gi cases

1. GI Cases in Surgery
Surgery Campus Teaching
Session
Stage 5 Hospital Based Practice
2021
Dr. Antonio Jr. Villarivera
1

2. Objectives
• To be familiar with the clinical presentation of the different
common GI cases in surgery.
• To know the basic diagnostic and management principles
for these cases.
2

3. Presentations & Conditions
• Core Presentations
– Abdominal pain
– Abdominal swelling
– Rectal bleeding
• Core Conditions
– Peritonitis, Diverticular disease, Pancreatitis, Appendicitis,
Bowel Obstruction, Acute Gallbladder Disease
3

4. Abdominal Pain
4

5. Abdominal Pain
• Pain and tenderness felt over the abdomen
• Abdominal pain is divided into visceral and parietal
components
• Progression to visceral pain parietal pain peritonitis
• Acute abdomen
– refers to the sudden onset of severe abdominal pain and
tenderness, a clinical presentation that often requires urgent
evaluation & therapy
5

6. Visceral Pain
• Tends to be vague and poorly localized
depending on its origin
– Foregut organs (stomach, duodenum, biliary
tract) produce pain in the epigastric region
– Midgut organs (most small bowel, appendix,
cecum) cause peri-umbilical pain
– Hindgut organs (most of colon & sigmoid)
and intraperitoneal portions of the GUT
cause pain initially in the suprapubic or
hypogastric area
• Due to distention of a hollow viscus
• Pain often described as dull, cramping &
aching

7. Parietal Pain
• Pain corresponds to irritation of the
segmental nerve roots innervating the
peritoneum
• Pain can be localized to the
dermatome superficial to the site of the
painful stimulus
• Pain tends to be better localized,
sharper, steady and constant
• Progression to visceral parietal
pain peritonitis
• Patient will often lie still

8. Referred Pain
• Pain perceived at a site distant
from the source of stimulus.
• Example: irritation of the
diaphragm may produce pain in
the shoulder
• Determining whether the pain is
visceral, parietal, or referred is
important and can usually be
done with a careful history.
8

9. Describing Abdominal Pain
9

12. Abdomen

13. SOCRATE
S
13

14. Abdominal Pain
• Site - Where is the pain? Or the maximal site of the pain.
• Onset - When did the pain start, and was it sudden or gradual?
Include also whether if it is progressive or regressive.
• Character - What is the pain like? An ache? Stabbing?
• Radiation - Does the pain radiate anywhere?
• Associations - Any other signs or symptoms associated with the
pain?
• Time course - Does the pain follow any pattern?
• Exacerbating/Relieving factors - Does anything change the pain?
• Severity - How bad is the pain?

15. Abdominal Pain
15

16. Abdominal Pain
16

17. Abdominal Pain
17

18. Abdominal Swelling
18

19. Abdominal Swelling
• Also called abdominal distention
• Can be due to various causes
both medical and surgical
• Examples:
– Excessive fluid (ascites)
– Accumulation of air (bowel
obstruction)
– Others: mass, blood, gastric/bowel
contents (acute pancreatitis,
perforated peptic ulcer, trauma
leading to peritonitis)
19

20. Abdominal Swelling
• Evaluation requires careful history and complete physical
examination
• Investigations should be focused on finding the cause of the
problem
– Blood investigations (FBC, U&Es, etc….)
– Imaging investigations (abdominal x-ray, CT scan)
• Management depends on the underlying pathology
– Conservative
– Surgical management
20

21. Rectal Bleeding
21

22. Rectal Bleeding
* Important to as much as possible quantify the bleeding
• Fresh blood (hematochezia)
– Can indicate a possible lower GI
bleed
– Possible causes include a GI
malignancy, diverticulosis,
hemorrhoids, angiodysplasia,
colitis, etc
• Black tarry stools (melena)
– Can indicate a possible upper
GI bleed
– Possible causes can be divided
into variceal & non variceal (ie.
PUD) causes
22

23. 23

24. Diagnostic Work Up
• Upper GI bleed
– Oesophagogastroduodenoscopy (OGDS)
• Lower GI bleed
– Colonoscopy
• appropriate for minimal to moderate bleeding
– Angiography
• Can detect bleeding in the range of 0.5-1ml/min; generally used for
diagnosis of ongoing bleeding; can also offer therapeutic options (ie.
vasopressin infusion)
– RBC tagging (scintigraphy)
• most sensitive (90%) but least accurate in terms of localization (40-
60%); able to detect 0.1ml/min bleeding
24

25. 25

26. 26

27. Management
• Resuscitate and stabilize patient (ie. ABCDE)
• Treatment would depend on the cause of the bleeding
– Medications
– Endoscopic maneuvers
– Surgery
• Hemodynamic instability despite resuscitation (>6 units of transfusion)
• Failure of endoscopic measures
• Recurrent bleed after initial stabilization (up to 2 attempts)
• Shock with recurrent hemorrhage
• Continued slow bleed requiring >3 units/day of transfusion
27

28. Core Conditions
• Peritonitis
• Diverticular disease
• Pancreatitis
• Appendicitis
• Bowel obstruction
• Acute gallbladder disease
28

29. Peritonitis
• Peritoneal inflammation of any cause
• May affect the entire abdominal cavity
(visceral or parietal peritoneum)
• Characterized by severe tenderness to
palpation, with or without rebound
tenderness, and guarding on PE
• Often due to an inflammatory insult (gm (-
) infection w/enteric organisms or
anaerobes)
• Can result from noninfectious
inflammation (ie. pancreatitis) 29

30. Primary Peritonitis
• Occurs when microbes invade the
normally sterile confines of the
peritoneal cavity via hematogenous
dissemination from a distant source of
infection or direct inoculation
• Common among patients who retain
large amounts of peritoneal fluid
(ascites, renal failure on peritoneal
dialysis)
• Infections are mostly monobacterial
• Rarely require surgical intervention
30

31. Secondary Peritonitis
• Due to contamination of the peritoneal
cavity (2’ to perforation or severe
inflammation and infection of an intra-
abdominal organ)
• Ex: appendicitis, perforation of any portion
of the gastrointestinal tract, or
diverticulitis.
• Therapy often requires source control to
resect or repair the diseased segment,
debridement of necrotic, infected tissue
and debris (surgery)
• Also administer antimicrobials 31

32. Diverticular Disease
32

33. Definitions
• Diverticular disease: presence of diverticula with
mild abdominal pain or tenderness and no
systemic symptoms.
• Diverticulosis: presence of diverticula w/o
symptoms.
• Diverticulitis: diverticula associated with
inflammation and infection.
• Acute diverticulitis: sudden inflammation or
infection associated with diverticula.
• Complicated acute diverticulitis: presence of
complications associated with inflamed or infected
diverticula (abscess, fistula, stricture perforation
and sepsis) 33

34. Pathophysiology
• Disease of the elderly (over 50% of patients >50 years old are
affected rising to 70% by 80 years of age.
• Most occur in the sigmoid colon (50%)
• The most accepted theory is that a lack of dietary fiber results in
smaller stool volume, requiring high intraluminal pressure and
high colonic wall tension for propulsion.
• Chronic contraction then results in muscular hypertrophy  colon
acts like separate segments instead of functioning as a
continuous tube (segmentation).
34

35. Pathophysiology
• Segmentation causes high
pressures that are directed
radially toward the colon wall
rather than propulsive waves that
move stool distally.
• The high radial pressures
directed against the bowel wall
creates the diverticula
35

36. Clinical Presentation
• Diverticulosis: asymptomatic; may present with
lower GI bleed without abdominal pain
• Diverticular disease: intermittent pain at the left
lower quadrant of the abdomen (most common)
• Others:
– Constipation and diarrhoea
– Occasional large rectal bleeds often described
as bright red bleeding (hematochezia)
– Some people (Asian origin) pain and may be in
the right lower quadrant
– Presentation maybe similar with irritable bowel
syndrome, colitis and malignancy.
36

37. Clinical Presentation
• Acute diverticulitis- sudden
inflammation or infection
associated with diverticula.
• Symptoms include constant
abdominal pain, usually severe
and localising in the left lower
quadrant.
• Other features, including fever,
may also be present.
• Tends to develop complications
complicated acute diverticulitis 37

38. Clinical Presentation
• Complicated acute diverticulitis: presence
of complications associated with inflamed
or infected diverticula:
– Rigid abdomen & guarding perforation
peritonitis
– Tender mass in the left lower abdomen is
suggestive of a phlegmon or abscess
– Abdominal distention & inability to pass
flatus bowel obstruction
– Presence of fecaluria, pneumaturia
bladder/vaginal fistula

39. Investigations
• Endoscopy via flexible sigmoidoscopy/ colonoscopy or CT
colonography
• Abdominal x-ray
– Useful to rule out other similar cases; ie. intestinal obstruction
• Complicated acute diverticulitis
– CT scan (contrast/non-contrast)- identifies location of the infection,
extent of the inflammatory process, presence of an abscess &
involvement of other organs
– Can aid in draining abscesses via percutaneous CT guided
approach
– Alternative imaging modalities: MRI, ultrasound
– Others: FBC, U&Es, CRP 39

40. 40

41. Management
• Diverticulosis:
– No treatment needed, balanced diet, increase
fluid intake, consider bulk-forming laxatives if
constipated, do exercise & stop smoking
• Diverticular disease:
– Balanced diet, increase fluid intake, consider
bulk-forming laxatives if constipated, exercise &
stop smoking
– Paracetamol for pain relief and anti-spasmodic
for abdominal cramping
– If persistent or no response to treatment,
consider other causes and investigate and
manage appropriately

42. Management
• Patients who have acute diverticulitis who are systemically well:
– Consider not giving antibiotics
– Offer Paracetamol for pain
– Advise patient to return if condition persists
• Patients who have acute diverticulitis BUT are systemically
unwell, immunosuppressed or has significant co-morbidities:
– Give antibiotics (oral antibiotics for no complications; IV antibiotics for
complicated cases; review after 48 hours; watch out for sepsis)
– For patients with uncomplicated acute diverticulitis (CT confirmed),
review need for antibiotics & discharge if warranted
• For recurrent attacks of diverticulitis, consider surgical treatment

43. Management
• Complicated acute diverticulitis:
– Abscess formation:
• IV antibiotics & follow guidelines for sepsis
• Do imaging (CT, MRI, ultrasound)
• Consider percutaneous drainage (culture & sensitivity for the abscess)
• Monitor for improvement/deterioration and management appropriately
– Bowel perforation:
• Surgery (laparoscopic or open)
• Do extensive lavage if with fecal peritonitis
• Decide if can do primary anastomosis or damage control surgery
(Hartman’s procedure)
43

44. Pancreatitis
44

45. Definitions
• Acute pancreatitis- sudden
inflammation of the pancreas
associated with little or no
fibrosis.
• Chronic pancreatitis- a
continuing, chronic,
inflammatory process of the
pancreas, characterized by
irreversible morphologic
changes

46. Acute Pancreatitis
• Hallmark is inflammation associated
with little or no fibrosis.
• Ranges from a mild self-limiting
inflammation of the pancreas to
critical disease (25%) characterized
by infected pancreatic necrosis,
multiple organ failure and high-risk
mortality risk (25%)
• Approximately 56 cases per 100,000
people per year (UK); approx. 5%
overall mortality rate
46

47. Pathophysiology
• Most common causes are due to
gallstones (50%) and alcohol (25%)
• If these have been excluded,
investigate other possible causes
(25%) such as:
– metabolic causes (such as
hypercalcaemia or hyperlipidaemia)
– prescription drugs
– microlithiasis
– hereditary causes; autoimmune
pancreatitis
– ampullary or pancreatic tumours

48. Clinical Presentation
• Cardinal symptom is epigastric
and/or periumbilical pain that
radiates to the back
• May also have nausea, vomiting,
fever, tachycardia
• Typically, the pain is often constant
• Presentation may be variable:
– From mild, self-limiting abdominal
discomfort to a patient with shock &
with an “acute abdomen"
48

49. Investigations
• Diagnosis confirmed by elevated blood lipase or amylase
levels, (if not raised, CT may help confirm pancreatic
inflammation)
• Blood examinations;
– Amylase, lipase levels (*there is no significant correlation between the
magnitude of serum amylase elevation and severity of pancreatitis)
– Others: FBC, ABGs, ESR/CRP, LFTs, serum electrolytes, lipid profile
• Imaging:
– CT scan: to assess severity and for complications
– Abdominal/chest X-ray: to rule out other conditions
– Ultrasound and ERCP
49

50. Management
• Acute pancreatitis
– Fluid resuscitation
– Pain management
– Nutritional support
– Do not offer prophylactic antimicrobials to people with acute
pancreatitis (based on NICE guidelines)
– Therapeutic ERCP
– Monitor & manage local complications
• Severe infected pancreatic necrosis
• Pseudocyst formation
50

51. Chronic Pancreatitis
• An incurable, chronic
inflammatory condition that is
multifactorial in its etiology and
highly variable in its
presentation
• Prolonged inflammatory process
leads to fibrosis, cyst formation
and pancreatic duct stricture
• Presents as signs and
symptoms of pancreatic
insufficiency 51

52. Pathophysiology
• Most common cause is excessive intake of alcohol (over
many years) repeated attacks pancreatic damage
chronic pancreatitis
• In children the most common cause is cystic fibrosis
• Other less common causes include the following:
– Smoking, autoimmune chronic pancreatitis, inheriting a faulty
gene (hereditary pancreatitis), trauma/injury to the pancreas,
pancreatic duct obstruction (gallstone), radiotherapy to the
abdomen, idiopathic (no cause can be identified)
52

53. Clinical Presentation
• Repeated episodes of abdominal pain
– Described as a burning or shooting pain
and may last for several hours or days
– Nausea & vomiting may be present
• Episodes become more frequent as
condition progresses
• Eventually patients develop pancreatic
insufficiency
– Stools becomes greasy (steatorrhea)
– Weight loss, loss of appetite, jaundice, DM
53

54. Investigations
• Consider chronic pancreatitis as a possible diagnosis for patients
presenting with chronic/recurrent episodes of upper abdominal
pain
• Investigations may include the following:
– CT scan, ultrasound scan, upper GI endoscopy, endoscopic
ultrasound, MRCP
– Biopsy (if cannot rule out malignancy)
– Secretin stimulation test (aka pancreatic function test)
54

55. Management
• Treatment geared towards controlling/managing symptoms.
– Lifestyle changes (stopping drinking alcohol & quit smoking
– Pain medications
– Surgery (managing intractable symptoms like pain & presence of
complications)
• Complications:
– Painful inflammatory mass, obstructed pancreatic duct obstruction,
biliary or duodenal obstruction
– Ascites or pleural effusion
– Type 3 DM & pancreatic carcinoma
55

56. Appendicitis
56

57. Appendicitis
• Definition
• Pathophysiology
• Clinical Presentation
– History
– Physical Examination
• Diagnosis & Differentials
• Management
57

58. Bowel Obstruction
58

59. Definitions
• Complete obstruction
• Open-loop obstruction
• Closed-loop obstruction
• Simple obstruction
• Strangulation
59

60. Complete Obstruction
• Bowel lumen is completely
obstructed
• No distal passage of stool or air
• Can be only partial, meaning the
bowel lumen is narrowed and
there is some distal passage of
bowel contents
60

61. Open & Closed Loop Obstruction
• Open Loop Obstruction: when
proximal decompression is possible
via emesis or nasogastric tube
(NGT)
• Closed-loop obstruction: when both
proximal and distal bowels are
obstructed; common causes include
bowel incarceration in a hernia sac
or intestinal torsion
61

62. Closed Loop Obstruction
• Example is a sigmoid carcinoma
with a competent ileocecal valve
• Both proximal & distal ends are
‘obstructed’ forming a ‘closed loop’
• Runs the risk of perforation usually
at the caecum where the bowel is
thinnest and widest; (more
than12cm requires urgent
decompression)
62

63. Strangulated Obstruction
• Simple obstruction: no
compromise of blood flow to the
bowel
• Strangulation involves
compromise of blood flow with
inevitable bowel necrosis (pain is
more severe)
• May present with signs &
symptoms of peritonitis (board-like
rigidity on abdominal palpation,
fever, leucocytosis, etc…) 63

64. Causes
• Small Bowel Obstruction
– Post operative adhesions
– Strangulated inguinal hernia
– Small bowel volvulus
– Small bowel neoplasms
– Miscellaneous
• Large Bowel Obstruction
– Carcinoma of colon
– Volvulus (sigmoid)
– Diverticular disease
– Others:
• Crohn’s stricture, gallstone
ileus, intussusception,
foreign body
64

65. Clinical Presentation
• Generalized abdominal pain
• Vomiting and abdominal distention
(may depend on the level of
obstruction)
• Inability to pass out gas or flatus
(complete obstruction)
• Physical examination shows
abdominal distention and ‘metallic’
tinkling sounds on auscultation
• When bowels become non-viable
hypoactive bowel sounds
65

66. Clinical Presentation
• Proximal small bowel obstruction
– frequent, profuse vomiting, central abdominal pain, there may
be minimal distension
• Distal small bowel obstruction
– Colicky abdominal pain, moderate vomiting (vomitus may be
feculent), moderate distension
• Large bowel obstruction
– abdominal distension, pain is more constant, minimal vomiting
66

67. Diagnosis
• Abdominal X-ray
– Useful for identifying dilated loops of bowel
– Often includes supine and upright plain radiographs of the
abdomen and an upright chest radiograph
• CT scan
– For non-specific and uncertain cases in which clinical and
radiographic findings are inconclusive
67

68. Small Bowel Obstruction
• > 3cms; recognized by the visible
valvulae conniventes (arrowheads
passing across the width of the
lumen)
• The central position of the loops is
another clue
• Presence of air fluid levels (on
upright x-ray)
68

69. Large Bowel Obstruction
• The colon can be identified by its
peripheral location
• If obstructed:
– >6cms in diameter with the
presence of haustral folds that are
widely spaced
– The caecal diameter is > 9 cms
69

70. Management
• Decision should be based on the cause, site, duration of
onset, type of obstruction (simple, closed loop,
strangulated) & status of the patient
70

71. Management
• Initial non-operative management (no peritoneal signs)
like in small bowel obstruction due to post op
adhesions:
– Can decompress bowels initially
– Decompress (insert NGT & monitor for character and amount
of output)
– Nil by mouth
– Resuscitate with IVF (insert catheter; monitor I&O)
– Antibiotics
– Monitor for improvement or deterioration & treat accordingly
71

72. Management
• Surgery in cases of
– Strangulation (signs of vascular compromise)
– Closed loop obstruction (especially with impending rupture)
– Generalized peritonitis
– Failure to improve despite conservative management
72

73. Acute Gallbladder Disease
73

74. Definitions
• Cholelithiasis- stones in the gallbladder
• Cholecystitis- inflammation of the
gallbladder
– most commonly due to a stone obstructing the
cystic duct
– acalculous cholecystitis: acute inflammation of
the GB due to stasis & ischemia
inflammatory response in the gallbladder wall
(multifactorial in etiology)
• Choledocholithiasis- presence of stones in
the biliary tree (common bile duct)
• Cholangitis- inflammation of the biliary tree
74

75. Pathophysiology
• Majority of cholecystitis are due to stones inside the gallbladder
– Gallstones form as a result of solids settling out of solution.
– The major organic solutes in bile are bilirubin, bile salts,
phospholipids, and cholesterol
– Classified by their cholesterol (cholesterol stones or pigment stones)
• Acalculous cholecystitis results from gallbladder stasis and
ischemia, causing a local inflammatory response in the
gallbladder wall.
– May involve multiple risk factors including specific primary infections
75

76. Clinical Presentation
• Cholelithiasis- may asymptomatic
• Cholecystitis often presents with:
– Pain at the epigastric or right upper
quadrant (biliary colic) radiating to the
back/scapula
– Nausea, vomiting & feeling of bloatedness
– Exacerbated by eating fatty foods
– Patients generally suffer discrete, recurrent
attacks of pain, between which they feel well
– If untreated 2/3 develop chronic
noninfectious inflammation of the
gallbladder wall 76

77. Clinical Presentation
• PE may reveal mild right upper quadrant
tenderness during an episode of pain.
• If the patient is pain free, the physical
examination is usually unremarkable
77

78. Clinical Presentation
• Acute Cholecystitis
– Starts as an attack of biliary colic, BUT
pain does not subside (caused by a stone
obstructing the cystic duct)
– Pain is more severe, patient is often
febrile, complains of anorexia, nausea,
and vomiting
– On PE: focal tenderness and guarding are
usually present in the right upper quadrant
– (+) Murphy’s sign is characteristic
78

79. Investigations
• Imaging investigations:
– Ultrasound
– MRCP if ultrasound is inconclusive
and the bile duct is dilated or
abnormal LFTs
• Consider endoscopic ultrasound
(EUS) if MRCP does not allow a
diagnosis to be made
• Blood exams:
– LFTs, FBC, U&Es, etc…
79

80. Management
• Asymptomatic patients
reassurance
– Exceptions: diabetics, renal transplant
patients, porcelain gallbladder
• Symptomatic patients surgery
(laparoscopic/open surgery)
– Requires taking out the gallbladder
together with the stones
• Acalculous cholecystitis
– Majority are acutely unwell may need
ICU support & monitoring
– Decide on cholecystectomy vs
drainage
80

81. Special Consideration
• Acute Cholangitis- ascending
bacterial infection associated with
partial or complete obstruction of the
CBD
• Obstruction bile stasis bacterial
overgrowth cholangitis
• Most common cause: gallstones
(others: malignant strictures,
parasites, instrumentation of the bile
ducts)
• Common organisms :E. coli and
Klebsiella pneumoniae 81

82. Clinical Presentation
• May present from mild, intermittent,
self-limited disease to fulminant
potentially life-threatening septicemia
• Most common presentation is fever,
epigastric or right upper quadrant pain,
and jaundice (Charcot’s triad) 2/3 of
patients
• May deteriorate with hypotension &
disorientation (Reynolds’ pentad: fever,
jaundice, right upper quadrant pain, septic
shock, and mental status changes).

83. Diagnosis
• Ultrasound
– Useful to document presence of gallbladder
stones, demonstrate dilated ducts, and
possibly pinpoint the site/cause of obstruction
• Alternatives: endoscopic retrograde
cholangiopancreatography (ERCP) or PTC
(percutaneous transhepatic cholangiogram)
• Liver function tests (LFTS)
– Shows hyperbilirubinemia, significant
elevations especially with the ALPs and
GGTs
• FBC shows leukocytosis 83

84. Management
• Initial treatment includes IV antibiotics &
fluid resuscitation (may require ICU
monitoring)
• About 15% of patients will not respond to
antibiotics and fluid resuscitation
emergency biliary decompression may be
required
• Decompression may be accomplished
endoscopically via percutaneous
transhepatic biliary drainage or by surgery

85. Special Considerations
• Choledocholithiasis- stones in
the common bile duct (CBD)
– Often presents as a
complication of a pre-existing
cholelithiasis
– Patients present with
obstructive jaundice, tea-
colored urine and grayish
stools
– Investigations include an
ultrasound, and LFTs
(showing ALP & GGT
elevations)

86. 86

87. 87

88. Summary
CONDITION HISTORY & PHYSICAL EXAMINATION
Symptomatic Cholelithiasis RUQ pain radiating to the back after fatty meals,
resolves within a few hours, female, multigravida, obese
Acute Cholecystitis Severe RUQ pain radiating to back +/− scapular pain,
persistent pain, fever, tachycardia, (+) Murphy’s sign
Choledocholithiasis RUQ pain with jaundice but no systemic inflammatory
signs (no fever or leukocytosis)
Acute Cholangitis Persistent RUQ pain, fever, jaundice (Charcot’s triad); if
with mental status changes & hypotension (Reynold’s
pentad)
88

89. End of Session
Any Questions??
89

90. End of Session
Thank You
90