5th year medical student seminar, general surgery, acute biliary infections

1. ADAMA HOSPITAL MEDICAL COLLEGE
Department of Surgery
Seminar presentation on common biliary tract
infections
(Acute cholecystitis and cholangitis )
MODERATOR-- DR.ABDURAHMAN (MD, General surgeon)
Presenters- Jemal Argo
Hussein Abiti
Kalkidan Feyera
January/2021

2. Outline of presentation
• Objectives
• Surgical anatomy and physiology
• Acute cholecystitis
• Acute ascending cholangities

3. Objectives
After the end of the seminar the participants will be able to
 Explain the anatomy and physiology of the biliary
system
Describe the clinical picture, how to approach and
manage a patient with acute cholecystitis
Describe the clinical picture, how to approach and
manage a patient with an ascending cholangities

4. Surgical anatomy of the biliary system

5. Gall bladder and the biliary ducts

6. Artery, veins and nerves

7. Calot’s triangle

8. Calot’s triangle anomalies
Tortuous common hepatic artery Tortuous right hepatic artery

9. Bile
• Produced and excreted by the liver at a rate of
40 mL/hour.
• Helps for emulsification of fatty food and
facilitate their absorptions

10. Bile…
• Contain : -
– About 95% of water, bile salts ( chenodeoxycholic
acids, ursodeoxycholic acid)
– Phospholipids, cholesterol and bilirubin.
• About 95 % of bile salts are reabsorbed in the
terminal ileum (enterohepatic circulation)

11. GB functions
• Storage of bile (about 50% of liver secretion) –
release in response of CCK
• Concentrating of bile – by active absorptions
of H20, Na, Cl, HCO3- , and Ca.
• Mucus production (about 20 ml/day) – can
form mucocele when cystic duct is completely
obstructed.

12. • The storage and release of bile from GB is
controlled by autonomic NS:
– GB contract in response to CCK and vagal
stimulations to release its content.
– Sympathetics causes its relaxation and sphincter
constrictions, so that bile storage

13. Approach to and management of
common biliary infections
• Acute cholecystitis --- hussein
• Acute cholengitis---- kalkidan

14. Acute cholecystitis
• It is an inflammation of GB
• Obstruction of the cystic duct by a gallstone is
the initiating event
• Based on underlying cause, it can be
– Calculus – in about 90 - 95 % of cases
– Acalculus -- 5- 10 % of cases

15. Epidemiology
• Develops in 1%–3% of patients with
symptomatic gallstones
• Most frequently in patients aged 18 – 44 yrs
• Female predominance
• ACC was the second most common
gastrointestinal reason for hospital admission.

16. Pathogenesis of ACC
• Unresolved cystic duct obstruction.
• GB distention, inflammation, and edema of the
GB wall
• Spontaneous resolution of symptom and recur
on the other time----- chronic cholecystitis
• Without resolution of the obstruction, the
gallbladder will progress to ischemia and
necrosis

17. Pathogenesis…..
• Thrombosis of cystic artery….. gangrenous
cholecystitis
• When complicated by infection with a gas-
forming organism ---- acute emphysematous
cholecystitis
• This may end up in perforations --- chemical
peritonitis

18. Clinical presentation
• History
– Severe, constant RUQ or epigastrisc pain
sometimes with radiation to the the right shoulder
and back between scapula
– Hx of Preceding bilary colic
– Anorexia ,Nausea, vomiting
– Fever

19. Epigastric and RUQ is the most
common site of biliary pain.
Common sites of pain Common sites of radiation

20. Physical examination:
• General appearance:
– Acute sick looking
– Limitation of mov’t to ease pain
• Vital signs: fever, tachycardia
• Abdominal examination: guarding, tenderness
over the RUQ, postive murphy sign
– A mass, the gallbladder and adherent omentum
may be palpable

21. • A 45 year-old women in ER presenting with a
compliant of 10 hrs duration of progressively
worsening RUQ pain that is associated with
LGIF, chills, nausea and one episode vomiting
of ingested mater.
• What other Hx you want to hear ?
– Pain chxts….
– Any Hx of jaundice ?

22. DDx of RUQ abdominal pain…?
• Acute cholecystitis
• Acute cholangitis
• Acute pancreatitis
• Perforated PUD
• Acute appendicitis
• Ruptured AAA
• Acute mesenteric ischemia
• MI

23. DDx…..
• Right lobe pneumonia
• Hepatitis
• Liver abscess
• Acute pyelonephritis
• Intestinal obstruction
• Diverticulitis

24. • Laboratory investigation:
– CBC - mild to moderate leukocytosis
• Normal WBC does not rule out the diagnosis
• An unusually high WBC count (>20,000 cells/mm3)
suggests a complicated form of cholecystitis
– BG and Rh
– Liver enzymes - mild elevations

25. • Imaging:
– U/S
– HIDA scan
– Plain abdominal X-ray
– CT-scan
– ERCP
– MRCP

27. US….

28. HIDA scan

29. • On chest X-ray, abnormal gas may present in
the right upper abdomen.

30. From TG-2018

31. Diagnosis
• Early diagnosis reduces both mortality and
morbidity:
– History
– Physical exam…
– Investigation

32. Diagnosis of acute cholecystitis
• TG13/18 criteria required for definitive
diagnosis :
– Presence of one local signs of inflammation
– Presence of one systemic signs of inflammation,
and
– Confirmation by imaging findings
• Sensitivity and specificity to 91.2% and
96.9%, respectively.

35. Management of acute cholecystitis
• Management principles include:
– Conservative mgmt followed by definitive mgmt.
– Definitive management is cholecystectomy.
• Early cholecystectomy
• Delayed cholecystectomy

36. Conservative mgmt:
• Experience shows that, in more than 90% of
cases, the symptoms of acute cholecystitis
subside with the following conservative
measures:
– IV fluids
– IV antibiotics
– Analgesics

37. Conservative measure…
• Admit the pt
• Keep NPO: put on IV fluid (replace deficit if
septics/hypotension; 2-3L with in one hour for adult,
20ml/kg bolus for pediatrics), then MF
• Put on IV antibiotics ( that cover G-ve and anaerobic)
– Ceftriaxone 1 gm IV Bid and metronidazole 500mg IV Tid
• Give analgesics … tramadol 50 - 100 mg IV Tid,
diclofenac 75mg iv Bid
• Give cemitidine 400 mg IV Bid (prophylaxis to prevent
stress gastric ulcer)

38. Cont’d….
• NG-tube suctions
• Antismasmodics
• Monitoring
– Adequacy of UOP hourly
– Vital sign is monitored q 30 min over 2-3 days
until the pt become well
• Deciding on the next mgmt plan

39. • The timing of surgery in acute cholecystitis
remains controversial
• Either to go for early or interval
cholecystectomy depends on:
– Time of presentation
– Patient clinical conditions
– Severity grade as per Tokyo guideline and
– Surgeon decision

40. Mgmt algorithm of acute cholecystitis

41. Based on Tokyo Guideline:
• The current recommendations are
– Mild
• Early cholecystectomy (after the patient is resuscitated)
– Moderate - Severe :
 Conservative management with antibiotics and
cholecystostomy tube as needed.
 Surgical treatment when conservative treatments fail.

42. Early Cholecystectomy :
• Can be performed when pre-OP diagnosis is
established, the pts hemodynamic is stabilized
and complication excluded.
– Mainly if the patient present with in 72 hrs of onset
of pain.
– If mild or moderate grade of acute cholecystitis
• It shortens the total hospital stay, and no need
of second admission.

43. Interval cholecystectomy:
• Delayed presentation, intense local inflammatory
process that can cause adhesion of GB to local
structure and makes surgery not feasible.
• Surgery is associated with a higher incidence of
complications and a higher conversion rate.
• The aim of delaying surgery is to give time for
inflammation to settle down.
• Patient is resuscitated and discharged with
appointment
• Then elective cholecystectomy on the best time
after 6 -12 weeks.

44. • Surgical options:
– Laparoscopic
– Open

45. Laparoscopic cholecystectomy
• The gold standard procedure for acute
cholecystitis.
• It is safe and effective, even in the setting of
acute and sometimes severe inflammation.
• The conversion rate to an open
cholecystectomy is < 5%

46. • In general early laparoscopic cholecystectomy
is preferable to delayed laparoscopic
cholecystectomy in patients with ACC as long
as it is completed within 10 days of onset of
symptoms.
• Open cholecystectomy must remain an option
in particularly difficult cases, or in patients
suspected of having intra-abdominal
adhesions, perforations, peritonitis

47. Emergency cholecystectomy (5-10%)
• When pts condition is deteriorating despite
conservative mgmt, or if there is feature of
perforation or generalized peritonitis ,
empyema, acalculus cholecystitis ----- go for
emergency cholecystectomy

48. Cholecystostomy
• When patients are medically unfit for surgery
due to the severity of their illness ( grade-III)
or medical comorbidities (Eg: those cannot
tolerate GA), they can be treated with
antibiotics and biliary decompression with
cholecystostomy tube placement, which is
usually effective in stabilizing the patient.

49. • Option of cholecystostomy:
– Percutaneous appraoch (Done under US guidance)
• Transhepatic
• Transperitoneal /laparoscopic
– Open cholecystostomy
• Relative contraindications:
– Coagulopathy
– Ascitis

50. • For those who do recover after
cholecystostomy, the tube can be removed
once the track is mature (approximately 4
weeks) and cholangiography through it shows
a patent cystic duct.
• Elective laparoscopic cholecystectomy can be
scheduled within approximately 6 to 8 weeks,
assuming their medical fitness recovers.

51. • Failure to improve after cholecystostomy may
be due to gangrene of the gallbladder or
perforation, in which case, damage control
surgery (open cholecystectomy done)
• There are no reports providing quality
scientific evidence on the best timing for
surgery after percutaneous cholecystostomy.

52. Acute acalculous cholecystitis
• Acute cholecystitis in the absence of stones
• Account for 5-10% of AC
• The pathophysiologic mechanism is poorly
understood, but thought to occur due to bile stasis
and ischemia in the setting of critical illness.
• But, associated with certain risk factors:
– Older age, critical illness, burns, trauma, shock, sepsis,
recent surgery, ICU admissions
– Prolonged use of TPN
– Prolonged fasting
– Immunosuppression.

53. • Presentation is usually more fulminant than ACC,
may progress to empyema, gangrene and
perforation.
• An open procedure is generally preferred.
• But, mortality rate of early cholecystectomy for
acalculous cholecystitis is up to 40%.
• Therefore; percutaneous drainage and delaying
laparotomy is advised .
– 90% of patients will improve with percutaneous
drainage.

54. Complications
• In about 5% to 10% ischemia and necrosis of the
gallbladder wall -- > Gangrenous cholecystitis
• Secondary bacterial contamination in 15% to 30%
of patients ( E.coli, Kleibsela, …)  Empyma of
GB
– Emphysematous cholecystitis (pseudomonas…)
• Mirrizzi syndrome
• Acute cholengitis
• Gallstone ileus
• Chronic cholecystitis

55. • Perforations
– Chemical peritonitis
– Cholecystoenteric fistula (gas in the lumen or wall
of GB on CT or x-ray)
– Intrahepatic abscess

56. Mirrizi syndrome

57. Chronic Cholecystitis
• Recurrent attacks of biliary colic, with only
temporary occlusion of the cystic duct, can
cause inflammation and scarring of the
gallbladder leading to fibrosis and shrinkage
(a histological diagnosis)
• The presentation is that of symptomatic
cholelithiasis, or biliary colic.

58. Thickening, scarring and fibrosis of
GB

59. Emphysematous cholecystitis
• It is an inflammation caused by gas forming
bacteria, and has a high perforation rate.
• Mainly in patients with DM
• It causes potentially fatal complications
including
– Intra-abdominal abscess
– Generalized peritonitis
– Gas gangrene of the abdominal wall, and
– Sepsis

60. • Its clinical course is often extremely rapid
• Classified as moderate cholecystitis in TG13
• Intramural or luminal gas is often present in
gangrenous cholecystitis
• Plain CT (non contrast enhanced) is the most
useful method for diagnosing emphysematous
cholecystitis than any other imaging.

61. Emperic antimicrobial therapy
• Empiric therapy is defined as antimicrobial
therapy until the cultures and susceptibility
testing results are available.
– Broad spectrum agents thought to cover at least G-
ves and GI aerobes and anaerobes
• Once culture result available, shifting to
antimicrobial targeting the specific susceptible
organism (De-escalation)

64. Acute Cholangitis
64

65. • Acute cholangitis is an ascending bacterial infection
associated with partial or complete obstruction of the
bile ducts.
• It is one of the main complications of choledochal
stones.
65

66. • Hepatic bile is sterile, and bile in the bile ducts is kept
sterile by
continuous antegrade flow flushing action of bile
because sphincter of Oddi normally forms an effective
mechanical barrier to duodenal reflux and ascending
bacterial infection.
The bacteriostatic activity of bile salts and
the presence of antibacterial substances in bile,
such as IgA and biliary mucous
66

67. • Mechanical hindrance to bile flow facilitates
ascending bacterial contamination from the bowel.
• Positive bile cultures are common in the presence of
bile duct stones as well as with other causes of
obstruction.
• Biliary bacterial contamination alone does not lead to
clinical cholangitis; the combination of both
•significant bacterial contamination and
•biliary obstruction is required for its development.
67

68. Gallstones are the most common cause of obstruction
in cholangitis.
Other causes include
primary sclerosing cholangitis,
benign and malignant strictures,
parasites,
instrumentation of the ducts, and
Indwelling stents,.
68

69. • The most common organisms cultured from bile in
patients with cholangitis include
•E coli,
•Klebsiella pneumoniae,
•Enterobacter,
•Streptococcus faecalis, and
•Bacteroides fragilis.
69

70. Pathophysiology
• Acute cholangitis occurs when biliary obstruction
results in bile backing up and becoming infected.
• This blockage elevate s pressure within the biliary
system and results in the infected bile being flushed
into systemic circulation, inducing a systemic
inflammatory response.
• The patient can develop septicemia if this situation
continues.
• Severe AC can lead to organ failure due to
septicemia;
70

71. Clinical Manifestations
• Cholangitis may present as anything from a mild, self-
limited episode to a fulminant, potentially life-
threatening septicemia.
• Patients with gallstone-induced cholangitis are most
commonly older and female.
• The most common presentation is fever, epigastric or
right upper quadrant pain, and jaundice.
• These classic symptoms, known as Charcot’s triad,
are present in about two-thirds of patients (50 to75 %)
71

72. • The illness can progress rapidly with the development
of shock and altered mental status, known as
Reynolds’ pentad (e.g. fever, jaundice, right upper
quadrant pain, septic shock, and mental status
changes).
• However, the presentation may be atypical, with little
if any fever, jaundice, or pain. This occurs most
commonly in the elderly, who may have
unremarkable symptoms until the process is already
quite advanced
72

73. • Acute cholangitis has long been diagnosed on the
basis of Charcot ’s triad, which relies on clinical signs
and symptoms.
• Although Charcot’ s triad is highly specific for acute
cholangitis, studies have reported its sensitivity to be
50 to 70%.
• To compensate for the low sensitivity of Charcot’ s
triad, the Tokyo guideline diagnostic criteria were
introduced based on Charcot’ s triad with the
addition of blood test and imaging findings
73

74. 74

75. aSTD: upper limit of normal value
75

76. Severity grading criteria for Acute
cholangitis
• It’s mportant for
predicting prognosis and
determining a treatment strategy, especially
identifying patients that require early biliary
drainage.
• The TG13/18 severity grading criteria allow
assessment based on
• clinical signs and symptoms and
• routine blood tests
76

77. Grade III (severe) acute cholangitis
Grade III acute cholangitis is defined as acute cholangitis
that is associated with the onset of dysfunction at least in
any one of the following organs/systems:
1. Cardiovascular dysfunction: hypotension requiring
dopamine ≥5 micg/kg per min, or any dose of
norepinephrine.
2. Neurological dysfunction: disturbance of consciousness.
77

78. Cont...
3. Respiratory dysfunction: PaO2/FiO2 ratio <
300
4. Renal dysfunction: oliguria, serum
creatinine >2.0 mg/dl
5. Hepatic dysfunction: PT-INR >1.5
6. Hematological dysfunction: platelet count
<100,000/mm3
78

79. Grade II (moderate) acute cholangitis
Grade II acute cholangitis is associated with any
two of the following conditions:
1. Abnormal WBC count (>12,000/mm3,
<4,000/mm3)
2. High fever (≥39°C)
3. Age (≥75 years old)
4. Hyperbilirubinemia (total bilirubin ≥5 mg/dl)
5. Hypoalbuminemia (<STDaX0.7)
79

80. Grade I (mild) acute cholangitis
• Grade I acute cholangitis does not meet the criteria
of Grade III (severe) or Grade II (moderate) acute
cholangitis at initial diagnosis.
80

81. Patient approach
81

82. DDX
Biliary leaks
Acute Cholecystitis
Appendicitis
Acute Pancreatitis,
Liver abscess
Infected choledochal cysts
Recurrent pyogenic cholangitis
Intestinal perforation
Right lower lobe pneumonia/empyema
82

83. Hx of fever, chils, right upper quadrant pain, yellowish
discoloration , itching sensation, clay colored stool, cola
colored urine
Hx of complications: change in mentation, reduced uop
Hx of a history of biliary disease such as gallstones,
previous biliary procedures, laparascopic cholecystectomy
placement of a biliary stent.
Hx of alcohol intake, position dependent pain,
Hx of pain migration
Hx of contact with jaundice patient, msp hx
Hx of similar illnness in the past
83

84. Physical examination
GA
V/S: BP, temprature
HEENT: conjunictiva, sclera, buccal mucosa,
Chest: signs of pneumonia
Abdominal : organ of foci
IGS: cold extremity, pallor, capilary refilling
CNS : mentation
84

85. Laboratory tests
• Routine laboratory tests typically reveal
CBC: an elevated white blood cell count with
neutrophil predominance, and
LFT & Liver enzymes: a cholestatic pattern of
liver test abnormalities, hyperbilirubinemia
(predominantly conjugated) , and elevation of
alkaline phosphatase and transaminases.
85

86. Imaging findings
• diagnostic imaging is considered a method to
directly identify biliary stenosis /blockage that can
cause Acute cholangitis or
 describe dilatation of the bile duct that can be used
as an indirect finding in support of a diagnosis
•Abdominal ultrasound ,
•(CT), and
•(MRI) / (MRCP)
• ERCP is performed for the purposes of treatment
(drainage), but is not suitable as first choice for
diagnostic purposes. 86

87. Abdominal ultrasound
• can readily detect
abnormal dilation of the bile duct ,
identify the Bile duct stones present as highly echoic
nodular lesions that cast an acoustic shadow,
 malignant stenosis of the bile duct, the mass around
the stenosed bile duct can be identified as a normal,
low-echo region.
• abdominal ultrasound has high specificity but
insufficient sensitivity
87

88. Identification of the cause of acute cholangitis by
abdominal ultrasound.
Stone in the common bile duct in a patient with acute cholangitis.
The stone can be seen as hyperechoic nodule with slight
acoustic shadow in the intrapancreatic common bile duct .
88

89. Cholangitis caused by cancer of the pancreatic head. The
bile duct is clearly dilated and the duct is abruptly blocked
by a tumor of the pancreatic head
89

90. • CT imaging
clearly identify bile duct dilatation and
contribute to much better diagnoses of the cause of
biliary stenosis (e.g. biliary carcinoma, pancreatic
cancer, or sclerosing cholangitis). diagnosing local
complications (e.g. liver abscess or portal vein
thrombosis)
90

91. • MRI/MRCP are generally only used for imaging
when a diagnosis proves difficult or uncertain with
abdominal ultrasound or CT.
can delineate the bile duct and
for identifying malignant disease or bile duct stones
causing biliary obstruction
91

92. Management of Acute cholangitis
Should follow these principles:
1. Early diagnosis,
2. Vigorous resuscitation and hemodynamic support,
3. Broad-spectrum IV antibiotics to cover enteric
organisms and anaerobes,
4. Relief of biliary obstruction (decompression)
92

93. 1. Supportive
 Admit to the hospital for evaluation and
treatment.
 Classify the patient as severe, moderate or
mild according to TG13/18 grading
 keep the patient NPO
 Fluid managment
 IV antibiotic covering gm +ve,-ve and anaerobe
Ceftriaxone 1g BID plus metronidazol 500mg
TID ,duration 4-7 days after source control but
minimium of 2wks if strept
 Follow up, v/s, abdominal tenderness, uop
93

94. • Most patients (85%) will clinically improve over the
ensuing 12 to 24 hours.
• Imaging of the biliary tree by ultrasound (US),
computed tomography (CT), magnetic resonance
cholangiography (MRC) is indicated to diagnose the
location and cause of the underlying biliary obstruction
• Patients with acute cholangitis who do not respond to
the initial medical treatment (general supportive care
and antimicrobial therapy) undergo rapid biliary
decompression
94

95. 2. Definitive management, biliary decompression
Depends on underlying cause
 Removal of CBD stones, resection of tumor,
excision of choledochal cyst
For unresectable tumor, self expandable metal
stent(SEMS)
ERCP + sphincterotomy: diagnostic and therapeutic
PTC with catheter drainage: if ERCP not available
or unsuccessful
 and T-tube
placement if above fails
 Cholecystectomy
95

96. Biliary drainage
 Biliary drainage can then be performed on an
elective basis.
 In 15 to 20 percent of cases, cholangitis fails to settle
over the first 24 hours with conservative therapy
alone, requiring urgent biliary decompression.
96

97. Biliary drainage…
• Indications for urgent biliary decompression include:
1. Persistent abdominal pain
2. Hypotension despite adequate resuscitation
3. Fever greater than 39ºC
4. Mental confusion, which is a predictor of poor
outcome
97

98. • Patients who have suffered an episode of acute cholangitis
related to gallstone disease should be recommended to undergo
elective cholecystectomy approximately 6 weeks after the
resolution of their cholangitis.
• Those whose cholangitis was related to another cause of biliary
obstruction should be followed and treated for the specific
etiology of their obstruction but do not necessarily require
cholecystectomy
• Patients with indwelling stents and cholangitis usually require
repeated imaging and stent exchange to mitigate the risk of
recurrent infections.
98

99. Prognosis
• Most patients will respond to biliary decompression
and supportive measures.
• However, Patients with cholangitis can deteriorate
rapidly and may require intensive care unit monitoring
and vasopressor support.
• In the current era, acute cholangitis is associated with
an overall mortality rate of approximately 5%.
• When associated with renal failure, cardiac
impairment, hepatic abscesses, and malignancies, the
morbidity and mortality rates are much higher
reaching up to 50%.
99

100. References
• Bailey and Love’s Short Practice of Surgery: 27th edition
• Schwartz’s Principles of Surgery: 11th edition
• Tokyo Guidelines 13/18
• Uptodate 21.6
• Sabiston Textbook of Surgery: The Biological Basis of
Modern Surgical Practice, 20th edition
100

101. Thank
You !
101