GASTRIC
ANALYSIS
Analysis of gastric secretions usually
implies measurement of total output. However, detection of other components
such as blood or lactic acid, which are not normally found in gastric contents,
may be of clinical significance.
There are no definite cut–off points
for anacidity, normal acidity and hypersecretion. Only at the extremes of
secretion, such as anacidity in the patient with pernicious anemia or hypersecretion
of acid that occurs in the patient with Zollinger–Ellison syndrome, can any
underlying disease be diagnosed with certainty.
Importance of Gastric Analysis
1. Determination
of whether a patient is capable of secreting any gastric acid.
2. Diagnosis
of patients with symptoms of peptic ulcer disease
3. Diagnosis
of Zollinger–Ellison syndrome
Total gastric acid was
originally defined as the sum of combined acid and free acid. Combined
acid is that fraction complexed with physiologic buffers such as proteins
and salts and free acid is that part that exceeds the buffering
capacity of gastric fluid.
Collection of specimen
1. The
patient must fast overnight for 12 hours; intake of food and liquid, smoking
and physical exertion are prohibited.
2. The
patient is intubated with a nasogastric tube, and the tip of the tube is
positioned in the lowest portion of the stomach.
3. Residual
gastric fluid is first aspirated and then discarded and then four samples are
collected at 15 minutes intervals.
4. After
the collection of the basal acid secretions, the patient is given a gastric
stimulant. The synthetic peptide pentagastrin, which is a strong
stimulus for HCl secretion is used.
5. Gastric
secretions are again collected in four 15 minute sampling period.
6. After
the collection of gastric fluid, the volume and pH of each sample are measured
and recorded.
7. Particulate
matter, if present, is removed by centrifuging of the sample.
8. Each
sample is next titrated with 0.1 M NaOH with phenolphthalein as the end–point
color indicator. The volume of NaOH used to titrate the sample is recorded.
9. The
mEq of acid secreted for each collection period is calculated according to the
following formula:
Volume of NaOH
(L) x
Total
volume of specimen (mL) x
Molarity of NaOH x 1000
mEq
Volume
of gastric fluid titrated (mL) mole
=
mEq of acid secreted for each collection period
10. For
basal acid output, the two highest values obtained are used in the following
formula to calculate the mEq of acid per hour:
Basal I + Basal
II
= mEq of acid secreted per hour in basal condition
0.5
11. The
mEq of acid produced per hour after pentagastrin stimulation is calculated by
summing the mEq of acid secreted in each 15 minutes sample (Stim I + Stim II +
Stim III + Stim IV).
Normal value = 20
– 100 ml / 12 hours fast
·
Basal pH values of 6.0 or
greater are most likely due to subnormal parietal cell activity and may be
associated with pernicious anemia, gastric carcinoma, rheumatoid arthritis and
myxedam. The pH of gastric secretion after pentagastrin stimulation should be
less than 2.0.
Acid output in
basal state and after stimulation:
Subject
Basal
Acid output Maximal Acid
Output
(mmol / hr) (mmol / hr)
Normal adult
male 2.2 – 2.7 14 – 42
under 30
Over 30 2.2 –
2.7 3 –
33
Normal adult
female 1.0 – 1.5 7 – 20
SCHILLING TEST
The Schilling Test for absorption of
Vitamin B12 evaluates both gastric and intestinal function. There
are three ways of performing Schilling Test. Tests of B12 absorption
should first be done with an oral dose of B12 then with intrinsic
factor and B12, and finally, if bacterial overgrowth is suspected,
after a course of treatment with broad spectrum antibiotics. The urinary
excretion and the double isotope techniques are used to perform the test.
1. Urinary
Excretion Technique
a. Vitamin
B12 radiolabeled with Cobalt–57 or Cobalt–58 is taken orally. A test
dose of 1 mg is most frequently used since this dose is within the physiologic
range of Vitamin B12 absorption capacity of the gastrointestinal
tract.
b. One
to two hours after ingestion of the radiolabeled B12, 100 mg of non–radioactive B12 is given via intramuscular injection. This non–radioactive
B12 given saturates the body’s binding sites for B12
preventing any of the radiolabeled B12 that might be absorbed from
being stored. Any of the radiolabeled B12 that is absorbed is thus
excreted into the urine.
c. Urine
is collected for 24 hours after the oral dose of B12 and the
radioactivity counted. The amount of radioactive B12 excreted in the
urine is determined as a percentage of the original dose. Since the test relies
on urinary excretion of B12 that is absorbed is thus excreted into
the urine.
d. In
patients whom radiolabeled B12 is not absorbed, the Schilling test
may be repeated except this time radiolabeled B12 is given in
conjunction with intrinsic factor. Urine is collected as before and the
percentage of the original dose of B12 excreted of B12 is
now normal. A deficiency of intrinsic factor is the cause of B12
deficiency. If the renal excretion of B12 is still abnormal after
the administration of B12 and intrinsic factor, an absorptive defect
for vitamin B12 may be present. This may be seen in patients with
bacterial overgrowth in the small intestine. If bacterial overgrowth is
suspected, patients are given a course of broad spectrum antibiotic therapy and
the Schilling test is repeated.
2. Double
Isotope Technique
a. A
dual isotope test has been devised that uses two isotopes of cobalt (Cobalt–57
and Cobalt–58), each of which is used to make a different preparation of
radiolabeled B12.
b. One
preparation contains free radiolabeled B12; the other contains
intrinsic factor that is bound to radiolabeled B12 in vitro.
c. One
hour after the administration of the two preparations, a loading dose of B12
is administered intramuscularly as the conventional Schilling test.
d. Urine
is collected over the next 24 hours, and the ratio of the two isotopes in urine
is measured.
e. Use
of the two preparations allows one to discriminate between failure to produce
endogenous intrinsic factor (associated with pernicious anemia) and failure to
absorb B12 bound to intrinsic factor (associated with ileal disease)
as a cause of B12 deficiency.
Sensitivity = for pernicious anemia = 83%
= for ileal disease =
67%
D–XYLOSE
ABSORPTION TEST
D–xylose is a pentose sugar not
normally present in blood. Taken orally, D–xylose is passively absorbed in the
proximal small intestine and is not metabolized by the liver. Most of that which
is absorbed is eliminated via the kidneys. Thus, the amount of D–xylose
excreted into the urine over a specified time period after ingestion is
directly correlated with the amount absorbed in the gastrointestinal tract.
Procedure of the test
1. Patient
should fast before starting the test
2. Immediately
before receiving D–xylose, the patient should avoid and discard any urine.
Although the amount of D–xylose is given is variable, a 25 g dose appears to be
adequate.
3. After
administration of the sugar, all urine voided over the next 5 hours is
collected.
4. Blood
is also collected.
5. Blood
samples are usually collected at one hour in children and 2 hours after administration
in adults.
6. The
amount of D–xylose present in the urine and blood is measured by a quantitative
assay
a. Performed
using a urine or PFF specimen
b. These
samples are mixed with p–bromoaniline in acid medium
c. In
the presence of acid, D–xylose is dehydrated to furforol, which in turn condenses
with p–bromoaniline, forming a pink complex that has a maximum absorption of
520 nm.
d. Reaction
of non–specific chromogens with p–bromoaniline is minimized by the addition of
thiourea to the reaction mixture, which is an antioxidant and helps prevent the
formation of interfering colored compounds.
Sources of
error:
a. Patients
with renal insufficiency who cannot excrete D–xylose into the urine may be
falsely classified as having malabsorption. This problem can be overcome by
measurement of D–xylose in blood.
b. In
addition to malabsorption, low concentrations of urine and plasma D– xylose may
be seen in patients with ascites, thyroid disease, vomiting and delayed gastric
emptying.
c. Incomplete
urine collection and metabolism of D–xylose by microorganisms in urine.
d. Increase
in urine D–xylose is seen if urine contains increased galactose or glucose
concentrations.
Reference ranges
for D–xylose in urine and blood
Specimen Concentration
mg/dl mmol
/ L
Blood
Child (dose, 0.5 g/lb)
1 hour >30 >2.00
Adult (dose, 25 grams)
1 hour 21
– 57 1.4 – 3.8
2 hours 32
– 58 2.13 – 3.86
3 hours 19
– 42 1.27 – 2.8
4 hours 11
– 29 0.73 – 1.93
5 hours 6
– 18 0.40 – 1.20
Urine (5 hours
collection)
Child,
16 – 33% of ingested dose
Adult
(dose, 25 grams) >4 >26.64
>65
years old >3.5 >23.31
FECAL FAT
The determination of fecal fat is
performed in the evaluation of malabsorption due to pancreatic or intestinal
dysfunction. The fat content of feces in normal individuals consists primarily
of fatty acids, fatty acid salts (soap) and neutral fats. Tests of fecal fat
excretion are affected by disorders that influence digestion in the intestinal
lumen as well as processes affecting absorption of fats by the mucosa. Although
determination of fecal fat is useful for identifying the presence of
steatorrhea, it does not reveal its cause.
1.
Screening test
Average number
of fat droplets Approximate
fat content
10 5
20 10
30 15
35 20
>40 >30
2.
Quantitative
measurement
a. Collection
of specimen is done for three consecutive days.
b. Two
days before starting the test, the patient consumes a diet containing
approximately 100 g of fat per day. Ingestion of other triglyceride– containing
compounds, such as castor oil or cod liver oil, should be avoided during this
time.
c. Ingestion
of capsules containing markers such as chromic oxide, congo red, charcoal or
barium sulfate may be used to keep track of the transit time. Contamination of
feces with urine should be avoided.
d. Van
de Kamer titration method
(1) Fats
are converted to soaps by boiling a preweighed fecal sample in alcoholic
potassium hydroxide
(2) The
soap are next converted to fatty acids by the addition of hydrochloric acid and
then extracted into petroleum ether.
(3) An
aliquot is evaporated and the remaining residue dissolved in ethanol.
(4) After
a standard dietary intake of 100 grams of fat per day, normal individuals
should excrete less than 6 grams of fat per 24 hours period.
SWEAT CHLORIDE
The determination of chloride
concentrations in sweat of patients with cystic fibrosis is an extremely
reliable tool for the diagnosis of the disease when performed correctly. Sweat
for chloride determination is collected after iontophoretic delivery of pilocarpine
to the skin.
Pilocarpine is a drug
that stimulates sweating when introduced to the skin. At least 100 mg of sweat
is required for quantitation. Lower yields of sweat may result in unreliable
results because chloride concentration varies with rate of sweating and
accurate measurement may be difficult owing to insufficient chloride amounts.
Infants less than 3 weeks of age may show abnormally increased sweat chloride
concentration and testing should therefore be delayed in these individuals.
Procedure of the test:
1. Sweat
is collected by iontophoresis.
2. Pilocarpine
is introduced into the skin by applying gauze square to the anterior surface of
the forearm, which has been moistened with a 4 mg/dl solution of pilocarpine
nitrate.
3. A
second gauze square, moistened with a solution of potassium sulfate, is
attached to the posterior surface of the forearm.
4. The
positive electrode of the iontophoresis power supply is fastened to the gauze
moistened with pilocarpine and the negative electrode fastened to the gauze
moistened with potassium sulfate. A 2mA current is applied for 5 minutes.
5. After
iontophoresis, the gauze squares are removed and the skin thoroughly cleaned
with distilled water and dried.
6. The
actual sweat collection process begins with the placement of dry, preweighed
gauze square over each of the pilocarpine–treated areas.
7. Each
square is covered with parafilm or a plastic sheet and sealed to the skin with
tape.
8. After
approximately 30 minutes of sweat collection, the gauze is removed with forceps
and placed in a preweighed vial.
9. The
vial and gauze are weighed and the tare is subtracted to obtain the actual
weigh of sweat collected.
10. The
concentration of chloride in sweat is determined with the use of approximate
titrating equipment.
Sweat chloride concentration:
Normal 0 – 35 mmol/L
Ambiguous
35 – 60 mmol/L
Cystic
fibrosis 60 – 200 mmol/L
Sources of error
1.
Falsely
decreased value
a. Patients
with cystic fibrosis who are salt depleted as a result of vomiting, diarrhea or
gastric suction.
2.
False positive
results
a. Patients
without cystic fibrosis who have electrolyte imbalances associated with
meconium ileus, hypothyroidism, congestive heart failure and some types of
renal disease that result in increased sweat chloride concentration.
Precaution in specimen
collection
1. Patients
who are malnourished or dehydrated may not produce adequate amounts of sweat
for analysis.
2. All
sweat chloride measurements should be done in duplicate.
3. Patients
who have a positive initial finding should be repeated.
SERUM GASTRIN
Several commercial kit preparations
are available for measurement of serum gastrin. Most use a double–antibody
separation technique that does not measure the same components of gastrin.
Thus, the biologic equivalence of the different immunoassay cannot be ensured.
The ideal antibody would detect all gastrin components. This point is well
illustrated by measurement of gastrin in gastrinoma patients in whom G–34 is
the predominant form of gastrin. Since most assays use antibody directed toward
G–17, measurement of gastrin in patients with gastrinoma should be expressed in
terms of G–17 equivalents.
CLINICAL
SIGNIFICANCE OF G.I. FUNCTION TEST
1.
Lactase
deficiency
is the most common derangement of carbohydrate digestion and may be inherited
as a congenital defect or acquired in later life. Infants with congenital
lactase deficiency present with profuse watery diarrhea soon after the
introduction of milk. Unless the disease is quickly identified and lactose
withdrawn from the diet; infants may die of dehydration.
Lactose that
remains in the intestinal lumen of patients with lactase deficiency increases
the osmotic pressure of the luminal contents. Fermentation of lactose by bacteria
in the lower small intestine and colon results in the production of gas as well
as lactic acid and fatty acid which also add to the osmotic effect. The osmotic
retention of water in the intestinal lumen leads to diarrhea. Thus, lactase
deficiency results in abdominal discomfort, cramps flatulence, diarrhea–associated
dehydration and electrolyte imbalances.
2.
Malabsorption occurs as a
result of maldigestion of foodstuffs. This form of malabsorption usually
results from pancreatic diseases such as chronic pancreatitis or fibrocystic
disease of the pancreas. Malabsorption resulting from normal digestion but
inadequate assimilation of foodstuffs may result from competition by bacteria
or altered bacterial flora, from obstruction to the flow of lymph, from
diminished mucosal surface area, or from rapid transit of small bowel contents.
The presence
of fat in stool, steatorrhea, is a major sign of malabsorption. Patients with
severe forms of fat malabsorption frequently develop calcium oxalate kidney
stones because of enhanced absorption of dietary oxalate. The increased
absorption of oxalate occurs as a result of increased fatty acid
concentrations, which bind calcium and thus prevent the precipitation of oxalate
by free calcium, which normally occurs. Another mechanism contributing to
increased absorption of oxalate is the result of solubilization of oxalate by
dihydroxy bile acids. In those forms of steatorrhea in which large amounts of
dihydroxy bile acids reach the colon, passive absorption of oxalate is greatly
increased.
3.
Zollinger–Ellison
syndrome,
also known as gastrinoma occurs as the result of gastrin–secreting
tumors of the pancreas or rarely the upper small intestine. Gastrin is released
from these tumors at a high continuous rate that is not altered by intake of
food. The high rate of gastrin secretion results in hypersecretion of gastic
acid by the parietal cells. The low duodenal pH that results causes
inactivation of pancreatic enzymes, leading to maldigestion and erodes the
intestinal mucosa, producing ulceration. When secreted in very large amounts,
gastrin may inhibit absorption of fluid and electrolytes by the intestine. The
resulting large volume of fluid in the intestine, coupled with the decreased
intestinal transit time, contributes to the diarrhea seen in these patients.
4.
Menetrier
disease
is an uncommon condition characterized by hyperplasia of the surface cells of
gastric mucosa. The disease is most often encountered in men in the fourth to
sixth decade of life and is of unknown cause. The hyperplasia of the surface
mucosal cells is associated with gastric hyposecretion and anacidity, and there
is excessive loss of gastric protein.
5.
Cystic
fibrosis
is among the most lethal genetic pediatric disorders. The incidence of
heterozygote carriers is estimated to be approximately 1 in 20. The
symptomatology may range from mild to severe, and onset may be at birth or may
not become evident until years later. Usually, the disorder is discovered
between the second and twelfth months of life. Affected individuals usually
present with malodorous steatorrhea and chronic pulmonary infection.
6.
Crohn’s
disease
is a chronic inflammatory disorder of the intestine of unknown etiology. It
most commonly affects the ileocecal area, although it may involve virtually any
part of the gastrointestinal tract.
No comments:
Post a Comment