Altered Urinary and Stool Elimination

General Introduction to Altered Elimination

• Conceptual Approach: This material focuses on the mechanisms of disease regarding urinary and stool elimination, specifically addressing altered states caused by neural, vascular, muscular, and hormonal influences.

• Functional Requirement: For effective elimination, the movement of urine from its production to its exit—as well as the movement of fecal matter—must be both patent and functional.

Altered Urinary Elimination Mechanisms

Altered Motility

• Definition: Characterized by reduced contraction of hollow structures.

• Consequences of Motility Failure:

  • Stasis of Filtrate: Reduced movement promotes the stasis of filtrate within the renal tubules.

  • Stasis of Urine: Stasis in the bladder promotes the growth of bacteria and subsequent infection in the kidneys.

• Effects of Stasis:

  • Altered Reabsorption and Secretion: Leads to increased sodium concentration and low pH.

  • Casts Formation: Stasis leads to the precipitation of urinary fluid components and obstruction.

  • Specific Cast Types and Pathologies:

    • Red Blood Cells (RBCs) in Casts: Indicates glomerulonephritis (inflammation of the glomerulus).

    • Epithelial Cells in Casts: Indicates acute tubular necrosis (sloughing of tubular cells).

    • White Blood Cells (WBCs) in Casts: Indicates pyelonephritis (kidney infection and inflammation).

Altered Neuromuscular Function

• Definition: Impaired neural control of urinary elimination or an inappropriate muscle response, such as failed peristalsis of the renal tubules.

• Impaired Neural Control Factors:

  • Involves neurons within the peripheral and central nervous systems.

  • Disruption in neurotransmitter production and availability.

  • Poor coordination of neural impulses from initiation to action.

• Outcomes of Neuromuscular Alteration:

  • Failure of Stimulus: Leads to limited or absent ability to eliminate urine, resulting in urinary retention.

  • Exaggerated Response: Leads to the premature release of urine, resulting in urinary incontinence.

Altered Perfusion

1. Decreased Perfusion:

   • Causes: Excessive constriction of arterioles, inadequate vascular volume, or obstructed patency of the arterial supply (e.g., an embolism).

   • Effect on Oxygen: Decreased oxygen delivery damages renal structures as they cannot meet metabolic demands.

   • Result: Loss of functional tissue through necrosis, which manifests as pain, bleeding, and obstruction of venous system branches.

2. Enhanced Perfusion:

   • Definition: Increased blood flow causing an additional workload.

   • Consequence: May stress the individual organ system.

Altered Patency or Obstruction

• Definition: The blockage of physiological structures, characterized by a buildup of pressure behind the blockage.

• Immediate Consequences:

  • Blockage of urine flow.

  • Dilation of structures proximal to the obstruction.

  • Injury to renal anatomy.

• Causes of Blockage:

  • Precipitation of substances in smaller lumen structures (e.g., casts).

  • Structural blockage: Polyps or tumors.

  • Mechanical obstructions: Urine precipitation, scar tissue, adhesions, or inflammation.

• Specific Obstructive Conditions:

  • Hydroureter: Accumulation of fluid in the urinary ureter due to complete ureteral obstruction.

  • Hydronephrosis: Increased hydrostatic pressure extending up to the renal pelvis and tubules.

    • Leads to impaired renal function.

    • Fluid escapes from tubules into the surrounding capillary system.

    • Impaired excretion of sodium, urea, and water.

  • Structural Damage: Prolonged or severe pressure causes permanent structural damage and impaired function.

Clinical Manifestations and Diagnosis of Altered Urinary Elimination

General Manifestations

• Altered urinary volume and composition.

• Bleeding and Pain.

• General malaise and fever.

• Gastrointestinal (GI) symptoms.

Pain Sensation Profiling

• Mechanism: Stimulated by stretching and inflammation in the renal capsule rather than the kidney tissue itself.

• Renal Capsule Pain: Sensed as dull and persistent.

• Urinary System Pain (remaining parts): Sensed as intermittent and sharp.

Infection Manifestations

• Symptoms include general malaise, anorexia, fever, nausea, and vomiting.

• Ascending Infection: Potential for renal structural damage, which affects the organ's ability to produce urine.

Diagnostic Procedures

• Urinalysis: Microscopic and macroscopic analysis.

• Urinary Electrolytes: Used to monitor homeostasis, though normal values are not strictly standardized as kidneys dynamically maintain plasma levels.

• Glomerular Filtration Rate (GFR) and Creatinine Clearance: Measurements of nephron function.

• Radiographic Testing:

  • Intravenous Pyelogram (IVP): Intravenous injection of radiocontrast medium to visualize kidneys, ureters, and bladder.

  • Voiding Cystourethrogram (VCUG): X-ray of the bladder and urethra using contrast inserted via a catheter; uses fluoroscopy to determine ureteral reflux and bladder configuration during voiding.

  • Renal Angiogram: Contrast injected into the renal artery via the aorta to diagnose renal artery stenosis or vascular obstructions.

  • Renal Ultrasound: Determines kidney size, hydroureter, cysts, obstructions, or fluid collection. Doppler ultrasound is specifically used for renal artery flow.

Treatment Foundations

• Treatment depends on the underlying cause and is often focused on fluid balance regulation.

• Supplemental Fluids: Used to correct body fluid deficit.

• Diuretics: Used to correct body fluid excess.

Altered Stool Elimination Mechanisms

Large Intestine Function

• The large intestine is responsible for the final retrieval of water and electrolytes from fecal matter.

• It facilitates the absorption of vitamins produced by intestinal bacterial flora.

• Defecation: The process of fecal matter moving forward and propelling intestinal contents towards the anus.

Motility Alterations

• Increased Motility (Diarrhea):

  • Shortened transit time.

  • Impairs nutrition by preventing adequate nutrient and water absorption.

  • Enhances loss of water and electrolytes.

• Decreased Motility (Constipation):

  • Slowed, increased transit time.

  • Prolongs storage time in the large intestine.

  • Promotes enhanced loss of fluid from fecal matter (making it harder).

  • Risk of obstruction and potential return of waste products to circulation.

• Bacterial Influence on Motility:

  • Promoters of Motility: Lactobacillus acidophilus, Bifidobacterium bifidum.

  • Inhibitors of Motility: Escherichia coli.

Altered Neuromuscular Function (Bowel)

• Impairment Causes: Abdominal surgery, electrolyte imbalances, peritonitis, spinal trauma, narcotic analgesia, and emotional stress.

• Effects of Reduced Activity:

  • Stool remains longer in the large intestine, more water is removed, and stool becomes harder.

  • Impaired passing of flatus leads to abdominal distention, pain, and obstruction.

• Exaggerated Response: Passing stool unexpectedly (bowel incontinence).

• Enhanced Function: Exercise promotes peristalsis and bowel elimination.

Altered Perfusion (Bowel)

1. Decreased Perfusion: Ischemia manifested by pain and altered bowel function.

   • Local causes: Clots, pressure from space-occupying masses, or erosion of vessels (ulceration/trauma).

   • Global causes: Blood is redistributed away from the digestive system to vital organs.

2. Excessive Perfusion Demands: Typically caused by infection.

Appendicitis: A Case Study in Altered Perfusion/Patency

• Fecal material and infectious bacteria become trapped in the appendix.

• Inability to empty content leads to acute inflammation.

• Appendix swells, squeezing off venous drainage.

• Leads to ischemia and necrosis.

• Rupture: Bacterial feces leak into the peritoneum, causing peritonitis.

Altered Patency (Bowel Obstruction)

• Space-Occupying Lesions: Tumors, polyps, or impacted feces.

• Non-Space-Occupying Lesions: Herniation, adhesion, volvulus, and intussusception.

• Clinical Presentation: Characterized by abdominal distention, pain, loss of fluids/electrolytes via vomiting, gas/fluid accumulation, ischemia, necrosis, perforation, and sepsis.

General Manifestations and Diagnosis of Altered Bowel Elimination

Visual and Auditory Assessment

• Bowel Sounds (Auscultation): Reflection of intermittent smooth muscle contractions. Quality, location, and frequency indicate peristaltic function (e.g., increased in diarrhea).

• Abdominal Appearance: Should be soft and flat. Increase in size suggests trapped gas (hardening) or accumulation of fluid/feces.

Stool Characteristics

• Diarrhea: Loose, watery stools due to inflammation, infection, or high motility.

• Constipation: Absence of movement due to impaired mobility or obstruction.

• Color Indicators:

  • Bright Red Blood around Stool: Hemorrhoids.

  • Large Frank Red Blood: Internal bleeding (e.g., colon cancer).

  • Light Colored: Malabsorption syndromes or hepatitis (absence of bile).

  • Black Stool (Melena): Bleeding higher up in the GI system.

• Texture: Watery, hard, stringy, fatty, or foul-smelling.

Other Systemic Symptoms

• Pain: Mechanical, inflammatory, or ischemic.

• Anorexia, Nausea, Vomiting: General indicators of GI distress.

• Fever: Indicates infection or peritonitis.

Diagnostic Techniques

• Stool Analysis: Microscopic culture for bacteria/parasites; fat content analysis for malabsorption.

• Occult Blood Testing:

  • Guaiac Test: Chemical solution applied to a sample; blue color change indicates blood.

  • Immunochemical Method: Uses antibodies against human hemoglobin.

• Imaging and Visualization:

  • Barium Enema: Radiograph using contrast inserted via anus to visualize diverticulitis, motility, obstruction, and colon dimensions.

  • Sigmoidoscopy: Flexible tube inserted to view the rectum and lower colon.

  • Colonoscopy: Flexible tube inserted to view the entire colon from the small intestine to the rectum.

Treatment of Altered Bowel Elimination

Treating Diarrhea

1. Antimotility Agents: Slow passage to promote water removal (useful for chronic conditions).

2. Adsorbents: Move causing factors out of the stool (may also remove essential products).

3. Anti-Secretory/Antibiotics: Reduce inflammatory response and fluid movement into the intestine.

4. Bulk-forming Agents: Absorb excess fluid to firm the stool.

Treating Constipation

• Lifestyle interventions: Exercise, high dietary fiber, and adequate fluid intake.

• Stool Softeners: Promote moisture without stimulant effects.

• Laxatives and Enemas: Enemas involve fluid injection into the lower bowel via the rectum.

• Surgical Treatment: For mechanical/obstructive abnormalities.

• Bowel Training: For neuromuscular functional alterations.

Epidemiology of Intestinal Conditions (Table 16.4)