Transcript Cm * gastro, block 5 exam 1, lectures 1-12

So far I finished lecture 1-7
Lectures 8-12 are coming.
Lecture 3 – I cut and pasted slides I thought might be important
There are __ total slides.
There are 70 title slides.
1
1.
2.
3.
4.
Bacteria responsible for caries
Vitamins and tooth growth / development
Cariogenic and non-cariogenic foods
Pathogenesis of caries with xerostomia
2
Question

A 4 year old presents with the findings seen in the
picture. Which bacteria would you expect to be most
responsible for these findings?
A.
B.
C.
D.
E.
Clostridium difficile
Streptococcus mutans
Lactobacillus casein
Actinomyces species
Peptostreptococcus mutans
3
Caries
Pathophysiology

Bacteria
 Steptococcus mutans most prevalent
 Streptococcus sanguis
 Streptococcus sobrinus
 Lactobacilus casein



Metabolize carbohydrates in the mouth producing organic
acids as a byproduct
Produce sticky polymers called fructans and glucans which
bind the bacteria to the smooth enamel surface and form the
bulk and matrix of the biofilm
Joined by thin, branched Actinomyces, gram-positive
bacteria, that add to the complex network of early plaque
4
Question

Which of the following supplements or vitamins is
required for development of the mineral component
of enamel and dentin?
A.
B.
C.
D.
E.
Fluoride
Vitamin A
Vitamin C
Vitamin D
Xylitol
5
Fluoride
Four primary actions on teeth
1. When incorporated into enamel and dentin along with calcium and
phosphorous it forms fluoroapatite which is more resistant to acid
challenge than hydroxyapatite
2. It promotes repair and remineralization of tooth surfaces with early
signs of decay
3. It helps to reverse the decay process while promoting the
development of a tooth surface that has increased resistance to
decay
4. Helps to deter the harmful effects of bacteria in the oral cavity by
interfering with the formation and function of the microorganisms
6
Can you answer the following?

A patient was asking about nutrition and dental health.
Which of the following breakfasts would you recommend
because of the least cariogenic properties?
A.
B.
C.
D.
E.
Aged cheddar cheese omelet
Oatmeal with brown sugar
A whole banana
Toast with a glass of skim milk
Waffle House #1 with orange juice
7
Anticariogenic Foods





Prevent plaque from recognizing a cariogenic food when it is
eaten first
Cheese particularly, aged cheddar, Monterey Jack and Swiss
cheeses (which contain casein, calcium and phosphate)
Xylitol (a 5-carbon sugar alcohol, sweetener in sugarless
gum) cannot be metabolized the same way as 6-carbon
sugars. It also replaces fermentable CHO in the diet. S.
mutans is actually inhibited by xylitol
May increase salivation or have antimicrobial activity
Casein phosphopeptide-amorphous calcium phosphate
(CPP-ACP; Recaldent) is a substance that promotes
remineralization of enamel surfaces
8
1. Bacteria responsible for caries
9
Caries
Pathophysiology

Bacteria
 Steptococcus mutans most prevalent
 Streptococcus sanguis
 Streptococcus sobrinus
 Lactobacilus casein



Metabolize carbohydrates in the mouth producing organic
acids as a byproduct
Produce sticky polymers called fructans and glucans which
bind the bacteria to the smooth enamel surface and form the
bulk and matrix of the biofilm
Joined by thin, branched Actinomyces, gram-positive
bacteria, that add to the complex network of early plaque
10
The Decay Process
Begins with the production of acids as a byproduct of
bacterial metabolism in plaque which is a sticky,
gelatinous mass that adheres to teeth and gingiva
 Composed of bacteria, salivary proteins, polysaccharides
and lipids
 Most common bacteria – S. mutans prefers sucrose, the
most common sugar consumed in the diets of children
and adults

11
2. Vitamins and tooth growth /
development
12
Introduction
Tooth development
During pregnancy, maternal nutrition must supply
preeruptive teeth with the appropriate building materials
 Primary tooth development begins at 2-3 months’
gestation. Mineralization begins at ~ 4 months’ gestation
thru preteen years
 Posteruption diet and nutrient intake continue to affect
tooth development, mineralization, enamel development
and strength

13
Introduction
Anatomy of a tooth

Enamel
 Keratin (requires Vit. A)

Dentin
 Collagen (requires Vit. C)

Mineral component of enamel and
dentin is hydroxyapatite (requires
Vit. D)
14
3. Cariogenic and non-cariogenic foods
15
3a. Cariogenic foods
16
Cariogenic Foods
 Refers
to the caries-promoting properties of a
diet, food or beverage
 Cariogenicity of a food is dependent on:
 the form in which it occurs,
 its nutrient composition,
 when it is eaten in relation to other foods and fluids,
 the duration of the exposure to the teeth,
 and the frequency with which it is eaten
17
Cariogenic foods
 Found
in 3 of the 5 MyPlate food groups
 Grains: crackers, chips, hot & cold cereals, breads, pretzels
 Fruits (fresh, dried, canned) and fruit juices
○ Fruit with high water content less cariogenic
○ Bananas and dried fruit more cariogenic
 Dairy products sweetened with fructose, sucrose or other sugar.
 However, dairy products are rich in calcium which has an alkaline
nature and may have a positive influence in reducing the
cariogenic potential of the food
Glucose, fructose and lactose, sucrose, maltose stimulate cariogenic bacterial activity
18
Cariogenic foods
All dietary forms of sugars including honey, molasses,
brown sugar, corn syrup solids, high-fructose corn syrup,
maple syrup have cariogenic potential and can be used
by bacteria to produce organic acid
 Be aware of hidden sugars!
 Learn and teach your patients how to identify them on
food labels

 E.g. agave nectar, dextrose, xylose, invert sugar, sorghum
19
Cariogenic foods
20
Cariostatic Foods
 Do
not contribute to decay, are not
metabolized by microorganisms
 Do not decrease salivary pH <5.5 within 30
minutes
 Include foods such as proteins,
meat, fish, eggs, poultry;
most vegetables, fats,
sugarless gums
21
3b. Non-cariogenic foods
22
Anticariogenic Foods





Prevent plaque from recognizing a cariogenic food when it is
eaten first
Cheese particularly, aged cheddar, Monterey Jack and Swiss
cheeses (which contain casein, calcium and phosphate)
Xylitol (a 5-carbon sugar alcohol, sweetener in sugarless
gum) cannot be metabolized the same way as 6-carbon
sugars. It also replaces fermentable CHO in the diet. S.
mutans is actually inhibited by xylitol
May increase salivation or have antimicrobial activity
Casein phosphopeptide-amorphous calcium phosphate
(CPP-ACP; Recaldent) is a substance that promotes
remineralization of enamel surfaces
23
4. Pathogenesis of caries with xerostomia
24
Roles of Saliva
Clears food from around teeth
 Provides buffering action to neutralize bacterial
metabolism

 via bicarbonate-carbonic acid and phosphate buffer systems

Supersaturated with calcium and phosphorus
 Once pH is restored, remineralization can occur
 If fluoride is present, minerals are deposited in the form of
fluoroapatite
25
Xerostomia (dry mouth)  pathogenesis of
caries
Flip-flop everything from the previous slide
Without saliva,
 Food cannot be cleared from the mouth
 Bacterial meteabolism cannot be buffed (i.e. bicarb,
phosphate buffering system) back to normal pH
 Abnormal pH prevents remineralization via calcium
and phosphorus

26
1.
2.
3.
4.
5.
Causes of PUD
Treatments for PUD
Uncomplicated vs. complicated ulcers
Treatment for perforated ulcers
ZE syndrome clinical findings
27
1. Causes of PUD
28
Etiology
Microbes - H. pylori (#1 risk factor)
 Drugs/toxins - NSAIDs, ASA, Biphosphonates,
corticosteroids, cocaine and alcohol
 Ischemia - Mesentaric vascular occlusion, P. Vera
 Hyperacidic syndromes - Zollinger-Ellison
 Systemic inflammation - Crohn’s disease
 Stress ulceration
 Radiation Gastritis

29
2. Treatments for PUD
30
Drugs to treat PUD

Antacids – Maalox, Mylanta, Tums, etc.
 Use for occ. dyspepsia

H-2 blockers – ranitidine, cimetidine, famotidine, etc.
 Use for chronic dyspepsia
PPI’s – pantoprazole, omeprazole, lansoprazole,
esomezole, etc.
 Mucosal protective agents –

 Sulcrafate – helpful adjunct esp., with smokers
 Misoprostol - Prostaglandin analog – use with NSAIDS, but
contraindicated with pregnancy.
 Bismuth subsalicylate (BSS) – use with H. pylori
31
Management
32
3. Uncomplicated vs. complicated ulcers
33
3a. Uncomplicated ulcers
34
Key Signs and Symptoms of PUD
UNCOMPLICATED ULCER





No symptoms (“silent ulcer” in up to 40% of cases)
Epigastric pain - Pain may radiate to the back, thorax,
other parts of abdomen (cephalad most likely, caudad
least likely)
Pain may be nocturnal (most specific), “painful hunger”
relieved by food, or continuous (least specific)
Nausea & Vomiting
Heartburn (mimics or associated with gastroesophageal
reflex)
35
3b. Complicated ulcers
36
Surgical Indications
Surgical Treatment Recommendations for Complications
Related to Peptic Duodenal Ulcer Disease
Intractable: Parietal cell vagotomy ± antrectomy
 Bleeding: Oversewing of bleeding vessel with treatment of
H. pylori
 Perforation: Patch closure with treatment of H. pylori
 Obstruction: Rule out malignancy and gastrojejunostomy
with treatment of H. pylori

37
4. Treatment for perforated ulcers
38
Surgical Indications
Surgical Treatment Recommendations for Complications
Related to Peptic Duodenal Ulcer Disease
 Intractable: Parietal cell vagotomy ± antrectomy
 Bleeding: Oversewing of bleeding vessel with treatment of
H. pylori
 Perforation: Patch closure with treatment of H. pylori
 Obstruction: Rule out malignancy and gastrojejunostomy
with treatment of H. pylori
39
5. ZE syndrome clinical findings
40

Zollinger-Ellison Syndrome: <1% of pts

Triad- gastric acid hypersecretion, severe PUD and
non-Beta cell tumor of the pancreas
 Caused by gastrin secreting endocrine tumor found usually in the




pancreas or proximal small bowel.
Associated with multiple endocrine neoplasias, esp.
hyperparathyroidism.
Pts will have elevated serum gastrin levels ( greater than 1000pg/ml is
diagnostic)and abnormal secretin testing.
CT or MRI will usually confirm the presence of the tumor (usually
benign)
Pts will frequently have a secretory diarrhea, as well.
Hypergastrinemic syndromes
41
I have cut and pasted some slides from Dr. Stewart’s lecture
She emphasized a few things
42
UMBILICAL HERNIA
Spontaneous closure
by age 1 year
 Large defects by 5-6 yo

 Size of the fascial
defect, NOT the
degree of protrusion,
is most indicative of
whether spontaneous
closure will occur
43
OMPHALOCELE




herniation of abdominal contents
into the base of the umbilical cord
abdominal cavity underdeveloped
defect may vary from <2-10 cm
sac is covered with peritoneum and
amnion without overlying skin
 + intestines
 + liver and intestines

embryologic etiology uncertain
 Persistent primitive body stalk
 Failure of retraction
 Failure of complete lateral folding
44
Omphalocele: Epidemiology
Occurs in approximately 1:4,000
live births
 + intestines 1/5,000
 + liver and intestines 1/10,000


High incidence of congenital
abnormalities (50 to 70 percent )
 Trisomy 13, 18, 21 most common
 Cardiac defects
 GI
45
Omphalocele: Diagnosis

Elevated maternal serum
alpha-fetoprotein
concentration (MSAFP) is
elevated in 70%

2nd trimester ultrasound
46
GASTROSCHISIS
Full thickness defect in the
abdominal wall
 Small defect
 Does not involve the umbilical
cord
 Contains small bowel, maybe
portions of stomach or colon
 Viscera are not protected by
the peritoneal sac
 Exact cause is uncertain

 defective formation or disruption
of the body wall in the embryonic
period, with subsequent
herniation of bowel
47
Gastroschisis: Treatment

Management in delivery room (same as omphalocele)
 Preserve heat and minimize insensible fluid loss – use sterile bowel
bag to reduce insensible fluid losses
 Orogastric tube to decompress the stomach
 Stabilize the airway
 IV access

Surgical repair EMERGENT (unlike omphalocele)
 Primary closure
 Staged closure
○ Dacron-reinforced silastic silo
 Prolonged TPN may be necessary
 “Gentle touch”
○ Slower process allowing gravity to reduce bowel before closure
48
Abdominal Wall Defects: Gastroschisis vs.
Omphalocele
GASTROSCHISIS
OMPHALOCELE
Defect
Open
Membrane covered
Defect Size
2-5 cm
1-15 cm
Umbilical Cord
Left of defect
Center of membrane
Bowel
Serositis, edema, matted
Normal
Assc Anomalies
10%
60%
Prognosis
70-90%
20-70%
IUGR (intrauterine growth
restriction)
Common
Less Common
Other organs
Rare (stomach, colon)
Liver often out
49
PRUNE BELLY SYNDROME

Absence of major abdominal
muscles
 Result of severe urethral
obstruction in early fetal life
or a genetic component
affecting mesodermal
development

Characteristic association
 deficient abdominal muscles
 undescended testes
 urinary tract abnormalities
50
Prune Belly Syndrome: Prognosis
1/3 are stillborn or die in the first few
months from pulmonary hypoplasia
 30% long term survivors develop end
stage renal disease from renal
dysplasia or complications of infection
and reflux
 depends on degree of pulmonary
hypoplasia and renal dysplasia

51
CONGENITAL DIPHRAGMATIC HERNIA





Developmental defect of the
diaphragm that allows abdominal
viscera to herniate into the chest
Incidence 1/ 2,000-5,000 live births
Females:male, 2:1
Etiology may be congenital or
traumatic
80-90% occur on the Left
BochdaLek type

2-6% occur on the Right side
MoRgani type
52
Congenital Diaphragmatic Hernia:
Pathology
Structural diaphragmatic defect
 Limiting factor for survival is the associated
pulmonary hypoplasia
 Lung hypoplasia was believed to be solely due to
compression by abdominal contents
 Pulmonary hypoplasia may precede the development of
the diaphragmatic defect

53
Congenital Diaphragmatic Hernia:
Presentation
 Respiratory
distress within the first several hours
after birth
 Level of distress consistent with the degree of pulmonary
hypoplasia and persistent pulmonary hypertension
 Increased
chest wall diameter with barrel-shaped chest
 Scaphoid abdomen
 Absence of breath sounds on the ipsilateral side
 Bowel sounds auscultated in the chest
 Heartbeat (PMI) displaced away from the hernia if there
is a shift in the mediastinum
54
Congenital Diaphragmatic Hernia:
Treatment
Management





Avoid blow-by oxygen and bag mask ventilation
Immediate endotracheal intubation
Ventilatory support with low airway pressure to minimize lung injury
May include ECMO
Nasogastric tube placed in the stomach connected to continuous suction for
decompression
 UAC and UVC (if possible)
 IVF and inotropes if necessary to support blood pressure
Surgical repair
 Delayed until resolution of early pulmonary insufficiency and acute pulmonary
hypertension
55
ESOPHAGEAL ATRESIA

Most frequent congenital anomaly of the esophagus
(1/
4,000)
> 90% present with a Tracheoesophageal fistula
> 90% survival rate
Exact cause unknown (defect of foregut septation)
Associated features include advanced maternal age,
European ethnicity, obesity, low socioeconomic status
and tobacco smoking.
 50% of infants are non-syndromic without other
anomalies, the rest have associated anomalies, most
frequently VATER/VACTERL or CHARGE.




56
Esophageal Atresia +/- TEF: Presentation





h/o polyhydramnios
Neonate presents with frothing or bubbling at the mouth and
nose after birth. Also, coughing, cyanosis and respiratory
distress.
Feeding exacerbates symptoms, causing regurgitation which may
lead to aspiration.
Aspiration of gastric contents via a distal fistula causes more severe
pneumonitis than aspiration of oropharyngeal secretions from the
blind upper pouch.
Infants with an isolated TEF in the absence of EA (H-type fistula)
may come to medical attention later in life with a history of
chronic respiratory problems, including refractory bronchospasm and
recurrent pneumonias.
57
DUODENAL ATRESIA
1/10,000 live births
 25-40% of all intestinal atresias
 30% associated chromosomal anomaly (primarily
Trisomy 21)

Causes
 Intrinsic defect of bowel formation
 failed recanalization of the intestinal lumen during
gestation
58
MALROTATION AND VOLVULUS
True incidence of malrotation
unknown as many cases
asymptomatic for life
 Symptomatic malrotation 1/6000
 90% present in the first 2
months
 75% < 1 month old
 can present at any age
 30 – 60% have an associated
anomaly

59
Malrotation: Diagnosis
Flat and upright x-ray:
 Bowel loops at the site of the liver
 Naso/orogastric tube located in an abnormally postioned duodenum
 “Double bubble” sign – showing distention of the stomach and duodenum
 With complete volvulus – dilated loops of bowel with air-fluid levels proximally and
absence of gas distally
Upper GI Series (gold standard):


abnormal duodenum with corkscrew appearance
Duodenal obstruction (classic “beak” appearance with volvulus)
Ultrasound
Barium enema
CT
60
1.
2.
3.
4.
Pyloric stenosis metabolic disorders
GE reflux treatments – non-medicinal
Treating dehydration/metabolic derangements in GI disorders
Normal course of GE reflux in infants
61
Key points
• Pyloric Stenosis
• Hypochloremic, hypokalemic, metabolic alkalosis
• Diagnostic modality of choice- US (ultrasound)
• Correct dehydration and metabolic derangements- 1.5
times the calculated maintenance rate
• GERD Treatment
• Adjust feeding volumes and frequency
• Thickening of feeds with rice cereal
• Usually resolves by age 12mo-18 mo
62
QUESTION
Which of the following results would you expect to
see in this infant with the diagnosis of pyloric
stenosis?
 A. Na+ 142, K+ 4.2, Cl- 108, CO2 27
 B. Na+ 128, K+ 6.8, Cl-98, CO2 13
 C. Na+ 137, K+ 5.2, Cl- 111, CO2 17
 D. Na+ 138, K+ 3.1, Cl- 89, C02 37
 E. Na+ 150, K+3.1, Cl- 99, CO2 17

63
Question?
 What
historical piece of information can be
considered normal infant behavior?
A. Regurgitation and vomiting 30-40 minutes after feedings
B. Arching and stiffening with vomiting
C. Aversion to feeding
D. Choking when vomiting/spitting
E. Increasing infant irritability
64
Question?

Which of the following is not an exacerbating factor
for GER in children?
○ A. Supine position
○ B. Secondary smoke exposure
○ C. Overfeeding
○ D. Breastfeeding
○ E. Increased respiratory effort (ie: cough)
65
1. Pyloric stenosis metabolic disorders
66
Pyloric Stenosis - Labs/Radiographs

Complete Metabolic Panel
 Hypochloremic, hypokalemic, metabolic alkalosis
 Hyperbilirubinemia (5%-14%) = icteropyloric syndrome

Ultrasound
 Diagnostic modality of choice
 Allows earlier diagnosis for those infants without palpable
olive on exam

Barium Studies – String sign
67
2. GE reflux treatments – non-medicinal
68
Key points
• Pyloric Stenosis
• Hypochloremic, hypokalemic, metabolic alkalosis
• Diagnostic modality of choice- US (ultrasound)
• Correct dehydration and metabolic derangements- 1.5
times the calculated maintenance rate
• GERD Treatment
• Adjust feeding volumes and frequency
• Thickening of feeds with rice cereal
• Usually resolves by age 12mo-18 mo
69
GERD Treatment - Infants
Most infants do not need any treatment for
“asymptomatic” GER
 Dietary changes

 Adjust feeding volumes and frequency
 Thickening of feeds with rice cereal
 Trial of hypoallergenic diet (exclude dairy or soy proteins)

Positioning
 Prone positions and upright carried positions can minimize
reflux

Pharmacology
70
GERD - older children and adolescents
Treatment

Conservative therapy and lifestyle changes
 Avoid tobacco smoke
 Avoid acidic or reflux inducing foods
 Weight reduction
 ? Left side position and head elevation during sleep

Pharmacology
 Acid suppression (see next slide)
71
3. Treating dehydration/metabolic
derangements in GI disorders
72
Key points
• Pyloric Stenosis
• Hypochloremic, hypokalemic, metabolic alkalosis
• Diagnostic modality of choice- US (ultrasound)
• Correct dehydration and metabolic
derangements - 1.5 times the calculated
maintenance rate
• GERD Treatment
• Adjust feeding volumes and frequency
• Thickening of feeds with rice cereal
• Usually resolves by age 12mo-18 mo
73
Pyloric Stenosis - Treatment

Correct dehydration and metabolic derangements
 Correction of alkalosis
 1.5 times the calculated maintenance rate

Pyloromyotomy
74
4. Normal course of GE reflux in infants
75
GERD
Peaks at 4 months
 Usually resolves by age 12mo-18 mo

 90% by 12 months
Likely genetic and environmental predispositions
 More common in:

 Premature infants
 Children with neuromuscular disorders
○ i.e. muscular dystrophy, cerebral palsy, and children with Down
syndrome
76
1.
2.
3.
4.
5.
Locations of salivary stones
Infectious causes of siladenitis
Illnesses associated with siladenitis
Complications of parotidectomy
Causes of bilateral parotid swelling in kids
77
1. Locations of salivary stones
78
Salivary Stones

Location
 Most are submandibular (80%)

Composition
 Most are calcium
○ Dr. Orr said this is a good EXAM Question:
 What distinguishes submandibular stones from salivary stones?
- Submandibular stones ARE calcified
- Salivary stones are NOT calcified
 Uric acid
79
2. Infectious causes of siladenitis
80
Sialadenitis – Infectious Etiology
Organisms involved
 S.
aureus - most common
Streptococcus
 Coliforms
 Anaerobes

81
3. Illnesses associated with siladenitis
82
Sialadenitis – Etiology
Usually after duct obstruction
 Hyposecretion states

 Sjogren’s Syndrome
 Prior radiation treatment to oral cavity
Most common in parotid gland
 Typical patient is 50-60 years old
 Can be seen in younger patients with anorexia

83
Sialadenitis – Atypical … DON’T MEMORIZE








Viral infections – paramyxovirus, influenza, coxsackie, adenovirus, HIV
Atypical bacteria – mycobacterium TB, non-TB mycobacterium,bartonella,
actinomycosis
Autoimmune – Sjorgen’s syndrome
Granulomatous – parotid gland sarcoidosis, Crohn’s disease
Radiation (I-131)
Endocrine – Acromegaly, alcoholism, diabetes insipidus, diabetes mellitus,
hypothyroidism, cirrhosis of the liver, uremia
Medications – Antihypertensives, Iodine, Isoprenaline, Lead, Mercury,
Naproxen, Oxyphenbutazone, Sulfisoxazole, Thiocyanate (from sodium
nitroprusside), Propylthiouracil, Valproic acid
Nutritional problems - Beriberi (B1 – thiamine deficiency), Bulimia, Malnutrition,
Pellagra (B3 – Niacin deficiency), Amylophagia, Vitamin A deficiency
84
4. Complications of parotidectomy
85
Salivary Gland Tumors – Benign

Treatment is excision (parotidectomy)
 Picking the right surgeon is critical

Complications of parotid surgery
 Facial nerve paralysis or paresis
 Greater auricular nerve damage
 Gustatory sweating (Frey’s syndrome)
 Salivary fistula (uncommon and usually subsides with
conservative treatment)
86
5. Causes of bilateral parotid swelling in
kids
87
Viral Sialadenitis
Typical case is mumps (paramyxovirus)
 Usually will see bilateral swelling and
tenderness
 Other viruses

 Influenza
 Coxsackie
 Adenovirus
 HIV – diffuse non-tender enlargement of all
glands

Treatment is supportive
88
1.
2.
3.
4.
Differentials for dysphagia
Surgical intervention for Zenkers
EGD findings for Plummer-Vinson
Gold standard for diagnosis and treatment procedures for achalasia
89
1. Differentials for dysphagia
90
Pathology
Zenker’s Diverticulum
 Eosinophilic Esophagitis
 Infectious Esophagitis
 Achalasia
 Diffuse Esophageal Spasm
 Plummer-Vinson Syndrome
 Boorhave’s Syndrome

91
2. Surgical intervention for Zenkers
92
Zenker’s Diverticulum

Barium Esophagram (Dx study of choice)

Therapy:
 Surgery – Zenker’s is a surgical disorder
Diverticulectomy + Myotomy
Myotomy + Diverticulopexy
Dohlman Procedure (Endoscopic Stapling and Division)
All Involve Division of the Cricopharyngeus Muscle for
Successful Treatment!!
1.
2.
3.
93
3. EGD findings for Plummer-Vinson
94
Plummer-Vinson Syndrome
Triad: Dysphagia, IDA, Esophageal Webs
 Typically in Postmenopausal Women
 Labs: hypochromic, microcytic anemia
 Endoscopy: Esophageal Webs (Cervical Esophagus)
 Tx: Oral Iron Supplements

PREMALIGNANT CONDITION
 SQUAMOUS CELL CA

95
4. Gold standard for diagnosis and
treatment procedures for achalasia
96
Achalasia
Greek Root: chalan = “to loosen”
 Etiology: Unknown
 Secondary Effect of Etiology:

 Loss of ganglionic cells in Myenteric Plexus
 Interruption of vagal n. innervation of LES, which
mediates relaxation
FAILURE OF LES RELXATION
INNEFFECTIVE PERISTALSIS
97
4a. Gold standard for diagnosis of
achalasia
98
Achalasia - Dx
Esophagram: “Bird’s Beak”
 Manometry (Gold Standard): Hypertensive LES
 EGD: Confirms Hypertensive LES, rules out
concomitant pathology

99
4b. Gold standard for treatment procedures
for achalasia.
100
Achalasia Tx
Treatment:


Not Curative
Endoscopic / Surgical Txs are
Palliative

 SL nitroglycerin
 Nitrates
 Calcium channel blocker

Relieve Obstruction
Prevent GERD
Achieve Long-Term Results
Endoscopic:
 Pneumatic dilation
 Botox injection
Principles of Tx:



Medical:

Surgical:
 Heller Myotomy with
Fundoplication (Standard)
 Esophagectomy
(Megaesophagus “sigmoid”, failed
myotomy, undilatable reflux
stricture)
101
1.
2.
3.
4.
5.
Most common risk factor for esophageal cancer
Treatment for H pylori
Treatments for esophageal cancer by stage
Best modality to diagnose esophageal cancer
Risk factors for gastric cancer (body or distal stomach)
102
1. Most common risk factor for esophageal
cancer
103
Risk Factor Summary - LEARN THIS
Factor
SCC
Adeno
Tobacco
+++
++
Alcohol
+++
-
Barrett’s
-
++++
Weekly reflux S’s
-
+++
Achalasia
+++
-
Obesity
-
++
Caustic injury
++++
-
Head/neck CA
++++
-
Poverty
++
-
Breast radiation
+++
+++
104
Risk Factors

Tobacco and Alcohol
 Per previous slide, if you have to pick one, I would
choose TOBACCO.
Achalasia
 Chronic Strictures
 Barrett’s Esophagus
 Environmental

105
2. Treatment for H pylori
106
Treatment of H Pylori
There are many schemes for treating H. pylori infection;
however, an optimal treatment has not been defined, and
there is not a single antibiotic treatment that can
eradicate it.
 Historically, a combination of various antibiotics has been
used to eradicate the infection. The antibiotics used
include clarithromycin, amoxicillin, metronidazole,
tetracycline, fluoroquinolones, tinidazole, and others.
These antibiotics are often used in combination with
antisecretory agents, such as PPIs, or with bismuth salts.

107
Up To Date guidelines – EXAM!!
TRIPLE THERAPY:
PPI + Clarithromycin + Amoxicillin
(substitute metro for PCN allergy)



The regimen most commonly recommended for first line treatment of
H. pylori is triple therapy with a proton pump inhibitor (PPI)
amoxicillin (1 g twice daily), and clarithromycin (500 mg twice daily)
for 7 to 14 days. We suggest treatment for 10 days to two weeks.
Metronidazole (500 mg twice daily) can be substituted for amoxicillin
in penicillin-allergic individuals.
A longer duration of treatment (14 versus 7 days) may be more
effective in curing infection but this remains controversial
108
EXAM!!!
QUADRUPLE THERAPY = PPI + Bismuth + metro + TCN

Quadruple therapy consists of a PPI, combined with bismuth (525
mg four times daily) and two antibiotics (eg, metronidazole 250
mg four times daily and tetracycline 500 mg four times daily)
given for 10 to 14 days. Quadruple therapy is appropriate as
initial therapy in areas in which the prevalence of resistance to
clarithromycin or metronidazole is ≥15 percent, or in patients with
recent or repeated exposure to clarithromycin or metronidazole
[18]. If tetracycline is not available, doxycycline (100 mg twice
daily) may be substituted
109
3. Treatments for esophageal cancer by
stage
110
Treatment

Treatment options vary according to stage, patient
performance status and local expertise
111
Treatment Stage 0-1
CA in situ or tumors limited to the
mucosa
 Esophageal Sparing Procedures

 Endoscopic mucosal resection
 Phototherapy
 RFA
No role for Chemo or XRT
 Conservative or Minimally
Invasive Resection

112
Treatment Stage 2-3
Higher potential for lymph node involvement
 Surgery alone is insufficient if N+ disease

 Neoadjuvant = Preoperative Treatment (SEE NEXT SLIDE)
T2N0 patients
 Definitive chemoradiation (no surgery) may be used
in selected patients – usually with SCC

113
What is adjuvant therapy?
Chemo +/- radiation given AFTER “curative” surgery
 Rationale: High risk patients with R0 resection might
have microscopic (undetected) metastases. Giving
chemo or radiation at this point is typically more
effective then waiting until metastases are manifest.
 Disadvantage: Some patients might have been cured
by surgery alone and are treated unnecessarily [Key:
Use guidelines for risk stratification to discuss options
with patients]

114
What is Neoadjuvant therapy?
Chemo +/- radiation BEFORE surgery
 Advantages:







Objective measurement of chemotherapy effectiveness
Possible organ preservation (rectum, breast…)
Patient has best functional state
XRT given to tissues that have not been devascularized
Possible survival advantage
Disadvantages:
 Delays surgery
 Possibly increased surgical complications
 Patients “want cancer out”
115
Treatment Stage 4
Non regional lymph node metastases (e.g. cervical or
celiac axis)
 Distant metastases
 Palliative chemotherapy
 Palliative resection - rarely
 Stenting
 Brachytherapy
 Photodynamic Therapy

116
4. Best modality to diagnose esophageal
cancer
117
Diagnosis
EGD with Biopsy
 Barium Swallow

EGD with Biopsy is the primary
diagnostic modality and allows
histologic evaluation as well as
anatomic evaluation of location,
position related to GE junction, and
evaluation of the stomach as potential
conduit or need for resection
118
Diagnosis
EGD with biopsy
 CT scan
 PET scan
 EUS

119
5. Risk factors for gastric cancer (body or
distal stomach)
120
Risk Factors

Environmental
 H.
Pylori
Diet – nitrosamines (smoked meat)
 Tobacco
 Genetic Predisposition
 Pernicious Anemia

 Vit B 12 deficiency
○ Due to cell change in stomach
 Low acid environments
121
Japan: Gastric cancer accounts for 50% of cancer
deaths – also high in Chile, Costa Rica, Hungary,
Portugal, and Romania (a very diverse group
geographically and ethnically)
 Migration to low risk areas decreases risk

H
pylori infection is probably the
biggest risk factor

Nitrosamine ingestion in animal models is
associated with gastric cancer
122
H pylori

Unequivocally linked to gastritis and gastric cancer

Associated with cancers
in the body and
distal stomach but not GE junction (these are
related to reflux)
 In North America 50% of adults older than 50 years
are seropositive for H pylori, but relatively few
develop gastric cancer
123
1.
2.
3.
4.
5.
First steps in treatment
Findings and chances of rebleeds
Rare causes of upper GI bleeds
Mortality in UGI bleeds
Steps to treatment of esophageal varices
124
1. First steps in treatment
125
Goals & Objectives
 Assess
the severity of the UGI bleeding
 Initiate resuscitative efforts
 Localization of the site of hemorrhage
 Define the Etiology
 Explain the treatment
126
Presentation
 UGI
bleeding is defined as bleeding from a
 source in the esophagus, stomach, or duodenum and may
be overt or occult
 Hematemesis - vomiting blood or coffee grounds
 Melena - black or tarry stools (needs minimum of 50ml and
transit time of at least 14 hours)
- the passage of bright red, bloody stools;
suggests brisk and major bleeding
 Hematochezia
127
Resuscitation
 Assess
Hemodynamic status
 Fluid resuscitation
 Gastric lavage
 CBC, Bmp, Coagulation studies
128
2. Findings and chances of rebleeding
129
Endoscopic Stigmata of Hemorrhage
 Finding
Rebleeding rate
 Arterial
70-90%
40-50%
10-20%
5%
spurting
 Visible vessel
 Adherent clot
 Clear base
80%
40%
20%
5%
130
2. Findings and chances of rebleeds
131
3. Rare causes of upper GI bleeds
132
133
134
4. Mortality in UGI bleeds
135
136
5. Steps to treatment of esophageal varices
137
Natural history of esophageal varices
138
139
140
Management of active variceal bleeding
141
Endoscopic variceal ligation (D)
142
Octreotide for active variceal hemorrhage
143
144
145
Transjugular intrahepatic portosystemic shunts TIPS
146
Surgical shunts
147
1.
2.
3.
4.
Manometric findings with GERD
Stepwise treatment and workup of GERD
Define sliding hiatal hernias
Treatment options for Barrett’s
148
1. Manometric findings with GERD
149
Esophageal Manometry
Used to evaluate the physiology of the esophagus
 Determines if there are any esophageal motility
disorders
 Helpful in evaluating the LES pressures
 Aids in determination of appropriate surgical
intervention

150
LES Pathophysiology
Three Mechanisms of Incompetence:
Transient LES Relaxation w/o Anatomic Abnormality {Physiologic}
2. LES Hypotension w/o Anatomic Abnormality {Physiologic}
3. LES Distortion Inclusive of (but not limited to) hiatal hernia {Anatomic}
1.
Severity of GERD dependent upon a 2-hit phenomenon to the
GEJ
151
Transient LES relaxationor permanent LES
HoTN (i.e. LES pressure < 10 mmHg)

Monometry





Hooked to monitors
Swallow water
Probe measures pressure of
esophagus all the way down
to the stomach
Top to bottom = proximal to
distal
Normal range = 10-30
mmHg
152
2. Stepwise treatment and workup of GERD
153
154
Initial Management of GERD
Lifestyle Modifications:
Lose Weight
 Exercise
 Avoid spicy / citrus / acidic foods
 Don’t eat within 3 hrs of bedtime
 Don’t recline after meals
 Don’t overeat
 Avoid tight garments
 Stop smoking and drinking
 Manage the medications

155
Medical Management of GERD
 Majority
of GERD sufferers never seek medical
attention
 Of those who do, almost all have self medicated
with antacids or OTC H₂-Blockers
 Most physicians start with PPI (proton pump inhibitor)
after lifestyle modification
156
Management of GERD
Typical Reflux should respond to medical therapy
 Atypical Reflux should respond with ease of ‘typical’
symptoms. Will the atypical symptoms respond?
 If yes, diagnosis is likely GERD
 If medical therapy results in transient improvement, often
therapy is continued with anti-histamine + PPI or twicedaily PPIs

157
When Should I do more with GERD?

Alarming Features:
 Dysphagia – r/o malignancy / strictures
 Weight Loss
Non-Responders to acid suppression
 Refractory symptoms

ENDOSCOPY
158
Ph Probe utilization
 pH




Probe monitoring = GOLD STANDARD
Measures only acid (not biliary reflux)
Either wired or wireless (bravo probe)
Measures: time < pH 4, # of episodes, longest episode, % of
symptomatic events
Demeester Score (Normal < 18-20)
159
Esophageal Manometry
Used to evaluate the physiology of the esophagus
 Determines if there are any esophageal motility disorders
 Helpful in evaluating the LES pressures
 Aids in determination of appropriate surgical intervention

160
Surgical Treatment of GERD

Refractory Cases

Must have Objective Clinical Evidence
 Esophagram
 EGD
 pH Monitoring
 +/- manometry
 Gastric Emptying Study
161
Surgical Treatment of GERD
Laparoscopic, Open Transabdominal, Transthoracic
Approaches
 Laparoscopic Nissen Fundoplication
 Parial Fundoplication

 Dor vs Toupet vs Belsey Mark IV
162
3. Define sliding hiatal hernias
163
Hiatal Hernia
1(A): Sliding, GE
Junction above hiatus
 Type


 MOST COMMON
Type 2 (B): Rolling GE Junction
in abdomen but stomach above
hiatus
Type 3 (B): BOTH GE Junction
and Stomach above hiatus
 TREATED MOST OFTEN
164
4. Treatment options for Barrett’s
165
Barrett’s Esophagus
Replacement of normal striated squamous epithelium
with metaplastic columnar epithelium. Intestinal
Metaplasia must be present in the tubular esophagus
to confirm diagnosis.
 Surgeons Definition:

 Displacement of the S-C junction proximal to the GE
junction
166
167
Barrett’s Esophagus
(Metaplasia)
Dysplasia
Cancer
168
169
1.
2.
Presentation of intussusception / volvulus / necrotizing enterocolitis / malrotation
Long term complications of necrotizing enterocolitis
170
1. Presentation of intussusception /
volvulus / necrotizing enterocolitis /
malrotation
171
1a. Presentation of intussusception
172
Intussusception

Portion of the alimentary tract is telescoped into an
adjacent segment
 i.e. inversion of one portion of the intestine within another





3 mo- 6 years of age- most common
Most common abdominal emergency in children <2 yr
The incidence varies from 1 to 4/1,000 live births
Male to female ratio is 3 : 1
Intestinal infarction, perforation, peritonitis, and death
173
Etiology and Epidemiology

2-8% of patients, recognizable lead points for the
intussusception-more common in children >2 yr. Basically, the
following help localize the point of intussusception
 Meckel diverticulum
 intestinal polyp
 neurofibroma
 intestinal duplication cysts
 hemangioma
 malignant conditions such as lymphoma



Henoch-Schönlein purpura, hemophilia, cystic fibrosis
Postoperative-within several days
Intrauterine intussusception, premature infants-rare
174
Clinical Manifestations
Severe paroxysmal colicky pain- sudden onset
Accompanied by straining efforts with legs and knees flexed and
loud cries
 May initially be comfortable and play normally
 Lethargy - moaning sounds
 Shock like state, with fever
 Vomiting

 Early phase, frequent vomiting
 Later phase, vomits becomes bile stained

Stools
 Normal 1st few hours
 Currant jelly stool- 1st 12 hr
175
Clinical Manifestations
 The classic triad of (<15% of patient)
1. Pain,
2. Palpable sausage-shaped abdominal mass,
3. Currant jelly stool

Recurrent intussusception is noted in 5-8%
 more common after hydrostatic than surgical reduction

Chronic intussusception, with or after acute enteritis
176
1b. Presentation of malrotation/volvulus
177
Small Bowel Volvulus
 Surgical
emergency- delay cause short gut or
death
 Incomplete rotation of the embryonic bowel
 Vascular supply of the small intestine flowing
through a narrow pedicle of mesentery
 Twist about its base cutting off blood flow
 First symptom- dull, aching abdominal pain
 Obstructive- acutely inflamed abdomen
Pediatrics in Review 2010;31;135
178
Malrotation
179
UpToDate.com
180
181
Clinical Presentation and Diagnosis
Presents early, before 1 year of age
 Bile-stained emesis and pain - think surgical
emergency
 Rectal bleeding is a late sign
 Occasionally- malabsorption
 Protein-losing enteropathy - associated with bacterial
overgrowth
 A plain radiograph may show a dilated stomach and
proximal duodenum

182
183
Diagnosis
 Primary
test for a volvulus is a contrast
upper gastrointestinal study
 Doppler ultrasonography has been used to
detect volvulus and malrotation
 The bowel must be untwisted before
vascular necrosis occurs- appendectomy
184
1c. Presentation of necrotizing enterocolitis
185
Neonatal Necrotizing Enterocolitis
 The
most common life-threatening emergency of
the gastrointestinal tract in the newborn period
 Various degrees of mucosal or transmural
necrosis
 The cause is most likely multifactorial
 The incidence1-5% of infants in NICU
 Both incidence and case fatality rates increase
with decreasing birth weight and gestational age
186
Pathology and Pathogenesis






Most frequently- the distal part of the ileum and the proximal segment of colon
are involved
Gangrene may extend from the stomach to the rectum
The greatest risk factor prematurity “Risk Factors” –
The triad
 intestinal ischemia (injury)
 enteral nutrition (metabolic substrate)
 bacterial translocation
Interaction between loss of
 mucosal integrity due to a variety of factors (ischemia, infection, inflammation)
 the host's response to that injury (circulatory, immunologic, inflammatory)
 leading to necrosis of the affected area
Coagulation necrosis
187
Necrotizing Enterocolitis in Term Infant

“secondary” disease; seen more frequently in infants
with history of
 Birth asphyxia
 Down syndrome
 Congenital heart disease
 Rotavirus infections
 Hirschsprung disease
188
CLINICAL MANIFESTATIONS
Gastrointestinal:
 Abdominal distention
 Abdominal tenderness
 Feeding intolerance
 Delayed gastric emptying
 Vomiting
 Occult/gross blood in stool25%
 Change in stool
pattern/diarrhea
 Abdominal mass
 Erythema of abdominal wall
Systemic:
 Lethargy
 Apnea/respiratory distress
 Temperature instability
 “Not right”
 Acidosis (metabolic and/or
respiratory)
 Glucose instability
 Poor perfusion/shock
 Disseminated intravascular
coagulopathy
 Positive results of blood cultures
189
190
191
2. Long term complications of necrotizing
enterocolitis
192
Prognosis
Medical management fails- 20-40% of patients
 Mortality 10-30%
 Early postoperative complications

 Wound infection, dehiscence, and stomal problems

Later complications
 Intestinal strictures 10%
 Short-bowel syndrome (malabsorption, growth failure,
malnutrition)

Complications related to central venous catheters
(sepsis, thrombosis), and cholestatic jaundice
193
1.
2.
3.
4.
Location of Meckels diverticulum and presentation signs/symptoms
Define obturator sign
Management of appendicitis
Mesenteric lymphadenitis presentation
194
1. Location of Meckels diverticulum and
presentation signs/symptoms
195
Meckel’s diverticulum
Most common true diverticulum of the GI tract
 Congenital diverticulum that results from incomplete
closure of the omphalomesenteric duct (vitelline duct)

 Located
near the terminal ileum
Vary in length from 1 to 12 cm
 Often contain heterotrophic gastric or pancreatic
tissue
 About 2% of the general population has a meckel’s
diverticulum

2. Define obturator sign
197
Physical exam
Dunphy’s sign – coughing exacerbates the RLQ pain
 Rovsing’s sign – Pain in the RLQ during palpation in
the LLQ

 Pain on release of palpation (rebound pain)
 Obturator’s
sign - Pain with internal
rotation of the hip

McBurney’s point – point located 1/3 of the distance
along a line drawn from anterior iliac spine to
umbilicus.
3. Management of appendicitis
199
Work up
Labs: elevated WBC. 10% normal. Really high WBC >20K
suspect perforation and abscess.
 Plain film may see appendicolith, but should not be ordered
as a matter of routine
 Ultrasound is very good but requires special expertise from
the radiologist and a thin patient (pediatrics).
 MRI is very good but more time consuming and cumbersome
to obtain. Used primarily in pregnant women as a way to
avoid radiation to the fetus.

 CT
scan is the gold standard
CT scan for appendicitis








Sensitivity, specificity, positive predictive value and
negative predictive value are all likely > 90 %
Effective test with no contrast, IV contrast, Oral contrast
or rectal contrast
Is easily readable by non – radiologist
Distended appendix > 7mm
Fecolith
Circumferential wall thickening and enhancement (halo)
Fat stranding in surrounding tissue.
Free fluid or abscess
Use of CT scans has drastically reduced the negative
appendectomy rate
 Before performing surgery, surgeons run a CT scan
 As a result, CT scans prevent surgeons from
needlessly removing an appendix

202
Negative appendectomy rate in the era of CT:
an 18 year perspective (radiology aug 2010
Harvard)
Review of appendectomies two time periods 2003-2007
and 1990-1994
 Studied negative appendectomy rate, number of
appendectomies and CT scans
 Between these two time frames negative appendectomy
rate decreased from 23% to 1%. Annual number of
appendectomies decreased from 217 to 119 per year and
preoperative CT increased from 1% to 97.5%

Making the diagnosis of acute appendicitis: do more preoperative CT scans mean
fewer negative appendectomies? A 10 year study. (Radiology, 2010 Feb;254(2):460468)


Looked at the frequency of preoperative CT in the evaluation of patients
suspected of having appendicitis (925 patients)
18.5% of patients underwent preoperative CT in 1998, 93.2% of patients
underwent preoperative CT in 2007.
 Negative
appendectomy rate for women < 45 went
from 42.9% to 7.1%.



For all men and women > 45 no change (men NAR 10%, women >45 NAR
8.7%)
Increase in the use of CT scan coincided with decrease in negative
appendectomy in young women but not men and older women
Shift to thin slices decreased the incidence of false positive diagnosis.
Treatment of appendicitis
Surgery: open and laparoscopic
 Antibiotics
 Timing of surgery
 Management of ruptured appendicitis

Surgery
Open appendectomy transverse RLQ incision (Rockey –
Davis), muscle splitting incision reduces pain.
 For a ruptured appendix sometimes a midline laparotomy
incision may be used
 Inflamed firm appendix is felt and delivered into the field.
The mesenteric artery is divided with clamps and tied.
And the base of the appendix is divided and tied as it
enters into the cecum.
 Difficulties: Obese patients. Appendix is in an unusual
location. If the patient does not have appendicitis limited
visualization of abdomen

Laparoscopic appendectomy
Three ports: one camera and two working ports.
 Mesentery divided with vascular stapler and appendix
is divided with bowel stapler. Appendix is placed in a
bag and brought out one of the port sites.

Conclusions
 Antibiotics
as primary treatment probably
works 90% of time
Rupture may be managed with drainage and antibiotics
 No clear indication for interval appendectomy
 Somewhere around 5-10% of people will have a
recurrence after treatment with antibiotics alone
(uncomplicated and ruptured appendicitis)

Management of ruptured appendicitis
Ruptured appendicitis is a medical emergency not a
surgical emergency
 Admit. Fluid. Foley. Antibiotics. Drain abscess
 Drain abscess in OR or sometimes interventional
radiologist can drain via CT guidance.
 Not worried about the appendix
 Can take many weeks or months to get over
 May need an interval appendectomy at a later date

Conclusions
Risk of rupture was < 2% in patients with less than 36
hours of untreated symptoms.
 With untreated symptoms beyond 36 hours risk of
rupture rose to and remained steady at 5% for each
ensuing 12 hour period

Summary
Probably very low risk of rupture (<2%) during first 36
hours
 Probably makes no difference if you operate within
the first 2 hours or wait 12 hours (If you start
antibiotics once diagnosis is made)
 Patient interval likely has bigger influence than
hospital interval.

4. Mesenteric lymphadenitis presentation
212
Mesenteric lymphadenitis
It is one of the most common causes of acute
abdominal pain in young adults and children
 The lymph nodes involved in mesenteric
lymphadenitis are those that drain the ileocecal region
 Nodes are enlarged, discrete, soft and pink.
 Histologically the nodes show a pattern of reactive
hyperplasia and tend to be sterile with culturing
 Theory is that the nodes are reacting to something
absorbed in the terminal ileum.

Ct scan of mesenteric lymphadenitis
Clinical manifestations of mesenteric
lymphadenitis
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Often there has been a recent illness: sore throat, upper
respiratory tract infection.
Pain is usually first symptom
Pain is located in RLQ but is less focal and more diffuse than
appendicitis
Nausea and vomiting occur in one third of patients
20% of patients will have enlarged lymphadenopathy
elsewhere
Low grade fever and WBC common
Older literature showed up to 20% of people operated on for
appendicitis actually had mesenteric lymphadenitis
Requires no specific treatment
1.
2.
3.
4.
5.
Metabolic abnormalities with SBO
Venous drainage to the small bowel
Anatomy of volvulus
Complications of SBO
Location of acute mesenteric ischemia
216
1. Metabolic abnormalities with SBO
217
Signs and Symptoms of SBO
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Crampy abdominal pain (intestinal colic)
Hyperactive bowel sounds
Abdominal distension: proximal vs distal
Nausea
Vomiting: bilious in nature.
 Early symptom with proximal obstruction
 Late with distal obstruction
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Lack of bowel function
 Dehydration
 Lab abnormalities
 Hemo concentration, elevated creatinine, metabolic
alkalosis, hypo chloremia (cl-), hypo kalemia (K+)
2. Venous drainage to the small bowel
219
Vascular Anatomy
Venous outflow = portal
vein and liver
- Arcades  drain into
SMV (parallel to SMA)
 splenic vein (under
pancreas)  portal
vein (drains bowel) 
into liver
- IVC drains legs, pelvis
3. Anatomy of volvulus
221
Sigmoid volvulus
Volvulus: torsion or twisting of a loop of intestine
causing obstruction
 Xray shows “bent inner tube” in RUQ
 Responsible for 8% of bowel obstructions
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 Most
common segment of colon to be involved
in a volvulus
More common in the elderly, debilitated and those
with a history of chronic constipation
 Can progress onto gangrene
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Bird’s beak sign for sigmoid volvulus
Gangrene of sigmoid colon
Cecal volvulus
Less common
 Younger patients
 The patients are often institutionalized and debilitated
with neurologic and psychiatric conditions, such as
Parkinson disease and schizophrenia
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Cecal volvulus
4. Complications of SBO
227
Strangulation
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When you have a bowel obstruction that leads to
compromise of blood flow to the small bowel. Most
often starts with venous outflow obstruction which can
lead to arterial inflow to stop. The resulting ischemia
of small bowel leads to gangrene and death of the
obstructed segment of bowel
Gangrenous small bowel
5. Location of acute mesenteric ischemia
230
Mesenteric ischemia
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Definition: Injury to small bowel due to inadequate blood
flow
Acute or chronic problem
Arterial or Venous cause
Operative or non operative treatment
Most cases of acute ischemia are caused by an embolus
typically from the heart. Patients with atrial fibrillation or
MI with mural thrombus. Embolism from a cardiac tumor
like atrial myxoma is another cause. Acute venous
thrombosis can occur secondary to hyper coagulable
state.
Etiology has 4 distinct categories , each associated with group
risk factors , signs and symptoms,
1. Arterial embolus – most common 40%
2. Arterial thrombosis – 25%
3. Non occlusive mesenteric ischemia -25%
4. Mesenteric venous thrombosis – 5-10%
 Regardless of the mechanism, the disease follows the same
course. Depending on the cause and severity of the
impairment of the bowel blood supply, the morphologic pattern
can be arbitrarily subdivided into 3 groups: (1) transmural
infarction, (2) mural infarction in which the injury extends from
the mucosa into the muscularis, and (3) mucosal infarction in
which ischemic damage is confined to the mucosa
 Mortality rates climb to 70% once infarction has occurred
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