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ACUTE KIDNEY INJURY Nadine Soliman Year 3 Teaching 3rdyearclinicalteaching@gmail.comWhat we’re covering today: AKI • Pre-renal • Renal HistoryT aking Examination • Post-renal Sepsis • Definition Progress Style • Management Questions OSCETipsAKIAKI- Definition • An acute drop in kidney function.It is diagnosed by measuring the serum creatinine. • Multiple different causes • Affects the function of the kidney- specifically the ability to control fluid and maintain electrolyte and acid-bases balance. • What two values do we use to stage an AKI? • Serum Creatinine • Urine Output • NICE Guidelines to define AKI • Rise in creatinine of ≥ 25 micromol/L in 48 hours • Rise in creatinine of ≥ 50% in 7 days • Urine output of < 0.5ml/kg/hour for > 6 hoursKidney Function • Creatinine -> breakdown product of creatine • Creatine kinase-> enzyme which breaks down creatine to produce energy • Why do we use creatinine to estimate kidney function (eGFR)? • It is not reabsorbed and very negligible amount secreted by the kidney tubules • What is the limitation of creatinine? • Creatinine is a product of muscular metabolism -> amount of creatinine will vary among individuals based on their muscle mass • eGFR is calculated using serum creatinine,age,ethnicity and gender in a formula -> more accurate • Remember that a small rise in serum creatinine can cause a massive drop of glomerular filtration rate function.AKI StagingRisk Factors for AKI Consider the possibility of an acute kidney injury in patients that are suffering with an acute illness such as infection or having a surgical operation. Risk factors that would predispose them to developing acute kidney injury include: • Chronic kidney disease • Heart failure • Diabetes • Liver disease • Older age (above 65 years) • Cognitive impairment • Nephrotoxic medications such as NSAIDS and ACE inhibitors • Use of a contrast medium during CT scansCauses ofAKI • How do we split the causes of AKI? • Pre-Renal • Reduced blood flow to the kidney,leading to ischemia and damage • Renal • Anything targeting the kidneys • Post-Renal • Obstruction which stops the patient from passing urine leading to backup and damagePrerenal AKI •Most common cause ofAKI- approx.70% •Reduced blood flow to the kidneys -> reduced filtration by the glomerulus and also ischaemia causing damage to the kidneys 1. Reduced volume eg dehydration,sepsis Can you name a few causes of prerenal AKI? 2. Reduced Cardiac Output eg HF 3. Widespread vasodilation eg sepsis or hypovolemic •Presents with Raised Urea,Creatinine, shock Potassium 4. Renal vascular pathology eg renal artery stenosis •Sometimes if there is ischaemia & renal damage as a result or if the patient is on certain meds,this can result in acute tubular necrosis (ATN) -> intrinsicAKI What is a typical finding in the urine sample? Muddy brown casts- these are the dead cells •Urine output stages in ATN:early- oliguria,intermediate- not oliguric,stable creatinine,recovery- polyuria (beware can lead to hypovolaemia)Renal AKI •In renal AKI,the pathology depends on which structure is affected: What are the four different structures that can be affected? • Glomerulus- glomerulonephritides ie nephrotic and nephritic syndromes • Tubule Acute tubular necrosis • Interstitium –Acute interstitial nephritis- • mostly drug induced eg NSAIDs,diuretics,penicillin.AKI plus eosinophilia • Blood supply to the kidney tissue itself eg HUS,TTPPost renal AKI •Any obstruction from the renal pelvis to the urethra •Raised pressure due to backflow of urine -> Raised pressure in the Bowman’s capsule -> Reduced filtration at the glomerulus Can you name a few causes of post renal AKI? • Kidney stones • Stricture • Cancer • BPH • Urinary catheter that’s blocked • Medications such as anti cholinergics What would be your first line investigation? Renal USSInvestigations Urinalysis for protein,blood,leucocytes,nitrites and glucose. • Leucocytes and nitrites suggest infection • Protein and blood suggest acute nephritis (but can be positive in infection) • Glucose suggests diabetes Ultrasound of the urinary tract is used to look for obstruction.It is not necessary if an alternative cause is found for the AKI. ECG- HYPERKALEMIA Biopsy for some types of renal glomerulonephritisAKIT reatment Treat Complications Treat Underlying Cause • HYPERKALEMIA • PRE RENAL • Protect Myocardium • Fluid Resuscitation • Remove Potassium • RENAL • PULMONARY OEDEMA • Diuretics • Immunosuppression • ACIDOSIS • POST RENAL • Bicarbonate • Nephrostomy tube • Dialysis • Catheter AKI can occur in at risk patients (CKD, renal transplant,,hopovolaemic,elderly) with contrast use. Risk ofAKI can be reduced by giving saline before and after the contrast Management • Diuretics •Mnemonic SALFORD: • ACEi/ARBs/ ØSepsis 6 • Aminoglycosides • Metformin ØACE inhibitors -> think of the DAAMN drugs -> What does this stand for? • NSAIDs Hyperkalaemia ØLab tests-> creatinine and U&Es -> What are you particularly worried about with those? ØFluid status –are they responding? ØObstruction- renal USS ØRenal referral- transplant,Stage 3 AKI,anuria,CKD 4 and 5 What is the treatment? ØDip urine – before catheter • Calcium glucuronate- stabilises the cardiac membranes • Insulin/dextrose infusion and Salbutamol- reduce potassium Hyperkalaemia Fluid overload,heart failure and pulmonary oedema Complications Metabolic acidosis Uraemia (high urea) can lead to encephalopathy or pericarditisSEPSIS Shock Shock essentially means hypoperfusion ➔ Cardiogenic shock (due to heart problems) ➔ Hypovolemic shock (caused by too little blood volume) ➔ Anaphylactic shock (caused by allergic reaction) ➔ Septic shock (due to infections) ➔ Neurogenic shock (caused by damage to the nervous system)How do you know the patient is septic? Other signs on examination: • Signs of potential sources such as cellulitis,discharge from a The National EarlyW arning Score (NEWS) is wound,cough or dysuria used in the UK to pick up the signs of sepsis. • Non-blanching rash can indicate meningococcal septicaemia This involves checking physical observations • Reduced urine output and their consciousness level: • Mottled skin • Cyanosis • Temperature • Arrhythmias such as new onsetatrial fibrillation • Heart rate There are a few key points worth being aware of: • High respiratory rate (tachypnoea) is often the first sign of sepsis • Respiratory rate (>22) • Elderly patients often present with confusion or drowsiness or • Oxygen saturations simply“off legs” • Blood pressure (SBP <100) • Neutropenic or immunosuppressed patients may have normal observations and temperature despite being life threatening • Consciousness level unwell •Septic shock->hypotension that is refractory to fluids and vasopressors being needed to maintain a MeanArterial Pressure of 65 and above plus the patient has a lactate of 2 or moreSepsis Pathophysiology: Infection leads to inflammation (activation of inflammatory cells) -> affects the endothelium lining of blood vessels-> vasodilation and leaky capillaries Signs and Symptoms: •S&S of the infection Less blood in the intravascular compartment-> tissue ischaemia •Fever Dysregulation of the coagulation cascade -> •Capillary refill>2s prothrombotic state.DIC is often associated with sepsis •Tachycardia and hypotension •Confusion Blood lactate rises due to hypoperfusion of tissues •Purpuric rash (non-blanching) that starves the tissues of oxygen causing them to switch toanaerobic respiration.A waste product of anaerobic respiration is lactate.Sepsis- Risk StratificationInvestigations Arrange blood tests for patients with suspected sepsis: • Full blood count to assess cell count including white cells and neutrophils • U&Es to assess kidney function and for acute kidney Other investigation: injury •Bedside- Urinalysis,Sputum,Swabs,LP?, • LFTs to assess liver function and for possible source of lines? infection •Bloods- Serial blood gases,FBC,U&Es,LFTs, • CRP to assess inflammation CRP ,Coagulation screen • Clotting to assess for disseminated intravascular •Imaging- CXR,CT,USS,Echo (depending coagulopathy (DIC) on what the suspected source of infection is) • Blood cultures to assess for bacteraemia • Blood gas to assess lactate,pH and glucose • Remember to always take blood cultures before Sepsis Management: giving antibiotics • hourntibiotics should be given within the golden SEPSIS 6 T ake 3 Give 3 1.Blood cultures 1. Oxygen 2.Urine Output 2. IV Fluids 3. IVAntibiotics (Broad 3.Lactate Spectrum)PROGRESS STYLE QUESTIONS Q1 Na- 135-145 K- 3.5-5.0 Urea- 2.5-7.0 Creatinine- 60-120Q2 Q3 Urea- 2.5-7.0 Creatinine- 60-120Q4Q5Q6 What is your next step in management?Q7Q8Q9OSCETIPSHistoryT aking As we now all know,AKI is usually secondary to a cause. PMH: In your history,you want to find out the cause(s) of the•Heart failure,CKD,diabetes AKI. •Previous AKI Risk factors: •Immunosuppressed- HIV? •Features of sepsis (fever,confusion,very unwell) •Long term line or indwelling catheter •Systems review- infection,MI,bleed,recent surgery,fall •BPH/Prostate cancer •Vomiting and diarrhoea? Meds: •Any abdominal pain with inability to pass urine? LUTS? •Any nephrotoxic drug? New meds? Herbal meds? Over (obstruction) the counter? Exposure to contrast recently? •Frothy or blood in urine? •Are they usually well hydrated? •Joint pain/swelling and rash Examination Again there is no specific examination in the handbook for AKI because of the various causes. Depending on what the station asks you or what your suspicions are,you will perform the appropriate examinations accordingly •Hydration status-> signs of dehydration or overload (prerenal AKI) •Abdominal examination-> Checking for a palpable bladder,balloting kidneys and listening for renal bruits (renal artery stenosis)Investigations Bedside- •Obs Urea:Creatinine ratio • Pre renal- >100 •Urine dip and MC&S (esp microscopy looking for casts),urinary sodium • Renal- < 40 • Post rena- 40-100 •Catheter for urine output Bloods- •FBC,CRP ,U&Es,serum creatinine,cultures,specific antibodies and complements,urea:creatinine ratio Imaging- •Renal US Special test- •Renal biopsy AKI can occur in at risk patients (CKD, renal transplant,,hopovolaemic,elderly) with contrast use. Risk ofAKI can be reduced by giving saline before and after the contrast Management • Diuretics •Mnemonic SALFORD: • ACEi/ARBs/ ØSepsis 6 • Aminoglycosides • Metformin ØACE inhibitors -> think of the DAAMN drugs -> What does this stand for? • NSAIDs Hyperkalaemia ØLab tests-> creatinine and U&Es -> What are you particularly worried about with those? ØFluid status –are they responding? ØObstruction- renal USS ØRenal referral- transplant,Stage 3 AKI,anuria,CKD 4 and 5 What is the treatment? ØDip urine – before catheter • Calcium glucuronate- stabilises the cardiac membranes • Insulin/dextrose infusion and Salbutamol- reduce potassiumResources https://zerotofinals.com/medicine/infectiousdisease/sepsis/ https://zerotofinals.com/medicine/renal/aki/THANKYOU FOR LISTENING! ANY QUESTIONS? 3rdyearclinicalteaching@gmail.com