OVERVIEW OF ACUTE CHOLECYSTITIS

1. AETIOPATHOGENESIS AND
MANAGEMENT
OF
ACUTE CHOLECYSTITIS
PRESENTER:
EZEAKU CHIZOWA
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2. 2

3. OUTLINE
• INTRODUCTION
• ANATOMY/PHYSIOLOGY
• AETIOLOGY/ RISK FACTORS
• PATHOGENESIS/PATHOLOGY
• MANAGEMENT
• COMPLICATIONS
• PROGNOSIS
• LOCAL EXPERIENCE/FUTURE TRENDS
• CONCLUSION
• REFERENCE
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4. INTRODUCTION
• Acute cholecystitis is the inflammation of the gallbladder that occurs
most commonly because of an obstruction of the cystic duct from
stone.
• It is classified as
• Acute calculous cholecystitis(90%)
• Acute acalculous cholecystitis(10%)
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5. Anatomy
• It is a pear-shaped structure, 7.5–12 cm long, with a
normal capacity of about 25–30 mL. Lies on the underside
of the liver.
• May embedded within the liver substance to being
suspended by a mesentry
• Blood supply-cystic artery, an accessory cystic artery arises
from the gastroduodenal artery.
• Anatomical variations (Moynihan’s hump’.)
• Venous drainage-multiple small veins in the gall bladder
bed into the liver substance, cystic vein(uncommon)
• Lymphatics drainage- cystic lymph node of Lund, nodes in
portal hepatis and coeliac plexus
• Nerve supply- parasympathetic (hepatic branch of anterior
vagal trunk), sympathetic (cell bodies of coeliac ganglion)
• CALOT TRIANGLE(IMPORTANT SURGICAL LANDMARK)
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6. Moynihan’s hump
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7. Physiology
• The gall bladder is a reservoir for bile.
• The second function of the gall bladder is
concentration of bile by active absorption of
water, sodium chloride and bicarbonate by the
mucous membrane of the gall bladder.
• The third function of the gall bladder is the
secretion of mucus – approximately 20 mL is
produced per day.
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8. EPIDEMIOLOGY
• Patients are commonly 30 to 60years.
• The incidence increases with age.
• Linked to changing androgen-to-estrogen ratios in elderly men.
• Male :Female = 2:3 (Calculous cholecystitis)
• Acalculous cholecystitis observed more often in elderly men.
• Increased prevalence in people of Scandinavian, Hispanic populations,
less common among individuals from sub-Saharan Africa and Asia.
• Generally more prevalent in whites than black.
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9. AETIOLOGY(CALCULOUS CHOLECYSTITIS)
• Two principal agents are implicated:
• An inflammatory element
• Bacterial(70%) -E.coli, Streptococci,salmonella,staphylococci, C. welchii)
• or chemical(30%)
• An obstructive element
• Cholelithiasis (about 99%)
• Neoplasm (1%)
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10. AETIOLOGY(ACALCULOUS CHOLECYSTITIS)
• The exact cause is unknown. Several theories exist
• Seen in conditions associated with biliary stasis.
• Injury may be the result of retained concentrated bile, an extreme
noxious substance.
• Role of organisms and their endotoxins –demonstrated to abolish the
contractile response to CCK, cause necrosis ,hemorrhage ,extensive
mucosal loss and area of fibrin deposition in the gallbladder wall.
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11. Risk factors(acute calculous cholecystitis)
• Mirrors those for cholelithiasis, and include the following:
• Female sex
• Certain ethnic groups
• Obesity or rapid weight loss
• Drugs (especially hormonal therapy in women)
• Pregnancy
• Increasing age
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12. Risk factors(acute acalculous cholecystitis)
• Seen in conditions associated with bliary stasis:
• Critical illness
• Multiple major trauma/ surgery
• Extensive burns
• Prolonged total parenteral nutrition (TPN)
• Drug overdosage
• Multiple blood transfusions
• Starvation
• Cardiac events,including myocardial infarction
• Sickle cell disease
• Patients with AIDS, who have CMV, cryptosporidiosis,or microsporidiosis 12

13. Pathogenesis
• When a stone becomes impacted in the cystic duct or Hartmann’s
pouch.
• Obstruction causes stasis, oedema of the wall, bacterial invasion and
wall thickening.
• Events may then take one of several
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14. • 1. The mucous membrane may
become lifted away from the
sides of a stone wedged in the
neck of the gall bladder, making
it possible for the stone to slip
back into the gall bladder.
• So that the muco-purulent
contents of the bladder drain
into the common bile duct .
• The attack is then temporarily
arrested.
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15. • 2. Occasionally the impaction
may persist with resulting
empyema of the gall bladder.
• 3. Rarely the distended gall
bladder may perforate.
Usually in diabetics and old
patients over 60-70 with
atherosclerosis.
• A local abscess or general
peritonitis is the result of
perforation.
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16. • 4.Calculous impaction with inflammation and
oedema causes reduction of blood flow rendering
the gall bladder not only more susceptible to
infection but may precipitate gangrene.
• 5. In severe haemorrhagic cholecystitis, the mucosa
becomes partly necrotic and with obstruction to the
cystic duct persisting, empyema is the result.
• 6.Transmural inflammation of the serosa leads to
local peritonitis and this could progress to produce
an inflammatory mass
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17. • 6.An inflammatory mass that develops
around a stone impacted in Hartman's
pouch.
• This often spreads to adjacent
structures, including the common
hepatic duct resulting in Mirizzi
syndrome, cholangitis and other
attendant complications -
pericholecystitis, abscess,
cholecystocholedochal fistula,
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18. Pathology
• Gallbladder is distended with oedematous friable wall, containing
friable wall. Areas of necrosis and patchy gangrene may be seen.
• Mucosa shows ulceration and necrosis.
• Lumen contains infected fluid/infected bile or frank pus.
• Histology shows areas of focal necrosis, venous congestion with influx
of neutrophils.
• May be superimposed on a histology picture of chronic cholecystitis-
fibrosis, mucosal flattening, mucosal herniation(Rokitansky-Aschoff
sinuses)
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19. Management
• History
• Physical examination
• Differentials
• Investigations
• Treatment
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20. History
• BIODATA-Female, 30 to 60 years, elderly male
• Prsenting Complaint-
• The main symptom is a upper abdominal pain,. It is felt in the right hypochondrium or
epiastrium,and often radiates close to the tip of the right scapula. Gradual or sudden in
onset,
• Continuous, lasting more than 6 hours, and is exacerbated by fatty meals.
• Associatied features:
• nausea and vomiting, fever, flatulent dyspepsia, transient jaundice, abdominal mass.
• Previous history:
• flatulent dyspepsia or previous attacks of gallstone colic, weight gain, OCP use
• History of risk factors
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21. Physical examination
• General- painful distress ,febrile, jaundice, dehydration
• Abdomen:
• INSPECTION
• fullness in the right hypochondrium(Zackary Cope’s sign).
• PALPATION
• Tenderness,rebound tenderness,guarding or rigidity on the right hypochondrium
• Mass …….(inflammatory mass)
• Murphy’s sign
• Boas’ sign
• PERCUSSION
• a dull area just beneath the costal margin may suggest an inflammatory mass
• AUSCULTATION
• Absent bowel sound seen in peritonitis
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22. Differentials
• Mucocele of the gallbladder
• Cholangitis
• Biliary colic
• Gallbladder ca
• Hiatus hernia
• Acute appendicitis,(especially high retrocecal appendix)
• Acute pancreatitis
• Acute pyelonephritis,
• Hepatitis,
• Acute exacerbation of peptic ulcer,
• Myocardial infarction,
• Pneumonia
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23. INVESTIGATIONS
• To confirm the diagnosis
• Abdominal ultrasound, Liver function test, plain abdominal xray,
• Others: HIDA scan, CT scan, ERCP
• To workup patient for treatment
• Fbc +diff, urinalysis, SEUCr, CXR,ECG(for elderly)
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24. Abdominal ultrasound
• 95% specificity and 85% sensivity.
• Diagnostic criteria includes:
• calculi with acoustic shadowing
• Gall bladder(GB) wall thickening >4mm
• Sonographic murphy’s sign
• Serosal edema (halo sign)
• Pericholecystic fluid collection
• Hypervascularity of the GB wall on colour flow and Doppler
• Intraluminal-wall desquamation, resulting in lacelike lumen
• Distension of gallbladder (about 93% of patient with GB volume >70ml have AC)
• Best done after a fast of at least 8hours.
• Visualise surrounding organs eg pancreas, liver.
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25. ULTRASOUND SCAN
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26. • Liver Function Test
• Slight elevation of serum transaminase, alkaline phosphatase and bilirubin.
• Plain Abdominal xray
• 10% of gall stones are radio-opaque.
• Gas within the gallbladder
• emphysematous cholecystitis, calculi just passed into the duodenum
• Diffuse calcification (Porcelain gallbladder)
• FBC +Diff
• Leucocytosis with a left shift
• Urinalysis
• Rule out pyelonephritis,bilirubinuria(obstructive jaundice)
• SEUCr
• Normal or deranged in dehydration
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27. PLAIN XRAY
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28. • HIDA Scan(hepatoimunodiacetic acid)spec 85-95%,sens 90-100%
• Non visualization of gallbladder is diagnostic.
• CT Scan(less sensitive than USS)
• Wall thickness>4mm, pericholecystic fluid,subserosal edema,intramural gas,
and sloughed mucosa.
• ERCP
• Outline biliary tract, locate and retrieve stones,passage of stent
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29. CT Scan showing stone at the neck of the
gallbladder
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30. Treatment Options
• Two school of thought
• Conservative management and interval cholecystectomy(at 6weeks )
• Early cholecystectomy(within 72hrs of onset of illness)
• Emergency cholecystectomy
• Percutaneous cholecystostomy with interval cholecystectomy
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31. Conservative management and interval cholecystectomy
• The argument in favour of this approach is that:
• (a) Majority of patients settle on conservative measures.
• (b)Dissection of the inflamed area could lead to spread of infection.
• ( c) The inflammatory vascular congestion does not make for a dry field;
anatomical anomalies may, not be readily evident.
• (d) Patients at risk from perforation are frequently identifiable (diabetic and aged
individuals) and the signs of incipient perforation are readily recognizable.
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32. Indications for conservative management
• Afebrile with stable vital signs.
• No evidence of obstruction by lab values.
• No evidence of CBD obstruction on ultrasonography.
• No underlying medical problems(advanced age, pregnancy,
immunocompromised).
• Prompt follow up care.
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33. Conservative Management
• Rest inflamed gall bladder!
• NPO , Nasogastric aspiration, replacement of fluid and electrolytes.
• Anticholinergics- reduce gastric and pancreatic secretion,relaxes sphincter of Oddi.
• I.M. Propantheline 15mg 8hrly; I.M. Atropine 0.6mg 8 hrly (rapid response)
• Analgesics
• I.M. pethidine lOOmg, I.M. Tramadol 100mg, NSAIDS-Ibuprofen.
• DO NOT USE MORPHINE!- causes spasms of sphincter of Oddi.
• Antibiotics
• Broad spectrum and bacteriocidal, covering common organisms encountered.
• 3rd generation cephalosporns are agents of chioce. Aminoglycosides nay be used.
• Interval cholecystectomy done after 6 -10 weeks 33

34. Contra-indications to conservative treatment
• Worsening vital signs.
• Spreading pain and tenderness- signs of incipient perforation.
• Spreading gangrene of the gall bladder with redness and oedema of the
overlying skin.
• Presence of an inflammatory mass in the right hypochondrium.
• Mucocele of the gallbladder(swelling without fever).
• Detection of gas in the extrabiliary system.
• Detection of intestinal obstruction.
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35. Early cholecystectomy(within 72hrs of onset of illness)
• Recent studies has shown that early cholecystectomy following diagnosis and
conservative management has shown clear benefits over delayed. This
includes:
• Lesser hospital stay.
• Lesser cost of treatment.
• Also there is no increase in the morbidity from iatrogenic ductal injury or
missed stones; nor is the mortality, when done within 3days.
• In addition ,approximately 20% of patient admitted for conservative
management failed to respond before planned interval cholecystectomy,
necessitating early surgery.
• Best done using the retrograde technique and is covered by a short pre- and
post-operative (24h)course of broad-spectrum bactericidal antibiotics.
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36. Emergency cholecystectomy
• This is indicated in
• Failed conservative management or worsening of symptoms
• Empyema gallbladder
• Emphysematous gallbladder
• Gall bladder perforation
• Elderly
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37. Percutaneous cholecystostomy with interval cholecystectomy
• Indicated in
• Critically ill patient with prohibitive high operative risk.
• Elderly with serious comorbid conditions.
• Patient with acute acalculous cholecystitis.
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38. Cholecystectomy
• There are two methods
• Laparoscopic cholecystectomy
• This is the standard treatment of care for the surgical treatment of
cholecystitis.
• Open cholecystectomy
• Commonly done in our environment .
• Conversion from laparoscopic approach(4%)
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39. Open cholecystectomy
• Preoperative preparation: hx ,exam, lab ,informed consent
• General anaesthesia with endotracheal intubation is recommended
• Supine position
• Routine skin prep and prophylactic antibiotics
• Incision
• Right paramedian incision, Right upper transverse incision (Kocher incision)
• Techniques
• Retrograde technique
• Fundus-first technique
• Identification and safe dissection of Calot’s triangle
• Skin closure
• Post operative care
• NG tube(significant infection,ileus) post op antibiotics , analgesics, diet soon as tolerated. 39

40. Complications of cholecystectomy
• Bleeding from cystic artery or gallbladder bed
• reoperation
• Injury to common bile duct
• Stenting, bile duct reconstruction
• Bile leakage from cystic duct or gallbladder
• Mgt- ERCP, T-tube
• Biliary peritonitis
• Biliary stricture, stenosis and subsequent obstructive jaundice
• Early onset (passage of guidewire,balloon dilatation with stent insertion)
• Late (immediate Roux-en- Y choledochojejunostomy)
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41. Complications of cholecystectomy
• Post-cholecystectomy syndrome
• Is the persistence of symptoms following cholecystectomy
• This is attributed to residual common duct stones, residual cystic duct stump,
damage to biliary tree, autonomic nerve neuromas of the stump.
• This is best performed by MRCP or ERCP, the latter which has the added
advantage that if a stone is in the common bile duct it can be removed.
• Post-cholecystectomy choledocholithiasis
• Endoscopic papillotomy is the preferred first technique with a
sphincterotomy, removal of the stones using a Dormia basket or the
placement of a stent if stone removal is not possible.
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42. Cholecystostomy
• This relatively minor procedure may be performed as an emergency
measure in unfit patients in whom cholecystectomy is indicated.
• Frequently done under ultrasound guidiance under local anesthesia with
some sedation.
• The fundus of the gall bladder is opened, any impacted stones extracted
with forceps and a self retaining catheter (e.g. De- pezzer, Malecot or
Foley) inserted and brought to the exterior through a separate stab
incision. Left for several weeks.
• Tubogram may be done to check for residual stones, biliary anatomy
• More than 50% remain asymptomatic after 5years and not every patient
requires subsequent cholecystectomy.
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43. CHOLECYSTOSTOMY
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44. Complications of Cholecystitis
• Perforation
• Peritonitis
• Pericholecystic abscess
• Empyema gallbladder
• Cholangitis
• Gangrenous gallbladder
• Chronic cholecystitis
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45. Prognosis
• The overall reported mortality of acute cholecystitis is 2-3 % with
much higher figures (10%) in patients over 70.
• This is largely due to incidental cardiorespiratory disease and
complications.
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46. Local experience
• Open cholecystectomy still remains the procedure of choice mainly
due to unavailability of laparoscopic technology and expertise.
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47. Future trend
• Endoscopic treatment
• Endoscopic ultrasound-guided transmural cholecystostomy
• Studies indicates this procedure may be safe as an initial,interim, or definitive
treatment of patients with severe acute cholecystitis with high operative risk for
intermediate cholecystectomy
• Endoscopic gallbladder drainage
• Biliary obstruction and incomplete drainage with prior intervention
• Inaccessible ampulla
• Previous failed bile duct cannulation during ERCP.
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48. CONCLUSION
• Acute cholecystitis is a treated surgical condition, early diagnosis and
treatment is needed to avert complications.
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49. REFERENCE
• Bailey And Love's Short Practice of Surgery 26th edition
• Baja’s Principles and Practice of Surgery including Pathology of the
Tropics, 5th edition
• SRB's Manual of Surgery, 4th edition
• emedicine.medscape.com/article/cholecystitis
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