• Share
  • Email
  • Embed
  • Like
  • Save
  • Private Content
Aki
 

Aki

on

  • 771 views

eLecture By Dr.Moh'd Asim

eLecture By Dr.Moh'd Asim
ICU specialist- Meqat Qeneral Hospital
Medinah-KSA

Statistics

Views

Total Views
771
Views on SlideShare
771
Embed Views
0

Actions

Likes
0
Downloads
0
Comments
0

0 Embeds 0

No embeds

Accessibility

Categories

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

    Aki Aki Presentation Transcript

    • Acute Kidney Injury in Critical Care By: Dr. Muhammad Asim Fazal Meeqat General Hospital (ICU)
    • Objective• Definition of AKI• Classification of AKI• Epidemiology• Etiology of AKI• Management of AKI – Diagnosis of AKI – Treatment of AKI
    • Definition of AKI• There are more than 35 definitions of AKI (formerly acute renal failure) in literature! - shows the complexity of the problem.• Deterioration of renal function over a period of hours to days, resulting in • the failure of the kidney to excrete nitrogenous waste products and • to maintain fluid and electrolyte homeostasis
    • Classification of AKI• Can be Classified into 3 ways• 1* Oliguric / Non-Oliguric• 2* Pre-Renal / Renal / Post-Renal• 3* RIFLE Criteria
    • Oliguric / Non-Oliguric• Oliguric : AKI associated with decrease urine output (<400ml/24 hours)• Non-Oligguric: AKI associated with normal urine output (>400ml/24 hours)• Very simple classification but not much helpful except that non-oliguric AKI has better prognosis.
    • Acute Kidney Injury AKIPRERENAL INTRINSIC POSTRENAL
    • Acute Kidney Injury• PRERENAL: 40-80% – Volume loss/Sequestration – Impaired Cardiac Output – Hypotension (and potentially hypo-oncotic states)• Net result: glomerular hypoperfusion
    • Acute Kidney Injury• Prerenal Azotemia: fall in GFR secondary to renal hypoperfusion that potentially has rapid reversible component• Restoration of effective intravascular volume, perfusion pressure• By current detectable methods, AKI reverses with minimal evidence of tubular ischemia
    • Acute Kidney Injury• RENAL/INTRINSIC: 10-30% – Vascular disorders: – small vessel – large vessel – Glomerulonephritis – Interstitial disorders: – Inflammation – Tubular necrosis: – Ischemia – Toxin – Pigmenturia
    • Acute Kidney Injury• Prerenal and ATN encountered most often in the hospital setting: 70-75% in many studies• Most common diagnostic consideration is therefore between these two conditions• Prerenal: 1. Intravascular volume depletion 2. Hypotension 3. Edematous states 4. Localized renal ischemia• ATN: 1. All causes for prerenal, leading to post-ischemic ATN 2. Toxins
    • Postrenal azotemia• Stones• Blood clots• Papillary necrotic tissue• Urethral disease anatomic: posterior valve functional: anticholinergics, L-DOPA• Prostate disease• Bladder disease anatomic: cancer, schistosomiasis functional: neurogenic bladder
    • RIFLE Criteria– Risk • 1.5X increase in creatinine or UO < 0.5 ml/kg for 6 hours– Injury • 2X increase in creatinine or UO < 0.5 ml/kg for 12 hours– Failure • 3X increase in creatinine or UO < 0.3 ml/kg for 24 hours or anuria for 12 hours– Loss • Complete loss of function for more than 4 weeks– ESRD • Complete loss of function for more than 3 months
    • Epidemiology of AKI• AKI occurs in ≈ 7% of hospitalized patients. 36 – 67% of critically ill patients (depending on the definition). 5-6% of ICU patients with AKI require Renal Replacement Therapy.
    • Mortality• Dialysis requiring 40-90%• Increased mortality even in patients not requiring dialysis • 25% increase in creatinine associated with a mortality rate of 31% compared with 8% for matched patients without renal failure.
    • Etiology of AKI• Categorize the different causes of acute renal insufficiency. – Prerenal: volume depletion and relative hypotension – Vascular: Consider vasculitis, TTP, nephrosclerosis, renal artery stenosis – Glomerular: Consider the nephritic and nephrotic syndromes – Tubular/interstitial: Consider ATN, drugs, PCKD, myeloma, autoimmune disorders – Obstructive: Consider prostate disease, stones, metastatic cancer
    • • What are the most likely causes in hospitalized patients? – ATN (45%) – Prerenal (21%) – Acute on chronic kidney disease (13%) – Obstruction (10%) – Glomerulonephritis or vasculitis (4%) – Acute interstitial nephritis (2%) – Atheroemboli (1%)
    • Management of AKI• Consists of 2 Parts:• 1* Diagnosis of AKI• 2* Treatment of AKI History and Physical exam Detailed review of the chart, drugs administered, procedures done, hemodynamics during the procedures.
    • Diagnosis of AKI• The following tests can aid in the diagnosis and assessment of AKI:• Kidney function studies: Increased levels of blood urea nitrogen (BUN) and creatinine are the hallmarks of renal failure; the ratio of BUN to creatinine can exceed 20:1 in conditions that favor the enhanced reabsorption of urea, such as volume contraction (this suggests prerenal AKI)
    • • Complete blood count• Peripheral smear• Serologic tests: These may show evidence of conditions associated with AKI, such as schistocytes in disorders such as hemolytic- uremic syndrome and thrombotic thrombocytopenic purpura• Fractional excretion of sodium and urea
    • AKI: Diagnostic studies-urine• Urinalysis for sediment, casts• Response to volume repletion with return to baseline SCr 24-72 hr c/w prerenal event• Urine Na; FENa FENa (%) = UNa x SCr x 100 SNa x UCr – FENa < 1%: Prerenal – FENa 1-2%: Mixed – FENa > 2%: ATN• Hansel’s stain
    • Acute Kidney InjuryOTHER LABORATORY DATA• HCO3ˉ: anion gap, lactic acid, ketones• Serun Electrolytes especially serum K level• CPK/LDH/Uric acid/liver panel• Serologies: – Complement – ESR, RF, ANA, ANCA, AntiGBM – Electrophoresis• Toxicology studies
    • Acute Kidney InjuryIMAGING STUDIES• Ultrasound: evaluates renal size, able to detect masses, obstruction, stones.• Renal biopsy: Can be useful in identifying intrarenal causes of AKI
    • AKI: Acute Tubular Necrosis• Non-oliguric vs. Oliguric • Prognosis worse with oliguric ATN in most series• Ischemic insult: medulla most susceptible to hypoxic event, cellular ATP depletion, oxidative injury• AKI/ARF phase of ATN: 7-21 days on average• Recovery phase of ATN: also known as diuretic phase • High urine output (>3-4 L) • K, Mg, PO4 wasting• Associated with high FENa
    • Treatment of AKI• It cannot be overstated that the current treatment for AKI is mainly supportive in nature; no therapeutic modalities to date have shown efficacy in treating the condition.
    • • Maintenance of volume homeostasis and correction of biochemical abnormalities remain the primary goals of AKI treatment and may include the following measures:• Correction of fluid overload with furosemide• Correction of severe acidosis with bicarbonate administration, which can be important as a bridge to dialysis
    • • Correction of hyperkalemia• Correction of hematologic abnormalities (eg, anemia, uremic platelet dysfunction) with measures such as transfusions and administration of desmopressin as needed.
    • Dietary Modification• Dietary changes are an important facet of AKI treatment. Restriction of salt and fluid becomes crucial in the management of oliguric renal failure, wherein the kidneys do not adequately excrete either toxins or fluids.
    • • Because potassium and phosphorus are not excreted optimally in patients with AKI, blood levels of these electrolytes tend to be high.• Restriction of these elements in the diet may be necessary, with guidance from frequent measurements.
    • • In the polyuric phase of AKI, potassium and phosphorus may be depleted, so that patients may require dietary supplementation and IV replacement.
    • • Calculation of the nitrogen balance can be challenging, especially in the presence of volume contraction, hypercatabolic states, GI bleeding, and diarrheal disease.
    • • Critically ill patients should receive at least 1 g/kg/day protein but should avoid hyperalimentation, which can lead to an elevated blood urea nitrogen (BUN) level and water loss resulting in hypernatremia.
    • • Pharmacologic treatment of AKI has been attempted on an empiric basis, with varying success rates.
    • Avoid Nephrotoxic agents• In AKI, the kidneys are especially vulnerable to the toxic effects of various chemicals. All nephrotoxic agents (eg, radiocontrast agents, antibiotics with nephrotoxic potential, heavy metal preparations, cancer chemotherapeutic agents, nonsteroidal anti- inflammatory drugs [NSAIDs]) should be avoided or used with extreme caution.
    • • Similarly, all medications cleared by renal excretion should be avoided, or their doses should be adjusted appropriately.
    • Acute Kidney InjuryINDICATIONS FOR RENAL REPLACEMENT THERAPY• Consensus generally includes: 1. Refractory volume overload 2. Severe metabolic acidosis; HCO3 may be variable, but declining level of factor; also falling pH to 7.1- 7.2 3. Hyperkalemia, with levels > 6.5, or documented rapid rise refractory to medical therapy 4. Major uremic target organ manifestations i.e. pericarditis, progressive neuropathy, seizure 5. Platelet dysfunction, bleeding diasthesis 6. AKI in setting of dialyzable drug/toxin
    • Acute Kidney InjuryINDICATIONS FOR RENAL REPLACEMENT THERAPY• Despite modalities available (IHD, CRRT) mortality remains 50% for AKI in critically ill patients• Clinicians will generally opt for RRT induction prior to development of the above symptoms; BUN of 80-100 in absence of other sx’s sometimes is a indication, but practices vary• While concept of prophylactic RRT has been around since 1950-60’s, its benefit remains uncertain, whether due to dose, timing, modality – Studies based on BUN criteria – Studies based on volume removal/ultrafiltration in cardiac patients rather than high-dose diuretics• No benefit proven of IHD vs CRRT
    • CRRT• CRRT may have a role in patients who are hemodynamically unstable and who have had prolonged renal failure after a stroke or liver failure.• Such patients may not tolerate the rapid shift of fluid and electrolytes caused during conventional hemodialysis.
    • Acute Kidney Injury: conclusions• Major advances in understanding AKI, but no clear definition that guides research on prophylaxis, prognosis• AKI still carries high M/M risk, especially in ICU setting• Improving volume status, hemodynamics rapidly aids in minimizing ischemic AKI risk; volume resuscitation, relief of urinary obstruction can be done concurrently• Patient history, hosp chart review, PEx coupled with routine labs, UA may establish cause in 40-60% of AKI• Serologies and consideration of Bx are also adjuncts
    • THANKYOU