ACUTE ABDOMEN

The term “acute abdomen” refers to an amalgamation signs and symptoms of abdominal pain and
tenderness, a clinical presentation that often requires emergency surgical therapy.

The most common examples of acute abdomen.

1. Intra-abdominal haemorrage
1. Abdominal trauma→ rupture or compression of organs (spleen, liver, small
intestines)
2. Arterial aneurysms
3. Ectopic preg rupture
2. Infection
1. Appendicitis
2. Cholecystitis
3. Meckel’s diverticulitis
4. Psoas abscess
3. Perforation
1. Perforated GI ulcer
4. Ileus
1. adhesion of small and large bowels
2. IBS
3. GI malignanacy
4. volvulus of colon (cecum)
5. incarcerated hernia
5. Ischaemia
1. strangulation hernia
2. burger’s disease
3. mesenteric embuli/ thrombi
Detailed abdominal examination for acute abdomen:

1. Anamnesis:
◦ Pain and tenderness→ MC complaint (intensity prop to lvl of damage)
▪ excruciating→ perforation or ischaemia
▪ progressive→ infectious
▪ colicky→ obstruction
2. Physical Examination:
◦ Inspection:
▪ contour of abdomen: scaphoid, distended, flat
▪ scars
▪ masses
◦ Auscultation:
▪ no bowel sound= ileus
▪ hyperactive bowel sounds= enteritis
◦ Percussion:
▪ tympanic→ gas distention→ intraabdominal air, ascities, inflammation
◦ Palpation: ID organomegaly, locate masses
▪ superficial palp: normal→painful
▪ deep palp: locate masses
▪ focal pain→ early disease process
▪ diffuse pain→ late presentation
 ▪ DRE→ pelvic pain, intraluminal blood
3. Imaging and Dx:
◦ CT: GOLD standard
◦ Abdominal XRAY: air in peritoneal cavity (as little as 1ml)
◦ US: gallstones, uterus and ovary abdormalities, diamaeter and thickness of
gallbladder and bile ducts. NOT USEFUL IF THERE IS AIR IN INTESTINES.
ACUTE APPENDICITIS.

This is the sudden and severe inflammation of the appendix. N.B. The significance of the
appendix to the surgeon lies in its importance as the most common cause of the acute abdomen!
Acute inflammatory process of the appendix (appendicitis) is the most common general surgical
emergency, and early surgical intervention improves outcomes.

Aetiologies:

• Obstruction of the lumen is believed to be the major cause of acute appendicitis. This may
be caused by inspissated stool (fecalith or appendicolith), lymphoid hyperplasia,
vegetable matter or seeds, parasites.
• The lumen of the appendix is small in relation to its length and this configuration may
predispose to closed-loop obstruction.
• Obstruction of the appendiceal lumen → to bacterial overgrowth → continued secretion of
mucus leads → intraluminal distention and increased wall pressure.

Pathophysiology of appendicitis:

1. Obstruction of lumen
2. Bacterial overgrowth + mucus hyper-secretion
3. Intra-luminal distension → increased appendicular wall pressure
4. Vicseral pain + impaired lymphatic and venous drainage
5. Mucosal ischaemia (arterial compromise)
6. Localised inflammatory process→ local pain + gangrene + perforation
7. Perforation is open or closed
1. open: peritonitis, septic shock
2. closed: intra-abdominal abscess
Clinical Presentation. Anamnesis.

• The history begins with central abdominal pain of a visceral type (ill-localised), usually
around the umbilicus or epigastrium.
• The pain may be accompanied by a variable amount of gastrointestinal symptoms like
nausea, vomiting and anorexia. There is obstipation prior to pain. Diarrhoea in association
with perforation.
• As the organ becomes inflamed, local peritoneal irritation causes parietal peritoneum and
somatic pain felt in the right iliac fossa→ localised pain. Although right lower quadrant pain
is one of the most sensitive signs of acute appendicitis, variations in the anatomic location of
the appendix may account for the differing presentations of the somatic phase of pain!
Physical Findings: Inspection
 • Patients with acute appendicitis typically look ill and are lying still in bed.
• A coated tongue and foul breath accompanied by mild pyrexia (≈38 C).
• N.B. Absence of the general features, citing above, does not exclude appendicitis!
Palpation

• Local tenderness and guarding in the right lower quadrant. The appendix is in its most
common position is medial to the caecum and the exact location of the tenderness is at
McBurney's point (the junction of the middle and outer thirds of a line which joins the
umbilicus to the anterior superior iliac spine). However, local tenderness and guarding vary
in position of the appendix. They are often much reduced in retroileal or particularly
retrocecal appendicitis, and may be absent if the organ is in the pelvis.
• Pelvic examination is especially helpful when the inflamed appendix is in the pelvis.
Rectal examination is usually sufficient, but in young women, where pelvic inflammatory
disease is a possibility, a vaginal examination is done to attempt to localise the side of
maximum tenderness.
• Sings:
◦ ROSVING SIGN
▪ pressure in left iliac fossa→ pain in right iliac fossa
◦ OBTURATOR SING
▪ pain on internal rotation of right hip→ pelvic appendicitis
◦ OILIOPSOAS SIGN
▪ pain on extension of hip→ retroceal appendicitis
◦ DUNPHY SIGN
▪ increased pain with any movement (coughing)
◦ BLUMBURG SIGN
▪ rebound tenderness
• If there is perforation: pain is intense and diffuse + gaurding and rigidity+ blumburg +ve and
increased HR & TEMP

Diagnosis. Experienced clinicians accurately diagnose appendicitis based on a combination of

history and physical examination. Tenderness over the site of the appendix is the hallmark in
the diagnosis “acute appendicitis”. The differential diagnosis of appendicitis can include almost
all causes of abdominal pain.

Tx

Non perforated

Appendectomy

• Open→ McBurney’s incision (emergency)

• Laprascopic
Perforated

• OR + ressusciatation with fluids

• Laprotomy → midline inscision
• Appendectomy
• Antibiotics
MECKEL’S DIVERTICULUM

Anatomy

• Meckel's diverticulum is a true diverticulum (involves all layers of the intestine) of

variable size derived from the intestinal remnant of the yolk stalk (omphalomesenteric
duct). It is a vestigue of the embryonic vitelline duct (connects yolk sac to the lumen of the
midgut).
• This is the most common congenital anomaly of the small intestine – incidence of
Meckel’s diverticulum is 1 % to 3 % in general population.
• Typically, it is found on the antimesenteric border of the terminal ileum approximately
40 to 50 cm from the ileocecal valve in adults.
• About 25% of the diverticula have a fibrous or vascular attachment to the anterior
abdominal wall at the umbilicus.
• Approximately half of the examined diverticula during autopsy reveal the presence of
heterotopic gastric, duodenal, pancreatic, and colonic tissue within the gastric
diverticulum.
In about 75% of patients with symptomatic diverticula, gastric mucosa is present. When
symptoms occur, bleeding or perforation is generally the result of peptic ulceration of the adjacent
ileal mucosa, not from the diverticulum itself.

Clinical presentation

Most Meckel’s diverticula are asymptomatic (incidentally discovered during autopsy, laparotomy,
or barium studies) unless associated complications arise. The risk of developing a complication
related to Meckel’s diverticulum decreases with age.

1. Gastrointestinal bleeding.

◦ It is the most common clinical presentation of Meckel’s. The peptic ulcer occurs on
the mesenteric border of the adjacent ileal mucosa, and the presentation is of pain
and lower small-bowel bleeding (almost always in children or young adults).
◦ Confirmation of peptic ulcer origin in a Meckel's diverticulum can sometimes be
obtained by radionuclide scanning with 99mTc sodium pertechnetate. Contrast
studies and endoscopy have a limited role when the problem is hemorrhage from a
Meckel's diverticulum.
◦ Treatment choices include surgical resection of the diverticulum and the involved
small bowel.
2. Perforation.

◦ Peptic ulcer on the mesenteric border of the adjacent ileal mucosa may cause of ileal
perforation with clinical features of severe acute peritonitis.
◦ Perforation may also be the result of foreign bodies into the diverticulum (most
commonly parts of bones).
◦ The treatment in cases with perforation is emergency laparotomy.
3. Diverticulitis.

◦ About one third of patients with symptomatic Meckel's diverticulum have acute
diverticulitis.
 ◦ Similar to appendicitis, intra-luminal obstruction in a Meckel's diverticulum can
lead: distal inflammation→ gangrene→ perforation.
◦ Peptic ulceration causes inflammation and perforation with the development of
peritonitis.
4. N.B. The signs and symptoms of Meckel's diverticulitis are indistinguishable from
appendicitis, and emergency abdominal exploration is both diagnostic and therapeutic!

5. Small intestinal obstruction, caused by Meckel’s diverticulum.

◦ Intestinal obstruction associated with omphalomesenteric duct anomalies usually

results from either intussusception or volvulus:
▪ Volvulus **around an abnormal attachment between the Meckel’s
diverticulum and the abdominal wall.
▪ Volvulus around its longitudinal axis.
◦ Emergency operation must be performed in cases of small intestinal obstruction.
6. Enteroliths and foreign bodies.

◦ Enteroliths is a rare complication.

◦ They are formed in a narrow-necked diverticula where there is stasis.
◦ Enteroliths and foreign bodies may be:
▪ Associated with diverticulitis
▪ May result in bowel obstruction
▪ Or may evoke hemorrhage from local pressure necrosis.
◦ Plain abdominal films that show calculi as well as small-bowel cause obstruction
diagnostic confusion with gallstone ileus.
Management

• An asymptomatic diverticulum discovered at exploration for another reason is removed by

simple diverticulectomy.
• Symptomatic diverticula are dealt with according to the complications that they cause.
CROHN’S DISEASE

Definition

• Crohn’s disease is a chronic idiopathic, transmural inflammatory disease of the

gastrointestinal tract.
• Crohn’s disease can involve any part of the alimentary tract from the mouth to the anus
but most commonly affects the small intestine and colon.
Macroscopic and the Histological Features

• Chronic granulomatous inflammation of the ileum (ddx tuberculosis).

• Subsequently, the terms: 1) regional enteritis 2) terminal ileitis and 3) granulomatous
enteritis has been used, but the eponymous term 'Crohn's disease' is preferable, since it does
not imply an anatomic site nor the presence of granulomas.
Pathology

• The small intestine is affected in at least 70% of all patients with the disease. Of these,
about 1/2 have ileal involvement alone and the rest will have associated colonic disease—
usually affecting the right colon.
There is a transmural granulomatous inflammation with noncaseating granulomas formation.
 • Granulomas, fissures, ulcers, and fibrosis of the intestinal wall are gross appearance and
they may lead to stricturing of the small intestine.
• N.B. Granulomas, with giant cell formation, are the hallmark of the disease – the exact
diagnosis of Crohn’s disease can be established only by histological examination!
Progression of the disease.

1. Acute stage: transmural abscesses and perforation of the intestine wall.

2. Subacute stage: granulomas and ulcers onto the intestinal mucosa are produced
3. Chronic stage: fibrotic transformation of the intestine wall with:
1. granulomas and ulcers onto the intestinal mucosa
2. intestinal fistulas: between segments of the small intestine; between the small
intestine and the urinary bladder; between the small intestine and the skin surface
(external fistulas).
Acute clinical presentation

• The Crohn’s disease is expressed with periods of exacerbations and remissions.

• Most commonly, in acute stage of the disease clinical presentation is similar to acute
appendicitis – abdominal pain is the most frequent symptom. Diarrhea that contains blood
(melena) is the second most common presentation of the disease – because of mucosal
ulcers.
• N.B. Crohn’s disease can mimic inflammatory and neoplastic lesions of gastro-intestinal
tract**!**
Complications.

1. Significant intestinal bleeding;

2. Acute peritonitis – because of small intestine perforation;
3. Bowel obstruction;
4. Symptoms of intestine fistulas.
Management.

• Since Crohn's disease cannot be cured, the role of the clinician is to control the
inflammation, to correct nutritional deficiencies, and to ameliorate symptoms.

• These aims will frequently involve surgery and, indeed, 70% to 75 % of patients will require
at least one operation during their lifetime. Thus, management of these patients requires
close co-operation between physicians and surgeons.

• In general, medical treatment should be in accordance with the symptoms.

• Corticosteroids have been beneficial in the induction of remission in active Crohn’s

disease but are ineffective in maintaining remission in Crohn’s disease.

• Indications for surgical treatment:

The indications for operation are limited to complications that include:

◦ intestinal obstruction (the most common indication for surgical therapy),

◦ intestinal perforation with fistula formation or abscess,
◦ free perforation,
◦ gastrointestinal bleeding,
 ◦ urologic complications,
◦ failure or intolerance of steroid therapy,
◦ cancer,
◦ perianal disease.
• N.B. It is important that operative treatment of a complication is limited to the segment of
bowel involved with the complication!

• N.B. No attempt should be made to resect more bowels, even though evident disease may be
apparent in them**!**

• N.B. The decision to perform a primary anastomosis versus initial ostomy formation with
delayed reconstruction can be a difficult one for those with Crohn’s disease!