2020_AKI assess AND interventions

Acute kidney injury: assess, intervention And nurse’s role Saowaros Parinyachitta, M.N.S., APN Acute dialysis unit









Content • Background • AKI definition, cause, detection of AKI, Risk factor to AKI • Assess of AKI patients • KDIQO 2012 & Intervention for AKI • Management in AKI • Prevention • Management • Renal replacement therapy in critically ill

Background • Acute kidney injury (previously known as acute renal failure: ARF) →wide spectrum of injury to the kidneys, not just kidney failure • ~18% of all hospital admissions have AKI • Inpatient AKI-related mortality ~ 25 - 30% • ~ 20 - 30% of cases of AKI are preventable • Prevention could save up to 12,000 lives each year • NHS costs related to AKI ~ £434 - £620 million/year www.nice.org.uk

NCEPOD: Key findings June 2009 • AKI avoidable in 14% of cases • Only 50% of pts received “good care” • Post admission AKI: poor recognition & care • 24% not receive adequate senior review • Quality of care in this group was judged to be less good • 85% not have documented evidence of critical care outreach involvement

https://www.nephrocheck.com/aki-detection-urgency/

https://www.nephrocheck.com/aki-detection-urgency/

https://www.nephrocheck.com/aki-detection-urgency/

Background: prevention and early identification • AKI →identified by close monitoring Cr & urine output • AKI →prevented by early recognition and treatment of underlying cause, for example: • Early treatment of infections/sepsis • Early treatment/prevention of dehydration • Correcting hypovolaemia • AKI →prevented by: • Monitoring use of drugs →NSAIDs & ACE inhibitors • Taking care with at-risk pts →iodinated contrast agents with scans

Epidemiology of AKI in ICU • Acute Kidney Injury (AKI) ~20% of ICU pts • 5% of general hospital population • 25% of ICU case → require RRT • AKI →multifactorial • Sepsis • Hypotension • Drugs • Mortality rate up to ~ 80% (some studies)

Definition: AKI • Lack of consensus definition of AKI in the past • Acute Dialysis Quality Initiative (ADQI) • RIFLE criteria • Graded risks of injury • Has been validated in variety of critically ill populations • Acute Kidney Injury Network (AKIN) –Modified RIFLE criteria –Diagnostic and staging criteria for injury –Acute Kidney Injury to describe all levels of injury

Definition of AKI • A sudden, sustained, and usually reversible decrease in the glomerular filtration rate (GFR) occurring over a period of hours to days. > 30 definitions used in published studies

KDOQI clinical practice guideline for AKI

Relationships and definitions of kidney diseases and disorders





KDIGO Definition of AKI ( 2012 ) Defined by any of the following: • Increase in SCr by ≥0.3 mg/dL within 48 hours • Increase in Scr by ≥1.5 times baseline, which is known or presumed to have occurred within the prior seven days • Urine volume <0.5 mL/kg/h for 6 hours

Clinic Annals of Internal Medicine 7 November 2017

AJKD 2016

BUN and Creatinine as a marker of AKI But have limitations??

Limitations of serum creatinine and BUN • Change when extracellular volume depletion or decreased kidney blood flow Influenced by other factors, which are not directly related to kidney damage, such as:  age  sex  body mass  nutritional status

Limitations of Serum creatinine and BUN cont…  Elevated serum Cr → are not specific for AKI and require differentiation from other pre-renal or extra-renal causes.  Serum Cr → not specific for renal tubular lesions, pathogenetically related to AKI development.  Reflect the loss of glomerular filtration function, accompanying the development of AKI.

Limitations of serum creatinine and BUN cont…  Increases in serum Cr →detected later than the actual GFR changes as Cr accumulates over time  Serum CR → poor marker of kidney dysfunction as changes in its concentrations are neither sensitive nor specific in response to slight GFR alterations  Changes in serum Cr become apparent only when the kidneys have lost ≥50% of functional capacity

What is a biomarker? “ a characteristics that is objectively measured and evaluated as an indicator of normal biological process, pathogenic process, or pharmacologic response to a therapeutic intervention”. Test Biomarker Height Growth Urinary dipsticks for nitrites Proteinuria UTI Anti-GBM Ab Disease severity in IgA nephropathy Good pastures syndrome

Ideal Biomarker AKI  Non – invasive  Easily obtainable  Measurable using standardized assays  Fast results  Reasonable cost to perform

Possible roles for novel kidney injury biomarkers Ismaili Z Al et al., Ped Nephrol , 2010

AKI Bio-Markers • Cystatin C • Microalbumin • N-Acety-β-Glucose-Amidase (NAG) • Kidney Injury Molecule-1 ( KIM-1) • Neutrophil Gelatinase-Associated Lipocalcin (NGAL) • IL-18 • Liver Fatty Acid Binding Protein

AKI

Pre renal Intra renal Post renal



Kathryn E Griffith RCGP Representative for Kidney Care Member of Think Kidneys NHS England AKI Project Board







80% 10-15% 5%

Causes of AKI by region and how common • Pre-renal-Due to reduced blood supply to the kidney (Hypovolaemia) due to dehydration, D/V, drugs, sepsis, bleeding, cardiac problems, hypotension, etc 80% • Renal –Damage to Kidney by; infection/inflammation e.g nephritis, vasculitis. Hypoxia due to prolonged hypovolemia, Drugs toxic to kidneys such as Gentamicin, NSAID e.g ibuprofen, iodinated contrast Toxins, Rhabdomyolysis etc 10%-15% • Post renal- Kidney stones, obstructed ureters, urethral obstruction, prostate problems 5%

Cause of AKI and example •“Pre renal states” Decreased kidney perfusion • Hypovolemia: Increased losses (hemorrhage, burns, massive vomiting or diarrhea), poor oral intake or dehydration • Reduced cardiac output: Heart failure, cardiac tamponade, massive pulmonary embolism • Renal vasomodulation/shunting: Medications (NSAID, ACEi/ARB, cyclosporine, iodinated contrast), hypercalcemia, hepatorenal syndrome, abdominal compartment syndrome • Systemic vasodilation: Sepsis, SIRS, hepatorenal syndrome

•Intra renal cause • Vascular: Renal artery stenosis, arterial/venous cross-clamping • Microvascular: TTP, HUS, aHUS, DIC, APS, malignant hypertension, scleroderma renal crisis, preeclampsia/HELLP syndrome: H- hemolysis EL- elevated liver enzymes LP- low platelets counts, drug-induced), cholesterol emboli • Tubulointerstitium: AIN medications, infection, lymphoproliferative disease; pigment nephropathy: rhabdomyolysis, massive hemolysis (hemoglobin); crystal nephropathy: uric acid, acyclovir, sulfonamides, protease inhibitors (indinavir, azatanavir), methotrexate, ethylene glycol, acute phosphate nephropathy, oxalate nephropathy; myeloma- associated AKI (cast nephropathy); ATN: ischemia (shock, sepsis), inflammatory (sepsis, burns)

• Glomerular: Rapidly progressive (crescentic) GN: anti– glomerular basement membrane; immune complex diseases: IgA nephropathy, post infectious, lupus, mixed cryoglobuminemia with MPGN; pauci immune GN: ANCA- associated vasculitides: GPA, MPA, EGPA (Churg-Strauss); ANCA-negative; nephrotic-range proteinuria with associated AKI: HIV-associated nephropathy (secondary FSGS); other causes of nephrotic-range proteinuria that commonly associate with AKI: minimal change disease with ATN/AIN; membranous nephropathy + crescentic GN or renal vein thrombosis; myeloma + multiple different pathologies, but in particular light chain cast nephropathy

•Post renal causes • Bladder outlet Benign prostatic hypertrophy, cancer, strictures, blood clots Ureteral Bilateral obstruction (or unilateral with one kidney): stones, malignancy, retroperitoneal fibrosis Renal pelvis Papillary necrosis (NSAIDs), stones

Evolution of acute kidney injury

Who are risk ?

Identifying patients with risks for AKI • Elderly patients > 65 years of age • CKD →eGFR<60 ml/min • Liver Disease, Diabetes, Past History of AKI • Recent use of Nephrotoxins: example  NSAID-e.g ibuprofen,  ACE-I e.g ramipril, ARB e.g losartan  Spironolactone,  Metformin,  Iodinated contrast  Aminoglycosides, eg gentamicin • Cardiovascular disease e.g MI, stroke, peripheral vascular disease, HF

CCSAP 2017 Book 2

Common medications which can contribute to, or are affected by, AKI • UK Renal Pharmacy Group – AKI Medicines Optimisation Toolkit (March 2012) • Consider Acute Nephrotoxic Drug Action Contrast media ACE Inhibitors NSAID’S Diuretics ARB’s

Patients at risk of AKI due to illness •Oliguria urine output <0.5ml/kg /hr •Dehydration, bleeding, diarrhoea and vomiting (D/V) •High/deteriorating early warning scores EWS >/= 3 •Infection or sepsis •Fall, prolonged stay on floor-toxins from muscle crush toxic to kidneys- Rhabdomyolysis •Urinary obstruction •Emergency surgery especially intra-abdominal •Cognitive or neurological impairment that limits access to fluids- dehydration e.g dementia, stroke