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MEDICOSURGICAL NURSING
BSC LECTURE NOTES
Course tutor: Dr Kehbila Jules

Management of Gastrointestinal Emergencies

1. Acute Gastrointestinal Bleeding

Causes of upper GI (UGI) bleeding include (70-80% of all GI bleeding:
■ Gastric or duodenal ulcers including stress ulcers; may be nonsteroidal anti-inflammatory drug (NSAIDs) related
■ Peptic ulcer disease, gastritis, or esophagitis ■ Esophagogastric varices
■ Mallory-Weiss tear ■ Neoplasms ■ Liver disorders
Causes of lower GI bleeding include (20-30% of all GI bleeding):
■ Diverticulosis ■ Infectious colitis ■ Bowel disease or trauma
■ Neoplasm ■ Hemorrhoids or anorectal disorders
Pathophysiology
■ Constriction of peripheral arteries → ↓ blood flow to skin and kidneys → renal failure;
↓ blood flow to GI tract → mesenteric insufficiency →bowel infarction and liver necrosis;
↓ blood flow to coronary arteries → myocardial infarction (MI), pulmonary edema, heart failure, and dysrhythmias;
↓ blood flow to brain → confusion, anxiety, restlessness, stupor, and coma.
■ Acute massive GI bleed → ↓ blood volume → ↓ cardiac output → ↓ BP, HR → hypovolemic shock and multiple organ
dysfunction.
■ Metabolic acidosis and lactic acid accumulation → anoxia and respiratory failure.
Clinical Presentation
■ Hematemesis: Bright red or brown, coffee-ground emesis ■ Melena: Black, tarry stools
■ Hematochezia: Maroon-colored stools or bright red blood
■ Hypotension: May be orthostatic, light headedness, fainting
■ Tachycardia: ■ Cardiac dysrhythmias ■ Tachypnea, shortness of breath, chest pain
■ Pallor, apprehension, confusion, lethargy, weakness ■ ↓ urine output, urine concentration
■ bowel sounds, diarrhea ■ Stupor and coma if large blood loss
■ Multiple organ dysfunction if severe blood loss and hypovolemic shock
Diagnostic Tests
■ CBC, platelets, and coagulation studies
■ Serum chemistries, liver function tests, kidney function test
■ Arterial blood gases (ABGs) or pulse oximetry ■ UGI series
■ Abdominal x-ray or CT of abdomen ■ Barium enema
■ GI bleeding scan ■ Endoscopy
■ Colonoscopy or sigmoidoscopy
Management
■ Monitor vital signs and hemodynamics status
■ Monitor for cardiac dysrhythmias.
■ Assess respiratory status and ABGs or pulse oximetry. Administer O2 via cannula, mask, or mechanical ventilation.
Assess for signs of hypoxia.
■ Insert nasogastric (NG) tube and set at low intermittent suction. Lavage as necessary. Assess color and amount of
drainage. Note bright red to coffee-ground drainage. Keep patient NPO if active bleeding. Start clear liquids when
bleeding stops.
■ Assess bowel sounds; assess abdomen for distention and palpate for pain.
■ Administer IV fluids, colloids, crystalloids, blood, and blood products.
■ Note amount and color of feces.
■ Insert Foley catheter. Monitor intake and output. Assess fluid and electrolyte balance.
■ Administer histamine blockers or proton pump inhibitors. Consider misoprostol (prostaglandin analog),
anticholinergics, or mucosal protective agents.
■ Administer IV or intra-arterial vasopressin with caution.
■ If coagulopathy is present ( partial thromboplastin time [PTT]), administer vitamin K and fresh frozen plasma.
■ Administer tranexamic acid (Cyklokapron) if excessive bleeding and decreased fibrinolysis.
■ A specific protocol of medications is ordered if patient is Helicobacter pylori positive.
■ Provide emotional support to patient and family. Relieve anxiety and pain.
■ Prepare patient for possible endoscopic or surgical procedures:
■ Laser phototherapy
■ Endoscopic thermal or injection therapy
■ Intra-arterial embolization
■ Vagotomy, pyloroplasty, or total or partial gastrectomy

Hepatic Failure
Hepatic failure is defined as loss of liver function which occurs when there is a loss of 60% of hepatocytes. It may be
chronic or acute and can lead to hepatic encephalopathy.. Acute liver failure usually occurs in people with no previous
history of liver disease unlike chronic liver which occurs in previous liver problems like cirrhosis.

Causes of hepatic failure include:

■ Cirrhosis of the liver ■ Hepatitis A, hepatitis B, hepatitis C, and Epstein-Barr virus
■ IV drug use, cocaine use, and acetaminophen toxicity ■ Repeated environmental and hepatotoxin exposure
■ Malignancy ■ Hypoperfusion of the liver
■ Metabolic disorders: Reye’s syndrome, Wilson’s disease
■ Malnutrition, diabetes mellitus, chronic cholestatic disease, and hypertriglyceridemia
■ drugs including acetaminophen overdose
■ Postoperatively: jejunoileal bypass, partial hepatectomy, liver transplant failure

Pathophysiology
■ Severe liver impairment such as necrosis or ↓ blood supply to liver → toxic substances accumulating in the blood.
■ Impaired bilirubin conjugation, ↓ clotting factors, ↓ glucose synthesis, ↓ lactate clearance → jaundice, coagulopathies,
hypoglycemia, and metabolic acidosis.
■ Decreased macrophages in liver → risk of infection and spleen enlargement.→
■ Hypoalbuminemia, fluid and electrolyte imbalances, acute portal hypertension → development of ascites.

■ Hepatic failure may progress to hepatic encephalopathy.

Clinical Presentation
■ Jaundice, ascites, edema, and pruritus ■ Malnutrition, nausea, vomiting, and anorexia
■ Weakness, fatigue, and confusion ■ Hyperventilation, respiratory alkalosis, dyspnea, pleural effusion, and hypoxemia
■ Hypokalemia and hypo- or hypernatremia ■ Palmar erythema, spider nevi, and bruising
■ Asterixis: Liver flap (patient extends arms → wrist dorsiflexes downward involuntarily)
■ metabolic acidosis, hypoglycemia, hypokalemia, and hyponatremia
■ Gallstones, malnutrition, light-colored stools, and dark urine
■ Diarrhea and steatorrhea (fatty, greasy, foul-smelling stools)
■ Hepatic encephalopathy: Drowsiness, confusion, delirium or coma, inappropriate behavior, fetor hepaticus (breath odor)
Diagnostic Tests
■ CT scan or ultrasound ■ Serum chemistries, bilirubin, and albumin
■ AST, ALT, and cholesterol ■ Ammonia levels
■ CBC and platelets ■ ABGs or pulse oximetry
■ PT, PTT, plasmin, plasminogen, fibrin, and fibrin-split products
■ Urinalysis, urine bilirubin, and urine urobilinogen
Nursing and Medical Management
■ Administer lactulose orally or rectally.
■ Administer diuretics such as furosemide (Lasix) if ascites present. Monitor intake and output. Prepare patient for
paracentesis.
■ Measure abdominal girth; weigh daily. ■ Monitor for cardiac dysrhythmias.
■ Provide stress ulcer prophylaxis. Elevate head of bed 20°–30°. Assess for signs of GI bleeding.
■ Administer vitamin K and platelets. Avoid frequent venipunctures. ■ Treat fever and control BP.
■ Correct fluid and electrolyte imbalances. Prevent and correct hypokalemia, which increases renal ammonia production
→ ammonia across the blood-brain barrier.
■ Prevent infection. Administer prophylactic antibiotics. Consider rifaximin (Xifaxan).
■ Assess neurological status, level of consciousness, Glasgow Coma Scale score, and response to verbal and noxious
stimuli.
■ Assess for signs of increased intracranial pressure (ICP). Administer mannitol.
■ Assess respiratory status, and monitor ABGs or pulse oximetry. Correct hypercapnia and hypoxemia via O2
administration or mechanical ventilation.
■ Provide continuous renal replacement therapy (CRRT) if renal failure present.
■ Avoid benzodiazepines and other sedatives that may mask symptoms.
■ Use physical restraints as necessary. Provide reality orientation. Institute measures for patient safety.
■ Administer medications with caution. Adjust dosage per liver function tests.
■ Provide a low-protein, low-sodium diet. Restrict fluids as necessary. Consider enteral feeding or total parenteral
nutrition (TPN) if oral intake insufficient. Assess for hypoglycemia. Monitor serum albumin, electrolytes, and liver
function tests.
■ Prevent intravascular volume depletion through IV fluids, colloids, and crystalloids. Avoid lactated Ringer’s solution.
■ Monitor ammonia levels ■ Provide comfort measures and emotional support.
■ Prepare patient for TIPS to ↓ portal hypertension, prevent rebleeding from varices, and ↓ formation of ascites.
■ Prepare patient for liver transplantation if necessary.
Complications
■ Cerebral edema and increased ICP, and low cerebral perfusion pressure ■ Cardiac dysrhythmias and coagulopathy
■ Respiratory depression, acute respiratory failure, and respiratory arrest ■ Sepsis and circulatory failure
■ Acute renal failure ■ Hypoxemia, metabolic acidosis, and electrolyte imbalances
■ Hypoglycemia ■ GI bleeding
■ Hepatic failure may progress to hepatic encephalopathy → death.
■ The severity of hepatic encephalopathy is evaluated according to the following grades:
■ Grade 1: Euphoria or anxiety, shortened attention span
■ Grade 2: Lethargy, apathy, subtle personality change, inappropriate behavior, minimal disorientation to time or place
■ Grade 3: Somnolence to semistupor, responds to verbal stimuli, confusion
■ Grade 4: Coma, unresponsive to stimuli

Acute Pancreatitis
Pancreatitis is an inflammation of the pancreas that can be categorized into edematous interstitial pancreatitis and acute
necrotizing pancreatitis. 10%–20% of cases of pancreatitis are idiopathic and have no etiologic factor. Causes of
pancreatitis include: ( recall I GETSMASHED)
■ Alcoholism
■ Gallstones, biliary disease, and hypertriglyceridemia
■ Infection (e.g., mumps, ischemia)
■ Blunt abdominal trauma and surgical trauma
■ Hyperparathyroidism, hypercalcemia, and hyperthyroidism
■ Systemic lupus erythematosus and vasculitis
■ Medications such as glucocoticoids, sulfanomides, tetracyclines, NSAIDs, furosemide, hydrochlorothiazide, and
estrogen
Pathophysiology
■ Trypsinogen is converted to trypsin (pancreatic enzymes) → destruction of ductal tissue and pancreatic cells →
autodigestion and fibrosis of the pancreas.
■ An increase in capillary permeability → leakage of fluid into the interstitium → edema, hypovolemia, hemorrhage,
pancreatic, and adipose tissue necrosis → third spacing of fluids → systemic inflammatory response syndrome (SIRS).
■ Obstruction of the pancreatic duct → reflux of bile into the pancreas → enzyme reaction.
■ Drugs and toxins → autodigestion and inflammation.
Clinical Presentation
■ Severe knife-like midepigastric or midabdominal pain that may radiate to the back; onset of pain is frequently 24–48
hours after a heavy meal or alcohol ingestion; pain may also be diffuse and difficult to localize
■ Nausea and vomiting
■ Fever, diaphoresis, and weakness
■ Tachypnea, ↓ BP, HR, and other symptoms of hypovolemic shock
■ Hypoactive or absent bowel sounds, and abdominal tenderness and Distention →
■ Ascites and jaundice if illness severe
■ Pancreatic hemorrhage → Grey Turner’s sign (gray-blue discoloration
of the flank) or Cullen’s sign (discoloration of the umbilical region)
■ Palpable abdominal mass if pseudocyst or abscess present
■ Hypocalcemia and hyperlipidemia
Diagnostic Tests
■ Serum amylaseand/or lipase >3 times the upper limit of normal
■ Abdominal flat plate or ultrasound of abdomen, CT, MRI, and endoscopic cholangiopancreatography
■ Chest x-ray to detect pleural effusions
■ Serum chemistries, including ↓ calcium, ↓ magnesium, bilirubin, glucose, ↓ potassium, liver enzymes, ↓ albumin, and
triglycerides
■ Urinalysis and urinary amylase (6.5–48.1 U/hr [SI units])
■ CBC ( WBC, hematocrit and hemoglobin may be or ↓), PT/PTT, C-reactive protein
■ ABGs to assess for hypoxemia and metabolic acidosis
Management
■ Administer analgesics; position patient in knee-chest position.
■ Consider prophylactic antibiotics. For necrotizing pancreatitis, administer imipenem-cilastatin (Primaxin) for its high
concentration of the drug in the pancreas.
■ Assess fluid and electrolyte balance. Note hypokalemia or hypocalcemia.
Administer IV fluids, crystalloids, and colloids. Monitor intake and output.
■ Assess nutritional status. Keep patient NPO initially. Consider TPN, or gastric or jejunal enteral feedings. Stress ulcer
prophylaxis.
■ Insert NG tube if vomiting, obstruction, or gastric distention is present. Provide frequent oral care.
■ Assess for metabolic acidosis.
■ Assess respiratory status and monitor ABGs or venous oxygen saturation. Administer O2 as needed.
■ Administer insulin if elevated blood glucose levels exist.
■ Assess abdomen for distention, rigidity, ascites, and increasing pain or rebound tenderness; auscultate bowel sounds and
measure abdominal girth.
■ Treat fever and monitor WBC count.
■ Assess vital signs. Monitor for cardiac arrhythmias.
■ Prepare patient for surgical debridement or pancreatic resection for necrotizing pancreatitis or drainage of pancreatic
pseudocyst or abscess.
Complications
■ Pancreatic abscess or pseudocyst formation, and bowel infarction
■ Acute lung injury (ALI), pleural effusion, atelectasis, pneumonia, pneumonitis, hypoxemia, respiratory failure, and
acute respiratory distress syndrome
■ Hypotension, pericardial effusion, myocardial depression, cardiac dysrhythmias, and disseminated intravascular
coagulation
■ Acute renal failure, ■ Hepatic dysfunction, obstructive jaundice, and paralytic ileus
■ Stress ulcers and esophageal varices → GI hemorrhage
■ Severe hemorrhage and shock ■ Multiorgan failure, sepsis, and death
Nursing Diagnosis
 Pain and discomfort related to edema, distention of the pancreas, and peritoneal irritation
 Imbalanced nutrition: less than body requirements related to inadequacy dietary intake, impaired absorption,
reduced food intake, and increased metabolic demands.
 Activity intolerance related to fatigue
 Ineffective breathing pattern related to severe pain, pulmonary infiltrates, pleural effusion and atelactasis
 Impaired skin integrity resulting from poor nutritional status, bed rest, surgical wound
 Fear in response to the diagnosis of pancreatitis
 Ineffective coping related to the diagnosis of pancreatitis
Nursing Management
The client should avoid oral intake to inhibit pancreatic stimulation and secretion of pancreatic enzymes.
 Total parenteral nutrition is administered to assist with metabolic stress.
Maintain fluid and electrolyte balance.
 Assess fluid and electrolyte status (e.g. skin turgor, mucous membranes, intake and output); and provide
replacement therapy as indicated.
Promote adequate nutrition.
 Assess nutritional status; monitor glucose levels; monitor IV therapy, provide a high-carbohydrate, low-protein,
low-fat diet when tolerate; and instruct the client to avoid spicy foods.
Maintain optimal respiratory status.
 Place the client in semi-Fowler’s position to decrease pressure on the diaphragm.
 Teach the client coughing and deep-breathing techniques.

Peritonitis
Peritonitis is the inflammation of the peritoneum, the serous membrane lining the abdominal cavity and covering the
viscera. It may be localized or generalized. Peritonitis is an example of acute abdomen.

Can be classified as acute or chronic, septic or aseptic, and primary or secondary

 Most common type is acute suppurative (septic) peritonitis secondary to visceral disease

Primary peritonitis is rare; as is chronic peritonitis (e.g. due to TB infection; although the incidence is highest in
patients receiving peritoneal dialysis)
Aseptic peritonitis is usually due to chemical (e.g. urine, bile, gastric contents, blood, meconium) or foreign
body irritants (e.g. starch, talc, cellulose) and will often develop into a secondary septic peritonitis
Primary peritonitis, otherwise known as spontaneous bacterial peritonitis, most commonly occur inpatients with
cirrhosis and clinically significant ascites.
Secondary peritonitis most commonly occurs as a result of spillage of intestinal, biliary, or urinary tract contents into the
peritoneal space as a result of perforation, suppuration, or ischemic injury. Patients at risk for developing secondary
peritonitis include those with recent abdominal surgery, a perforated ulcer or colon, a ruptured appendix or viscus, a
bowel obstruction, a gangrenous bowel, or ischemic bowel disease.

Pathophysiology
Inflammation, bacterial infection, ischemia, tumor, and trauma → leakage of contents from the abdominal organs into the
abdominal cavity → tissue edema → fluid in peritoneal cavity.
Clinical Presentation
■ Abdominal pain that increases with movement such as coughing and flexing the hips; rebound tenderness, guarding, and
abdominal rigidity (washboard abdomen); Blumberg’s sign: Pressing a hand on the abdomen elicits pain, but pain
increases when releasing the hand as the peritoneum moves back into place
■ Air and fluid in the bowel ■ Abdominal distention, hyperactive → hypoactive bowel sounds → paralytic ileus
■ Nausea and vomiting ■ Fever and HR
Diagnostic Tests
■ CBC: assess for leukocytosis, and ↓ hemoglobin and hematocrit
■ Serum chemistries ■ Abdominal x-ray
■ Peritoneal lavage or peritoneal aspiration, and culture and sensitivity studies of peritoneal fluid or peritoneal effluent
Complications
■ Fluid and electrolyte imbalance, ↓ CVP, hypovolemia → shock → acute renal failure
■ Intestinal obstruction due to bowel adhesions ■ Peritoneal abscess ■ Sepsis
Management
■ Administer antibiotics. Obtain blood cultures to assess for sepsis.
■ Obtain peritoneal effluent cultures.
■ Provide fluid and electrolyte replacement. Monitor intake and output.
■ Administer analgesics and antiemetics. Place patient on side with knees flexed. →
■ Monitor vital signs. Assess for ↓ BP and HR. Provide cardiac monitoring.
■ Assess respiratory status. Administer O2 as indicated by ABGs or pulse oximetry.
■ Assess abdomen for pain and distention. Auscultate bowel sounds.
■ Perform surgery to remove infected material and correct the cause.

Bowel obstruction

An interruption in the normal passage of bowel contents.

Etiology
 Mechanical bowel obstruction: an interruption in the normal passage of intestinal contents due to a structural
barrier (e.g., bowel cancer, adhesions)
 Paralytic ileus: a temporary impairment of peristalsis in the absence of a mechanical obstruction

Degree of obstruction
 Partial bowel obstruction: bowel obstruction in which passage of some intestinal content through the blocked
segment is possible
 Complete bowel obstruction: total interruption of the passage of intestinal contents
 Closed loop obstruction: a type of complete mechanical bowel obstruction in which a segment of bowel is
occluded at two contiguous points (e.g., volvulus)

Site of obstruction
 Small bowel obstruction (SBO): obstruction occurring in the duodenum, jejunum, or ileum
 Large bowel obstruction (LBO): obstruction occurring in the cecum, colon, or rectum

Progression
 Simple bowel obstruction: obstruction without evidence of bowel ischemia
 Strangulated bowel obstruction: obstruction with compromised intestinal blood flow, resulting in bowel
ischemia

Functional bowel obstruction, or paralytic ileus, is a temporary disturbance of peristalsis in the absence of
mechanical obstruction. Postoperative ileus is the most common cause of paralytic ileus, which can also be caused
by metabolic disturbances (e.g., hypokalemia), endocrinopathies (e.g., hypothyroidism), and certain drugs (e.g.,
anticholinergics). Mechanical bowel obstruction is classified according to the location as either small bowel
obstruction (SBO) or large bowel obstruction (LBO) and, depending on the severity of obstruction, as either partial or
complete. The most common cause of SBO is postoperative bowel adhesions, while the most common cause of LBO
is malignant tumors.

INFLAMMATORY BOWEL DISEASE

Definition
 The term inflammatory bowel disease (IBD) is used to identify two chronic inflammatory GI disorders; regional
enteritis (i.e. Crohn’s disease) and ulcerative colitis.
Risk Factors
 Food additivies
 Tobacco
 Radiation exposure
 Immunologic influences
 Hereditary

Pathophysiology

Regional enteritis
 Is a subacute and chronic inflammation that extends through layers of the bowel walls from the intestinal
mucosa. Fistula, fissures, and abscesses extend into the peritoneum, but segments of normal intestinal tissue
occur between the inflammations.

Ulcerative colitis
 Is an inflammatory disease of the submucosal layer of the colon and rectum characterized by continuously
occurring ulcerations and shedding of intestinal epithelium. Fat deposits and muscular hypertrophy result in a
narrow, short, and thickened bowel.

Assessment/Clinical Manifestations/Signs and Symptoms

Regional enteritis
 Abdominal tenderness and pain, typically colicky and increased after meals
 Diarrhea, flatulence, and steatorrhea
 Fever, malaise, and anorexia
 Signs of nutritional deficits
 Perianal fistulas and abscesses
  Usually occurs in ileum and ascending colon

Ulcerative colitis
 Severe diarrhea containing pus, blood and mucosa
 Abdominal cramping and tenderness, fever
 Anorexia and weight loss
 Usually occurs in the descending colon and rectum

Laboratory and diagnostic study findings:

Regional enteritis
 Barium study of the upper GI tract, the most conclusive diagnostic test, reveals the classic “string sign” on a X-
ray study of the terminal ileum indicating constriction of a segment of intestine.
 Barium enema shows ulceration and “cobblestone” appearance because of fissures surrounded by submucosal
edema.
 Colonoscopy visualizes distinct ulceration separated by relatively normal mucosa in the ileum and ascending
colon.
 Computed tomography scan shows bowel wall thickening and fistula tracts.

Ulcerative colitis
 Barium enema shows mucosal irregularities, shortening of the bowel, and dilation of bowel loops
 Colonoscopy shows friable mucosa with pseudopolyps or ulcers in the descending colon and sigmoid colon.
 Stool analysis is positive for blood. Entemoeba histolytica, which causes dysentery, must be ruled out.

Medical Management
 Surgery may include total colectomy with ileostomy; segmental colectomy with anastomosis, subtotal
colectomy; total colectomy with continent ilestomy, and total colectomy with ileoanal anastomosis.

Nursing Management

Enhance nutritional status.

 Promote nursing care of the client who is receiving nothing by mouth, receiving oral fluids, or on total parenteral
nutrition during an acute exacerbation.
 Assess for fluid and electrolyte imbalance. Administer IV fluids and electrolytes as indicated.
 Encourage a low-residue, high-protein, high-calorie diet with supplemental vitamin therapy and iron
replacement.
 Implement measures to treat diarrhea or constipation.

Minimize pain.
 Address and mediate the client’s pain. Promote intermittent rest periods and bed rest when the client has acute
exacerbations.

Promote client and family teaching.

 Encourage the client to seek psychotherapy to determine the factors that distress the client and how to deal
with these factors to preventexacerbations.
Provide client teaching covering:
 The importance of good nutrition and adequate fluid intake
 Stress-management techniques
 Perianal skin care
 The need for follow-up visits to the health care provider

Administer medications, which include antidiarrheals, corticosteroids, antibiotics, antispasmodics, and anticholinergic
and opioid analgesics.

Abdominal hernias
Definition

Abdominal hernias are defined as the abnormal protrusion of intra-abdominal contents through
congenital/acquired areas of weakness in the abdominal wall.

Classification

The four categories of anatomically-classified abdominal hernias include the following:

1. ventral hernias: (e.g., epigastric, umbilical, incisional, spigelian hernias),

2. groin hernias: (inguinal and femoral hernias),
3. pelvic hernias (obturator, sciatic, and perineal hernias),
4. flank/lumbar hernias: Incisional hernias, Lumbar hernias(superior and inferior).
Risk factors
 Mechanical causes such as not lifting heavy weights correctly, hard coughing, incorrect posture or blows
to the abdomen.
 Conditions that increase pressure in the abdominal cavity such as obesity, constipation, chronic lung
disease and fluid build-up in the abdomen (ascites).
 Muscle weakness: congenital or acquired via overexertion, poor nutrition or smoking, for example.
 Gender M>F - Age, - Pregnancy -Previous hernia
 Prematurity and low birth weight

Clinical features

Reducible hernia

 Hernial contents completely return to the abdominal cavity through the abdominal wall defect on lying
down or upon application of mild external pressure. They have a positive cough reflex
o Most reducible hernias manifest as an asymptomatic nontender mass.

Irreducible/incarcerated hernia

 Hernial contents become adhered to the hernial sac and cannot be reduced into the abdominal cavity.
 o Irreducible nontender mass
o Visible cough impulse present
o May decrease partially on lying down
o Increased risk of obstruction and strangulation

Obstructed hernia

 The abdominal wall defect acts as a tourniquet around the hernial contents, causing edema and distension of
the hernial contents.

 Acute pain at the site of the hernia

 Absent cough impulse

Strangulated hernia

 Ischemia and necrosis of the hernial contents due to compromised vascular supply
o Acute pain at the site of the hernia

o Features of bowel obstruction (if the hernial content is bowel)

o Signs of strangulation
 A tender, irreducible hernia, Absent cough impulse, Edematous, erythematous, warm overlying
skin
  Toxic appearance, fever, signs of sepsis
  May lead to intestinal gangrene
  Fatal if left untreated

Diagnosis

Usually a clinical diagnosis

Utrasound, CT scan, X-ray, if hernia proves difficult to diagnose

Management

Treatment
 Surgical hernia repair is recommended for the management of most abdominal hernias.
o Surgery: open or laparoscopic tension-free closure of the abdominal wall defect with/without a mesh

o Elective surgery is indicated in reducible and incarcerated hernias.

o Emergency surgery is indicated in obstructed or strangulated hernias.
 Conservative management (observation) is indicated in:
o Congenital umbilical hernia in children < 5 years of age
o Asymptomatic wide-necked hernias in patients with high operative risk: A truss or corset may be
considered in these patients to decrease the risk of obstruction and strangulation
Bowel Obstruction

An interruption in the normal passage of bowel contents.

Etiology
 Mechanical bowel obstruction: an interruption in the normal passage of intestinal contents due to a structural
barrier (e.g., bowel cancer, adhesions)
 Paralytic ileus: a temporary impairment of peristalsis in the absence of a mechanical obstruction

Degree of obstruction
 Partial bowel obstruction: bowel obstruction in which passage of some intestinal content through the blocked
segment is possible
 Complete bowel obstruction: total interruption of the passage of intestinal contents
 Closed loop obstruction: a type of complete mechanical bowel obstruction in which a segment of bowel is
occluded at two contiguous points (e.g., volvulus)

Site of obstruction
 Small bowel obstruction (SBO): obstruction occurring in the duodenum, jejunum, or ileum
 Large bowel obstruction (LBO): obstruction occurring in the cecum, colon, or rectum

Progression
 Simple bowel obstruction: obstruction without evidence of bowel ischemia
 Strangulated bowel obstruction: obstruction with compromised intestinal blood flow, resulting in bowel
ischemia

Etiology

Small bowel obstruction Large bowel obstruction

 Malignant tumors (e.g., colorectal
carcinoma): most common cause
 Adhesions (e.g., prior abdominal surgery, abdominal of LBO
Most
tuberculosis): most common cause of SBO
common  Volvulus: second most common
causes cause of LBO
 Incarcerated hernias: second most common cause of SBO

Other  Meckel diverticulum  Diverticulitis

causes
 Strictures (e.g., Crohn disease)  Adhesions (e.g., postoperative,
prior abdominal surgery)
 Malignant tumors or metastases
 Strictures (e.g., inflammatory
 Gall stone ileus bowel disease, congenital
 Superior mesenteric artery syndrome (bowel obstruction strictures)
due to compression of the third portion of the duodenum  Fecal impaction
in between the aorta and the superior mesenteric artery)
 Foreign body impaction
 Small bowel obstruction Large bowel obstruction
 Foreign body impaction
 Tumor
 Internal hernia

 Congenital intestinal atresia (e.g., duodenal  Hirschsprung disease

atresia, jejunal atresia)
 Congenital strictures and bands (e.g., Ladd
Specific to infants  Intussusception (e.g., secondary to Meckel bands in intestinal malrotation)
and children diverticulum)
 Meconium ileus
 Congenital strictures and bands (e.g., Ladd
bands in intestinal malrotation)  Rectal atresia

Pathophysiology
Bowel obstruction → stasis of luminal contents and gas proximal to the obstruction → ↑ intraluminal pressure,
which leads to the following:
 Gaseous abdominal distention → sequestration of fluids within the distended bowel loops (third
spacing) → dehydration and hypovolemia
 Vomiting → loss of fluid and Na+, K+, H+, and Cl- → hypokalemia, metabolic alkalosis, and
hypovolemia
 Compression of intestinal veins and lymphatics → bowel wall edema → compression of intestinal
arterioles and capillaries → bowel ischemia
o → ↑ Bowel wall permeability → translocation of intestinal microbes to the peritoneal cavity →
sepsis
o → Necrosis and perforation of the bowel wall → peritonitis
o → Anaerobic metabolism and lysis of ischemic cells → accumulation of lactic acid and release
of intracellular K+→ metabolic acidosis and hyperkalemia

Clinical features

Clinical features SBO LBO

Abdominal pain  Colicky, periumbilical  Colicky or constant

Nausea/vomiting  Early-onset  Late-onset

 Large volume
 Bilious  Initially bilious
 Progresses to fecal vomiting (presence of feces in
 vomitus)

Constipation or  Late-onset in proximal SBO  early-onset in distal LBO

obstipation

Abdominal distension Typically less significant than in LBO Early and significant abdominal distention
Examination findings  Dehydration and possible hypovolemia (hypotension, dry mucous membranes)
 Diffuse abdominal tenderness
 Tympanic percussion
 Increased high-pitched, tinkling bowel sounds (early) or absent bowel sounds (late)
 Collapsed, empty rectum on digital rectal examination

Diagnostics

In the workup of suspected mechanical bowel obstruction, imaging(like X ray, CT scan, MRI) allows for quick
confirmation of the diagnosis as well as detection of conditions requiring immediate surgery (e.g., perforation).
Laboratory tests(serum electrolytes, FBC, may further help to assess the severity of the condition (e.g.,
electrolyte imbalance due to vomiting).

Treatment
Conservative management
 Indications
o Partial bowel obstruction cases
o Complete bowel obstruction with no signs of ischemia/necrosis or signs of clinical deterioration
 
 Measures
 Fluid resuscitation, correction of electrolyte imbalance
 Intestinal decompression: nasogastric tube insertion
  Bowel rest (NPO)
 Administration of IV analgesics and antiemetics
 Gradual increase of oral intake, starting with clear fluids, can be initiated once the abdominal pain and
distention subside and bowel sounds return to normal.
 Etiology-specific treatments
 Fecal impaction: stool evacuation (manual disimpaction, distal softening/washout with enemas or
suppositories, proximal softening/washout with oral solutions such as polyethylene glycol or sodium
phosphate)
 Sigmoid volvulus with no signs of strangulation: rigid/flexible sigmoidoscopic detorsion.

Surgery
It is indicated in strangulation, perforation, persistent obstruction.

Paralytic ileus
Definition

 Paralytic ileus: temporarily impaired peristalsis of the gastrointestinal tract in the absence of mechanical
obstruction

Etiology
  Intra-abdominal surgery (postoperative ileus)
 Abdominal trauma (e.g., due to retroperitoneal hemorrhage)
 Endocrine abnormalities (e.g., hypothyroidism, porphyria, uremia)
 Electrolyte disturbances (e.g., hypokalemia)
 Neuropathy (e.g., diabetes mellitus, spinal injury)
 Neurosurgical procedures (e.g., spinal surgery)
 Vascular diseases (e.g., mesenteric ischemia)
 Peritonitis
 Inflammation of intra-abdominal organs (e.g., appendicitis, cholecystitis, pancreatitis, severe
gastroenteritis)
 Medications (e.g., anticholinergics, opioids, antidepressants)

Pathophysiology

 Stressful stimuli to the bowel (e.g., surgery, peritonitis) → sympathetic nervous system activation →
decreased/arrested peristalsis
 Inflammation or intraoperative manipulation → local release of nitric oxide → relaxation of intestinal smooth
muscles → decreased/arrested peristalsis
 Decreased/arrested peristalsis → bowel wall distention → progresses as detailed above in mechanical bowel
obstruction

Clinical features

Same as for mechanical but for non colicky pain and decresed bowel sounds.

Treatment

 Conservative treatment: in patients with no signs of localized or diffuse sepsis (e.g., appendicitis,
secondary peritonitis)
o Bowel rest

o Nasogastric tube insertion

o IV fluids and electrolyte repletion
o Stop or decrease causative medications (e.g., opioids).
o Gradual increase in enteral feeding as tolerated by the patient
o Early postoperative ambulation (although still recommended to prevent DVT) and use of
prokinetics have not been proven to improve peristalsis.
 Surgical intervention: in patients with signs of peritonitis (e.g., appendectomy, exploratory laparotomy