Elimination

Concepts

• Priority concept for this chapter: Elimination
• Interrelated concepts: Fluid and electrolyte balance; Acid–base balance; Immunity; Pain

Pyelonephritis

• Pathophysiology: bacterial infection that starts in the bladder and moves upward to infect the kidneys
• Acute vs chronic:
  • Acute: active bacterial infection
  • Chronic: repeated or continued upper urinary tract infections; almost exclusively in patients with anatomic urinary tract abnormalities
• Complications: abscesses can develop on kidneys

Etiology and Genetic Risk (Pyelonephritis)

• Acute etiology: results from bacterial infection with or without obstruction or reflux
• Chronic etiology: usually with structural deformities, urinary stasis, obstruction, or reflux
• Common organisms: Escherichia coli or Enterococcus faecalis

Incidence and Prevalence

• Most common in young females who are sexually active
• Common in the second trimester and beginning of the third trimester in pregnant females

Recognize Cues: Assessment (Pyelonephritis)

• History: ask about recurrent UTIs, diabetes, stone disease, GU defects, reduced immunity, kidney function
• Imaging considerations: ensure woman is not pregnant before radiographic imaging
• Physical assessment/signs: inspect flanks and palpate costovertebral angle (CVA) for pain, edema, redness
• Psychosocial assessment: anxiety, embarrassment, guilt

Key Features

• ACUTE PYELONEPHRITIS:
  • Fever; Chills
  • Tachycardia and tachypnea
  • Flank, back, or loin pain
  • Tenderness at CVA
  • Abdominal, often colicky, discomfort
• CHRONIC PYELONEPHRITIS:
  • Hypertension
  • Inability to conserve sodium
  • Decreased urine-concentrating ability, nocturia
  • Tendency to develop hyperkalemia and acidosis
  • Nausea and vomiting
  • General malaise or fatigue
  • Burning, urgency, or frequency of urination; nocturia
  • Recent cystitis or treatment for UTI

Recognize Cues: Assessment (Cont.)

• Laboratory assessment:
  • Urinalysis
  • Blood cultures
  • WBC count with differential
  • C-reactive protein
  • ESR
  • BUN, creatinine, GFR
• Imaging assessment:
  • KUB or CT
• Other diagnostic assessment:
  • Antibody-coated bacteria in urine
  • Radionuclide renal scan

Analyze Cues and Prioritize Hypotheses

• Priority collaborative problems:
  • Pain (flank and abdominal) due to inflammation and infection
  • Potential for chronic kidney disease (CKD) due to kidney tissue destruction

Planning and Implementation

• Managing pain
• Nonsurgical management: Acetaminophen; antibiotics (IV usually)
• Catheter replacement
• Nutritional changes
• Surgical management: Pyelolithotomy; nephrectomy; ureteral diversion or reimplantation of the ureters
• Preventing CKD: Blood pressure control; nephrology referral

Care Coordination and Transition Management

• Self-management education: drug regimen; adequate fluid intake; disease recurrence; coping mechanisms
• Health care resources: community outreach; interprofessional care

Evaluate Outcomes

• Outcome indicators:
  • Pain is controlled
  • Patient is knowledgeable about disease, treatment, and interventions to prevent or reduce CKD progression

Acute Glomerulonephritis

• Definitions:
  • Primary: involve the kidneys primarily
  • Secondary: kidney involvement is part of a systemic disorder
• Pathophysiology: develops suddenly from an excess immune response within kidney tissues
• Cause: usually infectious

Recognize Cues: Assessment (Acute Glomerulonephritis)

• History: recent infections, illnesses, surgery, systemic diseases
• Physical assessment/signs: edema (facial, eyelids, hands); hypertension (fluid overload); dark urine; oliguria; dysuria

Recognize Cues: Assessment (Cont.)

• Laboratory assessment:
  • Urinalysis: hematuria, proteinuria
  • 24-hour urine collection: total protein
  • Serum albumin: decreased
  • Serum creatinine: elevated
  • BUN: elevated
  • GFR: may be decreased
• Other diagnostic assessment:
  • Kidney biopsy: precise diagnosis if needed

Take Actions: Interventions (Acute Glomerulonephritis)

• Managing infection: appropriate antibiotic therapy; infection control
• Preventing complications: fluid and electrolyte balance; antihypertensive drugs
• Providing education: weight and blood pressure daily; drug regimen/side effects

Chronic Glomerulonephritis

• Course: develops over years to decades
• Symptoms: mild proteinuria, hematuria, hypertension, fatigue, occasional edema
• Cause: exact cause not known

Recognize Cues: Assessment (Chronic Glomerulonephritis)

• History: other health problems; recent infection; fatigue; elimination patterns
• Physical: systemic circulatory overload; lung crackles; uremic symptoms (slurred speech, ataxia, tremors)
• Psychosocial: uncertainty, loss, fear

Diagnostic assessment (Chronic Glomerulonephritis)

• Urinalysis: protein
• GFR: decreased
• Serum creatinine: elevated
• BUN: elevated
• Sodium and phosphate levels
• ABGs: acidosis
• Imaging: kidney biopsy if needed

Take Actions: Interventions (Chronic Glomerulonephritis)

• Slow progression and prevent complications
• Dietary changes; fluid intake; drug therapy
• Ultimately dialysis or transplantation

Nephrotic Syndrome

• Pathophysiology: Glomerular permeability increases; allows larger molecules to pass into urine
• Consequences: massive loss of protein into urine, edema, decreased plasma albumin levels
• Most common cause: altered immunity with inflammation

Interprofessional Collaborative Care (Nephrotic Syndrome)

• Main feature: increased protein elimination with severe proteinuria
• Treatments:
  • ACE inhibitors (ACEIs): decrease protein loss
  • Heparin: reduce vascular defects and improve kidney function
  • Dietary changes: protein may need to be limited
  • Mild diuretics: control edema and fluid retention
  • Sodium restriction: control edema and fluid retention
  • Hydration status: vascular dehydration common

Nephrosclerosis

• Definition: degenerative disorder from changes in kidney blood vessels
• Pathophysiology: nephron blood vessels thicken; narrowed lumens; decreased kidney blood flow
• Associations: hypertension, atherosclerosis, diabetes mellitus
• Prognosis: may be reversible or progress to ESRD
• Genetic link: APOL1 allele

Interprofessional Care (Nephrosclerosis)

• Hypertension control: ACE inhibitors and diuretics
• Goal: reduce albuminuria

Polycystic Kidney Disease (PKD)

• Genetics: fluid-filled cysts develop in nephrons
• Common clinical features: hypertension, abdominal fullness and pain, cyst bleeding, hematuria, kidney stone formation, infections, systemic disease

Etiology and Genetic Risk (PKD)

• Inheritance:
  • Autosomal-dominant trait or autosomal-recessive trait
  • Autosomal-dominant PKD is the most common inherited kidney disease

Recognize Cues: Assessment (PKD)

• History: family history; pain; constipation; urine changes; hypertension; headaches
• Physical: distended abdomen; flank pain; cyst rupture may cause bright red/cola-colored urine
• Psychosocial: uncertainty, loss, fear

Recognize Cues: Assessment (Cont.)

• Diagnostic assessment:
  • Ultrasonography: primary diagnostic method
  • MRI or CT: tissue oxygenation and inflammation data
  • Urinalysis: may show proteinuria, hematuria, bacteria

Take Actions: Interventions (PKD)

• Blood pressure management: ACEIs
• Pain management: acetaminophen; opioids
• Sodium restriction: less than 2 g/day
• Slowing CKD progression: tolvatpan? (tolvaptan); protein restriction

Renovascular Disease

• Pathophysiology: processes affecting renal arteries narrow lumen; greatly reduce renal blood flow
• Epidemiology: often in people over 50 with sudden onset HTN
• Common causes: atherosclerosis or vascular hyperplasia
• Other causes: thrombosis; renal vessel aneurysms

Recognize Cues: Assessment (Renovascular Disease)

• Key features: significant, difficult-to-control hypertension; poorly controlled diabetes or sustained hyperglycemia; elevated serum creatinine; decreased GFR
• Diagnosis: MRA; renal ultrasound; radionuclide imaging; renal arteriography

Take Action (Renovascular Disease)

• Interventions: tailored to defect type; extent of narrowing; condition of surrounding vessels
• Drug therapy: multiple antihypertensives as needed
• Endovascular techniques: stenting
• Renal artery bypass surgery

Diabetic Nephropathy

• Definition: vascular complication of diabetes mellitus
• Significance: leading cause of chronic kidney disease worldwide
• Severity: related to degree of hyperglycemia
• Management: the same as for CKD

Renal Cell Carcinoma

• Nature: adenocarcinoma of the kidney; most common kidney cancer
• Paraneoplastic syndromes: anemia; erythrocytosis; hypercalcemia; liver dysfunction; hormone changes; hypertension
• Metastasis pattern: adrenal gland, liver, lungs, long bones, or other kidney

Recognize Cues: Assessment (Renal Cell Carcinoma)

• History: age; genetic factors; exposure to heavy metals; weight loss; urinary changes; abdominal pain; fever
• Signs: flank pain; visible blood in urine (late sign); kidney mass
• Skin: pallor/ashen gray appearance; darkening of nipples; gynecomastia in men
• Diagnostics: urinalysis; hematologic studies; serum creatinine; BUN; CT; MRI; ultrasound; kidney biopsy

Take Action: Interventions (Renal Cell Carcinoma)

• Goals: prevent metastasis; manage complications
• Nonsurgical: cryoablation; immunotherapies
• Surgical: nephrectomy (main option)
• Postoperative monitoring: assess for hemorrhage and adrenal insufficiency (hypotension; decreased urine output; altered consciousness)

Kidney Trauma

• Etiology: penetrating wounds, blunt injuries, urologic procedures
• Classification: five grades depending on severity

Recognize Cues: Assessment (Kidney Trauma)

• History: mechanism of injury
• Assess: pain, urine output, circulation
• Diagnostics: urinalysis; H&H; ultrasound; CT; KUB

Take Actions: Interventions (Kidney Trauma)

• Nonsurgical management
• Drug therapy: bleeding prevention or control
• Fluid therapy: restore circulating blood volume
• Interventional radiology: drain collections or embolize area
• Surgical management: angiographic embolization; laparotomy; nephrectomy

Care Coordination and Transition Management (Kidney Trauma)

• Teach how to assess for infection and complications; contact health care provider if symptoms arise

Concepts (Revisited): The priority concept is Elimination; Interrelated concepts: Acid–base balance; Fluid and electrolyte balance; Immunity; Perfusion

Acute Kidney Injury (AKI)

• Pathophysiology: rapid reduction in kidney function leading to failure to maintain waste elimination, fluid/electrolyte balance, and acid–base balance
• Onset: occurs over a few hours to days; typically in the acute care setting
• Definition (current):
  • Increase in serum creatinine by
    $0.3~ ext{mg/dL} ext{ or more within } 48~ ext{hours}$
  • OR increase in serum creatinine to
    $1.5 imes ext{baseline}$
  • OR urine output <
    $0.5~ ext{mL/kg/hr} ext{ for } 6~ ext{hours}$

Etiology (AKI)

• Reduced perfusion to kidneys; damage to kidney tissue; obstruction of urine outflow
• Risk factors: shock; cardiac surgery; hypotension; prolonged mechanical ventilation; sepsis
• Higher risk: older adults or adults with chronic diseases

Causes of AKI (Source categorization)

• PRE-RENAL: Impaired perfusion (Cardiac failure; Sepsis; Blood loss; Dehydration)
• RENAL: Glomerulonephritis; Small-vessel vasculitis; Acute tubular necrosis; Drugs; Toxins; Interstitial nephritis
• POST-RENAL: Urinary calculi; Retroperitoneal fibrosis; Benign prostatic enlargement; Prostate cancer; Cervical cancer; Urethral stricture/valves; Meatal stenosis/phimosis

Health Promotion / Disease Prevention (AKI)

• Promote hydration: drink 2–3 L of water daily for healthy adults
• Avoid exposure to nephrotoxic drugs

Recognize Cues: Assessment (AKI)

• History: changes in urine appearance, frequency, volume; recent surgery, trauma, transfusions, allergic reactions; drug history (antibiotics, NSAIDs, contrast); coexisting conditions (DM, sepsis, PVD, liver disorder)
• Immunity-mediated AKI: influenza, colds, gastroenteritis, sore throats
• Anticipate AKI after hypotension or shock
• History of urinary obstructive problems

Recognize Cues: Assessment (Cont.)

• Physical: hourly urine output; signs of azotemia and oliguria; fluid overload signs (pulmonary crackles, edema, confusion, dyspnea); vital signs for hypoperfusion/hypoxemia

Laboratory assessment (AKI)

• Creatinine, BUN: elevated
• Blood electrolytes: abnormal
• Urine tests: abnormal specific gravity; sediment
• Imaging: US, CT, pelvis/kidneys KUB; MAG3 nuclear scan
• Kidney biopsy: uncertain diagnosis or immune response possible

Take Action (AKI)

• Avoid hypotension; maintain normal fluid balance
• Reduce exposure to nephrotoxic agents and drugs
• Frequent laboratory monitoring; monitor I/O
• Drug therapy: diuretics; fluid challenges
• Nutrition: dietician consultation for protein and calorie needs; supplements; parenteral routes as needed

Kidney Replacement Therapy (KRT)

• Definition: supportive strategy to purify blood, substituting for kidney function
• Indications: symptomatic uremia; persistent or rapidly rising hyperkalemia; severe metabolic acidosis; fluid overload impairing tissue perfusion
• Modalities: Intermittent and continuous hemodialysis (HD); peritoneal dialysis (PD)
• Access: temporary central venous catheter needed for initial access

Chronic Kidney Disease (CKD)

• Pathophysiology: progressive, irreversible disorder lasting > 3 months; can progress to end-stage kidney disease (ESKD)
• Terminology: Azotemia = buildup of nitrogen-based wastes in blood; Uremia = azotemia with symptoms (muscle cramps, vomiting, edema, paresthesias)

Stages of CKD

• Five stages by GFR category:
  • Stage 1: GFR > 90
  • Stage 2: GFR 89–60
  • Stage 3: GFR 59–30
  • Stage 4: GFR 29–15
  • Stage 5: GFR < 15

Body System Changes in CKD

• Kidney: abnormal urine production; extracellular volume overload
• Metabolic: disrupted fluid/electrolyte and acid–base balance
• Cardiac: hypertension; hyperlipidemia; heart failure; pericarditis
• Hematologic and immunity: anemia; infection risk
• GI: halitosis; stomatitis; peptic ulcers
• Cognitive and functional: mental status changes; risk of drug toxicity

Etiology and Genetic Risk (CKD)

• >100 different disease processes can cause progressive kidney function loss
• Two main causes leading to dialysis or transplantation: Hypertension and Diabetes mellitus

Incidence and Prevalence (CKD)

• About 15% of adults in the U.S. have CKD
• Most with CKD do not know they have it

Health Promotion / Disease Prevention (CKD)

• Control diseases that lead to CKD
• Dietary adjustments: sodium, protein, cholesterol restriction
• Weight management: BMI 22–25 kg/m^2
• Smoking cessation; exercise 30–60 minutes most days; limit alcohol

Recognize Cues: Assessment (CKD)

• History: weight changes; medical history of kidney/urologic origin; drug use; dietary habits; GI/GU problems; energy changes; family history
• Physical: neurologic changes (lethargy, seizures, neuropathy, fatigue); CV signs (fluid overload, HTN, heart failure, pericarditis, potassium dysrhythmias); respiratory symptoms (dyspnea); hematologic signs (anemia, abnormal bleeding); skeletal signs (osteodystrophy, calcium absorption issues); urine changes (oliguria, color changes, proteinuria, hematuria); skin signs (jaundice, pruritus, uremic frost, bruises)

Recognize Cues: Assessment (Cont.)

• Psychosocial: anxiety, fear; coping mechanisms; may need mental health support

Laboratory & Imaging (CKD)

• Lab: Creatinine, BUN; electrolytes (Na, K, Ca, P, bicarbonate); Hemoglobin/hematocrit; GFR; Urinalysis
• Imaging: X-ray findings (not always abnormal); Kidney or CT scans

Analyze Cues & Prioritize Hypotheses (CKD)

• Priority collaborative problems: Fluid overload; Decreased cardiac function; Weight loss; Potential for injury; Potential for psychosocial compromise

Generate Solutions and Take Actions (CKD)

• Managing fluid volume: diuretics; fluid restriction; daily weights
• Improving cardiac function: ACEIs, calcium channel blockers (CCBs); BP monitoring
• Nutrition: dietician referral; protein/sodium/potassium/phosphate restriction; vitamin/mineral supplementation
• Preventing injury: transfer techniques; drug toxicity/levels; bone monitoring; infection risks; bleeding precautions
• Minimizing psychosocial compromise: sleep improvement; disease education; manage depression/anxiety

Hemodialysis

• Purpose: remove excess fluids and waste; restore fluid/electrolyte and acid–base balance
• Mechanism: pass patient’s blood through an artificial semipermeable membrane
• Indication: stage 4–5 CKD with life-threatening manifestations or persistent discomfort

Hemodialysis Patient Selection

• Criteria: symptoms due to disturbances of fluid/electrolyte and waste/toxin accumulation
• Common trigger: uremic symptoms (nausea, vomiting, confusion, seizures) or severe bleeding
• Other criteria: irreversible kidney failure when other therapies are unacceptable/ineffective; no disorders complicating HD; patient values and ability to maintain roles at home/work/school

Hemodialysis Setting and Procedure

• Setting: hospital-based if recently started or complicated; otherwise community/freestanding center
• Process: blood and dialysate flow in opposite directions across a semipermeable membrane; diffusion removes wastes and reestablishes balance; duration is preset

Hemodialysis System

• Components: dialyzer, dialysate, vascular access, HD machine
• Safety: built-in monitoring of vital signs, flows, pressures, delivered dialysis dose, plasma volume, and temperature

Hemodialysis Anticoagulation and Vascular Access

• Anticoagulation: heparin delivered into the circuit; remains active 4–6 hours after dialysis
• Vascular access: internal AV fistula or AV graft for long-term HD
• AV fistula: surgically connect an artery to a vein; maturation ~2–3 months or longer
• AV graft: synthetic material; used if fistula does not develop or complications prevent use

AV Fistula vs AV Graft (Diagrammatic description)

• Fistula: native connection between artery and vein (e.g., radial artery to cubital vein)
• Graft: synthetic conduit (e.g., loop/cubital/branchial configurations)

Caring for the Patient with an AV Fistula or AV Graft

• Do not take blood pressure readings on access limb
• Do not perform venipunctures or IVs in access limb
• Palpate for thrills and auscultate bruits every 4 hours while awake
• Assess distal pulses and limb circulation
• Elevate affected limb after surgery; encourage ROM exercises
• Monitor for bleeding at needle sites and infection signs
• Do not carry heavy objects or place pressure on the access arm; avoid sleeping with weight on it

Vascular Access Complications

• Thrombosis: most frequent complication; can be reopened with thrombolytic drugs
• Infections from cannulation
• Aneurysms: from repeated needle punctures
• Ischemia/steal syndrome: reduced arterial flow to tissues distal to fistula
• High-output heart failure risk due to shunted blood

Temporary Vascular Access

• Special catheters for immediate HD
• Sites: subclavian, internal jugular, or femoral vein
• Size: much smaller; 4–8 hours session duration
• Subcutaneous devices may provide temporary access; mechanism opens with needle insertion and closes after removal

Hemodialysis Nursing Care

• Determine which drugs to hold until after HD
• Monitor for post-dialysis side effects (hypotension, headache, N/V)
• Record vital signs and post-dialysis weight
• Avoid invasive procedures for 4–6 hours after dialysis due to anticoagulation

Hemodialysis Complications

• Hypotension; dialysis disequilibrium syndrome
• Cardiac events in patients with cardiovascular disease
• Reactions to dialyzers (dialyzer reactions) during first-time filter use

Peritoneal Dialysis (PD)

• Mechanism: exchanges in the peritoneal cavity; slower than HD; less common today (<10% of dialysis population)

Peritoneal Dialysis: Patient Selection and Procedure

• Selection: good for those who cannot tolerate anticoagulation or have vascular access problems; provides flexibility
• Procedure: Silastic catheter placed in the abdomen
• Process: fill 1–2 L dialysate by gravity over 10–20 minutes; dwell time prescribed; drain by gravity into drainage bag

Peritoneal Dialysis: Process and Additives

• Diffusion and osmosis across peritoneal membrane
• Dialysate may include heparin to prevent catheter/ tubing clotting
• Dialysate may contain potassium and antibiotics as needed

Peritoneal Dialysis Complications

• Peritonitis: major complication; often due to connection site contamination
• Pain during inflow initially
• Exit-site and tunnel infections
• Poor dialysate flow often related to constipation
• Fibrin clot formation after catheter placement or with peritonitis
• Other: bleeding, bowel perforation

Nursing Care for Peritoneal Dialysis

• Baseline vital signs; monitor weight (pre/post drain) to assess dry weight
• Monitor catheter exit-site dressings for wetness during procedure
• Monitor blood glucose in patients absorbing glucose from PD
• Maintain accurate inflow and outflow records for fluid balance

Kidney Transplantation

• Candidate selection criteria: advanced kidney disease; reasonable life expectancy; medically and surgically fit
• Waiting list: in the U.S. generally when GFR < 20 mL/min
• Donors: living donors (best graft survival); non-heart-beating donors; cadaveric donors

Kidney Transplantation Procedure

• Preoperative care: immunologic studies; dialysis 24 hours before surgery; blood transfusion before surgery
• Operative procedures: donor status-dependent; failed kidneys may be left in place unless infected or enlarged/painful
• New kidney is placed in the right or left anterior iliac fossa

Kidney Transplantation Procedure (Cont.)

• Postoperative care: urologic management with catheter for decompression; hourly urine output for 48 hours; continuous bladder irrigation if prescribed; monitor input/output; urine may be pink-tinged initially
• Complications: rejection (most serious); thrombosis; renal artery stenosis (may require balloon angioplasty); wound problems/strictures

Types of Kidney Transplant Rejection

• Acute rejection: 1 week to any time after surgery; oliguria or anuria; increased BP; enlarged, tender kidney
• Chronic rejection: months to years; gradual rise in BUN/serum creatinine; electrolytes changes; fatigue
• Hyperacute rejection: within 48 hours; fever and hypertension; pain at transplant site

Care Coordination and Transition Management (Transplant)

• Home care: dietary needs; vascular access needs; equipment
• Self-management education: drug therapy; potential complications
• Resources: support groups; community support

Evaluate Outcomes (Overall CKD/Transplant Context)

• Maintain appropriate fluid and electrolyte balance
• Maintain adequate nutritional status
• Avoid infection at vascular access site
• Use effective coping strategies
• Prevent or slow systemic complications of CKD (osteodystrophy)
• Assess for absence of anxiety or depression

Health Promotion / Disease Prevention (AKI and CKD contexts)

• Maintain hydration; limit nephrotoxic exposure
• Manage chronic diseases (HTN, diabetes) to prevent CKD progression

Key Formulas and Numerical References

• AKI diagnostic thresholds:
  • ext{Increase in serum creatinine}
    riangle ext{Cr} \ge 0.3~ ext{mg/dL in } 48~ ext{hours}
  • OR $ext{Cr}_{ ext{baseline}} imes 1.5$ or more
  • Urine output: V_{ ext{urine}} < 0.5~rac{\text{mL}}{\text{kg}\cdot \text{hour}} ext{ for } 6~\text{hours}
• CKD stages (GFR, mL/min):
  • Stage 1: GFR > 90
  • Stage 2: GFR 89–60
  • Stage 3: GFR 59–30
  • Stage 4: GFR 29–15
  • Stage 5: GFR < 15
• Sodium restriction (CKD): less than 2 g/day
• PD fill volumes: usually 1–2 L of dialysate per exchange
• Dialysate anticoagulation duration: heparin remains active 4–6 hours after dialysis
• Immunosuppression-related considerations (transplant): clinical vigilance for rejection, thrombosis, stenosis