Approach to acute abdomen

1. Acute Abdomen and
appendicitis

2. Outline
• Introduction
• causes (DDX)
• Approach
-History taking
-physical examination
°Clinical presentation
*Acute Appendicitis

3. What is Acute Abdomen?
• It is sudden severe attack of abdominal pain to
such an extent that patient is in severe agony
and often in shock.
• It is in many cases a medical emergency,
requiring urgent and specific diagnosis and
surgery.
• Because there is progressive underlying intra-
abdominal disorder, undue delay in diagnosis
and treatment adversely affect outcome.

4. Causes of acute Abdomen?
INTRA-ABDOMINAL CAUSES
Inflammation—Acute appendicitis, acute cholecystitis,
acute salpingitis, acute diverticulitis, acute Crohn’s, acute
mesenteric adenitis, primary acute peritonitis.
 Perforation of bowel
 Acute intestinal obstruction – In the lumen (roundworm,
gallstones),
in the wall (stricture, intussusception, tumour),
outside wall (hernia, bands, adhesions, volvulus).

5. Con.t

 Mesenteric vessel occlusion by thrombosis or
embolism.
 Haemorrhage—Ruptured ectopic gestation, ruptured
tropical spleen like malarial, ruptured aortic
aneurysm.
 Torsions—Twisted ovarian cyst, twisted splenic
pedicle.
 Colicky causes—Ureteric, biliary, intestinal, appendiccular.

6. Con.t
EXTRA-ABDOMINAL CAUSES
• In the abdominal wall—Abdominal wall abscess,
Meleney’s spreading gangrene, rupture of
abdominal wall muscles, inferior epigastric artery
tear and haematoma foformation
• In thorax – Lobar pneumonia, diaphragmatic
pleurisy, pericarditis, angina pectoris, coronary
disease.
•
•

7. Con.t
• Retroperitoneal causes—Acute pyelonephritis,
retroperitoneal lymphadenitis and lymphangitis,
ruptured aortic aneurysm.
• Diseases of spine, spinal cord and intercostal nerves
•
• – Pott’s tuberculous spine, gastric crisis of Tabes dorsalis,
herpes zoster of intercostal nerves with neuralgia.
• Other causes – Malaria, typhoid, porphyria, diabetic
crisis, sickle cell disease, purpura, haemophilia, etc.

8. Approach to Acute Abdomen
• The first step is to obtain a history from the
patient. But even before that, initial observations
provide clues to the direction which the history
should take; general appearance, gait, position in
bed, facial expression, tone of the speech.
• History of pain, Fever, chills and rigors are
important in acute abdomen.
• History of jaundice may be significant in acute
chole cystitis, pancreatitis.

9. Con.t
History taking should be in this order:
Presenting complaint
Duration of the presenting complaint
History of the presenting complaint
Past history
Drug history and allergies
Social history,Family history,Review of the
systems.

10. Con.t
Physical Examination
• Observation of the patient’s general
condition is useful even before starting to
take the history, especially in the emergency
situation.
• If a patient resorts to the knee–elbow
position to get relief from pain, it indicates
that the pain is of pancreatic origin.

12. Con.t
Inspection
In a patient with acute abdominal pain, always
check to see if the abdominal wall moves with
respiration. If only the thorax moves then
peritonitis should be suspected.
• Grey Turner’s sign
• Cullen’s sign

14. Con.t
Plapation
 Signs of parietal peritoneal irritation (tenderness,
guarding, rebound tenderness, rigidity)
 Abdominal masses
Percussion
Percussion is a very sensitive and refined method of testing
for rebound tenderness. If the patient winces with pain
on ababdoial percussion it denotes underlying peritonitis.

15. Con.t
Auscultation
 Not heared during generalized peritonitis
 High-pitched bowel sounds are heard during early stages of
mechanical intestinal obstruction.
 A succussion splash is found most often in patients with gastric
stasis due to gastric outlet obstruction.

16. Clinical presentation of Acute
Abdomen
Pain
Pain is the most common presentation of acute abdomen.
• Mode of onset of pain
• Change in position of pain or spread of pain
• aggravating and relieving factors:
• Type of pain;
• Visceral Pain: dull and aching in character, poorly localized and
arises from distention or spasm of fibers innervating the wall
of hollow or solid organs.
• Parietal Pain: sharp, very well localized and arises from
irritation of somatically innervated parietal peritoneal.
• Referred Pain: aching and perceived to be near the surface of
the body.

17. Con.t
Vomiting
• Character
• frequency
• quantity and nature of the vomitus
• History of haematemesis
• after feeling of pain or simultaneously.

18. Con.t
Bowel Habits
 diarrhoea
 constipation
 Bloody putrid stool
Abdominal Distention
often presents with fullness of abdomen which is gradually
progressive and is associated with constipation and vomiting.

19. Acute appendicitis
One of the most common surgical emergencies
encountered by general surgeons.
It is inflammation of the Appendix.

20. Eitology
• 1, Altered diet (Decreased dietary fibre and increased
consumption of refined carbohydrates)
• 2, Familial susceptibility (individuals with long
retrocecal appendix)
3, Obstruction of the lumen of appendix (Faecoliths,
stricture, foreign body, roundworm or threadworm.)
(4) Distal colonic obstruction.
(5) Abuse of purgatives
*out of all this "faecoliths" is the comonest cause.

21. Types
• 1, Acute non-obstructive
appendicitis:(Inflammation of the mucus
membrane)
• 2, Acute obstructive appendicitis: pus collects and
it become blackish, gangrenous, oedematous and
rapidly progresses leading to perforation either at
the tip or at the base of the appendix.
• 3, Recurrent appendicitis
• 4, Subacute appendicitis

23. Clinical features
• It is rare before the age of two, common in
children and other age groups.
• Pain: Visceral pain starts around the umbilicus
due to distension of the appendix, later after few
hours somatic pain occurs in right iliac fossa due
to irritation of parietal peritoneum by the
inflamed apappendix.
Pain eventually becomes severe and diffuse
which signifies spread of infection into the general
peritoneal cavity.

24. Con.t
• Vomiting: Due to reflex pylorospasm
• Constipation is the usual feature but diarrhoea
can occur if appendix is in post-ileal or pelvic
positions.
• Urinary frequency: Inflamed appendix may
come in contact with bladder and can cause
bladder irritation.
• _x0000_Fever, tachycardia, foetor oris are
other features_x0000_

25. How to diagnose A. Appendicitis ?

26. Rebound
Tenderness /
Release Sign /
Blumberg’s Sign
When the hand is abruptly
removed to spring back the
abdominal muscles to its original
position, patient winces with
pain.

27. Rovsing’s Sign
When pressed in the left iliac
fossa intestine gets pushed
towards right iliac fossa pressing
the inflamed appendix causing
tenderness in right iliac fossa
which is adefinitive feature of
acute appendicitis.

28. Cope’s Psoas
Test
Retrocaecal appendicitis irritates
psoas major muscle causing
flexion of right hip joint. Patient
develops pain when this muscle
is stretched by hyperextending
the hip joint with patient turning
towards his left side.

29. Cope’s
Obturator Test
Stretching of the obturator
internus muscle by internally
rotating the hip joint will cause
pain if inflamed appendix is in
pelvic position and gets irritated
by the obturator internus
muscle.

30. Baldwing’s
Test/Sign
Flank is pressed with hand and
with knee extended patient
raises his right hip from the bed
to cause contraction of psoas
major muscle which irritates
inflamed retrocaecal appendix to
develop pain.

31. DDX

32. Alvarado Scoring System

33. Investigation
• The diagnosis of acute appendicitis is
essentially clinical;_

34. Management
Surgery
The surgical procedure for the removal of the
appendix is called an appendectomy.
Open appendectomy: This procedure consists of
the removal of the infected appendix through a
single large incision in the lower right area of the
abdomen. The incision in a laparotomy is usually
2 to 3 inches (51 to 76 mm) long. Under general
Anesthesia

35. Con.t
• Laparoscopic Appendoctomy
• This surgical procedure consists of making
three to four incisions in the abdomen, each
0.25 to 0.5 inches (6.4 to 12.7 mm) long. This
type of appendectomy is made by inserting a
special surgical tool called a laparoscope into
one of the incisions

36. Acute Pancreatitis

37. Outline
• Definition
• Etiology
• Pathophysiology
• Clinical manifestations
• Investigation
• Management

38. • Definition
– It is an inflammatory disorder of the pancreas that is
characterized by edema and when severe necrosis.
– Ranges from mild self limiting inflammation to sever
critical disease
• Etiology
– Gallstones(present in the 6th decade) and alcohol(present
in the 3rd or 4th decade) accounting for up to 80% of cases
– Gender difference is related with etiology

39. Gallstones
• Transient incompetence caused by the
passage of a stone through the shinicter of
oddi might allow duodenal fluid and bile to
reflux into the pancreatic duct
• Gallstone obstructing the pancreatic duct
leading to ductal hypertension-> minor ductal
disruption->extravasation of pancreatic juice

40. Alcohol
• Ethanol acts on acinar and stellate cells
• Ethanol induced spasm of sphincter of oddi
• Ethanol also induce ductal permeability
• Ethanol increases the protein content of
pancreatic juice and decreases bicarbonate
levels and trypsin inhibitor concentration.

41. Other causes
• Iatrogenic
• Hereditary pancreatitis
• Drugs
• Hyperlipidemia
• Tumors
• Idiopathic

42. Pathophysiology
• Begins with the activation of digestive
zymogens inside acinar cells -> cell injury
• Severity determined by events that occur after
acinar cell injury.
• Physiologic protective mxs
– Inactive precursors
– Separation of site of production and activation of
enzymes
– Trypsin inhibitors in pancreas

44. Clinical Presentation and Diagnosis
• Acute onset of severe constant epigastric pain
that often radiates through to the mid back
• Nausea, repeated vomiting
• elevation of serum amylase/lipase(>3x upper
limit of normal)
• In some cases urinary clearance of pancreatic
enzymes
• Imaging(usually CT scan) only required when the
above diagnostic criteria are not met

45. Clinical Signs
• Abdominal tenderness
• Cullen’s sign
• Grey Turner’s sign
• Tetany

46. Investigations
• Serum amylase level
• Serum lipase level
• Urinalaysis
• Contrast enhanced CT scanning

47. Classification of Severity
Revised Atlanta Criteria Determinant Based Classification

48. Management
• Initial assessment (first 4 hours)
– IV Analgesia
• For mild pain- NSAIDS
• For severe pain – Opoids ; avoid morphine
– Fluid resuscitation
• Reassessment (4-6 hrs)
– Assess response to fluid resuscitation
– Determine etiology
– ERCP if concomitant cholangitis is present
– Commence enteral nutrition

49. Cont.
• Managing local complication
– Percutaneous catheter drainage in patients with
suspected infected complications
• Indication for laparotomy
– Failed step up approach
– Acute abdomen(ischemia or perforation)
– Sever abdominal compartment syndrome
• Cholecystectomy to prevent gallstone
pancreatitis recurrence

50. Cholelithiasis
• Often asymptomatic.
• Most common symptom is biliary colic which
usually develops 1-2 hours after fatty meal
• Gallbladder contraction forces the stone against
the orifice of the cystic duct->rise in intraluminal
pressure and pain
• Dull pressure like discomfort in the RUQ or
epigastrium that may radiate to the back and
right shoulder

51. Acute Cholecystitis
• Inflammation of the gallbladder.
• Calculous cholecystitis 90-95% of cases
• Can occur without gallstones :- Acalculous
cholecystitis

53. Risk Factors
• Calculous cholecystitis
– Risk factor for gallstones
• Female
• Obesity
• >age, px, crohn’s disease …
– Previous gallbladder attacks
• Acalculous cholecystitis
– Mostly seen in ICU patients
– Usually associated with major illness such as
polytrauma, burns, major surgery, elderly with DM

54. Complications
• Gangrene
• Cholcystoenteric fistula

55. Clinical manifestations
• In contrast to biliary colic, the pain of acute
cholecystitis doesn’t subside(may persist for
several days)
• Patient is often febrile, complains of anorexia,
nausea or vomiting and maybe reluctant to
move as the inflammatory process creates
focal peritonitis.

56. Clinical signs
• Tenderness and guarding often present in the
RUQ
• A mass, gallbladder and adherant omentum is
occasionally palpable
• Positive murphy’s sign
• Boa’s sign:- an area ofof hyperesthesia between
the 9th and 11th ribs posteriorly on the right
side
• Jaundice- indicates Mirizzi’s syndrome

57. Investigation
• WBC count
• Blood and urine sugar estimation to rule out DM
• Bilirubin level
• Abdominal ultrasound- most commonly used
• Pericholecystic fluid
• GB wall thickening
• Dilation of bile duct
• Sonographic murphy’s sign
• HIDA
• CT scan

58. Management
• IV fluids, broad spectrum antibiotics and analgesia
• Cholecystectomy is the definitive treatment.
• Early cholecystectomy performed with in 72 hours of
illness is preferred over delayed one that is
performed 6-10 weeks after onset of the illness
• Laparoscopic cholecystectomy is preferred
• Unfit for surgery patients are treated with antibiotics
with cholecystectomy scheduled for 2 months later

59. Peptic Ulcer Disease
59

60. Outline
• Introduction to PUD
• Etiology and Pathogenesis of PUD
• Clinical manifestaions of PUD
• Investigations
• Complication
• Rx of Peptic Ulcer Disease
60

61.  It is defined as : A circumscribed ulceration
of gastrointestinal mucosa occurring in
areas exposed to acid and pepsin and
most often caused by Helicobacter
pylori infection.
 gastric ulcer : the ulcer that occurs in the stomach
lining ,some of them may be malignant
 duodenal ulcer : most often seen in first portion of
duodenum (>95%)
61
2.PEPTIC ULCER DISEASE(PUD)

62. Etiology and Pathogenesis
• Imbalance between aggressive factors and defensive factors
cause ulcer

63. Etiologies
● H.pylori
● NSAIDs
● Smoking
● Stress
● Hypersecretory states
ZE syndrome, Systemic mastocytosis, G cell
hyperplasia
● Radiation therapy

64. Clinical Manifestations
• Abdominal pain (90%)
– nonradiating, burning, epigastrium
 Nausea
 Vomiting
 bloating,
 weight loss,
 stool positive for occult blood,
 and anemia.
64

65. 65
Modified Johnson classification of GU

66. Investigation
66
• Laboratory to R/O other condition: CBC, Liver
chimistry, electrolytes, amylase
• Serum Gastrin level
• Endoscopy or contrast radiography
• H.pylori testing
-invasive or endoscopical(RUT,
Histopathology, culture)
-non invasive(UBT, serology)

67. Complication
 bleeding,
 perforation, and
 obstruction.
67

68. Perforated Peptic Ulcer
• Focal defects in the gastric or duodenal
mucosa that extend into the submucosa or
deeper

69. Perforated Peptic Ulcer
Stages of PUD Perforation
1st phase - Stage of chemical peritonitis
• within 2 hours of onset
2nd phase - Stage of reaction (illusion)
• Between 2-6 hours
3rd phase - Stage of diffuse bacterial peritonitis
• After 6 hours

70. Clinical feature of perforated PUD
• Abdominal pain
– Duodenal ulcer
– Gastric ulcer
• Anemia, stool color change
• Vomiting with/without hematemesis
• Active ulcer can perforate
– Severe stabbing/penetrating agonizing
epigasric pain that even the patient
recognize the exact time of the incident 
later generalized

71. Management
 Rx GOALS
Medical
• PPI
• high dose H2RAs and
sucralfate
• Antacids
ƚ stop smoking alcohol
and NSAIDs (aspirin).
71

72. Indications for
surgery in PUD
Management
 Surgical
• bleeding,
• perforation,
• obstruction, and
• intractability
72

73. The goals of operation
To prevent gastric acid secretion
• Achieved by:
• l.anterctomy- removal of the gastrin-secretion
portion of stomach
• 2.vagotomy alone decrease the acid secretion
by 50%
• 3.Combination of vagotomy and anterectomy
decrease acid secretion by 85%

74. 74

75. 75
Antrectomy

76. 76

77. urolithiasis

78. outline
• Definition
• Pathogenesis
• Risk factors
• Clinical feature
• ComPlication
• Investigation
• Management

79. definition
• Urolithiasis(urethralstone)-a small ,hard deposit that forms
in the kidneys and is often painful when passed.
• Ureteric stone-stones come down from pelvis of the kidney and
may get impacted at any site of anatomical narrowing of ureter.

80. • Most stones pass
spontaneously from the
ureter but there are five
sites of narrowing where
the stones may be
arrested.
• Obstruction of urethral
lumen result in severe and
spasmodic pain which is
known as urethral colic.
NORMAL ANATOMICAL NARROWINGS OF URETER
Uretral orifice

81. pathogenesis

82. RISK factors of urolithiasis

83. Clinical feature
 Ureteric colic is an intermittent attack of pain which occurs when a
stone passes through the ureter.
• Pain in the loin radiating to groin: which is sever, colicky , intolerable
and lasts for a few hours. the pain may be aggravated by exercise
and relieved by rest.
• when stone descends in to lower ureter, pain radiates to testicles ,
labia majora , and to the upper portion of thigh due to the irritation
of genitofemoral nerve.

84. • Upper urinary tract obstruction-induce renal pain(renal colic) which
radiates from the flank anterioly toward umblicus.
• Right mid uretral obstruction-the pain is reffered to the RLQ of the
abdomen and may be misinterpreted as appendicitis.
• Left mid-ureteral obstruction-pain is referred to the LLQ and can
present in a similar way to diverticulitis.
• Stones lodged in the lower ureter, especially at the vesicoureteric
junction, may cause irritative bladder symptoms.

85.  Nausea and vomiting
 Hematuria
 Guardind and rigidity of the abdomen on physical
examination

86. complication
• Hydroureteronephrosis
• Urosepsis
• Infection
• Pyonephrosis
• Obstruction

87. Investigations
• Urine analysis
• Abdominal plain x-ray
• Intravenous pyelogram
• Non contrast helical CT-scan (gold standard)
• USG
• Urine culture
• Retrograde pyelography
• CBC…..

88. Management
• Pain- NSAIDs
•Surgical treatment
1.Ureteroscopic stone removal
2.Open surgery(ureterolithotomy)
•Non surgical treatment
1.Extracorporeal shock wave lithotripsy(ESWL)

89. Indications for surgical removal of
ureteric calculus
• Repeated attacks of pain and the stone is not moving
• Stone is enlarging
• Complete obstruction of the kidney
• Urine is infected
• Stone is too large to pass
• Stone is obstructing solitary kidney or there is bilateral
obstruction.

90. Prevention of renal stone disease
•Fluid management: 1.5L/day
• Dietary adjustments: red meat to be avoided (rich in uric acid)
• Ultrasound to be done once in 6 months

91. Acute Ischaemic
conditions

92. Mesentric Ischaemia
• Decreased or blocked blood flow to the
intestine
• Realtively uncommon
• High prevalence in advanced age group

93. Types
1. Acute mesentric ischemia
Causes - thrombosis
- embolism
- vasoconstriction
2. Chronic mesentric ischemia
Causes -atheroscelerosis
3.Non-occlusive mesentric ischemia
Causes -viseral hypoperfusion and vasosapsm
-global hypoperfusion: MI, shock
- pt’s with co-morbidities

94. Clinical Mamifestations
• Acute mesentric ischemia
- Sudden onset abdominal cramp
- Bloody diarrhea
- Fever
- Nausea
- Vomiting
- Abdominal Distension
- Diffuse/ Rebound tenderness
- Rigidity

95. • Chronic mesentric ischemia-
- postprandial abdomibal pain
- persistent nausea
- occasionally diarrhea may coexist

96. • Non-occlusive mesentric ischemia
-abdominal pain
- in the absence of abdominal pain, progressive
abdominal distension. with acidosis maybe an
early sign of ischemia

97. Diagnostic Evaluation
• CBC
• Serum amylase
• Abdominal x-ray
• CT scan
• Arteriography
• Ultrasound
• Stool testing for occult blood

98. Management
• Initial management
- Fluid resuscitation
- Systemic anticoagulation with heparin
• Appropriate antibiotics
• Operative management

99. • In chronic mesentric ischemia the goal is to
revascularize mesentric circulation and
prevent development of bowel infarction
• Mesentric occlusive disease can be treated by
transaortic endarterectomy or mesentric
artery bypass.

100. • Ischemic Colitis
-Most commonly from non-occlusive causes
-splenic flexure and cecum has poor tolerance to
hypoperfusion
- May occur in healthy young individuals from
vasospasm due to extreme exercise or illicit drug
use

101. - Less abdominal pain than small bowel
ischemia
- Pt’s recover with conseravtive management,
normalization of the collateral flow and
resolution of the precipitating factors.