Altered Elimination Notes

Altered Elimination

Chapter 18 Learning Outcomes

Define and use key terms.
Describe the processes of urine and stool production and elimination.
Identify the role of neural, motor, endocrine, and physical processes in altered elimination.
Outline the processes involved in altered elimination.
Characterize the clinical manifestations in altered urinary and gastrointestinal elimination.
Recognize health conditions that can precipitate impaired elimination.
Detail alterations in systemic organ systems as a response to altered elimination.
List the common diagnostic procedures used to identify altered urinary and bowel elimination.
Describe treatments used in altered urinary and bowel elimination.
Apply concepts of altered elimination to select clinical models.

Key Terms

Acute tubular necrosis
Ampullary cancer
Anal canal
Anorexia
Anuria
Anus
Appendicitis
Appendix
Arteriovenous (AV) fistula
Arteriovenous shunt
Auscultation
Bladder training
Bowel obstruction
Bowel resection
Burch procedure
Casts
Cecum
Chyme
Colon
Colostomy
Constipation
Costovertebral angle (CVA)
Countercurrent exchanger
Countercurrent mechanism
Countercurrent multiplier
Defecation
Defecation reflex
Detrusor muscle
Diarrhea
Diverticula
Diverticular disease
Diverticulitis
Diverticulosis
Diverticulum
Enteric nervous system
Enuresis
Evacuation
External anal sphincter
External urethral sphincter
Extracorporeal shockwave lithotripsy (ESWL)
Feces
Filtrate
Flatus
Frank
Frequency
Functional fecal incontinence
Functional incontinence
Functional nonretentive fecal incontinence
Functional retentive fecal incontinence
Glomerular filtration rate (GFR)
Glomerulus
Guaiac test
Haustra
Hematuria
Hemodialysis
Hemorrhoids
Heparin
Hydronephrosis
Hydroureter
Incontinence
Internal anal sphincter
Internal urethral sphincter
Intestinal flora
Large intestine
Macroscopic analysis
Macula densa
Marshall-Marchetti-Krantz (MMK) procedure
Mass movements
Meconium
Meissner plexus
Melena
Microscopic analysis
Micturition
Myenteric plexus
Nephron
Nephroscope
Nephrostomy tube
Nocturia
Occult
Oliguria
Overactive bladder
Overflow incontinence
Paralytic ileus
Percutaneous nephrolithotomy
Peristalsis
Peritoneal dialysis
Peritonitis
Polycystic kidney disease (PKD)
Precipitation
Pyelonephritis
Re-anastomosis
Rectum
Renal calculi
Retention
Rome III criteria
Segmental movement
Sling procedure
Steatorrhea
Stercobilin
Stool
Stress incontinence
Struvite
Taeniae coli
Tension-free vaginal tape (TVT) procedure
Trigone
Ureteroscopic stone removal
Ureters
Urethra
Urge incontinence
Urgency
Urinary bladder
Urinary incontinence
Urine
Urine dipstick
Urodynamic testing
Urolithiasis
Valsalva maneuver
Venipuncture
Voiding diary

Introduction

Urinary system: secretes wastes and regulates body fluids.
Nephrons: functional units of kidneys, form urine through filtration, reabsorption, and secretion.
Digestive system: absorbs nutrients and eliminates wastes, begins at the mouth and ends at the anus
Both systems work together to maintain homeostasis.
Maintaining homeostasis requires balance and coordination of body systems.
Urine and stool (feces) are waste products excreted after nutrients are extracted from food and liquids.
Impaired waste elimination leads to clinical manifestations and pathophysiologic alterations.
Altered urinary and gastrointestinal (GI) elimination and their clinical manifestations are described in Modules 1 and 2.
Application of these altered processes is considered in Module 3, selected clinical models of altered elimination.

Module 1 Altered Urinary Elimination

Elimination requires motility and patency of structures for waste movement.
Processes are regulated by neuromuscular signaling and influenced by transport functions and perfusion.
Regulation of body fluid and acid-base balance are primary roles of the kidneys.
Water and ion movement across renal tubules, closely associated with vasculature, allows fluid and waste secretion in urine.

Urine Production Process

Urine is a waste product produced by the kidneys, stored in the bladder, and excreted via the urethra.
This process involves neural, motor, and hormonal mechanisms.
Basic processes of the renal system include:
- Regulation of body fluid volume and composition
- Elimination of metabolic wastes
- Synthesis, release, or activation of hormones
  - Erythropoietin
  - Renin
  - Vitamin D
- Regulation of blood pressure

URINE PRODUCTION

Nephron: functional unit of the kidney, composed of the renal corpuscle (glomerulus and Bowman capsule), proximal tubule, loop of Henle, distal tubule, and collecting duct.
Glomerulus: capillary network.
There are both cortical and medullary nephrons in each kidney.
Role of the nephron:
- Filter water-soluble substances from the blood
- Reabsorb filtered nutrients, water, and electrolytes
- Secrete waste
The kidneys process 20% to 25% of the cardiac output, approximately 1,000
ormal{mL} of blood per minute.
Blood enters the kidney through the renal artery, dividing into interlobular arteries, arcuate arteries, afferent arterioles, and glomerular capillaries.
Blood entering the glomerular capillaries via the afferent arteriole is filtered, resulting in fluid called filtrate.
Filtrate enters Bowman capsule, then the renal tubular system.
Blood remaining in the glomerular capillaries exits the glomerulus via the efferent arteriole, which branches into peritubular capillaries.
Peritubular capillaries surround the proximal and distal tubules.
Vasa recta: additional capillaries surrounding the loop of Henle deep within the medulla; important in concentrating urine through exchange of water and solutes from the filtrate flowing in the opposite direction of the blood (countercurrent exchanger).
Blood travels into the interlobular venules and veins and returns to the venous circulation via the renal vein.
Filtrate travels from Bowman capsule to the proximal tubule, where the majority of sodium is reabsorbed back into the blood.
Other reabsorbed substances include glucose, potassium, amino acids, HCO3, PO4, urea, and water. Hydrogen is secreted from the resulting isotonic fluid.
Fluid moves down the loop of Henle where it is progressively more concentrated (countercurrent multiplier).
Water is reabsorbed and sodium diffuses into the descending limb, with sodium actively reabsorbed in the ascending limb.
Countercurrent mechanism: involves the countercurrent exchanger and countercurrent multiplier; responsible for maintaining the vertical gradient in the interstitium.
In the distal tubule, sodium (through the actions of the hormone, aldosterone) and HCO_3^- are reabsorbed.
Macula densa: epithelial cells adjacent to the distal tubule, provide information about sodium content in the filtrate to the cells of the juxtaglomerular apparatus, regulating aldosterone release via the renin-angiotensin-aldosterone system (RAAS).
Secretion of potassium, urea, hydrogen, and ammonia (NH_3) occurs; the remaining filtrate moves into the collecting duct.
In the collecting duct, additional water is reabsorbed in an antidiuretic hormone dependent mechanism, in addition to sodium, hydrogen, potassium, and NH_3.
The end product produced by the nephron is urine, which is transported via the ureters to the bladder, where it is stored until it is eliminated through the urethra.

URINE REMOVAL

Urine enters the ureters via the renal pelvis, promoting flow out of the kidneys.
Ureters: composed of smooth muscle fibers that propel the urine to the bladder by peristalsis.
Urine enters the bladder via the trigone.
Trigone: triangular, smooth area at the base of the bladder between the openings of the two ureters and the urethra (opening to the exterior), serving as a functional sphincter, which prevents urine from moving in a retrograde manner back into the ureter from the bladder.
Urinary bladder: muscular organ lined with transitional epithelium and innervated by the pelvic nerves.
Body of the bladder: composed of the detrusor muscle (smooth muscle).
Filling of the bladder activates sensory stretch receptors, and the generated action potential is transmitted to the sacral region of the spinal cord.
Contraction of the detrusor muscle is stimulated by parasympathetic cholinergic motor fibers.
Relaxation of the bladder neck muscle, the internal urethral sphincter (composed of a ring of circular smooth muscle), promotes release of urine from the bladder (micturition).
Somatic control of the external urethral sphincter (skeletal muscle) innervated by the pudendal nerve allows for voluntary release of urine.
Tonic contraction of the smooth muscle of the urethra prevents urine leakage until pressure in the bladder exceeds threshold.
Urethral length differs between sexes; the female urethra is much shorter than the male urethra, which spans the length of the penis.

Micturition Reflex

Stimulation of stretch receptors in bladder walls transmits impulse to the sacral spinal cord.
Neural impulse ascends from the sacral cord segments to the micturition center in the pons of the brain.
Neural impulse descends from the micturition center, initiating contraction of the detrusor muscle and relaxation of the internal urethral sphincter.
Voluntary relaxation of the external urethral sphincter stimulates urine release.

Urine Characteristics

Urine: clear yellow fluid composed primarily of water, containing water-soluble wastes.
Total volume produced: approximately 750 to 2,000
ormal{mL} over a 24-hour period; varies depending on fluid intake, medications, and health conditions.
Slight ammonia odor from the breakdown of urea.
Variations in color, derived from urochrome pigments, indicate hydration status.
Concentrated, dark, strong-smelling urine may indicate dehydration, whereas dilute, pale-colored urine may indicate increased fluid volume.

Urine Samples

Random collection
- May be taken at any time of the day
- No special preparation required
Clean-catch
- Requires special cleansing of the external urethral orifice
- Midstream urine collection (urine collected does not include fluid from the initial or final urinary stream)
Bladder catheterization
- Sterile insertion of a catheter through the external urethral orifice, through the urethra, and into the bladder to collect urine sample
Suprapubic aspiration
- Insertion of a sterile needle transabdominally into the bladder for urine collection

Urine Analysis

Macroscopic analysis: visual assessment of color and clarity.
- Biochemical analyses can be obtained by testing urine with a urine dipstick. Color changes indicate the absence or presence of substances in urine.
  - pH
  - Specific gravity
  - Protein
  - Glucose
  - Ketones
  - Nitrite
  - Leukocyte esterase
Microscopic analysis: performed using a specially prepared urine sample.
- A small sample (10 to 15
  ormal{mL}) of urine is centrifuged for approximately 10 minutes until the sediment forms at the bottom of the test tube.
- All but a small amount of fluid is removed, and the sediment is resuspended in the remaining fluid.
- The sample is stained with dye and placed onto a glass slide with a coverslip for viewing under the microscope.
- Low-power examination can detect crystals, casts, squamous cells, and other large components.
- High-power examination can detect crystals, cells (white blood cells [WBCs] and red blood cells [RBCS]), and bacteria.
- The number of specific sediment components seen under microscopic examination can be quantified. The degree of magnification is also indicated and is determined with low-power field (LPF) or high-power field (HPF).
- Several fields, or areas, are counted and then averaged to provide an accurate estimate.
- Urine should be free of glucose, ketones, nitrite, bacteria, leukocyte esterase, crystals, stones, and significant amounts of protein. Casts, structures consisting of a protein meshwork of entrapped cells formed in the distal tubules and collecting ducts, are also absent in normal urine.
- Epithelial cells may be present in small numbers but increased amounts may indicate pathology.

ALTERED URINARY ELIMINATION

Elimination involves interplay of neural, vascular, muscular, and hormonal influences.
Structures involved in urine movement must be patent and functional.

Processes of Altered Urinary Elimination

Alteration in motility, neuromuscular function, vascular insufficiency, and obstruction are most commonly associated with altered urinary elimination.

ALTERATION IN URINARY MOTILITY

Can promote stasis of filtrate in the renal tubules and urine in the bladder.
Casts may form due to low flow rate, increased sodium concentration, and low pH.
Precipitation of urinary fluid components may cause blockage of essential renal structures.
Trapping of RBCs within casts may indicate glomerulonephritis.
Epithelial cells may indicate shedding of tubular cells causing acute tubular necrosis.
WBCs may indicate pyelonephritis, kidney inflammation.
Stasis of urine in the bladder may promote bacterial growth, leading to local and ascending infection in the kidneys.

ALTERATION IN URINARY NEUROMUSCULAR FUNCTION

May result in urinary retention (incomplete emptying) or incontinence (involuntary urine leakage).
Impaired neural control may involve neurons of the peripheral and central nervous systems, neurotransmitter production, and coordination of neural impulses.
Failure to provide appropriate stimulus for the desired response will result in a limited or absent ability to eliminate urine. Exaggerated responses may prompt stimulation to prematurely release urine.
Muscles must have the ability to respond to a generated neural impulse to achieve the intended effect. Muscle functions involved in urinary elimination include peristalsis in the renal tubules and contraction or relaxation of smooth and skeletal muscles.
Conscious control of urinary elimination may be impaired as a consequence of altered mobility and the resulting reduction in toileting independence.

ALTERATION IN URINARY PERFUSION

Inadequate arterial blood supply results in ischemia and infarction.
Decreased oxygen delivery by arterial blood supply may result in damage to renal structures due to inability to meet metabolic demands.
Decreased perfusion leading to impaired oxygenation of tissue may be due to excessive constriction of arterioles, inadequate vascular volume, or obstructed patency of the arterial supply, as occurs with an embolism.
Loss of functional tissue through necrosis leads to pain, bleeding, and obstruction of the venous system branches that drain the affected tissue.
Enhanced perfusion represents additional workload and has the potential to stress the individual organ system.

ALTERATION IN URINARY PATENCY

Blockage of urinary passageways may result in obstruction.
Consequences of obstruction are influenced by:
- Degree of the obstruction (complete or partial)
- Duration of the obstruction
- Acuity or chronicity of the condition
Obstructions are characterized by a buildup of pressure behind the blockage. Prolonged or severe pressure results in structural damage and impaired function.
Due to mechanical obstruction of the arterial or venous system, tissues may not be perfused, causing ischemia and necrosis.
Blockage may be caused by precipitation of substances in smaller lumen structures, or structural blockage resulting from endogenous or exogenous sources such as polyps or tumors.
Physical obstructions may result from urine precipitation, scar tissue or adhesions, tumor, or inflammation.
Obstruction of the renal and urinary systems impedes urine flow.
Dilation of the structures proximal to the obstruction causes dilation and stasis, leading to infection and structural damage.
Hydroureter: accumulation of fluid in the urinary ureter, a consequence of complete ureteral obstruction.
Increased hydrostatic pressure extends up to the renal pelvis and tubules, leading to hydronephrosis.
Glomerular filtration rate (GFR): rate of filtrate formation as blood passes through the glomerulus, used to measure how well the kidneys are functioning.
In hydroureter, the GFR decreases, reflecting impairment of renal function. Fluid escapes from the tubules into the surrounding capillary system.
Excretion of sodium, urea, and water is impaired. Local hormonal responses to promote renal perfusion are effective for a short time.
Impaired perfusion develops within 24 hours, leading to ischemia, tubular atrophy, and damaged glomeruli if the condition is not corrected.
Sequelae include infection, sepsis, and loss of renal function leading to renal failure.

General Manifestations of Altered Urinary Elimination

Impairment of urinary elimination results in a variety of clinical manifestations. Specific manifestations are related to the underlying pathology.
Generally, manifestations include:
- Altered volume of urine
- Altered urine characteristics
- Bleeding
- Pain
- Distension
- Anorexia
- Nausea
- Vomiting
- Fever
Urinary volume may be increased or decreased. In the case of obstruction or damage to the renal structures themselves, oliguria (scanty urine production) or anuria (absent urine production) may be seen.
Other conditions may be associated with increased urine output and are often the result of hormonal stimulation of a compensatory response or regulation of fluid balance.
Urine composition may also be altered, reflecting the origin of the pathology. An analysis of urine associated with kidney disorders is detailed in Table 18.3. Hematuria, evidenced by frank bleeding or clots, can be identified based on urine color. Small amounts of blood require microscopic detection.
Pain is a frequent symptom associated with altered renal and urinary function. Renal and ureteral nociceptors transmit pain impulses to the spinal cord between T10 and L1. The associated dermatomes include the lower abdomen anteriorly and posteriorly at the level of the costovertebral angle (CVA) or flank area. Most nociceptive receptors are located in the renal capsule rather than in the kidney itself and are stimulated by stretching and inflammation. Stretching induced by distension produces the sensation of dull, persistent pain. In contrast, many pain receptors are located in the remaining parts of the descending urinary system. The pain sensations from this region are usually intermittent and sharp.
Infection is characterized by feelings of general malaise, anorexia, and fever. Infection in the lower urinary tract is presented as a clinical model in Chapter 5 to illustrate the typical pathology, clinical manifestations, diagnosis, and treatment of this condition. Ascending infection of the pathogen through the ureters into the kidneys represents the potential for renal structural damage, significantly affecting the ability to produce urine. Nausea and vomiting may occur in ascending infection or systemic illness, such as pyelonephritis.

Diagnosis of Conditions of the Renal and Urinary Systems

Diagnosing altered elimination processes is important to prevent further damage to involved organs. Both the cause and effect of altered elimination are critical to the effective management and treatment of individuals with these conditions.
Microscopic and macroscopic urinalysis provides a useful resource for diagnosing conditions resulting in altered elimination. Normal values for urinary electrolytes are not standardized because the kidneys function dynamically to maintain electrolyte homeostasis in the plasma. Calculation of and creatinine clearance indicates nephron function.
Radiographic diagnostic testing useful in the determination of anatomic and functional anomalies includes:
- Intravenous pyelogram (IVP): Intravenous injection of a radiocontrast dye to allow radiographic visualization of the kidneys, ureters, and bladder.
- Voiding cystourethrogram (VCUG): X-ray examination of the bladder and urethra completed after insertion of contrast dye into the bladder via a urinary catheter. Fluoroscopy is used to determine ureteral reflux and bladder/urethra configuration during voiding.
- Renal angiogram: Contrast dye injected into the renal artery via the aorta to diagnose renal artery stenosis or intrarenal vascular obstructions.
- Renal ultrasound: Noninvasive image produced by sound waves. Useful in determining kidney size, hydroureter, cysts, obstructions, or fluid collection. Renal artery flow can also be determined with Doppler ultrasound.

Treatment of Altered Urinary Elimination

Treatment of conditions contributing to altered urinary elimination is determined by the condition underlying the clinical manifestations. A thorough review of medical history, description of symptoms, physical examination, and diagnostic testing may be necessary to specify treatment.
Altered urinary elimination is often associated with impaired regulation of fluid balance. Control of fluid balance through administration of supplemental fluids to correct body fluid deficit or the use of diuretics to correct body fluid excess may be indicated.

Research Note

Kidney cancer, also called renal cell carcinoma, is now being treated with immunotherapy.
Bevacizumab (Avastin): monoclonal antibody that inhibits blood vessel growth in tumors by targeting the VEGF/VEGFR pathway.
Aldesleukin (Proleukin): cytokine that targets the IL-2/IL-2R pathway
Avelumab (Bavencio): checkpoint inhibitor that targets the PD-1/PD-L1 pathway
Ipilimumab (Yervoy): checkpoint inhibitor that targets the CTLA-4 pathway
Nivolumab (Opdivo): checkpoint inhibitor that targets the PD-1/PD-L1 pathway
Pembrolizumab (Keytruda): checkpoint inhibitor that targets the PD-1/PD-L1 pathway

Module 2 Alteration in Stool Elimination

Processes of Stool Elimination

Involves organs of the digestive (gastrointestinal) system.
Final processes of stool production and elimination occur in the large intestine after nutrient extraction.
Large intestine: hollow organ in the abdominal cavity, beginning at the end of the ileum of the small intestine and terminating at the anus.
- Nearly 5 ormal{ft} long and 3 ormal{in} wide; divided into three segments:
  1. Cecum: pouchlike structure to which the appendix attaches.
  2. Colon: largest segment, subdivided into ascending, transverse, descending, and sigmoid portions.
  3. Rectum: ends at the anal canal.
- Ileocecal valve: directs flow of fecal matter from the ileum to the cecum.
- Diameter of the large intestine reduces as it progresses toward the rectum, where the colon dilates.
- Superior and inferior mesenteric arteries supply blood to the large intestine.
- Autonomic nervous system provides primary neural control of the gastrointestinal tract.

STOOL ELIMINATION PROCESS

Food ingestion begins the digestive processes and results in stool excretion.
Bowel motility, perfusion, patency, and response to neural signals are critical to stool elimination.

Stool Production

Stool is a product of digestion. As digestive processes continue throughout the length of large intestine, fecal matter entering at the cecum via the ileocecal valve is propelled toward the rectum for excretion.
Water and electrolytes are removed from the fecal matter as it moves through the large intestine.
Continued processing results in stool (feces).
Large intestine functional responses are related to the rate at which contents move.
- Faster movement allows less time for intestinal processes.
- Slower movement leads to extended time.
Large intestine: final site for establishing water and electrolyte balance.
- Of the 7 to 10
  ormal{L} of water entering the small intestine, only 1 to 1.5
  ormal{L} enters the large intestine daily.
- Final product, stool, includes approximately 100 to 200
  ormal{mL} of water.
- Absorption of water and electrolytes occurs in and around the epithelial cells that line the large intestine.
Chyme: semiliquid mixture of partially digested food formed in the small intestine; altered from a liquid to a semisolid form in the ascending and transverse large intestine segments.
Indigestible carbohydrates, including dietary fiber, as well as remaining sodium, magnesium, and chloride are retained within the intestines.
Time from ingestion to elimination: 2 to 5 days, dependent on dietary intake of nutrients.
Most water is reabsorbed along with several B complex vitamins and vitamin K, much of which is produced by intestinal bacteria.
Remaining fecal matter: combines with intestinal mucus and resident bacteria (intestinal flora) and becomes stool (feces).
Greatest concentration of GI bacteria resides in the large colon. Complex intestinal flora contains primarily anaerobic bacterial organisms, though composition among adults is variable and in large part dependent on diet.
Food provides energy and carbon for intestinal bacteria.
Intestinal bacteria break down some remaining dietary fiber, releasing short chain fatty acids used by epithelial cells of the colon.
Resident intestinal flora protect the intestine from harmful pathogens by maintaining local homeostatic balance.

Stool Evacuation

Stool is stored in the large intestine until evacuation (defecation).
- Contents of the intestine take approximately 18 hours to pass from the proximal end of the large intestine to the distal end.
Continuous inner layer of circular smooth muscle of the muscularis externa is surrounded by an outer, discontinuous layer of longitudinal smooth muscle.
Contraction of smooth muscle occurs through sliding filament mechanism.
Longitudinal muscle forms three distinct bands known as taeniae coli. When contracted, haustra (pouches) are created.
Contraction of longitudinal and circular smooth muscles propels stool through the intestine.
Closeness of smooth muscle fibers makes it easier for action potentials to be transmitted to adjacent fibers, propagating the nerve impulse along the length of the large intestine.
Peristalsis: caused by squeezing of circular fibers, promotes forward movement of intestine contents.
Circular fiber contraction and relaxation occurs at different locations, producing segmental movement of the large intestine.
Mass movements: strong peristaltic contraction, occur three to four times a day, propelling stool.
Muscle fibers are innervated locally by the enteric nervous system, including the myenteric plexus (Auerbach plexus) found between the longitudinal and circular muscle layers and the Meissner plexus, located in the submucosa.
Myenteric impulses control gastrointestinal movement, while the Meissner plexus transmits sensory impulses through stretch receptors.
Both systems are involved in the reflexes necessary for stool movement and evacuation.
Myenteric plexus stimulation promotes increased tonic contractions as well as increased intensity, rate, and velocity of rhythmic contractions; induced via colon distension.
Enteric nervous system is modulated by the autonomic nervous system.
- Sympathetic stimulation via the sacral nerves of the spinal cord has an inhibitory effect.
- Parasympathetic stimulation serves an excitatory function via the vagus nerve.
Two sphincters: involved in defecation.
- Internal anal sphincter: thick layer of smooth muscle, tonically constricted because of sympathetic control.
- External anal sphincter: skeletal muscle, surrounds the internal anal sphincter and is innervated by the pudendal nerve (somatic nervous system), providing voluntary control.
- Movement of stool into the rectum stimulates the reflex to defecate (defecation reflex). Parasympathetic stimulation prompts relaxation of the internal anal sphincter. Voluntary relaxation of the external anal sphincter allows for conscious control of defecation.
Defecation is often assisted by the Valsalva maneuver-conscious contractions of abdominal muscles and forced exhalation against a closed glottis. This generation of intra-abdominal pressure forces the diaphragm and chest muscles against the glottis, stimulates the vagus nerve, and assists in stool evacuation.

Defecation Reflex

Stimulation of stretch receptors in the rectal wall transmits sensory impulse to the sacral spinal cord.
Sensory neurons synapse on parasympathetic nerves, promoting relaxation of the internal anal sphincter (smooth muscle).
Interneuron stimulation promotes contraction of abdominal muscles.
Motor signal from the cerebral cortex stimulates opening of the external anal sphincter (skeletal muscle).
Defecation assisted by voluntary contractions of the abdominal muscles.

Stool Characteristics

One of the main functions of the large intestine is compaction of feces.
Water is absorbed as the fecal matter moves along the length of the large intestine, and the solid matter in the feces becomes more compact. Approximately 400 to 800
ormal{mL} of water, along with sodium, chloride, and bicarbonate, are absorbed out of the large intestine and approximately 5
ormal{mEq} potassium is secreted into the lumen of the large intestine daily.
Constituents of stool include approximately 100
ormal{mL} of water and 25 to 50
ormal{g} of solids consisting of remaining unabsorbed nutrients, shed epithelial cells, bile pigments, bacteria (30%), fat (10% to 20%), undigested dietary fiber (30%), and inorganic solids (20%). Water comprises approximately 75% of stool content.
Normal adult stool appears firm and moist. The characteristic brown color is derived from the bilirubin pigment in bile, stercobilin. Chemical reactions resulting in the breakdown of fecal components during digestion produce compounds, including hydrogen sulfide, that provide the characteristic odor of feces.
Upon defecation, stool is soft, moist, and semisolid. Formed in the shape of the rectum, stool averages approximately 1
ormal{in.} in diameter and should be easy to pass. The amount and frequency of defecation is variable among individuals, though the average for adults is 200 to 300
ormal{g} stool once per day.
Newborns and infants differences in stool characteristics can be explained by the major sources of oral intake during development.
In utero, the fetus swallows amniotic fluid, which passes through the gastrointestinal tract. Peristalsis and stool production typically occurs in the developing fetus. Normally, the fetus does not pass stool in utero but is expected to pass the first stool in the early newborn period after birth. This first stool, meconium, represents the digestion of amniotic fluid and is black, sticky, and odorless.
Once feedings are begun, the stool transitions to reflect the newborn's main source of oral intake. Breastfed babies have stool that is soft, unformed, and yellow. The odor is mild and uncharacteristic of a normal fecal scent. Babies fed artificial milk, or formula, have light brown stools. Frequency of bowel movements is often increased in breastfed babies due to the efficient digestion of breast milk, compared to the less frequent stooling patterns characteristic of formula-fed babies. As table foods and supplemental liquids are introduced in late infancy, stool patterns alter to reflect the composition of these ingested foods.

STOOL ANALYSIS

Based upon elimination patterns and characteristics. Laboratory analysis may include microscopic examination or chemical evaluation.
Color, consistency, volume, shape, and odor should be consistent with characteristics described previously. Stool should be free of blood, mucus, pus, and harmful parasites. Stool pH should be 6, and it should contain less than 2 mg of reducing factors (i.e., sugars).

Altered Bowel Elimination

Impaired large intestine function may alter water and electrolyte reabsorption from the fecal matter in the cecum.
Absorption of vitamins produced by intestinal bacterial flora may also be altered if there is impaired function of the large intestine.
Social and personal concerns regarding alteration in bowel elimination may impact quality of life. Social norms and rules of defecating may represent a major source of stress for individuals.

PROCESSES OF ALTERED BOWEL ELIMINATION

Forward movement of fecal matter is essential, propelling the intestinal contents toward the anus, leaving the body as stool through the process of defecation.
Impaired bowel elimination often results from alterations in bowel motility, neuromuscular function, perfusion, or patency.

Alteration in Bowel Motility

Motility of the large intestine determines the rate at which fecal matter passes through for evacuation.
Increased motility may impair nutrition, preventing adequate time for nutrient and water absorption, and it may enhance loss of water and electrolytes.
Decreased motility prolongs storage time in the large intestine, increasing fluid loss from fecal matter, forming hard stools, and potentially promoting the return of waste products to the circulation.
Composition of bacterial intestinal flora may also influence motility within the large intestine, with Lactobacillus acidophilus and Bifidobacterium bifidum promoting motility, and Escherichia coli inhibiting motility.
Diarrhea and constipation are the most common clinical manifestations of altered motility in the large intestine.
Factors that alter the transit time of stool also present potential stressors for stool elimination.
Certain foods may irritate the intestine, enhancing the speed at which the feces moves from the cecum to the anus. Shortened transit time limits water absorption, leading to stool that is less formed due to increased water content. Such stools are often passed with more frequency and urgency.
Some individuals respond to particular foods with a slowed transit time, leading to increased water movement out of the feces. The result is often hard, formed stools with reduced frequency in elimination.

Alteration in Bowel Neuromuscular Function

Coordination of neurologic and muscular functions is essential to optimal bowel function. Any alteration in neural signal transduction or muscle responsiveness may result in altered bowel function.
Impaired function associated with loss of propulsive activity may result from abdominal surgery, electrolyte imbalances affecting contractile function, peritonitis, or spinal trauma. Impaired motility is often seen as a side effect of narcotic analgesia.
Emotional stress may alter stool elimination processes due to central nervous system influence.
Reduced activity may also slow the process of stool elimination. Walking, running, swimming, and other active movements enhance neuromuscular activity and coordination in the large intestine, promoting peristalsis and bowel elimination.
Loss of mobility often serves as a stressor to bowel elimination, leading to reduced intestinal smooth muscle contractions. The longer feces remains in the large intestine, the more water is removed, and stool becomes harder. Further, intestinal gas passed through the anus (flatus) builds up, leading to abdominal distension and pain if not released.