1 / 63

A cute K idney I njury

A cute K idney I njury. Dr. M. A. Al-Odat Jordanian board of medicine S.R. of ICU KSMC. Definition. There is NO sharp definition of AKI . Traditionally defined as:

egan
Download Presentation

A cute K idney I njury

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Acute Kidney Injury Dr. M. A. Al-Odat Jordanian board of medicine S.R. of ICU KSMC

  2. Definition There is NO sharp definition of AKI. Traditionally defined as: Abrupt loss of kidney function that results in the retention of urea and other nitrogenous waste products, and dysregulation of extracellular volume and electrolytes.

  3. AKI-RIFLE Criteria GFR Criteria Urine Output Criteria Increased creatinine x1.5 or GFR decrease > 25% UO < .5ml/kg/h x 6 hr Risk High Sensitivity Increased creatinine x2 or GFR decrease > 50% UO < .5ml/kg/h x 12 hr Injury Increase creatinine x3 or GFR decrease > 75% UO < .3ml/kg/h x 24 hr or Anuria x 12 hrs Failure High Specificity Persistent ARF** = complete loss of kidney function > 4 weeks Loss End Stage Kidney Disease (> 3 months) ESKD

  4. Limitations The change in serum creatinine during acute renal failure does not directly correlate with the actual change in glomerular filtration rate, which alters the assignment of that patient to a particular RIFLE level.

  5. Given these limitations, a modification of the RIFLE criteria has been proposed by the Acute Kidney Injury Network.

  6. RIFLE and AKIN staging criteria for AKI ______________________________________________________________ RIFLE AKIN Serum Cr Urine Output Stage Stage Criteria Criteria ______________________________________________________________ Risk 1 Increase in Scr of 1.5-2x < 0.5 ml/kg/hr baseline or increase >0.3 for 6 hrs Injury 2 Increase in Scr of 2-3x < 0.5 ml/kg/hr baseline for 12 hrs Failure 3 Increase in Scr of more < 0.3 ml/kg/hr than 3x baseline or Scr >4 for 24 hr with an acute rise of > 0.5 or anuria for 12 hr Loss Persistent renal failure > 4 wk ESRD Persistent renal failure > 3 mo

  7. Problems with Creatinine • Serum creatinine does not accurately reflect the GFR in a patient who is not in steady state. • Creatinine is removed by dialysis. As a result, it is usually not possible to assess kidney function by measuring the serum creatinine once dialysis is initiated. • In the early stages of severe acute renal failure, the serum creatinine may be low even though the actual (not estimated) GFR is markedly reduced since there may not have been sufficient time for the creatinine to accumulate.

  8. Abnormal BUN:Cr ratio • BUN: Cr > 15 • High protein intake. • Catabolic states. • Tissue necrosis. • Corticosteroids. • Tetracyclines. • Sepsis. • Volume loss. • Low cardiac output. • Obstructive uropathy. • BUN:Cr < 15 • Advanced liver disease. • Rhabdomyloysis. • Cimetidine. • Ketones. • Methyldopa. • Barbiturates. • Cotrimexazole

  9. Pre-Renal (reduced renal perfusion): • 1) hypovolaemia: • hypotension • Diarrhea/vomiting • Blood loss • Third space loss • Inadequate intake • 2) Reduced effective circulating volume: • Cardiac failure • Septic shock • Cirrhosis • 3) Drugs: • ACE-I • NSAIDs • 4) Renal artery stenosis • Renal: • Glomerular: • Glomerulonephritis • 2) Tubular: • Ischaemic ATN • Nephrotoxic ATN • Myeloma cast nephropathy • 3) Tubulointerstesial: • Drugs • Myeloma • Sarcoid • 4) Vascular Causes of AKI • Post Renal: • Urethral stricture • Prostatic hyperplasia/malignany • Kidney stones • Renal papillary necrosis • Retroperitoneal fibrosis • Carcinoma of cervix

  10. Epidemiology Of AKI

  11. 67% of critical care patients have AKI • 12% class R • 27% class I • 28% class F • More than half of patients with class R will progress to either class I or F • 5% of patients in general intensive cares will require RRT • 10-20% of surviving patients require ongoing RRT beyond hospital discharge Hoste et al Crit Care 2006

  12. AKI and Mortality • RIFLE class F have a mortality of 57% • RIFLE class I 45% • RIFLE class R 21 % • Compared to 8.4% of patients without AKI Ostermann M, Chang RW: CCM 2007

  13. Epidemiology of AKI in the ICUSaudi Arabia Clinical spectrum of acute renal failure Saudi Arabia. Ghacha R, Sinha AK, Al-Khursani IA. Saudi J Kidney Dis Transpl. • Acute tubular necrosis (67.5%) • Obstructive uropathy (30%) • Mortality rate was 26%

  14. Epidemiology of AKI in the ICUSaudi Arabia Epidemiology of acute renal failure in hospitalized patients: experience from southern Saudi Arabia. Al-Homrany M. East Mediterr Health J. 2003 • Acute tubular necrosis 62% • sepsis (24.7%) • ischemia (12.7%) • rhabdomyolysis (10.7%) • drugs (7.3%) • malaria and snake-bites (4.6%). • Overall, 40% died

  15. Clinical Picture • The clinical picture of the cause. • General signs/symptoms, including decreased or no urine output, flank pain, edema, hypertension, discolored urine, anorexia, vomiting, mental status changes or seizures. • Many patients are asymptomatic and are noted on routine examination to have an elevated plasma creatinine concentration or an abnormal urinalysis. • laboratory findings due to the renal injury.

  16. Clinical PicturePre-Renal • History and clinical picture of the cause. • Tahycardia. • Hypotension/Orthostatic hypotension. • Dryness of mucocutaneous membranes. • Oliguria ( < 400 ml/d). • Anuria ( < 50 ml/d).

  17. Clinical PicturePre-Renal • Hypovolaemia: - blood loss - Third space loss: pancreatitis, GIT obstruction, hypoalbuminaemia. • Cardiovascular: - infarction, tamponade, arrythmias, valvular diseases • Distributive: - sepsis, cirrhosis, hepatorenal syndrome. • Local renal causes: - renal artery stenosis, malignant hypertension. • Certain medications

  18. Clinical PicturePre-Renal: Medications • NSAIDs, ACE-I, Cocaine, Cyclosporines. • Alteration of renal perfusion, and glomerular haemodynamics. • failure of glomerular pressure autoregulation. • Predisposing factors: - CHF - liver cirrhosis - nephrotic syndrome - hypovolaemia - atherosclerosis - Age.

  19. Clinical PicturePre-Renal: Medications • AKI associated with ACE-I should prompt investigation to rule out bilateral renal artery stenosis.

  20. Clinical PictureRenal • History and clinical picture of the cause. • Acute glomerulonephritis: vasculitis, SLE, endocarditis, cryoglobulinaemia, anti-glomerular basment membrane disease. • Acute interstitial nephritis: sarcoidosis, myeloprolifrative disorders. • Acute tubular necrosis: ischaemia, sepsis, nephrotoxins, drugs, contrast, rhabdomyolysis, myoglobin/ haemoglobin.

  21. Clinical PictureRenal • The most common cause of AKI in hospitalized patient is intrinsic renal failure due to ATN. • Polypharmacy is common among most patients with chronic diseases and hospitalized patients. • Allergic interstitial nephritis should be strongly considered in all patients with AKI. • Rhabdomyolysis . • Contrast induced AKI.

  22. Mechanisms of ATN

  23. Medications causes of allergic interstitial nephritis • Penicillines • Cephasporines • Sulfonamides • Rifampin • Ciprofloxacin • NSAIDs • Thiazide diuretics • Loop diuretics • Cimetidine • Phenytoin • Allopurinol • Chinese herb

  24. Pathophysiology of Rhabdomyolysis

  25. Clinical PictureRenal: contrast induced AKI • Contrast induced AKI is predominantly via acute vasoconstriction. • Risk factors: GFR < 35 ml/min, diabetic nephropathy, severe CHF, large volume of contrast, preexisting hypotension/hypokalaemia.

  26. Pathophysiology of contrast inducedacute kidney injury

  27. Prevention of contrast induced AKI • Administration of crystalloid(1-1.5mL/Kg/hr for 8-12 hours before a procedure) remains the safest, most efficacious, and cost-effective method of preventing contrast induced nephropathy. • Administration of acetylcysteine in two 600mg doses the day along with saline infusion for patients with stable chronic renal insufficiency(Cr~2.0mg/dL). • Type of Contrast.

  28. Clinical PicturePost-Renal • Total absence of urine (anuria) is primarily observed with bilateral ureteral obstruction/ urethral obstruction. • Loin or flank pain. • Prostatic hyperplasia/malignancy (male). • Carcinoma of cervix (female).

  29. Evaluation of AKI

  30. Evaluation of AKI • Intravascular volume status is the most important factor in the evaluation of AKI. A decrease in urinary volume is often one of the initial clinical findings in AKI. • The most important laboratory test for a patient with AKI is urine analysis. • Both urinary sediment and urinary indices in combination with serum values can often be extremely helpful in determining the cause of AKI.

  31. Urine analysis in AKI • RBC, RBC cast, Protienuria: - Glomerulonephritis – vasculitis - thrombotic microangiopathy. • WBC, WBC casts: - Pyelonephritis - Interstitial nephritis. • Eosinphilurea: - Glomerulonephritis - Atheroemboli - Allergic interstitial nephritis • Pigmented casts, renal tubular epithelium: - ATN - Haemoglobinurea – myoglobinurea • Crystallurea: - Uric Acid - Drugs - Toxins.

  32. RBC cast Granular cast Hyaline cast Granular cast Granular cast WBC cast Oval fat body and Hyaline cast WBC cast

  33. Urinary Sediment of ATN

  34. GUIDELINE OF URINARY INDICES

  35. Typical Urine Findings in Conditions that cause AKI Condition Dipstick test Sediment analysis Uosmo FENa Pre-renal -ve, trace few hyaline casts >500 <1 Azotaemia Ischaemic mild to mod. Pigmented granular <350 >1 ATN proteinuria cast Nephrotoxins mild-mod prot. Pigmented gran. Cast <350 >1 A. Interstitial mild-mod prot, WBC, WBC casts, Eosin. <350 >1 Nephritis hemoglobin, WBC Eosin. Casts, RBC A. Glomerulo mod-severe prot. RBC, RBC casts >500 <1 Nephritis hemoglobin Post-renal -ve, trace, WBC crystals, RBC < 350 >1 Azotaemia hemoglobin

  36. Radiologic Studies : • Ultrasonography is most common. • Safe, easy to use, informative. • Principally required to assess urinary tract obstruction, kidney stones, renal cyst or mass. • CT scan.

  37. Renal Biopsy • Indications : Isolated glomerular hematuria with proteinuria, nephrotic syndrome, acute nephritic syndrome, unexplained acute or rapidly progressive renal failure. • Contraindications: Uncorrectable bleeding diathesis, Small kidneys (indicative of chronic irreversible disease), Severe hypertension, multiple, bilateral cysts or a renal tumor, hydronephrosis, Active renal or perirenal infection, uncooperative patient. • Complications: Bleeding.

  38. Biomarkers • Neutrophil gelatinase–associated lipocalin (NGAL) is up-regulated in proximal tubular cells immediately following ischemic injury. • Interleukin-18 (IL-18) is a proinflammatory cytokine that is activated in proximal renal tubules following injury. • Cystatin C is a better marker of GFR than serum creatinine, and could identify the development of AKI 1 to 2 days before elevation in serum creatinine.

  39. Management • The goal of any focused evaluation of AKI is immediate correction of its reversible causes. • Recognition and relief of urinary outlet obstruction should be given the highest priority, especially for patient with anuria.

  40. Management • Support of renal perfusion with either volume infusion or therapeutics that improve renal oxygen delivery should be considered before any attempt to improve urinary flow. • Urinary indices should be examined before diuretic intervention.

  41. Management Renal Replacement therapy remains the cornerstone of management of patients with severe AKI Nephron Clin Pract 2009;112:c222-c229

  42. Indications of RRT • Anuria or Oliguria (UOP < 200 ml/12 hrs.) • Hyperkalaemia (K > 6.5 mmol/L). • Severe Acidaemia (pH < 7.1). • Azotaemia ( Urea > 30 mmol/L). • Clinically significant organ oedema (particularly Lungs). • Uraemic: encephalopathy, pericarditis, neuropathy, myopathy. • Severe dysnatraenia (Na >160 or < 115 mmol/L) • Drug over dose with dialysable product. • Hyperthermia.

  43. Pharmacologic treatments under study: • Dopamine: no benefit • Atrial Natriuretic Peptide (ANP) or ANP-analogue (Anaritide): promising • Human Insulin like growth factor 1: no benefit • Erythropoietin • Intensive Insulin Therapy (IIT).

  44. Case Scenario

  45. Case 1 26 yo F is involved in a RTA, with multiple fractures, blunt chest and abdominal trauma. She was briefly hypotensive on arrival to ED, received 6L NS and normalized BP. Non contrast CT showed small retroperitoneal hematoma. On day#2 her SCr is 0.9 mg/dl, lipase is elevated and tense abdominal distension is noted. US showed massive ascites. UOP drops to <20 cc/hr despite of 10 L total IV intake. On day#3, SCr is 2.1mg/dl, CVP is 17, UNa is 10 meq/L, with a bland sediment. What is the cause of her AKI? What bedside diagnostic test and therapeutic intervention is indicated?

  46. Bladder pressure was 29 mmHg UOP and SCr improved with emergent paracenthesis. Dx: Abdominal Compartment Syndrome causing decreased renal perfusion from increased renal vein pressure.

  47. Case 2 59 yo M, hx liver transplant in 2001 and acute on chronic rejection, now decompensatedESLD, is admitted with worsening ascites, hepatic encephalopathy and GI bleed (which is now controlled). The only medications he has been receiving are Lactulose and omeprazole. He has been hemodynamically stable with average BP~100/70 mmHg. He had a 3.5 L paracenthesis on day 2. His SCr has been slowly rising from 1.2 to 4.7 mg/dl within the 2nd to 4th day of admission and his UOP has dropped to 150 cc/day. His daily FeNa is <1% despite of 2 L fluid challenge. His Urine sediment is blend. His renal US is normal. What is the cause of his AKI?

  48. Patient required HD. He had a second liver transplant and came off HD after the surgery with stable SCr of 1.4 mg/dl. Dx: Hepatorenal Syndrome (HRS)

  49. Case 3 54 yo F with CAD, on statin, started a new exercise program with intense weight training. She was brought to ED with neck pain, and LL weakness. VS stable, normal UOP, with dry mucosa. LL muscle strength 2/5 bilaterally. BUN 40 mg/dl, creatinine=8 mg/dl. FeNa 1.5%. Renal US normal. UA: 1.010, 3+ blood, few RBCs, few granular casts. What would be the next test to order? What may be the cause of her AKI?

  50. Her CPK=57,700 She was treated with IV NaHCO3 gtt to alkalinize urine to PH>6.5 . Her UOP remained normal but she required HD for uremia. Dx: ATN due to Rhabdomyolysis

More Related