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, Pathophysiology of abdominal pain
Types of pain:
1. Visceral pain
a. Generalised dull pain
b. Mediated by sympathetic nervous system
c. The visceral peritoneum and the viscera are insensitive to mechanical,
thermal or chemical stimulation, and can therefore be handled, cut or
cauterized painlessly. However, they are sensitive to tension, whether due Page |
to overdistension or traction on mesenteries, visceral muscle spasm and 4
ischaemia.
d. Irritation of foregut structures (the lower oesophagus to the second part of
the duodenum) is usually felt in the epigastric area.
e. Pain from midgut structures (the second part of the duodenum to the
splenic flexure) is felt around the umbilicus.
f. Pain from hindgut structures (the splenic flexure to the rectum) is felt in the
hypogastrium.
2. Somatic pain
a. Well localised sharp pain
b. The parietal peritoneum covers the anterior and posterior abdominal walls,
the undersurface of the diaphragm and the pelvic cavity.
c. Its nerve supply is derived from somatic nerves supplying the abdominal wall
musculature and the skin (T5–L2). The exception to this is the diaphragmatic
portion, which is supplied centrally by afferent nerves in the phrenic nerve
(C3–C5), and peripherally in the lower six intercostal and subcostal nerves.
d. The parietal peritoneum is sensitive to mechanical, thermal or chemical
stimulation, and cannot be handled, cut or cauterized painlessly → reflex
contraction of the corresponding segmental area of muscle, causing rigidity
of the abdominal wall (guarding) and hyperaesthesia of the overlying skin.
e. When the diaphragmatic portion of the parietal peritoneum is irritated peripherally, there will be pain, tenderness and
rigidity in the distribution of the lower spinal nerves, but when it is irritated centrally, pain is referred to the cutaneous
distribution of C3, 4 and 5 (i.e. the shoulder area.)
Causes of pain:
- Inflammation
o Infection
o Non-infective e.g. chemical, ischaemic, trauma, immune
- Perforation
- Obstruction
Peritonitis pathophysiology
- May be classified according to extent (either localized or generalized)
- Generalized peritonitis common causes
o Perforation of an intra-abdominal viscus → chemical spillage
o Ischaemia → generalised bowel inflammation
▪ Inflammation of the peritoneum results in an increase in its blood supply and local oedema formation. There is
transudation of fluid into the peritoneal cavity, followed by the accumulation of a protein-rich fibrinous exudate.
▪ In the normal state, the greater omentum constantly alters its position within the abdominal cavity as a result of
intestinal peristalsis and abdominal muscle contraction. In the presence of inflammation, the greater omentum
will adhere to and surround the abnormal organ. The fibrinous exudate effectively glues the omentum to the
inflamed viscus, walling it off and preventing the further spread of inflammation.
▪ In addition, the exudate inhibits intestinal peristalsis, resulting in a paralytic ileus which also limits the spread of
the inflammation and infection. As a result of the ileus, fluid accumulates within the lumen of the intestine and,
along with the formation of large volumes of intra-peritoneal transudate and exudate, this will lead to a decrease
in the intravascular volume, producing the clinical features of hypovolaemia.
- Localised peritonitis most common cause
o Cholecystitis
o Appendicitis (irritation of parietal peritoneum by inflamed structures)
Obstruction pathophysiology:
- The smooth muscle in the wall of the obstructed viscus will contract reflexly in an effort to overcome the impedance. This reflex
contraction produces ‘colicky abdominal pain’.
- The exception to this rule is ‘biliary colic’. The gallbladder and biliary system has little smooth muscle in its wall and attempts at
contraction tend to be more continuous than ‘colicky’.
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