From StudyingMed

< AH1
Jump to: navigation, search

See Lawson's page 130 AH1. & Jayraj's notes

Case 1

NB - read case as this presentation is "classic appendicitis"

  • Differentials:
    • Acute appendicitis
    • Ectopic pregnancy --> ask about last normal menstrual period, enquire about recent sexual activity
    • Mittelschmerz pain --> menstrual associated
    • Pelvic inflammatory disease
    • Ureteric colic
    • Meckel's diverticulum - outpouching of ileum: 2% of people
      • Obstruction can cause same presentation as appendicitis
    • Mesenteric lymphadenitis (young children) - follow gastroenteritis; enlarged/tender lymph nodes can cause right iliac fossa pain
  • Examination
    • Guarding - the muscles of the anterior wall go into spasm to prevent stretch of that part of the abdomen to prevent damage to underlying organs
      • Reflex response to peritonitis
      • Involuntary - prevent stretch of parietal peritoneum; can cause rigidity
    • Rebound tenderness
      • Increase in pain when release hand
      • Less cruel: elicit similar sign by percussing lightly on the area
    • All of the above are associated with peritonitis - different to bowel obstruction
  • Blood test
    • leucocytosis (systemic inflammatory response) and higher ESR (due to release of fibrinogen/other high molecular weight proteins from the liver; anticoagulated tube of blood, let it settle for an hour, measure mm of red cell sedimentation in an hour). CRP - acute phase protein from liver
      • nonspecific
    • suggests appendicitis but not confirmatory (other states e.g. cholecystitis produce the same picture
    • The reason why appendicitis first starts off with epigastric is because a viscus does not have somatic innervation, only autonomic innervation. As such, inflammation and pain is referred to the dermatome supplied by the same spinal segment supplying it. When the



  • Investigations to help you diagnose appendicitis:
    • Usually done on clinical grounds.
    • Imaging only done if there is doubt about the diagnosis.
      • CT is the most sensitive and specific, more so than ultrasound or MRI,. In obese patients, MRIs of the abdomen can be obscured by mesenteric fat, leading to false-negative results.
    • Pregnancy must be ruled out via β-HCG urine test.
    • CT scan (but may not be appropriate in young children, as they’d have to be anesthetised).
    • Ultrasound (good only if you have a good ultrasonography, not good in obese people, CT better for less skilled technician)
    • Plain abdominal x-ray is useless

 ===Pathogenesis of appendicitis==

  • Usually caused by some sort of obstruction first (e.g. by faecolith - hardened piece of faecal matter obstructing lumen).
    • Other obstructions: Obstruction outside the wall = carcinoma of the colon. Can also have obstructions in the wall.
  • Continued mucin secretion distal to the obstruction, leading to increased luminal pressure, distension and stretching of the wall (which is relatively inelastic). Favours bacterial proliferation, which are normally present in the appendicoel lumen (e.g. E coli and bacteroides).
  • Small venules and capillaries become thrombosed while arterioles remain open, leading to congestion. This is because pressure of the lumen > venous pressure. This results in ischaemic injury, particularly to the mucosa (most metabolically active part) --> bacterial invasion of mucosa --> acute inflammatory response in mucosa --> exudate in appendiceal wall and lumen
  • The inflammation involves the serosa of the appendix, and also the parietal peritoneum in the region.
  • Mucin provides environment which favours bacterial growth.
  • If inflammation spreads to mesoappendix, it can involve the appendicoel artery or vein - thrombosis of those vessels -> gangrene (necrosis with putrefaction by bacteria --> green/black appearance)
  • Gangrenous appendix could rupture --> pus and bacteria spill into peritoneal cavity

Complications

  • Periappendiceal abscess – the greater omentum adheres to the fibrinosuppurative exudate on the surface of the inflamed appendix, walling off the organ in an appendiceal mass. If gangrene of the organ develops, with subsequent perforation, pus accumulates within the mass and forms an abscess.
    • Very difficult to remove the appendix in an appendicoel mass
  • Inflamed appendix may adhere to greater omentum [fi
  • Generalised peritonitis has a high mortality rate because of septic shock. It is more likely to occur in young children (shorter greater omentum, thus less likely to wall off the appendix) and the elderly (in whom diagnosis is often delayed due to impaired reflex responses to pain).
  • Portal pyaemia is uncommon, but can be caused by bacteria entering the appendiceal vein and travelling to the liver to cause abscesses.
  • Worst case scenario: Rupture --> no localisation to greater omentum --> spread of infection to peritoneal cavity --> hypotension [+ abdominal guarding and rigidity + septic shock (bacterial toxins rapidly absorbed into the circulation - LPS endotoxin causes massive release of IL1 and TNFa --> vasodilation--> lower TPR and lower BP)
    • Can also exude a lot of fluid into the peritoneal cavity in peritonitis --> hypovolemic shock
    • Generalised abdominal pain of peritonitis is associated with rigidity/guarding
  • If they survive peritonitis --> abscesses in suphrenic or pelvic areas (remaining pus in peritoneum)
  • Common: wound infection and delayed wound healing, or opening up of wound [particularly in gangrenous or perforation of appendix]
  • Long term complications: adhesions (fibrous bands left over from inflammation) --> trap a loop of bowel --> bowel obstruction

Gross of appendicitis

  • This is appendicitis.
  • The yellow shows an inflamed appendix with mesenteric fat with the characteristics of inflammation – vasodilation and congestion of vessels, with swelling.
    • This makes it macroscopically red
  • The blue - haemorrhage.
  • The bit towards the right is fibrinosuppurative exudate – this leads to irritation of the parietal peritoneum lining the anterior abdominal wall, causing localised pain, tenderness and guarding.

Differentials information

This woman presents with abdominal pain associated with loss of appetite, which shifted to the right iliac fossa, and now has guarding and rigidity in that region. These clinical features are classically seen in acute appendicitis.

With regard to the other alternatives:

Mesenteric lymphadenitis typically occurs in young children following viral gastroenteritis, and may be associated with signs and symptoms that are difficult to distinguish from acute appendicitis. However, in view of this woman's age and the absence of a history of gastroenteritis, this is NOT the most likely diagnosis in this case.

Pelvic inflammatory disease is unlikely in this case because this woman is not sexually active. PID also typically presents with a high fever, unlike the low grade fever in this case.

Urinary tract infection (UTI) may present with urinary frequency and dysuria (cystitis) or loin pain and fever (pyelonephritis). The diagnosis is unlikely in this case, in view of the presence of tenderness and guarding in the right iliac fossa, as well as the absence of urinary symptoms.

Ectopic pregnancy may present with pain, tenderness and guarding in the right iliac fossa. However, in view of this woman's lack of sexual activity and normal menstrual period three weeks ago, the diagnosis is unlikely in this case.

Investigations of appendicitis

A helical CT scan would be the most useful imaging test in this case. It is considered to be more sensitive and specific than ultrasound for the diagnosis of appendicitis in obese patients. Please refer to the Diagnostic Imaging Pathways website for further information.

With regard to the other alternatives:

In general, MRI is not considered to be a first line investigation for appendicitis. In any case, abdominal MRI is unlikely to be useful in this case, because in this obese woman the appendiceal wall might be obscured by mesenteric fat, leading to a false-negative result. For more information, please refer to an article on MRI in appendicitis in eMedicine.

In many centres, an abdominal ultrasound is the preferred imaging investigation for the diagnosis of appendicitis. However, this test is less sensitive in obese patients, such as this woman. Another drawback of ultrasound is its operator dependence. Please refer to the Diagnostic Imaging Pathways website for more information.

An abdominal X-ray is rarely useful for imaging the appendix. Please refer to an article on abdominal radiography in eMedicine for more information.

Low grade fever = between 37.5°C and 38.2°C

Histo of appendicitis

This is an acutely inflamed appendix. All the features of acute inflammation are present throughout the appendiceal wall, extending into the mesoappendix (neutrophilic infiltration through to the muscularis externa is necessary to confirm the diagnosis histopathologically) - vasodilatation, congestion and haemorrhage, as well as a fibrinosuppurative exudate.

The regions will now be shown.


Mesoappendix = mesentery attaching appendix to ileum :)

Complications of gangrenous appendix

Periappendiceal abscess is the most likely outcome. The reason for this is that in an otherwise healthy adult with ongoing appendicitis, the greater omentum typically adheres to fibrinosuppurative exudate on the surface of the inflamed appendix, thereby walling off the organ in a periappendiceal mass. In this situation, if gangrene develops and subsequent perforation occurs, pus accumulates within the periappendiceal mass, forming a periappendiceal abscess.

Generalised peritonitis is a feared complication of gangrenous appendicitis, with a high mortality rate as a consequence of hypovolaemic shock and sepsis. This complication is more likely to occur in young children (whose greater omentum is shorter, and therefore less likely to wall off the appendix) and the elderly (in whom diagnosis is often delayed due to impaired reflex responses to pain).

Portal pyaemia is an uncommon complication of appendicitis, caused by bacteria entering the appendiceal vein, and travelling via the portal system to the liver to cause liver abscesses. This is not necessarily a consequence of gangrene, i.e. it can occur in fibrinosuppurative appendicitis.

  • Appendix: dilated, yellowed/discoloured distally, proximally firm and thick walled, wall distally is tissue thin and on the verge of perforation
    • Scanty fibrinous exudate on surface of appendix
    • Contents of appendix = fecal material and pus
    • Cause of appendicitis is sometimes a cancer. Commonest is carcinoid.
  • Distal end = inspissated fecal material

Slide

  • Haemorrhage and pus within the lumen of the appendix
  • Almost all of the epithelium has been lost to ulceration, only a few islands remaining
  • The normal structure of the wall is changed - vasodilation, neutrophils. Lymphoid follicles disrupted by inflammation
  • Muscularis:
  • Inflammation affecting mucosa/submucosa of the appendix from gastroenteritis, but true appendicitis is inflammation extending into the muscularis - if you see vasodilation/neutrophils extending into this layer = diagnostic - outside of this is fibrinosuppurative exudate
  • In this case, inflammation extends into the mesoappendix
  • Colicky abdo pain presentation: visceral pain
    • Visceral pain is referred to the dermatome that corresponds to embryonic origin of the structure - in this case the midgut (T12) - so it's referred to this level, umbilicus, midline, poorly localised
      • Colicky because of obstruction of appendicoel lumen and periodic contractions
    • Pain shifted because inflammation spread to serosal surface of appendix, irritated parietal peritoneum --> somatic pain fibres. Very localised, associated with reflex abdo muscle contraction --> guarding or rigidity
    • Anorexia (consistent with appendicitis) = reflex affect of visceral pain affecting gut --> causes pylorus to go into spasm. If they vomit, they only do it once. Recurrent vomiting is not consistent with the diagnosis.
    • Constipation -- cease peristalsis as result of visceral pain

Pathogenesis map

Case 2

Acute pancreatitis

Acute pancreatitis is the most likely diagnosis in this case, based on the history of a preceding alcoholic binge, epigastric pain radiating straight through to the back, and an elevated level of plasma lipase, which is more specific for the diagnosis than elevated plasma amylase (please see eMedicine for more details).

Pancreatitis results from intrapancreatic activation of zymogens, with subsequent injury to the pancreas and surrounding tissues (by proteases including trypsin, chymotrypsin and elastase), cell membranes (phospholipase) and fat stores in adipocytes (lipase). The disease typically presents with severe epigastric pain which characteristically radiates to the back.

Gallstone impaction in the ampulla of Vater and alcohol abuse are the two most common causes of acute pancreatitis in developed nations.

With regard to the other alternatives:

Ruptured abdominal aortic aneurysm characteristically presents in older age groups, and is also associated with severe hypotension and a pulsatile mass in the epigastrium.

Perforated peptic ulcer classically presents with generalised peritonitis (although it may be localised to the epigastrium on some occasions), caused by irritation of the peritoneum by gastric acid. Also, the pain is typically of suden onset, as opposed to the gradual onset of pain in this case.

Viral gastroenteritis is characterised by symptoms of vomiting, diarrhea and abdominal cramping. In the absence of those symptoms, so this is an unlikely diagnosis in this case.

Acute cholecystitis is characterised by pain and tenderness in the upper right quadrant, as well as fever. Occasionally, perforation of an inflamed gallbladder can result in epigastric or generalised peritonitis. The absence of fever and right upper quadrant tenderness is against the diagnosis in this case.

Enzymes from pancreatitis:

Amylase is responsible for digestion of complex carbohydrates, but does not injure host tissues.

Parenchymal necrosis in pancreatitis is caused by:

1. Enzymatic injury to cell membranes (phospholipase) and proteolytic digestion (trypsin, chymotrypsin); and 2. Oxygen radicals and proteolytic enzymes released by neutrophils as part of the acute inflammatory response.

The above processes primarily result in liquefactive necrosis, with potential loss of pancreatic structure.

Lipase can degrade triglyceride stored in adipocytes, causing liberation of free fatty acids and complexing with calcium salts, leading to enzymatic fat necrosis.

Elastase can degrade arterial walls, resulting in potentially fatal internal haemorrhage.

Case

  • Alcoholic, epigastric pain going through to the back. Guarding rigidity = peritonitis. Bowel sounds absence - reflex effect of peritonitis
  • Lipase for clinical chemistry - produced by exocrine pancreas along with
    • Amylase
    • Trypsin, chymotrypsin
    • Elastase
    • Phospholipase
  • These enzymes are released when the pancreas is inflamed. They are released into the circulation
  • Previously amylase was used as a marker for pancreatitis. Now lipase is used - more specific, stays elevated for longer - better for late presentations
  • Most common causes of pancreatitis: alcohol and gallstones
  • Need to distinguish between conditions requiring surgery (e.g. AAA or perforated peptic ulcer) vs not surgery. Elevated lipase excludes requirement for surgery
  • Differentials -
    • Acute pancreatitis – epigastric pain following alcoholic binge, radiating to the back with rise in plasma lipase and amylase. Results from inappropriate activation of pancreatic zymogens with
    • Acute cholecystitis – typically RUQ pain with fever. But can cause generalised peritonitis if perforated.
    • Perforated peptic ulcer – classically presents with generalised peritonitis (although may be localised to epigastrium), caused by irritation of the peritoneum by gastric acid. Pain in such cases is sudden rather than gradual.
    • Ruptured AAA – presents in older ages, associated with severe hypotension and pulsatile mass in the epigastrium.
    • Viral gastroenteritis – vomiting, diarrhoea and abdominal cramping.
  • Hypotensive: 1. exudation of fluid 2. sepsis (bacteria infect necrotic pancreas) 3. paralytic ileus (loss of fluid to the bowel - third space loss) 4. vasodilation throughout the body (chymotrypsin). Note that hyperglycaemia/osmotic diuresis is uncommon unless diabetic
    • Note that there is a functional defect in insulin secretion --> high BSL acutely
  • Low Ca: enzymatic fat necrosis
  • Patient’s blood results:
    • Elevated amylase and lipase are indicators of pancreatic involvement.
    • Lipase is more sensitive and specific for pancreatic disease, and remains elevated for longer.
    • The patient’s azotaemia (increased urea and creatinine) is probably secondary to shock, decreased renal perfusion.
    • BSLisupduetothepatient’sinabilitytoproduceinsulin.
  • Histology
    • Autolytic change - basement membrane intact but separated from the epithelium
    • Surrounding inflammation
    • Necrosis in peripancreatic tissue
    • Basophilic staining of former adipose tissue, but the cells have lost their nuclei and have basophilic staining material in cytoplasm. This is enzymatic fat necrosis = release of phospholipase from pancreatic acini destroying cell membrane. Lipase degrade TG into FFA and glycerol. Saponification: form a calcium salt with free calcium in the serum. This man had so much enzymatic fat necrosis occuring --> sequester a lot of calcium, hence low serum calcium
    • Can form a pseudocyst following acute pancreatitis --> ongoing pain/complications
  • Acute pancreatitis is related to autodigestion – by proteases that destroy tissue (trypsin, chemotrypsin) and blood vessels (elastase), phospholipases which cause cellular necrosis, and lipases that cause fat necrosis.
    • Furthermore, oxygen radicals and proteases released by neutrophils as part of the acute inflammatory response also causes damage.
    • Results in liquefactive necrosis (transformation of the cells into a liquid vicous mass) with distortions of pancreatic tissue.
    • Notethatamylasedoesnotcausedamagetohosttissues.
    • Lipases degrade triglycerides stored in adipocytes, releasing these fatty acids which can complex with calcium salts (saponification), leading to fat necrosis.
      • Causes of pancreatitis: gall stones, viruses (parvovirus, mumps), alcohol (destroys ducts and inappropriate activation of enzymes) and trauma.
      • In the macroscopic specimen on the right, there is an area of liquefactive necrosis and haemorrhage in the head of the pancreas, along with patchy fat necrosis.
      • Acute pancreatitis is often complicated by hypotension, due to a combination of:
    • Exudation into the peritoneal cavity;
    • Haemorrhage due to injury of arterial walls by elastase;
    • Sequestration of fluid in the bowel due to paralytic ileus - "third space loss"; o Complicating bacterial infection, resulting in sepsis; and
    • Activation of the kallikrein system by circulating trypsin, resulting in formation of bradykinin, leading to systemic arteriolar vasodilation.
      • In non-diabetics, even though insulin secretion might be impaired in acute pancreatitis, blood glucose levels rarely reach a level that would result in glycosuria and osmotic diuresis.
  • Mechanism for acute pancreatitis and activation of enzymes
    1. Obstruction of ducts: gallstones, lodging in ampulla of vater, block pancreatic ductal system, ischaemic injury to acinar cells and release of enzymes. Ductal obstruction can also occur due to alcohol (increases viscosity of mucinous secretions --> increased )
    2. Direct acinar injury - alcohol, drugs, trauma (e.g. steering wheel in car crash), viruses (mumps)
    3. Unique to alcohol: defective intracellular transport of enzymes - proenzymes are transported to a lysosome where they're cleaved into the active enzyme --> cell injury
  • Enzymes cause digestion of normal tissues
  • Complications acute pancreatitis: shock, ards, acute renal failure, DIC, pancreatic abscess, pancreatic pseudocyst (walling off of inflammation), duodenal obstruction (swollen pancreatic head).
    • Chronic pancreatitis (due to lots of alcohol over a long time - usually acute exac. on chronic): exocrine failure (malabsorption, weight loss, steathorrea), endocrine function (diabetes; when >90% beta cells lost), duct obstruction and pain, pseudocyst.

Common Complications from Acute Pancreatitis

  • ARDS due to systemic release of inflammatory mediators that cause sequestration and activation of neutrophils in pulmonary vasculature, leading to subsequent injury via release of oxygen radicals and proteases.
    • Systemic release of pancreatic enzymes, such as phospholipase A2, might contribute to ARDS via degradation of pumonary surfactant.
  • Following acute pancreatitis, a pancreatic pseudocyst may result from walling off of a collection of exuded fluid containing pancreatic enzymes within the lesser sac. Pseudocysts typically develop over several weeks - the fluid is initially contained by granulation tissue.
  • In acute pancreatitis, hypocalcaemia occurs primarily due to enzymatic fat necrosis, leading to sequestration of calcium via precipitation of calcium soaps in the abdominal cavity.
  • DIC can occur as a consequence of release into the bloodstream of tissue factor (thromboplastin) from injured pancreatic tissue, resulting in widespread microthrombi in microvascular beds (leading to multiple organ dysfunction), as well as consumption of platelets and clotting factors (leading to a bleeding diathesis).
  • Sepsis complicating acute pancreatitis may also induces DIC via systemic release of TNF-alpha, which initiates release of tissue factor, as well as activating endothelial cells.
    • Diabetes mellitus is not a typical complication of acute pancreatitis, because it requires more than 90% of beta islet cells to be destroyed. However, there may be transient beta islet cell dysfunction, resulting in short-term hyperglycaemia. Progressive destruction and scarring of the pancreas in chronic pancreatitis is more likely to be complicated by both pancreatic endocrine and exocrine failure.
  • Chronic Pancreatitis
    • Characterised by severe epigastric pain radiating to the back, resulting from pancreatic duct obstruction or repeated episodes of acute pancreatitis. It leads to atrophy of the exocrine pancreas, scarring and destruction and failure. This progresses onto weight loss and steatorrhoea.
      • Can cause diabetes, jaundice and malabsorption syndromes.


Case 3

  • Peritonitis RUQ (tenderness/rigidity).
  • Acute cholecystitis with gram negative sepsis: NB most people survive
  • Gross specimen
    • Not consistent with the history: gallbladder wall is scarred and contracted (been affected by chronic process). Most people presenting with acute cholecystitis that is really acute on chronic (e.g. epigastric pain after meal, fatty food intolerance etc. Acute exacerbation = big stone that blocks the neck of the gallbladder) - but not this lady.
  • Obstruction to bile outflow leads to inflammation of the gall bladder. This is because bile contains lecithin, cholesterol and bile. Lecithin can be enzymatically converted into lysolecithin, which is toxic to the gall bladder epithelium.
    • However, cholecystitis can occur without gall stones– e.g. typhoid fever and shock (reduced perfusion of gall-bladder leading to ischaemia and infection).
  • Bacteria can migrate to the inflamed tissues and cause suppurative bacterial infection. This can lead to gram-negative sepsis.
  • Risk factor for gall stones:
    • Obesity (more cholesterol secreted into bile). Family history.
    • Gender(oestrogencausesmorecholesteroltobesecretedintobile).
    • Haemolytic anaemia which cause pigment stones (excess Br in bile).
    • Fat, forty, female, fertile (high E), fair, flatulence
      • Increased cholesterol secreted into bile --> supersaturated bile --> gallstone
    • There are also pigmy gallstones (bilirubin gallstones). This is caused by haemolysis (e.g. haemolytic anaemia e.g. thalassemia)
  • Complications of acute cholecystitis
    • Tendstoresolvein7-10days.
    • Empyema of the gall-bladder.
    • Gallbladder gangrene: Most common complication, particularly in elderly patients and diabetes. Causes a sepsis-like picture.
    • Subsequent perforation: Occurs after gangrene; and perforate into the surrounding to form an abscess, or into the peritoneum to cause generalised peritonitis, or into the bowel to form a cholecystoenteric fistula.
    • Emphysematous cholecystitis: Secondary infection by gas-forming organisms e.g. E. coli, precipitating gangrene and perforation.
    • Obstruction of other parts of the biliary tree can cause irritation there – e.g. pancreatitis if the ampulla of Vater is obstructed and obstructive jaundice.
    • Repeated injury predisposes to cancer.
  • Key Features of Acute Cholecystitis

**Thickened wall due to oedema and inflammation.

    • Dilated and congested blood vessels.
    • No evidence here of chronic changes in the wall (unusual because patients tend to present with acute-on-chronic cholecystitis).
  • Clinical presentation of gallstones
    • May be asymptomatic for years
    • Very common (10%) in western society
    • Biliary colic (transient obstruction)
    • Acute cholecystitis - obstruction of cystic duct
    • Obstruct bile duct - obstructive jaundice
    • Acute pancreatitis - obstruct ampulla of vater
  • Complication: empyema of the gallbladder
    • Wall of gallbladder may be gangrenous and perforate --> peritonitis
    • Sepsis
    • Ascending cholangitis
  • Recommend removal of gallbladder after symptomatic problem because it is the main cause of cancer of the gallbladder. Exclusively occurs in gallstones people and has a poor prognosis
  • U/S: intense
    • US very good for gallstones in GB, not so good for in bile duct
    • Gallbladder bed inflamed and more echogenic than normal

Virtual slide

  • Top = columnar epithelium: absorptive, concentrates bile
  • Laminar propria underneath, then a layer of oblique SM for contractions
  • Inflammation in gallbladder wall - vasodilation and congestion of vessels, lots of neutrophils and fibrinosuppurative exudate, thickening wall of GB, extends throughout adventitia onto serosa.
    • Inflammation on serosa causes murphy's sign: breath in while palpating underneath right costal margin, and as GB makes contact with anterior wall, they catch their breath due to pain
  • Ulceration on surface, loss of epithelium
  • No evidence here of chronic changes in the wall (unusual because patients tend to present

with acute-on-chronic cholecystitis).

Case 5

  • Vomiting and upper abdo pain, vomiting brown fluid, and absolute constipation (no faeces, no gas)
    • High pitched tinkling bowel sounds
  • Small right sided inducible femoral hernia (know how to tell the difference between femoral and inguinal hernia)
    • Inguinal hernias generally have a larger hernial orifice, less likely to cause bowel trapping/obstruction than femoral hernia
  • Continuity of peritoneal cavity has been lost: loss of impulse on coughing (check it out)
  • This is small bowel because it has plicae circulares (small circulation bands of muscle forming a ladder pattern), and there are no haustrations
  • Decubitus X-ray demonstrates multiple air fluid levels = bowe obstruction
  • Classical features of complete mechanical bowel obstruction
    • Colicky abdo pain
    • Abdominal distension/vomiting
    • Absolute constipation
  • in this case it's due to a piece of small bowel being trapped in a hernial orifice
  • bowel loop trapped: venous return is stopped, bowel swells, pressure builds up, very little arterial inflow, causes ischaemic injury, causes cessation of peristalsis causing obstruction proximally
  • Removed necrotic bowel just in time to prevent faeculant peritonitis.
  • Histo: bottom part of bowel (trapped) - epithelium has lost integrity, haemorrhagic, necrosis. Submucosa is viable as is muscularis
  • Surgically remove the obstructed bowel and anastamose
  • Causes of small bowel obstruction
    • Herniation
    • Adhesions
    • Intussusception
    • Volvulus
  • Causes of large bowel obstruction: cancer, diverticular disease, sigmoid volvulus