Intestinal diseases Notes

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 osms.it/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 osms.it/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 osms.it/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 osms.it/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 osms.it/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 osms.it/viral-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 osms.it/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 osms.it/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 osms.it/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) osms.it/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 osms.it/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) osms.it/necrotizing-enterocolitis 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 osms.it/ischemia-and-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 osms.it/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