DIAGNOSTIC PROCEDURES

IN GI DISEASES

Dr Syed Ayesha Fatema

MD Medicine
Associate professor
PG dept of Moalijat
ZVMUMCH Pune
 DIAGNOSTIC PROCEDURES
IN GI DISEASES
The diagnostic tests can be divided into several
categories:
 • Structural tests

 • Functional tests

 • Tests for Helicobacter pylori

 • Special blood tests

 • Special stool tests

DIAGNOSTIC PROCEDURES IN GI
DISEASES

FUNCTIONAL TESTS
 A number of dynamic tests can be used to investigate aspects of
gut function, including digestion, absorption, inflammation and
epithelial permeability.

 In the assessment of suspected malabsorption, blood tests (full

blood count, erythrocyte sedimentation rate (ESR), folate, B 12,
iron status, albumin, calcium and phosphate) are essential, and
endoscopy is undertaken to obtain mucosal biopsies.
SOME OF THE MORE COMMONLY USED TESTS ARE LISTED IN
BOX 22.10 IN DAVIDSON'S
 SEHCAT
 A SeHCAT scan is a diagnostic procedure, which looks
at the function of the bowel.
 It involves swallowing a capsule containing a very
slightly radioactive tracer and imaging with a special
camera shortly after swallowing the capsule and after a
week.
 This then shows which percentage of bile acid was
absorbed, and thus whether the patient has BAM.

https://www.ncbi.nlm.nih.gov/books/NBK262912/
 Tauroselcholic acid is a bile acid analogue which shows
identical physiological behaviour with naturally
occurring bile acid conjugates.
 Following oral administration in normal subjects,
approximately 95% of the labelled bile acid is absorbed,
mainly by the terminal ileum during each enterohepatic
cycle.
 The distribution of activity is almost entirely confined to
the lumen of the biliary ducts, gut and liver.
GUT HORMONES
 FUNCTIONAL TESTS

I. • Tests for motility

II. • 24 hour pH monitoring
III. • Tests for acid output
IV. • Tests for malabsorption
 I. TESTS FOR GIT MOTILITY
 A range of diverse radiological, manometric and radioisotopic
tests exist for investigation of gut motility but many are research
tests of limited value in daily clinical practice.
 Oesophageal motility

 Gastric emptying

 Small intestinal transit

 Colonic and anorectal motility

 OESOPHAGEAL MOTILITY
 A careful barium swallow can give useful information about
oesophageal motility. Video fluoroscopy, with joint assessment by a
speech and language therapist and a radiologist, may be necessary
in difficult cases.
 Oesophageal manometry (Fig. 22.1, p. 852 Davidson's), often in
conjunction with 24-hour pH measurements, is of value in
diagnosing cases of refractory gastro-oesophageal reflux, achalasia
and non-cardiac chest pain.
 ESOPHAGEAL MANOMETRY
Indications  Diffuse esophageal spasm,
1. Oropharyngeal dysphagia with  Nutcracker esophagus,

normal structural studies  Hypertensive LES,

 Cricopharyngeal achalasia,  Collagen vascular disease,

 Pharyngeo-UES  Amyloidosis,

dyscoordination  Hypothyroidism, etc.

2. Esophageal dysphagia with 3. Noncardiac chest pain

normal structural studies
 Primary esophageal body
dysmotility e.g.

 Achalasia,
 TESTS FOR GIT MOTILITY
 A range of diverse radiological, manometric and radioisotopic
tests exist for investigation of gut motility but many are research
tests of limited value in daily clinical practice.
 Oesophageal motility

 Gastric emptying

 Small intestinal transit

 Colonic and anorectal motility

 GASTRIC EMPTYING

 Delayed gastric emptying (gastroparesis) causes persistent

nausea, vomiting, bloating or early satiety.
 Endoscopy and barium studies are often normal.

 Normal gastric emptying rates for solids are highly variable but
approximately 50% leaves the stomach by 90 minutes (t½).
 Calculating the amount of radioisotope retained in the stomach
after a test meal containing solids and liquids labelled with
different isotopes (Box 22.11) may reveal the diagnosis.
 TESTS FOR GIT MOTILITY
 Oesophageal motility
 Gastric emptying

 Small intestinal transit

 Colonic and anorectal motility

 SMALL INTESTINAL TRANSIT

 This is much more difficult to quantify and is seldom necessary in

clinical practice.
 Barium follow-through examination can give a rough estimate by
noting the time taken for contrast to reach the terminal ileum
(normally 90 minutes or less).
 Orocaecal transit can be assessed by the lactulose-hydrogen breath
test. (SIBO) https://www.youtube.com/watch?v=FEMs9N8kZ5Q
 Lactulose is a disaccharide which normally reaches the colon
intact; here, breakdown by colonic bacteria results in hydrogen
production.
 The time at which this occurs, as measured in expired air, is a
measure of orocaecal transit.
 TESTS FOR GIT MOTILITY
 Oesophageal motility
 Gastric emptying

 Small intestinal transit

 Colonic and anorectal motility

 COLONIC AND ANORECTAL MOTILITY

 A plain abdominal X-ray taken on day 5 after ingestion of

different-shaped inert plastic pellets on days 1-3 gives an
estimate of whole gut transit time.
 The test is useful in the evaluation of chronic constipation when
the position of any retained pellets can be observed, and helps
to differentiate cases of slow transit from those due to
obstructed defecation.
 The mechanism of defecation and anorectal function can be
assessed by anorectal manometry, electrophysiological tests and
defecating proctography.
 ANORECTAL MANOMETRY
 Anorectal manometry is a test performed to evaluate patients with
constipation or fecal incontinence.
 This test measures the pressures of the anal sphincter muscles, the
sensation in the rectum, and the neural reflexes that are needed for
normal bowel movements.
 This technique is helpful in evaluating the anorectal sphincter
mechanism.
 Contraindicated in the presence of an anal fissure, since the resting
anal pressure is abnormally high.

 https://www.youtube.com/watch?v=Z_arAAlTlmI
(Anorectal Manometry Test, Live Patient Demo & Training)
https://www.youtube.com/watch?v=vxpkXiIYcgU

https://www.youtube.com/watch?v=VI5sSo1TfGM
 II. 24 HOUR PH MONITORING
Indications
 • Patients with non cardiac chest pain

 • Refractory acid reflux symptoms: evaluate

treatment efficacy
 • Pre and post-operative evaluation of antireflux

surgery
 • Patients with atypical presentations of acid reflux

(ENT, pulmonary)
 Methods for the measure of gastric acid secretion include
invasive and non-invasive tests.
 The gold-standard to measure the acid output is the
collection of gastric acid after in basal condition (Basal
Acid Output, B.A.O.) and after an i.m. injection of
pentagastrin (Maximal Acid Output, M.A.O.).
 However, direct measurement of gastric acid production
is out of order in clinical practice, but many GI
symptoms are claimed to be related with acid disorders
and empirically cured.
 III. GASTRIC ACID SECRETION TEST

Definition
 The stomach acid test is used to measure the amount of acid in the
stomach.
 It also measures the level of acidity in stomach contents.

How the Test is Performed

 The test is done as a patient have not eaten for a while so fluid is
all that remains in the stomach.
 Stomach fluid is removed through a tube that is inserted into the
stomach through the esophagus.
 A hormone called gastrin may be injected into your body.

 This is done to test the ability of the cells in the stomach to release
acid.
 The stomach contents are then removed and analyzed.
Normal Results
 The normal volume of the stomach fluid is 20 to 100 mL and
the pH is acidic (1.5 to 3.5).
 These numbers are converted to actual acid production in units
of milliequivalents per hour (mEq/hr) in some cases.
 Note: Normal value ranges may vary slightly depending on the
lab doing the test.
What Abnormal Results Mean
 Abnormal results may indicate:

 Increased levels of gastrin can cause increased release of acid

and may lead to ulcers (Zollinger-Ellison syndrome).
 The presence of bile in the stomach indicates material is backing
up from the small intestine (duodenum).
 This may be normal.

 It may also happen after part of the stomach is removed with

surgery.
 The determination of serum pepsinogen I (sPGI) is
regarded as reliable gastric secretory parameter.
 The possibility to evaluate gastric acid secretion levels
by simple measurement a serum markers has significant
clinical implications in daily practice.
DIAGNOSTIC ALGORITHM IF GASTRIC ACID HYPERSECRETION
SUSPECTED
 IV. TESTS FOR
MALABSORPTION
 Serum screening tests for malabsorption
 S. Calcium,
 Albumin,
 Iron,
 Vitamin B12,
 Folate,
 Carotene,
 Prothrombin time
 Quantitative fecal fat determination
 D-xylose absorption test

 Small bowel biopsy

 Schilling test for Vitamin B12 Absorption

 Hydrogen Breath Test for lactose intolerance

 DIAGNOSTIC PROCEDURES
IN GI DISEASES
The diagnostic tests can be divided into several
categories:
 • Structural tests

 • Functional tests

 • Tests for infection Helicobacter pylori

 • Special blood tests

 • Special stool tests

DIAGNOSTIC PROCEDURES IN GI DISEASES

TESTS FOR INFECTION HELICOBACTER

PYLORI
 TESTS OF INFECTION
 Bacterial cultures
 Stool cultures are essential in the investigation of diarrhoea,
especially when it is acute or bloody, to identify pathogenic
organisms.
 Serology

 Detection of antibodies plays a limited role in the diagnosis of

gastrointestinal infection caused by organisms such as H.
pylori, Salmonella species and Entamoeba histolytica.
 Breath tests

 invasive and Non-invasive breath tests for H. pylori infection

and
 Breath tests for suspected small intestinal bacterial overgrowth.
 TESTS FOR HELICOBACTER PYLORI
Non-invasive
 C13 or C14 Urea Breath Test

 H. pylori IgG titer (serology)

 Stool antigene for H Pylori

Invasive
 Gastric mucosal biopsy

 Rapid Urease test

DIAGNOSTIC PROCEDURES IN GI DISEASES

SPECIAL BLOOD TESTS AND STOOL TESTS

 DIAGNOSTIC PROCEDURES
IN GI DISEASES
The diagnostic tests can be divided into several
categories:
 • Structural tests

 • Functional tests

 • Tests for Helicobacter pylori

 • Special blood tests

 • Special stool tests

 BLOOD TESTS

 • Liver function tests (LFT’S)

 • Hepatitis serology

 • S. Amylase & Lipase

 • Alfa-Feto Protein (AFP)

 • Carcino-Embryonic Antigen (CEA)

 INTRODUCTION

 Liver function tests (LFTs) are among the most commonly

ordered blood tests in both primary and secondary care.
 The ability to interpret LFTs is, therefore, an important skill to
develop.
 This guide provides a structured approach to the interpretation
of LFTs which you should be able to apply in most
circumstances.
WHY CHECK LFTS?

LFTs are requested for two primary reasons:

 To confirm a clinical suspicion of potential liver injury or
disease.
 To distinguish between hepatocellular injury (hepatic
jaundice) and cholestasis (post-hepatic or obstructive
jaundice).
 WHAT BLOOD TESTS ARE USED TO ASSESS LIVER
FUNCTION?

 Alanine transaminase (ALT)

 Aspartate aminotransferase (AST)

 Alkaline phosphatase (ALP)

 Gamma-glutamyltransferase (GGT)

 Bilirubin

 Albumin

 Prothrombin time (PT)

Hint: ALT, AST, ALP and GGT are used to distinguish between
hepatocellular damage and cholestasis. Bilirubin, albumin and
PT are used to assess the liver’s synthetic function.
 the reference ranges for LFTs, however, these often vary
between laboratories, so make sure to check your local
guidelines.

Blood test Reference range

ALT 3-40 iu/l

AST 3-30 IU/l

ALP 30-100 umol/l

GGT 8-60 u/l

Bilirubin 3-17 umol/l

Albumin 35-50 g/l

PT 10-14 seconds
 STEP 1 – ASSESS ALT AND ALP

 Assess if ALT and/or ALP is raised:

 If the ALT is raised, decide if this is a more than a 10-fold
rise (↑↑) or less than a 10-fold rise (↑).
 If the ALP is raised, decide if this is a more than a 3-fold rise
(↑↑) or less than a 3-fold rise (↑).
 STEP 2 – COMPARE ALT AND ALP LEVELS

Key facts about ALT and ALP

 ALT is found in high concentrations within hepatocytes and
enters the blood following hepatocellular injury.
 It is, therefore, a useful marker of hepatocellular injury.

 ALP is particularly concentrated in the liver, bile duct and bone

tissues.
 ALP is often raised in liver pathology due to increased synthesis
in response to cholestasis. As a result, ALP is a useful indirect
marker of cholestasis.
HOW DO WE COMPARE THE RISE IN ALT AND ALP?

 A greater than 10-fold increase in ALT and a less than 3-

fold increase in ALP suggests
a predominantly hepatocellular injury.
 A less than 10-fold increase in ALT and a more than 3-fold
increase in ALP suggests cholestasis.
 It is possible to have a mixed picture involving
both hepatocellular injury and cholestasis.
 WHAT ABOUT GAMMA-GLUTAMYL
TRANSFERASE?
 If there is a rise in ALP, it is important to review the level of
gamma-glutamyl transferase (GGT).
 A raised GGT can be suggestive of biliary epithelial damage
and bile flow obstruction.
 It can also be raised in response to alcohol and drugs such as
phenytoin.
 A markedly raised ALP with a raised GGT is highly suggestive
of cholestasis.
 ISOLATED RISE OF ALP
 A raised ALP in the absence of a raised GGT should raise your suspicion of non-
hepatobiliary pathology. Alkaline phosphatase is also present in bone and
therefore anything that leads to increased bone breakdown can elevate ALP.

CAUSES OF AN ISOLATED RISE IN ALP INCLUDE:

 Bony metastases or primary bone tumors (e.g. sarcoma)

 Vitamin D deficiency

 Recent bone fractures

 Renal osteodystrophy

Hint: Compare to what degree the ALT and ALP are raised. If
ALT is raised markedly compared to the ALP, this is primarily
a hepatocellular pattern of injury. If ALP is raised markedly
compared to ALT, this is primarily a cholestatic pattern of
What if the patient is jaundiced but ALT and
ALP levels are normal?

 An isolated rise in bilirubin is suggestive of a pre-hepatic cause

of jaundice.
 Causes of an isolated rise in bilirubin include:

 Gilbert’s syndrome: the most common cause.

 Haemolysis: check a blood film, full blood count,
reticulocyte count, haptoglobin and LDH levels to confirm.
STEP 3- ASSESS HEPATIC FUNCTION

The liver’s main synthetic functions include:

 Conjugation and elimination of bilirubin

 Synthesis of albumin

 Synthesis of clotting factors

 Gluconeogenesis

Investigations that can be used to assess synthetic

liver function include:
 Serum bilirubin

 Serum albumin

 Prothrombin time (PT)

 Serum blood glucose

The combination of the colour of urine and stools can
give an indication as to the cause of jaundice:
 Normal urine + normal stools = pre-hepatic cause

 Dark urine + normal stools = hepatic cause

 Dark urine + pale stools = post-hepatic cause (obstructive)

Causes of unconjugated hyperbilirubinaemia include:
 Haemolysis (e.g. haemolytic anaemia)

 Impaired hepatic uptake (e.g. drugs, congestive cardiac failure)

 Impaired conjugation (e.g. Gilbert’s syndrome)

Causes of conjugated hyperbilirubinaemia include:

 Hepatocellular injury

 Cholestasis
 ALBUMIN
 Albumin is synthesised in the liver and helps to bind water,
cations, fatty acids and bilirubin.
 It also plays a key role in maintaining the oncotic pressure of
blood.
Albumin levels can fall due to:
 Liver disease resulting in a decreased production of albumin (e.g.
cirrhosis).
 Inflammation triggering an acute phase response which
temporarily decreases the liver’s production of albumin.
 Excessive loss of albumin due to protein-losing enteropathies or
nephrotic syndrome.
 Prothrombin time
 Prothrombin time (PT) is a measure of the blood’s
coagulation tendency, specifically assessing the extrinsic
pathway.
 In the absence of other secondary causes such as
anticoagulant drug use and vitamin K deficiency, an
increased PT can indicate liver disease and dysfunction.
 The liver is responsible for the synthesis of clotting factors,
therefore hepatic pathology can impair this process resulting
in increased Prothrombin time.
 AST/ALT ratio
 The AST/ALT ratio can be used to determine the likely
cause of LFT derangement:
 ALT > AST is associated with chronic liver disease

 AST > ALT is associated with cirrhosis and acute

alcoholic hepatitis
 STEP 5- COMMON PATTERNS OF LFT
DERANGEMENT

 The table on next slide demonstrates the typical LFT

patterns associated with acute hepatocellular damage,
chronic hepatocellular damage and cholestasis.
 A single arrow (↑) refers to a mild impairment and a double
arrow (↑↑) refers to severe impairment.
 ACUTE CHRONIC
HEPATOCELLULA HEPATOCELLUL
R DAMAGE AR DAMAGE
CHOLESTASIS

ALT ↑↑ Normal or ↑ Normal or ↑

ALP Normal or ↑ Normal or ↑ ↑↑

GGT Normal or ↑ Normal or ↑ ↑↑

Bilirubin ↑ or ↑↑ Normal or ↑ ↑↑
 STEP 6- WHAT TO DO NEXT
Once the pattern of LFT derangement has been established, it is crucial to
determine the cause.

Common causes of acute hepatocellular injury include:

 Poisoning (paracetamol overdose)

 Infection (Hepatitis A and B)

 Liver ischaemia

Common causes of chronic hepatocellular injury include:

 Alcoholic fatty liver disease

 Non-alcoholic fatty liver disease

 Chronic infection (Hepatitis B or C)

 Primary biliary cirrhosis

Less common causes of chronic hepatocellular injury include:

 Alpha-1 antitrypsin deficiency

 Wilson’s disease

 Haemochromatosis
 THE LIVER SCREEN
A ‘liver screen’ is a batch of investigations focused on ruling
underlying causes of liver disease in or out. A
typical liver screen includes:

 Coagulation screen  p-ANCA (antineutrophil cytoplasmic

 LFTs antibodies)
 Hepatitis serology (A/B/C)  Immunoglobulins – IgM/IgG
 Epstein-Barr Virus (EBV)  Alpha-1 Antitrypsin (to rule out
alpha-1 antitrypsin deficiency)
 Cytomegalovirus (CMV)
 Serum Copper (to rule out Wilson’s
 Anti-mitochondrial antibody (AMA)
disease)
 Anti-smooth muscle antibody
 Ceruloplasmin (to rule out Wilson’s
(ASMA)
disease)
 Anti-liver/kidney microsomal
 Ferritin (to rule out
antibodies (Anti-LKM)
haemochromatosis)
 Anti-nuclear antibody (ANA)