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Copy of Acute Kidney Injury
Transcript of Copy of Acute Kidney Injury
AMK Qs Definition
Relevant anatomy – kidneys
Causes of AKI according to classification
Relevant pathophysiology – KEY!!!!
AMK Qs Define AKI The old name was Acute Renal Failure.
It is an abrupt and sustained decline in glomerular filtration rate (GFR) which leads to uraemia (accumulation of nitrogenous waste - urea, uric acid, creatinine etc. in the blood)
So what is GFR? Relevant anatomy and
physiology Classification of AKI AKI - CAUSES Pre-renal - due to renal hypoperfusion Blood flow - __% of cardiac output?
What are some of the normal functions of the kidney?
Filtration of nitrogenous wastes, urea
Regulation of fluid balance and maintenance of intravascular volume
Production of EPO
Production of urine PATHOPHYSIOLOGY – PRE-RENAL Q. So, what are these mechanisms to restore perfusion pressure and their effects?
A: The aim is to restore intravascular volume
Activation of Renin-Angiotension-Aldosterone (RAAS) system
Release of Anti-diuretic hormone (ADH)
This increases Na+ and H2O retention ACE-i and ARBs reduce the effects of renin on renal blood flow which can combine with diuretics to cause pre-renal AKI in people with reduced blood flow due to large vessel or small vessel kidney disease.
NSAIDs reduce renal blood flow through inhibition of prostaglandin synthesis. Renal - due to damage to renal parenchyma Pathophysiology of Acute Tubular Necrosis Post-renal - urinary tract obstruction INVESTIGATIONS CLINICAL FEATURES SYMPTOMS Urine output - oliguria or anuria.
Abdomen: may reveal a large, painless bladder typical of chronic urinary retention
Pallor, rash, bruising: may suggest inflammatory or vascular disease, emboli or DIC
Pericardial rub CLINICAL FEATURES SIGNS MANAGEMENT ABC approach.
Get specialist help early.
Identify underlying cause.
Optimise cardiac output and renal blood flow
Review drugs: stop nephrotoxic agents; adjust doses/concentrations where appropriate.
Accurately monitor fluid balance and daily body weight.
Optimise nutritional support: adequate calories, minimal nitrogenous waste production, potassium restriction.
Identify and aggressively treat infection; minimise indwelling lines; remove bladder catheter if anuric.
Identify and treat bleeding tendency: avoid aspirin.
Initiate dialysis before uraemic complications emerge. COMPLICATIONS Hyperkalaemia
Uraemia (urea, creatinine)
Bleeding ECG changes according to severity
Tall tented T-waves
Gets worse >> asystole.
IV Calcium gluconate 10ml of 10% solution, repeat until ECG improves. (cardioprotective)
IV insulin (10 units) + glucose (50ml of 50% solution) – drives K into cells.
Salbutamol 2.5mg nebs (drives K into cells)
Haemodialysis HYPERKALAEMIA Symptoms and signs:
Pink frothy sputum
↑pulse, ↑JVP; wheeze (cardiac asthma)
Sit pt upright
100% O2 (if no PMHx of lung disease)
Morphine 2.5 mg IV + metocloperamide 10mg IV
Furosemide 120-250mg IV over 60 mins
Haemodialysis PULMONARY OEDEMA Impaired hameostasis due to ↑ urea and made worse by underlying cause.
PPI or H2 antagonist
If actively bleeding:
FFP + platelets
Blood transfusion to get Hb>10g/dL.
Desmopressin (to increase ↑fVIII activity, normalise bleeding time) BLEEDING
Refractory pulmonary oedema
Persistent hyperkalaemia (>7mmol/L)
Severe metabolic acidosis (pH<7.2 or BE<10)
Uraemic pericarditis (pericardial rub) INDICATIONS FOR DIALYSIS AMK QUESTIONS A 78 year old woman has a bowel resection procedure for her colon carcinoma. Postoperatively, her urine output is low and blood results at the end of her second day show urea 12.3 mmol/L and creatinine 172 umol/L. What is the most likely cause of renal failure in this scenario?
A. Analgesic nephropathy
B. Renal metastases
D. Post-surgical rhabdomyolysis
E. Urinary retention
F. Don't know Q1 A 26 year old woman is admitted to ED complaining of pain across her back. She became unwell 2 days ago when she started to develop a fever and an ache in her back. The pain has become progressively more severe. She has vomited twice in the last 6 hours. She has a PMHx of cystitis 3 months ago. On examination, she appears unwell and flushed. Her temperature is 39.5C. Her HR is 120bpm, BP 104/68mmHg. Her abdomen is generally tender but most markedly in both loins. Bowel sounds are normal. CVS and RS exams are unremarkable. Her WCC is 25.2x10/L, urea 14.2mmol/L, CRP 316mg/L. Urinalysis is ++ protein, +++blood and +++nitrites. Urine microscopy shows > 50 RBCs and >50 WCCs. AXR is normal. What is the most likely diagnosis in this patient? Why do you get nitrites?
C. Nephrotic syndrome
D. Ruptured ectopic pregnancy
E. Aortic aneurysm dissection
F. Don't know Q2 A 76 year old man presents to his GP with a history of difficulty passing urine with hesitancy, poor stream and occasional pain of 3 months duration. He also has nocturia. No finding on examination. Urinalysis shows + blood, + protein. Serum creatinine is high at 560umol/L. The man is referred to hospital where they notice that he has a palpable bladder and a smooth, enlarged prostate on examination. What is the most likely cause of this man’s symptoms?
A. Renal calculus
B. Nephrotic syndrome
D. Obstructive uropathy secondary to enlarged prostate (BPH)
E. Nephrotic syndrome
F. Don't know Q3 Ans. C. dehydration. She had normal renal function pre-op and it only changed post-op. urinary retention might be likely in elderly males with PMHx of BPH. In these cases, all you need to do is catherisation and replace fluids Ans. B. Pyelonephritis. More common in F>M. Occurs due to ascent of bacteria up to urinary tract.
Pregnancy, DM, immunosuppression and structurally abnormal urinary tracts increase the likelihood of ascending infection. Fever (upto 40C), anorexia, nausea and vomiting are common systemic symptoms. Some pts can have preceding symptoms of lower UTI symptoms ie. Dysuria, urinary frequency, urgency, haematuria) but they do not always occur.
Elderly pts often present with non-specific symptoms and confusion. It can mimic othe rconditions such as appendicitis, acute cholecystitis, pancreatitis. There is marked tenderness over kidneys anteriorly and posteriorly. If untreated >> septic shock.
Blood, protein, nitirties suggest inflammation of urinary tract secondary to bacterial infection. So once, appropriate Ix has been done, start pt on an appropriate antibiotic regime.
If pt has obstructive uropathy, then infection ca lead to pyonephrosis with severe loin pain, fever, septic shock and renal failure. Ans. D. Obstructive uropathy secondary to BPH. USS of abdomen and pelvis shows bilateral hydronephrosis, hydroureter and enlarged prostate. Bilateral small kidneys or cortical thinning would suggest long-standing obstruction (chronic retention). Serum PSA should be done – high PA can suggest possible prostate ca…although, this is notoriously high post PR exam/catheterisation.
Management – immediate bladder catherisation to relieve obstruction. If this is difficult, you need to call urology team and insert suprapubic catheter. Fluid balance must be monitored as pt. is likely THANKS FOR LISTENING!!! Pathophysiology Made Incredibly Easy. 4th Ed. Pp.303-307
Oxford Handbook of Clinical Medicine pp. 298-299
Craig J, Molony D.Evidence Based Nephrology. Pp.71-88, 97-110.
Bain S, Stephens J. Core Clincal Cases: Medicine and Medical Specialities. 2nd Ed.
Bath J, Morgan R, Patel M. EMQs and SBAs for Medical Finals. 2nd Ed.
Pattison J, Rees P, Williams G. 100 Cases in Clinical Medicine.
Malik I, Ramrakha P. “Best of Five” Clinical Scenarios for the MRCP Part 1. Volume 1
Structure and Function of the Nephron RLO. EMILY. E-learning Support Group. Peninsula College of Medicine and Dentistry https://eres-pcmd.plymouth.ac.uk/elsg/eresources_gateway/rlo_menu_template/index.php?id=63 (accessed 19th March 2013) REFERENCES CONCLUDING REMARKS... SUMMARY Causes
Pre-renal: renal hypoperfusion
Renal: renal parenychmal damage – intrinsic damage
Post-renal: urinary tract obstruction
reduced urine output, nausea, vomiting,
Dehydration, distended abdomen of chronic urinary retention
Key investigations: FBC, U+E, Urine dip, USS, Creatinine
ABC approach, optimise renal perfusion, stop nephrotoxins
Get specialist help early.
Watch out for complications, treat infection and find underlying cause. Davidson E, Foulkes A, Longmore M, Mafi A, Wilkinson A. Renal Medicine in Oxford Handbook of Clincal Medicine. 8th Ed. Oxford. Oxford University Press; 2010. p298-299
Goddard J, Stewart L, Turner A. Kidney and urinary tract disease. In: Colledge N, Ralston S (eds.) Davidson’s Principles and Practice of Medicine. 21st ed. Edinburgh. Churchill Livingstone Elsevier; 2010. p482-487
Structure and Function of the Nephron RLO. EMILY. E-learning Support Group. Peninsula College of Medicine and Dentistry https://eres-pcmd.plymouth.ac.uk/elsg/eresources_gateway/rlo_menu_template/index.php?id=63 FURTHER READING For more in-depth information on anatomy at the cellular level and basic physiology, use this link: -
THE END Please use the model(s) of the kidney provided to familiarise yourself with the anatomy during this section. For a quick guide to navigating through this presentation, please click on the
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