Abdominal Flashcards

1
Q

What are the main types and locations of primary colorectal cancers?

A

The majority of colorectal cancers are adenocarcinomas derived from epithelial cells. Less common types of primary malignant colorectal tumours are carcinoid tumours, GI stromal cell tumours, and lymphomas.

The rectum is the most common site in the large bowel, accounting for 1/3 of all large bowel cancers, although the sigmoid colon in the most common site in the colon.

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2
Q

What are the risk factors for Colorectal Cancer?

A
  • Increasing age is the greatest risk factor for sporadic colorectal adenocarcinoma, with 99% occurring in people aged 40 or over.
  • Family history (APC mutation)
  • Lynch syndrome (Hereditary Non-Polyposis Colorectal Cancer) accounts for 5% of colorectal cancers.
  • Familial adenomatous polyposis (FAP)
  • Diet (high fat, low fibre)
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3
Q

What are the clinical features of Colorectal Cancer?

A

Red flag symptoms are common. They include:

  • Rectal bleeding
  • Change in bowel habit - increased frequency or looser stools is the most common symptom

Although weight loss and anorexia are uncommon.

Right sided carcinomas present with iron deficiency anaemia, usually with dark blood mixed in with stool. There may also be a RIF mass.

Left sided (commonest) carcinomas present with increasing frequency/looser stools, rectal bleeding (bright red blood coating stool) with or without mucus. Can also present as intestinal obstruction due to constricting neoplasm.

Rectal: Tenesmus, worm-like stool with other signs? There is a palpable rectal mass in up to 80% of patients.

Anal: Pain, pruritus ani, and mass felt.

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4
Q

Describe the NHS colorectal cancer screening programme

A

The NHS now has a national screening programme offering screening every 2 years to all men and women aged 60 to 74 years in England.

  • Eligible patients are sent Faecal Immunochemical Test (FIT) tests through the post

a type of faecal occult blood (FOB) test which uses antibodies that specifically recognise human haemoglobin (Hb)

Patients with abnormal results are offered a colonoscopy:

  • 5 out of 10 patients will have a normal exam
  • 4 out of 10 patients will be found to have polyps which may be removed due to their premalignant potential
  • 1 out of 10 patients will be found to have cancer
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5
Q

What are the investigations for Colorectal Cancer?

A

FBC may show microscopic anaemia (iron deficiency). LTFs and U&Es are often normal.

  • CEA (Carcinoembryonic Antigen) is a tumour marker elevated in only 40%-80% of patients.

Occult blood is often present and detected by faecal immunochemical test (FIT).

Sigmoidoscopy will reveal tumours in the rectosigmoid region and allow biopsy. Even if tumour is not detected, the presence of blood or slime coming down from above is strongly suspicious of a malignant disease.

Colonoscopy and biopsy is necessary.

CT thorax, abdomen and pelvis may be indicated in some patients.

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6
Q

Describe the management of Colorectal Cancer

A

Management centres around surgery:

  • Pre-operative: The bowel is cleared by enemas and oral stimulant laxatives (e.g. Picolax). Metronidazole and gentamicin are given at time of surgery.
  • Operative: The principle of operative treatment is wide resection of the growth together with its regional lymphatics.
    • In the unobstructed case, the bowel can be prepared beforehand and primary resection with restoration of continuity can be achieved.
    • In cases of obstruction, the primary goal is to relieve obstruction and so a Hartmann’s procedure can be performed. Primary restoration can occur at a different time.
  • Post-operative: Adjuvant chemotherapy with 5-fluorouracil (5-FU) in combination with folinic acid may reduce the risk of recurrent disease, and may prologue survival for metastatic disease.
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7
Q

Describe the surgical options for of colorectal cancer

A
  • Typically for a lesion in the right colon a right hemicolectomy is performed, with an ileocolic anastomosis.
  • For a lesion in the left colon, a left hemicolectomy or sigmoid colectomy is performed, with anastomosis of the colon to the rectum.
  • In an emergency situation, with unprepared bowel, a Hartmann’s operation can be performed with the formation of an end colostomy and the rectum oversewn or brought to surface.
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8
Q

What is the definition and classification of Mechanical Intestinal Obstruction?

A

Intestinal obstruction is a restriction to the normal passage of intestinal contents. It may be divided into two main groups: paralytic and mechanical. This page will discuss mechanical intestinal obstruction.

Classification

Mechanical bowel obstruction can be classified in various ways:

  • Speed of onset:
    • Can be acute which has a rapid onset and severe symptoms
    • Can be chronic which has insidious onset and less severe symptoms, for example due to carcinoma.
    • Can be acute-on-chronic which is the rapid development of obstruction in the background of chronic bowel obstruction.
  • Site:
    • Can be low/large bowel
    • Can be high/small bowel
  • Simple (no damage to blood supply) or strangulated (blood supply compromised)
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9
Q

What is the aetiology of Mechanical Intestinal Obstruction?

A

The aetiology can also be structured in different ways. One way is thinking about it by causes in the lumen, in the wall, or outside the wall:

  • Intraluminal causes include:
    • Impaction of faeces or worms
    • Intussusception
    • Gallstone ‘ileus’ (remember not really ileus)
  • Intramural causes include:
    • Tumours
    • Strictures such as from IBD, surgery, diverticulitis.
    • Congenital atresia
  • Extramural causes include:
    • Hernias
    • Volvulus
    • Adhesions
    • Extrinsic compression due to abscesses, haematomas, non-colonic tumours etc.
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10
Q

What are the common causes of small and large bowel obstruction?

A

Small bowel obstruction is commonly due to:

  • Adhesions (60%) - abdominal surgery is becoming increasingly common, which can commonly lead to adhesions.
  • Hernias

Large bowel obstruction is commonly due to:

  • Tumours (60%)
  • Diverticular stricture (20%)
  • Volvulus (5%)
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11
Q

What are the causes of intestinal obstruction in neonates and infants?

A
  • Neonatal: congenital atresia and stenosis (e.g. duodenal atresia), imperforate anus, volvulus neonatorum, Hirschsprung’s disease and meconium ileus.
  • Infants: intussusception, Hirschsprung’s disease, strangulated hernia and obstruction due to Meckel’s diverticulum.
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12
Q

What are the causes of intestinal obstruction in young adults/middle aged and the elderly?

A
  • Young adults and middle age: strangulated hernia, adhesions and bands, Crohn’s disease.
  • The elderly: strangulated hernia, carcinoma of the colon, colonic diverticulitis, impacted faeces.
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13
Q

What are the cardinal symptoms of Mechanical Intestinal Obstruction?

A

There are four cardinal features of bowel obstruction:

  1. Colicky abdominal pain: usually the first symptom. Small bowel pain tends to be periumbilical, whereas large bowel tends to be suprapubic.
  2. Abdominal distention: usually more pronounced in large bowel obstruction. With a small bowel obstruction that has little proximal bowel there may not be much to distant.
  3. Absolute constipation is an early feature in large bowel obstruction, but a late feature in small bowel obstruction - in fact the patient may pass a single normal stool after onset of small bowel obstruction as the distal bowel empties.
  4. Vomiting is more a early feature of small bowel obstruction and may be absent large or chronic bowel obstruction. In the late stages of intestinal obstruction, the vomiting becomes faeculent but not faecal. The faeculent vomiting is due to bacterial decomposition of the stagnant contents of the obstructed small intestine.
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14
Q

What are the examination features of intestinal obstruction?

A
  • The patient may be dehydrated if vomiting has been copious. They are in pain and may be rolling about with colic.
  • The pulse is usually elevated, but the temperature is frequently normal.
    • A raised temperature and a tachycardia suggest strangulation.
  • The abdomen is distended and visible peristalsis may be present.
  • The abdomen is tender and you may feel a mass.
  • Bowel sounds are usually accentuated and tinkling.
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15
Q

What must you look out for/perform if suspecting intestinal obstruction?

A

During inspection it is important to look carefully for three features:

  1. The presence of a strangulated external hernia, which may require a careful search in the case of a small strangulated femoral hernia in a very obese and distended patient, and
  2. The presence of an abdominal scar. Intestinal obstruction in the presence of this evidence of a previous operation immediately suggests adhesions or a band as the cause.
  3. Perform a rectal examination. It may reveal an obstructing mass in the pouch of Douglas, the apex of an intussusception or faecal impaction.
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16
Q

What are the investigations for Mechanical Intestinal Obstruction?

A
17
Q

Describe the management of Mechanical Intestinal Obstruction

A

Conservative

  1. Gastric aspiration by means of nasogastric suction. This helps to decompress the bowel and prevent asipration.
  2. Intravenous fluid replacement - a lot of fluid may be required. Hartmann’s solution or normal saline are given, with potassium if this is low and renal function satisfactory.
  3. Antibiotic therapy is commenced if intestinal strangulation is likely (or is found at operation).

Gastrografin can be therapeutic and help resolve bowel obstruction. If the contrast does not pass the through the bowel in 8 hours, it is unlikely conservative management would suffice, and surgery should be considered.

Operative

The affected bowel is carefully inspected to determine its viability. Doubtful bowel may recover after relief of the obstruction. It should be reassessed after it has been left for a few minutes wrapped up in a warm wet pack.

  • Small bowel: Conservative management is successful in 65- 80% of cases and surgical intervention is only considered for those patients who do not improve with conservative management. Generally small bowel can be resected and primary anastomosis performed with safety because of its excellent blood supply.
  • Large bowel obstruction is treated by resection of the obstructing lesion, with a primary ileocolic anastomosis in the case of obstructing lesions proximal to the splenic flexure. Left-sided lesions are managed by excision of the affected segment and exteriorizing the two ends of colon as a temporary colostomy and mucous fistula(Hartmann’s procedure). This is due to poorer blood supply of the large bowel and the fact that a colonic primary anastomosis is very liable to leak in the presence of obstruction.
18
Q

What are the complications for mechanical bowel obstruction?

A

Bowel ischaemia

Bowel perforation leading to faecal peritonitis (high mortality)

Dehydration and renal impairment

19
Q

What is the aetiology of peritonitis?

A
20
Q

What are the clinical features of peritonitis?

A

When the visceral peritoneum becomes inflammed, it presents as a generalised and severe constant abdominal pain due to the poor localisation of pain from the visceral peritoneum. The pain may become localised after (with the involvement of the somatically innervated parietal peritoneum).

Irritation of the diaphragm may be accompanied by shoulder tip pain.

Vomiting is frequent.

The pain is exacerbated by movement and coughing.

On Examination

Peritonitis is associated with guarding or rigidity of the abdominal muscles. If peritonitis involves the whole abdomen, the patient would typically present with a board-like, rigid, tender abdomen with absent bowel sounds. Rebound tenderness is a sign of peritonitis, as sudden removal of the hand causes pain due to movement of the peritoneum.

Patient also tends to be generally unwell and may have signs of dehydration.

21
Q

What are the potential complications of peritonitis?

A

Early: Septic shock, respiratory or multiorgan failure, paralytic ileus, would infection, abscesses.

Late: Incisional hernia, adhesions.

22
Q

What are the investigations for peritonitis?

A

Blood tests and ABG should be ordered, looking for acidosis or respiratory failure). Amylase may be raised in acute pancreatitis and prevent unnecessary surgery.

CXR may show pneumoperitoneum indicating a Gastrointestinal Perforation.

AXR may reveal cause such as Intestinal Obstruction.

USS or CT abdomen and laparotomy can be done to investigate underlying cause.

If the patient has ascites, perform an Ascitic tap and cell count (diagnostic of SBP if >250 neutrophils/mm3). The bacteria should be gram stained and cultured.

23
Q

Describe the management of peritonitis

A

Localised

Treatment will depend on underlying cause, may be surgery or I.V antibiotics.

General

  • A-E resuscitation to restore fluid and electrolyte status and oxygenation.
  • I.V antibiotics is necessary - specificity to treat broad spectrum of bowel organisms such as a cephalosporin and metronidazole.
  • NG tube to aspirate the gastric contents, preventing inhalation of vomit.

Any localised collection of pus requires drainage, and later surgery may be required for the evacuation of residual abscesses, e.g. subphrenic or pelvic collections.

Treat the cause and perform a peritoneal washing with copious irrigation to remove all seropurulent exudate.

Spontaneous Bacterial Peritonitis

Medical treatment with quinolone antibiotic or cefuroxime and metronidazole combination.

24
Q

What is the aetiology of gastrointestinal perforation?

A
  • Large bowel mainly caused by diverticulitis and colorectal carcinoma. Perforated appendix is the most common complication of appendicitis. Other causes include volvulus, ulcerative colitis (toxic megacolon), trauma, radiation enteritis and complications of operations.
  • Gastroduodenal is most commonly caused by a perforated gastric or duodenal ulcer and rarely gastric carcinoma.
  • Small bowel (rare) caused by trauma, infection, Crohn’s disease, lymphoma, vasculitis, radiation enteritis.
  • Oesophagus - Boerhaave’s syndrome is rupture following forcible vomiting against a closed glottis. OGD can also rarely cause perforation.
25
Q

What are the clinical features of gastrointestinal perforation?

A

Large Bowel

Patients usually present with sudden onset abdominal pain due to peritonitis. There may be weight loss and signs of colorectal carcinoma.

Gastroduodenal

Sudden onset and severe epigastric pain, worse on movement. The pain later becomes generalised. In the elderly, the presentation may not be as acute, instead presenting as epigastric discomfort.

There may be signs of gastric malignancy such as weight loss and nausea. More commonly signs of peptic ulcer disease such as dyspepsia, dysphagia etc.

Oesophageal

Severe pain following an episode of violent vomiting. Pain may be in the neck or chest and dysphagia develops soon after.

On Examination

  • Patient is unwell with signs of shock, pyrexia, pallor and dehydration
  • Signs of localised or general peritonitis with abdominal rigidity and guarding, reduced or absent bowel sounds
  • Loss of liver dullness due to overlying gas
26
Q

What are the investigations for gastrointestinal perforation?

A

Bloods: Amylase may be raised in peritonitis, but if >3x normal then pancreatitis should be suspected).

CXR may show subdiaphragmatic free gas (common)

AXR can show abnormal gas shadows in tissues or in the bowel wall. A lateral decubitus film can demonstrate intraperitoneal gas.

27
Q

Describe the management of gastrointestinal perforation

A

Resuscitate patient with fluid and electrolyte correction as well as IV antibiotics (cephalosporin or metronidazole). Analgesia, urinary catheter and central line as required.

Conservative

Usually reserved for those who are a high anaesthetic risk.

Surgical

Laparotomy - identification of site of perforation and peritoneal lavage.

Resection of the involved colon, usually part of a Hartmann’s procedure if large bowel.

If gastroduodenal, then biopsy the perforated ulcer (to examine for carcinoma). Close the perforation with an omental patch.

28
Q

What are the potential complications of gastrointestinal perforation?

A

Large and small bowel: Peritonitis.

Oesophageal: Mediastinitis, shock, overwhelming sepsis and death.

29
Q

What is the definition and epidemiology of paralytic ileus?

A

Obstructions are subdivided into mechanical and paralytic, the latter produced by lack of intestinal motility. Paralytic (or adynamic or neurogenic) ileus can be defined as a state of atony of the intestine. This can be produced by a large number of factors, sometimes coexisting.

30
Q

What is the aetiology of paralytic ileus?

A

Aetiology:

  • Peritonitis - perhaps due to toxic paralysis of intrinsic nerve plexuses. There may be associated mechanical obstruction.
  • Metabolic factors such as severe potassium depletion, uraemia, and diabetic coma.
  • Drugs - particularly heavy doses of anticholinergic drugs and antiparkinsonian drugs.
  • Post-operative - some degree of paralytic ileus occurs after every laparotomy. Aetiology is complex, including sympatric overactivation, the effects of manipulation of the bowel, potassium depletion, irritation from blood or associated peritonitis. Does not last for more than 48 hours; paralytic ileus that does last for more than 48 hours postoperatively probably has some other aetiological factor present.
31
Q

What are the clinical features of paralytic ileus?

A

Paralytic ileus is most commonly seen in the post-operative stage of peritonitis or of major abdominal surgery.

  • It can cause hypovolaemia and electrolyte disturbances BEFORE nausea and vomiting becomes apparent.
  • There is abdominal distension, absolute constipation and effortless vomiting.
  • Pain is not present, apart from the discomfort of the laparotomy wound and the abdominal distension.

On examination, the patient is anxious and uncomfortable. The abdomen is distended, silent and tender.

32
Q

Differentiation of paralytic ileus from mechanical obstruction is important because paralytic ileus is treated conservatively and mechanical obstruction is treated with urgent laparotomy. How can they be differentiated clinically?

A
  • Duration. Paralytic ileus rarely lasts more than 3 or 4 days; persistence of symptoms after this time is suspicious of mechanical obstruction.
  • Bowel sounds. The presence of bowel sounds is important. An absolutely silent abdomen is diagnostic of paralytic ileus, whereas noisy bowel sounds indicate mechanical obstruction.
  • Pain. Paralytic ileus is relatively painless, whereas colicky abdominal pain is present in mechanical obstruction.
  • Timing. If symptoms commence after the patient has already passed flatus or had a bowel action, it is very likely that a mechanical obstruction has supervened. The other possibility to consider is that there has been a leakage from an anastomosis and that peritonitis is now present.
  • X-ray appearances. A plain X-ray of the abdomen showing a localized loop of distended small intestine without gas shadows in the colon or rectum is strongly suggestive of mechanical obstruction, in contrast to the diffuse appearance of gas throughout the small and large bowel in paralytic ileus.
33
Q

Describe the management of paralytic ileus

A
  • Nasogastric suction is employed to remove swallowed air and prevent gaseous distension. The aspiration of fluid also helps to relieve the associated gastric dilatation.
  • Intravenous fluid and electrolyte therapy is instituted with careful biochemical control.
  • Pethidine, which has relatively little effect on intestinal motility compared with the other opioids, may be used to allay discomfort, and is combined with a phenothiazine such as prochlorperazine for nausea.

Eventually, patience is rewarded and recovery from the ileus will occur unless it is secondary to some underlying cause, such as infection.

In the absence of any evidence of mechanical obstruction or infection, prolonged stubborn ileus is occasionally treated pharmacologically:

  • Motility stimulants such as metoclopramide, together with erythromycin (which stimulates the motilin receptor), may be tried. Metoclopramide is a dopamine antagonist that stimulates gastric emptying and small intestinal transit.