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ACUTE ABDOMINAL PAIN
Dr M du Plessis
Dept of Chemical Pathology
University of Pretoria
23 May 2001
DEFINITION:
“Acute abdominal pain”:
- Presentation with a history of undiagnosed abdominal pain,
- Lasting less than 1 week,
- Excluding abdominal trauma or strangulated hernia.
COMMON CAUSES OF THE ACUTE ABDOMEN:
Table 1:
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APPROACH TO DIAGNOSIS AND TREATMENT OF
ACUTE ABDOMINAL PAIN:
IMPORTANCE OF CORRECT DIAGNOSIS:
- For correct treatment.
- Emergency surgery may be life-saving/ contra-indicated.
APPROACH TO DIAGNOSIS:
- Careful and proper HISTORY.
- PHYSICAL EXAMINATION:
o Careful pelvic and rectal examinations: Pelvic peritonitis due
to appendicitis, diverticulitis, twisted ovarian cyst, pelvic
inflammation.
- FURTHER INVESTIGATIONS:
o Full blood count:
  wbc > 20, in favour of viscus perforation, but also
seen with pancreatitis, acute cholesistitis, pelvic
inflammatory disease, intestinal infarction.
o Urine analysis:
 State of hydration, rule out severe renal disease, DM
or urinary infection.
o Plain X-ray of the abdomen:
 Diagnostic in cases of intestinal perforation or
obstruction.
o Peritoneal lavage:
 Blunt abdominal trauma.
o Ultrasonography:
 Preferred in absence of trauma.
 Useful for detection of  gallbladder or pancreas,
presence of gallstones, ovarian pathology, or a tubal
pregnancy.
o Laporoscopy:
 Helpful in diagnosing pelvic conditions (ovarian cysts,
tubal pregnancy, salpingitis) and acute appendicitis.
o CT scan:
 May demonstrate an  pancreas, ruptured spleen, or
thickened colonic wall and streaking of mesocolon
characteristic of diverticulitis.
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CLINICAL BIOCHEMISTRY has only a limited role:
o Useful for general support of patient:
 UKE (urea, creatinine, electrolytes)
 Glucose
o Differential diagnosis of
 Acute pancreatitis,
 Acute porphyria
 Ectopic pregnancy.
ACUTE PANCREATITIS:
Acute pancreatitis is an acute inflammatory condition of the pancreas
which may have a self-limiting short course, or may be fatal.
Ethiology:
Table 2:
Pathogenesis:
Structural damage to the pancreas allows release of pancreatic enzymes
(amylase, lipase, proteases) which then attack and damage local healthy
pancreatic tissue.
The initiating events that cause premature enzyme activation (protrypsin)
and uncontrolled release is not known, but hypotheses include:
- Altered composition of secretions causing protein plugs and back
pressure
- Back pressure or toxic substances (lysolecithin) causing
intracellular disruptions and premature enzyme activation.
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Clinical picture:
Abdominal pain:
- severe, sudden onset, upper half of abdomen
- may radiate to the back
- accompanied by nausea and vomiting
- fever is often present
- shock may develop
LABORATORY INVESTIGATION OF ACUTE
PANCREATITIS:
A. Associated biochemical abnormalities, prognostic
indicators, not diagnostic of pancreatitis:
1. Liver function tests:
-
Biliary tract disease (cholecystitis, cholelithiasis, common bile duct
stones) associated with 30-75% of cases:  D-Bili,  ALP,  GGT.
Alcohol is the other major cause of pancreatitis:  GGT, and other
liver function tests depending on stage of liver disease.
2. Serum UKE (electrolyte and renal function tests):
-
Renal failure is associated with moderate hyperamylasaemia (< 3
times URL) due to  clearance.
Acute pancreatitis can cause acute renal failure.
Electrolyte abnormalities due to vomiting and dehydration:
o HypoNa, HypoK, metabolic alkalosis.
Metabolic (lactate) acidosis due to shock.
3. Serum lipids:
-
Cause: Familial hyperlipidaemia ( TGS > 10 mmol/l) is associated
with a high incidence of acute pancreatitis.
Consequence: Temporary hypertriglyceridaemia may occur during an
acute attack of pancreatitis, particularly if alcohol-related.
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4. Serum calcium:
-
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Hypocalcaemia: (50% of acute pancreatitis) (transient, 1.7-2.0
mmol/l, asymptomatic)
o Lipase release by damaged pancreatic cells cause release of
FFA that cause sequestration of Ca2+ by formation of soaps.
o Hypoalbuminaemia as a result of shock.
o Associated hypoMg (alcoholics with poor diet)
o Release of unidentified substances that block PTH action on
bone resorption and/or inhibit PTH secretion.
Long-standing hypercalcemia (eg primary hyperparathyroidism) may
be a minor cause of pancreatitis.
5. Plasma glucose:
-
-
Normal P-Glucose: hormonal balance, both glucagons and insulin .
If  P-Glucose:
o Temporary: Stress ( catecholamines)
o Persisting: Significant loss of normal pancreatic tissue – poor
prognosis.
30-60% of patients with DKA have an associated hyperamylasaemia
(? Reduced renal clearance).
B. Diagnostic tests:
1. Amylase:
-
-
Source: Pancreas (main plasma source), salivary glands, lung, ovary,
fallopian tubes, prostate.
Low molecular weight: excreted by kidney (filtered by glomeruli,
reabsorbed by proximal tubules).
Following an acute attack of pancreatitis:
o Amylase rises in 2-12- h,
o Reaches a max at 12-24 h,
o Returns to normal within 3 days.
Major drawbacks of Serum Amylase:
o Not specific for pancreatic disease (other causes – table 3):
o In proven pancreatitis the degree of elevation does not
correlate with clinical severity/cause.
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o S-Amylase in severe hemorrhagic or chronic pancreatitis may
be normal or only slightly .
o A very  S-Amylase (> 10 times URL) supports the diagnosis
of pancreatitis.
o Moderate elevations (< 3 times URL) can also be seen with
extra-pancreatic causes, and rarely assist the differential
diagnosis of acute abdomen.
If S-Amylase remains  or rises following an acute attack of
pancreatitis, it is suggestive of the formation of a pancreatic
pseudocyst.
-
Table 3: Extra-pancreatic causes of  S-Amylase:
-
Urinary amylase:
o If S-Amylase is , determination of U-Amylase does not
provide additional information.
o Useful if high clinical suspicion of pancreatitis, with onset of
abdominal pain 2-3 days earlier.
o A low or normal U-Amylase in association with  S-Amylase:
 Renal failure
 Macroamylasaemia (high MW complex of amylase and
IgA,  renal clearance)
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o Amylase:creatinine ratio (spot urine):
 U-Amy/S-Amy X S-Creat/U-Creat X 100%
 Normal < 7%
 Increased (> 7%):
 Acute pancreatitis ( tubular reabsorption)
 Non-pancreatic causes:
o CRF, DKA, severe burns, bile duct
surgery.
2. Isoamylase
-
-
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2 distinct isoenzymes of amylase:
o Pancreatic (P): pancreas.
o Salivary (S): salivary glands, Fallopian tubes, some tumours
of lung and ovary.
Most extra-pancreatic causes of  S-Amylase are due to secondary
pancreatitis, and isoenzyme determination will not be of value to
distinguish them from primary causes.
Methods for emergency determination have been developed:
o Not robust enough for routine use.
o In practice no advantage over total S-Amylase.
3. Lipase
-
-
Released into intestinal lumen for digestion of triacylglycerol.
S-Lipase is barely detectable in normal individual.
Rises in parallel with S-Amylase in acute pancreatitis.
Drawbacks are similar to S-Amylase:
o Not specific for pancreatic disease
o Intra-abdominal extra-pancreatic causes of secondary
pancreatitis cause  S-Amylase and  S-Lipase.
o Extra-pancreatic sources of lipase:
 Lipoprotein lipase, liver, intestine.
o Also increased with renal failure ( catabolism).
Possible advantages over S-Amylase:
o Normal in macroamylasaemia.
o Normal in  S-Amylase due to non-pancreatic origin: eg
Fallopian tube or salivary gland diseases.
o Falls slower than S-Amylase and therefore remains raised
for longer following an acute attack.
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4. Trypsin
-
Present in circulation bound to 1-antitrypsin and 2-macroglobulin,
and as the zymogen trypsinogen.
Increased amount enters blood stream in acute pancreatitis
Difficult to measure because of complexes
Similar diagnostic accuracy as S-Amylase.
5. New markers:
-
S-Elastase
Phospholipase A2
Not significantly better than amylase.
6. Choice of test for diagnosis of acute pancreatitis
-
-
Diagnostic utility is similar for S-Amylase, and S-Lipase.
o Good sensitivity (> 90%), with poor specificity (~ 80%).
o  specificity: increasing decision-point to above URL
determined on healthy individuals:
 2 times URL for S-Amylase
 3 times URL for S-Lipase.
o Determination of S-Lipase adds little if any benefit to
determination of S-Amylase in cases of acute pancreatitis
with normal S-Amylase.
S-Amylase is most widely used as single test.
Additional determinations are limited to:
o S-Lipase: Establish whether an  S-Amylase is of pancreatic
origin.
o U-Amylase: persistently  S-Amylase in asymptomatic person
– to exclude macroamylasaemia.
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ACUTE PORPHYRIA:
-
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Acute porphyria is a rare cause of the acute abdomen.
Diagnosis may be suggested:
o History: association of abdominal pain with ingestion of a
drug known to provoke acute attacks eg anaesthesia
(barbiturates), steroids, sulphas, pregnancy,
premenstruation, stress, fasting, alcohol.
o Observation of dark red urine/ on standing.
Important to exclude because surgery is contra-indicated and
anaesthesia may be life-threatening.
Porphyrias responsible for acute attacks:
o Acute intermittent porphyria (AIP)
o Porphyria variegata (PV)
o Congenital coproporphyria (CCP)
Clinical picture of acute attack:
o Abdominal pain
o Neurological:
 Psychiatric disturbances (depression, psychosis)
 Peripheral neuropathy (myalgia, weakness,
paraesthesia)
o Cardiovascular: tachycardia, hypertension
o Electrolyte disturbances: SIADH (Syndrome of
inappropriate ADH = hypoNa)
o Skin involvement in PV and CCP.
Laboratory investigation:
o Determination of U-PBG (porphobilinogen) on random urine:
 If positive:
 Confirms acute attack of porphyria
 Send in stool and blood samples (EDTA-tube)
for determination of the type of porphyria.
 All samples should be protected against light.
 If negative: excludes acute porphyria.
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ECTOPIC PREGNANCY:
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Definition: Implantation of a fertilised ovum outside the uterus,
most often in Fallopian tube.
Although it is an uncommon cause of acute abdominal pain, it is
important to exclude in young women due to possibility of rupture
and intra-abdominal hemorrhage.
Laboratory investigation:
o Determination of serum -HCG:
o If positive: confirms diagnosis of pregnancy.
Ultrasonography (transabdominal/transvaginal)
o Gestational sac should be detectable in uterus above certain
cut-off value for HCG .
o If absent: confirms diagnosis of ectopic pregnancy.
REFERENCES:
1. Hooper J, Bangert SK. Clinical biochemistry in the investigation of
acute chest pain and the acute abdomen. In: Marshall WJ, Bangert
SK. Clinical Biochemistry Metabolic and Clinical Aspects. 1st Ed.
Churchill Livingstone, New York. 1995: 785-787.
2. Lott JA. The pancreas: function and chemical pathology. In: Kaplan
LA, Pesce AJ. Clinical Chemistry Theory, analysis, correlation. 3rd
Ed. Mosby, Missouri. 1996: 562-565.
3. Walmsley RN, White GH. A guide to diagnostic clinical chemistry.
3rd Ed. Blackwell Scientific Publications, London. 19994: 292-298.
4. Clave P, et al. Amylase, lipase, pancreatic isoamylase and
phospholypase A in diagnosis of acute pancreatitis. Clin Chem 1995;
41(8): 1129-1134.
5. Silen W. Abdominal pain. In: Fauci AS, et al. Harrison’s Principles of
Internal Medicine. 14th Ed. McGrawHill, New York. 1998, 65-68.