ACUTE ABDOMEN

Presenter : Meeraashini and Nitthiya Shan

Supervisor: Dr Alif
DEFINITION
 Acute attack of abdominal pain
- occur suddenly or gradually over a period of time
- presents symptom complex suggestive of a disease
- possibly life threatening
- require immediate or early intervention

 Underlying causes can be divided according to etiologies

or anatomy:
Obstruction
Infection
Inflammation
Hemorrhage
Ischemia
HISTORY
 Age
 Type of pain

 Onset

 Associated symptoms

 Previous surgical history

 Other relevant history

(Family history/Social history/Diet History)
PAIN
 TYPE OF PAIN
VISCERAL PAIN •Abdominal viscera and the visceral peritoneum receive
sensory fibres via symphathetic chain from T5 through L3
•Usually interpreted as dull, cramping,poorly localized
PARIETAL PAIN •Derives sensory fibers fromsomatic nerves from T6
through L1
•Usually sharp, sudden and well localized pain
REFERRED PAIN • When pain is felt at different regions having the same
segmental innervation as site of lesion.
•Epigastric : innervations by T6-T8,
stomach,duodenum,pancreas,liver, biliary tree, and
associated pariteal peritoneum
•Peri-umbilical: innervations byT9-T10,small intestine,
appendix,upper ureter
• Hypogastric : innervation by T11-T12,colon,
bladder,lower ureter and uterus
HISTORY
 Site
 Onset
 sudden or gradual
 Previous similar pain
 Character

 Radiation

 Associated symptoms
 Anorexia, abdominal distension, vomiting, diarrhea, constipation,
altered bowel habits, constitutional symptoms
 Timing

 Exacerbating and alleviating factors

 Severity

 Others significant history

EXAMINATION

Inspection
- General well being, then go for systemic.

Palpation
-Start away from site of pain. Identify ssx of peritonism

Percussion & Auscultation

Complete with genitalia, hernia orrifices and rectal examination.
BASIC INVESTIGATION.
 ECG
 Blood test.
- FBC
-RP
- VBG + Lactate
- LFT
- AMYLASE
- COAG PROFILE
- CARDIAC ENZYMES
 UFEME/ URINE DIASTHASE

 IMAGING
- CXR (erect)
- AXR
- USG
- CT/CECT
 ACUTE PERFORATED
APPENDICITIS GASTRIC ULCER

ACUTE ACUTE
CHOLECYSTITIS PANCREATITIS

INTESTINAL
OBSTRUCTION
ACUTE APPENDICITIS
 Inflammation of appendix
 Most common cause of acute abdomen

 APPENDIX:
- blind muscular tube with
mucosal,sub-mucosal,
muscular and
serosa layers.

Possible location of appendix

 HISTORY (Classical features)
 Migratory pain
 Nausea & Vomitting
 Fever
 Anorexia
 Diarrhea/ Constipation

 PHYSCIAL EXAMINATION (signs to look for)

 Tender over RIF ( most at Mc Burney’s point)
 Rovsing sign:
- RIF pain elicited with deep palpation of LIF
 Rebound Tenderness:
- Pain elicited upon sudden release of deep palpation at RIF
 Psoas sign : RIF pain when Right hip flexed/hyperextended
 Obturator sign : RIF pain with internal rotation of a flexed
right hip.
 Signs of peritonism : Generalised tenderness, rigid abdomen.
ALVARADO SCORE
INVESTIGATION MANAGEMENT

 FBC (wbc)  NBM with IVD

 RP
maintenance
 UFEME
 IV antibiotics
 UPT
 Analgesics
 COAG PROF
 Prep for operation
 ERECT CXR - optimize blood
 AXR parameters
 Appendectomy (open or
 Advanced imaging if indicated laparascopic)
(USG/CT)
POST OP COMPLICATIONS
 Complications from appendectomy:
--- SSI
--- Intra abdominal abscess
--- Adhesive intestinal obstruction
--- Ileus
--- Fecal Fistula
APPENDICULAR MASS
 Conservative treatment for appendix mass: Ochsner Sherren regime
 Omentum wraps around inflamed appendix resulting in localised
inflammatory process (phlegmon)
 Inadvertent surgery is difficult and dangerous (hard to find
appendix)
 Careful recording of the patient’s condition noting (1) pulse rate, (2)
extent of the mass and (3) spread of abdominal pain
 Symptomatic treatment as well as antibiotics, do contrast enhanced
CT
 When mass has reduced in size, patient is stable, do surgery (less
inflammation: easier)
 Exceptions: very young or very old patients, or patients with
suspected appendicular abscess (drained radiologically), clinical
deterioration (evidence of peritonitis)
PEFORATED PEPTIC ULCER
o Focal defects or breaks in mucosal lining of stomach or
duodenum more than 5mm in diameter with depth to
submucosa layers
o Imbalance between gastroduodenal mucosal defense
and acid hypersecretion
o Common site: First part of duodenum or gastric antrum
particularly over lesser curve
RISK FACTOR

 Helicobactor Pylori infection

 Chronic NSAIDs usage
 Gastroesophageal reflux
 Old age
 Smoking
 Chronic alcohol ingestion
 Stress
ANATOMY OF
STOMACH
Peptic ulcers occur when there is an alteration in the balance
between acid production and mucosal protective mechanisms.
 There are two major etiologies of this imbalance:
 H. pylori infection and NSAID use.
 CLINICAL PRESENTATION
 Commonly over anterior ulcers of duodenum
 In the initial phase within 2 h of onset, epigastric pain,
tachycardia and cool extremities are characteristic.
 In the second phase (within 2 to 12 h), pain becomes
generalized and is worse on movement. Typical signs such as
abdominal rigidity and right lower quadrant tenderness (as a
result of fluid tracking along the right paracolic gutter) may be
seen.
 In the third phase (more than 12 h), abdominal distension,
pyrexia and hypotension with acute circulatory collapse may be
evident.
Investigation
 FBC- leukocytosis/ anemia –chronic/acute blood loss
 Urinalysis

 Serum amylase

 LFT & RP

 Pregnancy test

 CXR erect-air under diaphragm

 Ultrasound

 CT scan/ with oral contrast. Leak confirms diagnosis

Diagnosis
 Upright chest radiographs will show pneumoperitoneum
(“free air”) in 80–90% of the cases.
 Ultrasound is less sensitive for detecting free air but could be
used to identify other indirect findings of perforation such as
free fluid and decreased peristalsis.
 Computerized tomography (CT) scans are more sensitive for
detecting pneumoperitoneum than the other modalities but
should ideally be performed at least 6 h following the onset
of symptoms.
 The use of oral contrast medium with CT scanning to identify
the site of perforation and the presence of ongoing leakage.
. Upright chest x-ray shows free air in about
80% of patients
MANAGEMENT
Initial management and priorities
• Stabilize patient
• Fluid resuscitations and blood transfusions if indicated
• Adequate analgesics
• Strict intake and output monitoring
• NBM, ryles tube
• Start proton pump inhibitors
• Start broad spectrum antibiotics
• IV Cefoperazone 2g Stat and 1g BD
• IV Metronidazole 500mg STAT and TDS
• Definitive management
• Exploratory laparotomy, primary repair and abdominal washout
Acute perforations of the duodenum are estimated to occur in 2% to
10% of patients with ulcers

 Surgery almost always indicated

 Conservative management should considered in patients who do
not have :
– generalized peritonitis
– hemodynamic instability
– free peritoneal perforation on a Gastrografin upper
gastrointestinal study
 Conservative management “Taylor method” consists of
nasogastric suction, intravenous drip, antibiotics and
repeated clinical assessment.

 A gastrograffin dye study is essential to confirm absence of

leakage in patients selected for non-operative management.

 If patients are clinically stable and improving, especially

with a sealed perforation, surgery may not be warranted.

 However, if they deteriorate, regardless of the presence and

size of the leak, urgent operation is indicated
Treatment options for perforated peptic ulcer
disease
 Omental patch closure

 Gastrectomy
Once operation is done
 Start pt on PPI life long

 Stop NSAIDS

 Eradication therapy

 Balanced diet
ACUTE CHOLECYSTITIS
 Inflammation of gall bladder

Calculous
cholecystitis
Etiology
Acalculous
cholecystitis
PRESENTATION
 Nausea, vomiting, low grade fever
 tachycardia

 right hypochondriac pain, colicky, radiate to shoulder, back

 guarding

 rigidity

 Murphy’s sign (arrest of inspiration with gentle pressure under

the right costal margin due to tenderness)
 Boas’s sign- hyperasthesia at 9th to 11th rib posteriorly on right
side-phrenic nerve irritation
 palpable tender gallbladder
INVESTIGATIONS
FBC : leucocytosis
Amylase : mildly raised
LFT : transaminitis, alp raised. bilirubin
RP
Septic workup
USG
CXR, KUB radiopaque stones, exclude
perf viscus
CT AP: fat stranding around gb, exclude
complication (empyema/perforation)
USG
• Sensitive
• Inexpensive
• Reliable
» Sensitivity 85%; Specificity 95%

What will you look in USG?

1.GallStone
2.Pericholecystic fluid
3.GB wall thickening
4.Sonographic murphy’s sign
MANAGEMENT OF
ACUTE CHOLECYSTITIS
1. NBM

2. RYLES TUBE ASPIRATE

3. IV FLUIDS
4.BROAD SPECTRUM
ANTIBIOTICS
5.IV ANALGESICS
6. OBSERVATION-
peritonism
7. SURGICAL
INTERVENTION
SURGICAL TREATMENT
CHOLECYSTECTOMY- either during
admission or 6 weeks after discharge
 open
 laparoscopic
OPEN CHOLECYSTECTOMY
LAPAROSCOPIC CHOLECYSTECTOMY
COURVOISIER’S LAW
 In presence of obstructive jaundice, a palpable GB is
usually NOT due to gallstone obstruction of CBD
 Most probably due to a growth in periampullary region
or head of pancreas.
 Exceptions :
- Double impaction of stone
- Stone with primary oriental cholangiohepatits
- Pancreatic calculus obstructing ampulla of vater
- Mucoele of GB
(A) Localised oedema around the pancreas
(B) Extensive fluid collections around the pancreas
Complications

*Systemic Complications
The systemic complications of acute pancreatitis tend to occur within
days of the initial onset:

•Disseminated Intravascular Coagulation (DIC)

•Acute Respiratory Distress Syndrome (ARDS)

•Hypocalcaemia
• Fat necrosis from released lipases, results in the release of free
fatty acids, which react with serum calcium to form chalky
deposits in fatty tissue

•Hyperglycaemia
• Secondary to destruction of islets of Langerhans and subsequent
disturbances to insulin metabolism
 Pancreatic Necrosis

 Pancreatic necrosis is prone to infection and should be suspected

if there is a clinical deterioration in the patient associated
with raised infection markers (or from positive blood culture
or changes of low density within the pancreas on CT).

 Definitive diagnosis of infected pancreatic necrosis can be

confirmed by a fine needle aspiration of the necrosis.
Pancreatic Pseudocyst
A pancreatic pseudocyst is a collection of fluid containing pancreatic
enzymes, blood, and necrotic tissue; they can occur anywhere within or
adjacent to the pancreas, however are usually seen in the lesser sac obstructing
the gastro-epiploic foramen by inflammatory adhesions.

They are typically formed weeks after the initial acute pancreatitis episode.
They lack an epithelial lining, therefore termed pseudocyst, and instead have
a vascular and fibrotic wall surrounding the collection.

Pseudocysts may be found incidentally on imaging or can present

with symptoms of mass effect, such as biliary obstruction or gastric outlet
obstruction.

They are prone to haemorrhage or rupture, and can become infected.

About 50% will spontaneously resolve, hence conservative management is
usually the initial treatment of choice.

Cysts which have been present for longer than 6 weeks are unlikely to resolve
spontaneously. Treatment options include surgical
debridement or endoscopic drainage (often into the stomach).
INTRODUCTION
Occurs when the normal flow of intestinal
contents is interrupted
It causes dilatation proximal to obstruction site
while distal to the blockage the bowel will
decompress as luminal contents are passed
CLASSIFICATION

1). EXTRAMURAL 1). PARALYTIC

2). INTRAMURAL ILEUS
3). INTRALUMINAL - POST
OPERATIVE
- INFLAMMATOR
Y
- METABOLIC
-
MECHANICAL
PATHOPHISIOLOGY
Bowel dilatation  overgrowth aerobic and anaerobic
organism  gas production (nitrogen + hydrogen
sulphide)
Bowel dilatation +obstruct  accumulation of
digestive juice  dehydration & electrolyte loss
Defective intestinal absorption
Losses as a result of vomiting
Sequestration in the bowel lumen
Transudation of fluid into peritoneal cavity
 STRANGULATION
Blood supply compromised  ischemic bowel emergency
CAUSES
DIRECT PRESSURE ON THE BOWEL WALL
HERNIA ORIFICES
ADHESIONS/ BANDS
INTERUPTTED MESENTERIC BLOOD FLOW
VOLVULUS
INTUSSUSCEPTION
INCREASE INTRALUMINAL PRESSURE
CLOSED- LOOP OBSTRUCTION
Special types of mechanical obstruction
INTERNAL HERNIA
Small intestine entrapped in retroperitoneal
fossae/ congenital mesenteric defect
OBSTRUCTION FROM ENTERIC
STRICTURE
2nd to tuberculosis and Crohn’s disease
BOLUS OBSTRUCTION
GALLSTONES, FOOD, TRICHOBEZOAR,
PHYTOBEZOAR, STERCOLITH, WORMS
ADHESIONS
POSTOPERATIVE
CAUSES
 Acute inflammation
 Sites of anastomoses,
reperitonealisation of raw
areas, trauma, ischaemia
 Foreign material
 Talc, starch, gauze, silk
 Infection
 Peritonitis, tuberculosis
 Chronic inflammatory
conditions
 Crohn’s disease
 Radiation enteritis
INTUSSUCEPTION
 one portion of the gut
invaginates into an
immediately adjacent
segment;
 it is the proximal into the
distal
 Most common in children
 Adult cases are secondary to
intestinal pathology, e.g.
polyp, Meckel’s diverticulum
 Ileocolic is the most common
variety
 Can lead to an ischemic
segment
VOLVULUS
TWISTING ROTATION OF A PORTION
OF BOWEL ABOUT ITS MESENTERY
OBSTRUCT TO LUMEN (>18O ‘
TORSION)
VASCULAR OCCLUSION IN
MESENTERY (>360’ TORSION)
May involve the small intestine, caecum
or sigmoid colon
neonatal midgut volvulus secondary to
midgut malrotation is life-threatening
The most common in adults is sigmoid
Surgery is required to prevent or relieve
ischaemia
history
4 cardinal signs
Abdominal pain
Nausea and vomting
Abdominal distension
Failure to pass flatus or
faeces
Others :
Dehydration, hypotension,
tachycardia, pyrexia,
abdominal tenderness,
empty rectum on DRE, high
pitched bowel sound.
ABDOMINAL PAIN
SMALL BOWEL :
periumbilical and colicky
comes in spasm
builds up in crescendo then
tappers off
regular pain at intervals of 2-3
minutes
LARGE BOWEL:
below the umbilicus & comes
at intervals of 6-10 minutes.
STRANGULATION
OBSTRUCTION
Severe & continuous pain
Vomiting
- The higher the obstruction, the vomiting is more severe
- In large bowel obstruction vomiting comes later and
sometimes patient may not vomit at all.
- As obstruction progresses the character of the vomitus alters
(digested food -> feculent material; as a result of the presence
of enteric bacterial overgrowth)
Abdominal distention
the more distal the obstruction,
the more distention of abdomen.
visible peristalsis may be present.
Constipation
may pass feces or flatus if early onset
occurs early in lower large bowel obstruction
occurs late in high small bowel obstruction
absolute constipation  complete intestinal obstruction
In high small bowel obstruction,;
vomiting occurs early and is profuse with rapid
dehydration.
Distension is minimal
In low small bowel obstruction
Vomiting is delayed. pain is predominant with central
distension.
In large bowel obstruction,
distension is early and pronounced. Pain is mild and
vomiting and dehydration are late.
investigation

FBC
Increase hematocrits value
Increase TWC
BUSEC
Hypokalemia, hyponatremia, hypocholaremia
ABG
alkalosis -> proximal obstruction (severe vomiting)
acidosis -> distal intestinal obstruction
(dehydration, ketosis and loss of alkaline secretion)
Radiological
AXR
Gas pattern
Fluid level
Masses shadow
Fecal pattern
Chest X-Ray
Elevated diaphragm
Air under diaphragm
Aspiration
USG:
to differentiate mechanical obstruction & paralytic
ileus,
poor visualization of gas filled structure,
only useful in selected patient ie pregnant, when CT
is contraindicated, in critically ill patients
 Free fluid
 Masses
 Mucosal folds
 Pattern of peristalsis

CT scan:
level of obstruction (transition point)
Causes (hernias, inflammatory changes, masses)
sign of strangulation, ischemia, perforation
Principles of treatment
Gastrointestinal drainage
Fluid and electrolytes replacement
Relief of obstruction
Surgical intervention
necessary for most cases
Need to be delayed until resuscitation is complete
Early management
ABC
Oxygen supply
fluid replacement with hartman or normal saline
Nasogastric decompression
KNBM
NG tube with free flow or 4hly aspirate
Close monitoring
BP, PR, Temp, Input/output, CVP
Antibiotic cover
Analgesia
Indication

of
Immediate intervention
surgery
 Evidence of strangulation
 Signs of peritonitis resulting from
perforation or ischemia
In the next 24-48H
Clear indication of no resolution of
obstruction (clinical or radiological)
Diagnosis is unclear in virgin abdomen
Adequate exposure by midline incision
then assess
the site of obstruction;
the nature of the obstruction;
the viability of the gut.