2020_AKI assess AND interventions

Potential cause of AKI Exposures Susceptibilities • Sepsis Exposures Susceptibilities • Dehydration or volume • Critical illness depletion • Circulatory shock • Burns • Advanced age • Trauma • Female gender • Cardiac surgery • Black race • CKD (especially with CPB) • Chronic disease • Major noncardiac • DM • Cancer surgery • Anemia • Nephrotoxic drugs • Radiocontrast agents • Poisonous plants and animals

Incidence: AKI By Age Hsu et al , JASN 2013, 24:37-42

AKI in high and low income countries Kidney International Reports (2017) 2, 544–558

Complications of AKI Metabolic CV Neuro Heme GI Infectious Metabolic Fluid Neuropath Anemia N&V UTI acidosis overload y Dementia Coag GI IV catheter Hyper K+ HTN anomalies bleeding sepsis Seizures Hypo Ca++ Arrhythmia Pneumonia s Hyperphosphat Pericarditis e hyper uremic Marini, J & Wheeler, A, Critical Care Medicine, 2010

AKI Presentation- Symptoms • Most patients have No Complaints/ nonspecific symptoms • Reduction of urine • Concentrated urine, deep yellow, brown etc • Dehydration or thirst • Nausea, vomiting • Abdominal pains and feeling generally unwell • Confusion and drowsiness

AKI Presentations- clinical signs • There may be NO clinical signs initially • Lower abdominal fullness and tenderness e.g urinary obstruction • Pallor- Anaemia e.g gastrointestinal bleeding Maleana, Haematemesis • Features of infection- fever, pneumonia, Urinary tract infection (UTI), cellulitis etc. • Haemoptysis, haematuria, vasculitis rash- renal AKI causes

AKI signs- Features of hypovolaemia; • Dry Mucous membranes • Loss of skin turgor (elasticity) • Tachycardia HR>90 b/min, BP<100 mmHg, postural drop of 20 mmhg with increase in RR • Respiratory rate(RR) >20 /min • Prolonged capillary refill time(CRT) >2s • Cold sweaty peripheries • Urine output < 0.5 ml/kg/h

Tests and Formulas for AKI • FENa - fractional excretion of sodium • Can help differentiate pre-renal from ATN • Measures percentage of filtered Na that is excreted • If <1%: prerenal, if >1%: ATN • Not accurate if pt has received diuretics • (PCr x UNa)/ (PNa x UCr) x 100% • Na = mEq/L Cr = mg/dl • Feurea – fractional excretion of urea • Better estimation if pt has had diuretics • (serumCr x urineUrea)/ (serumUrea x urineCr) x 100% • all units in mg/dl

Tests and Formulas for AKI • Urine to plasma creatinine ratio • Estimates tubular water resorption • Creatinine in filtrate is equal to that of plasma • Urine Cr increases as water, not Cr, is reabsorbed

Etiology Pre renal AKI Post renal ATN AIN AKI Serum BUN:Cr Dehydration, Ischemia, Allergic rxn; ratio hypoperfusion Obstruction nephrotoxins drug rxn Urine Na > 20:1 < 20:1 < 20:1 (mEq/L) > 20:1 FeNa < 20 > 20 Variable Variable < 1% > 1% Variable Variable 250 - 300 Variable Urine osms >500 < 400 (mosm/kg) Hyaline casts Muddy brown White cells, Nml or red casts, renal white cell casts, Urinary cells, white tubular casts +/- eosinophils sediment cells, or crystals

Common Diagnostics of AKI • Urinalysis • Renal ultrasound • Serum BUN/Cr • Gold standard • Urine Na+ • Will show obstructions, • FENa or FEurea hydronephrosis, kidney size • Urine osmolality • Urine to plasma Cr ratio • Consider CT abd/pelvis • Urine volume • Consider 24 hr urine collection

Acute kidney injury assessment

Assess of AKI Investigation Physical Examination History

History • Focus history on ascertaining the main causes of AKI (many patients have more than one cause of AKI): • Common causes • Sepsis • Hypoperfusion (hypotension, hypovolaemia, etc.) • Medications • Obstruction Royal College of Physicians of Edinburgh: NHS Kidney Care

History: Remember that there are many causes of AKI: • Pre-renal (functional) • Intrinsic renal • Post-renal • Hypovolemia, e.g. (damage) (functional) bleeding, • Prolonged • Renal stone gastrointestinal losses hypoperfusion disease • Sepsis causing tubular • Pelvic masses, e.g. • Cardiac arrhythmias injury cervical cancer • Myocardial infarction • Infiltrative disease, • Prostatic • Renal artery stenosis e.g. myeloma hypertrophy / • Nephrotoxins cancer • Glomerulonephritis • Urethral stricture • Interstitial nephritis • Rhabdomyolysis

AKI Causes:When to suspect Intrinsic Renal Disease

History (cont..) • Less common causes • (consider these if the common causes listed above are not obvious) • Intrinsic renal diseases • Glomerulonephritis • Vasculitis • Interstitial nephritis • Myeloma

History (cont..) • Hypoperfusion • Vomiting and/or :Clues from the history diarrhoea • Haemorrhage • Sepsis • Cardiac failure (acute or • Fever chronic) • Cough with sputum • Cardiac arrhythmias • Vomiting and diarrhoea • Diuretics (over diuresis) • Dysuria • Urinary catheter • Immunosuppression • (can predispose and also prevent rise in white cell count masking sepsis)

History (cont..) • Iodinated contrast agents (contrast-induced AKI) :Clues from the history • Any new medication • Medications • (some drugs can cause • Non-steroidal anti-inflammatory drugs interstitial nephritis, e.g. • (NSAIDs are nephrotoxic and can NSAIDs, proton pump also cause interstitial nephritis) inhibitors and antibiotics) • Angiotensin-converting enzyme inhibitors • Herbal remedies • (ACEi reduces renal blood flow) • (may contain nephrotoxic • Angiotensin receptor blockers compounds) • (ARBs reduces renal blood flow) • Gentamicin and vancomycin • Over the counter medications • (high levels of aminoglycosides are nephrotoxic)

History (cont..) :Clues from the history • Obstruction • History of kidney stones • Prostatic symptoms • (prostatic hypertrophy or malignancy) • Known single kidney • (obstruction of one ureter will cause AKI) • Pelvic malignancy

History (cont..) • Haemoptysis (vasculitis) • Red eye (uveitis in vasculitis) :Clues from the history • Back pain • Intrinsic renal disease • (bone pain may be a sign • Constitutional symptoms of myeloma – the lower • (fever and weight loss are non-specific back is a common site) but are features of vasculitis) • Joint pains (vasculitis) • Falls/immobility • Rashes (rhabdomyolysis) • (purpuric rashes or nodules may be a sign of vasculitis) • Neuropathies (vasculitis) • Nasal stuffiness • (sinus involvement in ANCA-associated vasculitis, e.g. granulomatosis with polyangiitis)

Examination : Aim to identify clues as to the cause, assess volume status and identify any complications • Identify the cause: • Intrinsic • Volume status examination • Pre-renal • Rash (vasculitis, interstitial nephritis) • Volume status examination • Red eye (vasculitis) • Evidence of sepsis, e.g. fever, • Red swollen joints (vasculitis) respiratory signs, surgical site, • Swollen limb (rhabdomyolysis) red swollen joints, cellulitis, indwelling urinary catheters, cannulae • Evidence of haemorrhage, e.g. haematemesis, melaena

Examination : • Identify the cause: • Post-renal • Tense ascites (intra-abdominal hypertension) • Palpable bladder • Large prostate

Examination : •Fluid status • Capillary refill (<3 s) • Pulse rate (tachycardia) • Blood pressure (lying and standing if patient able to stand safely) • Skin turgor (over clavicle) • Jugular venous pressure • Oedema (peripheral and pulmonary) • Fluid balance charts • Daily weights (trends in body weight are a sensitive indicator of volume status)

Examination : • Complications • Hyperkalaemia (potassium > 6.0 mmol/L) • Acidosis • Acute confusion (uraemic encephalopathy) • Pulmonary oedema • Pericarditis (pericardial friction rub)

Investigation: Aims to identify the cause and identify complications. All patients: • Biochemistry profile: • Full blood count • Urea • Look for evidence of • Liver function tests haemorrhage and sepsis • Electrolytes • Low platelets may occur with • Glucose sepsis or HUS/thrombotic • Creatinine thrombocytopenic purpura • Bone profile • Bicarbonate

Investigation: • Urinalysis Consider: (some case) • Blood and/or protein is abnormal • Cultures: • Urinary tract infection • blood and vasculitis must be • urine considered • wound • C-reactive protein (CRP) • Lactate (surrogate marker of shock and hypoperfusion) • Venous or arterial blood gas

Investigation: • Coagulation screen • Urine Bence-Jones protein (myeloma) • Creatine kinase (rhabdomyolysis) • Anti-neutrophil cytoplasmic antibody • Lactate dehydrogenase (LDH) • Blood film (HUS/TTP) (ANCA; vasculitis) • Serum and urine electrophoresis • Anti-nuclear antibody (ds DNA specific (myeloma) for SLE) • Serum free light chains (myeloma) • Complement (C3 and 4) • Anti-glomerular basement • Hepatitis B and C serology • Renal tract ultrasound membrane antibodies • CXR (Goodpastures disease) • ECG (hyperkalaemia, pericarditis, arrhythmia, ischaemia)

Prevention is the best for aki

Prevention AKI •Identify who are risk for AKI •Raise AKI awareness , treat the cause and limit AKI risk in “at risk” patient groups

Patients at risk of AKI in Community

Patients at risk of AKI in Community

• Fluid bolus: a rapid infusion to correct hypotensive shock. It typically includes the infusion of at least 500 ml over a maximum of 15 min • Fluid challenge: 100–200 ml over 5–10 min with reassessment to optimize tissue perfusion • Fluid infusion: continuous delivery of i.v. fluids to maintain homeostasis, replace losses, or prevent organ injury (e.g., prehydration before operation to prevent intraoperative hypotension or for contrast nephropathy) • Maintenance: fluid administration for the provision of fluids for patients who cannot meet their needs by oral route. This should be titrated to patient need and context, and should include replacement of ongoing losses. In a patient without ongoing losses, this should probably be no more than 1–2 m/kg per hour Kidney Int Rep (2017) 2, 544–558

• Daily fluid balance: daily sum of all intakes and outputs Cumulative fluid balance: sum total of fluid accumulation over a set period of time • Fluid overload: cumulative fluid balance expressed as a proportion of baseline body weight. A value of 10% is associated with adverse outcomes • Response: Achieving hemodynamic goal and/or improvement of UOP: >0.5 ml/kg per hour • Persistent AKI is characterized by the continuance of AKI by creatinine or urine output criteria (defined by KDIGO criteria) beyond 48 hours from onset. • Complete reversal of AKI by KDIGO criteria within 48 hours of the onset characterizes rapid reversal of AKI • AKD is defined as a condition wherein AKI Stage Ia or greater criteria is present 7 days (or more) after an exposure. a AKD that persists beyond 90 days is then considered CKD Kidney Int Rep (2017) 2, 544–558

Minimum treatment parameter requirements in community setting

Minimum treatment and parameter requirements in hospital





2.2.1:We recommend that patients be stratified for risk of AKI according to their susceptibilities and exposures. (1B) 2.2.2: Manage patients according to their susceptibilities and exposures to reduce the risk of AKI (see relevant guideline sections). (Not Graded) 2.2.3: Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI. (Not Graded) Individualize frequency and duration of monitoring based on patient risk and clinical course. (Not Graded)



3.1.1: In the absence of hemorrhagic shock, we suggest using isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume in patients at risk for AKI or with AKI. (2B) 3.1.2:We recommend the use of vasopressors in conjunction with fluids in patients with vasomotor shock with, or at risk for, AKI. (1C) Research recommendations There is a need to examine physiologic electrolyte solutions vs. saline in the prevention of AKI. Compare different types of vasopressors and different BP goals for prevention and treatment of AKI in hemodynamically unstable patients.



3.4.1:We recommend not using diuretics to prevent AKI. (1B) 3.4.2:We suggest not using diuretics to treat AKI, except in the management of volume overload. (2C) 3.5.1:We recommend not using low-dose dopamine to prevent or treat AKI. (1A) Research recommendation Given the potential to mitigate fluid overload but also to worsen renal function and possibly cause kidney injury, further study is required to clarify the safety of loop diuretics in the management of patients with AKI.

3.8.1:We suggest not using aminoglycosides for the treatment of infections unless no suitable, less nephrotoxic, therapeutic alternatives are available. (2A) 3.8.2:We suggest that, in patients with normal kidney function in steady state, aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens. (2B) 3.8.3:We recommend monitoring aminoglycoside drug levels when treatment with multiple daily dosing is used for more than 24 hours. (1A)

3.8.4:We suggest monitoring aminoglycoside drug levels when treatment with single-daily dosing is used for more than 48 hours.(2C) 3.8.5:We suggest using topical or local applications of aminoglycosides (e.g., respiratory aerosols, instilled antibiotic beads), rather than i.v. application, when feasible and suitable. (2B) 3.8.6:We suggest using lipid formulations of amphotericin B rather than conventional formulations of amphotericin B. (2A) 3.8.7: In the treatment of systemic mycoses or parasitic infections, we recommend using azole antifungal agents and/or the echinocandins rather than conventional amphotericin B, if equal therapeutic efficacy can be assumed. (1A)

4.1: Define and stage AKI after administration of intravascular contrast media (Not Graded) 4.1.1: In individuals who develop changes in kidney function after administration of intravascular contrast media, evaluate for CI-AKI as well as for other possible causes of AKI. (Not Graded) 4.2.1: Assess the risk for CI-AKI and, in particular, screen for pre- existing impairment of kidney function in all patients who are considered for a procedure that requires intravascular (i.v.or i.a.) administration of iodinated contrast medium. (Not Graded)

4.2.2: Consider alternative imaging methods in patients at increased risk for CI-AKI. (Not Graded) 4.3.1: Use the lowest possible dose of contrast medium in patients at risk for CI-AKI. (Not Graded) 4.3.2:We recommend using either iso-osmolar or low-osmolar iodinated contrast media, rather than high-osmolar iodinated contrast media in patients at increased risk of CI-AKI. (1B)

World J Nephrol 2017 May 6; 6(3): 86-99

4.4.1:We recommend i.v.volume expansion with either isotonic sodium chloride or sodium bicarbonate solutions, rather than no i.v.volume expansion, in patients at increased risk for CI-AKI. (1A) 4.4.2:We recommend not using oral fluids alone in patients at increased risk of CI-AKI. (1C) 4.4.3:We suggest using oral NAC, together with i.v.isotonic crystalloids, in patients at increased risk of CI-AKI. (2D) 4.4.4:We suggest not using theophylline to prevent CI-AKI. (2C) 4.4.5:We recommend not using fenoldopam to prevent CI-AKI. (1B) 4.5.1:We suggest not using prophylactic intermittent hemodialysis (IHD) or hemofiltration (HF) for contrast-media removal in patients at increased risk for CI-AKI. (2C)

5.1.1: Initiate RRT emergently when life-threatening changes in fluid, electrolyte, and acid-base balance exist. (Not Graded) 5.1.2: Consider the broader clinical context, the presence of conditions that can be modified with RRT, and trends of laboratory tests—rather than single urea and creatinine thresholds alone— when making the decision to start RRT. (Not Graded). 5.2.1: Discontinue RRT when it is no longer required, either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs, or because RRT is no longer consistent with the goals of care. (Not Graded). 5.2.2:We suggest not using diuretics to enhance kidney function recovery, or to reduce the duration or frequency of RRT. (2B)