Adult GI/GU Flashcards
Renal Replacement Therapies (Dialysis)
Indications
Indicated for AKI or ESRD as characterized by:
- Severe fluid and electrolyte imbalances (potassium, calcium/phosphorus inverted)
- Elevated serum creatinine
- Elevated serum potassium
- Acidosis
- Presence of uremic manifestations: N/V, fatigue, anorexia, weight loss, muscle cramps, pruritus, or changes in mental status (build up of waste)
- Patients with a GFR <10 mL/min
Continuous Renal Replacement Therapy (CRRT)
Indications
Vascular Access
Process
Indications
- Indicated for acutely ill patients with AKI or patients with severe fluid overload who are hemodynamically unstable**
Vascular Access
- Central venous double lumen catheter (CRRT) OR
- Single-lumen central venous line in combination with an arterial line
Process
- Blood from the patient flows through a highly permeable hemofilter which removes water and solutes, collectively termed ultrafiltrate
- As the blood returns to the patient, replacement fluid and electrolytes can be infused to replace the volume and solutes the patient needs to maintain stability
Continuous Renal Replacement Therapy (CRRT)
Complications
Mechanical Complications
Vascular access-related complications
- Bleeding, hematoma, thrombosis
- Infection
Extracorporeal circuit complications (filter complication)
- Premature filter clotting
- Air embolism
Hemodynamic Complications
- Hypothermia
- Hypotension: adjust the rate of the CRRT
Metabolic Complications
Acid-base abnormalities
- Metabolic acidosis - most likely
- Metabolic alkalosis
Electrolyte abnormalities
- Hypernatremia
- Hypophosphatemia
- Hypomagnesemia
- Hypocalcemia
- Hypokalemia
Pharmacological Complication -
- Rate changes -> kidneys filter medications
- Challenging antimicrobial dosing
Nursing Assessment for CRRT**
Frequent/hourly vital signs (usually q15 min, q30 min)
Hourly assessment of volume of filtrate (what is being filtered out)
- Increases may require modifications to maintain hemodynamic stability
- Decrease may indicate a clot or obstructed filter
Hemodialysis (HD)
Vascular Access**
Central venous double lumen catheter in the subclavian or internal jugular vein
- Used on a short-term basis (in patients with AKI requiring intermittent HD OR when waiting to secure long-term access)
- High risk of infection
Arteriovenous (AV) fistula (most common)
- Created by surgical anastomosis of an artery and vein (usually radial artery and cephalic vein) in the nondominant arm
- Fistula must “mature” prior to being suitable for dialysis, which can take several weeks
- Will usually use a central line while the AV is maturing
- Has a bulging and tortuous appearance under the skin
Arteriovenous (AV) graft
- A prosthetic graft is inserted between an artery and vein in the nondominant arm
- May be used more quickly than AV fistulas, but do not last as long and are more prone to infection
Hemodiaylsis
Process
Uses diffusion and filtration to remove waste products, electrolytes, and excess water from the body
Usually completed 3 times/week (M/W/F or T/Th/Sa) for 3-5 hours/session
Hemodialysis
Complications and treatments
Hypotension
- Due to the rapid removal of fluid from the vascular compartment
- Signs: light-headedness, nausea/vomiting, seizures, vision changes, chest pain r/t cardiac ischemia
- Treatment: decrease rate of fluid removal and replace fluid with IV NS
Muscle cramps (hypokalemia), Headache, Nausea, Dizziness, and Malaise
- Due to the rapid removal of electrolytes and water
- Treatment: reduce filtration rate or infuse NS bolus
Bleeding
- Due to altered platelet function associated with uremia and the use of heparin during the procedure
Systemic infection
- Higher risk of developing Hepatitis B, Hepatitis C, cytomegalovirus, and HIV
Dialysis-associated dementia
- Progressive, potentially incurable neurologic complication
- Thought to be due to aluminum present phosphate binders found in the dialysate solution as well as in oral phosphate binders
Dialysis disequilibrium syndrome
- Due to the very rapid changes in the composition of the extracellular fluid, causing a shift of fluid into the brain
- Signs of increased ICP: nausea/vomiting, confusion, restlessness, headaches, twitching, seizures
- Treatment: slow rate of dialysis and infuse hypertonic saline solution, albumin, or mannitol to draw fluid from the brain cells
Localized Complications
- Localized infection of the AV fistula or graft, can lead to systemic septicemia
- Clotting of AV fistula or graft, can lead to embolization
Nursing Assessment for Hemodialysis**
- Assess central venous double lumen catheter for evidence of bleeding or infection
- Monitor for drainage, surrounding erythema or edema, excessive pain
- Functional AV fistulas and grafts should have a palpable pulsation (“thrill”) and a bruit noted on auscultation
- Neurological assessment (dialysis disequilibrium syndrome)
- Systems assessment post-dialysis
- Monitor for muscle cramps, headache, nausea, dizziness, and malaise
Peritoneal Dialysis (PD)
Indications
Contraindications**
Indicated for patients who desire more control, who have had vascular access problems or who respond poorly to HD with hemodynamic instability
Contraindications
- History of multiple abdominal surgeries or chronic abdominal conditions (Crohns)
- Recurrent abdominal wall or inguinal hernias (increased abdominal pressure)
- Obesity with a large abdominal wall (lots more space for catheter to become dislodged or kinked)
- Pre-existing back problems or vertebral disease (weight of fluid will make back problems worse)
- Severe COPD (fluid filled cavity will push up lungs)
Peritoneal Dialysis (PD)
Access
Process
Access
- Permanent indwelling PD catheter
Process
- The membrane of the peritoneal cavity is used as a dialyzing layer
- Three Phases
1. Fill Phase
- Room-temperature sterile dialysate is instilled into the peritoneal cavity via the catheter
2. Dwell Phase
- Metabolic waste products and excess electrolytes diffuse into the dialysate while in remains in the abdomen
3. Drain Phase
- Gravity drains fluid out of the peritoneal cavity into a sterile bag
Three Forms of Peritoneal Dialysis
Continuous Ambulatory Peritoneal Dialysis (CAPD)
- Dialysate is infused into the abdomen 4-5 times per day with a dwell time of 4-6 hours
- Patients may be ambulatory during the dwell phase
Does not require machines
- If they skip it, it’s the equivalent of missing hemodialysis treatments
Automated Peritoneal Dialysis
- Uses a cycler to perform multiple overnight exchanges
- Machine is programmed to meet individual patient needs
- Allows patient to be dialysis-free during the day
Intermittent Peritoneal Dialysis
- Multiple short dwells utilizing automated technology
- 30-40 exchanges per week (30–60-minute exchanges)
Peritoneal Dialysis
Complications
Peritonitis**
- May result from contamination of the dialysate or tubing OR from bacteria in the intestine migrating into the peritoneal cavity
- Cloudy peritoneal effluent (or yellow/purulent) with an increased WBC count
- Severe abdominal pain, rigid abd pain, fever
- Treatment: antibiotics; may be given orally, IV, or intraperitoneally
- Repeated infections warrant removal of the PD catheter and a switch to HD
Catheter Infection
- Catheter site redness, tenderness, or drainage
- May result in abscess formation (and peritonitis) if not treated promptly and correctly
- Treatment: antibiotics
Abdominal Pain (causes)
- Intraperitoneal irritation from the low pH of the dialysate solution
- Tip of the catheter resting against the bladder, blow or peritoneum
- Accidental infusions of air
- Infusing dialysate too rapidly
- Infusing the dialysate at less than room temperature (cold)
Hyperglycemia and Increased Triglyceride Levels
- Glucose in the dialysate can be absorbed into the bloodstream causing hyperglycemia
- Insulin secreted in response to this hyperglycemia stimulates hepatic production of triglycerides
Outflow Problems (causes)
- Kinks in the catheter
- A fold in the abdomen compressing the catheter
- Migration of the catheter outside the peritoneal cavity
- Constipation or a full colon
Respiratory Compromise
- Repeated upward displacement of the diaphragm may cause atelectasis, pneumonia, and bronchitis
Protein Loss
- Peritoneal membrane is permeable to plasma proteins, amino acids and polypeptides which may result in excess protein loss
Nursing Assessment for Peritoneal Dialysis**
Monitor for complications
Monitor/Measure Abdominal girth
Monitor outflow
- Amount and COLOR
- Look for signs of infection (discolored/purulent outflow)
Acute Glomerulonephritis
Etiology
Patho
Inflammation of the glomeruli in the kidney* *Caused by autoimmune disorders or INFECTION
- Infection: Group A Beta-Hemolytic Streptococcus
- Throat (Strep Throat) or Skin (Impetigo)
*Occurs approximately 10 days after symptoms of infection present
*Most often seen in children and young adults
*Most patients fully recover if treated early
Patho
*Triggered by an immunologic mechanism
- Circulating antigens provoke the development of an antibody response
- Antigen-antibody complexes are deposited in the glomerular capillary walls
- Inflammatory changes in the glomeruli
- Vasoconstriction and decrease in plasma flow
*Glomeruli swell and glomerular capillaries are destroyed, increasing the permeability of the glomerulus basement membrane
- Blood and proteins leak into the urine
Acute Glomerulonephritis
Assessment, Clinical Presentation
- Edema/Fluid retention** (secondary to protein loss)
- Decreased urine output
- Cola colored urine (due to hematuria)**
- Mild hypertension (due to fluid retention)
- Fatigue, HA, pitting edema
Acute Glomerulonephritis
Lab Evaluations
Diagnosis
Lab Evaluation
*Urinalysis
- Protein (+)**
- WBC (+)
- Blood (+)**
* CMP
- Increased BUN
- Increased Creatinine
- Decreased GFR**
- Decreased Albumin
CBC
- Increased WBC
Diagnosis
- Based on history, physical exam, and lab findings
Acute Glomerulonephritis
Complications
Actual
- Fluid overload
- Hypertension
Potential
- If untreated or unresponsive to treatment, may develop acute or chronic kidney disease
Acute Glomeruloenphritis
Treatment
Based on the cause of the disease and the presenting symptoms
*Management of Infection: Antibiotics
- Penicillin**
*Treatment/Prevention of Complications
- Diuretics to treat HTN
- Fluid and sodium restriction
- Low protein diet (to prevent buildup of metabolic waste)
*Modulation of immune response
- Steroids
*Plasmapheresis
- Extracorporeal separation of the blood components to filter out immune complexes
- Filtered plasma is discarded while the RBCs and donor plasma are returned to the patient
*REST!!
Acute Glomeruloenphritis
Nursing Management
Nursing Management
- Monitor VS, Daily Weight, I&O
- Monitor dietary intake
- Administer medications as directed
Patient and Family Teaching
- Disease process
- Use of prescribed medications
- Emphasize medication adherence and completion of antibiotic regimen
- Dietary restrictions
- Infection prevention
Polycystic Kidney Disease
Etiology, Patho
Progressive disorder causing excessive growth of fluid-filled cysts in the kidneys, leading to complications over time!!
*Childhood: Autosomal recessive disorder
- May lead to ESRD as well as severe lung and liver dysfunction
*Adult: Autosomal dominant disorder
- Relatively common
- Lives dormant for many years – usually appears between the ages of 30-40
- Cysts not limited to kidneys – may also be present in liver, spleen, and pancreas
*Often found during workup of hypertension
Pathophysiology
- Genetic disorder that manifests in the cortex and medulla of both kidneys
- Large, thin-walled cysts develop as a result of repeated cell division
- Cysts become large and compress surrounding tissue, destroying underlying renal tissue
- Blood flow and nutrient supply to the kidneys is reduced
Polycystic Kidney Disease
Clinical Presentation, Assessment
- No clinical manifestations in the early stages
- First Symptom: Hypertension** (result of damage to the renal structures)
- Hematuria (due to rupture of cysts)
- Low back or flank pain
- Abdominal pain
- Headache
- Symptoms of obstruction to urinary flow
*UTI
*Increase in urinary frequency
*Urinary calculi - Positive CVA tenderness
Polycystic Kidney Disease
Lab evaluation, Radiologic evaluation, Diagnosis
*Urinalysis
- Blood (+)
- Bacteria (+)
*CBC
- Decreased H/H
CMP
- Increased BUN
- Increased Creatinine
- Increased Potassium
- Decreased Calcium
- Increased Phosphorus
*Genetic Testing
Radiology Evaluation
- Renal Ultrasound: used to evaluate for renal cysts
Inexpensive, non-invasive
- Abdominal CT scan: used visualize renal cysts and to evaluated for other complications related to PKD (i.e., cysts on the liver or other abdominal organs)
Diagnosis
- Often based on family history and presenting symptoms
- Confirmed with imaging (US, CT, etc.)
Polycystic Kidney Disease
Complications
Actual
- Hypertension
- Hematuria (if cysts have ruptured)
Potential
- Renal calculi and recurrent UTIs
- Heart valve abnormalities
- High risk for development of abdominal or cerebral aneurysms
- Liver and other GI organ/tract cysts
- Renal failure!!
Polycystic Kidney Disease
Medical Treatment
HTN Management
- ACE Inhibitors or ARBs
Pain Management
- Non-narcotic medications (Acetaminophen), no NSAIDs, Ibuprofen
- Narcotic medications
- Palliative nephrectomy if pain is too severe
UTI Management
- Antibiotics (rocpehin)
Renal Transplant considered the only curative measure
Polycystic Kidney Disease
Nursing Management
- Monitor VS, Daily weight, I&O
- Dietary Modification: Low potassium, phosphorus, protein, and sodium
- Fluid restriction
- Administer medications as directed
Patient and Family Teaching - Immediately report clinical manifestations of infection!!
- Dietary regimen
- Medication adherence
- Antihypertensives
- Antibiotic regimen completion
Acute Kidney Injury (AKI)
Patho
- Acute, rapid loss** of renal function that, in most cases, is reversible** if addressed in a responsive and timely manner
- Defined as azotemia** (an accumulation of nitrogenous waste products in the blood)
- Oliguria** (urine output of <400 mL/day) may or may not be present
- Patients without oliguria typically recover quicker
Acute Kidney Injury (AKI)
Three major cause categories
- Prerenal: Caused by decreased blood flow to the kidneys (BEFORE kidneys)
- Most common cause of AKI
- Decreased blood flow to the kidney causes the kidney to activate the renin-angiotensin-aldosterone system
- Result is low urine output and increased azotemia
- Ex: Hypovolemia**, decreased cardiac output decreased peripheral vascular resistance and vascular obstruction - Intrarenal Causes: Direct damage to the renal parenchymal tissues, resulting in impaired nephron functioning (IN KIDNEYS)
- Damage occurs as a result of prolonged ischemia, exposure to nephrotoxins (medications – ie., aminoglycoside antibiotics, NSAIDs), contrast dye, hemoglobin released from hemolyzed RBCs, or myoglobin released from necrotic muscle cells
- Acute glomerulonephritis
- Acute tubular necrosis (ATN)** - Postrenal Causes: caused by obstruction in the urinary tract below the kidneys (AFTER Kidneys)
- Obstruction causes reflux of urine into the renal pelvis
- Ex: urinary tract stones**, tumors, benign prostatic hypertrophy (BPH)
Phases of AKI
- Initiating Phase
- Begins with the precipitating event and continues until oliguria develops
- Lasts hours to days - Oliguric Phase
- Characterized by a urine output of <400mL/day that does not respond to fluid challenges or diuretics**
- Lasts up to 14 days or longer (the longer it lasts, the poorer the prognosis)
- Oliguria: <400 ml/day occurs within 1-7 days
- Urinalysis: casts, RBCs, - Diuretic Phase
- Occurs when the cause of the AKI has been corrected.
- Urine output increases rapidly** (even up to 5L per day
- Patient may experience dehydration and electrolyte imbalances because of the significant rapid fluid loss
- Lasts 1-3 weeks - Recovery Phase begins as the kidneys return to normal function
- Lasts from several months – 1 year
AKI
Clinical Presentation, Assessment
Signs of volume overload** due to decreased urine output
- Edema
- Pulmonary edema
- Shortness of breath
- Heart failure
- JVD
- Hypertension
- Chest pain or pressure
Anorexia and nausea
Constipation or diarrhea
Confusion
Seizures
Cues: Low BP, HR elevated, dizziness (lightheadedness), weakness, low urine output, HA, palpitations
AKI
Lab Evaluation
CBC
- Decreased H/H**
CMP
- Increased Potassium**
- Increased Phosphorus**
- Increased BUN**
- Increased Creatinine**
- Decreased Calcium**
- Decreased Sodium
ABG
- Decreased pH (Metabolic acidosis)
AKI
Complications
Fluid overload
Electrolyte imbalances
- Hyperkalemia**
- Can result in life-threatening dysrhythmias (V-fib, V-tach, asystole)
- EKG Changes
- Initial change is peaked T waves**
Worsening hyperkalemia indicated by widening of the QRS complex, loss of the P wave, and presence of the sine wave
AKI
Hyperkalemia Interventions
Stabilization of the myocardial cell membrane
- Calcium chloride or Calcium gluconate**
Intracellular movement of potassium
*IV Glucose followed by IV Insulin**
- Insulin facilitates movement of potassium
- Glucose given first to avoid hypoglycemia (does nothing else)
*Albuterol
- Can help lower K+, drives it into cell
*Bicarbonate**
- Drives K+ into cell
*Total body elimination of potassium
- Kayexalate**
- IV Lasix
- Emergent hemodialysis (central line)
AKI
Medical Treatment (medications, diet, etc)
*Focuses on eliminating the cause, preventing complications, and assisting in recovery
*Medications
- Diuretics: to treat fluid overload
*Nutrition
- Adequate carbohydrate, protein, and fat intake
- Sodium restriction
- Potassium restriction
*Dialysis
- May be considered in the short term
AKI
Nursing Management
Patient/Family Teaching
- Monitor VS, I&O
- Cardiac Monitoring: watch for EKG changes!
- Manage fluid balance
- Administer medications as directed
- Position, ambulation, cough, and deep-breathing exercises
- Monitor food intake
Patient and Family Teaching - Cause and treatment of AKI
- Avoid nephrotoxic meds
Chronic Kidney Disease (CKD)
Etiology, Patho
Progressive, irreversible loss of kidney function
Etiology
*Most common causes are diabetes and hypertension!!
*Other risk factors
- Hyperlipidemia
- Smoking
- Recreational drug use
- Chronic NSAID use
- Obesity
- Glomerulonephritis
- PKD
- Lupus
Pathophysiology
- Characterized by slow increases in BUN and Creatinine; longer onset than AKI
- Typically caused by a long-term disease or medical comorbidities
- May be the result of poorly managed AKI
CKI
Clinical Presentation, Assessment
Alterations in sodium and fluid balance!
- Hypertension
- Heart failure
- Pulmonary edema
Altered potassium excretion!
- Arrhythmias
Impaired Metabolic Waste Elimination!
- Uremia
- Nausea/vomiting
- Anorexia
- Headache
- Lethargy
- Fatigue
- Confusion
- Seizures
Due to altered calcium and phosphorus level!
- Bone breakdown
- Osteodystrophies
Due to endocrine dysfunction!
- Infertility
- Amenorrhea
- Hyperparathyroidism
Due to decreased production of erythropoietin!
- Chronic anemia
Cues: SOB, weakness, N/V, low UOP, confusion, gained 10 lbs in 2 weeks, fatigue
Resp: Kussmaul respirations (indicative of metabolic acidosis), crackles in lower lungs; Cardiac: S3; Abd: slightly distended; Extremities: 2+ edema
CKI
Labs, Radiology, Diagnosis
Lab Evaluation
*CBC
- Decreased H/H**
*CMP
- Decreased Sodium
- Increased Potassium**
- Increased Phosphate**
- Decreased Calcium**
- Decreased CO2
- Increased Creatinine**
- Increased BUN**
ABG
- Decreased pH (acidosis)
Urinalysis
- Increased Urine protein
Radiology Evaluation
- Renal Ultrasound
- Abdominal CT scan
Diagnosis
- Based on consistently elevated creatinine and decreased creatinine clearance
- Stages of CKD: Based on GFR and Protein in the urine
CKI Complications
Fluid Overload
Electrolyte Imbalances
Dysrhythmias
Anemia
Fragile bones – bones that fracture easily
CKI
Treatment
- Medications
- Nutrition
- Medications of concern
Focuses on maintaining remaining kidney function and preventing complications
Hyperkalemia
- Cleared via dialysis or by managing diet
When acutely elevated, decreased with medication therapy (Same as AKI)
Hypertension
- Target BP around 130/80
- Weight loss
- Avoiding alcohol and smoking
- Dietary modifications
- Meds: Diuretics, Beta blockers, CCBs, ACE inhibitors, ARBs
*Anemia
- Target: Hgb 11-12 g/dL and Hct 33-36%
- IV or SubQ Erythropoietin: Watch for HTN
- Oral iron supplements: Monitor for constipation and give stool softeners as needed
- Blood transfusions: Only if patient is actively bleeding or is symptomatic (dyspnea, fatigue, tachycardia, etc)
*Dyslipidemia
- Target: LDL <100 mg/dL, triglyceride <200 mg/dL
- Medication: Statins**
Renal Osteodystrophy
- Manage phosphorus and calcium levels
- Limit dietary phosphorus intake
- Medication: Phosphate Binders** (ie., calcium acetate) *Must be administered with each meal Monitor for constipation and give stool softeners as needed
Hypocalcemia
- Vitamin D and Calcium supplementation
Medication Management
- Patients may have delayed or decreased elimination of medications
- Dosages should be adjusted according to kidney function
*Specific medications of concern:
- Digoxin
- Antibiotics (aminoglycosides, penicillin, tetracycline)
- Pain medications
- NSAIDs
Nutrition
- Protein restriction
- Sodium restriction
- Potassium restriction
- Phosphorus restriction
- Vitamin Supplements
- Calcium
- Vitamin D
- Iron
Renal Replacement Therapy
- Hemodialysis**
- Peritoneal Dialysis**
Surgical Management
- Renal Transplantation
CKI Nursing Management
- Monitor VS, daily weight, I&O
- Cardiac monitoring
- Administer medications as directed
Nutrition management - Protein restriction
- Sodium restriction
- Potassium restriction
- Phosphorus restriction
- Vitamin Supplements
- Calcium
- Vitamin D
- Iron
Patient and Family Teaching - Disease process, progression, complications
- DO NOT miss dialysis appointments
- Dietary restrictions
- Avoid nephrotoxic medications
Renal Transplantation
Post-Op Care
*Evaluation of renal function.
*Transplant recipient requires close attention because the immunosuppressive drug therapy used to prevent tissue rejection impairs healing and increases the risk for infection.
*Assess urine output at least hourly during the first 48 hours.
- An abrupt decrease in UOP may indicate complications such as rejection, acute tubular necrosis (ATN), thrombosis, or obstruction.
*Urine color
- Urine is pink or blood-tinged right after surgery
- Gradually returns to normal over several days to several weeks
- Obtain daily urine specimens for urinalysis, glucose measurement, the presence of acetone, specific gravity measurement, and culture
*Monitor the patient’s fluid status
- Fluid overload can cause hypertension, heart failure, and pulmonary edema.
- Evaluate fluid status by weighing daily, measuring blood pressure every 2 to 4 hours, and strict I & O’s.
Renal Transplantation
Three Types of Rejection
Onset, Clinical Manifestations, Treatment
HYPERACUTE REJECTION
- Onset: Within 48 hours after surgery
- Clinical Manifestations
* Increased temperature
* Increased blood pressure
* Pain at transplant site
- Treatment: Immediate removal of the transplanted kidney
ACUTE REJECTION***
- Onset: 1 week - 2 years postop (Most common in first 2 weeks)
- Clinical Manifestations
* Oliguria or anuria
* Temperature over 100° F (37.8° C)
* Increased BP
* Enlarged, tender kidney
* Lethargy
* Elevated serum creatinine, BUN, potassium levels
* Fluid retention
- Treatment: Increased doses of immunosuppressive drugs
CHRONIC REJECTION
- Onset: Occurs gradually during a period of months to years
- Clinical Manifestations
* Gradual increase in BUN and serum creatinine levels
* Fluid retention
* Changes in serum electrolyte levels
* Fatigue
- Treatment: Conservative management until dialysis is required
Renal Transplantation
Post-Op Complications (besides rejection)
*Acute tubular necrosis (ATN)
- Result of hypoxic damage when transplantation is delayed after kidneys have been harvested.
- May need dialysis until adequate urine output returns and the BUN and creatinine levels normalize.
- Often difficult to distinguish from acute rejection.
*Thrombosis of the major renal blood vessels
- May occur during the first 2 to 3 days after the transplant
- A sudden decrease in UOP may signal impaired perfusion resulting from thrombosis.
*Renal artery stenosis
- May result in hypertension
- The involved artery may be repaired surgically or by balloon angioplasty in the radiology department.
*Infection
Renal Cancer
Etiology, Patho
*Most common type: renal cell carcinoma
*Occurs most often in males 50-70 years of age
*African Americans and American Indians have slightly higher rates
*Risk Factors
- Cigarette/cigar/pipe smoking
- Chewing tobacco
- First degree relative diagnosis
- Obesity
- Hypertension
- Exposure to certain substances (ie., asbestos, herbicides)
Pathophysiology
- Usually found in the cortex or pelvis of the kidney
- Tumors compress underlying tissue which may lead to compromised renal functioning
- Metastasis: Long bones, lungs, liver
Renal Cancer
Assessment, Clinical Presentation
- Most patients are asymptomatic early in the disease
- Classic Triad: flank mass, flank pain, hematuria**
- Weight loss
- Fatigue
- Hypertension
- Fever not related to infection
- Anemia
Assess: Left CVA tenderness, palpable swelling in left flank
Renal Cancer
Radiology Evaluation, Diagnosis
Radiology Evaluation
- Ultrasound: used to differentiate between a solid mass, tumor, and cysts
- CT scan
- MRI
Diagnosis
- Several studies needed (including those above)
- Renal biopsy
- Robson’s System of Staging
Renal Cancer
Complications
Pain
Reduced circulation/kidney perfusion
ESRD
Metastasis
Renal Cancer
Treatment
Medical Management
- Chemotherapy NOT effective**
- Immunotherapy used to boost the immune system to aid in the destruction of cancer cells
- Radiation therapy used as palliative treatment when metastasis is present
Surgical Management
- Typical treatment is a radical nephrectomy**
- Removal of the kidney, adrenal gland, and surrounding tissues
