Critical care Nursing

Acute Renal Failure Dr Naiema Gaber

The Learning outcomes1- Define acute renal failure (ARF).2- Explain the causes of ARF.3- Differentiate between the three types of ARF.4- Identify the clinical stages of ATN.5- Discuss the clinical manifestations of ARF.6- List the complications of ARF.7- Develop a plan for managing ARF.

Acute Renal Failure (ARF)Definition: Sudden deterioration in the ability of the kidneys to function ( to maintain fluid, solute or electrolyte homeostasis). It occurs over hrs or few days. It is Common in ICU patients (10-20%) Why?

ARF: Types, Causes and mortality1- Primary renal (intrarenal) disease: 33%Hemolytic uremic syndrome: 88%Obstructive uropathyRenal vein/artery thrombosisPrimary glomerulonephritis (RPGN)Overall mortality: 6%Most primary renal diseases develop RF gradually and do not need emergent dialysis

2-Extra-renal causes of ARF: 67% of totalOverall mortality: 62%!!

Data pooled from Ped. Nephrol. 7:703, 8:334, 6:470, and 7:434

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17

14

16

6

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Post-op heart or other heart failure32

Sepsis17

Cancer related14

Liver transplant or failure16

Trauma6

Other15

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ARF: What are the Risk factors for mortality?Multi-organ failureBacterial SepsisFungal sepsisHypotension/ vasopressorsVentilatory support Initiation of dialysis late in hospital courseOliguria /anuria: with oliguric ARF, mortality is > 50% compared to < 20% with non-oliguric ARF

Risk factors cont.Advanced age Co morbid conditions (heart failure, liver or kidney failure, diabetes) Contrast exposure (dehydrated, diabetic) Nephrotoxic medications (aminoglycosides, angiotensin enzyme inhibitors) Volume depletion (especially in diabetes) Rhabdomyolysis; surgery (cardiac surgery)

Types and causes of ARF

2- Renal

1- Prerenal

3-Postrenal

1- Prerenal azotemia (failure) Causes:Decreased circulatory volumeHypovolemiaGI losses (V/D, ileostomy, NG drainage)Hemorrhage (trauma, GI bleeding)Cutaneous losses (burns)Renal losses (diabetes insipidus or mellitus)Loss of fluids from intravascular spaceThird spacingSeptic (capillary leak) or anaphylactic shock.

Prerenal azotemia (failure) cont.Decreased local blood flow to kidneyRenal artery stenosis or RVTDrug-induced renal vasoconstrictioncyclosporin, tacrolimusHepatorenal syndromeDiminished cardiac outputCongestive Heart Failure (CHF)Arrhythmias, tamponade, etc.Cardiovascular surgery

Prerenal azotemia1-Decreased circulatory volume

A-Hypovolemia

B- Loss of fluids

2-Decreased local blood flow to kidneyA- Renal artery stenosis B- DrugC- Hepatorenal syndrome

3- Diminished cardiac outputA- (CHF)B- Arrhythmias, tamponade, etc.C- Cardiovascular surgery

2-Postrenal FailureKidney stone (usually UVJ)Ureteropelvic junction (UPJ) or UVJ obstructionBladder: as neurogenic bladder or fungus ballUrethra: posterior urethral valve; foreign bodyIatrogenic: obstructed Foley; narcotics

3- Intrinsic Acute Renal FailureAcute tubular necrosis (ATN)Prolonged Prerenal azotemia of any causeNephrotoxin-induced drugs (aminoglycosides; amphotericin)Primary Glomerular diseasesHemolytic uremic syndromeAll other forms of glomerulonephritis Intra-renal obstruction: tumor lysis syndrome

Clinical course of Acute Tubular Necrosis (ATN)I- Onset phase: (initiating) begins with an initial insult and lasts until cell injury occurs. It lasts from hours to days, the clinical manifestations in this phase include 1-decreased urine output 2-increased serum Creatinine. The major goal during this phase is to determine the cause

Clinical course of tubular Necrosis (ATN) contII- Oliguric phase or non oliguric phase (anuria) *Oliguria =

Diagnosis and Assessment of ARFIn history, seek clues regarding secondary causes - symptoms of CHF, liver disease, sepsis, systemic vacuitis, prodromal bloody diarrhea; birth asphyxia Check for symptoms of primary renal disease - UTI, gross hematuria, flank pain, Hx of strept infection, drug exposure ( aminoglycosides or narcotics) for bladder dysfunction

Assessment of ARF (Physical exam.) cont.Subjective: Dysuria, nausea, weakness, and fatigue Tachycardia and/or a drop in HR >15 b pm or drop in SBP >15mmHg with orthostatics indicate = dehydrationDecreased mental status =decreased perfusionRales =fluid overload, CHFAbdominal pain and distension = obstruction, UTIItching = azotemia

Assessment of ARF cont.During physical exam, look for secondary causesCauses of decreased effective circulatory volume - CHF, ascites, edema, sepsisSigns of systemic illness - (vasculitis, SLE): rash, arthritis, purpura Signs of obstructive uropathy: enlarged kidneys or bladder - CHECK FOLEY.

Assessment of ARF, Labs cont.UA: High specific gravity = dehydrationRBCs = UTI, urolithiasisWBCs, bacteria = UTICasts: RBC (glomerulonephritis), WBC (pyelonephritis), and epithelial cells and granular casts (ischemic damage)Electrolytes to assess for metabolic d/oUrine Na, CreatinineECG to look for peaked T waves, indicates Hyperkalemia

Assessment for ARF cont. BUN, Cr; CBC with platelets.Urine Analysis: hematuria, myoglobinuria, proteinuria, RBC casts, eosinophilsUrine indices (U-osm, U-CR, U-Na )Renal Ultra Sound (with Doppler flow to rule out renal vein thrombosis)Anti-DNA, ANA, renal biopsy

Nursing diagnosis for client having ARF Fluid volume excess related to decreased functionAlteration in cardiac output: decreased related to fluid volume excess.Altered nutrition: less than body requirements related to anorexia, nausea and vomiting.Impairment of skin integrity related to poor nutritional status, immobility and edema

Nursing diagnosis for client having ARF cont Anxiety related to unexpressed serious illness and current symptoms.Activity intolerance related to fatigue, anemia, retention of waste products and dialysis procedure.Sleep pattern disturbance related to decreased functioning of immune system.Knowledge deficit, disease and it management

Anticipated problems worsening the ARFAdjust medicines for renal insufficiencyAvoid Nephrotoxins if possibleAvoid intravascular volume depletion (especially in third-spacing or edematous patients)

Management of ARFVentilation and oxygenationCirculation / perfusionFluids /electrolytesMobilityProtection/safetySkin integrityNutritionComfort/ pain controlPsychological supportteaching

NB: Management of (ARF )To maintain Water balance

1- Assess the Volume status"Maintenance" is IRRELEVANT in ARF!!!If euvolemic, give insensible + losses + UOPIf volume overloaded, *concentrate all meds; limit oral intake *Need frequent check on weights and BP as well as accurate I/O *give insensible = 30 cc/100 kcal or 400cc/M2/day *If has any UOP, Lasix + ordered drugs may be effective

Once ARF stabilizes, fluid replacement should be equal to insensible losses (400) mL /day) plus urinary or other drainage losses to avoid hypervolemia

Management of ARF: General cont.Discontinue/re-dose nephrotoxic drugs Diet: *Eliminate potassium if serum level increased *Oral and IV amino acids *Provide nutrition with increased carbohydrates to decrease catabolism. *Total caloric intake of 35 to 50 kcal/kg/day should be maintained with most calories provided by carbohydrates (100 g/day).

Management of ARF: General contFoley catheterization for accurate output

Daily weight, monitor BP, labs

Correct easy bleeding with DDAVP, estrogen, and cryoprecipitate

Prednisone in acute interstitial nephritis may help

Mannitol - alkaline diuresis in Rhabdomyolysis

Management: PrerenalGoal is to restore BP and intravascular volumeFluid deficit:Fluid bolus with 500ml, recheck fluid status, repeat.Monitor vital signs and electrolytesNormal or increased fluid status:CHF: monitor O2 status. Lasix 20-80mg IV.Monitor diuresis, potassium status, daily weight

Management: PostrenalPlace Foley, note residual. If >400ml and discomfort is relieved, leave catheter in place.If Foley in place, Fluds with 20-30ml salineConsider stones or mass obstructionDaily weights, strict I/O

Management: RenalHyperkalemia:Continuous cardiac monitoringKayexalate 15 to 30g in 50-100ml 20% sorbitol PO q 3-4 hours or in 200ml 20% sorbitol PR q 4 hoursDialysis for failed kidneys: can remove 30-60 mEq/hrContrast dye:Creatinine peaks within 72 hours with slow recovery over 7 to 14 days with appropriate therapy. Aminoglycosides: higher risk: elderly, volume depletion, >5 days, large doses, preexisting liver disease, and preexisting renal insufficiency. Correct preexisting volume depletion and monitor drug levels

Indications for renal replacement therapyVolume overload Pulmonary edema, CHF, refractory HTNHyperkalemiaHyperphosphatemiaUremic side-effects: pericarditis, pleuritisMetabolic acidosisMental changes

Modes of renal replacement therapyPeritoneal dialysis - also gentle and don't need heparinization but slow and catheter may leak or not work.

Hemodialysis - very fast, but need big lines and systemic heparinization; causes hemodynamic instability and uremic dysequilibrium symptoms

Complications of ARFDeath (50%)Sepsis infection (leading cause of mortality)Hypertension exacerbated by fluid overload: Use antihypertensive that do not decrease renal blood flow).

Complications of ARF cont.Anemia is common, caused by increased red blood cell (RBC) loss and decreased RBC production.

Platelet dysfunction may occur secondary to the uremia and present as gastrointestinal (GI) bleeding.

Special CasesElderly: Elderly more susceptible to ARF (3.5 X more common)Creatinine clearance dependent on ageEvolution to acute tubular necrosis more common Pregnancy: Infected uterus Toxemia and related obstetric complications. Pregnant patients only group with a sharp drop in ARF mortality (1.7%)Pediatric: Congenital anomalies (e.g.,urethral valves, etc)

Review questions1-Intrarenal acute renal failure can be due toa- dehydration and increased cardiac outputb- calculi in the ureters and hypovolimic shockc- antibiotics and radiocontrst dye administrationd-obstructed Foley catheter and prostate hypertrophy

(c)

(b)

2-During which phase of acute tubular necrosis (ATN) are Hyperkalemia, gastrointestinal bleeding, infection, and vascular volume overload major potential problemsa-onset b-oliguric c-diureticd-recovery

(c)

3- Decreased erythropoietin production in renal failure results ina- decreased RBC survivalb-impaired white blood cell functionc- decreased red blood cell productiond-an inability of platelets to function properly

Clinical Case #1 Ali is a 15 year old male who presented with URI (upper Respiratory Infection) symptoms, then headache, vomiting, abdominal pain, knee pain, edema, and a purpuric rash on his legs. He had not voided for 24 hours.What is the diagnosis? ARF? What the lab. Investigations that confirm the diagnosis?

Physical exam and labsBP was 152/94. Heart and lung exams were normal. IndicatehypertensionA urinalysis revealed hematuria and proteinuria. BUN and Creatinine were 76 and 8.0. Albumin was 3.1 indicate ARF

Fluid management in ARF (Clinical Case #1) This kid weighs 70 kg. What percent maintenance should you run his IV at?NO FLUIDS - Hes fluid overloaded and hypertensive he doesnt need any fluidHow were the maintenance calculations derived? What goes into the formula?Insensible + UOP = maintenance=400 cc only

Fluid management in ARF (Clinical Case #1) cont.If this kid had an albumin of 1.0 and mucus membranes were very dry, what fluids would you give him?

Bolus of NS like any other dehydrated kid but cautiouslyNow you have the kid euvolemic by exam but still has no UOP. Hes NPO though, so what fluid rate should you run now?

Insensible loss 400 cc+ UOP = maintenance = 400 cc

2-Hypertension management(Clinical Case #1) High blood pressure could be from volume overload or from intrinsic renal disease

If has volume overload, need to directly vasodilate (calcium channel blockers, clonidine,, nitropruside, etc

Goal is to prevent stroke or congestive heart failure

Back to Ali (Clinical case #1)K+ 6.5, Bicarb. 14Calcium 5.8, Phosphorus 9.3Hematocrit 30.3%, Platelets 280K

Interpret this results.

low bicarb. = Metabolic Acidosis

3-Acidosis management (Clinical case #1)Correct bicarbonate which is < 15Acidosis makes the kids feel terriblewatch -sodium and fluid overload-lowering ionized calcium levels (by increasing binding of calcium to albumin)

4-Anemia and uremic bleeding management (Clinical Case #1 ) Anemia results from lack of renal erythropoietin production + increased loss

Underlying disorder may also cause hemolysis or decreased RBC production (sepsis, leukemia)

Uremic PLT's do not function well, so have increased bleeding: treatment will causes transient improvement in PLT function.

Clinical Case #2Samira. is a 10 year-old with acute lymphocytic leukemia receiving chemotherapyHas fever, neutropenia and thrombocytopeniaUOP (Urinary output) is 1.2 cc/kg/hourOn clinical exam she has very moist mucus membranes BUN and Creatinine are 110 and 0.7. Albumin is 3.5

Assessment of clinical case #2Is she in renal failure?

Creatinine is normal, so NO!

Why is BUN so high?

Use of plasma BUN: Cr ratioIn pre-renal BUN :Cr > 20 usually

However, BUN may be increased disproportionately with blood products, excess amino acids in bleeding; increased catabolism as in case of treatment with steroids, fever.

(c)Mr. salem hasnt peed all night long!How is UO measured? a-By shift b- by hourc- Foley d- urinating on own?

For more information write three more questions

1-What is the trend over last 2-3 hours vs. last 24 hours?Oliguria =

Any questions???