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    Aki Inn Emergency

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    Hamza Dossa
    Acute kidney injury (AKI) is a common condition affecting 5-10% of hospitalized patients and up to 60% of intensive care unit patients. It is defined as an abrupt decrease in kidney function over a period of 7 days, which can be identified by an increase in serum creatinine of ≥0.3 mg/dL within 48 hours, or an increase of 1.5 times the baseline level. The main goals in managing AKI are to treat the underlying cause and prevent further kidney damage. Treatment involves fluid resuscitation, discontinuing nephrotoxic drugs, monitoring vital signs and urine output, and considering renal replacement therapy for severe cases.

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    Aki Inn Emergency

    Uploaded by

    Hamza Dossa
    12 views52 pages
    Acute kidney injury (AKI) is a common condition affecting 5-10% of hospitalized patients and up to 60% of intensive care unit patients. It is defined as an abrupt decrease in kidney function over a period of 7 days, which can be identified by an increase in serum creatinine of ≥0.3 mg/dL within 48 hours, or an increase of 1.5 times the baseline level. The main goals in managing AKI are to treat the underlying cause and prevent further kidney damage. Treatment involves fluid resuscitation, discontinuing nephrotoxic drugs, monitoring vital signs and urine output, and considering renal replacement therapy for severe cases.

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    ACUTE KIDNEY INJURY

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    aki inn emergency

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    Acute kidney injury (AKI) is a common condition affecting 5-10% of hospitalized patients and up to 60% of intensive care unit patients. It is defined as an abrupt decrease in kidney function over a period of 7 days, which can be identified by an increase in serum creatinine of ≥0.3 mg/dL within 48 hours, or an increase of 1.5 times the baseline level. The main goals in managing AKI are to treat the underlying cause and prevent further kidney damage. Treatment involves fluid resuscitation, discontinuing nephrotoxic drugs, monitoring vital signs and urine output, and considering renal replacement therapy for severe cases.

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    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    12 views52 pages

    Aki Inn Emergency

    Uploaded by

    Hamza Dossa
    Acute kidney injury (AKI) is a common condition affecting 5-10% of hospitalized patients and up to 60% of intensive care unit patients. It is defined as an abrupt decrease in kidney function over a period of 7 days, which can be identified by an increase in serum creatinine of ≥0.3 mg/dL within 48 hours, or an increase of 1.5 times the baseline level. The main goals in managing AKI are to treat the underlying cause and prevent further kidney damage. Treatment involves fluid resuscitation, discontinuing nephrotoxic drugs, monitoring vital signs and urine output, and considering renal replacement therapy for severe cases.

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    © All Rights Reserved
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    of 52

    Stepwise approach to

    Acute Kidney Injury


    in Emergency
    DR. SAMINA SHAMIM
    CONSULTANT NEPHROLOGY (FCPS)
    Outlines

    Background
    Epidimiology
    Definition
    Classification
    Consequences
    Emergency management of AKI
    Contrast associated AKI
     AKI of any stage 57% of patients.
     Severe (stage 2 or 3) AKI 39%
     Renal replacement therapy (RRT) 13.5%
    Mortality rates:
     (AKI-RRT) 40% to 55%
     Myocardial infarction in the ICU (20%),
     Sepsis without AKI (15%-25%)
     ARDS requiring mechanical ventilation (30%-40%).
    Background
     18th century Richard Bright described albuminuric end staged kidney disease termed bright’s disease

     Later Delafield by the 19th century further classified it as nephrosis and nephritis

     World War --- further noticing period

     By the 1950s the term ARF was established

     The term Acute Kidney Injury (AKI) became the preferred term in 2004 when ARF was redefined with
    the now widely accepted consensus criteria known as RIFLE
    DEFINITION

     AKI is characterized by the accumulation of


    creatinine, urea, and other unmeasured waste
    products after an abrupt decrease in kidney
    function
    AKI is defined as any of the following:
     Increase in SCr by ≥ 0.3 mg/dl (≥ 26.5 µmol/l) within 48 hours
    or
     Increase in SCr to ≥ 1.5 times baseline, which is known or presumed to have occurred
    within the prior 7 days;
    or
     Urine volume < 0.5ml/kg /hour for 6 hours
     AKI is common, affecting approximately 5% to
    10% of hospitalized patients and up to 60% of
    patients admitted to the intensive care unit (ICU).
    Even a minor increase in creatinine has great
    impact on mortality and morbidity .
    Classificcation of AKI
    Pathophysiology of AKI
    Management

    2 components

     Treat the underlying cause that leading to AKI


     Treat the AKI related events

     No single treatment that will modify the course of AKI from diffuse etiologies but certain
    universal measures are likely to be beneficial. These include maintenance of kidney
    perfusion, avoidance of nephrotoxic insults, and appropriate medication dosing
    Fluid Therapy.
    The most commonly used fluids are
     crystalloids ( 0.9 % saline . 0.45 % saline , ringers lactate , dextrose water , dextrose saline etc)
     Colloids (gelatins, human albumin, and hydroxyethyl starches (HES))
     Ideally, balanced crystalloid solutions should be used, as 0.9% saline is associated with hyperchloremic
    metabolic acidosis and worsening acid-base balance.
     High molecular weight HESs have been associated with an increased risk of AKI, greater need for RRT,
    and higher mortality and should therefore be avoided
     Although timely fluid resuscitation is important to prevent AKI in conditions associated with volume
    depletion, there is increasing evidence that excessive fluid administration can be harmful and lead to
    dysfunction of other organs and adverse outcomes .To avoid both hypo and hypervolemia, patients need
    to be assessed regularly, and fluid prescriptions should be individualized and tailored to the
    cardiovascular status of the patient.
     NS and balanced crystalloids are both reasonable options for IV fluids. However, emerging evidence,
    including the SMART and SALT-ED trials, may shift practice in favor of balanced crystalloids, namely
    Lactated Ringer’s, due to the potential benefits on mortality and renal function.
    High Risk 1 2 3
    Discontinue all nephrotoxic agents when possible

    Ensure volume status and perfusion pressure

    Consider functional hemodynamic monitoring

    Monitor Serum creatinine and urine output

    Avoid hyperglycemia

    Consider alternatives to radiocontrast procedures

    Non-invasive diagnostic workup

    Consider invasive diagnostic workup

    Check for changes in drug dosing

    Consider Renal Replacement Therapy

    Consider ICU admission

    Avoid subclavian catheters if possible


    Is there any role of Furesemide in AKI ?
     In a systematic review assessing the influence of diuretics in 876 patients, diuretics use was not associated
    with survival (relative risk 1.02; 95% CI 0.86–1.19) or with reduced need for RRT (RR 1.12; 95% CI 0.93–
    1.34)
    No differences were found in the proportion with worsening AKI (43.2% vs.
    37.1%, p = 0.6), kidney recovery (29.7% vs. 42.9%, p = 0.3), or RRT (27.0% s.
    28.6%, p = 0.8)
    Hyperkalemia treatment

    Clinical features Signs and symptoms are uncommon and tend to occur only when serum
    potassium is >7.0 meq/L include
     muscle weakness and ventricular arrhythmias.
     There are two major mechanisms of hyperkalemia:
     Increased potassium release from cells (eg, severe hyperglycemia, rhabdomyolysis)
     Reduced potassium excretion in urine (eg, hypoaldosteronism, kidney failure)
     Pseudohyperkalemia is a common cause of a reported elevation in serum potassium and
    must be excluded. It does not reflect true hyperkalemia and does not produce ECG
    changes.ECG manifestations
    The relationship between the degree of serum potassium elevation and ECG changes varies
    from patient to patient,
     Tall peaked T waves
     Shrinking and then loss of P waves.
     Widening of the QRS interval
     "sine wave," ventricular arrhythmia, and asystole
     ECG and place patients with hyperkalemic emergency on continuous cardiac monitoring.
     Give calcium gluconate 1000 mg (10 mL of 10% solution) or calcium chloride 500 to 1000 mg IV over
    two to three minutes to stabilize cardiac membranes.
     Give insulin and glucose to shift K+ intracellularly (give insulin only, without glucose, if serum
    glucose is >250 mg/dL [13.9 mmol/L]). A common regimen consists of a bolus injection of 10 units of
    regular insulin, followed immediately by 50 mL of 50% dextrose (25 g of glucose) over 5 minutes.
     Give therapy to remove potassium from the body.
     Remove potassium from the body Hemodialysis should be performed in patients with ESKD or severe
    kidney function impairment.
     Loop diuretics (in hypervolemia patients) or saline infusion with IV loop diuretics can be administered
    (eg, 40 mg of furosemide every 12 hours) to nonoliguric patients without severe kidney function
    impairment.
     A gastrointestinal cation exchanger (eg, sodium zirconium cyclosilicate 10 g orally or patiromer 8.4
    g ,Sodium polystyrene sulfonate (15 to 30 g orally) can be given, especially in patients with severe
    kidney function impairment in whom hemodialysis cannot be swiftly performed
    Metabolic acidosis
    Calculate bicarb deficit

     HCO3 deficit = TBW ( desired bic – actual bicarb )

     Replace 50% of the deficit


    Metabolic acidosis

    Iv bicarbonate Hemodyalysis Treat the cause


    Pulmonary edema
     Avoid hypertonic solutions including Bic
     Control blood pressures with nitrates
     Diuretics “ dose depend on clinical response”
     RRT ( Ultrafiltarion) for patients who do not respond to diuretics
    Uremic encephalopathy

    TME is a sign of advanced renal failure,


     encephalopathy typically occurs later in younger, otherwise healthy patients and sooner in older patients or those with underlying central
    nervous system disease.
     The dialyzable toxins responsible for uremic encephalopathy have not been unequivocally identified .
     Brain amino acid metabolism also may be impaired, causing an imbalance between excitatory and inhibitory neurotransmitters, or the
    accumulation of false neurotransmitters such as methylguanidine and "middle molecules"Uremic toxins".)
     Early clinical features of uremic encephalopathy include lethargy, irritability, disorientation, hallucinations, and rambling speech. Coma is
    unusual but may occur in patients with acute renal failure .Most uremic patients have mild diffuse weakness and show unsteadiness in
    their movements [8]. Tremor, myoclonus, and asterixis are common and tend to vary in parallel with mental status; tetany may be present.
    Rarely, focal signs such as hemiparesis or reflex asymmetry may occur [8]. Such focal signs tend to be transient, alternate from side to
    side, and resolve with hemodialysis.
     Generalized seizures may occur, particularly when uremia is acute, and myoclonus, psychosis, and coma can also be.Acute uremic
    encephalopathy reverses with dialysis, although a lag time of one to two days usually is required before mental status clears. Subtle
    cognitive difficulties may persist even after dialysis in patients with chronic renal failure. Failure to improve substantially following
    dialysis should alert the physician to other possible etiologies of encephalopathy. In most cases of dialysis disequilibrium syndrome,
    neurologic recovery is rapid and complete [1,6-8].
     Early clinical features of uremic encephalopathy include
     lethargy,
     irritability,
     disorientation, hallucinations, and rambling speech.
     Coma is unusual but may occur in patients with acute renal failure .
     Tremor, myoclonus, and asterixis are common and tend to vary in parallel with mental
    status; tetany may be present.
     Generalized seizures may occur, particularly when uremia is acute.
     Acute uremic encephalopathy reverses with dialysis, although a lag time of one to two
    days usually is required before mental status clears.
     Subtle cognitive difficulties may persist even after dialysis in patients with chronic renal
    failure.
     Failure to improve substantially following dialysis should alert the physician to other
    possible etiologies of encephalopathy.
     The EEG in uremia reflects the severity of encephalopathy. The most common EEG
    finding is prominence of slow waves.
     Intermittent frontal rhythmic theta activity and paroxysmal, bilateral, high-voltage delta
    waves also are frequent, and triphasic waves may appear in the frontal regions
     Epileptiform activity may be present in up to 14 percent of case
     Neuroimaging may be required to exclude the presence of a subdural hematoma
    Acute uremic encephalopathy reverses with dialysis, although a lag time of one to two days
    usually is required before mental status clears. Subtle cognitive difficulties may persist even
    after dialysis in patients with chronic renal failure.
    Failure to improve substantially following dialysis should alert the physician to other
    possible etiologies of encephalopathy. In most cases of dialysis disequilibrium syndrome,
    neurologic recovery is rapid and complete
    Dialysis indications
    Contrast associated AKI

     CA-AKI typically occurs within 48 h of receiving contrast with recovery expected, in


    most cases, over the next 5 days. 
    Management

     Management of CI-AKI aims primarily at prevention.


     Consideration should be given to alternative noncontrast studies if possible
     NSAIDS and other Nephrotoxins discontinued, ideally at least 24 hours before the procedure.
     Low- or iso-osmolar radiocontrast should be used, at the lowest possible volume required.
     Isotonic intravenous fluid administration reduces the risk for CI-AKI and should be used in those at elevated
    risk.
     Typical regimens consist of a 1-mL/kg/h infusion 12 hours before and 12 hours after contrast exposure, or
    3 mL/kg/ h 1 hour before and 1.5 mL/kg/h for 4 to 6 hours postprocedure.
     N-acetylcysteine vs placebo showed no benefit
     There have been a variety of other pharmacotherapies evaluated for CI-AKI prevention, none of which is clearly
    beneficial.
     Hemodialysis after administration of contrast is ineffective for preventing CI-AKI and may cause harm.
     Typical regimens consist of a 1-mL/kg/h infusion 12 hours before and 12 hours after
    contrast exposure, or 3 mL/kg/ h 1 hour before and 1.5 mL/kg/h for 4 to 6 hours
    postprocedure.
     N-acetylcysteine vs placebo showed no benefit
     There have been a variety of other pharmacotherapies evaluated for CI-AKI prevention,
    none of which is clearly beneficial.
     Hemodialysis after administration of contrast is ineffective for preventing CI-AKI
    and may cause harm.

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