ACUTE RENAL FAILURE.pptx for nursing students

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1. ACUTE RENAL FAILURE M. JENEFA SHINY MSC 2ND YEAR

2. Acute kidney injury (AKI), previously known as acute renal failure (acute kidney failure), is a sudden episode of kidney failure or kidney damage that happens within a few hours or a few days, as measured by glomerular filtration rate (GFR) Acute kidney injury (AKI) can be seen in up to 7% of hospital admissions and 30% of ICU admissions. INTRODUCTION

3. Acute kidney injury is defined as an abrupt (within 48 hours) reduction in kidney function based on an elevation in serum creatinine level, a reduction in urine output, the need for renal replacement therapy (dialysis), or a combination of these. DEFINITION

4. According to KDIGO (Kidney Disease: Improving Global Outcomes), AKI is the presence of any of the following  - Increase in serum creatinine by 0.3 mg/ dL or more (26.5 micromoles/L or more) within 48 hours; or Increase in serum creatinine to 1.5 times or more baseline within the prior seven days; or Urine volume less than 0.5 mL /kg/hour for at least 6 hours.

5. In 2004, the Acute Dialysis Quality Initiative group (ADQI) proposes the RIFLE classification of AKI. In 2007 - Acute Kidney Injury Network (AKIN) classification come out, based on the RIFLE system. CLASSIFICATION

6. RIFLE CRITERIA 1] RIFLE criteria define three grades of severity and two outcome classes. The most severe classification met by either criterion should be used 2] It describes acute kidney injury as an abrupt (within 48 hours) reduction in kidney function and separates renal dysfunction into categories in terms of the degree of renal insult 3] The degree of renal dysfunction, according to the RIFLE criteria, is determined by the worst value of either urine output or an assessment of the glomerular filtration rate (GFR)

7. Acute kidney injury classification

8. RIFLE Criteria

9. AKIN criteria Increase in sensitivity of the RIFLE criteria by recommending that a smaller change in serum creatinine (≥26.2 µmol/L) be used as a threshold to define the presence of AKI and identify patients with Stage 1 AKI (analogous to RIFLE-Risk) A time constraint of 48 h for the diagnosis of AKI was proposed. Any patients receiving renal replacement therapy (RRT) were to now be classified as Stage 3 AKI (RIFLE-Failure)

10. AKIN-Classification Category Serum creatinine Urine output Stage-1 Serum creatinine ≥ 150–200% from baseline <0.5 ml/kg/h for > 6 h Stage-2 Serum creatinine ≥ 200–300% from baseline <0.5 ml/kg/h for > 12 h Stage-3 Serum creatinine ≥ 300% from baseline OR serum creatinine ≥ 54 μmol /l with an acute rise of at least 44 μmol /l < 0.3 ml/kg/h for > 24 h or anuria for >12 h

11. CAUSES

12. Causes of Prerenal AKI 1 :-Intravascular volume depletion , 2:-Effective volume depletion from arterial underfilling a. Hemorrhage b. Renal fluid losses. c. Gastrointestinal fluid loss d. Skin loss of sweat e. Third-space losses Burns Traumatized tissue Peritonitis Pancreatitis 1 )Reduced cardiac output, a. Congestive heart failure b. Cardiogenic shock (e.g., acute MI) c. Pericardial effusion with tapenade d. Massive pulmonary embolism 2) Peripheral vasodilation , a. Gram-negative sepsis b. Antihypertensive medications c. Anaphylaxis D .Anesthesia e Cirrhosis & other liver diseases

13. 3:-Intrarenal hemodynamic changes A)Glomerular afferent arteriolar vasoconstriction NSAIDS(Prostaglandin inhibition) COX-2 (Prostaglandin inhibition) Cyclosporine Tacrolimus radiocontrast dye hypercalcemia B) Glomerular efferent arteriolar vasodilation ACE inhibitors ARBs

14. Causes of intrinsic AKI 2 Vascular—large vessels Vascular—small vessel s 3. Glomerular 1 . Tubular 4. Interstitial .

15. ACUTE TUBULAR NECROSIS

16. Acute tubular necrosis (ATN ) a. Renal ischemia(50%) b. Nephrotoxic drugs(35%) 1. Shock 2. Complications of surgery 3. Hemorrhage 4. Trauma 5. Gram-negative bacteremia 6. Pancreatitis 7. Postpartum hemorrhage 1.Antibiotics [e.g., aminoglycosides, vancomycin, amphotericin B, pentamidine, foscarnet, acyclovir] 2. Antineoplastic (e.g., cisplatin) 3. Iodine-containing x-ray contrast 4. Organic solvents ( CCl4) 5. Ethylene glycol (antifreeze) 6. Anesthetics (enflurane ) 1 . Myoglobin due to rhabdomyolysis 2. Hemoglobin (e.g., incompatible blood transfusion, acute falciparum malaria) 3. Uric acid (e.g., acute uric acid nephropathy) c. Endogenous toxins

17. Vascular—large vessels: Renal artery stenosis, thrombosis, or embolism a. Operative arterial cross-clamping b. Bilateral renal vein thrombosis Diseases of glomeruli and renal microvasculature Glomerulonephritis and vasculitis Hemolytic uremic syndrome Thrombotic thrombocytopenic purpura DIC Toxemia of pregnancy

18. a. Antibiotics, beta-lactam antibiotics rifampicin, sulfonamides, erythromycin, and ciprofloxacin B .Diuretics (e.g., furosemide, thiazides, chlorthalidone) c. NSAIDs d. Anticonvulsant drugs (e.g., phenytoin, carbamazepine) e. Allopurinol Acute interstitial nephritis(AIN) 1-Drug hypersensitivity 2-Infection associated-AIN a. Bacterial (i.e. Staphylococcus & Streptococcus) b. Viral (i.e. CMV &EBV) c. Tuberculosis d. fungal (i.e. candidiasis)

19. Causes Of Postrenal AKI B/L Ureteral obstruction- Intraureteral Extraureteral Bladder neck obstruction – BPH prostatic cancer Urethral obstruction

20. Advanced age Diabetes Liver disease Kidney diseases Heart failure High blood pressure RISK FACTORS

21. Cell injury: Decreased aerobic production of ATP from glucose and fatty acids Hyperglycemia, Hyperlipidemia Decreased energy production dyselectrolytemia and damage of renal epithelial cells Sudden restoration of renal blood flow (RBF) after ischemia→ release of 02 free radicals cell injury PATHOPHYSIOLOGY

22. Decreased GFR Due to decreased RBF and decreased glomerular capillary pressure. Prolonged vasoconstriction (impaired vasodilatory response and autoregulatory behavior) Intrinsic Acute Kidney Injury

23. Intratubular obstruction due to sloughed cells Sloughing and necrosis of tubular epithelial cells leading to obstruction and increased intraluminal pressure, which reduces globular filtration.

24. Failure of kidney to concentrate urine due to inability of injured kidneys to maintain high medullary solute gradient and loss of aquaporin 2, limiting water reabsorption from collecting duct.

25. 1. Onset phase : Kidney injury occurs. Features: Common triggering events such as significant blood loss, burns, fluid loss, diabetes insipidus Renal blood flow 25% of normal Tissue oxygenation 25% of normal Urine output below 0.5 ml/kg/hour Duration: Hours to days STAGES

26. 2. Oliguric ( anuric ) phase : Urine output decreases from renal tubule damage. Features: Urine output below 400 ml/day, possibly as low as 100 ml/day Increases in blood urea nitrogen (BUN) and creatinine levels Electrolyte disturbances, acidosis and fluid overload (from kidneys inability to excrete water) Duration: 8 to 14 days or longer, depending on the nature of the acute kidney injury and dialysis initiation

27. 3.Diuretic phase : The kidneys try to heal and urine output increases, but tubule scarring and damage occur. Features: Occurs when the cause of acute kidney injury is corrected Renal tubules scarring and edema Increased GFR ( glomerular filtration rate) Daily urine output above 400 ml Possible electrolyte depletion from excretion of more water and osmotic effects of high blood urea nitrogen (BUN) Duration: 7 to 14 days

28. 4.Recovery phase : Tubular edema resolves and renal function improves. Features: Decreased edema Normalization of fluid and electrolyte balance Return of GFR ( glomerular filtration rate) to 70% or 80% of normal Duration: Several months to 1 year.

29. Clinical presentation varies with the cause and severity of renal injury, and associated diseases. Most patients with mild to moderate acute kidney injury are asymptomatic and are identified on laboratory testing. Patients with severe cases, however, may be symptomatic and present with CLINICAL PRESENTATION

30. Prerenal AKI- H/O 1) Excessive Fluid Losses from vomiting or diarrhea; Intravascular space losses in burn and pancreatitis. 2) Compromised cardiac function in patients with congestive heart failure; recent myocardial infarction. 3) Liver cirrhosis and failure (hepatorenal syndrome); 4) Drugs- cyclosporine, NSAID, or ACE inhibitor use. Symptoms related to hypovolemia- increased thirst , decrease urine output, postural hypotension, dizziness, fatigue, Muscle cramp.

31. 1) Reduction in ECF volume a. Tachycardia b. Orthostatic hypotension c. Dry mucus membrane d. Absence of axillary sweat e. A recent reduction in body weight f. “ Tenting” of upper thorax skin when pinched between the fingers g. Jugular venous pulse not visible 2) Arterial underfilling with expanded ECF a. Elevated jugular venous pressure, b. Ascites, c. Peripheral edema d. CHF may be identified by Pulmonary crackles & S3 gallop e .Liver failure may be identified by Jaundice, palmer erythema, spider angiomas, decrease liver size. Physical findings

32. Intrinsic/Intrarenal AKI : H/O - 1) Use of Nephrotoxic agents, Current medications , Contrast agent. 2) Glomerular disease- Nephrotic / Nephritic syndrome with hematuria, edema and hypertension . 3) Tubular disease: ATN should be suspected in any patient presenting after a period of hypotension secondary to cardiac arrest, hemorrhage or sepsis. Physical finding : Peripheral edema Raised JVP Pulmonary rales Signs of uremia- Asterixis, myoclonus, pericardial rub.

33. POST RENAL FAILURE Usually occur in elderly male with prostatic obstruction. H/O – Urinary Frequency, urgency & Hesitancy PHYSICAL FINDINGS – a. Costovertebral Angle Tenderness b. Pelvic & Rectal Masses c. Prostatic Hypertrophy d. Distended Bladder

34. INVESTIGATIONS: Complete Blood Count , Blood urea, S. creatinine, Serum Na + /K + /Calcium /phosphate /uric acid CPK-MM -Rhabdomyolysis LDH -tumor lysis syndrome -acute urate nephropathy C-ANCA , P-ANCA, Complement level Anti GBM antibody Urine analysis IMAGING USG abdomen CT Abdomen Doppler USG Plain X-ray Abdomen MR angiography

35. Few Important biomarkers Neutrophil gelatinase -associated lipocalin (NGAL) Kidney injury molecule-1 (KIM-1) Interleukin (IL)-18 Cystatin C

36. Neutrophil gelatinase – associated lipocalin (NGAL) Most consistent biomarkers found during AKI. Normally very small amounts in kidney tubules Predominantly found in proliferating nuclear antigen–positive proximal tubule cells. Predicts the occurrence of AKI in paediatric and adult patients after cardiac surgery. Also predicts mobility and mortality in children who undergo cardiac surgery. Available methods… Urine NGAL ELISA Plasma NGAL Kit

37. Kidney Injury Molecule-1 (KIM-1) Trans-membrane receptor of unknown function. Undetectable in normal kidney tissue or urine. Markedly increased in Ichaemic and nephrotoxic proximal tubular cell injury Renal cell carcinoma. Higher urinary KIM-1 associated with worse outcome in established AKI. Also predicts graft loss in renal transplant patients. Useful in some studies to differentiate between AKI, CKD and normal patients.

38. Interleukin (IL) -18 Pro-inflammatory cytokine Mediates inflammatory process (recruits neutrophils ) during ischaemic and septic AKI. Can predict AKI 1 day ahead of serum creatinine . Independent predictor of mortality in the patients with acute respiratory distress syndrome .

39. Cystatin C cysteine protease inhibitor, secreted by all nucleated cells in plasma Freely filtered at the glomerulus and not secreted in the tubules Less influenced by factors other than GFR therefore change in serum and urinary cystatin C is more sensitive than a change in serum Cr in predicting changes in GFR Predicts the risk of AKI-associated morbidity Increase urinary cystatin C and alpha 1 - microglobulin are predictors of an unfavourable outcome in ATN. Has higher sensitivity and higher negative predictive value in determining GFR in CKD.

40. The clinical management goals for patients with AKI can be divided into three main categories: restoration of renal perfusion minimizing toxic effects correction of metabolic derangements Goals of management

41. Conservative medical management of ARF requires a. Complete fluid intake &output record b. Daily wt record c. Intravascular volume should be assessed clinically daily d. Frequent(3 times / week) measurement of serum Na/K, Bld. Urea ,s. creatinine ,calcium &phosphate. Put CVP line to measure CVP (10 - 12)cm of h20 Management

42. PHARMACOLOGICAL MANAGEMENT A.Diuretics – may be given in oliguric pt with volume overload . Initially I.V. Furosemide (40-120 mg) given as a bolus , if urine out put improves then continuous infusion of 10 to 20 mg/hour should be given. Diuretic therapy only converts oliguric AKI to non oliguric AKI, may simplify fluid management but does not improves renal outcome So, routine use of diuretics is not recommended in established AKI.

43. B . Renal-dose dopamine. Dopamine is a selective renal vasodilator. It elicits profound natriuresis and increases urine output. The renal selective dose is 1 to 3μg per kg per minute.

44. C . Avoidance of nephrotoxic drugs. Potentially nephrotoxic drugs and agents should be completely avoided in ARF—they perpetuate the renal injury. These include NSAIDs, ACE inhibitors, cyclosporine, tacrolimus, aminoglycosides, radiocontrast agents, amphotericin B, and chemotherapeutic agents. D.  Antibiotics may be needed to treat associated infections (predominantly only antibiotics excreted by the liver are used if there is no liver disease ( erythromycin, azithromycin , chloramphenicol ).

45. HYPERKALEMIA Restriction of dietary potassium. Discontinue K + supplements or K + -sparing diuretics. Calcium gluconate (10 mL of 10% solution over 3 min). Glucose (50 mL of 50% dextrose) + insulin (10 U regular insulin) IV. Inhaled beta-2 agonist therapy (10-20 mg of nebulized albuterol in 4 ml of normal saline over 10 min ) K + -binding resin (SPS 15-30gm with 33% sorbitol) Loop diuretics Sodium bicarbonate (150 mEq in 1L of D5W) IV infusion, if concmitant metabolic acidosis is present. Dialysis/hemofiltration

46. Metabolic acidosis Sodium bicarbonate (if HCO 3 - <15 mEq /L) Dialysis/ hemofiltration Hyperphosphatemia Restriction of dietary phosphate intake Phosphate-binding agents (calcium carbonate, calcium acetate, sevelamer )

47. Hypocalcemia Calcium carbonate (if symptomatic or sodium bicarbonate is to be administered).

48. Dialysis therapy The indications to start dialysis CLINICAL Anuria (< 50 mL/day) more than 3 days Uremic encephalopathy, Uremic pericarditis Uremic bleeding Volume overload Pulmonary edema BIOCHEMICAL S.Cr more than 6.7/dl BUN more than 100 mg/dl Metabolic Acidosis Hyperkalemia

49. Energy Requirements Calories : Provide adequate calories to prevent catabolism (muscle breakdown) without overloading the kidneys. The general recommendation is 20–30 kcal/kg/day, depending on the patient’s metabolic state. NUTRITION MANAGEMENT

50. Protein Management Non-Dialysis Patients : In early stages of AKI or when the patient is not undergoing dialysis, protein intake should be restricted to limit urea production (0.6–0.8 g/kg/day). Dialysis Patients : When a patient is on dialysis, protein needs increase due to the loss of amino acids during dialysis. In such cases, 1.0–1.5 g/kg/day is recommended. Catabolic Patients : In hypercatabolic patients, protein needs may go up to 1.5–2.0 g/kg/day, especially if on continuous renal replacement therapy (CRRT).

51. Sodium : Sodium intake is typically limited to 2–3 grams per day to avoid exacerbating fluid retention and hypertension. Potassium :Potassium intake should be restricted depending on serum levels, especially in non-dialysis patients. Phosphorus :The recommended dietary phosphorus intake is usually around 800–1,000 mg/day.

52. 1. Fluid volume excess related to decreased glomerular filtration rate, decreased urine output and sodium retention as evidenced by weight gain, edema, intake greater than output, changes in urine specific gravity, jugular vein distention and shortness of breath; orthopnea . NURSING MANAGEMENT

53. 2. Risk for decreased cardiac output related to fluid overload, fluid shifts, fluid deficit (excessive losses), and electrolyte imbalance (potassium, calcium),severe acidosis.

54. 3. Risk for decreased cardiac output related to fluid overload, fluid shifts, fluid deficit (excessive losses), and electrolyte imbalance (potassium, calcium),severe acidosis.

55. 4. Risk for infection related to depression of immunologic defenses (secondary to uremia), invasive procedures/ devices and changes in dietary intake/malnutrition

56. Pulmonary oedema Pericarditis Metabolic acidosis uremic encephalopathy hyperkalemia cardiac arythimias COMPLICATIONS

57. Prevention and nondialytic treatment of acute renal failure The last few years have seen a number of trials with acetylcysteine in the prevention of mainly radiocontrast nephropathy. Although the results are still conflicting, the majority indicates that acetylcysteine , when applied together with adequate volume expansion , may be a useful drug to incorporate in the standard treatment procedures in patients at risk for acute renal failure . JOURNAL INFORMATION

58. Davidson, principles and practice of medicine 2022, 24 th edition elsiever newyork Morton G. Patricia and fontaninek dorrie , 2018 critical care nursing a holistic approach international edition 11 th edition wolters kluwer publication h ttps://doi.org/10.3390/jcm13092455 Mehta RL, Kellum JA, Shah SV, et al. Acute Kidney Injury Network (AKIN): report of an initiative to improve outcomes in acute kidney injury. Crit Care . 2007;11(2):R31. Lameire , Norbert H.a ; De Vriese , An S.b ; Vanholder , Raymonda . Prevention and nondialytic treatment of acute renal failure. Current Opinion in Critical Care 9(6):p 481-490, December 2003. REFERENCE