Vivi Aanggelia

405100154

Definition of Acute
Abdomen
Any serious acute intra-abdominal
condition attended by pain,
tenderness, and muscular rigidity,
and for which emergency surgery
must be considered

Etiology of Acute Abdomen

Etiology of Acute Abdomen

Types of Abdominal Pain:

 Visceral pain comes from the abdominal viscera,

which are innervated by autonomic nerve fibers
and respond mainly to the sensations of distention
and muscular contractionnot to cutting, tearing,
or local irritation. Visceral pain is typically vague,
dull, and nauseating. It is poorly localized and
tends to be referred to areas corresponding to the
embryonic origin of the affected structure.
Foregut structures (stomach, duodenum, liver,
and pancreas) cause upper abdominal pain.
Midgut structures (small bowel, proximal colon,
and appendix) cause periumbilical pain.
Hindgut structures (distal colon and GU tract)
cause lower abdominal pain.

 Somatic pain comes from the

parietal peritoneum, which is
innervated by somatic nerves, which
respond to irritation from infectious,
chemical, or other inflammatory
processes. Somatic pain is sharp and
well localized.

 Referred pain is pain perceived

distant from its source and results
from convergence of nerve fibers at
the spinal cord. Common examples
of referred pain are scapular pain
due to biliary colic, groin pain due to
renal colic, and shoulder pain due to
blood or infection irritating the
diaphragm.

Somatic Pain

Visceral Pain

Receptor

Pain stimuli start in the parietal

peritoneum, which is
innervated by peripheral
nerves

Visceral peritoneum

Stimulus

Touch, pressure, heat,

inflammation

Traction, distention, & spasm

Mediation

CNS & interpreted at a

specific cortical location

Autonomic Nervous System

interpreted at the thalamic level
of the brain

Specifity

Precisely described as sharp,

knifelike, cutting

Vague, often dull, poorly

described

Localization

The pain is localized with great

accuracy by the patient, who
can often point to the site with
one finger

Poor and the patien is placing

the entire hand over the
involved region

Pathophysiology
Visceral pain

Somatic pain

Referred pain

comes from the abdominal

viscera, which are innervated by
autonomic nerve fibers and
respond mainly to the sensations
of distention and muscular
contractionnot to cutting,
tearing, or local irritation.

comes from the parietal

peritoneum, which is innervated
by somatic nerves, which respond
to irritation from infectious,
chemical, or other inflammatory
processes

perceived distant from its source

and results from convergence of
nerve fibers at the spinal cord

Visceral pain is typically vatigue,

dull, and nauseating

Somatic pain is sharp and well

localized.

Common examples of referred

pain are scapular pain due to
biliary colic, groin pain due to
renal colic, and shoulder pain due
to blood or infection irritating the
diaphragm.

Foregut structures (stomach,

duodenum, liver, and pancreas)
cause upper abdominal pain.
Midgut structures (small bowel,
proximal colon, and appendix)
cause periumbilical pain. Hindgut
structures (distal colon and GU
tract) cause lower abdominal
pain.

Projection Pain
Cause by sensoric nerves stimualtion
because injured or nerves
inflammation
Ex: phantom pain after amputation,
or localized peripheral pain in herpes
zoster

Continue Pain
Caused by peritoneum stimulation in
the parietal peritoneum and occur in
continuous time
Peritonitis localized pressure pain,
defense muscular to protect
inflammation area and avoid
movement or localized pressure

Cholic Pain
Caused by smooth muscle spasm in hollow
organs and usually cause by passage obstruction
in that organs (intestine obstruction, kidney
stone, bile stone, increase of intraluminer)
Appear by hypoxia, feels come and go, nausea to
emesis, and very nervous
Have specific TRIAS reccurent abdominal pain
followed by nausea or emesis and force
movement

Ischemic Pain
Very intensive, permanent, and not
reduce. This is sign of necrosis phase
is inisiated. Further more, general
intoxification will appear

Gradual, progressive pain

Colicky, crumpy, intermittent

pain

Sudden, severe pain

Referred Pain

Classification on Abdominal
Pain
Three main categories of abdominal
pain:
1. Intra-abdominal (arising from within the
abdomen cavity / retroperitoneum)
involves:

GI (Appendicitis, Diverticulitis, etc)

GU (Renal Colic, etc)
Gyn (Acute PID, Pregnancy, etc)
Vascular systems (AAA, Mesenteric Ischemia, etc)

Classification on Abdominal
Pain
2. Extra-abdominal (less common)
involves:

Cardiopulmonary (AMI, etc)

Abdominal wall (Hernia, Zoster etc)
Toxic-metabolic (DKA, OD, lead, etc)
Neurogenic pain (Zoster, etc)
Psychic (Anxiety, Depression, etc)

3. Nonspecific Abdominal pain not well

explained or described.

Historical features of
Abdominal Pain

Recent / current medications

Site
Nature & character
Duration
Intensity
Precipitating & relieving factors
Associated symptoms
Past hospitalizations
Past surgery
Chronic disease
Social history
Occupation / Toxic exposure (CO / lead)

Physical Examination of the

Abdomen
Note pts general appearance. Realize that
the intensity of the abdominal pain may
have no relationship to severity of illness.
One of the initial steps of the PE should be
obtaining and interpreting the vitals.
Pts with visceral pain are unable to lie still.
Pts with peritonitis like to stay immobile.

Physical Examination of the

Abdomen
INSPECT for distention, scars, masses,
rash.
AUSCULATE for hyperactive, obstructive,
absent, or normal bowel sounds.
PALPATION to look for guarding, rigidity,
rebound tenderness, organomegally, or
hernias.
Women should have pelvic exam (check
FHR if pregnant).
Anyone with a rectum should have rectal
exam (If no rectum check the ostomy).

Systemic Examination
Abdomen:
Inspection
- Scaphoid or flat in peptic ulcer
- Distended in ascites or intestinal
obstruction
- Visible peristalsis in a thin or
malnourished patient (with obstruction)

Systemic Examination
Palpation
Check for Hernia sites
Tenderness
Rebound tenderness
Guarding- involuntary spasm of muscles
during palpation
Rigidity- when abdominal muscles are
tense & board-like. Indicates peritonitis.

Systemic Examination
Local Right Iliac Fossa tenderness:
Acute appendicitis
Acute Salpingitis in females

Low grade, poorly localized tenderness:

Intestinal Obstruction

Tenderness out of proportion to examination:

Mesenteric Ischemia
Acute Pancreatitis

Flank Tenderness:
Perinephric Abscess
Retrocaecal Appendicitis

Important Signs in Patients with Abdominal Pain

Sign

Finding

Association

Cullen's sign

Bluish periumbilical
discoloration

Retroperitoneal haemorrhage

Kehr's sign

Severe left shoulder pain

Splenic rupture
Ectopic pregnancy rupture

McBurney's sign

Tenderness located 2/3 distance from

anterior iliac spine to umbilicus on right side

Murphy's sign

Abrupt interruption of inspiration on palpation

of right upper quadrant

Acute cholecystitis

Iliopsoas sign

Hyperextension of right hip causing abdominal pain

Appendicitis

Obturator's sign

Internal rotation of flexed right hip causing

abdominal pain

Appendicitis

Grey-Turner's
sign

Discoloration of the flank

Retroperitoneal haemorrhage

Chandelier sign

Manipulation of cervix causes patient to lift

buttocks off table

Pelvic inflammatory disease

Rovsing's sign

Right lower quadrant pain with palpation of

the left lower quadrant

Appendicitis

Appendicitis

Physical examination
Auscultation
BS
> 2min to confirm absent
High pitched, hyperactive or tinkling
Bruit in epigastrium

Systemic Examination
Rectum Examination:
- tenderness
- induration
- mass
- frank blood

Systemic Examination
Vagina Examination
- Bleeding
- Discharge
- Cervical motion tenderness
- Uterine Size or Contour

Laboratory Test

CBC (limited clinical utility)

BMP / CMP
UA / Urine culture
Lactic acid
LFT / Amylase / Lipase
CE / Troponin
HCG (quant / qual)
Stool Culture

Radiographic Test
Plain abdominal radiographs or
abdominal series has several
limitations and is subject to reader
interpretation.
CT scan in conjunction with
ultrasound is superior in identifying
any abnormality seen on plain film.

Evaluation
History in Patients with Acute Abdominal pain
Question

Potential Responses and Indications

Where is the pain?

See Fig 1

Where is the pain like?

Acute waves of sharp constricting pain that take the

breath away (renal or biliary colic)
Waves of dull pain with vomiting (intestinal
obstruction)
Colicky pain that becomes steady (appendicitis,
strangulating
intestinal
obstruction,
mesentric
ischemia)
Sharp, constant pain, worsened by movement
(peritonitis)
Tearingpain (dissecting aneurysm)
Dull ache (appendicitis, diverticulitis, pyelonephritis)

Have you had it before?

Yes suggests recurrent problems such as ulcer

disease, gallstone colic, diverticulitis, or mittelschmerz

Was the onset sudden?

Sudden : like a light switching on (perforated ulcer,

renal stone, ruptured ectopic pregnancy, torsion of
ovary or testis, some ruptured aneurysms)
Less sudden : most other causes
Severe

pain

(perforated

viscus,

kidney

stone,

Evaluation
History in Patients with Acute Abdominal pain
Question

Potential Responses and Indications

Right scapula (gallbladder pain)

Does the pain travel to any Left shoulder region (ruptured spleen, pancreatitis)
other part of the body?
Pubis or vagina (renal pain)
Back (ruptured aortic aneurysm)
What relieves the pain?

Antacids (peptic ulcer disease)

Lying as quietly as possible (peritonitis)

Vomiting precedes pain and is followed by diarrhea

(gastroenteritis)
Delayed vomiting, absent bowel movement and
What other symptoms occur flatus (acute intestinal obstruction; the delay
with the pain?
increases with a lower site of obstruction)
Severe vomiting precedes intense epigastric, left
chest, or shoulder pain (emetic perforation of the
intra-abdominal esophagus)

PERITONITIS

Acute Peritonitis
Is an inflammation of the peritoneum
May localized or diffuse in location,
acute or chronic in natural history,
infectious or aseptic in pathogenesis.
Acute peritonitis is associated with
decrease intestinal and motor
activitydistention of the intestinal
lumen with gas and fluid

Etiology and Pathophysiology

Medical procedures, such as peritoneal dialysis.
Peritoneal dialysis uses tubes (catheters) to remove waste products
from your blood when your kidneys can no longer adequately do so.
An infection may occur during peritoneal dialysis due to unclean
surroundings, poor hygiene or contaminated equipment.
A ruptured appendix, stomach ulcer or perforated
colon. Any of these conditions can allow bacteria to get into the
peritoneum through a hole in your gastrointestinal tract.
Pancreatitis. Inflammation of your pancreas (pancreatitis)
complicated by infection may lead to peritonitis if the bacteria spread
outside the pancreas.
Diverticulitis. Infection of small, bulging pouches in your
digestive tract (diverticulitis) may cause peritonitis if one of the
pouches ruptures, spilling intestinal waste into your abdomen.
Trauma. Injury or trauma may cause peritonitis by allowing
bacteria or chemicals from other parts of your body to enter the
peritoneum.

Etiology of Secondary
Peritonitis
Perforations or leaking of
other organs :
Pancreaspancreatitis
Gall bladdercholecystitis
Urinary bladdertrauma,
rupture
Liverbile leak after biopsy
Fallopian tubessalpingitis
Bleeding into the peritoneal
cavity
Disruption of integrity of
peritoneal cavity :
Trauma
Continuous ambulatory
peritoneal dialysis (indwelling
catheter)
Intraperitoneal
chemotherapy
Perinephric abscess
Iatrogenicpostoperative,

Perforations of bowel :
Trauma, blunt or
penetrating
Inflammation
Appendicitis
Diverticulitis
Peptic ulcer disease
Inflammatory bowel
disease
Iatrogenic
Endoscopic perforation
Anastomotic leaks
Catheter perforation
Vascular
Embolus
Ischemia
Obstructions
Adhesions
Strangulated hernias
Volvulus
Intussusception
Neoplasms
Ingested foreign body,

Risk Factors
The following factors may increase the risk for primary peritonitis:
Liver disease (cirrhosis)
Fluid in the abdomen
Weakened immune system
Pelvic inflammatory disease
Risk factors for secondary peritonitis include:
Appendicitis (inflammation of the appendix)
Stomach ulcers
Torn or twisted intestine
Pancreatitis
Inflammatory bowel disease, such as Crohn's disease or ulcerative
colitis
Injury caused by an operation
Peritoneal dialysis
Trauma

Etiology
Infectious agent
Penetrating wound
Foreign object that is/becomes
infected

Signs and Symptoms

The signs and symptoms of peritonitis include:
Swelling and tenderness in the abdomen
with pain ranging from dull aches to severe,
sharp pain
Fever and chills
Loss of appetite
Thirst
Nausea and vomiting
Limited urine output
Inability to pass gas or stool

Pathophysiology

Tests and Diagnosis

Peritoneal fluid analysis. Using a thin needle, your doctor
may take a sample of the fluid in your peritoneum (paracentesis). If
you have peritonitis, examination of this fluid may show an increased
white blood cell count, which typically indicates an infection or
inflammation. A culture of the fluid may also reveal the presence of
bacteria.
Blood tests. A sample of your blood may be drawn and sent
to a lab to check for a high white blood cell count. A blood culture
also may be performed to determine if there are bacteria in your
blood.
Imaging tests. Your doctor may want to use an X-ray to
check for holes or other perforations in your gastrointestinal tract.
Ultrasound may also be used. In some cases, your doctor may use a
computerized tomography (CT) scan instead of an X-ray.

Treatment
Antibiotics. You'll likely be given a course of
antibiotic medication to fight the infection and prevent it
from spreading. The type and duration of your antibiotic
therapy depend on the severity of your condition and the
kind of peritonitis you have.
Surgery. Surgical treatment is often necessary to
remove infected tissue, treat the underlying cause of the
infection and prevent the infection from spreading.
Other treatments. Depending on your signs and
symptoms, your treatment while in the hospital may include
pain medications, rehydration by intravenous (IV) fluids,
supplemental oxygen and, in some cases, a blood
transfusion.

Complications
ARDS
Kidney failure
Liver failure
Disseminated intravascular coagulation

Prognosis
With treatment, patients usually do well. Without treatment,

the outcome is usually poor.

Peritonitis can be life threatening and may cause a number of

different complications. Complications depend on the specific

type of peritonitis.

Mortality rates are <10% for uncomplicated peritonitis

associated with a perforated ulcer or ruptured appendix or

diverticulum in an otherwise healthy person. Mortality
rates of 40% have been reported for elderly people, those
with underlying illnesses, and when peritonitis has been
present for >48 h.

APPENDICITIS
Acute appendicitis: is an
inflammatory disease of the wall
of the vermiform appendix that
leads to trasnmural inflammation
and perforation and peritonitis

Appendicitis
Appendicitis is inflammation of the appendix.
Appendicitis is a painful swelling and infection of the
appendix.
Epidemiology
Appendicitis occurs in 7% of the US population, with
an incidence of 1.1 cases per 1000 people per year.
Some familial predisposition exists.
The incidence of appendicitis is approximately 1.4
times greater in men than in women. Anyone can get
appendicitis, but it is more common among people 10
to 30 years old.
Males and females are equally affected, except
between puberty and age 25, when males
predominate in a 3:2 ratio.

Pathogenesis
Acute appendicitis relates to obstruction of its
orifice, with secondary distention of the
lumen and bacterial invasion of the wall.
Mechanisms obstruction by fecaliths or solid
fecal material in the cecum is found in one
third of cases.
Tumors, parasites (enterobius vermicularis)
Foreign bodies
Lymphoid hyperplasia due to bacterial or viral
infection (salmonella or measles)
E.coli sterptococcus

Pathology
The appendix is congested, tense and
covered by a fibrionus exudate. Its lumen
often contains purulent material. Fecalith
may be evident.
Microscopically
Early cases mucuocal micro abscesses and a
purulent exudate in the lumen infections
progresses the entire wall become in filtrated
with neutrophils which eventually reach the
serosa perforation of the wall release he
luminal contents into the pritoneal cavity

Pathogenesis
Obstruction
Mucous cant be drained
Edema
Increase intraluminal pressure
Bacterial diapedesis
Mucosal Ulceration
Epigastric pain
Appendicitis acute focal

Pathogenesis
Mucous >>
Intraluminal pressure >>
Bacterial invasion of the
appendix wall
Vein obstruction
Peritonitis
Pain in RLQ
Appendicitis supurative acute

Pathogenesis
Bad arterial flow
Gangren
Appendicitic gangrenosa
Infark
Appendicitis perforation

Gangrenous Apendicitis

http://www.aafp.org/afp/991101ap/2027.htm

Clinical features
Typically manifested as epigastric or
periumbilical cramping pain, but the pain
may be diffuse or initially restricted to the
right lower quadrant.
Nausea, vomiting
Low grade fever and moderate
leukpocytosis.
The pain shift to the right lower quadrant,
where point tenderness is the rule.

SYMPTOMS OF APPENDICITIS IN
CHILDREN
Rupture appendix a child will feel pain
in some hours
A small child can not show the pain
location correctly
Vomiting with or without nausea
Fever 38,9 0C
Do not want to eat
Crying

CLINICAL PRESENTATION
The classic history of anorexia and periumbilical pain
followed by nausea, right lower quadrant (RLQ) pain,
and vomiting occurs in only 50% of cases.
Diarrhea or constipation is noted in as many as 18% of
patients and should not be used to discard the possibility
of appendicitis.
The most common symptom of appendicitis isabdominal
pain.
Typically, symptoms begin as periumbilical or
epigastric pain migrating to the right lower
quadrant (RLQ) of the abdomen.
Patients usually lie down, flex their hips, and draw
their knees up to reduce movements and to avoid
worsening their pain.
Usually, a fever is not present at this stage.

 The duration of symptoms is less than 48 hours in

approximately 80% of adults but tends to be longer in
elderly persons and in those with perforation.
Approximately 2% of patients report duration of pain in excess
of 2 weeks.
A history of similar pain is reported in as many as 23% of
cases, but this history of similar pain, in and of itself, should
not be used to rule out the possibility of appendicitis.
In addition to recording the history of the abdominal pain,
obtain a complete summary of the recent personal history
surrounding gastroenterologic, genitourinary, and pneumologic
conditions, as well as consider gynecologic history in female
patients.
An inflamed appendix near the urinary bladder or
ureter can cause irritative voiding symptoms and
hematuria or pyuria.
Cystitis in male patients is rare in the absence of
instrumentation.
Consider the possibility of an inflamed pelvic appendix in
male patients with apparent cystitis.
Also consider the possibility of appendicitis in pediatric or adult
patients who present with acute urinary retention

Examination
CT-scan
Barium Enema
Laparoskopi

PHYSICAL EXAMINATION
It is important to remember that the position of the
appendix is variable.
Of 100 patients undergoing 3-dimensional (3-D)
multidetector computed tomography (MDCT) scanning, the
base of the appendix was located at the McBurney
point in only 4% of patients; in 36%, the base was
within 3 cm of the point; in 28%, it was 3-5 cm from that
point; and, in 36% of patients, the base of the appendix
was more than 5 cm from the McBurney point.
The most specific physical findings in appendicitis are
rebound tenderness, pain on percussion, rigidity,
and guarding.
Rarely, left lower quadrant (LLQ) tenderness has been
the major manifestation in patients with situs inversus or in
patients with a lengthy appendix that extends into the LLQ.
Tenderness on palpation in the RLQ over the
McBurney point is the most important sign in these
patients.

Treatment
Surgical removal
IV fluids and antibiotics
Treatment of acute appendicitis is open or laparoscopic
appendectomy; because treatment delay increases mortality, a
negative appendectomy rate of 15% is considered acceptable.
The surgeon can usually remove the appendix even if
perforated.
A contraindication to appendectomy is inflammatory bowel
disease involving the cecum. However, in cases of terminal
ileitis and a normal cecum, the appendix should be removed.
Appendectomy should be preceded by IV antibiotics. Thirdgeneration cephalosporins are preferred.
For nonperforated appendicitis, no further antibiotics are
required. If the appendix is perforated, antibiotics should be
continued until the patient's temperature and WBC count have
normalized or continued for a fixed course, according to the
surgeon's preference.
If surgery is impossible, antibioticsalthough not curative
markedly improve the survival rate.

Treatment usually consists of

appendectomy (surgical
removal of the appendix).
How is appendicitis
treated?
Once a diagnosis of
appendicitis is made, an
appendectomy usually is
performed (surgical removal of
the appendix).
Antibiotics almost always are
begun prior to surgery and as
soon as appendicitis is
suspected. On the next several
slides we'll take a look at an
actual step-by-step
laparoscopic appendectomy
procedure being performed.

Step 1 of 8: The appendix is

located in the lower abdomen.
Appendectomy: Step 1 of 8.
This is a normal appendix in a
female patient found to have
an infection of the
reproductive organs. Since the
appendix serves no useful
function, it will be removed to
save her from getting
appendicitis in the future.

Step 2 of 8: The mesentery is divided

from the appendix.

Appendectomy: Step 2 of 8.
The next step is to free up the
appendix down to where it is
attached to the large bowel.
This requires dividing the
mesentery which contains the
blood vessels that supply the
appendix. Bipolar forceps apply
an electric current which seals
the blood vessels and prevents
bleeding.

Step 3 of 8: Scissors are used to free the

appendix
from its mesenteric attachment to the
abdomen and colon.
Appendectomy: Step 3 of 8.
Next, scissors are used to divide
the mesentery. Alternating
application of the bipolar
electrocautery forceps and
scissors allow complete
mobilization of the appendix
down to its base.

Step 4 of 8: The base of the

appendix is tied off using a
pre-tied suture.
Appendectomy: Step 4 of 8.
Now the base of the appendix
is tied off using a pre-tied
suture which is now being
positioned.

Step 5 of 8: The suture is now

tightened using a
fisherman's knot, which cannot loosen
on its own.
Appendectomy: Step 5 of 8.
The suture has now been
tightened and appears secure.
The knot is a fisherman's knot,
which can be tightened but will
not loosen on its own.

Step 6 of 8: The suture is cut

using scissors.
Appendectomy: Step 6
of 8.
As shown in this picture,
the suture is now cut with
the scissors.

Step 7 of 8: The appendix is

cut free and ready to be
removed.
Appendectomy: Step 7
of 8.
Using the same scissors,
the appendix is cut free
and ready to be removed.

Step 8 of 8: The operation is

complete and inspected.
Appendectomy: Step 8 of
8.
The operation is complete,
and the area is inspected
one final time to make sure
there is no bleeding.

An example of an infected appendix that has been

removed
(left) and the resulting incisional scar from an
appendectomy (right).

The complications of the

appendicitis are principally
related to perforation

Occurs in one third of children and young adults.

Periappendiceal abscesses are common, although
abscesses may develop anywhere in the abdominal
cavity
Fistulous tract may appear between the perforated
appendix and adjacent structure, including the small
and large bowel, bladder, vagina or abdominal wall.
Pylephlebitis and secondary hepatic abscesses may
occurs, because venous blood from the appendix
drains into the superior mesenteric vein
Diffuse peritonitis and septicemia are dangerous
sequelae
Wound infection most common complication of
acute appendicitis after surgry

Prognosis
Without surgery or antibiotics,
mortality is > 50%.
With early surgery, the mortality rate
is < 1%, and convalescence is
normally rapid and complete.
With complications (rupture and
development of an abscess or
peritonitis), the prognosis is worse:.

MECHANICAL INTESTINAL
OBSTRUCTION

Mechanical intestinal
obstruction
Intestinal obstruction is a restriction to
the normal passage of the intestinal
contents.
It may be divided into 2 main groups
Paralytic
Mechanical ileus

Speed of onset: acute, chronic, acute on chronic

Site: high or low
Nature: simple versus strangulating, and
aetilogy

Speed of onset
In acute obstruction: the symptoms
are insidious and slowly progressive
A chronic obstruction :may develop
acute symptoms as the obstruction
suddenly become complete

Site
Is classifies into high or low, which is
roughly synonymous with small or
large bowel obstruction

nature
Is divided into simple or
strangulated:
Simple obstruction-> occurs when the
bowel is occluded without damage to its
blood supply
Strangulating obstruction-> when the
blood supply of the involved segment of
intestine is cut off

Aetiology
Cause in the lumen : faecal impaction, gallstoneileus,
food bolus, parasites, intussusception
In the wall: congenital atresia, crohns disease, tumours,
divertivculitis of the colon
Outside the wall: strangulated hernia, volvulus and
obstruction due to adhesions or bands.
Neonatal : congenital atresia and stenosis, imperforate
anus, volvulus neonatorum, hirschsprungs disease,
strangulated hernia and meconium ileus
Infants : intussusception, hirschsprungs disease,
strangulated hernia and obstruction due to meckels
diverticulum
Young adults and middle age: atrangulated hernia,
adhesions and bands, crohns disease
The elderly : strangulated hernia, carcinoma of the bowel,
colonic diverticulitis, impacted faeces

Pathology
The bowel is obstructed by a simple
occlusion the intestine distal to the
obstruction rapidly empties and become
collapsed above the obstruction become
dilated (partly with gas and fluid poured out
by the intestinal wall together with gastric
biliary and pancreatic secretion increased
peristalsis in an attempt to overcome the
obstruction intestinal colic
As the bowel distends intestinal wall
becomes impaired and in extreme cases,
there may be mucocal ulceration and
eventually perforation

Pathology
In strangulating obstruction
The integrity of the mucosal barrier is lost
as ischemia progresses so bacteria and
theirs toxins can no longer be contained
within the lumen. transudation of
organisms into the peritoneal cavity rapidly
take place, with secondary peritonitis.
Unrelieved strangulation is followed by
gangrene of the ischemic bowel with
perforation

Clinical features
The four cardinal symptoms of intestinal obstruction
are the following
Colicky abdominal pain
Usually the first symptom of the intestinal obstruction and is
colicky in nature
In small bowel obstruction periumbilical
In distal colonic obstructionsuprapubic

Distension
Is marked in chronic large bowel obstruction and also in
volvulus of the sigmoid colon

Absolute constipation large bowel obstruction

Vomiting
Small bowel obstruction
Faecuent vomiting obstructed small intestine
True vomiting faeces gastrocolic fistula

ETIOLOGY
Mechanical obstructions

Non-mechanical obstruction

The bowel is physically

blocked and its contents
can not pass the point of
the obstruction.
This happens when the
bowel twists on itself
(volvulus) or as the result
of hernias, impacted
feces, abnormal tissue
growth, or the presence
of foreign bodies in the
intestines.

Called ileus or paralytic

ileus, occurs because
peristalsis stops.
Peristalsis is the rhythmic
contraction that moves
material through the
bowel.
Ileus is most often
associated with an
infection of the peritoneum
(the membrane lining the
abdomen). It is one of the
major causes of bowel
obstruction in infants and
children.

CAUSES OF INTESTINAL
OBSTRUCTION
Location

Causes

Colon

Tumors (usually in left colon), diverticulitis

(usually in sigmoid), volvulus of sigmoid
or cecum, fecal impaction, Hirschsprung's
disease

Duodenum
(Adults)

Cancer of the duodenum or head of

pancreas, ulcer disease

Duodenum
(Neonates)
Jejunum and ileum
(Adults)

Atresia, volvulus, bands, annular pancreas

Jejunum and Ileum

(Neonates)

Hernias, adhesions (common), tumors,

foreign body, Meckel's diverticulum,
Crohn's disease (uncommon), Ascaris
infestation, midgut volvulus,
intussusception by tumor (rare)
Meconium ileus, volvulus of a malrotated
gut, atresia, intussusception

SYMPTOMS
Small bowel

Abdominal cramps centered around

the umbilicus or in the epigastrium,
Vomiting
Obstipation (in patients with complete
obstruction)
Diarrhea (partial obstruction)
Severe, steady pain suggests that
strangulation has occurred. In the
absence of strangulation, the
abdomen is not tender
Hyperactive, high-pitched peristalsis
with rushes coinciding with cramps is
typical
Dilated loops of bowel are palpable
sometimes.
With infarction, the abdomen
becomes tender
Auscultation reveals a silent abdomen
or minimal peristalsis
Shock and oliguria (serious signs that
indicate either late simple obstruction
or strangulation)

Large bowel
Increasing constipation
leads to obstipation and
abdominal distention.
Vomiting may occur
(usually several hours
after onset of other
symptoms) but is not
common
Lower abdominal cramps
unproductive of feces
occur
No tenderness
The rectum is usually
empty.
A mass corresponding to
the site of an obstructing
tumor may be palpable.

Clinical examination

Vomiting has been copious

Colic
Pulse usually elevated
No fever
A raised temperature and a very
rapid pulse strangulation
Abdomen distended

Clinical examintaion
Inscpection
The presence of a strangulated external
hernia, which may require a careful search in
the case of the small strangulated femoral
hernia in a very obese and distended patient
The presence of an abdominal scar
Palpitation
Revelas generralized abdominal tenderness
a mass may be present
Bowel sound
Accentuated and tinkling

LAB EXAMINATIONS

X-rays
CT Scan
MRI
USG
Sigmoidoscope
CBC (Complete Blood Count)
Electrolytes
BUN (Blood Urea Nitrogen)
Urinalysis
Laboratory tests to exclude biliary or hepatic
disease
Phosphate level
Creatine kinase level
Liver panels

TREATMENTS
Non-Farmacologic :

Nasogastric tube
Rectal tube
Intravenous fluids
Repair the hernia to correct the
obstruction
Surgery complete obstructions

Farmacologic :
Antibiotics : pre and post operation

ILEUS
This abdominal x-ray shows a
stomach filled with fluid and a swollen
(distended) small bowel, caused by a
blockage (obstruction) in the
intestines. A solution containing a dye
(barium) that is visible on x-rays was
swallowed by the patient (upper GI
series).

Mechanical Ileus

Closed loop obstruction

Increasing distension of a loop of
bowel due to a combination of
complete obstruction distally and a
valve-like mechanism proximally
allowing the bowel to fill, but
preventing reflux back.
Most commonly seen with a left sided
colonic obstruction

 Closed loop obstruction is a specific type of

obstruction in which two points along the course of a
bowel are obstructed at a single location thus
forming a closed loop.
Usually this is due to adhesions, a twist of the
mesentery or internal herniation.
In the large bowel it is known as a volvulus.
In the small bowel it is simply known as small bowel
closed loop obstruction.
Especially in the small bowel the risk of strangulation
and bowel infarction is high with a mortality rate of
10-35%.

Adhesive obstruction

Volvulus
A twisting of a loop of the bowel
around its mesenteric axis, which
result in a combination of obstruction
together with occlusion of the main
vessels at the base of the involved
mesentery
Most commonly: sigmoid , caecum
and small intestine

Aetiology
An abnormally mobile loop of
intestine
An abnormally loaded loop
A loop fixed at its apex by adhesions
A loop of bowel with a narrow
mesenteric atachment

Sigmoid volvulus
Occurs usually in elderly and
Constipated patient
4 time more common in men than in
women
More common in Russia, Scandinavia
and central Africa
The loop of sigmoid colon usually twist
anticlockwise, from one half to three
turns.

Clinical features
Sudden onset of colicky pain with
characteristic gross and rapid dilatation
of the sigmoid loop
A plain X-ray enormously dilated oval
gas shadow on the left side bent inner
tube sign
Caecum is usually visible and dilated in
the right lower quadrant, distinguishing
it radiologically from caecal volvulus

treatment
Soft rectal tube
Laparotomy

Caecal volvulus
Associated with a congenital malrotation.
There is an acute pain in the right iliaca
focca with rapid abdominal distension
X-ray grossly dilated caecum, which is
often ectopically placed and its
frequently located in the left upper
quadrant of the abdomen
Treatment laparotomy, right
hemicolectomy

Small intestine volvulus in

adults
This may occrus where a loop of the
small intestine is fixed at its apex by
adhesions or by fibrous remnant of
the vitellointestinal duct
Treatment: early operations,

Neonatal intestinal
obstruction

Intestinal atresia
Volvulus nenatorum
Meconimun leus
Necratizing enteroolitis
Hirshcprungs disease
Anorectal atersias

Intestinal atresia
May be septum, complete or partial
or a complete gap, which may be
associated with a corresponding
defect In the mesentery.
Multiple segments may be involved
Treatment resection of the stricture
and anastomosis
High mortality

Intussusception
Prolapsed of one portion of the
intestine into the lumen of the
immediately adjoining bowel
The prolapsing or invaginating bowel
is called intussusception

Intussusception
Ileocolic the ileo ileal Intussusception
extends through the ileocaecal valve into
colon. 75%
Ielo-ileal the ileum is invaginated into the
adjacent ileum
Ileocaecal the ileocaecal valve is the apex
of the Intussusception
Colocolic the colon invaginating into an
adjacent colon (usually due to a protuding
tumours of the bowel wall)

Aetiology
90% occurs in infants or young children,
where there is usually no obvious cause.
A polyp, carnocoma , intestinal lymphoma
or an inverted Meckels diverticulum msay
form the apex of the Intussusception
Intussusception has its bloof supply cut off
by direct pressure of the outer layer and by
strectging of its suppling mesentery so that,
if untreates gangrene will occurs

Clinical features
Commonly aged between 3 and 12 months
Boys are affected twice as often as girls
Paroxysms of abdominal colic typified by
screaming and pallor
Vomiting and usually the passage of blood and or
slime perrectum givinng the appearance of red
currant jelly
Child pale and anxious and typical attack of
streaming
Palpitationsausage shaped tumours anywhere

Treatment in the infant

No operative
Barium is run per rectum
X-ray confirmation of the diagnosis is established
If the Intussusception is recent, it may be
completely reduced hydrostatically by the
pressure of the column of barium and this is
confirmed radiologically

Operative
Intussusception is reduced at laprotomy by
squeesing its apex backward out the containing
bowel.

ILEUS PARALITIK

 Ileus occurs from hypomotility of

the gastrointestinal tract in the
absence of mechanical bowel
obstruction.
Presumably, the muscle of the bowel
wall is transiently impaired and fails
to transport intestinal contents.
This lack of coordinated propulsive
action leads to the accumulation of
gas and fluids within the bowel.

Postoperative
ileus after an open
cholecystectomy.

Ogilvie pseudoobstruction in a
septic elderly
patient.
Note the
massive
dilatation of the
colon, especially
the right colon
and cecum.

PATOPHYSIOLOGY
According to some hypotheses,
postoperative ileus is mediated via
activation of inhibitory spinal reflex
arcs.
Anatomically, 3 distinct reflexes are
involved: ultrashort reflexes confined to the
bowel wall, short reflexes involving
prevertebral ganglia, and long reflexes
involving the spinal cord.
The surgical stress response leads to
systemic generation of endocrine and
inflammatory mediators that also promote
the development of ileus.

 Rat models have shown that laparotomy,

eventration, and bowel compression lead
to increased numbers of macrophages,
monocytes, dendritic cells, T cells,
natural killer cells, and mast cells, as
demonstrated by immunohistochemistry .
Macrophages residing in the muscularis
externa and mast cells are probably the key
players in this inflammatory cascade
Calcitonin generelated peptide, nitric oxide,
vasoactive intestinal peptide, and substance P
function as inhibitory neurotransmitters in the
bowel nervous system.

EPIDEMIOLOGY
Postoperative ileus occurs in
approximately 50% of patients who
undergo major abdominal surgery

CLININAL PRESENTATION
Patients with ileus typically have
vague, mild abdominal pain and
bloating.
They may report nausea, vomiting,
and poor appetite.
Abdominal cramping is usually not
present.
Patients may or may not continue to
pass flatus and stool.

PHYSICAL EXAMINATION
The abdomen may be distended and
tympanic, depending on the degree of
abdominal and bowel distention, and may
be tender.
A distinguishing feature is absent or
hypoactive bowel sounds, in contrast
to the high-pitched sound of obstruction.
The silent abdomen of ileus reveals no
discernible peristalsis or succussion
splash.

CAUSES
Most cases of ileus occur after intraabdominal operations.
Normal resumption of bowel activity after
abdominal surgery follows a predictable
pattern: the small bowel typically regains
function within hours; the stomach regains
activity in 1-2 days; and the colon regains
activity in 3-5 days.
Serial abdominal radiographs mapping the
distribution of radiopaque markers have
shown that the colonic gradient for resolution
of postoperative ileus is proximal to distal.

 Other causes of adynamic ileus are as

follows:
Sepsis
Drugs (eg, opioids, antacids, warfarin,
amitriptyline, chlorpromazine)
Metabolic (eg, low potassium, magnesium, or
sodium levels;anemia; hyposmolality)
Myocardial infarction
Pneumonia
Trauma (eg, fractured ribs, fractured spine)
Biliary colicand renal colic
Head injury and neurosurgical procedures
Intra-abdominal inflammation andperitonitis
Retroperitoneal hematomas

DIFFERENTIAL DIAGNOSE
The common differentials for ileus
are pseudo-obstruction, also
referred to as Ogilvie syndrome,
and mechanical bowel
obstruction.

Mechanical
bowel
obstruction
due to a left
colon
carcinoma.
Note the
paucity of
bowel gas
throughout

Contrast study,
in the same
patient as in
Media File 3,
showing the
classic "applecore" lesion of
colon
carcinoma.

TESTS
Laboratory studies and blood work should
focus on evaluations for infectious,
electrolytic, and metabolic
derangements.
On plain abdominal radiographs, ileus
appears as copious gas dilatation of the
small intestine and colon.
With enteroclysis, the contrast medium in
patients with paralytic ileus should reach the
cecum within 4 hours; if the contrast
medium remains stationary for longer than 4
hours, mechanical obstruction is suggested

TREATMENT
Patients should receive intravenous
hydration.
For patients with vomiting and distention,
use of a nasogastric tube provides
symptomatic relief; however, no studies in
the literature support the use of nasogastric
tubes to facilitate resolution of ileus.
For patients with protracted ileus,
mechanical obstruction must be excluded
with contrast studies.

 In one study, the amount of morphine

administered directly correlated with the
time elapsed before the return of bowel
sounds and the passage of flatus and
stool.
The use of postoperative narcotics can be
diminished by supplementation with
nonsteroidal anti-inflammatory drugs
(NSAIDs).
In addition to permitting lower narcotic doses
by providing pain relief, NSAIDS may improve
ileus by reducing local inflammation.

 The clinician must assess the

overall status of the patient and
evaluate for adequate oral
intake and good bowel function.
A patient's report of flatus, bowel
sounds, or stool passage may prove
misleading; therefore, clinicians must
not rely solely on self-reporting.

The presence of ileus does not preclude enteral feeding.

Postpyloric feeding into the small bowel can be cautiously performed.
Start feeds at one-quarter or one-half strength at a slow rate and gradually advance.
Having patients chew gum has been advocated as a means of promoting recovery
from postoperative ileus.
Chewing gum may constitute a form of sham feeding that stimulates gastrointestinal
motility.

DIET

 Meta-analyses have shown that gum

chewing can reduce the time to
first flatus and passage of feces,
and marginally decrease the length
of hospital stay after intestinal
surgery.

ACTIVITY
Conventional wisdom and wide practice
foster the notion that ambulation
stimulates bowel function and
improves postoperative ileus, although
this has not been shown in the literature.
Postoperative ambulation remains
beneficial in preventing the formation of
atelectasis,deep vein thrombosis, and
pneumonia but has no role in treating
ileus.

 Studies have shown that combinations of

thoracic epidurals containing
bupivacaine alone or in combination with
opioids improve postoperative ileus.
Continuous intravenous administration of
lidocaine during and after abdominal surgery
may decrease the duration of postoperative
ileus.
Peripherally selective opioid antagonists are
an option for the treatment of postoperative
ileus.
Methylnaltrexone (Relistor) and alvimopan
(Entereg) are approved by the Food and Drug
Administration

 Erythromycin, a motilin receptor

agonist, has been used for postoperative
gastric paresis but has not been shown
to be beneficial for ileus.
Metoclopramide (Reglan), a
dopaminergic antagonist, has antiemetic
and prokinetic activities, but data have
shown that the drug may actually
worsen ileus.

Slpingitis

Summary
Salpingitis is inflammation of the fallopian
tubes, triggered by bacterial infection.
This condition is a common cause of female
infertility because the inflammation can
damage the fallopian tubes.
Salpingitis is sometimes called pelvic
inflammatory disease (PID).
Salpingitis may have no symptoms, but
signs may include abnormal vaginal
discharge, spotting between periods,
painful periods, pain during ovulation or sex
and lower back pain.

 The fallopian tubes extend from the uterus, one on each side, and
both open near an ovary. During ovulation, the released egg (ovum)
enters a fallopian tube and is swept along by tiny hairs towards the
uterus.
Salpingitis is inflammation of the fallopian tubes. Almost all cases
are caused by bacterial infection, including sexually transmitted
diseases such as gonorrhoea and chlamydia. The inflammation
prompts extra fluid secretion or even pus to collect inside the
fallopian tube. Infection of one tube normally leads to infection of
the other, since the bacteria migrates via the nearby lymph vessels.
Salpingitis is one of the most common causes of female infertility.
Without prompt treatment, the infection may permanently damage
the fallopian tube so that the eggs released each menstrual cycle
can't meet up with sperm. Treatment options include antibiotics.
Salpingitis is sometimes called pelvic inflammatory disease (PID).
This umbrella term includes other infections of the female
reproductive system, including the uterus and ovaries.

Symptoms
In milder cases, salpingitis may have no symptoms. This
means the fallopian tubes may become damaged without
the woman even realising she has an infection. The
symptoms of salpingitis may include:
Abnormal vaginal discharge, such as unusual colour or smell
Spotting between periods
Dysmenorrhoea (painful periods)
Pain during ovulation
Uncomfortable or painful sexual intercourse
Fever
Abdominal pain on both sides
Lower back pain
Frequent urination
Nausea and vomiting
The symptoms usually appear after the menstrual period.

Acute and chronic

salpingitis
Salpingitis is usually categorised as either
acute or chronic. In acute salpingitis, the
fallopian tubes become red and swollen, and
secrete extra fluid so that the inner walls of
the tubes often stick together. The tubes may
also stick to nearby structures such as the
intestines. Sometimes, a fallopian tube may
fill and bloat with pus. In rare cases, the tube
ruptures and causes a dangerous infection of
the abdominal cavity (peritonitis). Chronic
salpingitis usually follows an acute attack. The
infection is milder, longer lasting and may not
produce many noticeable symptoms.

Most cases are caused

by bacteria
In nine out of 10 cases of salpingitis,
bacteria are the cause. Some of the most
common bacteria responsible for
salpingitis include:
Chlamydia
Gonococcus (which causes gonorrhoea)
Mycoplasma
Staphylococcus
Streptococcus.

Access to the
reproductive system
The bacteria must gain access to the
woman's reproductive system for infection
to take place. The bacteria can be
introduced in a number of ways, including:
Sexual intercourse
Insertion of an IUD (intra-uterine device)
Miscarriage
Abortion
Childbirth
Appendicitis.

RISK FACTORS
Male sexual partner with gonorrhea
or chlamydia
Multiple sexual partners
Past history of any sexually
transmitted disease
Past history of PID
Recent insertion of an IUD
Sexual activity during adolescence

Complications of
salpingitis

Without treatment, salpingitis can cause a range of complications,

including:
Further infection - the infection may spread to nearby
structures, such as the ovaries or uterus.
Infection of sex partners - the woman's partner or partners
may contract the bacteria and become infected too.
Tubo-ovarian abscess - about 15 per cent of women with
salpingitis develop an abscess, which requires hospitalisation.
Ectopic pregnancy - a blocked fallopian tube prevents the
fertilised egg from entering the uterus. The embryo then starts
growing inside the confined space of the fallopian tube. The risk of
ectopic pregnancy for a woman with prior salpingitis or other form
of pelvic inflammatory disease (PID) is around one in 20.
Infertility - the fallopian tube may become deformed or scarred
to such an extent that the egg and sperm are unable to meet.
After one bout of salpingitis or other PID, a woman's risk of
infertility is about 15 per cent. This rises to 50 per cent after three
bouts.

Diagnosis methods
Diagnosing salpingitis involves a number of tests,
including:
General examination - to check for localised
tenderness and enlarged lymph glands.
Pelvic examination - to check for tenderness and
discharge.
Blood tests - to check the white blood cell count
and other factors that indicate infection.
Mucus swab - a smear is taken to be cultured and
examined in a laboratory so that the type of
bacteria can be identified.
Laparoscopy - in some cases, the fallopian tubes
may need to be viewed by a slender instrument
inserted through abdominal incisions.

Treatment options
Treatment depends on the severity of
the condition, but may include:
Antibiotics - to kill the infection, which
is successful in around 85 percent of
cases.
Hospitalisation - including intravenous
administration of antibiotics.
Surgery - if the condition resists drug
treatment.

PREVENTION
Preventive measures include:
Get prompt treatment for sexually transmitted
diseases.
Practice safer sex behaviors. The only absolute
way to prevent an STD is to not have sex
(abstinence). Having a sexual relationship with only
one person (monogamous) can reduce the risk.
Use a condom every time you have sex.
You can reduce the risk of PID by getting regular
STD screening exams. Couples can be tested for
STDs before starting to have sex. Testing can detect
STDs that may not be producing symptoms yet.
All sexually active women ages 20 - 25 and younger
should be screened each year for chlamydia and
gonorrhea. All women with new sexual partners or
multiple partners should also be screened.