Download Acute Renal Failure

Acute Renal
Failure (Acute
Kidney Injury)
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Objectives
Acute Renal Failure ,Acute tubular Necrosis
(Definition)
Causes.
Clinical presentations.
Complications and Treatment.
Preventions.
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Acute Renal Failure (ARF)
ARF; also referred to as acute kidney injury (AKI) describes a
sudden and usually reversible loss of renal function, which
develops over days or weeks and is usually accompanied by a
reduction in urine volume.
 Azotaemia: retention of urea and other nitrogen compounds in
blood
 Uraemia : synonymous with azotaemia, also means uraemic
syndrome, i.e., the clinical manifestation of renal failure
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Classifications of Renal Failure
Acute versus chronic
Pre-renal, renal, post-renal
Anuric, oliguric, polyuric
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Acute Versus Chronic
• Acute
–
–
–
–
Sudden onset
Rapid reduction in urine output
Usually reversible
Tubular cell death and regeneration
• Chronic
– Progressive
– Not reversible
– Nephron loss
• 75% of function can be lost before its noticeable
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Acute Renal Failure
• Pre-renal = 55%
• Renal parenchymal (Intrinsic)= 40%
• Post-renal = 5-15%
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Causes of ARF
Prerenal
55%
Renal
40%
Pos-renal
5%
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Clinical assessment
•
There may be marked hypotension and signs of poor
peripheral perfusion, such as delayed capillary return.
It may occur without hypotension like in NSAIDs,
ACEI.
•
Not always the cause of reduced blood flow is clear
like in concealed blood loss can occur into the
gastrointestinal tract, following trauma or in to into the
pregnant uterus.
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Clinical assessment
•
In sepsis there is systemic circulatory vasodilation
hence relative underfilling of the arterial tree even
after fluid resuscitated.
•
The combination of sepsis with nephrotoxins such as
NSAIDs is a common cause of ARF.
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Clinical Manifestations
 Patients with AKI may report symptoms such as
anorexia, fatigue, nausea and vomiting, and pruritus, as
well as a decline in urine output or dark-colored urine.
 Furthermore, if the patient has become volume
overloaded, shortness of breath and dyspnea on exertion
may be noted.
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Clinical Manifestations
 On physical examination, findings such as asterixis,
myoclonus, or a pericardial rub may be evident.
 If volume overload is present, peripheral edema,
pulmonary crackles, and jugular venous distention may be
found.
 It is also not unusual for a patient to be entirely
asymptomatic, with advanced AKI discovered only by
laboratory testing.
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Management
1. Establish and correct the underlying cause of the ARF.
2. If hypovolaemia is present, restore blood volume as
rapidly as possible (with blood, plasma or isotonic saline
(0.9%), depending on what has been lost).
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Management
3. Optimise systemic critically ill patients may require inotropic
drugs to restore an effective blood pressure. Recent trials do not
support the use of low-dose dopamine in severely ill patients at
risk of ARF.
4. Correct metabolic acidosis:
-Restoration of blood volume will correct acidosis by restoring
kidney function.
-Sodium bicarbonate (e.g. 50 mL of 8.4%) may be used if acidosis
is severe to lessen hyperkalaemia.
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Prognosis

If treatment is given sufficiently early, renal
function will usually improve rapidly; in such
circumstances residual renal impairment is
unlikely. In some cases, however, treatment is
ineffective and renal failure becomes established.
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Established acute renal failure
 Established ARF may develop following severe or prolonged
underperfusion of the kidney (pre-renal ARF), when the
histological pattern of Acute tubular necrosis is usually seen.
 Differential diagnosis of acute renal failure in a haemodynamically stable,
non-septic patient
1.
2.
3.
4.
5.
Urinary tract obstruction should always be excluded by history,
Ultrasound.
Due to major vascular occlusion or small-vessel diseases .
Rapidly progressive glomerulonephritis (RPGN)
Acute interstitial nephritis.
Drugs and toxins (NSAIDs, ACE inhibitors, aminoglycosides),
(mushrooms, snake bite, paraquat, paracetamol).
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Acute tubular necrosis (ATN)
 ATN may result from
1. Ischaemia or
2. Nephrotoxicity, caused by chemical or bacterial toxins, or a
combination of these factors.
3. Drugs which are toxic to renal tubular cells include the
aminoglycoside antibiotics, such as gentamicin, the cytotoxic agent
cisplatin, and the antifungal drug amphotericin B.
Dead tubular cells may shed into the tubular lumen, leading to tubular
obstruction
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 During recovery, depending on the severity of the renal
damage and the rate of recovery, there is often a diuretic
phase in which urine output increases rapidly and remains
excessive for several days before returning to normal.
This is due in part to temporary loss of the medullary
concentration gradient, and which depends on continued
delivery of filtrate to the ascending limb of the loop of
Henle and active tubular transport.
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Urine findings in Prenal azotemia vs. Acute Renal
Failure
Prenal azotemia or
Glomerulonephritis
Acute renal failure or
Postrenal azotemia
Specific gravity
>1.018
<1.012
Urine osmolality
> 300 - 500
< 300 - 400
Urine Na (meq)
< 20 meq/l
> 40 meq/l
Urine/plasma creatinine
> 40
< 20
Renal failure index (U Na/ U/P creat)
<1
>2
Fractional excretion Na (U/P Na/ U/P
creat)x100
<1
>2
Response to fluid challenge
++
?
normal
hyaline cast brown granular
casts, cellular debris
Laboratory Tests
Urine sediment
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Complications
1. Expansion of extracellular fluid volume.
2. Hyperkalemia is a frequent complication of ARF; Coexistent
metabolic acidosis may exacerbate hyperkalemia by promoting
potassium efflux from cells. Hyperkalemia may be particularly
severe, even at the time of diagnosis, in patients with
rhabdomyolysis, hemolysis, and tumor lysis syndrome.
3. Metabolic acidosis, often with an increased anion gap. Acidosis
can be particularly severe when endogenous production of
hydrogen ions is increased by other mechanisms (e.g., diabetic or
fasting ketoacidosis; lactic acidosis complicating generalized tissue
hypoperfusion, liver disease, or sepsis; metabolism of ethylene
glycol or methanol).
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4. Hyperphosphatemia is an almost invariable complication of ARF.
Severe hyperphosphatemia may develop in highly catabolic patients
or following rhabdomyolysis, hemolysis, or tissue ischemia.
Metastatic deposition of calcium phosphate can lead to
hypocalcemia,
5. Anemia develops rapidly in ARF and is usually multifactorial in
origin. Contributing factors include impaired erythropoiesis,
hemolysis, bleeding, hemodilution, and reduced red cell survival
time.
6. Prolongation of the bleeding time is also common. Common
contributors to the bleeding diathesis include mild
thrombocytopenia, platelet dysfunction, and/or clotting factor
abnormalities (e.g., factor VIII dysfunction).
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7.Infection is a common and serious complication of ARF.
8.Cardiopulmonary complications of ARF include
arrhythmias, pericarditis and pericardial effusion, and
pulmonary edema.
9.Vigorous diuresis can occur during the recovery phase of
ARF.
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Investigations
1.
2.
3.
4.
5.
6.
Urea and creatinine.
Electrolytes.
Full blood count Clotting screen.
Urinalysis.
Renal ultrasound
Others; Albumin, Chest X-ray, Serology and ECG.
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Management
In the absence of dialysis, the most common
causes of death are
1.
Hyperkalaemia and
2.
Pulmonary oedema, followed by
3.
Infection and uraemia itself.
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Management of Ischemic and Nephrotoxic Acute Renal Failure
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
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Management of Ischemic and Nephrotoxic Acute Renal Failure
Management Issue
Therapy
Prevention and Treatment of Complications
Salt and water restriction
Intravascular volume
overload
Diuretics
Ultrafiltration
Restriction of enteral free water intake
Hyponatremia
Avoidance of hypotonic intravenous solutions, including
dextrose-containing solutions
Metabolic acidosis
Sodium bicarbonate (maintain serum bicarbonate >15
mmol/L or arterial pH >7.2)
Administration of other bases, e.g., THAM
Dialysis
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Hyperkalemia & EKG
•
•
•
•
•
•
•
K > 5.5 -6
Tall, peaked T’s
Wide QRS
Prolong PR
Diminished P
Prolonged QT
QRS-T merge – sine
wave
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Management Issue Therapy
Restriction of dietary K+ intake
Eliminate K+ supplements and K+-sparing diuretics
Hyperkalemia
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 β-agonist therapy to promote intracellular
mobilization
Calcium gluconate or calcium chloride (1 g) to stabilize the
myocardium
Dialysis
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Management Issue Therapy
Hypocalcemia
Calcium carbonate or gluconate (if symptomatic)
Hypermagnesemia Discontinue Mg++ containing antacids
Treatment usually not necessary if <890 µmol/L or <15mg/Dl
Hyperuricemia
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
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renal impairment
Absolute indications for dialysis include:
1.
2.
3.
4.
5.
6.
7.
8.
Marked volume overload.
Severe metabolic acidosis.
Hyperkalemia refractory to medical therapy.
Pericarditis.
Asterixis, Encephalopathy +Peripheral neuropathy.
PEM.
Anorexia, vomiting + nausea after exclusion of other causes.
blood urea levels of >100 mg/dL
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Prognosis
 In uncomplicated ARF mortality is low even when renal
replacement therapy is required. In ARF associated with
serious infection and multiple organ failure, mortality is
50-70%.
 Outcome is usually determined by the severity of the
underlying disorder and other complications, rather than
by renal failure itself.
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