CHOLECYSTITIS
DEFINITION
Refer gallstones.
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INCIDENCE
Refer gallstones.
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AETIOLOGY
Inflammation
Chemical irritation of an obstructed GB.
Then often infection.
- commonly E coli, then Klebsiella, occasionally enterococcus.
Rarely direct infection, eg w/ Salmonella typhi / staph cause acute
cholecystitis
without stones.
Idiopathic
Acalculous cholecystitis
- seen in severely ill, eg post major-op, septic, post-partum,
trauma,
burns,
multi-organ failure.
(see below)
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BIOLOGICAL BEHAVIOUR
Pathophysiology
GB / cystic duct becomes obstructed by a stone.
--> chemical irritation and inflammation.
--> usually sterile
Mucosal phospholipases activate lecithins.
Protective glycoprotein coat is disrupted
--> epithelium is exposed directly to detergent action of bile
salts.
With dysmotility, distention and resulting ischaemia of wall, gb
easily
gets infected.
- bacterial infection is late in the course.
--> worsening pain and systemic illness features appear.
As inflammation spreads transmurally, serosa becomes involved.
Irritates parietal peritoneum.
Causes localised features via somatic afferents.
Acalculous Cholecystitis
Usually seen in MODs pts in ICU; likely ischaemic basis.
- keep this possibility in mind
when
evaluating ICU pts who are septic with abN LFTs & tender
abdos.
Possibly dehydration and blood transfusions lead to an increased
pigment
load
- or GB stasis may follow hyperalimentation & ventilation.
--> bliary sludge, mucus production, obstruction w/out stones.
--> inflammation, ischaemia, bacterial contamination.
Complications
Continuation of the inflammatory process results in an empyema.
Nearby omentum, colon and duodenum become inflamed and adherent to
the
gallbladder (phlegmon).
Gall bladder may become gangrenous with local perforation.
- this is uncommon as blood supply good, and usually thick-walled
from
past inflammation.
--> gas in gallbladder wall and tree; emphysematous cholecystitis
A fistula may rarely form, into the associated bowel, usually the
duodenum.
--> rarely this may cause gallstone ileus at DJ flexure or distal
ileum.
Prognosis
Without medical attention, most attacks subside within 7-10 days,
often in 24hrs.
25% develop progressively severe symptoms.
In those that recover, repeat attacks are common.
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MANIFESTATIONS
Signs
Local
Often preceeding / superimposed features of cholelithiasis.
Often onset after a fatty meal --> gallstone entrapment.
Localised pain.
Sharp, localised to right hypochondrium.
- radiates to back / R shoulder
Exacerbated by moving or deep breathing.
Systemic
Nausea, vomiting common
Fever, chills, rigors, tachycardia.
Symptoms
Observe
Pain worst when the patient takes a deep breath.
Palpate
Tenderness and guarding in the right upper quadrant.
Murphy's sign may be present.
A mass may be felt if empyema has developed.
- if this stage is reached, pt will have a hyperdynamic circulation
of
sepsis.
Examine for jaundice and septic shock.
Acalculous
Tends to be more insidious
Less specific symptoms.
Underlying conditions obscure it.
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INVESTIGATIONS
Haematology
Us. mildly elevated WCC.
Biochemistry
Mirrizi's syndrome: large gallstone in cystic duct causing
compression of CHD.
High biliR = consider CBD obstruction.
- unless severe necrotizing cholecystitis; mildly elevated biliR.
Mildy elevated transaminases and alk phos can occur.
Clotting screen
Routine.
Cultures
If T>38.
Imaging
Ultrasound
Investigation of choice.
- wise to consider urgently if septic
Gallstones appear white with dark shadowing behind the stone.
- hyperechogenic, acoustic shadow behind stone; prominent as GB
cystic therefore exhibits acoustic enhancement normally.
Thickening of the gall bladder wall (>4mm) and pericholecystic
fluid
may indicate cholecystitis.
Ductal dilation suggests stone in duct.
CT
Can demonstrate features of GB pathology but not as sensitive as
sonography.
MRCP
As good as US; sensitive to fluid stasis and in demonstrating
pericholecystic fluid.
Very good for CBD stones.
Routinely useful (if available) to rule out CBD stones with ducts
dilated or biliR elevated.
- much safer than ERCP; obviates the need when half of these pts
have N tests.
HIDA
Can be undertaken.
But not often useful as false +ves when fasting.
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MANAGEMENT
Acute
IV fluids
Although sterile, infection can develop secondarily.
- antibiotics to cover gram -ves, eg. amoxyl, gent, metronidazole
- often dual therapy alone when not cholangitis, eg ceftriaxone and
metronidazole.
- in v. unwell pts consider tazosin.
Ceased when cholecystectomy performed.
Early vs Delayed Lap Chole?
Cochrane analysis of 5 trials has shown no difference in mortality,
bile duct injury, or conversion to open chole.
Early chole halts disease process and prevents complications.
Unless critically ill with hemodynamic instability or other active
problems that prohibit a safe operation, they should be considered.
- then consider cholecystostomy tube.
One safe way to manage a cholecystostomy tube
Maintain it for up to 3m
--> then insert contrast to check patency of cystic duct.
--> remove tube if patent.
--> then consider elective cholecystectomy.
But I have had patients with them fall out the next week and it goes
fine, so whatever.
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