Management of Patients with Renal Disorders

Nursing 230 Spring 2012 Presented by: Lorraine Sutphin RN, MSN

Fluid & Electrolyte Imbalances in Renal Disorders

y Fluid Overload: Occurs if the fluid intake exceeds the

amount that the kidneys can excrete y Fluid Volume Deficit: Occurs if the fluid intake is inadequate or volume is otherwise depleted

Nursing Management
y Daily Weights: Accurate indicator of fluid loss or gain

in acutely ill patients is accurate daily weights.

y 1-kg weight gain is equal to 1000 ml of retained

fluid

y Intake and Output (I&O) y Fluid taken in Parenterally and orally y Fluid output
y

Urine, vomiting, diarrhea, diaphoresis

In clinical practice, creatinine clearance or estimates of creatinine clearance based on the serum creatinine levels are used to measure GFR. Creatinine is produced naturally by the body (creatinine) is a break-down product of creatine phosphate, which is found in muscle). It is freely filtered by the glomerulus, but also actively secreted by the peritubular capillaries in very small amounts such that creatinine clearance overestimates actual GFR by 10-20%. This margin of error is acceptable, considering the ease with which creatinine clearance is measured. Unlike precise GFR measurements involving constant infusions of insulin, creatinine is already at a steady-state concentration in the blood, and so measuring creatinine clearance is much less cumbersome. However, creatinine estimates of GFR have their limitations. All of the estimating equations depend on a prediction of the 24-hour creatinine excretion rate, which is a function of muscle mass. One of the equations, the Cockcroft and Gault equation, does not account for race,.
4

Clinical Manifestations
y Table 44-1 y Insert the table here

Gerontological Considerations
y With advancing age the kidney is less able to respond

to acute fluid and electrolyte changes. y Elderly develop atypical and non-specific signs and symptoms of renal disturbances and fluid and electrolyte imbalances. y Fluid deficit in the elderly can lead to: constipation, falls, medication toxicity, urinary tract & respiratory infections, delirium, seizures, electrolyte imbalances, hyperthermia, and delayed wound healing

Renal Disorders Chronic Kidney Disease

y Chronic Kidney Disease (CKD) is an umbrella term

that describes kidney damage or a decrease in the glomerular filtration rate (GFR) for 3 or more months y CKD is associated with decreased quality of life, increased health care expenditures, and premature death. y Untreated CKD can result in end-stage renal disease(ESRD) y ESRD necessitates renal replacement therapy (dialysis or kidney transplantation)
7

Risk factors for CKD

y Cardiovascular disease y Diabetes y Hypertension y Obesity

16.8% of the US population aged 20 and older have CKD (CDC 2007)

Diabetes and CKD

y Diabetes is the primary cause of CKD y Between 25% & 40 % of Type 1 diabetics and 5%-40% of Type 2 diabetics develop kidney damage. y Diabetes is the leading cause of renal failure in patients starting renal replacement therapy y The second leading cause is hypertension followed by
y y y

Glomerular nephritis & pyleonephritis Polycystic-heredity or congenital disorders Renal cancers (U.S. Renal Data System, USRDS2007)

Pathophysiology
y There can be significant damage to the kidneys

without signs or symptoms. ( <20% functional nephrons leads to renal replacement) y The exact pathophysiology of CKD is not fully understood but the damage to the kidneys is thought to be caused by prolonged acute inflammation that is not organ specific and thus has subtle systemic manifestations. y What do you think this means??

10

Stages of Chronic Kidney Disease

y Stages are base of the glomerular filtration rate(GFR) y The National Kidney Foundation has classified CKD to include 5 y y y y y y

stagesStage 1 with normal or high GFR (GFR > 90 ml/min) Stage 2 Mild CKD (GFR = 60-89 ml/min) Stage 3 Moderate CKD (GFR = 30-59 ml/min) Stage 4 Severe CKD (GFR = 15-29 ml/min) Stage 5 End Stage CKD (GFR <15 ml/min) Dialysis or a kidney transplant needed in order to maintain health.

y Stage 5 results when the kidneys can not remove the body s metabolic

wastes or perform their regulatory mechanisms- this is when renal replacement therapy is required to sustain life. y Normal GFR is 125mL/min/1.73 (2)

11

Improving Patient Outcomes

y Screening and intervention are very important in order

to slow or stop the progression, not all patients with CKD will progress to Stage 5. y CKD increases the risk for cardiovascular disease- the leading cause of morbidity and mortality. y Treatment of hypertension, anemia, and hyperglycemia as well as detection of proteinuria will all help to slow the disease progression and improve patient outcomes.

12

Clinical Manifestations
y Elevated serum creatinine levels y Anemia: decreased erythropoietin production y Metabolic acidosis y Abnormalities in calcium and phosphorus y Fluid retention-edema & CHF y Abnormalities in electrolytes y Difficulty controlling hypertension

13

Assessment & Diagnostic Findings

y The GFR is the amount of fluid filtered through the

glomeruli per unit of time. (chapter 43)

y Creatinine Clearance is a measure of the amount of

creatinine the kidneys are able to clear in a 24 hour periody Normal values differ in men and women and in certain

races due to the difference in muscle mass

14

Medical Management
y Treatment of the underlying cause y Regular clinical & laboratory assessment y Maintain BP below 130/80 y Early referral for renal replacement therapy as indicated by renal status y Prevention of complications by controlling CV risks, treating hyperglycemia, treating anemia, smoking cessation, weight loss, exercise program and reduction in salt and alcohol consumption.

15

Gerontologic Considerations
y Changes in kidney function associated with aging predispose elderly patients to kidney dysfunction and renal failure. y Elderly have increased incidence of systemic diseases such as: atherosclerosis, hypertension, heart failure, diabetes, and cancer- all predisposing them to renal disease. y Acute problems need to be prevented whenever possible or recognized and treated to avoid kidney damage. y Nurses in all settings need to be alert to S/S of renal dysfunction in the elderly.
16

Gerontologic considerations cont.

y The elderly are frequently on multiple prescription and

over-the-counter medications. y Alterations in renal blood flow, glomerular filtration and renal clearance increase the risk for medicationassociated changes in renal function-precautions are indicated for all medications. y Dehydration can compromise marginal renal function and lead to renal failure so when elderly are on diuretics or are having diagnostic testing or procedures they need to have close monitoring.
17

Nephrosclerosis
y Hardening of the renal arteries y Caused by prolonged hypertension and diabetes.

y Major cause of CKD and ESRD

18

Pathophysiology of Nephrosclerosis
y Two types: y Malignant (accelerated) often associated with significant hypertension (DIASTOLIC BP > 130 mm Hg) y Usually occurs in young adults, twice as often in men as in women. y Damage occurs from patchy necrosis of the renal parenchyma, fibrosis occurs and glomeruli are destroyed y Progresses rapidly: without dialysis more then half of patients die within a few years from uremia (an excess of urea and other nitrogenous waste in the blood) y Benign: found in older adults, associated with atherosclerosis and hypertension
19

Assessment and Diagnostic Findings

y Symptoms are rare early in the disease y Protein and casts are seen in the urinalysis y Renal insufficiency and associated symptoms occur

late in the disease

20

Medical Management
y Aggressive antihypertensive therapy

y An angiotensen-converting enzyme (ACE) inhibitor

alone or in combination with other antihypertensive medications significantly reduces the incidence
y Why an ACE inhibitor?

21

Primary Glomerular Disease

y Diseases that cause destruction of the glomerulus are the 3rd most common cause of stage 5 CKD. y Antigen-antibody complexes form in the blood and become trapped in the glomerular capillaries y An inflammatory response ensues y Clinical manifestations of glomerular injury include y Proteinuria y Hematuria y GFR, sodium excretion y Edema y Hypertension
22

Acute Nephritic Syndrome

y The clinical manifestation of glomerular inflammation

y Glomerulonephritis is an inflammation of the

glomerular capillaries that can occur in acute and chronic forms

23

Pathophysiology
y Primary glomerular diseases include: y Postinfectious glomerulonephritis y Rapidly progressive glomerulonephritis y Membrane proliferative glomerulonephritis y Membranous glomerulonephritis
Causes of postinfectious glomerulonephritis are group A betahemolytic streptococcal infections of the throat that precedes the onset of glomerulonephritis by 2-3 weeks. Impetigo and acute viral infections , such as URI, mumps, varicella zoster virus, Epstein-Barr virus, hepatitis B and HIV infection
24

Sequence of Events in Acute Nephritic Syndrome

1. Antigen (group A beta-hemolytic streptococcus) 2. Antigen-antibody product 3. Deposition of antigen-antibody complex in glomerulus 4. Increased production of epithelial cells lining glomerulus 5. Leukocyte infiltration of the glomerulus 6. Thickening of the glomerular filtration membrane 7. Scarring & loss of glomerular filtration membrane 8. Decreased glomerular filtration rate (GFR)
Pg 1315 Brunner

25

CLINICAL MANIFESTATIONS
y Hematuria y Edema y Azotemia (an abnormal concentration of nitrogenous wastes in the blood) y Proteinuria (excessive e protein in the urine), this is caused by increased permeability of the glomerular membrane y Hypoalbuminemia, hyperlipidemia, & fatty casts in the urine y BUN & creatinine may increase as urine output decreases

26

Assessment & Diagnostic Findings

y Kidneys become large and edematous y Patients with and IgA mediated nephropathy have

elevated serum IgA levels

y Electron microscopy & immunofluroescent analysis

help identify the nature of the lesion, a kidney biopsy may be needed for definitive diagnosis.

27

Diagnostic Findings
y Patient improvement is identified by: y Increased urinary output y Protein & sediment in the urine decrease y Prognosis varies from full recovery to insidious development of chronic glomerulonephritis. y Some patients developed severe uremia(an excess of urea and other nitrogenous wastes in the blood) within weeks and require dialysis for survival.

28

Complications of Acute Glomerulonephritis

y Hypertensive encephalopathy: treatment is to

reduce the blood pressure without compromising renal function y Heart failure y Pulmonary edema Without treatment ESRD quickly develops-crescentshaped cells accumulate in the Bowman's capsule , disrupting the filtering surface. Treatment is plasmapheresis (plasma exchange) , high dose corticosteroids, and cytotoxic agents to reduce inflammatory response.
29

Medical Management of Acute Glomerulonephritis

y Treat Symptoms to minimize renal damage y Treat complications promptly y Treatment may include: y Corticosteroids y Manage hypertension y Control proteinuria y Treat underlying infections (streptococcal-penicillin is the drug of choice) y Dietary restrictions: protein with renal insuffiency and BUN. Restrict Na with CFH, HTN, edema
30

Nursing Management
y Hospital Care y Carbohydrates are provided liberally to provide energy and reduce the catabolism of protein. y I&O y Fluid is given based on daily weights and fluid losses
Insensible fluid loss is estimated: 300 ml from lungs, 600 ml from skin Proteinuria and microscopic hematuria may persist for months
y

Focus on patient education about the disease process, laboratory values and home care management
31

Promoting Home & Community Based Care

y Education is directed toward symptom management

and monitoring for complications y Fluid and dietary restrictions must be reviewed to avoid worsening of edema and hypertension.

32

Chronic Glomerulonephritis
y Chronic Glomerulonephritis may be caused by

repeated episodes of acute nephritic syndrome, hypertensive nephrosclerosis, , chronic tubulointerstitial injury or hemodynamically mediated glomerulosclerosis (decreased renal blood flow)

33

Pathophysiology Chronic Glomerulonephritis

y Kidneys reduced in size (replaced by fibrous tissue)

y Cortex layer shrinks to 1-2 mm in thickness. Bands of

scar tissue distort the remaining cortex making the surface rough and irregular.

34

Clinical Manifestations
y Many patients have no symptoms and the condition is

discovered when hypertension or elevated BUN and creatinine levels are detected. y Many patients report general symptoms of loss of weight and strength, increasing irritability, and increased nocturia. y Headaches, dizziness and gastrointestinal disturbances are also common y As the disease progresses signs of CKD and chronic renal failure may develop
35

Clinical Manifestations cont.

Patient appears poorly nourished Yellow-gray pigmentation of the skin Periorbital and dependent peripheral edema BP may be normal or severely elevated Retinal findings include: hemorrhage, exudates, narrowed arterioles y Anemia causes pale mucous membranes y Cardiomegaly, a gallop rhythm, distended neck veins and other S/S of hear failure maybe present y Crackles may be heard in the lung bases
y y y y y
36

Assessment and Diagnostic Findings

y Urinalysis Fixed Specific gravity of 1.010
y y

Proteinuria Urinary casts (protein secreted by damaged kidney tubules) As renal failure progresses the GFR falls below 50mL/min and the following changes occur:

37

Changes associated with a GFR 50mL/min

y Hyperkalemia y Metabolic acidosis from decreased acid secretion by the kidney y y y y y y

and inability to regenerate bicarbonate Anemia secondary to decreased erythropoietin (production of RBC s) Hypoalbuminemia with edema secondary to protein loss through the damaged glomerular membrane serum phosphorus due to decreased renal secretion of phosphorus serum calcium level (calcium binds to phosphorus to compensate for elevated phosphorus levels) Mental status changes Impaired nerve conduction due to electrolyte abnormalities and uremia.
38

Assessment and Diagnostic cont.

y CXR may show cardiac enlargement and pulmonary

edema y EKG-normal to evidence of left ventricular hypertrophy associated with hypertension and S/S associated with electrolyte imbalances such as tall, tented or peaked T waves associated with hyperkalemia y CT and MRI will show a decrease in size of the renal cortex

39

Medical Management of Chronic Glomerulonephritis

y Management of the symptoms guides the treatment: y Hypertension -restrict sodium and water intake, administer antihypertensive agents y Daily weights and diuretic medications to treat fluid overload y Proteins of high biologic value (eggs, dairy, meats) provide good nutrition-adequate calories are provided to spare protein to be used for tissue growth and repair y UTI s are treated promptly to prevent further renal damage y Dialysis may be initiated early in the disease to keep the patient in optimal physical condition, prevent fluid and electrolyte imbalances and to minimize the risks of complications of renal failure
40

Nursing Management of Chronic Glomerulonephritis

y Monitor the patient for common fluid and electrolyte

imbalances associated with renal disease. y Report changes in electrolyte status, cardiac and neurologic status promptly. y Anxiety levels are very high for both the patient and the family-provide emotional support and encourage them to verbalize their concerns, have their questions answered and explore their options.

41

Promoting Home and Community Based Care

y The nurse has a very important role in teaching patients and

families about the risks associated with noncompliance. y Follow up exams are essential- lab values are essential y Teaching dietary restrictions and providing literature and other resources for enhancing self care strategies is a very important nursing function. y The patient is instructed to inform all healthcare providers about the diagnosis of glomerulonephritis so that pharmacological therapy is based on altered renal function. y The National Kidney Foundation is an excellent source of valid evidence based educational materials http://www.kidney.org/
42

Nephrotic Syndrome
y Nephrotic syndrome is a type of renal failure

characterized by increased glomerular permeability and is manifested by massive proteinuria

43

Pathophysiology of Nephrotic Syndrome

y Occurs with many intrinsic renal diseases and

systemic diseases that cause glomerular damage.

y It is a constellation of clinical findings that result from

glomerular damage

44

Pathophysiology of Nephrotic Syndrome

Damaged glomerular capillary membrane Loss of Plasma protein (albumin) Stimulates synthesis of lipoproteins Hyperlipidemia Hypoalbuminemia
Decreased oncotic pressure Generalized Edema Activation of reninangiotensin system

Sodium retention Edema

45

Clinical Manifestations of Nephrotic Syndrome

y Edema-usually soft and pitting occurs around the eyes

(periorbital), in dependent areas (sacrum, ankles and hands), and in the abdomen (ascites)
y Irritability, malaise and headache are also common

46

Assessment and diagnostic Findings of nephrotic syndrome

y Proteinuria (predominately albumin exceeding 3.5

grams per day) is the hallmark of the diagnosis of nephrotic syndrome.

y Electrophoresis and immunoelectrophoresis may be

preformed on the urine to categorize the type of proteinuria

y A needle biopsy is needed to confirm the diagnosis

47

Complications of Nephritic Syndrome

y Infection (due to deficient immune response) y Thromboembolism (especially in the renal vein) y Pulmonary emboli y ARF due to hypovolemia y Accelerated atherosclerosis due to hyperlipidemia

48

Medical Management Nephrotic Syndrome

y The aim of treatment is to eliminate the underlying

disease state causing the proteinuria, thereby slowing the progression of CKD and relieving symptoms. y Diuretics for edema y Ace inhibitors to reduce proteinuria y Lipid lowering agents for hyperlipidemia

49

Nursing Management of Nephrotic syndrome

y Early in the disease nursing care is similar to that of

patients with glomerulonephritis y Progression of the disease may case ESRD and the care is then focused as such. y Patients with nephrotic syndrome need adequate teaching so that they understand the importance of compliance with medical regime and diet to keep the disease from progressing for as long as possible. y Patients must understand the importance of reporting changes in their condition to their healthcare provider.
50

Polycystic Kidney Disease

y PKD is a genetic disorder characterized by the growth of numerous cysts in the kidneys. y The cysts destroy the nephrons y The kidneys enlarge and the cysts replace the normal structures and destroy function leading to Kidney failure. y PKD and cystic diseases are the 5th leading cause of kidney failure. y Two major inherited forms of PKD exist: y Autosomal Dominant-90 % of cases develops between 30-40 years of age y Autosomal Recessive- rare begins early in life or in utero
51

Clinical Manifestations PKD

y S/S of PKD result from loss of renal function and the increasing size of the kidneys as the cysts grow. y About 50% of autosomal dominant PKD patients progress to CKD stage 5 and require renal replacement therapy y Renal damage can result in: y Hematuria y Polyuria y Hypertension y Renal calculi y Urinary tract infections y Proteinuria y Abdominal fullness and Flank pain due to the increased size
52

Assessment and Diagnostic Findings of PKD

y Genetic disease- careful family history y Palpation of the abdomen will reveal enlarged cystic

kidneys y Ultrasound of the kidney

53

Medical Management of PKD

y PKD has no cure and treatment is supportive. y Blood pressure control y Pain control y Antibiotics to treat infections y Renal replacement therapy y Genetic testing and counseling may be indicated After we already began the genetic testing, I began reading more about PKD and that is about the time I found the PKD Foundation website. I would caution that if I knew the facts that I have since learned, I am not so sure we would have agreed to do the genetic testing, and I fault all the doctors involved for not providing more genetic counseling before we did this. First, even if either of us does test positive, our "non symptomatic" case may be very different than our daughters. If we have a positive diagnosis in our medical records, we may have more difficulty in securing medical or life insurance in the future, and in reality, this will not accurately predict our daughter s outcome.

54

Renal Cancer
y Renal cancers account for 3% of cancers in adult men

and 2% of cancers in adult women in the U.S. ( ) y Risk Factors for Renal Cancer
Society 2009

American Cancer

y Gender : affects men more than women y Tobacco use y Occupational exposure to industrial chemicals, such as

petroleum products, heavy metals, and asbestos y Obesity y Unopposed estrogen therapy y PKD
55

Clinical Manifestations
y May be palpable as abdominal masses y Classic S/S that occur in only about 10% of patients y Hematuria y Mass in the flank y Pain y Symptoms from metastatic disease may be the first manifestations of renal tumors and include unexplained weight loss increasing weakness anemia
56

Assessment & Diagnostic Findings

y IV Urography y Cystoscopy y Renal angiograms y Ultrasound y CT scan

57

Medical Management
y Eradicate the tumor before metastasis occurs y Surgical Management: Nephrectomy y Renal Artery Embolization: in patients with metastatic disease the renal artery is occluded to impede the blood flow to the tumor and kill tumor cells. This decreases local blood supply making removal of the kidney easier. It also stimulates an immune response because infarction of the renal cell carcinoma releases tumor cell antigens that enhance the patients response to metastatic lesions. The procedure may also reduce the number of tumor cells released into the circulation during surgical manipulation.
58

Pharmacologic Therapy
y Renal cell carcinoma is refractory to most

chemotherapeutic agents y Treatment with biologic response modifiers such as interlukin-2 is effective when used in combination with lymphokine-activated killer cells. y A promising experimental approach is a vaccination to stimulate immune response with autologous tumor cells with Il-2, granulocyte-macrophage stimulating factor

59

Nursing Management
y Postoperative pain control y Maintain all drains, tubes and catheters y If immunosupressent agents are used monitor closely

for infection y Frequent incentive spirometery and deep breathing to prevent atelectasis and other pulmonary complications y Support to cope with the diagnosis and uncertain prognosis

60

Continuing Care
y Follow up care is essential to detect for signs of

metastases y If the patient had surgery a yearly physical examination including a CXR should be done because late metastases is not uncommon y All subsequent symptoms should be evaluated with the possibility of metastases in mind

61

Renal Failure
y Renal failure results when the the kidneys can not

remove the body s metabolic wastes or perform their regulatory functions. y The substances normally eliminated in urine accumulate in the body fluids as a result of impaired renal excretion affecting endocrine, metabolic, fluid and electrolyte and acid base balance. y Renal failure is a systemic disease and is a common final result of many kidney and urinary tract diseases. y Deaths from renal failure continue to rise.
62

Acute Renal Failure

y A rapid loss of renal function due to damage to the

kidneys

63

Pathophysiology of ARF
y Pathogenesis of ARF and olgiuria are not always known y Conditions that reduce renal blood flow to the kidney and can impair function: y Hypovolemia y Hypotension y Reduced cardiac output and heart failure y Obstruction of the kidney or lower urinary tract by tumor, blood clot or stone y Bilateral obstruction of the renal arteries or veins y IF THESE CONDITIONS ARE CORRECTED BEFORE THE KIDNEYS ARE PERMINATELT DAMAGED BUN and creatinine levels, olgiuria and other S/S may be reversed
64

Categories of Acute Renal Failure

y Prerenal ARF

this results from any type of condition outside the kidney that impedes blood flow to the renal vasculature (and subsequently causes a decrease in perfusion pressure to the glomerulus and oliguria). Although there is decreased perfusion to the glomerulus and other nephrons; they continue to function normally. With prompt correction of the underlying problem; the kidneys can return to full normal function at this stage.

65

Acute Renal Failure:

y Postrenal ARF

this is caused by a mechanical back up of urine into the renal pelvis. As with prerenal failure, prompt removal of the obstruction will allow the kidneys to return to normal function.

66

Acute Renal Failure

y Intrarenal ARF

y y y y

this results from anything that causes a direct insult to the kidneys (such as infection, glomerulonephritis, hypertension, diabetes). Acute tubular necrosis (ATN) is the most common intrarenal condition and accounts for approximately 75% to 90% of all intrarenal ARF. With ATN the epithelial layers of the nephrons (at the tubular portion of the kidneys) become damaged leading to changes in urine concentration, waste filtration, electrolytes and acid base balance. ATN most commonly occurs due to one of the following mechanisms: Nephrotoxic incident (chemicals can crystallize) Ischemic incident (decreased renal blood flow) Parenchymal damage Obstruction (due to the release of hemolyzed hemoglobin/myoglobin) (transfusion reaction)
67

Causes of ARF
Prerenal Failure:
y Volume depletion resulting from:
y y y

Hemorrhage Renal losses (diuretics, osmotic diuresis) Gastrointestinal losses(vomiting, diarrhea, nasogastric suction) Myocardial infarction Heart Failure Dysrhythmias Cardiogenic shock
68

y Impaired cardiac efficiency resulting from:

y y y y

Causes of ARF continued

Prerenal Failure causes continued: y Vasodilation resulting from:
y Sepsis y Anaphylaxis y Antihypertensive medications or other medications that

cause vasodialation

69

Causes of Intrarenal Failure

y Prolonged Renal Ischemia y Pigment nephropathy (associated with the breakdown of blood cells containing pigments that in turn occlude kidney structures) y Myglobinuria (trauma, crush injuries burns) y Hemoglobinuria (transfusion reaction, hemolytic anemia) y Nephrotoxic agents such as: y Aminoglycoside antibiotics (gentamycin, tobramycin) y Radiopaque contrast agents y Heavy metals (lead & mercury) y Solvents and chemicals (ethylene glycol, carbon tetrachloride, arsenic)
70

Nephrotoxic agents continued

y Nonsteroidal anti-inflammatory drugs (NSAIDs)
y Nonsteroidal anti-inflammatory drugs (NSAIDs) are known to be nephrotoxic

and may be associated with acute renal failure

y Angiotensin converting enzyme inhibitors (ACE

inhibitors)
y Renal impairment is a significant adverse effect of all ACE inhibitors, but the reason

is still unknown. Some suggest it is associated with their effect on angiotensin IImediated homeostatic functions, such as renal blood flow

y Infectious processes such as: y Acute pyelonephritis y Acute glomerulonephritis

71

Causes of Postrenal Failure

y Urinary tract obstruction, including: y Calculi(stones) y Tumors y Benign Prostetic Hyperplasia y Strictures y Blood clots

72

Phases of Acute Renal Failure

y There are four phases of ARF: initiation, oliguria,

diuresis, and recovery

y The initiation period begins with the initial insult and

ends when olgiuria develops. y The olgiuria period :

y

Increased serum concentration of the substances usually excreted (urea, creatinine, uric acid, intracellular cations, potassium and magnesium) The minimal amount of urine needed to rid the body of metabolic wastes products is 400 mL per day. Uremic symptoms appear & life-threatening conditions such as hyperkalemia develop.
73

Phases of Acute Renal Failure

Nonoliguric renal failure is when there is an accumulation of nitrogenous material yet the patient still produces normal amounts of urine (2 L per day or more) This form of ARF most often occurs after exposure to nephrotoxic agents, burns, traumatic injuries, and the use of halogenated anesthetic agents.

74

Phases of ARF
y Diuresis Period: y Gradual increase in urine output y Laboratory values stabalize and begin to return to normal (BUN and serum creatinine decrease) y The patient may still be uremic and may still have uremic symptoms even though the urine output may be normal or even excessive. The patients must be monitored closely during this phase, especially for dehydration. y ( What might dehydration do in this phase?)
75

Phases of ARF
y Recovery Phase: y The phase may take from 3- 12 months y Laboratory values return to the patients normal levels y A permanent reduction in the GFR of 1% to 3 % is common, it is not clinically significant.

76

Clinical Manifestations of ARF

y The patient will appear criticaly ill and lethargic y Dry skin and mucous membranes y CNS symptoms may include: y Drowsiness, headache, muscle twitching and seizures

77

Assessment & Diagnostic Findings of ARF

y Urine volume may be normal or scanty y Hematuria y Low specific gravity (normal value 1.010-1.025) (remember you y y y y y y y

are not clearing the uremic substances) One of the earliest signs of tubular damage is the inability to concentrate urine Renal CT and renal ultrasound are often preformed BUN increases GFR decreases Hyperkalemia Metabolic acidosis: patients can not rid their body of acid waste and additionally the renal buffering mechanisms are lost Decreased serum CO2 combining power and blood pH
78

Assessment & Diagnostic findings of ARF continued

y Increased blood phosphate concentrations y Decreased calcium levels from the compensatory

mechanisms of the elevated phosphate levels and a decreased absorption in the intestine. y Anemia from the decreased erythropoietin production, uremic GI lesions , reduced RBC life span and blood loss from the GI tract

79

Preventing Acute Renal Failure

1. Provide adequate hydration for patients at risk for dehydration including:
y Before, during and after surgery y Patients undergoing intensive diagnostic studies

requiering fluid restriction and contrast agents (barium enema, IVP) especially elderly patients who may have marginal renal reserve.

80

Preventing ARF
y Prevent and treat shock promptly with blood and fluid replacement y Monitor central venous and arterial pressures and hourly urine output y y y y y y y

of critically ill patients to detect the onset of renal failure as early as possible. Treat hypotension promptly Continually assess renal function (urine output and lab values) when appropriate AVOID TRANSFUSION REACTIONS Follow protocols when giving transfusions Detect and treat infections promptly Monitor wounds that may be precursors to sepsis Avoid indwelling urinary catheters when possible Monitor all drugs metabolized or excreted by the kidneys, avoid toxic drug effects

81

Preventing ARF
y Agents that reduce renal blood flow (long term

analgesic use) may cause renal insuffiency y Chronic use of NSAIDs can cause interstitial nephritis
y Patients with cirrhosis, heart failure, advanced age,

preexisting renal disease and simultanous administration of several nephrotoxic agents are at increased risk for ARF. y Radiocontrast induced nephropathy (CIN) is a major cause of hospital -acquired ARF. Patients undergo 1 million radiocontrast procedures in the US annually.
82

Preventing ARF cont.

y A creatinine level of greater than 2 mg/dL puts a

patient at high risk for CIN. y Limiting the patients exposure to nephrotoxic agents and contrast agents will reduce the risk. y Additionally, administration of N-acetylcysteine and sodium bicarbonate before and during the procedures reduces the risk. y Prehydration with saline is considered the most effective method to prevent CIN
83

Gerontological Considerations
y of all patients who develop ARF during

hospitalization are older than 60 years. y Supression of thirst, enforced bed rest and lack of access to drinking water and confusion all contribute to the older patients failure to consure adequate fluids and may lead to dehydration further complicating already decreased renal function. y Also remember poly-pharmacy y (Question increased use of NSAIDs for pain?)
84

Medical Management
y Eliminate the underlying cause y Maintain fluid balance y Avoid fluid excess y When indicated provide renal replacement therapy y Prerenal azotemia is treated by optimizing renal profusion y Postrenal azotemia is treated by relieving obstruction y Intrarenal azotemia is treated with supportive therapy, removal of causative agents, aggressive managemnet of pre and post renal failure and avoiding additional risks
85

Medical Management ARF cont

y Maintain Fluid Balance y Daily weights y CVP measurements y Serum and urine concentrations y Fluid losses y Blood pressure y Replace all fluids lost y Monitor for fluid excess: dyspnes, tachycardia, distended neck veins, lung sounds, edema, ( Mannitol, Lasix)
86

Medical Management cont. (ARF)

y Dialysis may be initiated to prevent complications of

ARF, such as hyperkalemia, metabolic acidosis, pericarditis, and pulmonary edema y Hemodialysis is a procedure where the patients blood circulates through a dialyzer to remove waste products and excess fluid. y Peritoneal Dialysis (PD) is a procedure that uses the peritoneal membrane as the semipermeable membrane to exchange fluid and solutes

87

Pharmacologic Therapy
y Hyperkatemia is the most life-threatening of the fluid

and electrolyte imbalances y Serial serum electrolyte levels are drawn. A potassium level of greater than 5 meq/L can cause EKG changes ( can you tell me what?) y Administration of Kayexalate (sodium polystyrene sulfonate) orally or by retention enema works by exchanging sodium ions for potassium ions in the intestional tract.

88

Pharmacologic Therapy cont.

y If the patient is hemodynamically unstable y IV dextrose 50% (D50) insulin and calcium

replacement may be given to shift potassium back into the cells. y Albuterol sulfate (Ventolin HFA) by nebulizer can laso lower potassium levels by 0.5 to 1.5 meq/L y Both of these methods are temporary so arrangements for dialysis need to be made

89

Pharmacologic Therapy cont.

y Diuretics are often used to control fluid volume, they

have not been shown to improve recovery from ARF. y Medications excreted by the kidneys must be reduced common examples are:
y Aminoglycosides y Digoxin y ACE inhibitors y Magnesium containing agents

90