Intestinal diseases Notes


Osmosis High-Yield Notes

This Osmosis High-Yield Note provides an overview of Intestinal diseases essentials. All Osmosis Notes are clearly laid-out and contain striking images, tables, and diagrams to help visual learners understand complex topics quickly and efficiently. Find more information about Intestinal diseases:

Intestinal adhesions

Ischemic colitis


Irritable bowel syndrome

Necrotizing enterocolitis

Small bowel ischemia and infarction



Diverticulosis and diverticulitis

Femoral hernia

Gallstone ileus


Inguinal hernia

NOTES NOTES INTESTINAL DISEASES GENERALLY, WHAT ARE THEY? PATHOLOGY & CAUSES ▪ Diseases preventing adequate digestive system function ▫ Often involve inflammation, stasis, obstruction, necrosis ▪ Various structural, functional etiologies SIGNS & SYMPTOMS ▪ Abdominal symptoms etiologicallydependent ▪ Abdominal pain, distension, constipation, bowel-habit change, hematochezia, nausea, vomiting ▪ Bulging abdominal mass (in hernia) DIAGNOSIS DIAGNOSTIC IMAGING TREATMENT ▪ See individual diseases MNEMONIC: APPENDICITIS Right lower-quadrant pain common differential Appendicitis/ Abscess Pelvic inflammatory disease (PID)/ Period pancreatitis Ectopic/ Endometriosis Neoplasia Diverticulitis Intussusception Crohn’s Disease/ Cyst (ovarian) IBD Torsion (ovary) Irritable Bowel Syndrome Stones ▪ CT scan, MRI, ultrasound OTHER DIAGNOSTICS ▪ Right lower-quadrant pain common differential (see mnemonic) OSMOSIS.ORG 263
APPENDICITIS PATHOLOGY & CAUSES SIGNS & SYMPTOMS ▪ Lumen obstruction → vestigial vermiform appendix inflammation ▪ Located at cecum base (near ileocecal valve) ▪ Obstruction → intraluminal content stasis → ↑ luminal, intramural pressure → thrombosis, occlusion small vessels, lymphatic flow stasis → ischemia, necrosis ▪ Excessive multiplication (gut flora) behind obstruction → immune system response → fibropurulent reaction → parietal peritoneum irritation ▪ Visceral nerve fiber stimulation → abdominal pain ▪ Abdominal pain ▫ Often begins in umbilical area → McBurney’s point (abdomen’s right lower-quadrant; one-third distance from anterior superior iliac spine, umbilicus) → progressive inflammation ▫ Rovsing’s sign: left lower-quadrant palpated → right lower-quadrant pain ▫ Psoas sign: right leg extended in leftside position → retrocecal appendix ▫ Obturator sign: right leg internally rotated in supine position → pelvic appendix ▪ Fever, anorexia, nausea, vomiting, diarrhea/ constipation ▪ In case of peritonitis ▫ Rebound tenderness at McBurney’s point ▫ Abdominal guarding (peritoneal irritation) CAUSES ▪ Obstruction ▫ Lymphoid hyperplasia (adolescence, viral infection), fecalith, foreign body (e.g. undigested seeds), pinworm infection, tumor (benign, malignant) RISK FACTORS ▪ 10–30 years old, family history, biologicallymale, cystic fibrosis comorbidity (children) COMPLICATIONS ▪ Appendix-supplying vessel compression → ischemia → appendix wall necrosis → bacterial invasion (wall) → appendix rupture → bacterial invasion (peritoneum) → peritonitis ▪ Periappendiceal abscess, subphrenic abscess, pylephlebitis, portal venous thrombosis, sepsis 264 OSMOSIS.ORG DIAGNOSIS DIAGNOSTIC IMAGING CT scan with IV contrast ▪ Increased appendix diameter ▪ Increased wall enhancement ▪ Severe ▫ Visible abscess, pus spillage Ultrasound (pregnancy, children) ▪ Visible, noncompressible, dilated appendix ▪ ↑ blood flow in appendix wall ▪ Visible appendicolith ▪ Right iliac fossa fluid collection
Chapter 34 Intestinal Diseases LAB RESULTS ▪ Neutrophilic leukocytosis ▫ ↑ with progression ▪ Mildly elevated serum bilirubin ▫ Perforation marker TREATMENT MEDICATIONS ▪ Antibiotics ▪ IV fluids, no food/water orally (NPO) SURGERY ▪ Removal (appendectomy) ▪ Abscess drainage Figure 34.1 Camera view of a laparoscopic appendicectomy being performed. The appendicectomy has been performed and the stump is visible on the right of the image, with the severed appendix reflected laterally. DIVERTICULITIS PATHOLOGY & CAUSES ▪ Inflamed diverticula; microperforation of diverticulum CAUSES ▪ Increased intraluminal pressure → erosion → inflammation, focal necrosis → micro/ macro perforation RISK FACTORS ▪ Diverticula present COMPLICATIONS ▪ Stricture, intestinal obstruction ▪ Diverticulum perforation ▫ Abscess, peritonitis ▪ Fistula formation ▫ Bladder communication ▫ Other organ communication (vagina, skin, other parts of bowel) ▫ Vesicoenteric fistula: pneumaturia (air in urine), fecaluria (stool in urine) SIGNS & SYMPTOMS ▪ Left lower-quadrant pain (often sigmoid colon); palpable abdominal mass; diarrhea/ constipation; nausea; vomiting; fever; urinary urgency/frequency/dysuria (inflamed sigmoid colon → bladder irritation) DIAGNOSIS DIAGNOSTIC IMAGING CT scan with contrast ▪ Inflammation → hyperdense tissue Abdominal X-ray ▪ Bowel obstruction ▪ Bowel perforation ▫ Free air LAB RESULTS ▪ Leukocytosis OSMOSIS.ORG 265
TREATMENT MEDICATIONS ▪ Uncomplicated ▫ Antibiotics, fluids, no food/water orally (NPO) SURGERY ▪ Resection ▫ Severe case/recurrence/complication OTHER INTERVENTIONS ▪ High-fiber diet ▫ Prevents recurrence Figure 34.2 Gross pathology of sigmoid diverticulosis. Notice how the diverticula appear either side of the longitudinal muscle. DIVERTICULOSIS ▪ Diverticulum (plural diverticula): outpouching of hollow anatomical structure wall ▫ Most frequent in large intestine (particularly sigmoid colon) ▪ Diverticulosis: multiple diverticula present (some areas) → mucosa/submucosa herniation predisposed → diverticulum formation ▫ Sigmoid colon: smallest diameter → highest pressure (Laplace’s Law: P∝1/D), most common location ▪ Outpouching: tend to form where intestinal wall-supplying blood vessels (i.e. vasa recta) traverse muscle layer TYPES RISK FACTORS PATHOLOGY & CAUSES True diverticulum ▪ All organ wall layers included (e.g. Meckel’s diverticulum) False (pseudo-) diverticulum ▪ Only mucosa, submucosa layers included ▫ Most common ▫ Colonic diverticula CAUSES ▪ Multifactorial pathogenesis from abnormal colonic motility ▪ Abnormal/exaggerated smooth muscle contractions → unequal intraluminal pressure distribution → high pressure 266 OSMOSIS.ORG ▪ Lifestyle: low-fiber diet, constipation; fatty food, red meat-rich diet; inactivity; smoking ▪ ↑ age ↑ risk ▪ Biologically-male ▪ Family history ▪ Obesity ▪ Connective tissue disorders ▫ Marfan syndrome ▫ Ehlers–Danlos syndrome ▫ Autosomal dominant polycystic kidney disease
Chapter 34 Intestinal Diseases COMPLICATIONS ▪ Blood vessel surrounding weakened outpouching ruptures → large intestine blood loss → bloody stool ▪ Inflammation (diverticulitis) ▪ Segmental colitis SIGNS & SYMPTOMS ▪ ▪ ▪ ▪ ▪ Often asymptomatic Vague abdominal pain, tenderness, bloating Occasional cramping Altered bowel habit (diarrhea/constipation) Rectal bleeding (hematochezia—fresh blood in stool) TREATMENT SURGERY ▪ Resection (if complications develop) OTHER INTERVENTIONS ▪ Lifestyle changes ▫ Diet (↑ fiber intake), avoid constipation, ↑ physical activity, smoking cessation DIAGNOSIS ▪ Often found incidentally DIAGNOSTIC IMAGING X-ray with barium enema ▪ Lower gastrointestinal series ▪ Directly shows pouches CT scan ▪ Visualization of colonic diverticula, thickening of the bowel wall thickening (> 4mm), an increase in soft tissue density within pericolonic Figure 34.3 Barium study demonstrating multiple diverticula. OTHER DIAGNOSTICS Colonoscopy, sigmoidoscopy ▪ Visible outpouching OSMOSIS.ORG 267
FEMORAL HERNIA PATHOLOGY & CAUSES ▪ Intestinal projection across femoral canal associated with femoral artery, vein; below inguinal ligament, lateral to pubic tubercle ▪ Abdominal contents enter hernia → may precipitate intestinal obstruction ▫ Most common cause worldwide ▫ Incarcerated/strangulated; severe abdominal pain, tenderness, erythema, fever, nausea, vomiting CAUSES ▪ Congenital, acquired ▪ Weakness/abnormal fascial opening in abdominal wall ▪ Usually includes properitoneal fat/omentum edge/small bowel loop RISK FACTORS ▪ Biologically-female, congenital disorder (embryological development → processus vaginalis obliteration failure), hernia (family history), obesity, pregnancy, frequent heavy lifting DIAGNOSIS DIAGNOSTIC IMAGING Ultrasound ▪ Variable echogenicity of tissue; movement of intra-abdominal structures in an inferior direction through the femoral canal CT scan ▪ Visualization of characteristic funnelshaped neck; protrusion through femoral ring COMPLICATIONS ▪ Narrow femoral canal ▫ ↑ incarceration/strangulation risk ▪ Compression of femoral vein ▪ Bowel obstruction SIGNS & SYMPTOMS ▪ Asymptomatic (commonly) ▪ Can manifest intestinal obstruction symptoms ▫ Bulging mass, pain, discomfort ▫ Supine: may resolve ▫ Valsalva maneuver (coughing/straining): worsens 268 OSMOSIS.ORG TREATMENT SURGERY ▪ Repair ▫ Open/laparoscopic (case-dependent) ▪ Early/elective repair ▫ Uncomplicated, asymptomatic hernia ▪ Urgent repair ▫ Complicated hernia (may require bowel resection)
Chapter 34 Intestinal Diseases GALLSTONE ILEUS PATHOLOGY & CAUSES ▪ Gastrointestinal motility (peristalsis) disruption → impaired bowel content propulsion ▪ Blockage → progressive intestine dilation blockage-proximal, decompression blockage-distal ▪ Gas accumulation (swallowed air, bacterial fermentation) → ↑ bowel distention ▪ Bowel wall edema → ↓ bowel content absorption → luminal fluid sequestration ▪ ↑ capillary permeability → transudative fluid loss from intestinal lumen into peritoneal cavity ▪ Emesis → fluid, electrolyte (Na, K, H, Cl) loss → metabolic alkalosis, hypovolemia ▪ Bowel dilation continues → ↓ intestinal wall tissue perfusion → ischemia, necrosis, bowel perforation TYPES Onset ▪ Acute: factors such as torsion, intussusception → sudden onset ▪ Chronic: factors such as tumor growth → prolonged onset ▪ Recurrent: often caused by adhesions → intermittent obstructions Extent ▪ Partial: some of intestinal lumen remains open ▪ Complete: total lumen obstruction Location ▪ Intrinsic: obstruction within bowel wall—e.g. inflammatory stricture, edema, hemorrhage, foreign body (ingested, parasite accumulation, large biliary calculus) ▪ Extrinsic: obstruction outside bowel wall— e.g. torsion, compression (hernia) Effect on intestinal wall ▪ Simple: no blood supply impairment ▪ Strangulated: blood supply cut off to bowel section ▪ Closed loop: obstruction occurs at each end of bowel section Type of factor ▪ Mechanical: obstruction caused by gallstone, neoplasm, adhesion, stricture, hematoma, meconium (in cystic fibrosis), medical device migration (PEG tube) ▪ Functional: intestinal musculature paralysis caused by trauma (surgery, blunt abdominal trauma), peritonitis, medication (opiates, anticholinergics) RISK FACTORS ▪ Surgery; bowel manipulation, anesthesia, postoperative opioids ▪ Hernia, neoplasm history, abdominal/pelvic irradiation, chronic inflammation, abdominal trauma COMPLICATIONS ▪ Fluid/electrolyte/acid-base imbalance; bowel strangulation, necrosis; perforation; sepsis SIGNS & SYMPTOMS ▪ Abdominal distension, cramping pain, constipation, nausea, vomiting ▪ Dehydration: tachycardia, dry mucous membranes, ↓ urine output ▪ Bowel sounds ▫ High-pitched “tinkling” sound auscultated: acute mechanical bowel obstruction ▫ Muffled, hypoactive bowel sounds: significant bowel distention association ▪ Abdominal percussion: hyperresonance/ tympany OSMOSIS.ORG 269
DIAGNOSIS DIAGNOSTIC IMAGING X-ray ▪ Small intestine, colon distension TREATMENT SURGERY ▪ Surgical intervention: e.g. release adhesions, complete obstructions, repair bowel OTHER INTERVENTIONS ▪ No food/water orally (NPO) ▪ Fluid, electrolyte replacement ▪ Parenteral feeding → nasogastric decompression Figure 34.4 A CT scan of the abdomen and pelvis in the coronal plane demonstrating a gallstone in the terminal ileum. If so large that it is unable to pass through the ileocecal valve, the gallstone will cause small bowel obstruction. GASTROENTERITIS PATHOLOGY & CAUSES ▪ Gastrointestinal tract viral infection (lasts 12 hours–3 days) ▪ Primary transmission ▫ Oral–fecal route ▪ Viruses → epithelium damage → osmotic diarrhea (> three stools daily), vomiting CAUSES ▪ Children: rotavirus (most common) ▪ Adult: norovirus (most common), astrovirus, adenoviruses RISK FACTORS ▪ ↑ morbidity ▫ Children, elderly, immunocompromised individuals 270 OSMOSIS.ORG ▪ Viral contact ▫ E.g. daycare center, cruise ship, closed community outbreak; contaminated food/water COMPLICATIONS ▪ Severe dehydration → altered mental status, weight loss SIGNS & SYMPTOMS ▪ Watery diarrhea; nausea; vomiting; abdominal cramps, pain; fever; malaise; dehydration (dry lips, skin turgor, tachycardia)
Chapter 34 Intestinal Diseases DIAGNOSIS LAB RESULTS ▪ Stool sample ▫ Excludes bacterial/parasitic etiology ▪ ↑ C-reactive protein (CRP), ↑ leukocytes ▪ Polymerase chain reaction (PCR) ▫ Stool, vomit: enzyme-linked immunosorbent assay (ELISA) performed for rotavirus TREATMENT Figure 34.5 A scanning electron micrograph of a cluster of Norwalk virus capsids. OTHER INTERVENTIONS ▪ Fluid replacement Prevention ▪ Hygiene practices, rotavirus vaccine INGUINAL HERNIAS PATHOLOGY & CAUSES Direct inguinal hernia ▪ Peritoneal sac; projects directly through inguinal triangle (AKA Hesselbach’s triangle) ▪ Projects medially to inferior epigastric vessels, lateral to rectus abdominis, pierces parietal peritoneum ▪ Hesselbach’s triangle composition: inguinal ligament (AKA Poupart’s ligament), rectus abdominis muscle (lateral border), inferior epigastric vessels ▪ Covered by external spermatic fascia Indirect inguinal hernia ▪ Most common hernia ▪ Intestinal projection through internal inguinal ring ▫ Location: spermatic cord (biologicallymale), round ligament (biologicallyfemale) exit the abdomen ▫ Testicular descent path: covered by three layers of spermatic fascia (three layers); external spermatic fascia (external oblique muscle fascia continuation); cremasteric muscle fascia; internal spermatic fascia (internal oblique muscle fascia continuation) CAUSES Indirect inguinal hernia ▪ Processus vaginalis closure failure (i.e. internal inguinal ring and processus vaginalis obliteration failure) RISK FACTORS Direct inguinal hernia ▪ Acquired, affects transversalis fascia ▫ Chronic intra-abdominal pressure ↑ (e.g. obesity, chronic cough, constipation, heavy lifting—occupational/recreational) ▪ Abdominal wall musculature atrophy OSMOSIS.ORG 271
(aging) ▪ Older, biologically-male individuals Indirect inguinal hernia ▪ Biologically-male individuals > biologicallyfemale individuals ▫ Biologically male: late right testicle descent ▫ Biologically female: asymmetric pelvis COMPLICATIONS Direct inguinal hernia ▪ Incarceration/strangulation potential Indirect inguinal hernia ▪ Can form hydrocele ▪ May precipitate intestinal obstruction ▪ Most common cause worldwide SIGNS & SYMPTOMS ▪ May be asymptomatic ▪ Bulging mass (indirect inguinal hernia, mass in groin), pain, discomfort ▫ Valsalva maneuver cessation/prone: may resolve ▪ Valsalva maneuver: worsens projection ▫ Coughing/straining DIAGNOSIS DIAGNOSTIC IMAGING Ultrasound ▪ Direct inguinal hernia ▫ Variable echogenicity of tissue; movement of intra-abdominal structures in an anterior direction through the Hesselbach triangle ▪ Indirect inguinal hernia ▫ Visualization through abdominal wall in biologically-female individuals CT scan ▪ Direct inguinal hernia ▫ Visualization of a protrusion with compressing inguinal canal contents; inguinal canal pushed into a semicircle of tissue that resembles a moon crescent ▪ Indirect inguinal hernia ▫ Identifies occult hernia/complications; hernia neck visualized superolateral to the inferior epigastric vessels OTHER DIAGNOSTICS ▪ Indirect inguinal hernia ▫ History, clinical exam; sufficient for majority of suspected inguinal hernias Direct inguinal hernia ▪ May precipitate intestinal obstruction ▫ Most common cause worldwide ▫ Incarcerated/strangulated: severe abdominal pain, tenderness, erythema, fever, nausea, vomiting Indirect inguinal hernia ▪ Visible bulge ▫ May be unapparent in biologicallyfemale individuals ▪ Incarcerated/strangulated ▫ Severe abdominal pain, tenderness, erythema, fever, nausea, vomiting Figure 34.6 Intraperitoneal view of an inguinal hernia during a laparoscopic hernia repair. The peritoneal cavity extends into the inginal canal, lateral to the epigastric vessels, making this an indirect hernia. 272 OSMOSIS.ORG
Chapter 34 Intestinal Diseases TREATMENT SURGERY Repair ▪ Open/laparoscopic (case-dependent) ▪ Elective repair ▫ Symptomatic hernias ▪ Direct inguinal hernia (asymptomatic) ▫ Monitor, surgical repair preferred Figure 34.7 Clinical appearance of a hernia in the groin. It is often not possible to distinguish between a direct and indirect hernia on clinical examination alone. Figure 34.8 A CT scan in the coronal plane demonstrating an indirect inguinal hernia. The proximal bowel is dilated, indicating a strangulated hernia causing obstruction. INTESTINAL ADHESIONS PATHOLOGY & CAUSES ▪ Fibrous tissue bands form physical attachment between intestines → ↓ intestinal motility ▪ Formed from scarred, post-trauma tissue ▪ Tissue injury → inflammation → fibrin deposits → fibrin connects parts left (similar to reconstructive “glue”) ▪ Adhesions extend between tissue if both parts have been injured, close proximity ▪ Initial fibrous adhesions dissolved by fibrinolytic enzymes ▪ Injury prevents enzyme secretion → macrophages, fibroblasts deposit collagen into adhesion → permanent CAUSES ▪ Surgery (most common), inflammation (cholecystitis, pancreatitis, peritonitis), endometriosis, pelvic inflammatory disease COMPLICATIONS ▪ Bowel obstruction, intestinal wall volvulus/ ischemia OSMOSIS.ORG 273
SIGNS & SYMPTOMS ▪ Abdominal pain, vomiting, bloating, constipation DIAGNOSIS DIAGNOSTIC IMAGING X-ray ▪ Detect obstruction; small intestine dilation CT scan, ultrasound ▪ Exclude other obstructive causes Figure 34.9 Intraoperative view of abdominal adhesions. TREATMENT SURGERY ▪ Surgical/laparoscopic adhesion excision INTUSSUSCEPTION PATHOLOGY & CAUSES ▪ Condition that occurs when part of intestine folds into adjacent section → obstruction ▪ Ileocecal region most commonly affected ▪ May be idiopathic/caused by abnormal structure (causes pathological lead point) → peristalsis causes one part of bowel to move ahead of adjacent section → bowel telescoping → ↑ pressure, impaired venous return → bleeding, bowel ischemia, infarction CAUSES ▪ Adults: abnormal growth (e.g. polyp, tumor) ▪ Infants: post-infection lymphoid hyperplasia (Peyer’s patches), Meckel’s diverticulum 274 OSMOSIS.ORG RISK FACTORS ▪ Most common < 24 months old, intestinal malrotation history, previous intussusception, intussusception in sibling, biologically male COMPLICATIONS ▪ Peritonitis, sepsis SIGNS & SYMPTOMS ▪ Intermittent abdominal pain (worsens with peristalsis) ▪ Guarding ▪ Straining efforts, draw knees toward chest ▪ Vomiting ▪ Sausage-like abdominal mass ▪ “Red currant jelly” stool (blood, mucus)
Chapter 34 Intestinal Diseases DIAGNOSIS TREATMENT DIAGNOSTIC IMAGING SURGERY Ultrasound, X-ray, CT scan ▪ Telescoped intestine: visualized as classic bull’s-eye image ▪ Intestinal obstruction signs OTHER INTERVENTIONS OTHER DIAGNOSTICS ▪ Free telescoped intestine portion → clear obstruction → remove necrotic tissue ▪ Reduction by air/hydrostatic contrast material enema (e.g. saline, barium) ▪ May be felt during digital rectal examination (children) IRRITABLE BOWEL SYNDROME (IBS) PATHOLOGY & CAUSES ▪ Chronic functional gastrointestinal system disorder; recurrent abdominal pain, impaired bowel motility ▫ No microscopic, macroscopic irregularities ▫ Constipation/diarrhea CAUSES ▪ Pathology not completely understood; likely multifactorial ▫ Visceral hypersensitivity: altered stimuli response ▫ Fecal flora alterations; bacterial overgrowth ▫ Food sensitivity: short-chain carbohydrates; ↑ water in bowel → smooth muscle spasm, diarrhea; metabolized by bacteria → gas → bloating, spasm, pain ▫ Psychosocial influence ▫ Genetic factor RISK FACTORS ▪ Biologically-female (region-dependent), previous gastroenteritis, stress SIGNS & SYMPTOMS ▪ Impaired bowel motility → diarrhea/ constipation ▪ Recurrent abdominal pain ▫ Bowel movement → improvement ▪ Bloating, nausea, mucus in stool DIAGNOSIS OTHER DIAGNOSTICS ▪ Based on predominant consistency of stool ▫ Diarrhea predominant, constipation predominant, mixed stool pattern, unclassified ▪ Organic disease exclusion “Rome IV” diagnostic criteria ▪ Abdominal pain ≥ one day weekly in last three months, associated with two/more of following ▫ Defecation → lessened pain ▫ Change in stool frequency ▫ Change in stool consistency OSMOSIS.ORG 275
TREATMENT ▪ No definitive cure MEDICATIONS ▪ Symptom-guided therapy ▫ Diarrhea predominant: drugs (e.g. loperamide) ▫ Constipation predominant: fiber supplementation, adequate fluid intake, osmotic laxatives ▫ Spasm, pain: antispasmodics OTHER INTERVENTIONS ▪ Stress management ▪ Diet modification ▫ Low fermentable oligo-, di-, monosaccharides/polyols diet (low FODMAPs diet) ▫ Avoid gas-producing food (caffeine, alcohol) ▫ Probiotics ▫ Physical activity ISCHEMIC COLITIS PATHOLOGY & CAUSES ▪ Inflammatory, ischemic condition; affects colon, most often splenic flexure, rectosigmoid junction ▪ Sudden blood flow ↓ → insufficient perfusion, oxygen/nutrient delivery to bowel → compromised cellular metabolism → ischemia, inflammation, infarction, necrosis → possible perforation ▪ Damaged, gangrenous mucosa promotes fluid/electrolyte loss → dehydration, shock, metabolic acidosis CAUSES ▪ Ischemia causes may be occlusive (embolic, thrombotic)/nonocclusive (↓ mesenteric circulation → severe hypotension, vasospasm) ▫ Usually acute, may be chronic disorder for marathon runners RISK FACTORS ▪ Any cause of ↓ perfusion/mesenteric arterial embolism, thrombosis/vasoconstriction ▫ Risk ↑ with age/comorbidities 276 OSMOSIS.ORG ▫ Hypercoagulable states (e.g. factor V Leiden) ▫ Biologically-female individuals ▫ Impaired perfusion (e.g. aortic surgery, myocardial infarction, hemodialysis) ▫ Vasculopathy ▫ Certain drugs (e.g. vasopressors) COMPLICATIONS ▪ Gangrenous bowel, stricture, pancolitis, colonic perforation, peritonitis, sepsis, shock, metabolic acidosis, multisystem organ failure, reperfusion injury, potentially fatal SIGNS & SYMPTOMS ▪ Symptomatology may be self-limiting ▪ Localized abdominal cramping, tenderness (usually left side) ▪ Loose, bloody stools, hematochezia ▪ ↓ bowel sounds ▪ Guarding, rebound tenderness ▪ Fever ▪ May develop shock signs (e.g. hypotension)
Chapter 34 Intestinal Diseases DIAGNOSIS ▪ Stool culture ▪ Identifies infectious etiology DIAGNOSTIC IMAGING X-ray/CT scan ▪ Abdominal; visualizes obstruction, perforation, pneumonitis ▫ Thumbprinting: segmented bowel edema/thickening pattern ▫ Double-halo pattern: mucosa, muscularis hyperdensity ▫ Pneumatosis coli, pneumoperitoneum indicates perforation TREATMENT MEDICATIONS ▪ Antibiotics ▫ Perforation/infection SURGERY ▪ Bowel resection ▫ Necrotic tissue Colonoscopy ▪ Visualizes ischemia: edema, erythema, friable mucosa ▪ Single-stripe sign: linear ulcer seen along longitudinal axis ▪ Submucosal hemorrhage: bluish nodules ▪ Biopsy: transmural fibrosis, mucosal atrophy LAB RESULTS ▪ Leukocytosis, thrombocytopenia, ↓ hemoglobin ▪ ↑ serum lactate, lactate dehydrogenase (LDH), creatine phosphokinase (CPK), amylase indicates tissue damage Figure 34.10 The endoscopic appearance of the colon in a case of ischemic colitis. There is mucosal edema and patchy erythema. OSMOSIS.ORG 277
OTHER INTERVENTIONS ▪ Circulatory support ▫ IV fluids, electrolytes ▪ Supplemental oxygen ▪ Bowel rest Figure 34.11 Histological appearance of the colon in an individual with ischemic colitis. There is mucosal necrosis, a sign that the condition is in its early stages at the time of biopsy. NECROTIZING ENTEROCOLITIS (NEC) PATHOLOGY & CAUSES ▪ Severe intestinal disorder: inflammation, ischemic necrosis ▫ Terminal ileum, colon (most often affected) ▪ Multifactorial pathology ▪ Preterm infants ▫ Immature gastrointestinal tract characterized by ↓ intercellular junction integrity + ↓ mucosal barrier → triggering event → normal intestinal microbiome dysbiosis → ↑ pathogenic bacterial growth → exaggerated immune system response → release of host cytokines, chemokines → tissue injury → necrosis ▪ Term infants ▫ Usually underlying condition adversely affecting intestinal perfusion 278 OSMOSIS.ORG RISK FACTORS ▪ Gestational age < 32 weeks ▪ Low birth weight < 2kg/4.41lbs ▪ Dysbiosis-contributing interventions ▫ Antibiotics, acid-reducing agents, feeding bovine milk formula ▪ Human milk promotes commensal bacteria growth, supports mucosal integrity ▪ Infections, gas-forming organism presence ▪ Underlying conditions ▫ Term infants (e.g. fetal growth restriction, perinatal hypoxia, congenital heart disease, gastrointestinal disorders, sepsis) COMPLICATIONS ▪ Bowel perforation, ileus, septic shock, metabolic acidosis, coagulopathy, respiratory failure ▪ Surgical complications
Chapter 34 Intestinal Diseases ▫ Strictures, short bowel syndrome ▪ ↑ impaired neurodevelopmental development risk ▪ High mortality rate SIGNS & SYMPTOMS ▪ Abrupt feeding tolerance change ▪ Abdominal distension, tenderness ▪ Erythema, crepitus, induration may also be present ▪ ↑ gastric residuals ▪ Vomiting (often bilious), bilious drainage from enteral feeding tubes ▪ Hematochezia ▪ Nonspecific findings ▫ Temperature instability, lethargy, apnea OTHER DIAGNOSTICS Surgery ▪ Through surgical/postmortem specimens ▫ Gross examination: gangrenous necrosis, hemorrhage, subserosal gas collection ▫ Histological examination: edema, hemorrhage, transmural necrosis, bacterial infiltration TREATMENT MEDICATIONS ▪ Empirical antimicrobial therapy SURGERY ▪ Exploratory laparotomy, bowel resection ▪ Primary peritoneal drainage (PPD) → ↓ intra-abdominal pressure OTHER INTERVENTIONS Figure 34.12 Gross pathology of necrotizing enterocolitis. ▪ Address complications (e.g. metabolic correction/hematologic abnormalities) ▪ Bowel rest with nasogastric intubation decompression ▪ Supplemental oxygen/mechanical ventilation ▪ Fluid replacement ▪ Inotropic support ▪ Total parenteral nutrition (TPN) DIAGNOSIS DIAGNOSTIC IMAGING Abdominal radiography, ultrasound ▪ Pneumatosis intestinalis, pneumoperitoneum/hepatobiliary gas LAB RESULTS ▪ Positive blood culture, ↓ platelets, ↓ red blood cells, disseminated intravascular coagulopathy evidence, ↑ serum lactate OSMOSIS.ORG 279
SMALL BOWEL ISCHEMIA & INFARCTION PATHOLOGY & CAUSES ▪ Serious small bowel condition; reduced blood flow, subsequent infarction; AKA mesenteric ischemia ▫ Collateral circulation network → small bowel especially vulnerable to widespread ischemic injury ▫ Hypoxia, subsequent reperfusion → tissue injury ▪ ↓ blood flow may be acute/chronic ▫ Acute: sudden ↓ small intestine perfusion ▫ Chronic: episodic ↓ digestion perfusion (often related to mesenteric atherosclerosis) ▪ Insufficient perfusion, oxygen/nutrient delivery to bowel → compromised cellular metabolism → ischemia, inflammation, transmural infarction, necrosis → bacterial transmigration + possible perforation ▪ Damaged, gangrenous mucosa promotes fluid/electrolyte loss → dehydration, shock, metabolic acidosis CAUSES ▪ Ischemia causes ▫ Occlusive (arterial/venous): embolic, thrombotic, tumor, volvulus, intussusception, hernia, atherosclerosis ▫ Nonocclusive: severe hypotension, vasospasm → ↓ mesenteric circulation RISK FACTORS ▪ Any cause of ↓ perfusion/mesenteric arterial embolism, thrombosis/vasoconstriction ▪ Cardiac disorders (e.g. arrhythmia, valvular disease → arterial emboli formation from heart; ↓ cardiac output, peripheral hypoperfusion) ▪ Procedures (e.g. cardiac catheterization, 280 OSMOSIS.ORG ▪ ▪ ▪ ▪ ▪ cardiopulmonary bypass surgery, hemodialysis → ↓ intestinal perfusion) Coagulative disorders Atherosclerotic occlusive disease Hypovolemia (e.g. dehydration, hemorrhage) Bowel strangulation (e.g. volvulus, incarcerated hernia) Vasoconstriction medications COMPLICATIONS ▪ Ileus, shock, metabolic acidosis, multisystem organ failure, high mortality SIGNS & SYMPTOMS ▪ Severe abdominal pain (often postprandial); nausea, vomiting; distended abdomen; guarding, rebound tenderness (develops later); ↓ bowel sounds; fever; feculent breath odor; rectal bleeding; may exhibit shock signs (e.g. hypotension) DIAGNOSIS DIAGNOSTIC IMAGING CT/magnetic resonance (MR) angiography ▪ Detects acute mesenteric ischemia Abdominal X-ray/CT scan ▪ Dilated bowel loops, bowel wall thickening, thumbprinting, intestinal pneumatosis, free intraperitoneal air LAB RESULTS ▪ Leukocytosis with left shift, ↑ hematocrit (dehydration, hemoconcentration) ▪ ↑ serum lactate, amylase, alkaline phosphatase
Chapter 34 Intestinal Diseases OTHER DIAGNOSTICS SURGERY ▪ Laparotomy ▫ Abdominal exploration ▪ Resection OTHER INTERVENTIONS TREATMENT ▪ Pain management ▪ Bowel rest with decompression MEDICATIONS ▪ Antibiotics ▪ Circulatory support ▫ IV fluids, electrolytes, inotropic medications VOLVULUS PATHOLOGY & CAUSES ▪ Intestinal obstruction ▫ Intestinal twisting/looping TYPES ▪ Classified by location Sigmoid volvulus (most common) ▪ Usually middle-aged/elderly individuals ▪ Causes include pregnancy, chronic constipation (e.g. Hirschsprung’s disease), intestinal adhesions Cecal volvulus ▪ Causes include impaired abdominal mesentery development, pregnancy, chronic constipation Midgut volvulus ▪ Usually infants/young children ▪ Caused by anomalous intestinal development (e.g. intestinal malrotation) COMPLICATIONS SIGNS & SYMPTOMS ▪ Abdominal tenderness, pain, distension, bilious vomiting, constipation, fever, auscultation (abnormal bowel sounds, often decreased), percussion (tympany), hematochezia (may indicate bowel ischemia, necrosis) DIAGNOSIS DIAGNOSTIC IMAGING X-ray ▪ Asses volvulus shape ▫ Bent inner tube sign (“coffee bean” sign) Barium enema ▪ May show “bird’s beak” shape (point of twisted bowel) ▪ Perforation suspected → barium contrast contraindicated CT scan ▪ Twisted mesentery (“whirlpool” sign) ▪ Mesenteric artery compression → intestinal wall ischemia, infarction ▪ Intestinal wall perforation, infection (e.g. diffuse peritonitis) OSMOSIS.ORG 281
TREATMENT SURGERY ▪ In case of midgut volvulus/ischemia/ necrosis; surgical resection if necessary OTHER INTERVENTIONS ▪ IV fluid replacement ▪ Bowel decompression ▫ Sigmoid volvulus: sigmoidoscopy ▫ Cecal volvulus: colonoscopy Figure 34.13 Abdominal radiograph demonstrating a massively dilated sigmoid colon in a case of sigmoid volvulus. Figure 34.14 3D CT virtual colonoscopy demonstrating sigmoid volvulus. 282 OSMOSIS.ORG

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