Disorders of the

Digestive System
Disorders of the Digestive
System
Sources of digestive problems
Mechanical
Nervous
Chemical
Hormonal
Eating Disorders
Anorexia
Chronic loss of
appetite
Possible emotional,
social factors
Anorexia Nervosa
Psychological disorder
Bulimia
Binge-purge syndrome
Causes of Anorexia

Anxiety, depression
Improper fit of dentures
Illness, physical discomfort
Constipation
Intestinal obstruction
Anorexia, Nursing
Implementation
Become familiar with patients eating
habits
Permit patient to choose own food
Don’t force patient to eat
Provide pleasant environment
Serve small portions
Dental Plaque and Caries
Erosive process that dissolves tooth
enamel
Medical management
Removal of affected area and
replace with dental material
Dental check ups
Fluoridated water
Nursing interventions
Teach patient oral care
Diet changes
Gingivititis
Inflammation of the gums
Symptoms
Bleeding, swollen, tender gums
Difficulty chewing
Causes
Accumulation of food between teeth
Vitamin deficiency
Anemia
Leukemia
Prevention
Brushing teeth & gums
Daily flossing
Adequate diet
Periodontitis
Untreated Periodontitis
Teeth loosen
Spreads to mandible
Prevention
Impeccable tooth & gum
Regular flossing
Adequate diet
Treatment
Drainage of abscess
Antibiotics
Extraction
Recurrent Aphthous Stomatitis
Multi system disorder
Painful ulcers
Mouth
Genitals
Uveal tract of the eye
Causes
Viruses, bacteria, fungus
Chemotherapy
Vitamin deficiency
Four Forms
Minor Type
Canker sores
Lesions are 2- 4 mm in diameter
Usually fewer than 5 in number
Recurrent Aphthous Stomatitis

Major Aphthous Stomatitis

Referred to as “Sutton’s disease”
10 mm or greater in diameter
They frequently occur in the
posterior portion of the mouth
Take four to six weeks to heal
These lesions may result in scarring
Herpetiform
Confused with herpes
Numerous, 1-2 mm ulcers, cropped
together
When the neutrophil count returns
to normal the lesions resolve
Recurrent Aphthous Stomatitis

Fourth form is known as Behçet's disease

Complex multi-system disorder including
Synovitis
Uveitis
Vasculitis
Meningoencephalitis
Oral and/or genital mucosa are the first manifestation
It is a rare, non-infectious disease
Very uncommon in North America and Europe
Half of the patients have evidence of immune
dysfunction
Recurrent Aphthous Stomatitis
Immune Dysfunction seen with Behçet's
disease
5-20% of Crohn's patients develop disease
Ulcerative colitis
Malabsorption syndromes
Gluten-sensitive enteropathy
HIV infection
The lesions appear to be more severe, more
painful and deeper
Cyclic neutropenia
Behcet’s
Herpes Simplex Virus
Acute viral infection
Two strains of herpes simplex virus
HSV-1 “Common cold sore”
Forms clusters of fluid filled blisters
HSV-2
Sexually transmitted
Can develop in and around the mouth or genitals
Shingles
Form along nerve path
Candidiasis
Etiology/Pathophysiology
Fungus normally present in the mouth, intestine,
vagina, and on the skin
Also referred to as thrush and moniliasis
Clinical manifestations/assessment
Small pearly-white patches on the mucous
membrane of the mouth
Thick white discharge from the vagina
Candidiasis
Causes
Cancer
Diabetes
Alcoholism
Treatment
Nystatin
Gentician Violet
OTC medications
Nursing care
Good hand washing
Bland or soft food for patient
Oral care
Education on medication administration
Mumps

Contagious viral infection of parotid

salivary glands
Possible complications
Inflammation of testicles
Sterility in males
MMR vaccine
Achalasia
Etiology/Pathophysiology
LES cannot relax (cardiospam)
Causes decreased motility of the lower portion of the
esophagus
Absence of peristalsis and dilation of the lower portion of
the esophagus
Decreased amount or no food can enter the stomach
The esophagus can hold as much as a liter
Possible causes
Nerve degeneration, esophageal dilation, and hypertrophy
Disruption of the normal neuromuscular activity of the
esophagus
Achalasia
Clinical manifestations/Assessment
Dysphagia-PRIMARY SYMPTOM
Regurgitation of food
Substernal chest pain
Loss of weight
Weakness
Poor skin turgor
Achalasia
Diagnostic tests
Radiologic studies- Esophagoscopy
Medical management
Medications: anticholinergics, nitrates,
and calcium channel blockers
Dilation of cardiac sphincter
Surgery-Cardiomyectomy
Gastroesophageal Reflux
Disease (GERD)
Etiology/Pathophysiology
Backward flow of gastric acid into the esophagus
Reduced LES pressure
Clinical manifestations
Pain may mimic angina
Heartburn (pyrosis) 20 min – 2 hrs after eating
Regurgitation
Dysphagia or odynophagia (painful swallowing)
Eructation (belching)
Cough
Wheezing
Hoarseness
Gastroesophageal Reflux
Disease (GERD)
Risk factors
Alcohol, tobacco, & smoking
Delayed gastric motility
Diagnostic tests to differentiate GERD from
angina
Esophageal motility
Bernstein tests evaluate LES function
pH monitoring for 24 hours to record reflux
episodes
Barium swallow & endoscopy to evaluate for
hiatal hernia
Gastroesophageal Reflux Disease
(GERD)
Medical management & Nursing interventions
Antacids or acid-blocking medications
Diet
4-6 small meals/day
Low fat, adequate protein
Remain upright for 1-2 hours after eating
Lifestyle
Eliminate smoking
Avoid constrictive clothing
HOB up at least 6-8 inches for sleep
Barrett’s Esophagus
Etiology/Pathophysiology
Cells in esophagus change to cells normally found in the
intestine (metaplasia)
Patients feel less discomfort as metaplastic cells are less
sensitive
Can’t cure, treat GERD
Medications
Antacids
GI stimulants
Histamine H2 antagonists
Proton pump inhibitors
Surgery
Fundoplication
Acute Gastritis
Etiology/Pathophysiology
Inflammation of the lining of the stomach
Associated with
Alcoholism & smoking
Bacteria & viruses
Chemical toxins
Stressful physical problems
Clinical manifestations
Fever
Headache
Epigastric pain
Nausea and vomiting
Coating of the tongue
Anorexia
Acute Gastritis
Long term
Changes in the mucosal lining that
interferes with acid and pepsin secretion
Gastritis usually resolves once the
offending agent is removed
Diagnostic tests
Stool for occult blood
WBC
Electrolytes
Acute Gastritis
Medical management
Antiemetics
Antacids
Antibiotics
IV fluids
NG tube
Nutritional Supplementation
Administration of blood
NPO until signs and symptoms subside
Nausea
Etiology/Pathophysiology
Feeling the urge to vomit
May occur independently or precede vomiting
Specific neural pathways not identified
Probably controlled by parts of brain that control
involuntary bodily functions
Signs and symptoms
Increased salivation
Diminished functional activities of the stomach
Altered small intestine motilility
Vomiting
Etiology/Pathophysiology
Forceful expulsion of gastric contents
Increased intrathoracic pressure
Increased intracranial pressure
Controlled by
Vomiting center (medulla)
– Initiates vomiting when stimulated
Chemo-receptor trigger zone
– Must be stimulated by a drug or toxin
Causes of Nausea & Vomiting
Stress, fear, and depression
Pain
Acute febrile illness
Medications
Food poisoning
Anesthesia
Diseases of the stomach
Intestinal obstruction
Pregnancy
Head injury
Nursing Implementation for
Nausea & Vomiting
Administer antiemetics
Monitor fluid & electrolyte
replacement
Protect patient from unpleasant sight
or smells
Attempt to keep stomach empty
Ventilate room
Observe & record the character and
quantity of emesis
Peptic Ulcers (PUD)
Gastric ulcers and duodenal ulcers
Ulcerations of the mucous membrane or deeper
structures of the GI tract
Most commonly occur in the stomach and
duodenum
Result of acid and pepsin imbalances
Chronic NSAID use
H. pylori
70% of patients with gastric ulcers
95% of patients with duodenal ulcers
Peptic Ulcers (PUD)
Gastric ulcer
In the distal half of the stomach
Bleed more, harder to control
Duodenal ulcers
May or may not be caused by hypersecretion of
gastrin
Ulceration occurs when the acid secretion exceeds
the buffering factors
More likely to have chronic bleeding and perforate
Peptic Ulcers (PUD)
Peptic Ulcers (PUD)
Clinical manifestations
Pain: Dull, burning, boring, or gnawing,
epigastric
Dyspepsia
Hematemesis
Melena
Diagnostic tests
Esophagogastroduodenoscopy (EGD)
Breath test for H. pylori
Peptic Ulcers (PUD)

Complications of peptic ulcers

Bleeding
Hematemesis
Melena
Gastric outlet obstruction
Peptic Ulcers (PUD)

Diagnosis
Esophagogastroduodenoscopy (EGD)
Visualize tissue and Biopsy if necessary
Wireless capsule endoscope
Complications
– Stool impaction
– Small bowel stricture
Peptic Ulcers (PUD)
Medical management/Nursing interventions
NG tube until bleeding subsides
Antacids
Histamine H2 receptor blockers
Proton pump inhibitor
Mucosal healing agents
Antibiotics
Anticolingerics
Reclining for 1 hour post meal
IV fluid
Diet
High in fat and carbohydrates
Low in protein and milk products
Small frequent meals
Limit coffee, tobacco, alcohol, and NSAID use
Peptic Ulcers (PUD)
Medical management/Nursing interventions
Surgery
Antrectomy-
Gastrodudodenostomy (Billroth I)
Gastrojejunostomy (Billroth II)
Total gastrectomy
Vagotomy
Pyloroplasty
Types of gastric resections with anastomoses.
A, Billroth I. B, Billroth II.
Peptic Ulcers
Complications after gastric surgery
Dumping syndrome
Eat 6 small meals a day
high in protein and
carbohydrates
Eat slowly and avoid fluid
with meals
Pernicious anemia
Iron deficiency anemia
Diarrhea

Rapid movement through intestines of

loose, watery stools resulting from
increased peristalsis
Causes:
Fecal impaction
Ulcerative colitis
Intestinal infections
Drugs
Diarrhea
Nursing implications
Meticulous skin care
Observe stool for color, odor, consistency, mucous,
blood, or pus
Administer anticholinergics
Reduce bowel spasticity
Administer anti-diarrheal agents
Mild diarrhea
Moderate diarrhea
Severe diarrhea (infectious agent)
Constipation
Etiology/Pathophysiology
Fecal mass in rectum
Water is absorbed and feces hardens
Painful to pass
Causes
Neurological conditions
Disease
Medications
Diet
Decreased activity
Ignoring the urge to defecate
Chronic laxative use
Constipation
Clinical manifestations/Assessment
Abdominal distention
Indigestion
Rectal pressure
Hard, dry stools
Decrease appetite
Rectal pressure
Intestinal rumbling
Constipation

Complications
Fecal impaction
Cardiac complications from straining
Dilation of colon (Megacolon)
Colonic mucosal atrophy
Fecal incontinence
Constipation
Treatment
High fiber diet
2-3 liters of fluid a day
Strengthening of abdominal muscles
Behavior changing
Diet
Whole grains
Fresh fruits
Vegetables
Constipation
Medications
Bulk forming agents
Absorb fluid and swell in the intestine and increase peristaltic action
Laxatives
Bulk forming, stool softeners, stimulant, and saline
Stool softeners
Detergent like drugs that permit easier penetration and mixing of
fats and fluids with the fecal mass
Stimulant
Increase the motility of GI tract by chemical irritation of the intestinal
mucosa
Golytely
Causes a large volume of water to be retained in the colon
Results in diarrhea within 30-60 minutes
Constipation
Enemas
Instilled directly into the lower colon
Retained in bowel
Cleansing
Types of enemas
Tap water
Saline
Soap
Oil
Medicated
Infection
Etiology/Pathophysiology
Invasion by pathogenic microorganisms
Person-to-person contact
Fecal-oral transmission
Long-term antibiotic therapy
Clinical manifestations
Rectal urgency
Tenesmus
Nausea, vomiting & diarrhea
Abdominal cramping
Fever
Infection

E-coli 0157:H7
Not part of normal human intestinal flora
Found in 1% of food cattle
Contaminated or under cooked meat or contaminated water
Signs and symptoms
Bloody diarrhea, abdominal cramping and tenderness
Avoid-anti-diarrheals and anti-mobility
C-Difficle
Complication of antibiotic because it inhibits the growth of normal
intestinal flora and allows for the overgrowth of C-Difficile
A toxin is produced that causes tissue damage in the intestine
Stop the offending antibiotic
Diagnosis-stool culture
Treatment-Flagyl or Vancomycin
Infection
Risk Factors
Recent travel to endemic area
Food borne Illness
Waterborne Illness
Day care exposure
High-risk sexual behavior
Antibiotic use within 6 months (C-
Difficile)
Infection
Diagnostic tests
Stool culture
Blood chemistry
Medical management/nursing interventions
Antibiotics
Fluid and electrolyte replacement
Kaopectate
Pepto-Bismol
Irritable Bowel Syndrome (IBS)
Etiology/Pathophysiology
Episodes of alteration in bowel function
Spastic and uncoordinated muscle
contractions of the colon
Related to eating coarse or highly seasoned
food
Clinical manifestations
Abdominal pain and distention relieved by BM
Frequent bowel movements
Sense of incomplete evacuation
Flatulence, constipation, and/or diarrhea
Irritable Bowel Syndrome (IBS)

Red Flags: Suggestive of other diagnosis

Nighttime Diarrhea
Nocturnal stool incontinence
Nocturnal awakening due to abdominal discomfort
Abdominal pain that interferes with normal sleep
Visible or occult blood in stool
Weight loss
Recurrent Fever
Family History of Colon Cancer
Family History of Inflammatory Bowel Disease
Laboratory abnormality
Leukocytosis
Anemia
Increased Erythrocyte Sedimentation Rate (ESR)
Irritable Bowel Syndrome (IBS)

Increase in functional diarrhea with

stress
Associated with psychiatric issues
Panic attacks
Chronic pelvic pain
Childhood sexual abuse
Diagnostic tests
History and physical examination
Often by exclusion
Irritable Bowel Syndrome (IBS)
Medical management & Nursing interventions
Diet and bulking agents
Education
Medications
Anticholinergics
Milk of Magnesia, fiber, or mineral oil
Opioids
Anti-anxiety drugs
Ulcerative Colitis
Etiology/Pathophysiology
Ulceration of the mucosa and submucosa of the
colon
Tiny abscesses form
Produce purulent drainage, slough the mucosa, and
ulcerations occur
Starts on the left and progresses to the right side of
colon
The capillaries become friable and bleed
bloody diarrhea
Pseudopolyps may turn cancerous
Scar tissue may form
Loss of elasticity and absorption abilities
Ulcerative Colitis
Clinical manifestations/Assessment
Diarrhea-pus and blood
15-20 stools per day
Fluid/electrolyte imbalance
Abdominal cramping
Involuntary leakage of stool
The urge to defecate lessons as scar tissue replaces
functional tissue
Weight loss and deficient nutrition
Megacolon
Ulcerative Colitis
Diagnostic tests
Barium studies
Colonoscopy & biopsy
Stool for occult blood
X-rays
Labs such as chemistries, CBC
Medical management/Nursing interventions
Diet
No milk products or spicy foods
High protein, high calorie
Total parenteral nutrition (TPN)
Stress control
Assist patient to find coping mechanisms
Ulcerative Colitis
Medical management/Nursing interventions
Medications
Azulfidine
Dipentum & Rowasa
Corticosteroids
Imodium
Anticholinergic drugs are avoided
Surgical interventions
Colon resection
Ileostomy
Ileoanal anastomosis
Proctocolectomy
Kock pouch
Crohn’s Disease
Etiology/Pathophysiology
Inflammation, fibrosis, scarring, and thickening of bowel wall
Inflammation of segments of the GI tract from mouth to anus
Possible association between Crohn’s and altered immune
mechanisms
Typically occurs in the small intestine (jejunum and terminal
ileum)
Clinical manifestations/Assessment
Weakness, loss of appetite, dehydration
Diarrhea, 3-4 daily, contain mucus and pus (steatorrhea)
Right lower abdominal pain
Anal fissures and/or fistulas
Anemia
Crohn’s Disease
Complications
Malabsorption
Pernicious anemia
Acid/base disturbance related to diarrhea
Fistulas may occur
Medical management/Nursing interventions
Diet
High protein
High in nutrients
Avoid lactose-containing foods, vegetables, caffeine,
beer, MSG, highly seasoned foods, carbonated
beverages, fatty foods
Crohn’s Disease
Medical management/Nursing interventions
Medications
Corticosteroids
Antibiotics
Anti-diarrheals
Antispasmodics
Enteric-coated fish oil capsules
B12 replacement
Surgery
Segmental resection of diseased bowel
Diagnostic tools
Small bowel barium
Colonoscopy with biopsy
Crohn’s Disease
Colon surgery and colostomy procedure
Colostomy and Bowel
Resections

Sigmoid Resection Right

with colostomy
Hemicoloctomy
Bowel Resections

Left Hemicolotomy Anterior

Recto
Sigmoidectomy
Appendicitis
Etiology/Pathophysiology
Inflammation of the vermiform appendix
Lumen of the appendix becomes obstructed
Clinical manifestations/Assessment
Rebound tenderness over McBurney’s point
Vomiting
Low-grade fever
Diagnostic tests
WBC
CT scan
Ultrasound
Appendicitis
Medical management/Nursing interventions
Laparoscopy
Appendectomy
Post-op complications
Peritonitis
Intra-abdominal abscess
Mechanical bowel obstruction
Diverticular Disease
Etiology/Pathophysiology
Diverticuli become inflamed
Fecal matter becomes stuck in the pouches
Perforation is a risk
Diverticulosis
Pouch-like herniations through the
muscular layer of the colon
Diverticulitis
Inflammation of one or more diverticuli
Diverticular Disease
Clinical manifestations/Assessment
Patient can become septic
Diverticulosis
May have few, if any, symptoms
Constipation, diarrhea, and/or flatulence
Pain in the left lower quadrant
Diverticulitis
Mild to severe pain in the left lower quadrant
Elevated WBC
Low-grade fever
Abdominal distention
Vomiting
Blood in stool
Diverticular Disease
Medical management/Nursing interventions
A temporary colostomy may be indicated with closure
in 6 weeks to 3 months
Diverticulosis with muscular atrophy
Low-residue diet; stool softeners
Bedrest
Diverticulosis with increased intracolonic pressure
and muscle thickening
High-fiber diet
Sulfa drugs
Antibiotics if indicated
Analgesics
Diverticular Disease
Medical management/Nursing interventions
Surgery
Hartmann’s pouch
Double-barrel transverse colostomy
Diverticulosis
Progression of Diverticular Disease
Diverticulitis
Umbilical Stoma & Stoma Infected
with Candida Albicans
Prolapsed Loop Colostomy
Colostomy Pouch
Colostomy Irrigation
Pancreatitis

Pancreatic enzymes back up into

pancreas
Can be fatal
Inflammation of the peritoneum following
infection
Localized
Generalized
Peritonitis
Etiology/Pathophysiology
Inflammation of the abdominal peritoneum
Bacterial contamination of the peritoneal cavity from
fecal matter or chemical irritation
Medical emergency
The prognosis for untreated peritonitis is very poor
Peritonitis
Causes
Internal perforation of the gastrointestinal
tract
Intestinal foreign body
Colonic diverticulum
A ruptured appendix
Peritonitis
Clinical manifestations/Assessment
Severe abdominal pain
May present in the fetal position with knees drawn up
Pain with movement
Nausea and vomiting
Abdomen is rigid
Tympanic or absent bowel sounds
Chills
Weakness
Weak rapid pulse
Fever
Hypotension
Peritonitis
Diagnostic tests
Flat plate of the abdomen
CT scan
Medical management
Semi-Fowler’s position
Surgery
Fecal contamination
Removal irritants
Parenteral antibiotics
NG tube
IV fluids
Meconium peritonitis
External Hernias
Etiology/Pathophysiology
Congenital or acquired weakness of the abdominal wall or
postoperative defect
Hernia is a protrusion of viscus through an abnormal
opening or weakened wall of the cavity in which it was
normally contained
Abdominal or Ventral
Femoral or inguinal
Umbilical
External Hernias
Clinical manifestations
Protrusion at umbilicus, groin or incision
Pain may or may not be present
Complications
Incarceration
Strangulation
Diagnostic tests
Radiographs
Palpation
External Hernias
Medical management/Nursing interventions
If no discomfort, hernia is left unrepaired,
unless it becomes strangulated or obstruction
occurs
Truss
Surgery
Synthetic mesh is applied to weakened area of the
abdominal wall
Umbilical Hernia
Hiatal Hernia

Etiology/Pathophysiology
Protrusion of the stomach and other abdominal
viscera through an opening in the membrane or tissue
of the diaphragm
Contributing factors: obesity, trauma, aging
Clinical manifestations/Assessment
Most people display few, if any, symptoms
Gastroesophageal reflux
Hiatal Hernia
Medical management/Nursing intervention
Head of bed should be slightly elevated when lying
down
Small frequent meals
OTC medications for GERD
Surgery
Posterior gastropexy
Transabdominal
fundoplication (Nissen)
Hiatal Hernia
Intestinal obstruction
Etiology/pathophysiology
Intestinal contents cannot pass
Partial or complete
Mechanical
Non-mechanical
Clinical manifestations/assessment
Vomiting; dehydration
Abdominal tenderness and distention
Constipation
Hiatal Hernia

Sliding hernia Rolling hernia

Intestinal Obstruction
Etiology/Pathophysiology
Mechanical
An occlusion of the lumen of the intestinal tract
– Adhesions, incarcerated hernias, impacted
feces, tumor, intussusception, volvulus,
strictures of inflammatory bowel disease
Non-mechanical
Neuromuscular or vascular disorder
– Paralytic ileus, trauma to the spine, mesenteric
thrombosis that reduces blood flow to the bowel
Intestinal Obstruction

Intestinal obstructions. A, Adhesions. B, Volvulus.

Intestinal Obstruction

Clinical manifestations/Assessment
Loud high pitched bowel sounds above the
obstruction and absent bowel sounds below
Inability to pass stool or gas
Vomiting, abdominal cramps, abdominal
distention
Diagnostic tests
Radiographic examinations
BUN, sodium, potassium,
hemoglobin and hematocrit
Intestinal Obstruction
Medical management/Nursing interventions
Evacuation of intestine
NG tube to decompress the bowel
Intestinal tube to evacuate the contents
Surgery
Required for mechanical obstructions
– Bowel resection
Hemorrhoids

Etiology/Pathophysiology
Varicosities (dilated anorectal vessels/veins)
External or internal
Contributing factors
– Straining with defecation, diarrhea,
constipation, pregnancy, obesity, CHF, portal
hypertension, family history, prolonged sitting
and standing
Anatomic abnormalities
Intrinsic weakness of anal blood vessels
Hemorrhoids
Clinical manifestations/Assessment
Varicosities in rectal area
Bright red bleeding with defecation
Pruritus
Rectal Pain
Prolapsed hemorrhoid
Fullness or mass sensation
Hemorrhoids
Diagnostic tests
Visual inspection
Digital Rectal Exam
Anoscopy
Differential Diagnosis
Fissure
Perirectal Abscess
Rectal Fistula
Condyloma
Rectal carcinoma
Hemorrhoids
Medical management/Nursing interventions
Bulk stool softeners
Hydrocortisone cream
Analgesic ointment
Sitz baths
Ligation
Sclerotherapy;
Cryotherapy
Infrared photocoagulation
Hemorrhoidectomy
Anal Fissure
Etiology/Pathophysiology
Linear ulceration or laceration of the skin of the anus
Usually caused by trauma
Lesions usually heal spontaneously
May be excised surgically
Usually follows trauma or diarrheal illness
Increased anodermal blood flow causes fissures
Affects young and middle-aged adults
Anal Fissure
Clinical manifestations/Assessment
Onset after forced hard bowel movement
Bright red rectal bleeding
Pain during bowel movement
Cut with sharp glass sensation
Pain persists for an hour after stooling
Avoid anoscopy if possible
Painful and usually not needed
Use local anesthesia if performed
Anal Fissure
Clinical manifestations/Assessment (continued)
Crack or crevice in anoderm at anal verge
Usually in canal midline (anterior or
posterior)
Lateral suggests other diagnosis
Best seen with lateral traction on opposite
buttock
Sentinel pile (distal skin tag)
Tag-like swelling of fissure end
Results from infection and edema
Anal Fistula
Etiology/Pathophysiology
Abnormal opening on the surface near the anus
Usually from a local abscess
Common in Crohn’s disease
Treated by a fistulectomy or fistulotomy
Perirectal abscess sequelae of rupture or
surgery
Anal Fissure
Anorectal cancer
Tuberculosis
Local radiation therapy
Lymphogranuloma venereum
Anal Fistula
Clinical manifestations/Assessment
Chronic seropurulent or mucus drainage from fistula
Communicating tract between perianal skin and anus
One or several external openings tracking toward
anus
Associated conditions
Perirectal Abscess