Acute Kidney Injury James Finnerty

Gross Anatomy Paired, retroperitoneal structures Upper Poles located between Tranverse Processes T____, lower poles descend to L____ Left typically higher Receives ___% of cardiac output Via Renal Artery, drains via Renal Vein

Microanatomy – The Nephron

Functions

Definition Clinically AKI is characterised by a rapid reduction in kidney function resulting in a failure to maintain fluid, electrolyte and acid-base homoeostasis One of: Serum creatinine rises by ≥ ___µmol/L within 48 hours  Serum creatinine rises ≥ ____ fold from the reference value, which is known presumed to have occurred within one week urine output is < ___ml/kg/hr for >6 consecutive hours (Normal urine output range _____/kg per hour) Renal Association Also associated with uraemia Usually Reversible

Epidemiology ___% of all inpatients develop acute renal failure. Risk Factors: Chronic Kidney Disease Heart failure Liver disease Cardiovascular disease (previous MI, stroke, PVD) Diabetes mellitus Recent use of nephrotoxins, e.g. _____________________________________________________________________________________________________________

Pre-Renal Hypotension Shock Hypovolaemia Haemorrhage, Vomiting Diarrhoea, Diuretics, dehydration Renal Glomerulus Glomerularnephritis Tubules Acute Tubular Necrosis Interstitium Nephritis (NSAIDS, gent, ACE) Vessels Vasculitis, coagulapathies Post Renal Obstruction Stone Tumour Prostate http://www.sciencedirect.com/science/article/pii/S1357303907001491 (Full list of Causes)

Signs and Symptoms Oliguria/ Anuria Fatigue Vomiting Pruritis Confusion SOB Peripheral oedema Oliguria/ Anuria http://www.oscestop.com/Hydration_exam.pdf (How to Assess fluid status)

Hx and Ex Volume status by checking: For possible underlying causes: Core temperature. Peripheral perfusion. Heart rate/blood pressure (and any postural changes). Jugular venous pressure. Moistness of mucous membranes, skin turgor. For possible underlying causes: Current symptoms, if the person is unwell (for example diarrhoea, vomiting, breathlessness). Any recent symptoms that may suggest an underlying obstructive cause (for example lower urinary tract symptoms, bloating from a pelvic mass, renal colic). Drug history Social history — including exposure to tropical diseases (e.g. malaria) and exposure to rodents (e.g. leptospirosis, hantavirus).

Investigations ________________ CXR Plasma sodium, potassium, urea, creatinine, glucose Urine dipstick, microscopy, biochemistry, culture (glomerulonephritis, acute pyelonephritis, and interstitial nephritis, tubular necrosis) ________________ “The most worrying findings are decreased or absent P-waves, PR prolongation, QRS widening, sine wave QRST, AV dissociation or asystole. It is often difficult to judge if T-waves are truly peaked and this finding on its own should not be an automatic indication for urgent therapy” CXR If a reference serum creatinine value is not available within 3 months (acceptable up to one year) and AKI is suspected repeat serum creatinine within 24 hours a reference serum creatinine value can be estimated from the nadir serum creatinine value if patient recovers from AKI

Complications Uraemia Fluid overload Hyperkalaemia Acidosis

Differential Diagnoses Abdominal aneurysm Alcohol toxicity Alcoholic ketoacidosis Chronic renal failure Dehydration Diabetic ketoacidosis Gastrointestinal (GI) bleeding Heart failure Obstructive uropathy Protein overloading Renal calculi Sickle cell anemia Steroid use

Management “Resuscitate patient with regards to their airway, breathing and circulation “ Get Senior help Treat Dangerous complications: Hyperkalaemia: _____________ Fluid Overload: _______________ Severe Acidosis: __________________ Severe Uraemia: _____________ Treat Underlying Cause: Give Saline (cautiously) Stop Nephrotoxic Drugs Monitor Urine Output (hourly) (Possibly) catheterise

Dialysis Indications for early dialysis: Hyperkalaemia refractory to treatment Pulmonary Oedema Severe metabolic acidosis refractory to treatment Uraemic encephalopathy Uraemic Pericarditis

Management Prevention: • Identify patients at risk (see AKI risk factors) •Optimise volume status •Treat sepsis promptly • Avoid nephrotoxins • Review medications, e.g. adjust drug doses, withhold antihypertensives if hypotensive • Reduce risk of contrast-induced AKI: • The risk of contrast-induced AKI is small in the general population • Patients at high risk are the acutely ill, with AKI/CKD, sepsis and hypovolaemia

Mortality Mortality is ______% in those patients with isolated renal failure This rises to 50-70% when ARF is precipitated by other organ failure