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Biliary diseases - Coggle Diagram

- - - - Usually dingle
      - Yellowish green
      - More than 2.5 cm
      - Nearly 100% cholesterol
      - Radiolucent
    - - Usually multiple with cholesterol core (60%)
      - Outer brown shell formed of ca bilirubinate, phosphate and palmitate (40%)
      - Laminated with faceted surface
      - Size 0.5-2.5 cm
      - Radioapaque in 15 % (ca content)
      - causedby infection
    - - Black pigment
        
        usually multiple
        
        tarry black with multiple spicules
        
        less than 2.5 cm
        
        50% radioopaque ( ca bilirubinate)
        
        in pt with hemolytic anemia or cirrhosis
      - Brown pigment
        
        multiple dark brown laminated
        
        less than 2.5 cm
        
        found in infection, stagnant bile and FB eg. stent
        
        Mostly radio-opaque ( ca bilirubinate mainly)
  - - - Disturbed bile salts/cholesterol ratio
        
        by bile salts and phospho lipid, cholesterol (water insoluble) form micelle aggregate them
        
        bile salts and phospholipid : cholesterol ratio is 25: 1
        
        any disturbance in this ratio >> supersaturated bile ( lithogenic bile)
        
        Factors disturbing this ratio
        
        Reduced bile salts pool
        
        oestrogens reduce bile salts concentration
        
        bile salts malabsorption in terminal ileum affect enterohepatic circulation as Crohn's, bypass procedure or DM ( autonomic neuoropathy)
        
        Diminshed hepatic synthesis in liver diseases
        
        Increase cholesterol synthsis
        
        Obesity, high dietary fat and high caloric diet
      - Stasis of bile
        
        Female hormones
        
        Progesteron >> relaxation & impaired GB emptying
        
        Oestrogen, oral contraceptive and repeated pregnancies >> increase gallstones incedince
        
        following trunkal vagotomy (GB denervation)
        
        DM
        
        Obesity
        
        long term parentral nutrition
        
        lack of oral intake prevent cholecystokinin release
    - - Haemolytic anemia
        
        Any condition w shorten life span of RBCs as (heridetary spherocytosis, thalassemia or prosthetic heart valves) assiciated with black pigment stones
      - Liver cirrhosis
        
        decrease bile acids secretion >> diminished uncojugated bilirubuin solubility
        
        assiciated with increased all gallstones incidence esp. black pigment stones
      - Infection
        
        brown pigment stones formation
        
        E. coli infection >> B- glucoronidase production >> hydrolyses bil. glucoronide to insoluble bilirubin ( precepitate ca bilirubinate)
  - - - CCC
        
        Thick walled and small ( contracted) GB
      - GB Carinoma
        
        long standing calcular dis. >> squamous metaplasia >> carcinoma
        
        90% of GB carcinoma pt. have gallstones
      - obstruction ( cystic duct or GB neck)
        
        Mucocele ( with sterile content)
        
        Infection
        
        cause ACC
        
        Severe inflammation produce empyema, gangrene or gallbladder perforation
    - - Migration CBD
        
        Cholangitis and liver cholegetic abscesses
        
        Acute pancreatitis
        
        The stone obstruct the common channel of CBD & pancreatic duct
        
        In many cases, no actual obstruction of the ampulla (unknown pancreatitis)
        
        Biliary cirrhosis
        
        In long standing intermittent obstruction
        
        Obstructive jaundice
        
        Causing bleeding tendency, septicaemia renal and hepatic failure
      - Migration to duodenum through a fistula ( rare)
        
        big stone > 2.5 cm pass though a fistula between GB and duodenum
        
        migrates and may impacted in the terminal ileum about 2 feetsfrom ileocecal valve
        
        this form of intestinal obstruction is called gallstone ileus
        
        Diagnosis is difficult as the patient is eldery and due to long history of biliary problem
  - - - biliary colic ( recurrent attacks)
        
        Recurrent severe upper abdominal pain may referred to back, right shoulder or right chest
        
        persistant increase in severity over 30 min.
        
        less than 5-6 hours ( longer suggests acute cholecystitis)
        
        precipitated by intake of fatty meal
        
        may be associated with nausea and vomitting
        
        Clinical ex. : right hypochondreal tenderness
        
        Murphy's sign +ve ( GB palpated while taking a deep breath>> the pt. 'll catch his breath)
        
        somtimes, misdiagnosed as peptic ulcer or chronic colitis
      - biliary dyspepsia ( with bloating and excessice eructation)
      - Reflex retrosternal pain ( cholecysto-cardiac link) : diagnosed as anginal pain
      - Complications : 1st presentation may be a complication as obstructive jaundice
  - - - conservative except if high complication rate
        
        High complication rate ( ttt by prophylactic cholecystectomy) :
        
        DM
        
        Congenital hemolytic anaemia
        
        Calcified GB ( porcelain)
        
        single stone > 3 cm
        
        Multiple tiny stones 2-3cm
    - - open or laparoscopic cholecystectomy
  - - - Inv. of choice
      - 98% detection of gallstones
      - detection of GB mural thickening ( indicate long standing recurrent inflammations )
      - detection of intra & extra hepatic biliary radicales ( may indicate CBD stone)
        
        MRCP
        
        accurate delienation of biliary tree
        
        verify prescence of CBD stones
- - - - With cholangitis
      - Without cholangitis
- - - - Cystic duct or GB neck obstruction by a stone (98%)
      - Consequent infection with Gram -ve bacilli
    - - Distended GB e' thick wall
      - loss of normal serosal lining bluish luster
      - covered by fibrinous deposits
      - wall : multiple micro abscesses
      - To localize infection : greater omentum, duodenum and colon become adherent to GB
    - - Resolution (commonest)
        
        Stone dislodges → obstruction relieved → resolution of inflammation
      - Persistent obstruction ( less common )
        
        Progressive GB distention → bl. Vessels thrombosis → wall gangrene
        
        GB perforation → localized or generalized peritonitis (0.5%)
        
        Acute emphysematous cholecystitis (in diabetic pt.) →due to anaerobic infection eg. Clostridia
        
        High virulent infection
        
        Accompanied by gas formation
        
        Leads to early GB gangrene
      - GB empyema
        
        Closed bag of pus
      - Recurrent attacks
        
        Lead to CCC
    - - Symptoms
        
        Initially diffuse colicky upper abdominal pain
        
        With serosal inflammation : pain becomes dull aching, persistent, localized to right hypochondrium
        
        Pain referred to right shoulder (due to irritation of under surface of diaphragm supplied by phrenic n. Sensory fibers
        
        Pain persisting more than 6 h.indicate acute cholecystitis
        
        Sometimes nausea and vomitting
      - Signs
        
        Pyrexia and tachycardia
        
        Right hypochondrial tenderness, rebound tenderness, guarding
        
        Difficult palpation of distended GB (tenderness and rigidity)
        
        Murphy's sign:
        Pt. Is asked to take a deep breath while applying pressure to right hypochondrium →he'll hold his
        
        Boas's sign:
        Right side hyperesthesia between 9th to 11th ribs posteriorly
        
        Mirrizzi's syndrome (rare):
        Impacted large stone in Hartmann's pouch may compress bile duct causing jaundice
    - - Perforated DU
      - Acute pancreatitis
      - High retrocececal appendices
      - Right pyelonephritis
      - Amoebic hepatitis
    - - Laboratory
        
        Bl. Picture: polymorphonuclear leucocytosis
        
        Liver function tests: usually normal
      - Imaging
        
        Abdominal US
        
        The most appropriate inv.
        
        Detect
        
        presence of gallstones
        
        distende GB
        
        thickened wall
        
        micro abscesses and serosal oedema
    - - Early cholecystectomy ( trend now)
        
        sure diagnosis
        
        fit patient
        
        experienced surgeon
        
        Advantage
        -Easy early surgery (within 3 days)
        -Avoid complications of acute cholecystitis
        -One hospital admission early return to work
      - Initial conservative ttt then cholecystectomy after 6 weeks
        
        NPO
        
        IV fliuds
        
        Abs against G-ve as ampicillin, cephalosporin
        
        Analgesic as NSAIDs or pethidine
        
        Follow up of pulse, temperature, tenderness and rigidity
        
        Most pt. Improve and return to elective cholecystectomy after 6 months ( after subside of inflammatory reaction)
        
        If not improved:
        
        Exploration+ cholecystectomy
        
        lf marked inflammation → cholecystostomy ( open fundus + remove stones + drain GB by a tube for 1 week) .. then cholecystectomy after 6 weeks
  - - - Major burn or major trauma patients
      - Patients on prolonged TPN
      - Complicate certain infections as brucellosis and typhoid