Small Intestines and Appendix - Anno

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Small Intestines and

Appendix
Surgical Considerations
RESOURCES
Schwartz, Textbook of Surgery 11e
Fadi S. Dahdaleh, David Heidt, and Kiran K. Turaga. The
Gabriel L. Martinez, MD, FPCS Appendix
American College of Surgeons Textbook of Surgery
Professor of Surgery Proceedings of the Mayo Clinic
World Journal of Surgery
Sabiston, Textbook of Surgery
Norton, Surgery: Basic Science and Clinical Evidence
Intended Learning Outcomes
At the end of the session, the student will be able to:

1. Recognize the structure, function and disease processes involving


the small intestines and the appendix.
2. Describe the clinical presentation of the various conditions involving
the small intestines and the appendix.
3. Choose the appropriate management plan for the various
conditions of the small intestines and appendix.
4. Diagnose and manage pathologic conditions related to the small
intestines and the appendix
The Small Intestines Histology
Anatomy
> tubular structure that extends from the Layers: mucosa (epithelium, lamina propia,
muscularis mucosae), submucosa, muscularis
pylorus to the cecum measuring about 4-
6 meters. propia, serosa
Duodenum – pylorus to Lig of Treitz>> Organized into villi/microvilli and crypts
(crypts of Liebekuhn) with multipotent stem
Jejunum (40%) >> ileum (60%) to cells.
ileocaecal Junction.
Cells are removed by apoptosis or by
> contains internal mucosal folds, the exfoliation every 2-5 days
plicae circulares or valvulae conniventes Cells: Enterocytes (absorption), Goblet
or valves of Kerckring that are visible (mucus production), Enteroendocrine
radiographically and help in the (regulatory agents), Paneth (growth factors,
distinction between SI and colon, on enzymes…)
abdominal radiographs* Peyer’s Patches – immune function
Small Intestines - Physiology Fat digestion and absorption –
Over 95% is in the form of long-chain
triglycerides. Over 94% of the ingested fats are
Digestion and absorption of food absorbed in the proximal jejunum.
Water and Electrolyte absorption Barrier and Immune Functions –
and secretion – 8-9L intake, 80% Gut-associated lymphoid tissue (GALT),
absorbed via paracellular or transcellular contains over 70% of the body’s immune
routes cells; Peyer’s Patches, Microfold (M) cells,
antigen presenting cells (APC)
Carbohydrate digestion and
absorption – pancreatic amylase is the Motility – regulated via intrinsic pacemaker
major enzyme in starch digestion (Interstitial cells of Cajal) and external
neurohumoral modulatory signals
Protein digestion and absorption –
50% of load derived endogenously
Small Bowel Obstruction - Classification
According to its anatomical Acute vs Chronic
relation to the wall: Partial vs Complete
1. intraluminal (e.g., foreign Simple vs Closed-loop
bodies, gallstones, or meconium)
Gangrenous vs Non-gangrenous
2. intramural (e.g., tumors,
Crohn’s disease–associated Incarcerated vs Strangulated
inflammatory strictures) Proximal (high) vs Distal (low)
3. extrinsic (e.g., adhesions, Vomiting Early onset vs Late onset
hernias, or carcinomatosis Distention Less vs more
Vomitus Bilious vs feculent
Small Bowel Obstruction - Etiologies
• Adhesions (primary, post-operative) Neoplasms
• Primary small bowel neoplasmsSecondary small bowel cancer (e.g., melanoma-derived
metastasis)
• Local invasion by intra-abdominal Carcinomatosis
• Malignancy (e.g., Desmoid tumors) Crohn’s disease
• Hernias Volvulus
• External (inguinal and femoral) Intussusception
• Internal (following Roux-en-Y Radiation-induced stricture
Gastric bypass surgery) Post-ischemic stricture
• Foreign body Gallstone ileus/Bouveret’s syndrome
• Diverticulitis Meckel’s diverticulum
• Hematoma Congenital abnormalities (e.g., webs,
duplications, and malrotation)
Small Bowel Obstruction - Pathophysiology
With onset of obstruction, gas and The intestinal motility is
fluid accumulate within the intestinal eventually reduced (hypoactive
lumen proximal to the site of bowel sounds). The luminal flora
obstruction. The intestinal activity of the small bowel changes.
increases to overcome the Translocation of these bacteria to
obstruction, accounting for the regional lymph nodes occurs
colicky pain and the diarrhea. (fever).
With ongoing gas and intraluminal With elevated intramural
fluid accumulation (loss of circulting pressure, intestinal microvascular
blood volume >>tachycardia), the perfusion is impaired (metabolic
bowel distends and intraluminal and acidosis, tachypnea) leading to
intramural pressures rise. intestinal ischemia and necrosis.
SBO – History and PE
Elements to obtain on history 5. Obtain a good pain history.
1. prior abdominal/pelvic Pain Mechanical Obstruction Ileus

operations (suggesting the Location Midabdomen Diffuse

presence of adhesions) Character Colicky but may diminish over Dull, poorly localized
time due to fatigue and atony
2. presence of other abdominal
disorders (e.g., intra-abdominal Severity Progressively severe mild

cancer or inflammatory bowel


disease). Upon examination, a meticulous
3. Previous abdominal irradiation search for hernias (particularly in
the inguinal and femoral regions)
4. Current medications and postop scars should be
conducted.
SBO – Clinical Presentation
The symptoms are colicky mid-
abdominal pain, nausea, vomiting, The signs include abdominal
and obstipation. Vomiting is a more distention and tenderness. . Bowel
prominent symptom with proximal sounds may be hyperactive initially,
obstruction than distal. but in late stages of bowel
obstruction, minimal bowel sounds
Character of vomitus is important as may be heard.
with bacterial overgrowth, the
vomitus is more feculent, suggesting
a more established (distal) Features of strangulated obstruction
obstruction. Continued passage of include abdominal pain often
flatus and/or stool beyond 6 to 12 disproportionate to the degree of
hours after onset of symptoms is abdominal findings, tachycardia,
characteristic of partial rather than localized abdominal tenderness, fever,
complete obstruction. marked leukocytosis, and acidosis
suggestive of intestinal ischemia.
SBO - Diagnosis
Goals
(a) distinguish mechanical obstruction
from ileus,
(b) determine the etiology of the
obstruction,
(c) discriminate partial from
complete/closed loop obstruction,
and
(d) discriminate simple from
strangulating obstruction.
(e) determine level of obstruction
SBO - Diagnosis The abdominal series consists of (a)
radiograph of the abdomen with the
patient in a supine position
(b) radiograph of the abdomen with the
patient in an upright position
(c) radiograph of the chest with the patient
in an upright position.
Features specific for SBO
1) dilated small bowel loops (>3 cm in
diameter),
2) air-fluid levels seen on upright films
3) a paucity of air in the colon.
SBO - Diagnosis
Computed Tomographic Scanning
with Contrast 80% to 90% sensitive and 70%
to 90% specific
Findings suggestive of SBO
1. discrete transition zone with
dilation of bowel proximally,
decompression of bowel distally,
2. intraluminal contrast that does
not pass beyond the transition
zone
The appearance of the contrast in the colon
3. colon containing little gas or fluid. within 24 hours of administration is predictive of
nonsurgical resolution of bowel obstruction with
a sensitivity of 92% and a specificity of 93%.
SBO - Diagnosis
CT scanning may also
Strangulation is suggested
provide evidence for the on x-rays by:
presence of closed-loop
obstruction and a) thickening of the bowel
wall,
strangulation.
b) pneumatosis intestinalis
Closed-loop obstruction is (air in the bowel wall),
suggested by the presence c) portal venous gas,
of a U-shaped or C-shaped
d) mesenteric haziness,
dilated bowel loop
associated with a radial e) poor uptake of
intravenous contrast into
distribution of mesenteric the wall of the affected
vessels converging toward bowel.
a torsion point.
SBO – Principles of Management
Small bowel obstruction is usually The stomach should be
associated with a marked depletion continuously evacuated of air and
of intravascular volume (due to fluid using a nasogastric tube (NGT).
decreased oral intake, vomiting, and sequestration Effective gastric decompression
of fluid in bowel lumen and wall). decreases nausea, distention, and
the risk of vomiting and aspiration.
Therefore, fluid resuscitation is
integral to treatment. Isotonic fluid
Broad-spectrum antibiotics are not
should be given intravenously, and indicated unless there is concern for
an indwelling bladder catheter be bowel ischemia and surgery is
placed to monitor urine output. planned.
SBO – Principles of Management
While a period of close observation Therefore, the goal is to operate
and non-operative management has before the onset of irreversible
been the mainstay of treatment for ischemia.
partial bowel obstruction, the
standard therapy for complete small
Most patients with partial small
bowel obstruction has generally been obstruction whose symptoms do not
expeditious surgery, with the dictum improve within 48 hours after
that “the sun should never rise and initiation of non-operative therapy
set on a complete bowel obstruction.” should be considered for surgery.
The rationale for favoring early
surgical intervention is to minimize
the risk for bowel strangulation Operative Goal: relieve the
obstruction and restore GIT continuity
SBO – Principles of Management
In hemodynamically stable patients,
Operative Option. short lengths of bowel of
The affected intestine should be questionable viability should be
examined, and nonviable bowel resected, and primary anastomosis
should be resected. Criteria of the remaining intestine should be
suggesting viability are normal color, performed.
peristalsis, and marginal arterial
pulsations. In borderline cases, a
Doppler probe may be used to check However, if the viability of a large
for pulsatile flow to the bowel, and proportion of the intestine is in
arterial perfusion can be verified by question, a concerted effort to
visualizing intravenously administered preserve intestinal tissue should be
fluorescein dye in the bowel wall made. A “second look” operation
under ultraviolet illumination. can be done later.
Small Bowel Obstruction
Outcomes Prevention
The perioperative mortality rate Good surgical technique, careful
associated with surgery for non- handling of tissue, and minimal use
strangulating small bowel obstruction and exposure of peritoneum to
is less than 5%, with most deaths foreign bodies, forms the
occurring in elderly patients with cornerstone of adhesion prevention.
significant comorbidities. Mortality
rates associated with surgery for
strangulated obstruction is higher, Use of hyaluronan-based agents,
highlighting the need for prompt such as Sperafilm has been clearly
intervention in this group shown to reduce the incidence of
postoperative bowel adhesions.
Gallstone Ileus from GuzmanC., et al. “Gallstone Ileus”. World J Gastrointest Surg. 2016 Jan 27; 8(1):65-76

A mechanical intestinal obstruction due to


gallstone impaction within the
gastrointestinal tract in a patient with a long
history of gallstone disease.
Nausea, vomiting, crampy abdominal pain
and variable distension are commonly
present.
Physical examination may be nonspecific.
The patients are often acutely ill, with signs
of dehydration, abdominal distension and
tenderness with high-pitched bowel sounds
and obstructive jaundice. Fever, toxicity and
physical signs of peritonitis may be noted if Treatment can be one-stage or multi-stage:
perforation of the intestinal wall takes enterolithotomy, cholecystectomy, closure of entero-
place. cholecystic fistula
Ileus and Intestinal Motility Disorders

Ileus and intestinal pseudo- Ileus is a temporary motility


obstruction are clinical syndromes disorder that is reversed with time
caused by impaired intestinal as the inciting factor is corrected.
motility and are characterized by
symptoms and signs of intestinal
obstruction in the absence of a Chronic intestinal pseudo-
lesion-causing mechanical obstruction comprises a spectrum
obstruction. of specific disorders associated
with irreversible intestinal
dysmotility.
Ileus - Etiologies
• Abdominal surgeryMesenteric ischemia
• Infection Myocardial infarction
• SepsisSpinal cord injury
• Intra-abdominal abscess Retroperitoneal hemorrhage
• Peritonitis Ureteral colic
• Pneumonia Hypothyroidism
• Electrolyte abnormalities Medications
• Hypokalemia Anticholinergics
• Hypomagnesemia Opiates
• Hypermagnesemia Phenothiazines
• Hyponatremia Calcium channel blockers
• Tricyclic antidepressants
Ileus - Pathophysiology
Return of normal motility:
Small-intestinal motility returns to
Among the proposed normal within 24-48 hours after
mechanisms responsible for laparotomy; gastric and colonic motility
returns to normal by 2 to 5 days.
this dysmotility are surgical Since small bowel motility returns
stress-induced sympathetic before colonic and gastric motility,
reflexes, inflammatory listening for bowel sounds is not a
reliable indicator that ileus has fully
response mediator release, resolved. Functional evidence of
and anesthetic/analgesic side coordinated gastrointestinal motility in
effects; each of which can the form of passing flatus or bowel
movement is a more useful indicator.
inhibit intestinal motility.
Ileus – Clinical Presentation and Diagnosis
Postoperative ileus is generally
The clinical presentation of ileus diagnosed if ileus persists beyond 5
resembles that of small bowel days postoperatively.
obstruction. Inability to tolerate • “two or more episodes of
liquids and solids by mouth, nausea, nausea/vomiting
and lack of flatus or bowel
• inability to tolerate oral diet over 24
movements are the most common h
symptoms. Vomiting and abdominal
distension may occur. Bowel sound • absence of flatus over 24 h
are usually diminished or absent, in • distension
contrast to the hyperactive bowel • radiologic confirmation
sounds that usually accompany occurring on or after day 4
mechanical small bowel obstruction. postoperatively
Ileus –Therapeutic Options
Limiting oral intake and correcting the Administration of nonsteroidal
underlying inciting factor. anti-inflammatory drugs such as
If vomiting or abdominal distention ketorolac and concomitant
are prominent, the stomach should be reductions in opioid dosing have
decompressed using a nasogastric been shown to reduce the
tube. duration of ileus.
Fluid and electrolytes should be Early postoperative feeding after
administered intravenously until ileus GI surgery is generally well
resolves. tolerated and can lead to reduced
If the duration of ileus is prolonged, postoperative ileus and a shorter
total parental nutrition (TPN) may be hospital stay. (ERAS protocol)
required
Postopoerative Ileus – Preventive Measures
Postoperative measures
Intraoperative measures
Minimize handling of the bowel Avoid nasogastric tubes
Laparoscopic approach, if possible Early enteral feeding
Restricted intraoperative fluid Epidural anesthesia, if indicated
administration
Restricted IV fluid administration
Correct electrolyte abnormalities
Consider mu-opiod antagonists
Chronic Intestinal Pseudo-obstruction
Primary Causes Secondary Causes
Familial types Smooth muscle disorders
Familial visceral myopathies (types I, II, and III) Collagen vascular diseases (e.g., scleroderma)
Familial visceral neuropathies (types I and II) Muscular dystrophies (e.g., myotonic
dystrophy)
Childhood visceral myopathies (types I and II)
Amyloidosis
Sporadic types Neurological disorders
Visceral myopathies Chagas disease, Parkinson’s disease, spinal
Visceral neuropathies cord injury
Pharmacological causes Endocrine disorders
Diabetes, hypothyroidism,
E.g., phenothiazines and tricyclic hypoparathyroidism
antidepressants
Miscellaneous disorders
Viral infections Radiation enteritis
Chronic Intestinal Pseudo-obstruction
The diagnosis of chronic The therapy of patients with
pseudo-obstruction is chronic intestinal pseudo-
suggested by clinical features obstruction focuses on palliation
and confirmed by radiographic of symptoms as well as fluid,
and manometric studies. electrolyte, and nutritional
management.
Diagnostic laparotomy or Surgery should be avoided if
laparoscopy with full-thickness possible. No standard therapies
biopsy of the small intestine are curative or will delay the
may be required to establish natural history of any of the
the specific underlying cause in specific disorders causing
suspected neural disorder. intestinal pseudo-obstruction.
Crohn’s Disease a chronic, idiopathic transmural inflammatory disease
with skip lesions that may affect any part of the alimentary tract, although there is
propensity to affect the distal small bowel.

The endoscopic pathological hallmark of Crohn’s


disease is focal, transmural inflammation of the
intestine. The earliest lesion characteristic of Crohn’s
disease is the aphthous ulcer. These superficial
ulcers are up to 3 mm in diameter and are
surrounded by a halo of erythema.
As disease progresses, aphthae coalesce into larger,
stellate-shaped ulcers. Linear or serpiginous ulcers
may form when multiple ulcers fuse in a direction
parallel to the longitudinal axis of the intestine. With
transverse coalescence of ulcers, a cobblestoned
appearance of the mucosa may arise.
Crohn’s Disease a chronic, idiopathic transmural inflammatory disease
with skipped lesions that may affect any part of the alimentary tract, although there is
propensity to affect the distal small bowel.

Serosal involvement results in adhesion of the inflamed bowel to other


loops of bowel or other adjacent organs. Transmural inflammation can
also result in fibrosis with stricture formation, intra-abdominal
abscesses, fistulas, and, rarely, free perforation.
Inflammation in Crohn’s disease can affect discontinuous portions of
intestine, so-called skip lesions that are separated by intervening
normal-appearing intestine.
Pathognomonic feature is “fat wrapping” of the serosa
Fat Wrapping in Crohn’s Disease
Crohn’s Disease – Clinical Presentation
The most common symptoms of The initial manifestation of Crohn’s
Crohn’s disease are abdominal pain, disease can consist of RLQ pain
diarrhea/steatorrhea mimicking the presentation of acute
(malabsorption), and weight loss. appendicitis.
The onset of symptoms is insidious, In some patients, the initial
and once present, their severity manifestation of Crohn’s disease is an
follows a waxing and waning course. acute abdomen related to small bowel
obstruction, intra-abdominal abscess,
Constitutional symptoms, like weight or free intestinal perforation. In other
loss and fever, or growth retardation patients, perianal abscesses and fistulas
in children, may also be prominent requiring surgical therapy may be the
and are occasionally the sole first manifestation of Crohn’s disease.
presenting features of the disease
Extraintestinal Manifestations – Crohn’s
• DermatologicHepatobiliary
Erythema nodosum Cholelithiasis
Pyoderma gangrenosum Primary sclerosing cholangitis
• Rheumatologic Pericholangitis
Peripheral arthritis Hepatic steatosis
Ankylosing spondylitis Urologic
Sacroiliitis Nephrolithiasis
• Ocular Ureteral obstruction Conjunctivitis, Uveitis/iritis, Episcleritis
• Miscellaneous
Thromboembolic disease, Vasculitis
Osteoporosis
Endocarditis, myocarditis, pleuropericarditis
Interstitial lung disease
Amyloidosis, Pancreatitis
Crohn’s Disease - Therapy
Because no curative therapies are available for Crohn’s disease, the goal of treatment is
to palliate symptoms rather than to achieve cure.

Medical Therapy. Surgery is generally reserved for


Pharmacologic agents used to treat patients whose disease is
unresponsive to aggressive medical
Crohn’s disease include antibiotics,
therapy or who develop
aminosalicylates, corticosteroids, complications of their disease.
immunomodulators, and biologic
therapies (monoclonal antibodies). One of the most common indications
for surgical intervention is intestinal
Antibiotics have an adjunctive role obstruction.
in the treatment of infectious An alternative to segmental resection
complications associated with for obstructing lesions is
Crohn’s disease. stricturoplasty.
Surgery for Crohn’s Disease
Acute onset of severe disease: Development of disease
Crohn’s colitis +/− toxic megacolon complications:
Failure of medical therapy: Obstruction
Persistent symptoms despite Perforation
long-term steroid use Complicated fistulas
Recurrence of symptoms when Hemorrhage
high-dose steroids are tapered Malignancy risk
Drug-induced complications
(Cushing’s disease, hpn)
Intestinal Fistula an abnormal communication between two
epithelialized surfaces
Clinical Presentation
Over 80% of enterocutaneous
fistulas represent iatrogenic Iatrogenic enterocutaneous fistulas
complications that occur as the usually become clinically evident
result of enterotomies or intestinal between the fifth and tenth
anastomotic dehiscences. postoperative days. Fever, leukocytosis,
prolonged ileus, abdominal tenderness,
Fistulas that arise spontaneously and wound infection are the initial
without antecedent iatrogenic signs.
injury are usually manifestations of There is drainage of enteric material
progression of underlying Crohn’s through the abdominal wound or
disease or cancer. existing drains. These fistulas are often
associated with intra-abdominal
abscesses.
Intestinal Fistula - Diagnosis

CT scanning following the If the anatomy of the fistula is


administration of enteral not clear on CT scanning, a
contrast is the most useful small bowel series or
initial test. Leakage of enteroclysis examination can
contrast material from the be obtained. This study is also
intestinal lumen can be useful to rule out the
observed. Intra-abdominal presence of intestinal
abscesses should be sought obstruction distal to the site
and drained percutaneously. of origin.
A fistulogram, in which
contrast is injected
under pressure through
a catheter placed
percutaneously into the
fistula tract, may offer
greater sensitivity in
localizing the fistula
origin
Closure of Fistula Fistulas have the potential to close
spontaneously.
Inhibitors of Spontaneous Closure
Foreign body within the fistula tract
Radiation enteritis
Infection/Inflammation at the fistula origin
Epithelialization of the fistula tract
Neoplasm at the fistula origin
Distal obstruction of the intestine
Closure of Fistula Fistulas have the potential to close
spontaneously.

Negative Impact Negative Impact


Patient factors Local Factors
Poor nutrition
Persistence of local
Medications /steroids
inflammation and sepsis
Etiological factors
Malignant fistula
Presence of a foreign body
(e.g., meshes or sutures)
Crohn’s disease fistula
Fistula in radiated fields Epithelialization of fistula tract
Fistula site – high output Fistula tract <2 cm
Gastric Distal obstruction to the fistula
Duodenal site
Therapy - The overall objectives are to increase the probability of spontaneous closure.

• 1. Stabilization. Fluid and 3. Decision. The available


electrolyte resuscitation is treatment options are
begun. Parenteral/enteral considered, and a time line
nutrition is provided. Sepsis for conservative measures
is controlled with antibiotics is determined (2-3 mos).
and drainage of abscesses.
The skin is protected from 4. Definitive Mgt. This
the fistula effluent with entails the surgical
ostomy appliances or fistula procedure and requires
drains. appropriate preoperative
planning and surgical
• 2. Investigation. The experience.
anatomy of the fistula is
defined. 5. Rehabilitation
Small Bowel Neoplasms
Benign neoplasms account for 30% to 50% of small bowel tumors and
include adenomas (most common), fibromas, lipomas, hemangiomas,
lymphangiomas, and neurofibromas.

Adenomas are histologically classified as tubular, villous, and tubulovillous.


Tubular adenomas have the least aggressive features. Villous adenomas
have the most aggressive features and tend to be large, sessile, and located
in the second portion of the duodenum. Malignant degeneration has been
reported to be present in up to 45% of villous adenomas by the time of
diagnosis.
Small Bowel Neoplasms
Low frequency of small-intestinal neoplasms maybe due to:
(a) dilution of environmental carcinogens in the liquid chyme
(b) rapid transit of chyme, limiting the contact time between carcinogens
and the intestinal mucosa;
(c) relatively low concentration of bacteria in small-intestinal chyme thus a
relatively low concentration of carcinogenic products of bacterial
metabolism;
(d) mucosal protection by secretory IgA and hydrolases;
(e) efficient epithelial cellular apoptotic mechanisms that serve to
eliminate clones harboring genetic mutations.
Small Bowel Neoplasms
Features of small intestinal malignancies

TUMOR TYPE CELL OF ORIGIN FREQUENCY PREDOMINANT SITE

Adenocarcinoma Epithelial cell 35–50% Duodenum


Carcinoid Enterochromaffin cell 20–40% Ileum
Lymphoma Lymphocyte 10–15% Ileum
GIST Interstitial cell of Cajal 10–15%
Small Bowel Neoplasms – Clinical Presentation

Most small-intestinal neoplasms are asymptomatic until they


become large. Partial small bowel obstruction, with associated
symptoms of crampy abdominal pain and distention, nausea, and
vomiting, is the most common mode of presentation. Obstruction
can be the result of either luminal narrowing by the tumor itself
or intussusception, with the tumor serving as the lead point.

Hemorrhage, usually indolent, is the second most common mode


of presentation.
Small Bowel Neoplasms

Gastroenteropancreatic Neuroendocrine Tumors (GEP-NETs or Carcinoid)

Carcinoid tumors of the small intestine are also usually


diagnosed after the development of metastatic disease. These
tumors are associated with a more aggressive behavior than the
more common appendiceal carcinoid tumors. Approximately
25% to 50% of patients with carcinoid tumor-derived liver
metastases will develop manifestations of the carcinoid
syndrome (diarrhea, flushing, hypotension, tachycardia, and
fibrosis of the endocardium and valves of the right heart).
Small Bowel Neoplasms - Lymphoma

Lymphoma may involve the small intestine primarily or as a


manifestation of disseminated systemic disease.
Primary small-intestinal lymphomas are most commonly located
in the ileum, which contains the highest concentration of
lymphoid tissue in the intestine.
Although partial small bowel obstruction is the most common
mode of presentation, 10% of patients with small-intestinal
lymphoma present with bowel perforation.
Small Bowel
Neoplasms
Gastrointestinal stromal tumors (GISTs) are the most common
mesenchymal tumors arising in the small intestine and comprise
the vast majority of tumors that were formerly classified as
leiomyomas, leiomyosarcomas, and smooth muscle tumors of the
intestine.
A defining feature of GISTs is their gain of function mutation of
proto-oncogene KIT, a receptor tyrosine kinase. The interstitial
cells of Cajal have been implicated as the cell of origin for GISTs.
KIT expression is assessed by staining the tissues for CD117
antigen, which is part of the KIT receptor and is present in 95% of
GISTs.
SB Neoplasms -
Diagnosis
Enterocolysis is reported to have a Tumors located in the duodenum can
sensitivity of over 90% in the detection be visualized and biopsied on EGD;
of small bowel tumors and is the test endoscopic ultrasonography (EUS)
of choice, particularly for tumors can offer additional information.
located in the distal small bowel.
Capsule endoscopy and double-
CT scanning can detect abnormalities balloon endoscopy have been used.
in 70% to 80% of cases with small CT and MR enterography are also
bowel tumor and assess for metastatic increasingly being utilized as
spread. Tumors associated with noninvasive tests to look for small
significant bleeding can be localized bowel masses. PET scans can also
with angiography or radioisotope- help assess metabolic activity of
tagged red blood cell (RBC) scans. lesions and risk of malignancy.
Small Bowel Neoplasm -
Therapy
In general, duodenal tumors less Duodenal adenomas occurring in the
than 1 cm in diameter are amenable setting of FAP require an especially
to endoscopic polypectomy. Lesions aggressive management. If surgery is
greater than 2 cm in diameter may required, pancreaticoduodenectomy
need to be removed surgically. is generally necessary because
Surgical options include adenomas in patients with FAP tend
transduodenal polypectomy and to be multiple and sessile, with a
segmental duodenal resection. predilection for the periampullary
Tumors located in the second portion region.
of the duodenum near the ampulla Surveillance endoscopy is the norm
of Vater may require postoperatively.
pancreaticoduodenectomy.
Small Bowel Neoplasm -
Therapy
The surgical therapy of jejunal and
ileal malignancies usually consists of
The goal of surgical therapy for
wide-local resection of the intestine
harboring the lesion. carcinoids is resection of all visible
disease. Localized small-intestinal
For adenocarcinomas, a wide excision carcinoid tumors should be treated
of corresponding mesentery is done to with segmental intestinal resection
achieve regional lymphadenectomy. and regional lymphadenectomy.
Chemotherapy has no proven efficacy Nodal metastases are present in 75%
in the adjuvant or palliative treatment to 90% of tumors larger than 3 cm in
of small-intestinal adenocarcinomas. diameter.
Small Bowel Neoplasm -
Therapy
Localized small-intestinal lymphoma Small-intestinal GISTs should be
should be treated with segmental treated with segmental intestinal
resection of the involved intestine resection. GISTs are rarely associated
and adjacent mesentery. If the small with lymph node metastases thus
intestine is diffusely affected by lymphadenectomy may not be
lymphoma, chemotherapy rather needed.
than surgical resection should be the GISTs are resistant to conventional
primary therapy. The value to chemotherapy agents. Imatinib
adjuvant chemotherapy after (Gleevec), a tyrosine kinase inhibitor
resection of localized lymphoma is with potent activity against tyrosine
controversial. kinase KIT, is used in those with
metastatic disease.
Radiation Enteritis -
Pathophysiology
Radiation induces cellular injury The intensity of injury is related to
directly and through the generation the dose of radiation administered,
of free radicals. The principal occurring in patients who have
mechanism of radiation-induced cell received at least 4500 cGy.
death is believed to be apoptosis Risk factors for acute radiation
resulting from free-radical–induced enteritis include conditions that may
breaks in double-stranded DNA. It limit splanchnic perfusion such as
impacts on rapidly proliferating hypertension, diabetes mellitus,
small-intestinal epithelium which is coronary artery disease, and
acutely susceptible to radiation- restricted mobility of the small
induced injury. (Bergonie and Tribondeau) intestine due to adhesions.
Radiation Enteritis - Pathophysiology
Injury is potentiated by concomitant Chronic radiation enteritis is
administration of chemotherapeutic characterized by a progressive
agents, such as doxorubicin, 5- occlusive vasculitis that leads to
fluorouracil, actinomycin D, and chronic ischemia and fibrosis that
methotrexate, that act as radiation- affects all layers of the intestinal
sensitizers. Because of the intestinal wall, rather than the mucosa alone.
epithelium’s capacity for These changes can lead to strictures,
regeneration, the mucosal injury that abscesses, and fistulas, which are
is characteristic of acute radiation responsible for the clinical
enteritis resolves after the cessation manifestations of chronic radiation
of radiation therapy. enteritis.
Radiation Enteritis – Clinical Presentation
The clinical manifestations of
chronic radiation enteritis usually
become evident within 2 years of
The most common manifestations of radiation administration. The most
acute radiation enteritis are nausea, common clinical presentations are
vomiting, diarrhea, and crampy diarrhea or one of partial small
abdominal pain. Symptoms are bowel obstruction with nausea,
generally transient and subside after vomiting, intermittent abdominal
the discontinuation of radiation distention, crampy abdominal pain,
therapy. and weight loss.
The terminal ileum is the most
frequently affected segment
Radiation Enteritis - Therapy

Most cases of acute radiation enteritis are self-limited. Supportive


therapy, including the administration of antiemetics, is usually
sufficient. Patients with diarrhea-induced dehydration may require
hospital admission and parenteral fluid administration.
Surgery for this condition is difficult, is associated with high morbidity
rates, and should be avoided in the absence of specific indications such
as high-grade obstruction, perforation, hemorrhage, intra-abdominal
abscesses, and fistulas. The goal of surgery is limited resection of
diseased intestine with primary anastomosis between healthy bowel
segments.
Meckel’s Diverticulum
unobliterated embryonic vitelline or omphalomesenteric duct

True diverticula that contains all Other abnormalities include:


the layers of the small intestines. 1) omphalo-mesenteric fistula,
Can contain heterotopic mucosa 2) enterocyst,
(gastric [60%], pancreatic acini or 3) fibrous band connecting the
islets [choristoma*], Brunner’s intestine to the umbilicus.
glands, colonic mucosa,
endometriosis, and hepatobiliary 4) remnant of the left vitelline
tissues) artery persisting to form a
mesodiverticular band tethering a
*choristoma is normal tissue growth in an abnormal location while a
Meckel’s diverticulum to the ileal
hamartoma is disorganized overgrowth of tissues in their normal mesentery.
location
Meckel’s Diverticulum – Clinical Presentation

Largely asymptomatic unless Intestinal Obstruction


associated complications arise:
1. Volvulus of the intestine around the
Bleeding (children) fibrous band attaching the diverticulum
Intestinal Obstruction to the umbilicus
(adults) 2. Entrapment of intestine by a
mesodiverticular band
Diverticulitis
3. Intussusception with the
Groin hernias (Littre’s) diverticulum acting as a lead point
Carcinoid tumor 4. Stricture secondary to chronic
Neuroendocrine tumor diverticulitis
Meckel’s Diverticulum
unobliterated embryonic vitelline or omphalomesenteric duct

Usually an incidental finding during The surgical treatment of


endoscopy, imaging or surgery. symptomatic Meckel’s diverticuli
should consist of diverticulectomy
Enterocolysis is associated with an with removal of associated bands.
accuracy of 75% but limited use.
If with bleeding, segmental
Radionuclide scans (99MTc– resection of ileum to include the
pertechnetate) can be helpful esp diverticulum and the adjacent ileal
with ectopic gastric mucosa. peptic ulcer.
Angiography can localize the site of If with tumor, perforation or
bleeding during acute hemorrhage inflamed base, do segmental ileal
resection.
Acquired Diverticula False diverticula; no muscularis
Acquired diverticuli are more Acquired diverticuli is hypothesized
common in the duodenum, and to be related to acquired
tend to be located near the abnormalities of intestinal smooth
ampulla; such diverticuli are muscle or dysregulated motility,
leading to herniation of mucosa and
known as periampullary,
submucosa through weakened
juxtapapillary, and perivaterian areas of muscularis. They can be
diverticuli. associated with bacterial
Acquired diverticuli in the jejunum overgrowth, leading to vitamin B12
or ileum are known as jejunoileal deficiency, megaloblastic anemia,
diverticuli. malabsorption, and steatorrhea.
Acquired Diverticula – Clinical Presentation
Usually asymptomatic unless Symptoms such as intermittent
associated complications arise: abdominal pain, flatulence,
intestinal obstruction, diarrhea, and constipation are
diverticulitis, hemorrhage, reported to be present in 10% to
perforation, and malabsorption. 30% of patients with jejunoileal
Periampullary duodenal diverticuli diverticuli.
may be associated with The relationship between these
choledocholithiasis, cholangitis, symptoms and the presence of
recurrent pancreatitis, and the diverticuli is still unclear.
sphincter of Oddi dysfunction.
Acquired Diverticula –
Therapy
Asymptomatic acquired Bleeding and obstruction related to
diverticuli should be left lateral duodenal diverticuli are
generally treated with
alone. Bacterial overgrowth diverticulectomy alone.
associated with acquired Complications related to medial
diverticuli is treated with duodenal diverticuli should be
antibiotics. managed nonoperatively.
Oversewing of bleeders can be
Segmental intestinal resection done.
for symptomatic diverticuli
Perforation can be managed with
located in the jejunum or wide drainage rather than complex
ileum. surgery.
Mesenteric Ischemia Embolus is the most common cause of
acute mesenteric ischemia. The embolic
Pathophysiologic mechanisms source is usually in the heart (left atrial or
leading to acute mesenteric ventricular thrombi or valvular lesions).
ischemia Acute arterial thrombosis is usually
superimposed on preexisting
atherosclerotic lesions.
1. Arterial embolus NOMI results from vasospasm and is
2. Arterial thrombosis usually diagnosed among critically ill
patients on vasopressor agents.
3. Vasospasm (also known as Mesenteric venous thrombosis is
nonocclusive mesenteric ischemia classified as primary if no etiologic factor
or NOMI) is identifiable, or as secondary if an
etiologic factor, such as heritary or
4. Venous thrombosis acquired coagulation disorders, is
identified.
Mesenteric Ischemia Postprandial abdominal pain is the
• Chronic mesenteric ischemia most prevalent symptom,
develops insidiously, allowing for producing a characteristic aversion
development of collateral circulation, to food (“food fear”) and weight
and, therefore, rarely leads to loss.
intestinal infarction. It results from
atherosclerotic lesions in the main Most patients with chronic
splanchnic arteries (celiac, superior mesenteric venous thrombosis are
and inferior mesenteric arteries). asymptomatic because of the
presence of extensive collateral
• A chronic form of mesenteric venous
venous drainage routes; this
thrombosis can involve the portal or
splenic veins and may lead to portal condition is usually discovered as
hypertension. an incidental finding on imaging
studies.
Mesenteric Ischemia
• Severe abdominal pain, out of proportion to the degree of tenderness
on examination is the hallmark of acute mesenteric ischemia,
regardless of the pathophysiologic mechanism. The pain is typically
perceived to be colicky and most severe in the midabdomen.
• Associated symptoms can include nausea, vomiting, and diarrhea.
• Physical findings are characteristically absent early in the course of
ischemia. With the onset of bowel infarction, abdominal distension,
peritonitis, and passage of bloody stools occur.
Tuberculous Ileitis
Most cases of TB ileitis (70%) are the result of the ingestion of infected
sputum from an active pulmonary TB, and are rarer as a result of
systemic spreading, the chest radiography result is normal in 70% of the
cases.
A barium examination shows shallow ulcers, thickened folds and
spasticity
The main complications are: Massive hematochezia, bowel obstruction,
necrosis and intestinal perforation, enterocutaneous fistula, ileoileal
fistula, ascites, purulent or stercoral peritonitis, mesenteric
lymphadenitis with intussusception, ileal loops or intestinal volvulus
Typhoid Ileitis

Fever of long duration with bradycardia (Faget sign) and leukopenia.


A complication of Typhoid Fever which is due to an infection caused by
Salmonella enterica subsp. Enterica.
Surgery is usually indicated if intestinal perforation occurs.
For surgical treatment, most surgeons prefer simple closure of the
perforation with drainage of the peritoneum. Small-bowel resection is
indicated for patients with multiple perforations. If antibiotic treatment
fails to eradicate the hepatobiliary carriage, the gallbladder should be
resected.
Obscure GI Bleeding - bleeding for which no source has been
identified by routine endoscopic studies (EGD and colonoscopy).

Overt GI bleeding refers to the Small intestinal angiodysplasias


presence of hematemesis, account for approximately 75% of
melena, or hematochezia. cases in adults, and neoplasms
Occult GI bleeding occurs in the account for approximately 10%.
absence of overt bleeding and is Meckel’s diverticulum is the most
identified on laboratory tests (e.g., common etiology of obscure GI
iron-deficiency anemia) or bleeding in children.
examination of the stool (FOBT) Endoscopy, RBC-tagging,
Angiography, Enterocolysis have
varied success.
Small Bowel Perforation
Among iatrogenic injuries, duodenal Other etiologies include infections
perforation during endoscopic retrograde (tuberculosis, typhoid, and CMV), Crohn’s
cholangiography (ERCP) with endoscopic disease, ischemia, drugs (NSAID-induced
sphincterotomy (ES) is the most common. ulcers), radiation-induced injury, Meckel’s
Stapfer classification and acquired diverticuli.
• Type I: Free bowel wall perforation Perforation of the jejunum and ileum
• Type II: Retroperitoneal duodenal causes overt s/s - abdominal pain,
perforation secondary to periampullary tenderness, and distention, fever and
injury (most common, nonsurgical tachycardia. Plain abdominal radiographs
management) may reveal free intraperitoneal air
• Type III: Perforation of the pancreatic or intraperitoneal perforations require
bile duct surgical repair (primary repair,
• Type IV: Retroperitoneal air alone diverticulization)
Chylous Ascites - accumulation of triglyceride-rich, milky or creamy
appearing peritoneal fluid, caused by the presence of intestinal lymph in the peritoneal cavity

Etiologic mechanisms Paracentesis is the most important


diagnostic test. Chyle is cloudy and turbid in
(a) exudation of chyle from dilated appearance; Fluid triglyceride concentrations
lymphatics on the wall of the above 110 mg/dL are diagnostic.
bowel and in the mesentery due to
Most patients respond to administration of a
obstruction of lymphatic vessels high-protein and low-fat diet supplemented
(b) direct leakage of chyle through a with medium-chain triglycerides.
lymphoperitoneal fistula due to Management is focused on evaluating and
trauma or surgery treating the underlying causes.
(c) exudation of chyle through the If leak can be localized, surgical repair can be
wall of dilated retroperitoneal undertaken.
lymphatic vessels
Intussusception - proximal segment of the intestine “telescopes”
into the lumen of the distal segment.

It is usually seen in the pediatric


population, where it is often an
idiopathic condition and treated
nonsurgically by radiological
reduction.
In adults, it is far less common and
usually has a distinct pathologic lead
point, which can be malignant in up
to one-half of cases.
Intussusception - proximal segment of the intestine “telescopes”
into the lumen of the distal segment.

Commonly present with a history of


intermittent abdominal pain and
signs and symptoms of bowel
obstruction. CT scan is the
investigation of choice, where a
“target sign” may be seen.
Treatment is surgical resection of the
involved segment and the lead point,
which needs to undergo pathological
evaluation to rule out an underlying
malignancy.
Pneumatosis Intestinalis - presence of gas within the bowel
wall
Pneumatosis intestinalis is The surgical interest in this
not a disease but merely a finding is the association of it
sign that can be idiopathic with bowel ischemia and
or associated with many infarction, both of which
intestinal or nonintestinal necessitate emergent
disorders, such as surgical intervention.
obstructive pulmonary
disease and asthma. Patients with this
radiological finding have to
be fully evaluated and
The pathogenesis of monitored closely to rule out
pneumatosis intestinalis is such intra-abdominal
not fully understood. catastrophes
Short Bowel Syndrome presence of less than 200 cm of residual
small bowel in adult patients

Clinically significant malabsorption occurs


Risk factors for development of short when >50% to 80% of the small intestine
bowel syndrome after massive small has been resected.
bowel resection 1. The colon can absorb short chain fatty
Small bowel length <200 cm acids.
2. An intact ileocecal valve prolongs
Absence of ileocecal valve contact time between nutrients and the
Absence of colon small-intestinal mucosa.
Diseased remaining bowel 3. Healthy residual small intestine is
associated with decreased severity of
(e.g., Crohn’s disease) malabsorption
Ileal resection 4. Resection of jejunum is better tolerated
than resection of ileum
Short Bowel Syndrome - Therapy
Medical Therapy Non-transplant surgical therapy
Management of the primary condition Operations designed to slow intestinal
precipitating the intestinal resection transit include segmental reversal of the small
bowel, interposition of a segment of colon
Repletion of fluid and electrolytes lost in between segments of small bowel, construction
the severe diarrhea that characteristically of small-intestinal valves, and electrical pacing
occurs of the small intestine.
Enteral nutrition should be gradually Intestinal lengthening procedures
introduced
Antimotility agents, like loperamide Intestinal Transplantation
hydrochloride or diphenoxylate, may be
Accepted indication for intestinal
administered to delay small-intestinal transit. transplantation is the presence of life-
Octreotide can reduce the volume of threatening complications attributable to
gastrointestinal secretions intestinal failure and/or long-term TPN therapy.
The Appendix • The appendix is a true
diverticulum of the cecum; it
measures 6 to 9 cm and derives its
blood supply from the
appendicular branch of the
ileocolic artery. It is intraperitoneal
and retrocecal in location.
• The appendiceal base can be
identified by tracing the
convergence of the taenia coli.
• Valve of the vermiform appendix is
also called Gerlach's valve.
The Appendix • The appendix act as a "safe house"
for beneficial bacteria.This
reservoir of bacteria could then
serve to repopulate the gut flora in
the digestive system or to boost it
following a milder gastrointestinal
illness.
• The appendix has been identified
as an important component of
mammalian mucosal immune
function, particularly B cell-
mediated immune responses and
extrathymically derived T cells.
Acute Appendicitis inflammation of the appendix mostly due
to obstruction of the appendiceal lumen
Affects any age but most common Classically starts as vague, poorly
at 10-19 years among males.
localized periumbilical pain with
Obstruction due to: nausea, vomiting and anorexia.
Fecalith After some time the pain increases
Food in severity and migrates to the RLQ,
associated with low grade fever and
Foreign bodies abdominal tenderness.
Parasites As the disease progresses, so do the
Calculi fever and abdominal tenderness.
Neoplasm The patient lays still in bed as
movement aggravates the pain.
Acute Appendicitis - Diagnosis
Appendicitis is a clinical diagnosis
based on History and PE. Murphy's Triad/sQuadrad*
Typical appendicitis includes Consists of "pain in the abdomen
several hours of generalized followed by nausea or vomiting,
abdominal pain that begins in the and general abdominal
region of the umbilicus or sensitiveness on the right side,
epigastrium with associated followed by an elevated body
anorexia, nausea, or vomiting. The temperature."
pain then "localizes" into the right
lower quadrant where the
tenderness increases in intensity.
Acute Appendicitis - Diagnosis
Most patients lay quite still due to parietal peritonitis.
Patients are generally have low-grade fever, (∼38.0°C [100.4°F]) with
signs of peritoneal irritation
>>Utilize scoring systems – Alvarado Score (MANTRELS)* or AIRS

If Equivocal Dx – use imaging aids (UTZ, CT, MRI)

Histopathologic hallmark – neutrophilic infiltration of the muscularis propia


Acute Appendicitis
Signs of Peritoneal Irritation-1
Aaron’s – sensation of pain or distress in the epigastric or Brittain’s – palpation of the RLQ produces retraction of
precordial region on pressure over McBurney’s point the right testicle in cases of gangrenous appendicitis.
Aure-Rozanova’s – increased pain on palpation with Dunphy’s – increased pain in RLQ with coughing
finger on right Petit’s triangle Gas stoppage – a feeling of fullness relieved by a bowel
Bartomier-Michelson – increased pain on palpation at movement; associated with retrocaecal appendicitis
right iliac region as the patient lies on his/her left side Gray’s – tenderness on pressure with the finger 1 ½
compared to lying supine inches below and to left of the umbilicus; also pain in
Bastedo’s – pain and tenderness on right iliac fossa or the shoulder.
McBurney’s point on inflation of the colon with air; Hamburger’s – patient refuses to eat (anorexia is 80%
seen in chronic cases. specific for appendicitis)
Blumberg’s – rebound tenderness; pain on abrupt Jack knife – sudden pressure over point of maximal
release of steady pressure over site of lesion. tenderness causes involuntary flexion of the thighs
Acute Appendicitis
Signs of Peritoneal Irritation-2
Kocher’s (Kosher’s) – pain in the umbilical region with Obturator – pain on passive internal rotation of the
subsequent shift to right iliac region. flexed thigh (due to contact between an inflammatory
La Roque’s/Liget’s – hyperesthesia over Sherren’s lesion and the obturator internus muscle).
triangle. Ott’s – pulling sensation felt when lying on left side.
Massouh’s – examiner performs a firm swish with index Psoas/Cope’s – flexion of or pain on hyperextension of
and middle finger across the abdomen from the xiphoid the hip (due to contact between inflammatory lesion
process to the left and the right iliac fossa. A positive and psoas muscle).
result is a grimace when the right side is examined. Rovsing’s/Gregory’s – contralateral tenderness; pressure
McBurney’s – tenderness over McBurney’s point. on the left side corresponding to the McBurney’s point
Mortola’s – pain on pinching the RLQ; severity of pain elicits pain over McBurney’s point in the right side
indicates degree of inflammation. (specific for appendicitis)
Acute Appendicitis
Signs of Peritoneal Irritation-3
Sitkovskiy/Rosenstein’s – increased pain over the right Tressder’s – assuming the prone position gives pain relief.
iliac region while patient lies on left side. Volkovitsch’s – relaxation and atrophy of the abdominal
Soresi’s – in supine position with thighs flexed, the muscle over the appendix in cases of chronic
patient coughs while examiner presses over the hepatic appendicitis.
flexure producing pain at McBurney’s point. Wachenheim-Reder’s – tenderness over the iliac fossa at
Sumner’s – slight increase in the tone of the abdominal the ileocaecal region on rectal palpation.
muscles is felt on gentle palpation of the iliac fossa. Widmer’s – temperature in the right axilla is distinctly
Treacherous Calm of De Falloy – “calm before the higher than that of the left axilla.
storm”; initial disappearance of abdominal pain among Markle sign or jar tenderness - pain in the right lower
patients with appendicitis, only to it to recur with quadrant of the abdomen is elicited by dropping from
greater severity and intensity associated with high standing on the toes to the heels with a jarring landing.
grade fever. Indicates a ruptured appendicitis.
Appendicitis
Appendicitis Inflammatory
The Scoring Systems Response Score (AIRS)
Vomiting1
Alvarado Score (MANTRELS) Pain (RLQ/right iliac fossa) 1
Guarding/Abdominal Defense
Migratory right iliac fossa pain 1 Low 1
Anorexia 1 Mild 2
Nausea and vomiting 1 Severe 3
Tenderness over RLQ 2 Temperature >38.50C 1 AIRS Score
Rebound Tenderness 1 Segmenters/Neutrophils
Elevation in temperature (fever) 1 70-84% 1 4-7 low
Leukocytosis 2 >85% 2 5-8 mild
Shift to the left (segmented neutrophils) 1 WBC/Leukocytes 9-12 high
10,000-14,900 1
<5 most probably NOT appendicitis Accuracy 97.2%
>15,000 2
5-6 equivocal; imaging studies needed C-Reactive Protein
>7 predictive of acute appendicitis 10-49 mg/dL 1
>50 mg/dL 2
Acute Appendicitis
Ancillary Lab Tests A urinalysis generally does not
show infection, but it is important
While there is no laboratory test for determining pregnancy status,
specific for appendicitis, a especially the possibility of an
complete blood count (CBC) is ectopic pregnancy in women of
done to check for signs of childbearing age.
infection. The urinalysis is also important for
ruling out a urinary tract infection
Due to its low sensitivity and
as the cause of abdominal pain.
specificity, on its own, WBC is not
seen as a good indicator of The presence of more than 20 WBC
appendicitis. per high-power field in the urine is
more suggestive of a urinary tract
disorder.
Acute Appendicitis
Ultrasonography
First choice due to radiation
concerns in children/pregnant px
Will show free fluid collection in
the right iliac fossa, along with a
dilated, noncompressible
appendix with increased blood
flow using color Doppler. Also
presence of echogenic mesenteric
fat around the appendix and the
acoustic shadowing of an
appendicolith.
Acute Appendicitis
Computed Tomography
First choice among adult patients. A
size of over 6 mm is both 95%
sensitive & specific for appendicitis.
Ancillary features such as increased
wall enhancement as compared to
adjacent bowel and inflammation of
the surrounding fat, or fat stranding,
can be supportive of the diagnosis
Acute Appendicitis
Magnetic Resonance Imaging
In pregnancy, it has been found to
be more useful during the second
and third trimester, particularly as
the enlarging uterus displaces the
appendix, making it difficult to find
by ultrasound.
The periappendiceal stranding that
is reflected on CT by fat stranding
on MRI appears as increased fluid
signal on T2 weighted sequences.
Acute Appendicitis
Management
Preoperative hydration
Prophylactic antibiotics
Appendectomy
(open/laparoscopic)
Non-operative with antibiotics but
will require an operation later.
Appendectomy with drainage for
abscess formation
Appendicitis
Clinico-pathological correlation //glm

Pathological Events Clinical Expression Rationale Other Data

Luminal Obstruction Nausea and vomiting, Anorexia Sympathetic ileus visceral peritoneum has the same
Dull, Periumbilical/epigastric pain Visceral pain nerve supply as the viscera it invests

Increased intraluminal pressure Pain migrates to RLQ, localized Somatic pain (parietal peritoneum Alvarado Score, AIRS
Compression of vessels in wall RLQ tenderness innervated by the same somatic Elevated C-reactive protein
Congestion of appendix ± Fever nerve as the region it lines) Elevated bilirubin, IL-6, procalcitonin
Early acute appendicitis Decreased venous return

Compression of intramural vessels Signs of peritoneal irritation Localized peritonitis Leukocytosis with shift to left
>>>Progressive ischemia (McBurney’s, Rovsing’s, etc.) Bacterial Translocation Hemoconcentration
Fibrin deposition Fever >380C
Acute appendicitis
Complicated appendicitis ± RLQ mass Periappendiceal phlegmon/ Fluid-Electrolyte problems
Gangrenous appendicitis High grade fever, diarrhea abscess Metabolic acidosis
Tachycardia, tachypnea Release of intraluminal pressure
Perforated appendicitis (72 hrs Temporary pain relief that recurs and contents
from onset) with greater intensity (“calm Generalized peritonitis
before the storm” a.k.a. “the
treacherous calm of De Faloy”)

Pylephlebitis (thrombophlebitis of Septic fever Sepsis syndrome Positive blood culture


the portal vein or any of its Jaundice, chills SIRS-MODS-MOF
branches (i.e. a portal vein Oliguria
thrombosis)
Special
Circumstances Atypical appendicitis – children and
Chronic or recurrent appendicitis the elderly; late diagnosis.
Patients with recurrent right lower Use Pediatric Appendicitis Score
quadrant abdominal pain not associated Older adult patients can have
with a febrile illness with imaging findings diminished inflammation and thus
suggestive of an appendicolith or dilated present with perforation or abscess
appendix. more frequently.
Stump Appendicitis Appendicitis in Pregnancy
Development of appendicitis in an Displaced point of maximal tenderness.
incompletely excised appendiceal stump RLQ tenderness on displacing uterus to
(greater than 0.5 cm stump length). the right (Brian’s sign)
Optimal management requires reexcision
of the appendiceal base, Risk of fetal loss as high as 36%.
Other Diseases of the Appendix
Gastroenteropancreatic Neuroendocrine Goblet Cell Carcinomas
Tumors (GEP-NETs or Carcinoid)
These lesions are adenocarcinoid with
Submucosal rubbery masses that are detected both adenocarcinoma and
incidentally; they are relatively indolent but can
develop nodal or hepatic metastases. neuroendocrine features. In the absence
For lesions that are less than 1 cm, a negative
of metastatic disease, a right
margin appendectomy is adequate. For tumors 2 hemicolectomy is generally appropriate.
cm or larger, a right hemicolectomy is
recommended. For lesions 1 to 2 cm in size, there
Lymphomas
is no consensus on a completion colectomy. A Usually non-Hodgkin’s and difficult to
right colectomy is often performed for diagnose preoperatively.
mesenteric invasion, enlarged nodes, or positive
or unclear margins. Measurement of serum Management includes an appendectomy
chromogranin A is recommended. in most cases.
Other Diseases of the Appendix
Adenocarcinoma Appendiceal Mucoceles and
Has three major histologic subtypes: Mucinous Neoplasms
mucinous adenocarcinoma, colonic Mucus-filled appendix that could be
adenocarcinoma, and adenocarcinoid. secondary to neoplastic or nonneoplastic
The most common mode of presentation for pathologies (mucosal hyperplasia, simple
appendiceal carcinoma is acute appendicitis. or retention cysts, mucinous
The recommended treatment for all patients cystadenomas, mucinous
with adenocarcinoma of the appendix is a cystadenocarcinoma).
formal right hemicolectomy.
Careful handling of a mucocele and the
Patients with appendiceal avoidance of rupture is vital because of
adenocarcinoma are at significant risk for the intraperitoneal spread of neoplastic
both synchronous and metachronous cells and subsequent development of
neoplasms. pseudomyxoma peritonei
Pseudomyxoma Peritonei Syndrome (PMP)

Occurs in peritoneal dissemination of appendiceal mucinous neoplasms,


gastric, ovarian, pancreatic, or colorectal primary tumors.
Cytoreductive surgery and hyperthermic intraperitoneal chemotherapy
(HIPEC) are considered the standard of care for patients with PMP
syndrome from appendiceal primaries.
The surgical technique involves parietal and visceral peritoniectomies, and
intraperitoneal administration of heated (42oC [108oF]) chemotherapy
(usually mitomycin) in the abdomen.
Take Home Messages for Appendicitis
1. Inflammation of the appendix is a significant public health problem
with a lifetime incidence of 8.6% in men and 6.7% in women, with
the highest incidence in the second and third decade of life; it
remains one of the most frequent emergent abdominal operations.
2. Acute Appendicitis is a clinical diagnosis. Scoring systems serve as
guides to the diagnosis.
3. In atypical presentations, laboratory data and imaging modalities
are used to rule out other diseases and guide management.
4. Appendectomy is the gold standard in the management of the
disease.
Group work and Tasking
Case Study
Three years ago, she noticed a decrease in
This 62 year-old obese female from the the intensity of the pains for about 3-4
foothills of the Sierra Madre Mountains, months. However, the pains recurred as
consults because of cramping abdominal abdominal cramping pains often associated
pains associated with nausea and vomiting. with nausea and vomiting lasting for a week
and mild to moderate grade fever.
Her symptoms started more than five years
ago as several episodes of colicky epigastric Three days prior to admission, she had
pains, radiating to the back which occurred abdominal cramps associated with vomiting
after heavy meals consisting of root crops, of previously taken food. One day prior to
vegetables and grilled or fried wild boar admission, the pain increased in intensity
meat. She thought it was just cases of and she noticed her vomitus smelled like
“impatso”. Being in the mountains, she feces; she experienced fever and chilly
relied on herbal medications given by the sensation. Her husband noticed distention
local arbularyo. of her abdomen and no bowel movement.
Group work and Tasking Abdominal Ultrasound
Case Study >Distended bowel loops; Acalculous thick-
Physical Examination walled gallbladder; >Normal liver and
T=38.2*C PR=102bpm RR=24 pancreas
cpm
BP= 100/70mmHg Abdominal
Pale conjunctivae, dry buccal
X-ray
mucosa
Flat neck veins
Clear breath sounds, regular
cardiac rhythm
Abdomen is tender, distended and
tympanitic with rushes and
borborymi on auscultation.
DRE: no feces in rectal vault, good
sphincter tone
Group work Your Case Your Tasks

Based on the data supplied herein:


1. What is your clinical impression of the case?
2. Describe the pathophysiology of the disease condition?
3. What other ancillary procedures will you request and why?
4. Create a management algorithm for this case.
5. Make a Reflection Paper regarding this activity.

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