Download Free Medical Acute Kidney Injury Generic Programme PowerPoint Presentation

Acute Kidney Injury Generic Programme PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Acute Kidney Injury Generic programme" by Dr Begho Obale.

This medical PowerPoint presentation talks about acute kidney injury (AKI) generic program which typically involves a set of guidelines and protocols that healthcare providers can follow when managing patients with AKI. The program aims to optimize patient care and outcomes, reduce complications, and improve overall patient satisfaction.

Tags : Acute Kidney Injury, Acute Kidney Injury generic program, critical care medicine, critical care medicine PowerPoint presentation

Published on : Mar 28, 2023 | Views : 1000 | Downloads : 2

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Acute Kidney Injury Generic programme Dr Begho Obale Associate Specialist Acute medicine
Slide 2-

1) Basic Functioning of the kidney
Slide 3-

Our Kidneys
Slide 4-

Basic anatomy and physiology Anatomy- 2 kidneys, measure 10-14cm in length, 5-6cm in width and 3-4cm in depth Found at the back of the abdomen(retroperitoneal)on either side of the of the vertebral column at level T12-L3 1300ml of blood which is 25% of the blood volume flows through the kidneys each minute The kidneys are made up of over a million nephrons each that carry out the functions of the kidneys of filtration, getting rid of wastes, toxins, excess water and acids etc. The kidney absorbs about 99.9% of all the glucose passing through it. Blood and protein molecules are large and hence not excreted in the urine except if there is inflammation or damage to the kidneys
Slide 5-

Cross section of Kidney(left) and nephron(middle and right)
Slide 6-

Function of the kidney Filter- excretion of creatinine, urea, drugs, toxins, salts, excess fluids etc. Control blood pressure – Renin angiotensin aldosterone system pH regulation-acidity control Fluid balance- stable blood volume, urine production, Endocrine gland-Vit D Produces Erythropoietin- Promotes red cell production
Slide 7-

2. What is Acute Kidney Injury( AKI)
Slide 8-

What is Acute Kidney Injury? Rapid/sudden deterioration in kidney function over a few hours to days in an unwell patient Resulting in a failure to excrete wastes, salts toxins, acids, excess fluids Commonest causes of AKI : Hypovolaemia (Includes dehydration) and Sepsis
Slide 9-

Hypovolaemia-is Reduced blood volume Common Causes: Dehydration- not eating/drinking , excess loss e.g. vomiting, diarrhoea( D/V), diuretics (water tablets) Sepsis, severe infection Bleeding- haematemesis, maleana, etc Hypotension- low blood pressure< 100mmhg Reduced cardiac output; Heart failure, Myocardial infarction (MI)(heart attack), Cardiac arrhythmia Drugs such as Ibuprofen, Ramipril, Losartan,(NSAID, ACE-I, ARB2) affect blood vessels in the glomerulus reducing blood supply in the nephron (kidney)
Slide 10-

Acute Kidney Injury is defined as: Increase in Serum Creatinine of 26mmol/l within 48hours Or An increase in Serum Creatinine of >/=1.5x above base line value within 1 week, Or Urine Output of <0.5ml/kg/h for over 6hours (oliguria)
Slide 11-

Acute Kidney Injury (AKI) The earliest sign of eminent AKI is reduced urine output, (identified within 2 hours) AKI is easily reversible if identified early Older patients can have a delay of up to 48hours to show a significant deterioration in blood test results e.g increased creatinine
Slide 12-

AKI the Facts 1:5 of all acute or emergency admissions 500,000 patients a year in UK suffer from AKI 1042 pts diagnosed with AKI 07/2015- MBHT All patients groups affected, especially elderly AKI 100x more dangerous than MRSA AKI cost the NHS over £1billion/year, Post discharge cost of £179 million/year
Slide 13-

AKI THE FACTS AKI inpatient mortality of 25-30% 100,000 AKI related inpatients deaths /year About 30% of these deaths could be prevented Early recognition, identification of risks and early treatment, could save 12,000- 40,000 lives/y and over £150m/y Patients may not recover fully- develop chronic Kidney disease (CKD), needing dialysis 40% of AKI starts newly in hospitalised patient Prolong hospital stay up to x2 longer(10 vs 4days
Slide 14-

ppt slide no 14 content not found
Slide 15-

Acute kidney injury stages
Slide 16-

AKI stages related to mortality Stage 1: <10% mortality– commonest stage(50% or more) urine output<0.5ml/kg/h over 6hours Stage 2: 20-30% mortality, urine <0.5ml/kg/h over 12h Stage 3: 30-50% mortality Urine<0.3ml/kg/h x24h or no urine x12h
Slide 17-

3. Identify Patients at risk of AKI
Slide 18-

Identifying patients with risks for AKI Elderly patients over 65years of age Chronic kidney disease CKD( [eGFR<60] Liver Disease, Diabetes, Past History of AKI Recent use of Nephrotoxins: NSAID-e.g ibuprofen, ACE-I e.g ramipril, ARB e.g losartan. Spironolactone, Metformin, Iodinated contrast Aminoglycosides, eg gentamicin Cardiovascular disease e.g Heart attack (MI), stroke, peripheral vascular disease, heart failure
Slide 19-

Patients at risk of AKI due to illness Oliguria urine output less than 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
Slide 20-

ppt slide no 20 content not found
Slide 21-

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 hypovoleamia, 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%
Slide 22-

Nephrotoxic drugs- recent use – account for 10%-20% of all AKI NSAID-e.g ibuprofen, voltarol ACE-I e.g ramipril, ARB e.g losartan. Spironolactone, Metformin, Iodinated contrast Aminoglycosides, eg gentamycin Some herbal remedies Causes renal damage especially if some associated causes of hypovolaemia or new increased drug dose Damage to the kidney by hypovolaemia or toxicity to kidney Advisable to stop drug as likely to make AKI worse
Slide 23-

4. Presentation of AKI( symptoms and signs)
Slide 24-

AKI Presentation- Symptoms Most patients have No Complaints/ nonspecific symptoms Reduction in the amount of urine passed Concentrated urine, deep yellow, brown etc Dehydration or thirst Nausea, vomiting Abdominal pains and feeling generally unwell. Confusion and drowsiness
Slide 25-

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
Slide 26-

AKI signs- Features of hypovolaemia; Dry Mucous membranes Loss of skin turgor (elasticity) Tachycardia HR>90b/min, BP<100mmhg, postural drop of 20mmhg with increase in RR Respiratory rate(RR) >20/min Prolonged capillary refill time(CRT) >2s Cold sweaty peripheries Urine output < 0.5ml/kg/h
Slide 27-

Effects of hypovolaemia Reduced cardiac output- tachycardia, ↓BP Vasoconstriction- results in cool clammy skin, pallor and poor Capillary refill time (CRT)>2s ↓kidney perfusion- oliguria,↑;acidosis, K, Cr Tissue hypoxia- ↑ Lactic acid production, metabolic acidosis, raised respiratory rate( RR) Reduced cerebral perfusion-confusion restless or unresponsiveness
Slide 28-

5.Assessing Urine Output
Slide 29-

HCSW/Nurses role in Assessing Urine output Find out when patient last made urine Calculate how many hours ago Weigh patient, (daily weights) Collect urine Calculate ml/kg/hr (Person weighing 60kg should make 60x0.5ml= 30ml/hour of urine) Urine output less than (<) 0.5ml/kg/hr indicate oliguria and high risk of AKI or established AKI
Slide 30-

Case 1 Mr J, 70yr old man, presented with D/V of 3 days duration, urine dark in colour, last made urine at 6am, 6hours ago, Pt weighs 80kg Produced 150ml of urine on admission What is his expected urine output? Is this output adequate? What will you do about this situation?
Slide 31-

Case 1 answer Weight 80kg Urine output/hr = 40ml ( 80x0.5=50% of weight) Urine output in 6h will be 40x6 = 240ml 150ml of urine is inadequate, <0.5ml/kg/h Inform Doctor as patient may need IV fluid Open fluid input/output chart Offer patient water if able to tolerate it
Slide 32-

Low urine output Can indicate Dehydration or hypovolaemia A drop in systolic BP of >40mmhg will reduce blood supply and oxygen to the kidney and reduce urine production, if prolonged>6h damage to kidney Damage to the kidney e.g nephrotoxic drugs Urinary obstruction- consider bladder scan Assess EWS, if >3 discuss with doctor, increase monitoring of vital signs Fluid balance chart- hydration, aim for urine output of >0.5ml/kg/h
Slide 33-

Fluid output Urine output- cardboard bottles /liners Urinary Catheter hourly volumes Fluid loss from diarrhoea, vomiting Ileostomy and colostomy output Loss from wound drains, weeping wounds etc Weigh wet beddings/pads 1000g extra= 1000ml Insensible loss from breathing and sweating 400-1000ml ( Add 500ml on current fluid balance)
Slide 34-

Patients needing input/output charts Raised EWS Receiving IV fluid treatment Patients treated for Sepsis or hypovolaemia Pre/Post surgical and post contrast procedures Patients with swallowing difficulties e.g NBM Increased fluid loss ie: stoma, vomiting, diarrhoea, drains Patients at ↑risk of AKI or with diagnosed AKI
Slide 35-

ppt slide no 35 content not found
Slide 36-

Fluid input Oral intake of fluids- measure of fluid taken in and not just amount offered Intravenous fluids administered Intravenous fluid volume in i.v Medication Nasogastric feeds volume Daily fluid requirement 25-30ml/kg/24h works at 1.5-2.5l/ day (maintenance fluid) 70kg person needs about 2100ml/day( 70x30ml) (use 25ml/kg for elderly 70kg patient = 1,750ml) Patients will need more if excess loss e.g D/V etc.
Slide 37-

Normal Fluid Balance…
Slide 38-

6. Urinalysis and other Investigations for AKI
Slide 39-

Urinalysis Blood and protein in the urine without nitrites indicates kidney inflammation or damage Absence of nitrites make urinary infection unlikely Send sample for microscopy culture and sensitivity If >/= 2+ protein, send sample for protein creatinine ratio Record all urinalysis report in patients notes Inform nurse or doctor of abnormal urine result
Slide 40-

Investigations for AKI Renal Function- U&E Venous gases, Bicarbonate (HCO3), Full blood count(FBC) Infection screen-CRP, ESR, Lactate, cultures- blood, urine Bone profile Liver function test (LFT), INR, Glucose Creatinine Kinase (CK)- if falls- Rhabdomyolysis
Slide 41-

Investigations 2 ECG- MI, changes for hyperkalaemia CXR- to check infection or pulmonary oedema USS within 6h if acute obstruction and sepsis -Pyonephrosis. USS within 12-24h if obstruction/ cause of AKI unknown or non resolving AKI 3
Slide 42-

7. Management
Slide 43-

Case 2 Jack 75y old man presented to A/E with fever and coughing green sputum for 4days , not eating or drinking He feels tired, lethargic and lightheaded, reduced urine output, dark urine PMH; Hypertension, Diabetes, arthritis, Drug Hx; Been taking Ramipril 10mg, Metformin 1g bd, Simvastatin 40mg od ,Amlodipine 10mg, Aspirin, OTC-over the counter Ibuprofen and paracetamol
Slide 44-

Case 2 cont o/e dehydrated, dry mucus membranes, loss of skin turgor , BP 100/55mmhg, 80/45 standing. Pulse 108/min, CRT 3s, Bladder not distended, T 38⁰ C, Resp- RR 22/min, Rt lung creps, Oxy sat 96% air, weight 70kg, 300ml urine in 12hr Investigations; Creatinine 400mmol/l(baseline 80mmol/l 7weeks ago) Urea 20mmol/l, K 4.9mmol/l, FBC normal, Urinalysis protein + blood +, no nitrite What are risk factors in this patient for AKI? What is the Minimum acceptable urine output/h, ?EWS , AKI stage? what will you do?
Slide 45-

Answers to Case 2- risks and stage Patients age Dehydration /hypovolaemia, hypotension Chest infection/ sepsis, Diabetes, Blood and protein in urine Nephrotoxic drugs-ramipril, metformin, ibuprofen Reduced urine output 300ml, <0.5ml/kg/h B) Expected minimum urine output is 420ml in 12 hours C) EWS>3, D) AKI Stage 3 due to sepsis Management- awareness patient is critically ill and at risk of complications of AKI
Slide 46-

Answer to Case 2 -management Intravenous cannula and take bloods for-Blood culture, bicarbonate and lactate , glucose Request a CXR I.V bolus of balanced crystalloid 500ml and reassess EWS, checking for improvement of EWS and hypovolaemia Request input from Dr in charge, use SBAR as patient likely to need i.v antibiotics and more i.v fluid boluses Stop nephrotoxic drugs- Ramipril, metformin and ibuprofen Withhold amlodipine as hypotensive
Slide 47-

Answer to Case 2 -management Record urinalysis results in notes, request culture, inform doctor or nurse (Send urine for legionella + pneumococcal antigen,- severe pneumonia) Consider catheterization as patient very unwell & AKI 3 Hourly monitoring of vital signs EWS >6 1-2 hourly monitoring of urine output as AKI 3 Repeat E&U and bicarbonate in 6hours
Slide 48-

9- Complications of AKI
Slide 49-

Complications of AKI Metabolic acidosis Fluid overload, pulmonary oedema Hyperkalaemia Uraemic pericarditis Uraemic encephalitis Dialysis or haemofiltration if these do not respond to standard treatment
Slide 50-

Consequences of persistent oliguria 1 Complications of AKI Deterioration in renal function- damage to kidney Deterioration in AKI stage progressing from 1 to 2 to 3 Increased risk of death Complications of AKI commoner in AKI 2/3 Accumulation of toxins e.g creatinine and urea Increase creatinine will cause increased stage of AKI, irritability, drowsy, confused Ureamia- vomiting. Also causes irritation of heart muscle-pericarditis which gives chest pain, worse on lying flat. Irritation to brain-encephalopathy causing confusion, disorientation, fits or coma
Slide 51-

Consequences of persistent oliguria 2 Complications of AKI Inability to excrete excess salts such as potassium with accumulation- Hyperkalaemia leads to abnormal heart rhythm and can cause a cardiac arrest Inability to excrete excess fluids- leads to fluid overload- increased weight, and fluid in the lungs- Pulmonary oedema, causing increased shortness of breath, cough with frothy phlegm, inability to lie flat Inability to excrete excess acid causes metabolic acidosis- increased respiratory rate, vomiting, confusion, hypotension, abnormal heart rhythm
Slide 52-

10. Role of Clinical support workers and Nurses in Management of AKI
Slide 53-

HCSW play a vital role in management of AKI Identifying patients at risk of AKI Analysing urinalysis in managing AKI Assessing urine output and identifying patients with or at risk of AKI if urine output < 0.5ml/kg/h Fluid balance- input/output interpretation Informing nurse or doctor of abnormal urinalysis or urine output <0.5ml/kg/h results Patient hydration Preventing inpatient AKI Reducing hospital stay and patient mortality
Slide 54-

Nurses role in improving AKI care Covers all the roles of the HCSW and also; Early recognition of acutely unwell patients, EWS monitoring and taking appropriate action Understanding stage of AKI on e-alert and responding appropriately with monitoring, management and doctor input Taking action if urine output <0.5ml/kg/h and discussion with doctors Withholding nephrotoxic medications and discussing with medical team
Slide 55-

HCSW/Nurses role in patient education Patient education on importance of hydration and monitoring of urine output as an important aspect of their care. Patient information-consider ideas when discussing with patient; - Acute illness such as sepsis, dehydration, or low blood pressure can prevent the kidneys from working effectively to rid the body of wastes and toxins(AKI )this can happen within hours or days AKI can be identified by reduced urine output within hours
Slide 56-

HCSW/Nurses role in patient education 2 AKI slows the response to treatment and a longer hospitalisation AKI is easily reversible by treating cause, ensuring good hydration evidenced by adequate urine output >0.5ml/kg/h e.g 30ml/h in 60kg person Good hydration and good urine output helps protect the kidneys, reverses AKI, better response to treatment, reduces duration of hospitalisation and better patient outcome
Slide 57-

HCSW/Nurses role in patient education 2 (Awareness encourages patient to cooperate/ help collect urine samples) (Patient awareness encourages effort to drink more fluid) Inform patient of cause of AKI and management plan, how to prevent this in future Drugs to withhold if dehydrated or sepsis- e.g ramipril, ibuprofen, metformin, furosemide etc. Advice about making effort to increase fluid intake if unwell and seeking help early if reduced urine production, dark urine, +/-dizzy on standing
Slide 58-

11. Summary AKI is a common problem affecting 5-15% of all hospitalised patients AKI associated with 100,000 inpatient deaths AKI is easily reversible/preventable if identified early by assessing for risk factors, treating cause and monitoring frequently, especially urine output and vital signs HCSW and nurses play a very important role in identifying, prevention and management of AKI
Slide 59-

Management of AKI- summary 1 Identify Identify risk factors for AKI Identify possible cause of AKI e.g dehydration, infection, medication, obstruction Stage of AKI on e-alert ( or urine output) Further investigations- bicarbonate, sepsis screen, USS as appropriate Monitoring Urinalysis- record result in notes, and appropriate action if abnormal Urine output; Weigh patient, minimum urine output/h= 0.5ml x weight. Assess urine output on admission and at least 4 hourly( 1-2hourly if AKI 2/3 or EWS>3, or inadequate urine output).
Slide 60-

Encourage hydration increased oral fluids or intravenous fluids Monitor fluid balance at least 4hourly or more often as above Monitor EWS at least 4hourly or 1-2hourly if AKI 2/3, poor urine output Request help if persistent low urine output or high EWS>3 for over 4hours Treatments Rehydration- oral or i.v fluids- balanced crystalloids e.g. Hartman's or 0.9% saline boluses to treat hypovolaemia till corrected signs and improved EWS. Maximum of 2l in 2-4 hours with doctor input. Otherwise maintenance fluids and extra to cover for excess loss
Slide 61-

Management of AKI Summary 2 Stop nephrotoxic drugs Reduce dose of some drugs e.g. enoxaparin Augmentin, long acting opiates etc. Treat precipitating cause e.g sepsis, hypovolaemia, obstruction Blood transfusion if hypovolaemia due to bleed Relief urinary obstruction with catheter Repeat E&U at 6-12hr initially, then at least daily Identify complications early and appropriate escalation Patient/carers advice and information
Slide 62-

Acknowledgement http://elearning.nice.org.uk/ National Institute for Health and Care Excellence (NICE) Acute Kidney injury An e-learning module for non- renal registered nurses and Health Care Support workers in all settings March 2014 NICE CG 169. National Institute for Health and Care Excellence. Clinical guideline 169: Acute kidney injury: prevention, detection and management of acute kidney injury up to the point of renal replacement therapy. 2013. NCEPOD 2009. Stewart J et al (editors). Adding insult to injury: a review of the care of patients who died in hospital with a primary diagnosis of acute kidney injury (acute renal failure). The National Confidential Enquiry into Patient Outcome and Death. 2009 www.thinkkidneys.nhs
Slide 63-

Quiz Q1- What is Acute Kidney Injury? A) A sudden or rapid deterioration in renal function over hours or days B) A rise in Creatinine of >26mmol/l within 48hours C) Urine output <0.5ml/kg/h for over 6 hours D) All of the above- definition of AKI
Slide 64-

Q 2 How many stages of AKI are there? A) 5 B) 3 C) 2
Slide 65-

Q3 How many people die from AKI in hospitals in the UK/ year A) 10,000 people B) A million people C) 100,000 people
Slide 66-

Q 4 Which of these are common causes of AKI A) Sepsis B) Dehydration C) Myeloma- very rare cause D) Hypovolaemia E) Rhabdomyolysis- rare cause
Slide 67-

Q5 Which of these drugs can damage the kidney(nephrotoxic) A) Ramipril B) Aspirin- safe C) Gentamicin D) Ibuprofen E) Gaviscon- safe
Slide 68-

Q6 Which of these measures are important in the management of AKI? A) Important to stop nephrotoxic drugs B) Record urinalysis results only if positive for blood and protein C) Monitor urine output and EWS more frequently such as 1-2 hourly in AKI 3 D) Treat cause of AKI E) New onset confusion, vomiting and shortness of breath in a patient with AKI 3 may indicate complication such as metabolic acidosis
Slide 69-

Q7 Which of these are complications of AKI? A) Hyperkalaemia- True B) Pulmonary oedema due to fluid overload- true C) Uraemic Encephalitis- True D) Death- True E) Diabetes- False
Slide 70-

Q 8 Which of these patients have got increased risk factors for AKI? A) Known history of Chronic Kidney disease B) Use of nephrotoxic drugs in past 7 days C) 56years old man attending eye clinic for cataract check( >65years) D) Patient admitted for emergency abdominal surgery E) Acutely ill patient with EWS of 6