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Recent onset of pain requiring medical attention

History in Patients with Acute Abdominal Pain
Question Potential Responses and Indications

Where is the pain? Depends on location

What is the pain like? Acute waves of sharp constricting pain that “take
the breath away” (renal or biliary colic)

Waves of dull pain with vomiting (intestinal

Colicky pain that becomes steady (appendicitis,
strangulating intestinal obstruction, mesenteric

Sharp, constant pain, worsened by movement

Tearing pain (dissecting aneurysm)

Dull ache (appendicitis, diverticulitis, pyelonephritis)

Have you had it before? Yes suggests recurrent problems such as ulcer
disease, gallstone colic, diverticulitis, or

Was the onset sudden? Sudden: “like a light switching on” (perforated ulcer,
renal stone, ruptured ectopic pregnancy, torsion of
ovary or testis, some ruptured aneurysms)

Less sudden: most other causes

How severe is the pain? Severe pain (perforated viscera, kidney stone,
peritonitis, pancreatitis)

Pain out of proportion to physical findings
(mesenteric ischemia)

Does the pain travel to any other part of Right scapula (gallbladder pain)
the body?
Left shoulder region (ruptured spleen, pancreatitis)

Pubis or vagina (renal pain)

Back (ruptured aortic aneurysm)

What relieves the pain? Antacids (peptic ulcer disease)

Lying as quietly as possible (peritonitis)

What other symptoms occur with the pain? Vomiting precedes pain and is followed by diarrhoea

Delayed vomiting, absent bowel movement and
flatus (acute intestinal obstruction; the delay
increases with a lower site of obstruction)

Severe vomiting precedes intense epigastric, left
chest, or shoulder pain (emetic perforation of the
intra-abdominal oesophagus)
Extra-abdominal causes of abdominal pain

Abdominal Pain
Mechanisms and physiology of abdominal pain

- Group III of A (fast pain fibres):
o cause bright, sharp, localised pain and
- Group IV or C fibres (slow pain fibres):
o Follows sharp pain with a dull, intense, diffuse, unpleasant sensation
caused by the latter fibres also called slow pain fibres.

The further from the brain the stimulus is applied; greater is the temporal separation of
the two components. Types of pain stimuli are mechanical, thermal, electrical, and

Nociceptive pain may be classified further in three types:
- Somatic pain
o conducted by somatic nerves
which are made up of both A
and C fibres
o may be superficial pain
which is sharp, distinct and
well localised
 Caused by injury to the
skin or superficial
 Cutaneous nociceptors
terminate just below
the skin, and due to the
high concentration of
nerve endings, produce a sharp, well-defined, localized pain of
short duration.
 e.g. minor wounds, and minor (first degree) burns.
o or deep pain from muscles, joints, parietal peritoneum which is poorly
 originates from ligaments, tendons, bones, blood vessels,
parietal peritoneum, and muscles
 The scarcity of pain receptors in these areas produces a dull,
aching, poorly-localized pain of longer duration than cutaneous
 The C fibres conducting the deep pain are connected to both
somatic motor as well as the ANS
• associated with reflex contraction or spasm of the
overlying skeletal muscle as well as autonomic symptoms
such as sweating, nausea and changes in blood pressure
 e.g. sprains, broken bones; irritation of parietal peritoneum is
associated with sweating, vomiting, hypotension
• Abdominal guarding occurs due to a reflex contraction of
the abdominal wall muscles, in response to a noxious
stimulus to the pain fibres of the same dermatome
- Visceral pain
o Conducted by the autonomic nerves (C fibres – symp. and parasymp.)
o no pain receptors in the visceral peritoneum, located within the capsule
of solid organs or submucous and myenteric plexus of the hollow
organs and are sensitive to distension greater
o Pain is always dull, poorly localised, unpleasant and associated with
nausea, vomiting and autonomic symptoms like sweating and changes
in blood pressure.
o Reflex spasmodic contractions of the local visceral smooth muscles
results in the colicky pain

Since deep somatic pain and visceral pain is poorly localised it may not be felt in the
viscera but in some somatic structure that may be a considerable distance away.

Referred Pain:

- The axons of primary afferent nociceptors enter the spinal cord via the dorsal
- Terminate in the dorsal horn of the spinal grey matter.
- The terminals of primary afferent axons contact spinal neurons that transmit
the pain signal to brain sites involved in pain perception.
- When primary afferents are activated by noxious stimuli, they release
glutamate from their terminals that excite the spinal cord neurons
o Primary afferent nociceptor terminals also release peptides, including
substance P and calcitonin gene-related peptide, which produce a
slower and longer-lasting excitation of the dorsal horn neurons.
- The axon of each primary afferent contacts many spinal neurons, and each
spinal neuron receives convergent inputs from many primary afferents.

Pain experienced at a distance from the site of the damaged area. The affected somatic
structure developed from the same embryonic segment or dermatome as the structure
in which the pain originates.

- Dermatomal Rule
o Pain felt at the tip of the shoulder, when the parietal peritoneum on the
inferior surface of the diaphragm is irritated (like cholecystitis). This
area of peritoneum is innervated by somatic nerves (C4) as is the skin
over the tip of the shoulder.
o pain from distension of the midgut is referred to the peri-umbilical area
- Sometimes the initial pain is due to hyperaemia (increased blood flow) or
distension of the viscera but as the pathology extends it may result in
stimulation of the adjacent parietal peritoneum.
- The nature and site of the pain may then shift from one site to
another, e.g. shifting pain in appendicitis which may initially start as
a dull pain around the umbilicus and then may shift and localise as a
sharp severe pain at McBurney’s point in the right iliac fossa.
- When visceral pain is both local and referred, it may appear to spread or
radiate from the viscera to the referred area e.g. radiation of pain from the
loin to groin following distension of the ureter.

Referred pain (error of projection) may be explained by the principles of convergence-
projection hypothesis. Convergence of sensory inputs to a single spinal pain-
transmission neuron is of great importance because it underlies the phenomenon of
referred pain.

- All spinal neurons that receive input from the viscera and deep
musculoskeletal structures also receive input from the skin.
- The convergence patterns are determined by the spinal segment of the
dorsal root ganglion that supplies the afferent innervations of a structure.
- e.g. the afferents that supply the central diaphragm are derived from the third
and fourth cervical dorsal root ganglia. Primary afferents with cell bodies in
these same ganglia supply the skin of the shoulder and lower neck. Thus,
sensory inputs from both the shoulder skin and the central diaphragm
converge on pain-transmission neurons in the third and fourth cervical spinal

Because of this convergence and the fact that the spinal neurons are most often
activated by inputs from the skin, activity evoked in spinal neurons by input from deep
structures is mislocalised by the patient to a place that is roughly coextensive with the
region of skin innervated by the same spinal segment.

The brain has no way of knowing the actual source of input and mistakenly "projects"
the sensation to the somatic structure.

Thus, inflammation near the central diaphragm is usually reported as discomfort near
the shoulder. This spatial displacement of pain sensation from the site of the injury that
produces it is known as referred pain.


- For history-taking
o Pain referred to abdomen from thorax, spine or genitalia is important to
clarify because diseases of upper abdominal cavity such as acute
cholecystitis or perforated ulcer are frequently associated with
intrathoracic complications
o The possibility of intrathoracic disease must be considered in every
patient with abdominal pain, especially if the pain is in the upper part
of the abdomen.
 Myocardial or pulmonary infarction, pneumonia, pericarditis, or
esophageal disease (the intrathoracic diseases that most often
masquerade as abdominal emergencies) will often provide
sufficient clues to establish the proper diagnosis.
• Diaphragmatic pleuritis resulting from pneumonia or
pulmonary infarction may cause pain in the right upper
quadrant and pain in the supraclavicular area, the latter
radiation to be distinguished from the referred subscapular
pain caused by acute distention of the extrahepatic biliary
o Palpation over the area of referred pain in the abdomen also does not
usually accentuate the pain and in many instances actually seems to
relieve it.
o Referred pain from the spine, which usually involves compression or
irritation of nerve roots, is characteristically intensified by certain
motions such as cough, sneeze, or strain and is associated with
hyperesthesia over the involved dermatomes.
o Pain referred to the abdomen from the testes or seminal vesicles is
generally accentuated by the slightest pressure on either of these

The Acute Abdomen – pathological causes of pain (4): Acute inflammation,
obstruction, ischaemia, and increased pressure within a solid organ.


• The common processes leading to intra-abdominal inflammation are bacterial
invasion, chemical irritation and ischaemia.

• Features of pain causes by inflammation depend on whether the organ affected is
intraperitoneal or extraperitoneal.

• Inflammation of intraperitoneal organs

o Results in localised peritonitis, caused by irritation of pain receptors in the
parietal (not visceral) peritoneum (peritoneal pain)

o Well localised, patient indicates position of pain with palm of hand or finger

o Aggravated by sudden movement – coughing; minimised by little
movement – lying still or using diaphragm not abdominal muscles for

 E.g. involvement of a segment of bowel with Crohn’s disease
(transmural inflammatory process) results in peritoneal pain

 Acute salpingitis (develops over period of hours)

 Acute appendicitis (intraperitoneal inflammation caused by
obstructive process): periumbilical due to obstruction of appendix
(visceral pain), then as inflammation becomes transmural pain
becomes peritoneal and moves to R iliac fossa over inflamed organ.

 Consequence of perforation of hollow viscera. Leakage of visceral
contents causes pain by chemical irritation. Degree of irritation –
depends on nature of leaking material. e.g. Gastric juice from a
perforated peptic ulcer or gas from perforated sigmoid colon
diverticulum (less irritation and less pain). Onset of pain in response
to chemical irritation is rapid. Whether pain is localised or
generalised depends on extent of spillage. i.e. max irritation is
around site of leakage (epigastric for peptic ulcer, and L iliac fossa
for perforated sigmoid diverticulum). Other causes of perforation are
ischaemia (progressing to infarction) and malignancy (perforated
gastric cancer)

 Ischaemic bowel – peritoneal part of pain is minor. Major component
of the pain is of visceral type. Peritoneal inflammation occurs only if
pain is transmural (most sensitive component of bowel wall to
ischaemia is mucosa). Except splenic infarct – pain is peritoneal in
type, not really visceral.

o Inflammation restricted to bowel mucosa, seen in Ulcerative Colitis,
doesn’t result in peritoneal pain.

o Inflammation of non-intraperitoneal organs: acute pancreatitis – chemical
irritation of retroperitoneal tissues and irritation of visceral nerves. Pain is
constant, severe, not aggravated by movement. If inflammatory process of
acute pancreatitis spreads anteriorly, patient will complain of peritoneal


• Bowel obstruction causes colicky pain unless there is a complication (gangrene,
2° infection or perforation causing pain to be continuous)

o Colic – severe, midline position.

 Epigastric if organ originated from foregut (down to the 2nd part of
the duodenum), periumbilical if the organ came from midgut (down
to splenic flexure of colon), and hypogastric if organ came from
hindgut (left colon and rectum)

 Sudden distension of the biliary tree produces a steady rather than
colicky type of pain; hence the term biliary colic is misleading.

• Onset of obstruction pain is related to speed of obstruction:

o Sudden occlusion (gall bladder outlet obstruction due to a stone or
volvulus of sigmoid colon) means onset of pain is over minutes.

o Slow progressing occlusion (obstructing cancer of sigmoid colon) means
onset is much slower.

o Intermittent occlusion (gall bladder outlet obstruction due to stone) means
intermittent pain

• Obstruction caused by luminal lesion (calculus), mural lesion (benign or
malignant tumour or fibrous stricture) or extraluminal lesion (fibrous band or
neck of hernia)

• Obstruction can occur anywhere along the lumen of GIT, resulting in proximal
distension and stasis; if obstructed bowel is open ended proximally, distension
progresses proximally. If lumen is closed proximally, luminal contents and organ
itself become infected (cholecystitis – inflammation of gall bladder, cholangitis –
inflammation of bile duct, appendicitis) or progressive distension can lead to
venous obstruction followed by arterial obstruction, then gangrene and
perforation (e.g. closed loop obstruction of bowel)

• Inadequate blood flow resulting in tissue death (infarction)

o Arterial ischaemia caused by arterial embolus to the bowel, thrombosis or
low output state.

 Sudden onset pain (over few min) and continuous (visceral pain)

o Venous ischaemia slower in onset
 When venous occlusion is complete, as occurs to a loop of bowel
strangulated by the neck of a hernia, the tissue drained by the
occluded vein becomes oedematous and engorged with blood, and
arterial obstruction and thrombosis may follow. With larger vein
occlusion by a thrombus (e.g. portal or superior mesenteric vein, or
occasionally volvulus of bowel), the occlusion may be incomplete
and alternative venous drainage may save the tissue from necrosis.
Acute major
mesenteric venous
obstruction causes
transudation of fluid
into peritoneal
cavity, which may be
evident as ascites.

o The pain of embolism or
thrombosis of the superior
mesenteric artery or that of
impending rupture of an
abdominal aortic aneurysm
certainly may be severe
and diffuse.

o Yet, just as frequently, the
patient with occlusion of
the superior mesenteric
artery has only mild
continuous diffuse pain for
2 or 3 days before vascular
collapse or findings of
peritoneal inflammation
appear. The early, seemingly insignificant discomfort is caused by
hyperperistalsis rather than peritoneal inflammation. Indeed, absence of
tenderness and rigidity in the presence of continuous, diffuse pain in a
patient likely to have vascular disease is quite characteristic of occlusion of
the superior mesenteric artery.

o Abdominal pain with radiation to the sacral region, flank, or genitalia
should always signal the possible presence of a rupturing abdominal aortic
aneurysm. This pain may persist over a period of several days before
rupture and collapse occur.


• Sudden swelling – pain of
visceral type due to stretching of
capsule of organ

o Dull and constant

o Severity depends on
degree of swelling

o Haemorrhage into ovarian
cyst, necrosis of hepatic
metastasis and hepatic
venous engorgement due
to acute R heart failure
Generalised abdominal pain

First issue: address whether patient has abdominal catastrophe – generalised
peritonitis, generalised tenderness, guarding, rebound tenderness, absence of bowel

Signs of shock (blood loss or hypovolemic shock) – tachycardia, hypotension, oliguria,
peripheral vasoconstriction (cool blue peripheral tissues and thready pulse), pallor
indicating blood loss

Signs of dehydration –

• dry tongue
• reduced skin turgor
• decreased eye turgor
• tachycardia
• possible arrhythmias
• Increased respiration
• Decreased sweating and
decreased capillary return
• Decreased urination
• Increased body
• Extreme fatigue
• Muscle cramps
• Headaches
• Nausea
• Tingling of the limbs

Conditions: Glossary

The typical syndrome will consist of
diffuse, cramping abdominal pain,
fever, and nausea, with hyperactive
bowel sounds and mild diffuse
abdominal tenderness. Bacterial
infections will cause higher fever,
watery diarrhea, and foul-smelling,
often bloody stools.

The patient is distended with stool
palpable through the abdominal wall
and only mild abdominal tenderness.
There will usually be a history of
absence of bowel movements for
several days although a small
amount of diarrhea may pass around the fecal obstruction.

Small bowel obstruction
The pain is colicky, severe, and poorly localized. Cramping pain occurs in short, intense waves
followed by complete absence of pain. Short pain-free intervals occur in proximal obstruction
and longer ones in distal. The patient is restless. Vomiting, which may become feculent, is
common in proximal obstruction. The abdomen is distended in distal obstruction, and the rectum
has an empty, “ballooned” feel. Tenderness to palpation is not impressive unless perforation has
occurred. High-pitched hyperactive bowel sounds are characteristic, but they may be hypoactive
or absent in 25%. Most patients (80%) have a history of prior abdominal surgery.

Large bowel obstruction
Constipation or change in bowel habits often precedes complete obstruction. Pain is felt below
the umbilicus. Distension is prominent, but pain is less severe than with small bowel obstruction.

Mesenteric ischemia
Acute vascular occlusion usually presents with severe midabdominal pain out of proportion to
the physical findings. The pain begins as colic, then progresses. In later stages, fever and
hypotension occur. An embolic substrate (atrial fibrillation or acute MI) is a key clue. The stool
should be hemoccult positive. “Intestinal angina” presents with recurrent colicky abdominal pain
and distension occurring 20 to 30 minutes after a meal and lasting 2 to 3 hours. This may
manifest itself as food aversion or a malabsorptive diarrhea/steatorrhea with prominent weight
loss. There is often a bruit in the upper abdomen.

There will be early vomiting, board-like abdominal rigidity, rebound tenderness, fever, and a
silent abdomen. The patient will lie absolutely still. The pain is often localized (e.g., appendicitis)
before becoming generalized.

Abdominal aortic dissection
The pain is migrating, severe, tearing, and radiating to the back. The patient will often be in
early shock, hypotensive, and restless. There may be a pulsating, enlarged, tender aorta
palpable through the abdomen. The femoral pulse may be absent. Loss of motor function and
sensation in one leg suggests dissection with spinal artery compromise.

Sickle cell crisis
Diffuse abdominal pain with peritoneal signs develops in a patient with sickle cell anemia.

Following a prodromal phase of anorexia and malaise, the icteric phase is dominated by right
upper quadrant pain and tenderness, fever, jaundice, nausea, dark urine, and light stools.

Biliary colic
Sudden onset of steady and severe pain lasting 15 minutes to hours occurs with acute
obstruction of the common bile or cystic duct. Cystic duct obstruction causes right upper
quadrant pain whereas common bile duct obstruction causes epigastric pain, early jaundice, and
prominent emesis. Pain may radiate to the scapula.

Peptic ulcer disease
Gnawing, aching, burning, or hunger pain in the epigastrium, relieved temporarily by food or
antacids, suggests this diagnosis. Radiation to the back suggests perforation into the pancreas.
Duodenal ulcer causes pain 1 to 2 hours after meals and at night.

Typically, the patient has dysuria, fever, nausea, and costovertebral angle tenderness although
presentation with poorly localized abdominal pain is not uncommon either.

Acute cholecystitis
Right upper quadrant pain radiates to the scapula and is accompanied by nausea, vomiting, and
fever. Murphy sign (inspiratory arrest on palpation over the gallbladder) is present, and a
distended gallbladder is palpable in 30%. There is often a background of biliary colic. Fever and
rigors herald a suppurative cholangitis.

Classically, it begins as poorly localized visceral pain in the periumbilical region, moving to the
right lower quadrant, where somatic pain is steadily progressive. There is localized tenderness
over McBurney’s point, with or without rebound tenderness. Anorexia/nausea and low-grade
fever are usually present.

Inflammatory bowel disease
Pain, fever, and diarrhea with blood or mucus accompany flares. Terminal ileitis in young adults
may simulate acute appendicitis. Crohn may be recognized by systemic signs, such as arthritis.

A sexually active woman presents with lower abdominal pain. Pelvic examination reveals yellow
discharge from the cervix, cervical motion pain (chandelier sign), or tender adnexa. An
exquisitely tender adnexal mass indicates a tubo-ovarian abscess.
Rectus abdominus muscle strain
The history will suggest strain or overuse. The pain is constant and aching and is exacerbated by
movement. There will be superficial tenderness over the rectus abdominis, and spasm may
mimic guarding. A hematoma may simulate a localized mass.

Ureteral calculus
Severe cramping flank pain radiates to the groin. The patient is pale and unable to find a
comfortable position. The urine will be dipstick positive for blood.

Ruptured corpus luteum cyst
Around the time of the menses, there occurs a sudden-onset, transient (hours), unilateral, lower
abdominal and adnexal pain and tenderness. It is less severe and more diffuse than appendicitis,
and it steadily improves on serial examination rather than worsening. A similar presentation
during midcycle occurs with rupture of a graafian follicle (mittelschmerz).

Ruptured ectopic pregnancy
A missed or late period (85%) with an adnexal mass may be the only clue; thus, a high index of
suspicion is needed. Rupture is accompanied by acute pain that may project to the shoulder,
accompanied by cervical bleeding, shock, and a full, boggy cul-de-sac. There is a prior history of
PID in 25%.

Ovarian torsion
The usual presentation is a young woman with acute onset of pain and a tender adnexal mass
but no fever.

Left upper quadrant pain boring through to the back, prominent nausea and vomiting, and a
history of heavy alcohol use or cholelithiasis are important clues. The patient sits up and leans
forward, or lies on the side in a knee-chest position. Rebound will be present just above the
umbilicus, and costovertebral angle tenderness occurs with inflammation of the tail of the
pancreas. Hiccups are often present.

Splenic infarction
Left upper quadrant pleuritic pain and tenderness occur in the setting of atrial fibrillation,
endocarditis, sickle cell anemia, or neoplastic splenic enlargement. There may be a localized
friction rub.

Myocardial infarction
Ischemia should be considered with upper abdominal pain although chest pain is usually
present. Nausea can be seen with inferior ischemia.

It presents subacutely with low-grade fever and left lower quadrant abdominal pain. A tender
mass with indistinct borders may be palpable on abdominal or rectal examination.

Sigmoid volvulus
Severe pain will suddenly occur while the patient is straining to defecate. Rapid, extreme left
upper quadrant distension occurs, with vertical peristalsis.