abnormal water, electrolyte and solute
balance.
Occurs over a period of hours to days.
Usually associated with oliguria. Some
patients develop non oliguric ARF eg. After
radiocontrast media.
It can be reversed with treatment of the
cause.
Acute-on top of chronic renal failure may
occur. 2
9. * Pre-renal failure :
- There is hypotension with signs of poor preripheral
perfusion.
- Postural hypotension.
- Signs of hypovolemia.
- Manifestations of the cause.
- Metabolic acidosis and ↑ K may be present.
* Established renal ARF :
- Oliguria (urine volume < 400ml/d) or anuria
(< 100ml/d).
- Disturbances of water, electrolyte and acid base
balance (↑ K, ↓ pH, Dilutional ↓ Na).
- Uremic features include anorexia, nausea, vomiting,
hiccough, acidotic breathing …. 10
10. * Post-renal (ARF) :
- Loin pain (which may be constant or intermittent)
- Complete anuria with bilateral obstruction or
complete obstruction of single kidney.
- Infection may → fever, septicaemia.
- Bladder outflow obstruction → Hesitancy, weak
urine stream, terminal drippling, re-tension with
overflow may occur
- Screening of urinary tract by sonar is essential.
11
11. Probable Causes of Acute Renal Failure
Based on the Findings of The History
History Probable causes of acute
renal failure
Review of systems
Pulmonary system
Sinus, upper respiratory or pulmonary Pulmonary-renal syndrome or vasculitis
symptoms
Cardiac system
Symptoms of heart failure Decreased renal perfusion
Intravenous drug abuse, prosthetic Endocarditis
valve or valvular disease
Gastrointestinal System
Diarrhea, vomiting or poor intake. Hypovolemia
Colicky abdominal pain radiating from Urolithiasis
flank to groin
Genitourinary System
Symptoms of benign prostatic Obstruction
hypertrophy.
Bone pain in the elderly Multiple myeloma or prostate cancer
Trauma or prolonged immobolization Rhabdomyolysis (pigment nepbropathy)12
12. (Cont.)
History Probable causes of acute
renal failure
Skin
Rash Allergic interstitial nephritis, vasculitis,
systemic lupus erythematosus,
atheroemboli or thrombotic
thrombocytopenic purpura.
Constitutional symptoms
Fever, weight loss, fatigue or anorexia Malignancy or vasculitis
Past medical history
Multiple sclerosis, diabetes mellitus Neurogenic bladder
or stroke
Past surgical history
Recent surgery or procedure Ischemia, atheroemboli, endocarditis
or exposure to contrast agent
Medication history
Angiotensin-converting enzyme Decreased renal perfusion, acute
inhobitors, nonsteroidal anti- tubular necrosis or allergic interstitial
inflammatory drugs, antibiotics or nephritis
acyclovir (Zovirax) 13
13. Probable Causes of Acute Renal Failure
Based on the Physical Findings
Physical Probable causes of acute renal failure
Examination
Vital signs
Temperature Possible infection.
Blood Hypertension: G.N or malignant hypertension.
pressure Hypotension: volume depletion or sepsis.
Weight loss or Hypovolemia or hypervolemia.
gain
Mouth Dehydration
Jugular veins Hypovolemia or hypervolemia
and axillae
(perspiration)
Pulmonary Signs of pneumonia, cavitations, pleurisy.
system
Heart New murmur of endocarditis or signs of
congestive heart failure
14
14. (Cont.)
Physical Probable causes of acute renal failure
Examination
Abdomen Bladder distention suggesting uretheral
obstruction
Pelvis Pelvic mass
Rectum Prostate enlargement
Skin Rash of interstitial nephritis, purpura of
microvascular disease, livedo reticularis
suggestive of atheroembolic disease, or splinter
hemorrhages or Osler’s nodes of endocarditis.
15
15. * Blood urea nitrogen and serum creatinine are
elevated.
* ABG, electrolytes, CBC, and serology.
* U/S kidneys (The size of the kidneys is usually
normal.
* Serology: ANA, ANCA, Anti DNA, HBV, HCV, Anti
GBM. Cryoglobulin, CK, urinary myoglobin.
16
16. * Urine analysis :
- Unremarkable in pre and post renal causes.
- Differentiates ATN vs. AIN. vs. AGN
Granular casts in ATN.
WBC casts in AIN.
RBC casts in AGN.
- Urine electrolytes (Na) and osmolality.
* Hansel stain for Eosinophiluria.
17
17. LAB Findings of Specific Types of
Acute Renal Failure
Findings on blood tests Diagnosis to consider
Very high uric acid level Suggestive of malignancy or tumor lysis
syndrome leading to uric acid crystals;
also seen in prerenal acute renal failure.
Elevated creatinine kinase or Rhabdomyolysis.
myoglobin levels
Elevated prostate-specific antigen Prostate cancer.
Abnormal serum protein Multiple myeloma.
electrophoresis
Low complement levels Systemic lupus erythematosus,
postinfectious glomerulophritis,
subacute bacterial endocarditis
Positive antineurtrophic Small-vessel vasculitis (Wegener’s
cytoplasmic antibody (ANCA) granulomatosis or polyartheritis nodosa)
18
18. LAB Findings of Specific Types of
Acute Renal Failure (Cont.)
Findings on blood tests Diagnosis to consider
Positive antinuclear antibody to Systemic lupus erythematosus
double-stranded DNA
Positive antibody to glomerular Goodpasture’s syndrome
basement membrane
Positive antibodies to streptolysin Poststreptocaccal glomerulonephritis.
O, streptokinase or hyaluronidase
Schistocytes on peripheral smear, Hemolytic uremic syndrome or
decreased hepatoglobin level, thrombotic thrombocytopenic purpura
elevated lactate dehydrogenase
level or elevated serum bilirubin
level
Low albumin levels Liver disease or nephrotic syndrome
19
19. Laboratory Findings in Acute Renal Failure To
Differentiate Pre-Renal from Renal Failure
Index Prerenal Azotemia Oliguric Acute Renal
Failure (ATN)
BUN/PCR Ratio > 20 : 1 10-15 : 1
Urine sodium (UNa) < 20 > 40
meg/L
Urine osmolality, > 500 < 350
mosmol/L H2O
Fractional excretion <1% >2%
of sodium
Response to Improvement No improvement
volume
Urinary Sediment Bland ATN: muddy brown granular
casts, cellular debris, tubular
epithelial cells
20
20. ARF is common in the ICU.
ARF is an independent factor for prognosis
in the ICU.
The incidence of ARF in the ICU 40-60%
compared to 1-3% in the ward.
ARF still has a mortality of 50% since it
occurs in very sick patients with multiorgan
failure.
21
21. Predisposing factors to ARF include old age
sepsis pre existing renal disease heart
disease and chronic liver disease.
Mechanical ventilation has an adverse effect
on renal blood flow and GFR and subsequent
renal function.
22
22. • Patients with ICU acquired ARF were classified
into the following :
A) According to the urine output:
- Oliguric (urine volume of < 400 ml/day).
- Nonoliguric (urine volume of > 400 ml/day).
- Anuric (urine volume of < 100 ml/day).
B) According to the cause:
1) Prerenal ARF.
2) Ischemic acute Tubular necrosis.
3) Nephrotoxic ARF (ATN or AIN).
4) Sepsis induced ARF.
5) Hepato-renal syndrome.
6) Other causes (e.g. obstructive uropathy,
pigment nephropathy, microangiopathies).
23
23. 1) Prerenal ARF was defined as ARF to renal
hypoperfusion with recovery after correction of
hemodynamic disturbances.
2) Ischemic Acute tubular necrosis (IATN) was
diagnosed when renal function did not improve after
correction of possible prerenal causes, and when
hepatorenal syndrome, vascular, interstitial,
glomerular and obstructive aetiologies were
excluded.
24
24. • Decreased renal perfusion was identified by
the following observations :
Any documented decline in blood pressure to less
than 90/60 mmHg.
Overt volume contraction on physical examination
(postural hypotension, decreased skin turgor, …),
and central venous pressure (CVP) less than 5 cm
H2O.
Clinically evident congestive heart failure with
improvement in renal function following
appropriate treatment of heart failure.
25
25. 3) Nephrotoxic ARF (either AIN or ATN)
Nephrotoxic Acute Interstitial Nephritis
(AIN): history of drug ingestion, fever, rash, or
arthralgias. Urinary increase in WBCs (frequently
eosirophiluria), WBC casts RBCs, and
proteinuria, with systemic eosinophilia, if
histologically demonstrated by renal biopsy or
when there was a high grade of clinical
suspicion.
26
26. Nephrotoxic Acute Tubular Necrosis
(ATN): was defined as ARF occurring after
administration of drugs known to cause ATN (e.g.
aminoglycosides, amphotericin, contrast media
etc …).
Concurrent administration of vancomycin &
aminoglycosides to critically ill septic
patients with normal renal function of
baseline induces mainly slight and transient
toxic tubular effects.
27
27. Radiographic contrast media, were determined to
be the cause of renal insufficiency when the
serum creatinine concentration increased – as
defined – within 72 hours following a radiologic
procedure employing these agents (e.g.
intravenous pyelogram – angiography – computed
tomography scan).
28
28. 4) Sepsis induced ARF was diagnosed if ARF is
associated with at least one of the following three
conditions:
Documented bacteremia.
A known focus of infection
Immunosuppression with neutropenia,
and at least two additional findings: rigors –
unexplained hyperventilation unexplained sudden
fall in blood pressure – abrupt rise in temperature to
more than 38C not due to transfusion reaction –
unexplained leukocytosis of more than 15.000 mm3.
29
29. 5) Hepatorenal syndrome was assigned as the
cause of renal failure if the patient had severe liver
failure (e.g. ascites – jaundice, hepatic
encephalopathy) – and a urine sodium concentration
less than 10 mEq/Liter, and the renal function did not
respond to a volume expansion.
30
30. 6) Other causes:
Obstruction was determined to be the cause of
renal failure if obstruction was present by
physical examination (as enlarged bladder) or by
radiological evaluation and if improvement in
renal function followed relief of obstruction.
31
31. Pigment induced-ARF, history suggestive of
rhabdomyolysis, urine dispstick positive for blood
(heme) without microscopic haematuria
hyperkalemia, hyperphosphatemia, hypocalcemia,
increased creatine kinase-MM fraction and serum
uric acid.
32
32. Atheroembolic ARF:
Associated with emboli of fragments of
atherosclerotic plaque from aorta and other large
arteries.
Diagnose by history, physical findings
(evidence of other embolic phenomena, ischemic
digits, “blue toe” syndrome, etc), low serum C3
and C4, peripheral eosinophiluria, rarely WBC
casts.
Commonly occur after intravasculer
procedures or cannulation (cardiac catheter,
CABG).
33
33. Number of patients admitted in different
ICUs with acquired ARF in each ICU
ICU No. of admitted No. & % of patients
patients with ICU acquired
ARF in each ICU
Medical ICU 1123 402 (35.7 %)
Gynecology ICU 431 98 (22.7 %)
Surgical ICU 336 53 (15.7 %)
Neurology ICU 116 17 (14.6 %)
Chest ICU 409 57 (13.9 %)
Coronary Care Unit 722 78 (10.1 %)
Cardiosurgery ICU 425 43 (10.1 %)
Total 3562 748 (21 %)
34
35. Number & Percentage of patient mortality
in each ICU
ICU No. of patients Mortality No. & %
with ICU acquired in each ICU
ARF
Medical ICU 402 261 (64.9 %)
Coronary Care Unit 78 20 (25.6 %)
Chest ICU 57 28 (49.1 %)
Neurology ICU 17 9 (52.9 %)
Surgical ICU 53 10 (18.8 %)
Cardiosurgery ICU 43 19 (44.1 %)
Gyne & obst. ICU 98 42 (42.8 %)
Total 748 389
36
36. * The initiation of RRT in patients with AKI prevents
uremia and immediate death from the adverse
complications of renal failure.
* It is possible that variations in the timing of
initiation, modalities, and/or dosing may affect
clinical outcomes.
* Multiple modalities of RRT are currently available.
These include intermittent hemodialysis (IHD),
continuous renal replacement therapies (CRRTs),
and hybrid therapies, such as sustained low-
efficiency dialysis (SLED). Despite these varied
techniques mortality in patients with ARF remains
high greater than 50% in severely ill patients. 37
37. 1. Indications for dialysis.
2. Timing of initiation of dialysis.
3. Optimal modality.
4. Optimal Dosing.
5. Discontinuation of therapy.
38
38. 1) Refractory fluid overload.
2) Hyperkalemia (plasma potassium concentration >
6.5 meq/L) or rapidly rising potassium levels.
3) Metabolic acidosis (pH less than 7.1).
4) Signs of uremia e.g. pericarditis and decline in
mental state.
5) Certain alcohol and drug intoxications.
* The likelihood of requiring RRT is increased in
patients with underlying CKD (Acute on top of
chronic).
39
39. Studies published during the 1960s and 1970s
suggested that improved outcomes were associated
with the initiation of hemodialysis when BUN reached
exceeded 150 to 200 mg/dL.
40
40. More recent studies have evaluated the relationship
between the timing of RRT initiation and clinical
outcomes. Several non-randomized studies have
reported that improved outcomes, including survival,
are associated with early versus late initiation of RRT.
It has been suggested that initiation of RRT dialysis
prior to the development of overt symptoms and signs
of renal failure due to AKI improves the outcome.
41
41. Can dialysis delay recovery
of renal function ?
There is at least theoretical concern that dialysis
might have detrimental effects on renal function.
Three factors may be important in this regard:
1) A reduction in urine output; Both removal of
excess volume and of urea contribute to a
reduction in or even cessation of the urine output.
The fall in urine output should not delay the
regeneration of tubules.
2) Induction of hypotension; Autoregulation is
impaired in ATN, because vascular endothelial
injury reduces the release of vasodilating
substances so recurrent ischemic tubular injury is
more likely to occur, thereby delaying the
restoration of function.
42
42. 3) Complement activation resulting from a blood-
dialysis membrane interaction, can lead to
neutrophilic infiltration into the kidney (and other
tissues) and prolonged acute kidney injury.
4) High flux membranes can enhance removal of
putative toxins and improve outcome, but may
also allow the back transport (from dialysate to
blood).
43
44. Principles of dialysis
Dialysis = diffusion =
passive movement of
solutes across a semi-
permeable membrane down
concentration gradient.
* Good for small molecules.
(Ultra) filtration =
convection = solute + fluid
removal across semi
permeable membrane down
a pressure gradient (solvent
drag).
* Better for removal of fluid Figure (1): Principles of dialysis
and medium-size molecules. (top panel) and filtration
(lower panel). 45
45. Principles of dialysis
Hemodialysis = solute passively diffuses down
concentration gradient.
Dialysate flows countercurrent to blood flow.
Urea, creatinine, K move from blood to dialysate.
Ca and bicarb move from dialysate to blood.
Ultrafiltration = This is the convective flow of water
and dissolved solutes down a pressure gradient
caused by hydrostatic or osmotic forces.
Hemodiafiltration = combination of dialysis and
ultrafiltration
46
46. Intermittent hemodialysis (IHD)
Oldest and most common technique.
Primarily diffusive treatment: blood and
dialysate are circulated in countercurrent manner.
Also some fluid removal by ultrafiltration due to
pressure driving through circuit.
Best for removal of small molecules.
Typically performed 4 hours 3x / wk or daily.
47
47. Continuous Renal Replacement
Therapy (CRRT)
CRRT strategies are particularly useful in haemo-
dynamically compromised patients with ARF.
They allow slow and gentle removal of solutes and
fluid, avoiding major intravascular fluid shifts and
minimizing electrolyte disturbances, hypotension and
arrhythmias.
Inflammatory mediators may also be continuously
removed by CRRT, so it may be useful in sepsis
syndrome.
48
49. Haemofiltration
Provides solute clearance by convection as
solutes are dragged down pressure gradient
with water.
It provides better removal of large MW solutes
e.g. B2-microglobulin, improved clearance of
low MW uraemic toxins and better
cardiovascular stability and Bp control than
HD.
Inflammatory markers are improved.
50
50. Sustained low-efficiency daily dialysis
(SLED):
Uses conventional dialysis machines but blood flow
of 100-200 ml/M and dialysate flow of only 100 ml/M
for 8-24 hr/D.
Major advantages: Flexibility of duration and
intensity, reduced costs.
Excellent tolerability, cardiovascular stability and
solute removal.
51
51. Slow continuous ultrafiltration ((SCUF):
Used for fluid removal in overloaded CHF patients
with refractory edema without severe renal failure.
Blood is driven through a highly permeable filter in a
venovenous mode to primarily remove water, not
solute.
The ultrafiltrate produced during membrane transit is
not replaced.
Haemodiafiltration (HDF):
Simultaneous use of HD and UF.
It is good with CVS instability.
It can remove the inflammatory mediators.
52
52. * Current data suggest that survival and recovery
of renal function are similar with both CRRT
and IHD.
* Advocates for CRRT have claimed that CRRT is
associated with the following advantages
compared with IHD:
1) Enhanced hemodynamic stability, in hemodynamically
unstable patients.
2) Increased net salt and water removal, thereby
permitting superior management of volume overload
and nutritional requirements.
53
53. 3) Enhanced clearance of inflammatory mediators, which
may provide benefit in septic patients, particularly
using convective modes of continuous therapy.
4) Among patients with acute brain injury or fulminant
hepatic failure, continuous therapy may be associated
with better preservation of cerebral perfusion.
54
54. Peritoneal dialysis:
Least useful form of CRRT in the ICU.
Diffusive treatment: Blood in capillaries of peritoneal
membrane exposed to dialysate in abdomen.
Continuous or intermittent.
Inefficient solute/ volume clearance if unstable or
poor intestinal blood flow.
Can’t use if intra-abdominal pathology – risk of
peritonitis.
Respiratory burden.
55
55. * Intermittent hemodialysis – Dosing in IHD is
based upon the dose delivered per session
plus the frequency of sessions.
* Improved survival was observed with a higher
Kt/V (greater than 1), which was particlarly
evident among patients with intermediate
levels of illness severity.
* Compared with every other day dialysis, daily
therapy was associated with a significant
reduction in mortality, fewer hypotensive
episodes during hemodialysis, and more rapid
resolution of acute renal failure.
56
56. * In contrast, the Acute Renal Failure Trial
Network (ATN) Study did NOT find a difference
in mortality associated with a more intensive
dosing strategy for renal replacement therapy.
* The Hanover Dialysis Outcome study compared
extended duration dialysis, provided for
approximately 8 hours per day, to a more
intensive regimen where additional 8-hour
treatment sessions were provided to maintain
the BUN < 42 mg/dL. No difference in survival
or recovery of kidney function was observed
with more intensive treatment.
57
57. • The Randomized Evaluation of Normal versus
Augmented Legal of RRT study and two meta-
analyses were performed. All studies found
that, compared with standard intensity dialysis,
higher intensity dialysis did not result in
improved survival or clinical benefits.
• It is recommended that IHD be provided 3
times/week with monitoring of the delivered
dose of therapy to ensure a minimum delivered
Kt/V of 1.2 per treatment.
58
58. RRT is usually continued until the patient
manifests evidence of recovery of kidney
function.
1. Increase in urine output.
2. A progressive decline in serum creatinine
concentration after initial attainment of stable values
(assessed daily during CRRT or predialysis in
patients managed with IHD) despite a constant dose
of renal support.
3. Measurement of creatinine clearance e.g. on six-
hour timed urine collections obtained when the urine
output exceeded 30 mL/hour based on an average
serum creatinine at the beginning and end of the
timed collection.
59
59. A precise level of kidney function needed to
allow discontinuation of renal support has not
been established; however,
Creatinine clearance < 12 mL/min → no discontinuation.
Creatinine clearance > 20 mL/min → discontinue.
Creatinine clearance 12 to 20 mL/min → optional.
60
60. 1) No drugs are currently available to enhance
or hasten renal recovery once ARF occurs.
2) There is now clear evidence that ARF is
associated with excess mortality, irrespective
of whether the patient requires renal
replacement therapy.
3) Hense prevention is the only powerful
tool to improve outcome of AKI.
61
61. Identification of patients at high risk to develop
AKI-Elderly, DM, HT. Sepsis etc ....
Non Pharmacological Pharmacological
Ensuring adequate Loop diuretics,
hydration (reversing Mannitol,
dehydration, Dopamine &
Maintenance of Fenoldopam.
adequate mean Natriuretic Peptides.
arterial pressure,
Minimizing exposure
to nephrotoxins.
62
62. NS, albumin, plasma ….
CVP = 8-12 cm H2O, MAP > 65 mmHg.
Optimal rate of infusion remain unclear and
should be individualized.
Target MAP ≥ 65 mmHg.
Which vasopressors to be used.
Role of low dose dopamine..
63
63. Noradrenaline is the drug of choice in AKI in
sepsis.
Norepinephrine has been demonstrated to
preserve splanchnic blood flow better than
dopamine.
Optimise fluid before starting vasopressors.
Low dose dopamine should not be used for
renal protection in severe sepsis.
64
64. Meta-analysis: Low-Dose Dopamine Increases
Urine Output but Does Not Prevent Renal
Dysfunction or Death
Low-dose dopamine offers transient
improvements in renal physiology, but no
good evidence shows that it offers
important clinical benefits to patients with
or at risk for acute renal failure.
65
65. In animal studies the use of mannitol and loop
diuretic minimize the degree of renal injury if
given at the time of ischemic injury.
Loop diuretics decrease the active Na
transport in the thick ascending loop
decreasing the energy requirement.
66
66. Increasing the urine output by loop diuretic
make the management easier but does not
affect cell injury or the severity of the renal
damage.
Loop diuretic increase the urine output in the
remaining nephrons and therefore huge
doses are required that may cause deafness.
67
67. ANP had been tried in experimental models
without any benefit despite their ability to
increase renal blood flow and Na excretion.
Calcium channel blockers decrease Ca influx
to the cells that lead to cell injury.
Most human studies were done on
established ATN.
68
68. Uncontrolled studies showed that those
patients who respond to diuretics or mannitol
may have better outcome but these patients
has less severe disease.
Controlled studies failed to show any
evidence that low dose dopamine have any
protection of cell injury in ischemic renal
damage. 69