Anatomy of the Jejunum and Ileum
General
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Jejunum + ileum = 6-7 m long
Jejunum
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Second part of the small intestine, the jejunum, begins at
the duodenojejunal flexure where the digestive tract
resumes an intra-peritoneal course.
Jejunum constituting approximately 2/5
Most of the jejunum lies in the left upper quadrant
Ileum
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Third part of the small intestine, the ileum, ends at the
ileocecal junction, the union of the terminal ileum and
the cecum
Ileum approximately 3/5
Most of the ileum lies in the right lower quadrant (RLQ)
The terminal ileum usually lies in the pelvis from which it
ascends, ending in the medial aspect of the cecum.
Differentiation between the jejunum and ileum
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Although no clear line of demarcation between the jejunum and ileum exists, they have distinctive
characteristics that are surgically important
Characteristics
Caliber
Wall
Colour
Vascularity
Vasa recta
Arcades
Fat in mesentry
Circular folds/ plicae circulares
Lymphoid nodules (Peyer’s patches)
Proximal Jejunum
2-4cm
Thick & heavy
Deeper red
Greater
Long
Few large loops
less
Large, tall, & closely packed
Few
Distal Ileum
2-3cm
Thin & light
Paler pink
Less
Short
Many short loops
More
Low & sparse, absent in distal part
Many
Mesentery
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The mesentery is a fan-shaped fold of
peritoneum that attaches the jejunum and
ileum to the posterior abdominal wall
The origin or root of the mesentery
(approximately 15 cm long) is directed
obliquely, inferiorly, and to the right
It extends from the duodenojejunal
junction on the left side of vertebra L2 to
the right sacroiliac joint (ileocolic
junction)
The average length of the mesentery from
its root to the intestinal border is 20 cm.
The root of the mesentery crosses
(successively):
o The ascending and inferior parts
of the duodenum
o Abdominal aorta
o IVC
o Right ureter
o Right psoas major
o Right testicular or ovarian vessels
Between the two layers of the mesentery are the superior
mesenteric vessels, lymph nodes, a variable amount of
fat, and autonomic nerves.
Blood supply
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Superior mesenteric artery (SMA) supplies the jejunum
and ileum via jejunal & ileal arteries
The SMA usually arises from the abdominal aorta at the
level of the L1 vertebra, approximately 1 cm inferior to
the celiac trunk
Runs between the layers of the mesentery, sending 15-18 branches to the jejunum and ileum
The arteries unite to form loops or arches, called arterial arcades
These give rise to straight arteries, called vasa recta
Venous drainage
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The superior mesenteric vein drains the jejunum and
ileum
It lies anterior and to the right of the SMA in the root of
the mesentery
The SMV ends posterior to the neck of the pancreas,
where it unites with the splenic vein to form the
hepatic portal vein
Lymphatics
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Specialized lymphatic vessels (lacteal) in the intestinal
villi that absorb fat are called lacteals.
They empty their milk-like fluid into the lymphatic
plexuses in the walls of the jejunum and ileum.
The lacteals drain in turn into lymphatic vessels
between the layers of the mesentery.
Within the mesentery, the lymph passes sequentially
through three groups of lymph nodes:
o Juxta-intestinal lymph nodes: located close to the
intestinal wall.
o Mesenteric lymph nodes: scattered among the
arterial arcades.
o Superior central nodes: located along the proximal
part of the SMA.
Efferent lymphatic vessels from the mesenteric lymph nodes
drain to the superior mesenteric lymph nodes.
Lymphatic vessels from the terminal ileum drain to the
ileocolic lymph nodes
Innervation
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Sympathetic inputs from T8-T10
o Reach the superior mesenteric nerve plexus through the sympathetic trunks and thoracic
abdominopelvic (greater, lesser, and least) splanchnic nerves.
o Sympathetic stimulation:
 ↓ peristaltic and secretory activity of the intestine
 Acts as a vasoconstrictor, reducing or stopping digestion and making blood (and
energy) available for “fleeing or fighting.”
Parasympathetic from posterior vagal trunk
o Parasympathetic stimulation :
 ↑peristaltic and secretory activity of the intestine
 Restoring the digestion process following a sympathetic reaction.
The small intestine also has sensory (visceral afferent) fibers
o nsensitive to most pain stimuli, including cutting and burning
o Sensitive to distension that is perceived as colic (spasmodic abdominal pains or “intestinal
cramps”).
Ileo-caecal junction
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The terminal ileum enters the cecum obliquely and partly
invaginates into it.
The ileal orifice enters the cecum between ileocolic lips
The folds that meet laterally forming ridges called the frenula of
the ileal orifice
The orifice is usually closed by tonic contraction, however,
appearing as an ileal papilla on the cecal side
The papilla probably serves as a relatively passive flap valve,
preventing reflux from the cecum into the ileum as contractions
occur to propel contents up the ascending colon and into the
transverse colon
Blood supply
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SMA gives off the ileocolic branch  ileal branch  supply the
junction
Venous drainage
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Veins follow the arteries
Histology of the Jejunum & Ileum
Consists of:
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Duodenum
Jejunum
Ileum
Digestion and absorption is enhanced
by:
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Length (4-6m)
Circular folds of mucosa and submucosa=plica
circulares
Fingerlike projections =villi
Invaginations of mucosa between villi= Crypts of
Liberkühn
Intestinal villi
Mucosa
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Epithelium (four types of cells):
o Absorption cells/Enterocytes: (90%)
 Simple columnar epithelium -microvilli (absorption)
o Goblet cells (10%)
 Mucin secretion
o Enteroendocrine/ Paneth cells: (0,5%)
 Secretes antimicrobial substances
o Endocrine cells (similar to stomach) and stem cells
Lamina propria
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Central part of villus
“Makes the villi stand up” Loose connective
tissue: collagen + elastic fibers
Vascular + lymphatic network: (Lacteal-blind
ending lymphatic capillary)
Smooth muscle fibers: from muscularis mucosae
(intermittent contraction)
Lymphocyte infiltration:
o Individual cells (plasma, eosinophils +
lymphocytes)
o Peyer’s patches=lymphoid aggregates (ileum)
o GALT structures
Layers of crypts of Lieberkühn
1. Epithelial layer
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Columnar epithelial cells
Stem cells
o Base of gland
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Paneth cells
o Base of gland
o Appear acidophilic
o Produce lysozyme (bactericidal/controls intestinal flora)
Goblet cells
Enteroendocrine cells
2. Muscularis mucosae
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Inner circular + outer longitudinal smooth muscle
3. Submucosa
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Loose connective tissue
Brunner’s glands-open into the bottom of the crypts of Lieberkühn-zymogen and mucous secretion
4. Muscularis externa
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Inner circular and an outer longitudinal smooth muscle
5. Serosa
A very low magnification of the duodenum demonstrating the layers.
1. Mucosa
2. Submucosa
3. Muscularis externa
4. Brunner's glands
5. Muscularis mucosae
6. Plica circularis
A higher magnification of the structures of the mucosa and submucosa.
1. Mucosa
2. Surface of duodenum
3. Submucosa
4. Mucinous glands of Brunner
5. Crypts of Lieberkuhn that invaginate from surface
6. Villi that extend from surface
A high magnification of the structures of the duodenum.
1. Villus
2. Simple columnar epithelium (enterocytes)
3. Surface of duodenum
4. Muscilaris mucosae
5. Lumen of Crypt
6. Crypts of Lieberkuhn that invaginate from surface
7. Lamina propria
A very high magnification of a part of a villus demonstating the structures.
1. Villus
2. Goblet cells
3. Connective tissue of the lamina propria
4. Simple columnar epithelium
A high magnification of the secretory ducts of Brunner's gland.
1. Villi
2. Crypts of Lieberkuhn
3. Secretory units of Brunner's gland
4. Secretory duct of Brunner's gland opening into the bottom of a crypt of
Lieberkuhn
5. Muscularis mucosae that are interrupted by secretory ducts
6. Surface of duodenum
A high magnification of the secretory units of Brunner's gland.
1. Crypts of Lieberkuhn
2. Muscularis mucosae
3. Mucinous secretory units
4. Submucosa
A very low magnification of a section through the ileum demonstrating the different layers and structures.
1. Mucosa
2. Villus
3. Muscularis externa
4. Submucosa
5. Ileum surface
A higher magnification of the ileum demonstrating structures of the mucosa.
1. Mucosa
2. Lamina propria
3. Simple columnar epithelium
4. Surface of ileum
5. Submucosa
6. Muscularis externa
7. Crypt of Lierberkuhn
8. Muscularis mucosae
A very high magnification of the ileum epithelium.
1. Lamina propria
2. Simple columnar epithelium
3. Microvilli
4. Goblet cell
5. Enterocyte
6. Basement membrane
A very high magnification of the outer layers of the ileum.
1. Submucosa
2. Mucosa
3. Muscularis mucosae
4. Serosa
5. Longitudinal smooth muscle layer
6. Sirkulêrverlopende gladdespierlaag
7. Mesothelium
A high magnification of a Peyer's patch in the ileum.
1. Submucosa of a plica circulares
2. Peyer's patch
3. Germinal center
Physiology - Small Intestine
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Length of small intestine ~ 300 cm
Length of colon ~ 80 cm
However, the effective functional surface area of the small intestine is ~ 600 fold greater as a result of
villi and microvilli.
The small intestine and colon are anatomically and functionally distinct:
o Villi are present in the small intestine, but absent in the colon.
o Nutrient digestion and absorption take place in the small intestine, but not the colon.
Functions of small intestinal epithelium: NB!!!!
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Nutrient digestion
o Small intestine has enzymes (lactase) to digests disaccharides  monosaccharides
Nutrient absorption
Fluid and electrolyte absorption and secretion:
o The small intestine absorbs ~ 7-8 L of fluid per day
o Dietary intake=1-2L per day
o Salivary, gastric, pancreatic, biliary and intestinal fluid= 6-7 L per day
Barrier and immune defence: synthesizes and secretes IgA
Synthesis and secretion of proteins: Apolipoproteins
Hormone production of several bioactive amines and peptides.
o The intestine is a large endocrine organ—produces several amines and peptides that serve as
paracrine and endocrine mediators of intestinal function.
No precise anatomic characteristics separate the duodenum, jejunum and ileum.
However, certain nutrients are absorbed exclusively in specific areas of the small intestine:
o VitB12 and bile acids in terminal ileum NB!
Disorders of Absorption
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From a clinical point of view Absorption can be increased or
decreased.
NOTE:
Ulcerative colitis  prevented by
smoking
Chron’s  if you smoke you
automatically get an another attack
Increased
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Only 2 clinical conditions lead to increased absorption NB!
o Hemochromatosis: Increased absorption of iron
o Wilson`s disease: Increased absorption of copper
Decreased
Specific malabsorption syndromes:
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Example is decreased vitamin B12 absorption in the terminal ileum due to absence of intrinsic factor
or ileal disease.
Most NB localised malabsorption syndrome:
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NOTE: NB!!
Local syndrome  specific presentation
General syndrome  general presentation
Terminal ileum: Crohn`s disease
Resection:
o Decreased absorption of vitamin B12
o Decreased absorption of bile acids. Decrease in bile acid pool.
o Need bile acids for fat absorption
o No bile acids, no fat absorption
o No fat absorption, no absorption of fat soluble vitamins: A, D, E, K
 VitA deficiency: Blindness
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VitD deficiency: Osteopenia, fractures
VitE deficiency: Neurological disease
VitK deficiency: Bleeding tendency
Generalised malabsorption
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Usually associated with steatorrhea–an increase in stool fat excretion > 6 % of dietary intake.
This can be due to pancreatic or small intestinal disease
Pancreatic causes
 Hereditary (atrophic, agenesis)
 Cystic fibrosis
 Chronic pancreatitis
 Resection
 After severe acute pancreatitis
Small intestinal causes
 Crohn`s disease
 Celiac`s disease
 Whipple`s disease
 Amyloidosis
 Lymphoma
 Scleroderma
 Vascular insufficiency
 Radiation
 Blind loop syndrome
 Bypass surgery
 Resection
How to you distinguish between the two
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D-Xylose absorption test to assess the integrity of the small intestinal mechanism of absorption.
Fecal elastase, fats to assess efficacy of digestion (pancreatic)
Physiological presentation of malabsorption:
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Chronic diarrhea (usually with steatorrhea)
Weight loss
Osteoporosis (vitD)
Bleeding tendency (vitK)
Blindness (VitA)
Neurological / peripheral neuropathy (vitE)
VitB12 malabsorption
o True pernicious anemia (pernicious = destructive)
o Ileal disease
o Anaemia
o Posterolateral sclerosis of spinal cord
o Dementia
o Jaundice due to haemolysis
Physiology - Colon
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The colon prepares waste material for controlled evacuation.
Colonic mucosa dehydrates the stool.
This decreases daily fecal volume from 1000 to 1500 ml delivered from the ileum to 100 to 200 ml
expelled from the rectum.
Dense bacterial colonization in the colon:
o This ferments undigested carbohydrates and short chain fatty acids.
Small bowel obstruction
Normal motility: electrical activity
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Slow waves – pacesetter potentials
Spike discharges – contractile potentials
Small bowel contractions
o Ring contractions
o Peristaltic contractions
Ileocaecal junction
NOTE: Dysentery  blood in stools (only Colon)
Introduction
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Most common surgical disorder
Barrier to aborel progress
Mechanical/dynamic
o Simple: lumen only
o Complicated (strangulated): compromised blood supply
Non-mechanical/adynamic (ileus)
o Neurogenic failure
o No barrier to progress of contents
o Poor peristalsis
o Gas throughout the bowel
o Non-operative management
Causes
Mechanical obstruction
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A BIG CHAV
Annular pancreas
Bezoars
Intussusception very common in children
Gall stone ileus
Carcinomatosis
Hernia
Adhesions
o Tough fibrous connective tissue
o Constricting bands
o Congenital or acquired
 Previous surgery
 Inflammation
 Infection
o Accounts for most cases (50-70%)
Volvulus
Adynamic obstruction
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Peritonitis
Mesenteric (vascular) occlusion
Pelvic fracture
Retroperitoneal haematoma
Metabolic disorder
o DKA
o Hyponatraemia
o Hypokalaemia
o Uraemia
PM PRM
Bezoars
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Accumulation of hair or vegetable
matter or a combination of the 2
which reduces nutritional absorption
Can form a complete cast of the
stomach and leads to malnutrition
Usually seen in females who eat their
hair and it remains undigested
Dx through barium examination
Tx with surgical removal through
gastrostomy
“Repunzel syndrome”
Pathophysiology
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Reactive hyperperistalsis bowel sounds
increase
Luminal distention
o Gas
o Fluid from GIT
Bacterial fermentation
Oedema & mural transudation
Volume contraction
Clinical features
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Pain
Distension
Vomiting
Constipation/obstipation
X-ray features
Bowel sounds
Tenderness
Temperature
Management
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Nasogastric suction
IV fluids
Correction of electrolytes
Monitoring
o Hydration
o Electrolytes
o Blood gas – pH & HCO3
o Pain & tenderness
o WBC
o Free intra-peritoneal gas
Removal of cause
Surgery
o Metabolic derangements
o Evidence of strangulation/ischaemia
o Peritonitis
o Non-resolution
o Hernia
o Cancer
Infective and malabsorptive diarrhoea
Diarrhoea
The means the stool has:
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Increased frequency, volume of stool
Decreased consistency
Children
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Numerous episodes first 5 years of life
Most infectious and self limiting
Can be associated significant complications and mortality
Other
o Acquired or inherited disorders of digestion and absorption
o Motility disturbances
o Drugs
o Food intolerances
Divided into: Chronic and acute
ACUTE GASTROENTERITIS
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Denotes infections GIT caused by bacterial, viral or paracytic infections
Many food-borne illnesses
Most common manifestation vomiting and diarrhoea
Associated systemic features abdominal pain, fever
The problem
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Diarrheal disorders 18% childhood deaths
Global mortality declining, overall incidence of diarrhoea remains the same
3-19% acute diarrhoea – persistent
Up to 50% of diarrhoea deaths due to persistent diarrhoea
Causes of Acute Diarrhoea
CANCER
Bacteria
 Salmonella
 Shigella
 Staphylococcus Aureus
 Vibrio cholera
 Yersinia enterocolitica
 Campylobacter jejuni
 E coli
 Clostridium Difficile
Viruses
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Parasitic infections
Protozoa
 Cryptosporidium
 Entamoeba
 Hystolytica
 Giardia Lamblia
 Microsporidium
 Isospora
Helminths
 Strongyloides stercoralis
 Trichuris trichura
 Schistosoma
 Trichinella
Caliciviruses
Astroviruses
Noroviruses
CMV
Enteric adenoviruses
Rotavirus
HSV
HIV
Differences in clinical presentation?
Viral
Bacterial
Example
Season
Rotavirus
Winter months
Shigella BUT Multiple pathogens isolated stool
Summer – bacterial contamination
Age
Presentation
6-24 months of age
Preceding respiratory symptoms and profuse
vomiting before onset diarrhoea
 Small intestinal mucosa damage
o Invade mucosal cells tips vili
o Shedding
o disaccharidase deficiency ↓carbohydrate digestion (osmotic
diarrhoea)
o ↓reabsorption fluid and electrolytes
< 6 months of age
Abrupt onset diarrhoea, prominent CNS symptoms, high
fever, no vomiting, blood and mucous in stools
 Adherence mucosal cell, damage
 Enterotoxin production
o stimulate secretion large amounts fluid and
electrolytes
o Toxigenic E.coli, Vibrio cholera
 Cytotoxin production
o Mucosal damage
 decreased absorptive surface
 Secondary inflammatory response ↑fluid
secretion
o Shigella dysentery type 1, campylobacter,
enteroinvasive E.coli
Mechanism
Presentation: Dehydration
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The loss of body water leads to compensatory mechanisms:
o Thirst
o Antidiuresis
o Catecholamine release of stress response
Continuing water loss will result in failure of compensation, at which stage the patient enters a state
of circulatory insufficiency.
The clinical features of dehydration evolve in a continuous spectrum
Features of dehydration
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Dry mouth and mucosa
Reduced urine, sweat and tears
Sunken eyes and fontanel
Reduced skin turgor
Acidotic breathing
Restlessness to irritability
Prolonged capillary filling time > 3 seconds
Hypotension and shock, tachycardia
Apathy to coma, convulsions
What advice regarding dehydration?
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Prevent
Replace amount that is lost in each vomit stool, +/- 15-30ml/kg additional to each feed
ORS small frequent quantities, teaspoon
Give as much as the child wants, 15-30 ml/kg/h
Once stronger, alert, pass urine, want food : offer small feed
Ongoing losses
How to prepare home-made solution? - WRITE IT DOWN FOR MOM
 8 teaspoons cane sugar
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½ teaspoon salt
1 L cleanest water
Presentation: Vomiting
Why do you get vomiting in gastroenteritis?
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Impaired gastric emptying
Starvation ketosis
Local irritation and stimulation CNX
Toxins – stimulation chemoreceptors vomiting center
What do we do when we have child? Resuscitation:
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Shock medical emergency: IV fluids
IV access : IV line, interosseus line
Ringer’s / 0.9% Saline: isotonic fluids
20ml /kg bolus
Reassess : another 10 – 20ml/kg bolus
½ Darrows 10-15ml/kg/h
What are the complications Diarrhoea?
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Dehydration  Shock
o ARF
o cerebral complications(hypoxic ischemia, cerebral vascular thrombosis),
o NEC part of the intestine dies
o Shock lung
Acidosis and electrolyte disturbance
Additional features
o Fever
o Convulsions
o Ileus
o Protein losing enteropathy
o Necrotizing enterocolitis
Dysfunction gut
o ↓ digestion and absorption nutrients
Complication: Convulsions
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Cerebral venous thrombosis
Fever
Hypoglycemia, hypo/hypernatremia
Meningitis, encephalitis
Cerebral edema rapid infusion hypotonic fluid
Toxins Shigella etc
Management of convulsion
 Prevent dehydration, continue feeds to allow maximal digestion and absorption
Which electrolytes lost in diarrhoeal stool? NB!
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Sodium
Potassium
Chloride
Bicarbonate
Clinical features electrolyte disturbance?
Hypokalemia:
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Weakness, hypotonia, paralysis, areflexia
Cardiac arythmias
Ileus
Older child inability to hold up head
Prolonged: renal tubular defects, reduced concentrating ability, interstitial nephritis
Hyponatremia
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< 125 mmol/l : Nausea, vomiting, muscle twitching, lethargy
< 115 mmol/l :Seizures and coma
Hypernatremia
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Osmotic gradient water from intracellular to extracellular compartment- masked clinical
signs dehydration
Symptoms of intracellular water loss from brain cells depressed sensorium, irritability,
convulsions
Severity depends on degree and rate of rise of plasma osmolality
Management and Advice
Constituents Oral Rehydration Solution (ORS)?
Advice regarding feeding?
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Maintaining nutrient intake important recovery
Continue milk feeds
Select solids easily digestable, bland and soft – starchy porridge, mashed banana
Small quantities at a time, as frequently as tolerated
Aim to restore normal intake 2nd-3rd day
Additional therapies
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Zinc beneficial
Antimotility agents like loperamide are contraindicated in children
Similarly, due to the potentially serious side effects (lethargy, dystonia, malignant
hyperpyrexia) of anti-emetics such as the phenothiazines they are of little value
Careful oral rehydration is usually sufficient
Ondansetron
o Selective serotoninergic 5HT3 receptor antagonist
o No sedative effect or extrapyramidal reactions
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Effective against placebo in relieving vomiting, reducing the need for intravenous fluids and
decreasing hospitalization
Antibiotic therapy
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If there is Dysentery  Ciprobay 15 mg/kg/dose bd po x 3 days
How to prevent gastroenteritis
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Hygiene and sanitation
Exclusive breastfeeding 6 months
Prevent malnutrition, early intervention
Immunizations – Measles, Rotarix
Chronic diarrhoea
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Passage of abnormal, unformed stools for 14 days or longer
Developing countries most common following acute episode
Other
o Inherited abnormalities intestinal mucosa
o Protein sensitisation
o Anatomic abnormalities
o Motility disturbances
o Immune deficiencies
o Chronic inflammatory disorders
Definitions
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Most cases acute diarrhoea self-limiting
Persisting diarrhoea > 7-14 days
o Risk factors: formula feeding, < 3/12 at onset, malnutrition, immune suppression,
associated illness, choice feeds during acute diarrhoea
Chronic diarrhoea
o 2-4 weeks without improvement
o Related acute infective onset: persisting diarrhoea spectrum
o Other cases: longstanding intestinal dysfunction, maldigestion and malabsorption
Disorders associated chronic childhood diarrhoea
Congenital
 Congenital Chloride diarrhoea
 Microvillus inclusion disease
 Epithelial displasia or Tufting
enteropathy
 Auto-immune enteropathy
Mucosal Damage and abnormalities
 Infections (viral, bacterial, protozoal)
 Post-enteritis enteropathy
 Celiac disease
 Protein-sensitive enteropathy
 Eosinophilic gastro-enteropathy
 Intestinal lymphangiectasia
Immune deficiency
 HIV
 Primary immune deficiency
Endocrine disorders
 VIP secreting tumours
 Zollinger-Ellison syndrome
 Carcinoid tumours
 Thyrotoxicosis
Pancreatic disorders
 Cystic fibrosis
 Schwachman-Diamond Syndrome
 Congenital lipase deficiency
Anatomic abnormalities
 Short bowel syndrome
 Stagnant loop syndrome
 Malrotation
Metabolic and endocrine abnormalities
 Acrodermatitis enterohepatica
 Abetalipoproteinaemia
 Wolman’s disease
 Hypoparathyroidism
 Hyperparathyroidism
Enzyme deficiencies
 Secondary disaccharidase deficiencies
 Adult-type lactase deficiency
 Congental disaccharidase deficiency
 Enterokinase deficiency
Other
 Small bowel bacterial overgrowth
4.
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3.
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1. NB!! Persistence dehydrating diarrhoea and FTT after acute onset
Risk factors
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
Immune deficiency
Onset of diarrhoea at less than 3 months
Measles
Malnutrition, Vit A and Zinc deficiency
Lack of breastfeeding
Environmental contamination with increased exposure to enteropathogens.
Cases of persistent diarrhoea (episodes that began acutely but last for at least 14 days)
account for 3-20% of all diarrhoeal episodes in children less than 5 years of age and up to
50% of all diarrhoeal deaths.
Why post enteritis persisting diarrhoea?
Persisting or new infection
 Malnutrition / HIV fail to clear infection
 Nosocomial infection overcrowded hospitals
 More than one pathogen
o Specific pathogens associated



o Cryptosporidium
o Giardia Lamblia
o EAggEC
Small intestinal bacterial overgrowth
o Unknown reasons
o Damage mucosa
o Deconjugation bile acids
Small intestinal mucosal damage
o Destruction villus mucosal cells  disaccharidase deficiency  carbohydrate
malabsorption (as cannot absorb as
o Osmotic agents bacterial action colon – aggrevate stool water losses
o Damaged mucosal surfaces  absorption intact foreign proteins  2 immunological
reaction host  further damage
o Decreased intestinal absorptive surface nutrients and fluids
Nutritional deterioration
o Nutrient loss related severity diarrhoea and cumulative
o >30g/kg/d nitrogen and energy loss too great for growth and tissue repair enterally
alone
o Vicious cycle diarrhoea  progressive  malnutrition  aggrevates diarrhoea
o Post enteritis enteropathy
2. Celiac disease (not done in class)




Genetically determined autoimmune enteropathy
Triggered exposure gluten
Manifest at any age
Wide range manifestations of variable severity
Gluten




Endosperm wheat, barley, rye
High content glutamine and proline
Resistant proteolytic enzymes GIT
Gluten-derived gliadin peptides
Clinical manifestations

Classical celiac disease: intestinal symptoms
o Diarrhoea +/- steatorrhea
o Constipation
o Anorexia
o Vomiting
o Abdominal pain
o Abdominal distention
o Weight loss
o Failure to thrive
Atypical Symptoms





Iron deficiency anemia
Rachitis, osteoporosis, dental enamel hypoplasia
Peripheral neuropathy, epilepsy, irritability
Short stature, delayed puberty, secondary hypoparathyroidism
Dermatitis herpetiformis, aloplecia areata, erythema nodosum


Ideopathic pulmonary hemosiderosis
Infertility, adverse pregnancy outcome, menstrual abnormalities
Diagnosis





Intestinal biopsy gold standard
Stepwise approach
o High degree clinical suspicion
o Age appropriate serological testing
Screening
o Symptoms
o First degree relative
o Associated diseases
All testing on gluten containing diet
GFD as diagnostic tool inappropriate
Which antibodies are celiac specific?



Endomysial antibody (EMA)
Transglutaminase 2- specific antibody (anti-TG2)
Deaminated gliadin-specific antibody (anti-DPG)
3. Non-dehydrating diarrhoea, FTT, appetite maintained (not done in class)






Exocrine pancreatic disorders
Good/increased appetite, bloated abdomen, foul smelling diarrhoea, undigested food
Cystic fibrosis most common disorder
F-elastase
Sweat test
Other: Schwachman, Diamond syndrome
4. Diarrhoea with normal hydration and nutrition (not done in class)




Motility disturbances, normal digestion and absorption
Toddler’s diarrhoea
– Healthy child
– 6m-4y
– Episodically
– Never at night, progressively more loose stools later day
– Family history bowel disturbance
Normal growth, physical exam, u+stool MCS, ESR, FBC
Reassurance
Diarrhoea in adults
Definition


3 or more bowel movements per day are considered to be abnormal
o Weight - above 200g/day
o Consistency - loose/watery
OR A CHANGE FROM USUAL PATTERN
Secretion is abnormal, not
absorption
Pathophysiology and mechanism


Is usually but not always a protective response to intestinal conditions
Usually is due to excess of stool water rather than a decrease in the water-holding capacity of faecal
solids
o Implying an abnormality in water transport within the gut
o Normally, the small intestine and colon absorb 99% of total water in transit
Types of diarrhoea
Osmotic  water




Disappears with fasting
Cessation of ingestion of the offending substance solves
NOTE: electrolyte absorption is not impaired in osmotic diarrhoea; thus, electrolyte concentrations in
stool water may be quite low
Ingestion of poorly absorbed account for most osmotic diarrhoeas:
o cations and anions
 Magnesium sulfate
 Magnesium phosphate
o absorbed sugars or sugar alcohols
 Mannitol
 Sorbitol (chewing gum!)
Secretory




Has many causes, the driving force for this is always:
o either net secretion of chloride or bicarbonate
o inhibition of net sodium absorption
Most common causes by far is infection
Enterotoxins from a host of infectious agent
o Primarily bacteria but also parasites and virus
o Interact with receptors modulating intestinal transport and lead to increased anion secretion
Other peptides
o Produced by endocrine tumours
 VIP
 Calcitonin
o Released from subepithelial neurons and inflammatory cells  cause secretory diarrhoea
by stimulating secretion by epithelial cells
Complex diarrhoea


Cases of pure secretory or pure osmotic diarrhoea are uncommon
Complex pathophysiology also may be observed in malabsorption syndromes and functional disorders
Clinical Classification
Time course (acute vs. chronic)


Acute diarrhoea (<4 weeks) usually are due to infectionsmost self-limiting/ easily treated
Chronic (>4weeks)
Volume (large vs. small)
Pathophysiology (secretory vs. osmotic)
Epidemiology
Stool characteristics (watery vs. fatty vs. inflammatory)



Chronic watery diarrhoea
o Infrequently due to ingestion of osmotically active substances that are poorly absorbed by the
intestine (osmotic diarrhoea)
o more commonly due to conditions causing secretory diarrhea
Chronic inflammatory diarrhoeas
o comprise a diverse group of
 infectious
 bacterial infections, such as:
o Tuberculosis, yersinosis
o Clostridium difficile– associated colitis

viral infections that ulcerate such as;
o cytomegalovirus ,herpes simplex

invasive parasitic such as strongyloidiasis
 idiopathic inflammatory
 neoplastic processes.
o Stools are characterized by the presence of

mucus and pus
 associated with ulceration of the mucosa. Such as in ulcerative colitis and Crohn's
disease
Fatty diarrhoea
o Malabsorption
 due to mucosal diseases
 celiac sprue
 Whipple's disease , typically produce fatty diarrhea.
 Short bowel syndrome or post resection
 Mesenteric ischemia
 may impair absorption of fat, but weight loss is often attributed to sitophobia
("fear of eating") due to postprandial pain
o Maldigestion
 due to pancreatic exocrine insufficiency inadequate duodenal bile acid concentration

produces steatorrhea.
Management



Dehydration
Nutrition
Fine tuned to The cause
o History - travel
o Physical examination
o Laboratory investigations
Chem Path - Lab evaluation of diarrhoea
Laboratory evaluation




Acute diarrhoea = production of loose stools +/- increased stool frequency for <2 weeks (chronic if >4 weeks)
Lab evaluation unnecessary for mild acute diarrhoea
Indicated for severe diarrhoea with fever, dysentery or if diarrheal illness is prolonged (>14 days)
Tests may include UEC, FBC, stool M,C+S and investigation for parasites
Lab tests for chronic diarrhoea







FBC, ESR, UEC, Ca2+, Mg, PO4, albumin, TP
Folate, vit B12, iron, LFT’s
Stool analysis
o MC+S for ova/parasites/leucocytes
o Faecal occult blood

Positive result suggests IBD, or neoplasm
o Faecal fat

Excessive fat excretion suggests malabsorption or maldigestion
o Faecal osmolality, Na+, K+ to calculate osmotic gap

OG = Osmolality – 2([Na+] + [K+])

>125 suggests osmotic diarrhoea

<50 suggests secretory diarrhoea
o Faecal pH

<5.6 suggests carbohydrate malabsorption
o Faecal laxative screening

Magnesium, phenolphthalein
Chronic secretory diarrhoea
o Exclude bacterial/parasitic infection
o Gastrin, VIP, 5HIAA, metanephrine, histamine, TSH
o Test for bacterial overgrowth only in selected patients
Chronic osmotic diarrhoea
o Most osmotic diarrhoea without steatorrhoea is due to poorly absorbable CHO or Mg salts
o In suspected lactose intolerance do hydrogen breath test or measure lactase in a mucosal biopsy
o Investigate possibility of sorbitol or fructose ingestion
Chronic inflammatory diarrhoea
o Small bowel follow-through and sigmoidoscopy/colonoscopy with biopsies for evaluation of IBD
o Stool culture to identify infectious causes of inflammation
Chronic fatty diarrhoea
o Assess pancreatic exocrine function by faecal elastase
o
Small bowel biopsy and aspirate of contents for culture
Special tests – CHO malabsorption


Hydrogen breath tests
o Bacterial overgrowth, CHO malabsorption
o Hydrogen measured in exhaled air in fasting pt
o Hydrogen measured in exhaled air after giving test sugar
D-Xylose Absorption Test
o Xylose is a five-C sugar that is absorbed in the small intestine and does not require intraluminal
digestion
o Used to differentiate between mucosal disease (in which absorption will be decreased) and pancreatic
disease
Special tests – fat malabsorption

Faecal elastase
o Random stool sample


o No need to discontinue enzymes
o Good sensitivity for moderate/severe pancreatic insufficiency
Faecal fat measurement
o Diet containing 50-150g fat per day for 3d prior to and during collection of stool for 72h into weighed
container
o Sample homogenised, fats extracted and measured
14C-triolein breath test
o Indirectly assesses pancreatic lipase activity in intestine
o 14C-labelled triglyceride triolein is ingested by fasting patient
o 14C-labelled CO2 is measured in exhaled air hourly for 6 hours thereafter
Special tests – Coeliac disease






Sensitivity to gluten (gliadin) in wheat/other cereals
Inflammation of SI with malabsorption
Measure antibodies while on gluten-containing diet
o IgA endomysial antibody (IgA EMA)
o IgA tissue transglutaminase antibody (IgA tTG)
o Anti-gliadin antibodies no longer advised
With selective IgA deficiency, do IgG tTG or EMA
At least 3 duodenal biopsies to confirm diagnosis
>99 % of pts have HLA DQ2 and/or DQ8
Special tests – Schilling test




Stage 1:
o
o
Stage 2:
o
Stage 3:
o
Stage 4:
o
o
Labelled B12 p.o. and unlabelled B12 IM as flushing dose
Measure labelled vit B12 in 24h urine collection
Give IF with vit B12 – will normalise in pernicious anaemia
Give pancreas extract with vit B12 – will normalise in pancreatic insufficiency
Repeat stage 1 after course of antibiotics – will normalise in bacterial overgrowth
If all 4 stages abnormal – ileal disease
Virology
Introduction


5 billion episodes of diarrhoeal disease globally every year
Improved public health infrastructure has led to ↓ frequency of bacterial & parasitic causes
of gastroenteritis BUT viral causes have not declined in an equal fashion
Etiologic agents




Viral gastroenteritis pathogens  all infect the intestine & induce gastrointestinal
symptoms
→ shared ability
NOT to be confused with enteric viruses (which infect the intestine but predominantly
produce manifestations at extraintestinal sites) e.g. enteroviruses, echoviruses,
coxsackieviruses, polioviruses, Hepatitis A and E
The medically important causes of viral gastroenteritis are:
o Rotavirus
o Astrovirus
o Norovirus
o Enteric Adenovirus
Epidemiology
Transmission



Faecal-oral
Person-to-person
Contaminated food and water
Risk groups


Increased exposure to virus
Increased susceptibility e.g. younger age or immunocompromised individuals
Clinical manifestations


Disease manifestations are clinically similar:
o Watery diarrhea → usually without blood/mucus
 Diarrhoea ranges from mild to severe
o Nausea & vomiting
o Abdominal cramps
o May be complicated by dehydration
Major differences are in onset and duration of symptoms
Gastroenteritis viruses
ROTAVIRUS
Family
Genus
Virus
Transmission
Incubation
Duration
Prevention
General
Season
Outbreak
At risk
Vaccines
Who should get
the rotavirus
vaccine?
Efficacy
Reoviridae
Rotavirus
Rotavirus
– faecal-oral
– ?respiratory droplets
short: 2 - 3 days
4-7 days
– Hygiene
– Vaccine
Most common cause of viral infantile diarrhoea in developing countries
Highly infectious
– 1012 per g faeces
– Resistant
Autumn → winter
– nosocomial
– child care centres
– homes for elderly
Children 6months  2years
– Rotarix - Attenuated human rotavirus vaccine derived from a G1P[8] strain
• Provides partial cross-protection against most other serotypes
• Included in South African EPI schedule
– RotaTeq - Pentavalent human-bovine rotavirus reassortant vaccine, contains only one G-type or Ptype protein from human strains—G1, G2, G3, G4, and P[8]
– WHO recommends universal immunisation of infants
– RotaTeq: 3 oral doses at 2, 4 & 6 months of age
• Catch-up: vaccination not to be initiated after 15 weeks of age
• Give last dose before 8 months of age in USA, 32 weeks in SA
– Rotarix: 2 oral doses at 2 & 4 months (6 and 14 weeks in SA)
• Catch-up: Initiate between 6 and 14 weeks of age, complete by 24 weeks
– HIV infected children?
• Rotarix found to be safe & immunogenic when administered to HIV+ infants
• If symptomatic, weigh risks & benefits
– Both vaccines protect (NOT 100%) against severe rotavirus gastroenteritis & hospitalisation for
rotavirus gastroenteritis
– Some cross-protection demonstrated against types not included in vaccine
ADENOVIRUS
Family
Genus
Virus
Adenoviridae
Mastadenovirus
Human adenovirus
Transmission
Incubation
Duration
Season
Outbreak
At risk
Vaccines
– 1011 per gram faeces
– Faecal-oral
– Person-to-person
7-8 days
- 6-7 days
- Prolong excretion
Midsummer peak
– Nosocomial
– Child care centres
Children <2years
NONE
ASTROVIRUS
Family
Genus
Virus
Transmission
Incubation
Duration
Season
Outbreak
At risk
Vaccines
Astroviridae
Astrovirus
Human astrovirus
– 1011 per gram faeces
– Faecal-oral
– Person-to-person
– Faecally contaminated
food and water
2 - 3 days
– 12 h – 3-4 days
– Prolonged excretion
Winter
– Nosocomial
– Child care centres
– Schools/old age homes
– 5 - 7% South Africa
– Children < 7 yrs
– Usually less severe than rotavirus
NONE
CALICIVIRUSES
Family
Genus
Virus
Epidemiology
Transmission
Incubation
Duration
Season
Outbreak
Caliciviridae
Norovirus
Sapovirus
limited/no cross
protection within genera
USA: Norovirus now most common cause of gastroenteritis among young children following rotavirus
immunisation
– Most common cause of epidemic viral gastroenteritis among all ages
– Extremely stable virus
• Resist heating to 60ᵒC
• Resist chlorine disinfection
– 106 per gram faeces
– Faecal-oral
– Person-to-person
– Aerosols of vomitus: high
rate of secondary spread
– Faecally contaminated food and water
1-3 days
1-4 days
– None
– Temperate climates: winter peak?
– Common source (e.g. shellfish)
– All age groups affected
– Nosocomial
– Child care centers
– Schools/old age homes
– Cruise ships
– Vomiting more prominent, more likely to be the sole presenting symptom compared to other types of
viral gastroenteritis
NONE
Clinical pic
Vaccines
Lab Diagnosis


Viral isolation
o Isolation difficult: NOT used for routine diagnosis
Serology
o Available for some viruses: NOT used for routine diagnosis
Management



Supportive care
o Rehydration
o Anti-motility drugs not recommended
Isolation or patient cohorting
Preventative measures
o Hand washing
o Appropriate diaper disposal
Physiologic complications of chronic vomiting
Face



Subconjunctival hemorrhage
Epistaxis
Due to chronic retching
Dental



Dental erosion
Cheilitis
Mucositis of hard palate and throat (long term can cause pre-malignancy)
Parotid gland


Parotid gland hypertrophy (Known as sialadenosis)
Exact cause unclear
Larynx




Hoarseness
Oedema
Telangiectasia
Polyp formation
Lower Oesophageal Sphincter



Chronic GORD
o Due to laxity of LES due to chronic retching
 Heartburn
 Odynophagia
 Stricture formation
o Mucosal tears—Mallory Weiss syndrome
Perforation of oesophagus—Boerhaave`s syndrome
Barrett`s oesophagus  adenocarcinoma
Elevated amylase levels


Hyperamylasemia
Secreted by salivary glands
Renal



Volume depletion
Resultant hyperaldosteronism (zona granulosum)
o Secondary vs primary (tumour) hyperaldosteronism
o Oedema Formation  Oedema formation can result from chronic vomiting due to
continued up regulation of aldosterone levels
This leads to hypokalaemia and alkalosis
o Also potassium and acid loss in vomitus
o Effects of hypokalaemia
 Muscle weakness
 Cardiac arrhythmia
Vomiting and Gastric Outlet Obstruction
Vomiting and regurgitation


Vomiting = active process where stomach content is actively expelled
Regurgitation associated with
o Achalasia
o Pouches
o Hiatus hernia
Gastric outlet obstruction
Caused by




PUD most common
Acute: edema in pyloric region
o Treat conservatively (Give nasogastric tube and treat with IV fluids)
Chronic: fibrosis
o May need surgery
Other:
o Hypertrophic pyloric stenosis (infants)
o Gastritis
o Antral stenosis (Acid ingestion)
o Gastric cancer
Pathophysiology





Stomach secreted acid (HCl) which is lost by vomiting
Develops alkalosis (increased pH)
Metabolic cause (loss of acid)
Dehydration (loss of volume)
Cells compensate (Potassium, hypokalemia)
Results in: hypochloremic, hypokalaemic metabolic alkalosis


Normal pH: 7.35-7.45
Henderson Hasselbach equation is used to determine pH
o Mortality
 Alkalosis:
 pH>7.55 = 45%
 pH >7.65 = 80%
 Acidosis:
 pH <7 = 60%
 pH <6.9 = 100%
Compensatory mechanisms



Body compensates for acidosis (metabolic processes produce acids)
…??
Commpensatory mechanisms
o Buffers
 Bloodstream has HCO3, PO4 and albumin that can bind H+ (acidosis)
 H + HCO£ = H2CO3 = H20 + CO2
o
o
 H + HPO4 = H2PO4
Respiratory
 Hypoventilation, increases CO2
 pCO2 + H20 = H2CO3 = H+ HCO3
 Increased HCO3
Renal
 Exchange H+ in tubule for K+, with increased K+ excretion (Hypokalemia)
 Reabsorb fluids for hypovolemia oliguria
Vomiting or nasogastric suction






Loss of HCL
Generation of HCO3
Excretion of NaHCO3 in urine
ECF contraction
Renin will increase angiotensin II and aldosterone
Excretion of K+: Kaliuresis
Symptoms


Non-specific
Low K+  weakness, myalgia, ECG changes, hypoventilation
Medical management

PUD:
o Reduced acid secretion: PPI, H2A
o Empty stomach: nasogastric tube for drainage
o Allow endoscopy and barium studies to confirm diagnosis]
Endoscopy




To establish Dx
Identify specific cause
Therapeutic
…?
Endoscopic balloon dilatation

Safe and effective alternative in management..?

Truncal vagotomy
o Need drainage procedure because with paralyse pylorus!
 Finneys pyroplasty
 Heineke-mikulicz pyloroplasty
Selective vagotomy
Highly selective vagotomy
o Only affects acid secreting parts of stomach
o Does not affect pylorus
o Recurrence rate quite high for PUD


Problems with gastric outlet obstruction




Chronic malnutrition
Need food
Give enterally (if feeding tube can be passed beyond obstruction) or paraenterally (TPN)
Increased complications (Adverse effects)
Surgical options



Bilroth I:
o Gastro-duodenostomy
Bilroth II
o Gastrojejunostomy
o Attach stomach to jejunum (bypass duodenum)
Roux – en-Y
o Gastrojejunostomy
o Attach jejunum to stomach and reattach duodenum to junum distally
TUMORS OF THE SMALL BOWEL
Benign and malignant tumours





Benign
Benign gist
Adenoma
Lipoma
Hamartomas
Hemangioma




Malignant
Adenocarcinoma
Carcinoid tumor
Malignant gist
Lymphoma
Introduction




Small bowel neoplasms are rare.
Only 5% of the all gastrointestinal tumors.
Small bowel has rapid transit of luminal content and high turnover rate of epithelial cells
which may minimize carcinogenic exposure.
The content is alkaline, the level of IgA is high in the intestinal wall and the bacterial count is
low.
Epidemiology






The mean age of the presentation is 62 years.
The highest incidence of the cancer in the Maori of New Zealand and ethnic Hawaiians.
AIDS CONTRIBUTED TO THE INCREASE OF LYMPHOMAS! (RSA)
Duodenal tumours are the most common per unit area.
Benign lesions are asymptomatic and identified at autopsy.
75% of symptomatic lesions that lead to surgery are malignant
Aetiology




Patients with Crohn’s disease and familial adenomatous polyposis are at higher risk for small
bowel neoplasms.
Mutations of the K-ras gene are commonly found.
Risk factors include hereditary nonpolyposis colorectal cancer, Peutz-Jeghers syndrome,
gluten sensitive enteropathyand biliary diversion (e.g. previous cholecystectomy).
Smoking, heavy alcohol consumption and consumption of red meat or salt-cured foods may
contribute to small bowel cancers.
Pathology


Benign lesions (polyps) are 10 times as common as malignant ones.
Lymphoma is now the most common primary malignant tumor of the small bowel.
Diagnosis


Correct preoperative diagnosis is made in only 20%.
CT enteroclysis has accuracy of about 90%.







Flexible endoscopy is useful for the duodenum and terminal ileum.
Push enteroscopy may take up to 8 hours to perform.
Capsule endoscopy –swallowed radiotelemetry capsule that transmit images of the bowel is
now more widely available.
Plain films ( X-Ray ) may confirm the presence of an obstruction. It doesn’t tell us the nature
of lesion. ( useless )
Angiography of value for vascular lesions.
CT abdomen useful for GIST and staging of malignant cancers.
Despite the sophisticated imaging and fancy diagnostic modalities, diagnosis often made at
laparotomy done as an elective or as an emergency procedure. (? diagnostic laparotomy )
BENIGN TUMORS
Types
GIST





Benign GIST is the most common tumor that produce symptoms.
GIST-Gastrointestinal stromal tumors arise from the interstitial cell of Cajal, an intestinal
pacemaker cell. On the microscopy: well-differentiated smooth muscle cells.
GIST may grow intraluminal, intramural and extramural.
These stromal tumors can cause bowel obstruction and bleed.
If mitotic count low (<2) imply benign disease. If mitotic count > 5 per 50 HPF or size > 5cm
imply malignancy.
Adenoma
 Adenoma is the most common tumor on autopsy (asymptomatic)
 Adenomas are benign polyps and may be true , villous and Brunner gland adenomas.
 Adenomas are usually solitary polyps and may cause symptoms by intussusception or
bleeding.
 Familial adenomatous polyposis is characterized by multiple intestinal and colonic polyps,
osteomas and subcutaneous fibromas. The polyps are true neoplasms and there is a
potential for periampullary duodenal cancer and colonic cancer.
Lipoma
Hamartomas
 Hamartoma may be solitary in patients who are free of associated anomalies.
 They are multiple in 50% of the cases.
 10% of Hamartomas take part in Peutz-Jeghers syndrome a familial disorder characterised
by diffuse gastrointestinal polyposis and mucocutaneous pigmentation.
 The classic pigmented lesions are small, 1 to 2-mm, brown or black spots located in the
circumoral region of the face, buccal mucosa, forearms, palms, soles, digits and perianal area
Hemangioma
 Hemangiomas are developmental malformations consisting of submucosal proliferation of
blood vessels.
 They can occur at any level of the gastrointestinal tract.
 Patients with Turner’s syndrome are likely to have hemangiomas of the intestine.
 The most common symptom is intestinal bleeding.
 Angiography and Tc-red blood cell scanning are useful for the diagnosis. Resection is
recommended.
Endometriosis can implant on the small bowel
Clinical findings




Symptoms are often vague and nonspecific, dyspepsia, anorexia, malaise and dull abdominal
pain (often intermittent and colicky).
Most are asymptomatic.
Benign small bowel tumors are the most common cause of the intussusception in adults.
Haemorrhage is the next most common symptom. Usually occult bleeding. Rarely
hematemesis and hematochezia.
Treatment



Surgical treatment is almost always indicated as the diagnosis cannot be made without
microscopic examination of the specimen. Also segmental resection and primary
anastomosis is needed to prevent complications.
Small lesions may be resected by enterotomy.
The search should be done for other lesions as they could be multiple.
MALIGNANT TUMORS
Types
Adenocarcinoma
 Often asymptomatic or causes only minimal symptoms. They may produce the typical
constricting apple-core lesions. Later may present with pain, weight loss, bleeding, anaemia
and obstruction
 Metastases are present in 80% of cases at the time of operation.
 Wide segmental resection of bowel and adjacent mesentery is done when possible.
 5 year survival is 25%.
Carcinoid tumor
 They arise from enterochromaffin cells and may be associated with multiple endocrine
neoplasia (MEN) type1 and 2. it produce serotonin, substance P, neurotensin, gastrin,
Somatostatin, motilin, secretin and pancreatic polypeptide.
 80% of those larger than 2 cm have metastatic spread.
 It presents with obstruction, pain, bleeding or the carcinoid syndrome. 10% of patients
presents with carcinoid syndrome and others develop it later.
Carcinoid syndrome
 It consists of cutaneous flushing, diarrhoea, bronchoconstriction and right sided cardiac
valvular disease due to collagen deposition.
 Biologically active substances secreted by carcinoids are usually inactivated in the liver, so
there are no above mentioned symptoms.
 Hepatic metastases or ovarian or bronchial carcinoids release these compounds directly into
the systemic circulation, where they produce symptoms.
 Serotonin production is causing diarrhoea.
 Asthmatic attacks are usually observed during the flushing symptom. Bradykinin and
serotonin are implicated.
 Serotonin is metabolised in the liver to the inactive 5-hydroxyindoleacetiacid (5-HIAA).
 Elevated urinary levels of 5-HIAA is the diagnostic hallmark of carcinoid syndrome.
 Chromogranin A is elevated in plasma and it is very useful in making the diagnosis.
 CT scan and Somatostatin receptor scintigraphy are useful localisation studies.



Octreotide/ Somatostatin inhibit release of gastrointestinal hormones. It relieves flushing,
wheezing and diarrhoea.
Carcinoid tumor is regarded as a “malignant neoplasm in slow motion” and it should be
resected aggressively. Isolated hepatic metastases should be resected.
5-year survival after resection is 70%. Median survival from the histologic diagnosis is 14
years.
Malignant GIST
 GIST mostly arise from muscularis propria and grow extramurally. It is greater than 5 cm
usually.
 Indications for surgery are bleeding and obstruction.
 GIST spread hematogenously and into adjacent tissues.
 Segmental bowel resection is indicated.
 Tyrosine kinase inhibitor imatinib mesylate gives a lot of hope in treatment of GIST.
Lymphoma
 It may involve small bowel primarily or as a manifestation of systemic disease.
 They are most commonly found in the ileum, where is the greatest concentration of
lymphoid tissue.
 AIDS patients have increased risk of getting it.
 Symptoms are pain, weight loss, nausea, vomiting and change in bowel habits. Perforation
occur in 25% of patients.
 Treatment is wide resection including regional lymph nodes, radiation and chemotherapy.
INFLAMMATORY BOWEL DISEASE
Crohn’s disease
Definition

Inflammatory condition of unknown etiology
o Any portion of the GIT, mouth to the perianal area.
o Transmural
Distribution





Oral
Gastroduodenal
ileum
Colon
Perianal
Epidemiology of IBD
Crohn’s Disease
Ulcerative Colitis
Incidence per 100 000
1-10
3-15
Prevalence per 100 000
20-100
50-80
Peak age of onset
15-30 2nd peak 50-80
15-30
Gender
M=F
Race
Whites > Blacks
Ethnic
Jewish>Non-Jewish
Smoking
+ CD & -UC
Appendectomy
Protective in UC
Genetics
Chromosome 16 (CD), 3,5,7,12,19
Presentation






Fatigue
Prolonged diarrhoea (NO BLOOD)
Abdominal pain
Fever
Weight loss
Physical signs
o Failure to thrive in children and young adults
o And others to discuss)
Laboratory



Full blood count
U&E
CRP


LFT
Serum B12 and schilling test
Imaging investigations







Structural Cause
Patterns
Could be normal
Straight abdominal X rays
Barium studies
Endoscopy
CT scans
Histology in Crohn’s

Granulomas – they tend to be deep so that an ordinary biopsy may be too superficial to expose them
– NON CASEATING
Complications and extraintestinal manifestations


Local
o Strictures
o Fistulae
o Abscesses
o Ulceration
No part of the body is spared! Extra- intestinal
o Crohn’s uveitis
o Crohn’s abscess CT
o Crohn’s fistula
o Episceleritis in IBD
o Erythema Nodosum in IBD
o Early Pyoderma gangrenosum
o Pyoderma gangrenosum
Management of Crohn’s


Acute Severe - Steroids
o IV steroids
o Oral steroids
o ASA
Complications
o Minimal surgery
Ulcerative colitis
Definition

Inflammation of unknown origin limited to the mucosa layer of the colon.
o Invariably involves the rectum.
o
Continuous.
Terms in colitis





Ulcerative proctitis
Distal colitis or proctosigmoiditis
Left sided colitis – not beyond splenic flexure
Extensive colitis – not as far as cecum
Pancolitis extends to cecum
Presentation



Rectal bleeding
Fever
Pallor
Imaging



Radiography
Endoscopy
What will be seen:
o Ulceration
o Lead pipe colon
o Endoscopic evolution of ulcerative colitis
o Contiguos ulceration
Management - Acute Severe





Inform surgeon on call
High dose IV steroids for 5 to 7 days
Monitor severity
o Number of stools, fever, wbc, platelets
Day 5 Cyclosporin
No response or getting worse do not hesitate to involve surgery
o In theory the condition is curable
Usual Management




Depends on severity
Area of Involvement
Patient response to different treatments and side effects
Dealing with complications
Management of left sided colitis
Toxic mega colon






Transverse colon 8-10cm
High fever
Pallor
Dehydration
MEDICAL/SURGICAL EMERGENCY
Intensive therapy
Management of severe pancolitis
Complications






Uveitis and episcleritis
Erythema nodosum and pyoderma gangrenosum
Arthritis large joints and ankylosing spondylitis (B27)
Sclerosing cholangitis
Lung disease, DVT
Autoimmune hemolytic anemia
Neoplasia in UC


Pancolitis
More than 8-10 years
Crohn’s vs Ulcerative colitis





CD involvement of small bowel
Sparing of the rectum by Crohn’s
Absence of gross bleeding in Crohn’s
Presence of bothersome perianal disease in Crohn’s
CD panmural with granuloma
Drugs
Steroid spairing drugs



ASA
Azathioprine
Methotrexate
Immunomodulatory drugs

Antibody to TNF
Other approaches


Antibiotics
o Metronidazole
o Quinolones
Probiotics
Conclusion


Long history of abdominal pain – think of Crohn’s
Long history of bloody diarrhea – think of Ulcerative colitis
Nuclear Medicine
GIT Bleeding

Massive haemorrhage in the lower GIT is defined as bleeding distal to the lig of trietz in excess of
30ml/hr
Causes




Diverticular disease
Angiodysplasia
Neoplasm
Trauma
Role of NM



Diagnosis
Localization
Prognosis
Radiopharmaceuticals



SC
Rapid clearance
Good target-tobackground
Liver and spleen mask
bleed
Bleeding rate 0.050.1ml/min
Limited imaging time
Labelling not a problem
Technetium Tc-99m RBC
Tc-99m Sulfur colloid (SC)
Other - Tc-99m albumin, In111 RBC
RBC
In Intravascular space 2448hrs
Poor target-to-background
Less liver and spleen
0.1-0.5ml/min
Intermittent bleeds - up to
24hrs
Problem of labelling
Technique
-in vivo
-Modified in vitro
-in vitro
Interventions
 Glucagon - smooth muscle relaxation  thus the tracer moves as slow as possible
Interpretation
NOTE: true bleed  it moves
 Focal uptake
and changes shape
 Change position - anterograde. Retrograde motion
 Changes intensity
 Severity
o Low - bleed seen after 1h , less intense density than the liver
o High - early appearance, equal to or more dense than the liver
 False positive
o Vascular neoplasm
o Horse-shoes kidney
o Varices
o Accessory spleen
o Vascular grafts
o Ischemic bowel
o Dilated abdominal aorta
o Inflammation
o AV malformation
 False negative
o Barium enema
o Small bleeds
o Intermittent bleeding
o Liver and spleen activity
Merckel’s diverticulum





Congenital remnant of omphalomesentric duct of the embryo
In terminal ileum
25%-40% asymptomatic
50% bleed by 2years
60% with gastric mucosa - histology parietal cells
Imaging

Tc-99m pertechnectate - localizes in gastric mucosal cells
Patient prep


Fasting
No Barium studies for 2 days
Interpretation



Focal uptake
Increases with time of intensity
False negative
o Ba enema
o Upper GI exam
o Small Merkel’s diverticulum
o
o
Ischemia or necrosis
Obscured by urinary activity
o
o
Strictures
Death
GE reflux


Common by 2 months
Complications
o FTT
o Pneumonia
Imaging





Tc-99m SC in milk feed
Burp patient
Stomach and thorax in FOV
Chest statics
Significant positives
o Reflux over 15s+
o Seen late
o Multiple episodes: Mild (<10), Mod (10-20) and Severe (>20)
o Pulmonary aspiration
Oesophageal transit



Achalasia
Diffuse oesophageal spasm
Nutcracker oesophagus
Imaging



Tc-99m SC in 10ml water or milk
ROI - upper, mild and lower oesophagus
Time activity curves
o Transit time <10s
o Infants should be cleared by 3.4s ± 1s
o 8-16years 4.6 ±1.9s
Gastric emptying
Imaging



Tc-99m in liquid or solid male
Liquid - exponential clearance
Solids - lag period followed by liber disappearance
o By 4hrs stomach should almost be empty
o By 6hrs stomach should be empty
Radiology: Small bowel obstruction
Small bowel obstruction





Mechanical obstruction
No treatment: 60% mortality
Treatment:
5% mortality
Symptoms
o Abdominal pain and cramps
o Nausea
o Vomiting
o ↓ Stools (constipation)
o ↑ High pitched bowel sounds
Late signs. Absent bowel sounds due to fatigued bowel
Common causes of obstruction
•
•
Extrinsic
– Adhesions
– Hernia
– Abscess
– Masses (neoplasms – polyps)
– Congenital malrotation: peritoneal bands  rare
Intrinsic
– Inside lumen
• Tumor
• Gallstones
• Foreign body
• Intussusceptions
– In the wall
• Strictures
• Inflammatory (Crohn’s)
• tumors etc
• Vascular insufficiency
• Atresia or stenosis
What to do
•
•
•
•
•
•
History & clinical examination!!!!
Abdominal radiograph (AXR)
CT Scan
Barium studies
Small bowel follow through
Enteroclysis
Questions to answer when looking at AXR
1.
2.
3.
4.
5.
6.
Is there obstruction or paralytic ileus?
At what level?
Partial / complete / closed loop?
Cause?
Is there strangulation?
Is there a perforation?
Common XR findings
•
•
No distal gas
– No gas in colon/rectum in complete obstruction
String of pearls
•
•
•
•
•
Valvulae conniventes
– Circular folds
Central location
Air fluid levels – caution
Distended small bowel loops down to obstruction
Lower obstruction: more loops tend to stack up as stepladder
CT
•
•
•
•
•
Used more than barium
Site and maybe the cause
No need for oral contrast and differentiate a prolonged obstruction where bowel is dilated and atonic
with abrupt site of narrowing
For ileus where dilated continue into colon and no abrupt narrowing of bowel
Small bowel faceses sign
– No normally solid faeces in small bowel traps air and can be seen
– Incomplete obstruction may not be clearly noted on CT and enteroclyses with CT may be the
answer
Causes of obstruction
•
•
•
•
•
•
•
Voluvulus
– Closed loop obstruction where mesentery twists and bowel dilates (proximal and distal
obstruction)
Hernia
– Can use CT but more clinical diagnosis
Tumour
Gall stone ileus
– Gallstone can cause obstruction in ileum
Bezoar
– Organic body in the bowel
Intusussception
– Bowel within the bowel
– Seen as coiled spring
Adynamic ileus
• Topic: To compare changes with that of Small bowel obstruction
• Rö sign in adynamic ileus is retention of gas and fluid in dilated large and small bowel with ↓ or
no bowel sounds
• No demonstrable point of obstruction
• Dilated stomach part of this complex – not seen in obstruction
• Possible causes
o Post surgery
o Peritonitis
o Electrolyte inbalance
o Acute chest disease (MI or CCF)
o Metabolic disorders
o Medication
• Variants
o Pancreatitis
o Appendicitis
o Acute cholecystitis