ABDOMINAL PAIN- Didactic Lectures- PPTs.pdf

CASE BASED LEARNING
ABDOMINAL PAIN
INTRODUCTION
Dr.B.Selvaraj MS;Mch;FICS;
Professor of Surgery
Melaka Manipal Medical College
Melaka 75150 Malaysia

ABDOMINAL PAIN- CAUSES
✓ Inflammation of a viscus
✓ Perforation of a viscus
✓ Obstruction of a viscus
✓ Infarction of a viscus
✓ Intra-abdominal hemorrhage or retroperitoneal hemorrhage
✓ Extra-abdominal or medical causes for acute abdominal pain like lower lobe
pneumonia and inferior wall MI

ABDOMINAL PAIN- HISTORY
SOCRATES = Nemonic
S - site
O - onset
C - characteristics
R - radiation
A – associated symptoms &
signs
T - timing
E - exacerbating/
alleviating
S - severity
✓ “S” stands for “site”. Which region/quadrant? Is
it a general sense of overall discomfort? The site
of pain helps you fine tune your subsequent
physical exam and diagnostic decision making.
✓ “O” stands for “onset”. When did the pain start?
Acute or insidious?
✓ “C” stands for “characteristics”. The pain may
be sharp, dull, heavy, etc. or a combination of
descriptions.

SOCRATES = Nemonic
S - site
O - onset
C - characteristics
R - radiation
signs
T - timing
E - exacerbating/
alleviating
S - severity
✓ “R”, which represents “radiation”. Ask if the
pain stays at the site they are describing or if it
travels somewhere else in the body. Ex:Ureteric
colic
✓ A” stands for associated symptoms. What other
symptoms are present and associated with the
pain? Ask do they also have nausea and/or
vomiting?
✓ "T" stands for timing. When does the pain
occur? Does it happen at specific times of the
day, or is it constant?

SOCRATES = Nemonic
S - site
O - onset
C - characteristics
R - radiation
signs
T - timing
E - exacerbating/
alleviating
S - severity
✓ “E” represents “exacerbating” factors; grouped
within this is also alleviating factors. The
patient should be probed as to what makes their
pain better or worse. Certain physical positions,
medications, etc. These factors can all provide
historical clues about the root cause.
✓ “S” stands for “severity”. In most hospitals this
is formulated on a 1 to 10 scale with 10 being
the most severe pain they’ve ever experienced.

ABDOMINAL PAIN
✓Somatic pain:
✓Originate from abdominal wall
and parietal peritoneum
✓Sharper and more distinct
✓Better localized
✓Sensitive to cutting,tearing,
burning and crushing
✓Visceral pain:
✓Originate from internal organs
and visceral peritoneum
✓Achy and crampy
✓Variable localization and
sensation
✓Not sensitive to cutting, tearing,
burning or crushing
✓Sensitive to stretching of walls of
hollow organs and capsule of
solid organs

ABDOMINAL PAIN
✓Shifting pain: Ex: Periumbilical pain shifting to RLQ in
Ac.appendicitis
✓Radiating pain: Ex: Pain radiating from loin to groin in ureteric
colic
✓Reffered pain: Ex: Pain felt at Lt shoulder in case of splenic
rupture

ABDOMINAL PAIN- GRADING
✓It is done by comparing a10cm line numbered 0 to 10 and this is
called Visual Analogue Scale- VAS
✓Minimum 0 means no pain
✓2 is mild pain
✓4 is discomforting pain
✓6 is distressing pain
✓8 is intense pain

AN OVRVIEW
“Surgical Educator”
Malaysia
ACUTE APPENDICITIS
RLQ PAIN

ACUTE APPENDICITIS
Objectives
ü Causes of RLQ Pain
ü Etiology
ü Pathology
ü Clinical features- Symptoms & Signs
ü Investigations
ü Scoring System
ü Treatment
ü Complications
ü Mindmap
ü Algorithm for RLQ Pain
ü Treatment Algorithm for Ac Appendicitis

ACUTE APPENDICITIS
Causes of RLQ Pain
üAcute Appendicitis
üEctopic Pregnancy
üTwisted Ovarian Cyst
üPelvic Inflammatory
Disease- PID
üEndometriosis
üTubo-Ovarian
Pathology
üMittlesmerz
In Females
üRt Ureteric Calculus
üPerforated DU-
Valentino Appendicitis
üAc Cholecystitis
üAc Pancreatitis
üCrohn’s Disease
üCecal Diverticulitis
üInferior Wall MI
üLower Lobe Pneumonia
In Males In Children
üIntussusception
üMeckel’s Diverticulitis
üMesenteric Lymphadenitis

ACUTE APPENDICITIS
ETIOLOGY
üObstructive:
1. Fecolith
2. Worms- Enterobious Vermicularis
3. Lymphoid Hyperplasia in Children
ü Non-Obstructive:
1. Catarrhal- infection

ACUTE APPENDICITIS
SYMPTOMS
MURPHY’S
TRIAD

ACUTE APPENDICITIS
SIGNS
üRIF Tenderness in McBurny’s
point
ü RIF Rebound Tenderness,
Release tenderness or
Blumberg’s sign
ü Guarding/Rigidity
ü Cope’s Psoas Test
ü Cope’s Obturator Test
ü Rovsing’s Sign
ü Hyperasthesia in Sherren’s
Triangle
Obturator Test

ACUTE APPENDICITIS
INVESTIGATIONS
üLab investigations:
1. Total WBC and Differential counts
2. C-Reactive Protein- CRP
2. Urine- FEME if positive for C&S
3. B- HCG to R/O pregnancy
ü Imaging studies:
1. CXR- Erect or AXR including both side diaphragm to R/O Pneumoperitoneum
2. USG-To R/O any other pathology in women of child bearing age group
3. USG-To confirm Appendicitis
4. CECT abdomen

ACUTE APPENDICITIS
USG ABDOMEN

ACUTE APPENDICITIS
CECT- ABDOMEN

ACUTE APPENDICITIS
ALVARADO’S
SCORING
üNemonic: MANTRELS
üIf Score is < 4- discharge patient
üIf Score is 5 to 7- admit for
observation
üIf Score is 8 to 10- Straight away
surgery

ACUTE APPENDICITIS
TREATMENT
ü If simple Appendicitis Open/Lap
Appendicectomy
ü If Perforated Appendicitis Exploratory
Laparotomy, Appendicectomy & Peritoneal
toileting
ü If Appendicular Abscess < 5cms USG
guided Needle aspiration or tube drain
If >5cms Open drain
ü If Appendicular Lump:
- Oschner’s Sherren’s Regimen of
Conservative treatment
- NPO
- IVF
- IV broad spectrum Antibiotics
- Analgesics & Anti-inflammatory drugs
- Vital Signs Q2H

ACUTE APPENDICITIS
COMPLICATIONS

ACUTE APPENDICITIS
Algorithm For RLQ PAIN

ACUTE APPENDICITIS
Algorithm For Ac Appendicitis

Peripheral Arterial Diseases(PAD)

ACUTE
CHOLECYSTITIS
RUQ PAIN
AN OVRVIEW
Malaysia

ACUTE CHOLECYSTITIS
 Causes for RUQ pain
 Epidemiology
 Etiology
 Pathology
 Clinical features
 Investigations
 Complications
 Treatment
 Mindmap
 Diagnostic Algorithm
 Treatment Algorithm

ACUTE CHOLECYSTITIS
-Epidemiology
 Cholecystitis is inflammation of the
gallbladder most commonly due to an
obstruction of the cystic duct by gallstones
arising from the gallbladder (cholelithiasis).
 Uncomplicated cholecystitis has an excellent
prognosis; the development of complications
such as perforation or gangrene renders a bad
prognosis.
 10%-20% of Americans have gallstones, and as
many as one third of these people develop
acute cholecystitis
 AGE: The incidence of cholecystitis increases
with age. Explanation for this is unclear.
 Sex distribution: Gallstones are 2-3 times
more frequent in females than in males,
resulting in a higher incidence of calculous
cholecystitis in females. Elevated progesterone
levels during pregnancy is the cause.
Acalculous cholecystitis is observed more often
in elderly men.
 Prevalence by race and ethinicity: More
common in people of Scandinavian descent,
Pima Indians, and Hispanic populations. In
the United States, white people have a higher
prevalence than black people.

ACUTE CHOLECYSTITIS
-ETIOLOGY
 Risk factors for Calculus Cholecystitis: 90%
- Female
- Fat- obese
- Fertile- Multigravida
- Forty- elderly
- Certain ethnic groups
- Certain drugs like HRT in females
 Risk factors for Acalculus Cholecystitis:
10%
- Critically ill patients
- Those who underwent major
surgery/trauma/Burns
- Severe Sepsis
- Prolonged fasting
- Long term TPN
- Sickle cell disease
- Immunocompromised patients- Diabetes & HIV
Admirand Triangle
 Percentages of saturation
of three elements in bile
lead to precipitation and
cholesterol stone formation
 These three elements are
cholesterol, lecithin and
bile salts.
 The normal ratio between
cholesterol and lecithin &
bille salt is 1: 30
 If this ratio comes below
1: 13 the cholesterol gets
precipitated and crystals
form.

ACUTE CHOLECYSTITIS
-PATHOLOGY
 90% of cases of cholecystitis involve
calculous cholecystitis, with the other
10% of cases representing acalculous
cholecystitis.
 Acute calculous cholecystitis is caused
by an obstruction of the cystic duct,
leading to distention of the gallbladder.
As the gallbladder becomes distended,
blood flow and lymphatic drainage are
compromised, leading to mucosal
ischemia and necrosis.
 Acalculous cholecystitis- exact
mechanism is unclear. Injury may be
the result of retained concentrated bile.
 Stage 1: stone lodges in cystic
duct; midepigastric colickypain
 Stage 2: stone impacts in cystic
duct; pain shift to RUQ;
radiation to right
scapula/shoulder
 Stage 3: bacterial invasion GB
wall; + Murphy sign; subsides if
stone falls out
 Stage 4: perforation

ACUTE CHOLECYSTITIS
- Clinical Features

ACUTE CHOLECYSTITIS
- INVESTIGATIONS
1. Gall stones with
posterior acoustic
shadow
2. Gall Bladder wall
thickness >4mms
3. Pericholecystic
fluid collection

ACUTE CHOLECYSTITIS
- INVESTIGATIONS
1. In Acalculus
Cholecystitis and
equivocal USG
2. Normal GB- will
take-up tracer
3. In Ac cholecystitis-
Tracer not taken
up by GB

ACUTE CHOLECYSTITIS
- INVESTIGATIONS

ACUTE CHOLECYSTITIS
- SEVERITY GRADING
A- American
A- Association
S- Surgery
T- Trauma

ACUTE CHOLECYSTITIS
- COMPLICATIONS

ACUTE CHOLECYSTITIS
- TREATMENT
 Most consider that it is safe to observe patients with
asymptomatic gallstones, with cholecystectomy
reserved for patients who develop symptoms or
complications
 If patients come within 3 days of onset of
symptoms Immediate Cholecystectomy
 If patients are going to come after 3 days of onset of
symptoms do conservative treatment to cool down
the inflammation first and do elective
Cholecystectomy after 45 days
 If severe Cholecystitis with comorbidities Do
percutaneous cholecystostomy. However, an interval
cholecystectomy will be required once the patient’s
condition has stablised.

ACUTE RUQ PAIN
- DIAGNOSTIC ALGORITHM

ACUTE CHOLECYSTITIS
- TREATMENT ALGORITHM

ACUTE
PANCREATITIS
EPIGASTRIC PAIN
AN OVRVIEW
Malaysia

ACUTE PANCREATITIS
ü Different causes for epigastric pain
ü Epidemiology
ü Classifications and definitions
ü Etiology
ü Pathology
ü Clinical features
ü Investigations
ü Assessment of severity
ü Treatment
ü Complications
ü Mindmap
ü Treatment Algorithm

ACUTE PANCREATITIS
D/D for Epigastric Pain

ACUTE PANCREATITIS
-Epidemiology
ü Pancreatitis is inflammation of the pancreas .
It is one of the most devastating conditions in
the abdomen.
ü More than 75% of cases of acute pancreatitis
are due to either gallstones or alcohol.
ü 80% to 85% of patients have mild and self-
limiting Pancreatitis, while 15% to 20% of
patients have severe Acute Pancreatitis
complicated by shock, sepsis, and MODS.
ü The overall mortality for AP is approximately
10% , but in its most severe form , it can
increase to 20% to 30 % .
ü The disease may occur at any age, with a
peak in young men and older women.
ü In the United States, more than 200,000
patients are hospitalized annually with acute
pancreatitis
ü It is the principal cause of approximately
3,200 deaths per year
ü Infection of pancreatic and peripancreatic
necrosis complicates 30% to 70% of cases of
acute necrotizing pancreatitis and occurs
during the second to third weeks after onset
of disease.

ACUTE PANCREATITIS
CLASSIFICATIONS AND DEFINITIONS
Atlanta classification of acute pancreatitis(1992)
ü Mild acute pancreatitis:
● no organ failure;
● no local or systemic complications.
ü Moderately severe acute pancreatitis:
● organ failure that resolves within 48 hours
(transient organ failure); and/or
● local or systemic complications without
persistent organ failure.
ü Severe acute pancreatitis:
● persistent organ failure (>48 hours);
● single organ failure
● multiple organ failure.

ACUTE PANCREATITIS
-ETIOLOGY
Nemonic: “I GET SMASHED”:
ü Idiopathic
ü Gallstones
ü Ethanol
ü Trauma
ü Scorpion bite
ü Mumps (viruses)
ü Autoimmune
ü Steroids
ü Hyperlipidemia
ü ERCP
ü Drugs like Azathioprine,Thiazide.Valproic acid
and Sulfasalazine.

ACUTE PANCREATITIS
-PATHOLOGY
Underlying Pathology: intrapancreatic activation of proteolytic enzymes

ACUTE PANCREATITIS
-Clinical Features
ü Severe epigastric pain radiating
straight to the back
ü This pain is relieved on bending
forwards
ü Anorexia, nausea and vomiting
ü Low grade fever
üMid-epigastric tenderness &
fullness (paralytic ileus)
üCullen’s sign ( peri-umbilical
discoloration)
üGrey Turner’s sign (discoloration
of flanks)
üFox’s sign ( discoloration around
inguinal ligament)
üEpigastric guarding
üPleural effusion
SYMPTOMS SIGNS

ACUTE PANCREATITIS
-INVESTIGATIONS
ü WBCs: ↑
ü Hct: ↑ (in dehydration)/ ↓ (in
hemorrhage)
ü ABG: metabolic & respiratory
acidosis + hypoxia
ü Urinary amylase: ↑
LAB INVESTIGATIONS
Serum
ü Lipase: ↑↑ (more specific &
sensitive)
ü Amylase: ↑↑↑ (less specific)
ü BUN, creatinine: ↑
ü Liver enzymes, bilirubin: ↑
ü Inflammatory markers (CRP,
IL-6, IL-8): ↑
ü Glucose: ↑
ü Ca2+: ↓

ACUTE PANCREATITIS
-INVESTIGATIONS
IMAGING INVESTIGATIONS- AXR
Sentinel loops Colon cut-off sign

ACUTE PANCREATITIS
-INVESTIGATIONS
IMAGING INVESTIGATIONS- USG
Pancreatitis with edema and Peripancreatic effusion

ACUTE PANCREATITIS
-INVESTIGATIONS
IMAGING INVESTIGATIONS- CECT
Dual phase CT scan is useful initial investigation to look for necrosis (however,
necrosis may not appear in initial 48 – 72 hrs)- If necrosis, won’t get “light up”

ACUTE PANCREATITIS
-INVESTIGATIONS
IMAGING INVESTIGATIONS- ERCP

ACUTE PANCREATITIS
ASSESSMENT OF SEVERITY
RANSON SCORING
At Admission
“GA LAW (Georgia law)”:
Glucose >200
Age > 55
LDH > 350
AST > 250
WBC > 16,000
After 48 hrs
“C HOBBS (Calvin and Hobbes)”:
Calcium <8 mg/dL
Hct drop of >10%
O2 <60 (PaO2)
Base deficit >4
Bun >5 increase
Sequestration >6 L
Score 0 to 2: 2% mortality

ACUTE PANCREATITIS
GLASGOW-IMRIE SCORING
ü Out of 8 criteria if more than 3 are
positive it is severe

ACUTE PANCREATITIS
BALTHAZAR CT SCORING

ACUTE PANCREATITIS
BISAP SCORING

ACUTE PANCREATITIS
TREATMENT
ü Admission to HDU/ICU
ü Analgesia Opioid analgesia
ü Aggressive fluid rehydration
ü Supplemental oxygen
ü Invasive monitoring of vital signs, central
venous pressure, urine output, blood gases
ü Frequent monitoring of haematological and
biochemical parameters (including liver and
renal function, clotting, serum calcium,
blood glucose)
ü Nasogastric drainage (only initially)
ü Antibiotics if cholangitis suspected;
prophylactic antibiotics can be considered
ü CT scan essential if organ failure, clinical
deterioration or signs of sepsis develop
ü ERCP within 72 hours for severe gallstone
pancreatitis or signs of cholangitis
ü Supportive therapy for organ failure if it
develops (inotropes, ventilatory support,
haemofiltration, etc.)
ü If nutritional support is required, consider
enteral (nasogastric) feeding
Early management of severe acute pancreatitis.

ACUTE PANCREATITIS
TREATMENT
ü Indications for surgery
Definitive diagnosis cannot be made
Pancreatic necrosis
Pancreatic abscess
Surgical management of severe acute pancreatitis.

ACUTE PANCREATITIS
COMPLICATIONS

ACUTE PANCREATITIS
TREATMENT ALGORITHM

PEPTIC ULCER
DISEASE
EPIGASTRIC PAIN
AN OVRVIEW
Malaysia

PEPTIC ULCER DISEASE
Different causes for epigastric pain
Applied Basic Sciences
Etiopathogenesis
Epidemiology
Clinical features
Investigations
Complications
Treatment
Mindmap
Treatment Algorithm

D/D for Epigastric Pain

Applied Anatomy
Celiac Axis:
Left Gastric
Common Hepatic
Splenic
-Rt Gastric from
Hepatic artery proper
-Rt Gastroepiploic
from Gastroduodenal
-Short Gastric from
Splenic artery

Applied Physiology
Chief cells
Pepsinogen
Parietal cells
Hydrochloric acid
and intrinsic factor
G cells Gastrin
D cells Somatostatin
Intrinsic factor is
needed for the
absorption of Vit B12
Autoimmune
destruction of
parietal cells causes
deficient B12
Pernicious Anemia
1. Gastrin from G cells
2. Acetylcholine from vagus
nerve
3. Histamine from paracrine
release via mast cells

ETIOPATHOGENESIS

EPIDEMIOLOGY
A peptic ulcer is a break in the epithelial
surface of the stomach or duodenum caused
by the action of gastric secretions (acid and
pepsin) and infection with Helicobacter
pylori.
Mucosal infection with Helicobacter pylori is
a major cause for PUD
Patients with duodenal ulcers have an
increased capacity for gastric acid secretion
relative to normal people.
Hemorrhage is the leading cause of death
associated with peptic ulcer.
Each year, approximately 300,000 t o 500,000
new cases of PUD occur.
Three to four million patients are self-
medicating for symptoms of PUD
30,000 surgeries are performed annually for
PUD .
The incidence and prevalence of PUD varies
based upon the presence of Helicobacter pylori
(H. pylori). Higher rates are found in countries
where H. pylori infection is higher
DUs occur two decades earlier than GUs,
particularly in males .

Clinical Features
Symptoms of Gastric ulcers
Male : female 3:1, peak incidence 50+
years.
Epigastric pain induced by eating.
Aversion to food because of pain
Nausea or vomiting.
Hemetemesis and Melenemesis
common
Weight loss.
Dyspepsia: Bloating and early satiety
Heartburn, which is a burning
sensation in the chest
Anemia from chronic blood loss.

Clinical Features
Symptoms of Duodenal ulcers and Type 2 Gastric
ulcers
Male : female 1:1, peak incidence 25–50 years.
Epigastric pain during fasting (hunger pain),
relieved by food/antacids, often nocturnal, typically
exhibits periodicity (i.e. recurs at regular intervals).
Nausea or vomiting.
Weight gain.
Dyspepsia: Bloating and early satiety
Boring back pain if ulcer is penetrating posteriorly
Haematemesis from ulcer penetrating
gastroduodenal artery posteriorly.
Peritonitis if perforation occurs with anterior DU.
Vomiting if gastric outlet obstruction (pyloric
stenosis) occurs (note succussion splash and watch
for hypokalaemic, hypochloraemic alkalosis).

Duodenal Ulcer Vs Gastric Ulcer

PUD- INVESTIGATIONS
Upper GI Endoscopy
Upper GI Endoscopy
“ Most sensitive and
specific test”

PUD- INVESTIGATIONS
Upper GI Endoscopy
Benign Gastric Ulcer Malignant Gastric Ulcer Resected Specimen

PUD- INVESTIGATIONS
H.Pylori Testing
NON-INVASIVE INVASIVE
H. pylori is a helical gram-
negative rod with flagella
that resides beneath the
mucous layer of stomach
& duodenum
Production of the enzyme
urease allows H. pylori to
survive in the acidic
environment of the
stomach.

PUD- INVESTIGATIONS
Contrast Radiology
Upper gastrointestinal radiology is not used
as much as in previous years, as endoscopy
is a more sensitive investigation
Computed tomography (CT) imaging with
oral contrast has also replaced contrast
radiology where anatomical information is
sought, eg large hiatus hernias of the
rolling type

PUD- COMPLICATIONS
Four major complications of peptic
ulcer disease (PUD)
- Bleeding,
-Perforation,
-Penetration,
-Obstruction.

PUD- TREATMENT
PPls are the gold
standard with80 to-90%
healing at 8 weeks (e.g.
omeprazole,
lansoprazole).
H2 antagonists have a
high recurrence rate
eg.Cimetidine, Ranitidine
PPIs need acidic
environment to get
activated. So, shouldn’t
combine with antacids
and H-2 blockers
Acid neutralizing & inhibitory drugs

PUD- TREATMENT
Cyto-Protective Drug H.Pylori Eradication
H.Pylori should be eradicated in all patients with
documented PUD
No single drug is effective in eradication
Combination of drugs should be given for 14 days
Triple therapy: H. pylori eradication (Rx:amoxicillin
500 mg,and clarithromycin 500 mg) and PPI (20 mg
omeprazole or 30 mg lansoprazole b.d.) for 7–14
days. Metronidazole may replace amoxicillin in
penicillin-allergic patients.
Quadruple therapy: bismuth, metronidazole,
tetracycline and PPI for 7–14 days.
The test of choice for documenting eradication is
Urea breath test

PUD- TREATMENT
- SURGERY
Elective for intractable GU: Billroth I gastrectomy.
Normal vagal innervation of stomach

PUD- TREATMENT
- SURGERY
Elective for intractable DU: Highly selective vagotomy
Selective Vagotomy
Truncal Vagotomy

PUD- TREATMENT
- SURGERY
Pyloric stenosis: Truncal vagotomy + Gastrojejunostomy
Truncal Vagotomy + Pyloroplasty

PUD- TREATMENT
- SURGERY
Gastric & duodenal ulcer perforation
For DU Perforation- Graham’s
omentopexy+Peritoneal toileting For GU Perforation- Graham’s omentopexy
+ Biopsy of the ulcer
+ Peritoneal toileting

PUD- TREATMENT
- SURGERY
Gastric & duodenal ulcer bleeding

TREATMENT ALGORITHM

SMALL BOWEL
OBSTRUCTION
GENERALISED ABDOMINAL PAIN
AN OVRVIEW
Malaysia

SMALL BOWEL OBSTRUCTION
✓ Different causes for generalized abdominal pain
✓ Epidemiology
✓ Etiology
✓ Pathology
✓ Clinical features
✓ Investigations
✓ Complications
✓ Treatment
✓ Mindmap
✓ Treatment Algorithm

D/D for Generalised Abdominal Pain

Epidemiology
✓ Stoppage of cranio- caudal propulsion of bowel
contents due to narrowing or complete
blockage of bowel lumen.
✓ Common surgical emergency, serious in nature
and demands early diagnosis and intervention
✓ SBO is more common and more severe than
LBO
✓ Post-op adhesion and obstructed inguinal
hernia are the two common causes
✓ The prevalence of small bowel obstruction is
approximately 100 - 500 per 100,000 - who
have not undergone previous abdominal
surgery.
✓ The prevalence of small bowel obstruction is
approximately 600 per 100,000 in patients who
have undergone previous abdominal surgery

ETIOLOGY

PATHOLOGY
In open-ended obstruction a one-point
obstruction interferes with the prograde
propulsion of bowel contents.
In closed loop obstruction the lumen of the bowel is
occluded at two points thus preventing prograde
and retrograde movement of bowel contents.

Clinical Features- Symptoms
QUARTET
✓ Colicky abdominal pain
✓ Bilious vomiting
✓ Abdominal distension
✓ Constipation/Obstipation

Clinical Features- Signs

INVESTIGATIONS- Labs

INVESTIGATIONS- Imaging
CXR- Erect to R/O Pneumoperitoneum
AXR-Erect
Multiple Air-Fluid levels
AXR- Supine
✓ Dilated bowel loops
>3cms
✓ Valvulae Conniventis
✓ No gas in colon

INVESTIGATIONS- Imaging USG abdomen
✓ Dilated bowel loops
✓ Fluid levels
✓ Mass

INVESTIGATIONS- Imaging CT abdomen

TREATMENT
Initial conservative management:
✓ NPO
✓ ½-hrly vitals monitoring
✓ Bladder catheterization
✓ Abdominal girth measurements
✓ IO (fluid input-output) chart
✓ NGT aspiration
✓ IV fluids
✓ Antibiotics

TREATMENT
Signs of recuperation:
✓ Relief from symptoms (pain & vomiting)
✓ Improvement of general condition & vitals
✓ Amount of aspirate ↓
✓ Abdominal girth ↓
✓ Return of bowel sounds
• Conservative management can be continued
if above are present
Indications for early surgical intervention
✓ Obstructed external hernia
✓ Clinical features suspicious of intestinal
strangulation
✓ Obstruction in a ‘virgin’ abdomen
Principles of surgical intervention for
obstruction
Management of:
✓ The segment at the site of obstruction
✓ The distended proximal bowel
✓ The underlying cause of obstruction

TREATMENT

PARALYTIC ILEUS
Clinical features:
✓ Abdominal distension + diffuse abdominal
discomfort
✓ Vomiting
✓ Silent/ high-pitched tinkling sound (on
auscultation)
Investigations
✓ Serum electrolytes, creatinine
✓ USG: dilated bowel loops
✓ Plain AXR: dilated bowel loops

MINDMAP

DIAGNOSTIC ALGORITHM

TREATMENT ALGORITHM

MESENTERIC
ISCHEMIA
AN OVRVIEW
Malaysia

MESENTERIC ISCHEMIA
 Different causes for generalized abdominal pain
 Etiology
 Pathology
 Epidemiology
 Clinical features
 Investigations
 Treatment
 Take home message
 Mindmap
 Treatment Algorithm

MESENTERIC ISCHEMIA

MESENTERIC ISCHEMIA
CLASSIFICATION- ETIOLOGY
 AMI-Acute Mesenteric Ischemia
-MAE- Arterial Embolus due to Atrial
Fibrillation- 40%
-MAT- Arterial Thrombus due to
Atheroscelerosis- 30%
-NOMI- Non-Occlusive Mesenteric Ischemia
due low volume blood flow – 15%
-MVT- Mesenteric Venous Thrombosis 15%
 CMI- Chronic Mesenteric Ischemia
-Atheroscelerosis 95%
-Aortic dissection, radiation, malignancy

MESENTERIC ISCHEMIA
PATHOLOGY
 The intestinal mucosa has a high metabolic
rate and, requiring more blood flow (normally
receiving 20 to 25% of cardiac output),
making it very sensitive to the effects of
decreased perfusion
 Ischemia disrupts the mucosal barrier,
allowing release of bacteria, toxins, and
vasoactive mediators, which in turn leads to
myocardial depression, SIRS,MODS and
death
 Mediator release may occur even before
complete infarction. Necrosis can occur as
soon as 6 h after the onset of symptoms which
eventually becomes transmural
 Hyper active phase severe abdominal pain
and passage of bloody stools. Many patients
get better and do not progress beyond this
 Paralytic phase follow if ischemia continues;
abdominal pain and tenderness becomes more,
bowel motility decreases, resulting in
abdominal bloating, no further bloody stools,
and absent bowel sounds on exam.
 Shock phase fluids start to leak through the
damaged colon. This can result in shock and
metabolic acidosis with dehydration, low blood
pressure, rapid heart rate, and confusion.

MESENTERIC ISCHEMIA
EPIDEMIOLOOGY
 Mesenteric ischemia is insufficient perfusion
of the mesentery to meet the metabolic
demands of the splanchnic system.
 Prompt diagnosis and treatment of this life-
threatening condition, with mortality rates
from 24% to 94% is important
 Despite the best efforts of modern medicine
mortality still exceeds 50%
 Acute mesenteric ischemia is different from
ischemic colitis, which involves only small
vessels and causes mainly mucosal necrosis
and bleeding.
 The overall incidence for Mesenteric Ischemia
is estimated at 12.9/100,000 person/year
 Incidence of Acute superior mesenteric artery
(SMA) occlusion (embolus/thrombus ratio =
1.4) is 70%
 Incidence of Mesenteric venous thrombosis
(MVT) is 15%
 Nonocclusive mesenteric ischemia (NOMI)
were found in 15%

MESENTERIC ISCHEMIA
Clinical Features
Acute Mesenteric Ischemia- AMI
- MAE: Mesenteric Arterial Embolism
- MAT: Mesenteric Arterial Thrombosis

MESENTERIC ISCHEMIA
Clinical Features
MVT- Mesenteric Vein Thrombosis NOMI- Non-Occlusive Mesenteric Ischemia

MESENTERIC ISCHEMIA
Clinical Features
Chronic Mesenteric Ischemia- CMI

MESENTERIC ISCHEMIA
Clinical Features

MESENTERIC ISCHEMIA
INESTIGATIONS- LABS
 White blood cell count >10.5 in 98%
 Lactic acid elevated 91%
 In very early stage these two may not be elevated
 However, in late cases both are elevated

MESENTERIC ISCHEMIA
INESTIGATIONS- CT Abdomen
SMA embolism. Axial contrast-enhanced CT
image shows the SMA trunk (white arrow), which
lacks contrast enhancement owing to an embolus.
The thrombosed SMA is dilated and is as large as
the adjacent SMV (black arrow).
(CT) showing dilated loops of small bowel with
thickened walls (black arrow), findings characteristic
of ischemic bowel due to thrombosis of the superior
mesenteric vein.

MESENTERIC ISCHEMIA
INESTIGATIONS- CT Angiography
CTA scan of acute mesenteric ischemia
secondary to occluded SMA from an
emboli. 3D reconstruction shows mid
occlusion of SMA.

MESENTERIC ISCHEMIA
TREATMENT
Acute Mesenteric Ischemia:
 If diagnosis is made during exploratory laparotomy, options
are surgical embolectomy, revascularization, and resection.
 A “second look” laparotomy may be needed to reassess the
viability of questionable areas of bowel.
 Patients with arterial embolism or venous thrombosis require
long-term anticoagulation with warfarin. Patients with
nonocclusive ischemia may be treated with antiplatelet
therapy.

MESENTERIC ISCHEMIA
TREATMENT
Chronic Mesenteric Ischemia:
 If diagnosis is made by angiography, infusion of
the vasodilator papaverine through the
angiography catheter may improve survival in both
occlusive and nonocclusive ischemia
 For arterial thrombosis, Catheter directed
thrombolysis, balloon angioplasty or surgical by-
pass surgery may be done
 Mesenteric venous thrombosis without signs of
peritonitis can be treated with papaverine followed
by anticoagulation with heparin and then
warfarin.

MESENTERIC ISCHEMIA
TAKE HOME MESSAGE
 Early diagnosis is critical because mortality increases significantly once
intestinal infarction has occurred.
 Initially, pain is severe but physical findings are minimal- Pain out of
proportion to physical findings
 Surgical exploration is often the best diagnostic measure for patients with
definite peritoneal signs.
 For other patients, mesenteric angiography or CT angiography is done.
 For AMI embolectomy, revascularization, and resection.
 For CMI thrombolysis, angioplasty or by-pass surgery

MESENTERIC ISCHEMIA
TREATMENT ALGORITHM

SIGMOIDVOLVULUS
AN OVRVIEW
Malaysia

SIGMOIDVOLVULUS
✓ Different causes for generalized abdominal pain
✓ Epidemiology
✓ Etiology- Risk Factors
✓ Pathology
✓ Clinical features- Symptoms & Signs
✓ Differential diagnosis
✓ Investigations
✓ Treatment
✓ Mindmap
✓ Diagnostic Algorithm
✓ Treatment Algorithm

SIGMOID VOLVULUS

SIGMOIDVOLVULUS
Epidemiology
✓ Volvulus occurs when a segment of colon
undergoes twisting along its own mesentery
(mesenterio-axial) resulting in obstruction.
✓ Twisting of 180 degrees results in clinical
obstruction, and further twisting to 360
degrees causes strangulation with venous
gangrene, ischemia, and eventual perforation.
✓ It is a closed loop obstruction
✓ Common in elderly and those who are taking
neuro-psychiatric drugs
✓ Sigmoid volvulus accounts for 5% of large
bowel obstruction in developed countries. and
10% to 50% in developing countries
✓ This is because of intake of high-fibre diet in
these countries
✓ Patients are often institutionalized and
debilitated due to underlying neurologic or
psychiatric disease and have a history of
constipation

SIGMOIDVOLVULUS
ETIOLOGY-Risk Factors
✓ Higher incidence in developing countries (attributed
to high fiber diets)
✓ Seen mostly in elderly, institutionalized male with
chronic neuropsychiatric conditions
✓ Long pelvic mesocolon
✓ Narrow attachment of pelvic meso-colon
✓ Overloaded pelvic colon- constipation
✓ A loop of bowel fixed at its apex by adhesions.

SIGMOIDVOLVULUS
PATHOLOGY
✓ The loop of sigmoid colon usually
undergoes twisting in an
anticlockwise direction from one
half to three turns.
✓ As the volvulized segment
enlarges, it becomes trapped in the
confines of the abdominal wall and
is unable to spontaneously detorse.

SIGMOIDVOLVULUS
Clinical Features- Symptoms & Signs
SYMPTOMS
✓ Abdominal pain (initially
left-sided, later diffuse)
✓ Enormous abdominal
distension (left iliac fossa
and then whole of abdomen)
✓ Obstipation
✓ Hiccough, retching
✓ Vomiting- late feature
SIGNS
✓ Tympanic abdomen
✓ Tyre-like consistency of abdomen
is diagnostic
✓ Empty rectal vault (on digital
rectal exam)
✓ Just distension of abdomen
without tenderness→Viable
bowel
✓ Generalised tenderness with
rebound tenderness→
Gangrenous bowel
✓ Rigid abdomen→ Bowel
perforation

SIGMOIDVOLVULUS
Clinical Features- Symptoms & Signs

SIGMOIDVOLVULUS
DIFFERENTIAL DIAGNOSIS
✓ Colorectal carcinoma causing
obstruction
✓ Toxic megacolon
✓ Colorectal strictures
✓ Hirschsprung's disease
✓ Caecal volvulus
✓ Paralytic ileus
✓ Ileosigmoid knotting
✓ Ogilvie's disease (colonic pseudo-
obstruction)- Dysfunction of Sacral
para-sympathetic nerves
✓ Acquired megacolon
✓ Giant colonic diverticulum

SIGMOIDVOLVULUS
INVESTIGATIONS
✓ Blood tests : FBC, Serum
Electrolytes
✓ RFT: Blood urea&Creatinine
✓ AXR- Erect is diagnostic
- Coffee-bean appearance
- Bent-inner tube sign
-Omega sign
- Frimann-Dhal sign

SIGMOIDVOLVULUS
INVESTIGATIONS
✓ Barium Enema:
- Bird’s beak appearance
- Ace of spade sign
✓ Upper end of Barium
column tapers into spirally-
twisted distal sigmoid colon

SIGMOIDVOLVULUS
INVESTIGATIONS
✓ CT Abdomen:
- whirl sign, which represents
tension on the tightly twisted
mesocolon by the afferent and
efferent limbs of the dilated colon.

SIGMOIDVOLVULUS
TREATMENT
Indication: Young patients without
signs of Ischemia
✓ Rigid/Flexible Sigmoidoscopy-
negotiate obstruction and
decompress proximal bowel
✓ Risk of recurrence >50%
✓ To prevent recurrence
-Percutaneous endoscopic
sigmoidopexy (Non-resectional)
- Mesosigmoidoplasty
-Sigmoid colectomy( Resectional)
Indication: Old patients with signs of
Ischemia
Exploratory laparotomy
✓ If bowel is viable
- Sigmoidopexy/Sigmoidectomy
✓ If bowel non-viable
- Paul-Mickulicz double barrel
colostomy
- Hartman’s procedure
✓ Never do primary anastomosis in an
emergency scenario for fear of
anastomotic leakage
CONSERVATIVE OPERATIVE
RESUSCITATION
-I.V.Fluids
-Antibiotics
-Bladder
Catheteris
ation

SIGMOIDVOLVULUS
TREATMENT
Paul-Mickulicz Double
barrel Colostomy
Hartman’s temporary End-
Colostomy

SIGMOIDVOLVULUS
DIAGNOSTIC ALGORITHM

SIGMOIDVOLVULS
TREATMENT ALGORITHM

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