Critical care Nursing

Acute Renal Failure

Dr Naiema Gaber

The Learning outcomes

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1- 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 mortality

1- Primary renal (intrarenal) disease: 33%
Hemolytic uremic syndrome: 88% Obstructive uropathy Renal vein/artery thrombosis Primary 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 total

Other Trauma 15% 6% Liver transplant or failure 16% Post-op heart or other heart failure 32%

Overall mortality: 62%!!

Cancer related 14%

Sepsis 17%

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

ARF: What are the Risk factors for mortality?

Multi-organ failure Bacterial Sepsis Fungal sepsis Hypotension/ vasopressors Ventilatory support Initiation of dialysis late in hospital course Oliguria /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

1- Prerenal 2- Renal

3-Postrenal

1- Prerenal azotemia (failure)

Causes:
Decreased circulatory volume
Hypovolemia
GI losses (V/D, ileostomy, NG drainage) Hemorrhage (trauma, GI bleeding) Cutaneous losses (burns) Renal losses (diabetes insipidus or mellitus)

Loss of fluids from intravascular space

Third spacing Septic (capillary leak) or anaphylactic shock.

Prerenal azotemia (failure) cont.

Decreased local blood flow to kidney
Renal artery stenosis or RVT Drug-induced renal vasoconstriction
cyclosporin, tacrolimus

Hepatorenal syndrome

Diminished cardiac output

Congestive Heart Failure (CHF) Arrhythmias, tamponade, etc. Cardiovascular surgery

Prerenal azotemia
1-Decreased circulatory volume

A-Hypovolemia B- Loss of fluids

2-Decreased local blood flow to kidney A- Renal artery stenosis B- Drug C- Hepatorenal syndrome

3- Diminished cardiac output A- (CHF) B- Arrhythmias, tamponade, etc. CCardiovascular surgery

2-Postrenal Failure
Kidney stone (usually UVJ) Ureteropelvic junction (UPJ) or UVJ obstruction Bladder: as neurogenic bladder or fungus ball Urethra: posterior urethral valve; foreign body Iatrogenic: obstructed Foley; narcotics

3- Intrinsic Acute Renal Failure

Acute tubular necrosis (ATN)
Prolonged Prerenal azotemia of any cause

Nephrotoxin-induced drugs (aminoglycosides; amphotericin) Primary Glomerular diseases

Hemolytic uremic syndrome All 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) cont

II- Oliguric phase or non oliguric phase (anuria)

*Oliguria = <400ml/24 hrs or <20ml/hr *Anuria = <50ml/24 hrs III- Diuretic phase: lasts 1-2 weeks. There is gradual increase in urine output and may lead to volume deficits and electrolytes imbalance. IV- Recovery phase: lasts from months to years. Renal function return to its normality.

Diagnosis and Assessment of ARF

In 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 = Decreased mental status

dehydration

perfusion Rales =fluid overload, CHF Abdominal pain and distension = obstruction, UTI Itching = azotemia

=decreased

Assessment of ARF cont.

During physical exam, look for secondary causes
Causes of decreased effective circulatory volume CHF, ascites, edema, sepsis Signs 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 = dehydration RBCs = UTI, urolithiasis WBCs, bacteria = UTI Casts: RBC (glomerulonephritis), WBC (pyelonephritis), and epithelial cells and granular casts (ischemic damage) Electrolytes to assess for metabolic d/o Urine Na, Creatinine ECG to look for peaked T waves, indicates Hyperkalemia

Assessment for ARF cont.

BUN, Cr; CBC with platelets. Urine Analysis: hematuria, myoglobinuria, proteinuria, RBC casts, eosinophils Urine 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 function Alteration 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 ARF Adjust medicines for renal insufficiency Avoid Nephrotoxins if possible Avoid intravascular volume depletion (especially in thirdspacing or edematous patients)

Management of ARF
Ventilation and oxygenation Circulation / perfusion Fluids /electrolytes Mobility Protection/safety Skin integrity Nutrition Comfort/ pain control Psychological support teaching

NB: Management of (ARF ) To maintain Water balance

1- Assess the Volume status "Maintenance" is IRRELEVANT in ARF!!! If euvolemic, give insensible + losses + UOP If 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 cont

Foley 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: Prerenal
Goal is to restore BP and intravascular volume Fluid deficit: Fluid bolus with 500ml, recheck fluid status, repeat. Monitor vital signs and electrolytes Normal or increased fluid status: CHF: monitor O2 status. Lasix 20-80mg IV. Monitor diuresis, potassium status, daily weight

Management: Postrenal
Place Foley, note residual. If >400ml and discomfort is relieved, leave catheter in place. If Foley in place, Fluds with 20-30ml saline Consider stones or mass obstruction Daily weights, strict I/O

Management: Renal
Hyperkalemia: Continuous cardiac monitoring Kayexalate 15 to 30g in 50-100ml 20% sorbitol PO q 3-4 hours or in 200ml 20% sorbitol PR q 4 hours Dialysis for failed kidneys: can remove 30-60 mEq/hr Contrast 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 therapy

Volume overload
Pulmonary edema, CHF, refractory HTN

Hyperkalemia Hyperphosphatemia Uremic side-effects: pericarditis, pleuritis Metabolic acidosis Mental changes

Modes of renal replacement therapy

Peritoneal 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 ARF
Death (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 Cases
Elderly:
Elderly more susceptible to ARF (3.5 X more common) Creatinine clearance dependent on age Evolution 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 questions
1-Intrarenal acute renal failure can be due to a- dehydration and increased cardiac output b- calculi in the ureters and hypovolimic shock c- antibiotics and radiocontrst dye administration d-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 problems a-onset b-oliguric c-diuretic d-recovery

(c)
3- Decreased erythropoietin production in renal failure results in a- decreased RBC survival b-impaired white blood cell function c- decreased red blood cell production d-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 labs

BP was 152/94. Heart and lung exams were normal. Indicate hypertension A 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 fluid

How 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 cautiously

Now 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. 14 Calcium 5.8, Phosphorus 9.3 Hematocrit 30.3%, Platelets 280K Interpret this results. low bicarb. = Metabolic Acidosis

3-Acidosis management (Clinical case #1)

Correct bicarbonate which is < 15 Acidosis makes the kids feel terrible watch -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 #2
Samira. is a 10 year-old with acute lymphocytic leukemia receiving chemotherapy Has fever, neutropenia and thrombocytopenia UOP (Urinary output) is 1.2 cc/kg/hour On clinical exam she has very moist mucus membranes BUN and Creatinine are 110 and 0.7. Albumin is 3.5

Assessment of clinical case #2

Is she in renal failure?

Creatinine is normal, so NO!

Why is BUN so high?

Use of plasma BUN: Cr ratio

In 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 hour c- 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 = <400ml/24 hrs or <20ml/hr Anuria = <50ml/24 hrs

2- does he has Recent surgery? 3- are therre any Other symptoms 4- is there any changes in vital signs?

Any questions???