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The Gallbladder

Surgery Clerkship
by

Jay Watsby

on 3 March 2015

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Transcript of The Gallbladder

CASE PRESENTATION
1.) HISTORY OF CHOLECYSTECTOMY
2.) CASE PRESENTATION
3.) EMBRYOLOGY
4.) PATHOLOGY OF THE GALLBLADDER AND RELATED DISORDERS
5.) REVIEW OF LITERATURE

HISTORY OF CHOLECYSTECTOMY
Jordan Whatley, MS3
New York Medical College

The Gallbladder
Antonio Benevieni, a pathologist in Florence, Italy creates first known report of gallstones in a woman who died with abdominal pain.
1420
1678
Cornelis Stalpert van der Wiel first incised the abdominal wall for bile drainage in a patient with an gangrenous cholecystitis with calculi and purulent peritonitis.
1667
Jean-Louis Petit, a French surgeon and inventor of the tourniquet, first suggests removal of gallstones and drainage of the gall bladder. 10 years later, he creates the first known cholecystocutaneous fistula.
1733
Cholecystostomy gains prominence as the definitive surgical treatment of gallstones after procedures accomplished by J. L. W. Thudichum, John Stough Bobbs, and Marion Simms. However, gallstones frequently recurred after cholecystostomy.
1859
Zambeccari and Teckoff performed cholecystostomies and cholecystectomies in dogs demonstrating that the gallbladder was unnecessary for life in animal models.
Recognizing the work of Zambeccari and Teckoff, Carl Langenbuch developed the technique of cholecystectomy via cadaveric dissection. At 27 years old, he performed the first known successful open cholecystectomy at Lazarus hospital in Berlin. The patient was a 43 year old man with a 16-year
history of biliary
colic.
1882
After decades of contention among surgeons, the cholecystectomy procedure overtook the cholecystostomy procedure as the standard of care for gallstones.
1897
Erich Mühe of Böblingen, Germany, performed the
first laparoscopic
cholecystectomy.
1985
SURGICAL
INTERVENTION
HOSPITALIZATION

Admitted to the MICU for severe anemia most likely secondary to postmenopausal bleeding where she was given packed RBCs until hemoglobin >8

Gynecology was consulted; Pelvic exam revealed trace vaginal bleeding and a 2 cm soft avascular mass extending from the anal canal; Hysteroscopic dilation and curettage with endometrial biopsy performed on 4/30/2013 which revealed inactive endometrium with stromal breakdown; Multiple fibroids in the cervical and endometrial canal were found on hysteroscopy; Postmenopausal bleeding attributed to fibroids; Gynecology recommended hysterectomy

Intraoperative surgical consult was made during hysteroscopy; anal polyp was excised and sent to pathology, which revealed a inflammatory cloacogenic polyp

After choledocholithiasis and ampullary adenoma was found on MRCP, patient was transferred to SICU for transduodenal excision of ampullary mass and common bile duct exploration

Additionally, colonoscopy was performed on 5/2/2013 which revealed a polyp
in the ascending colon; polyp was removed and sent to pathology,
which revealed a tubular adenoma
IMAGING
ED PRESENTATION
4/21/2013
HPI:
63 year-old woman presents to the ED with 1-month history of malaise, weakness, and painless jaundice, with occasional pale-colored, loose stool. Pt denied fever, abdominal pain, nausea, vomiting, urinary changes, blood in stool. She reports a 7-year history of abnormal vaginal bleeding. She has not seen a physician in 7 years.

PMH:
HTN, uterine fibroids

PSH:
C-section, uterine myomectomy

Medications:
None

Allergies:
NKDFA

Family History:
Father – died from stomach cancer; Paternal Grandmother – died from unspecified cancer

Social History:
Pt denied use of tobacco products, alcohol, illicit substances, and IV drug use at present or in past

Physical Exam:
moderate jaundice of the skin, icteric conjunctivae
Abdomen: soft, ND, NT, bowel sounds present and normal, negative Murphy’s sign,
no hepatosplenomegaly; healed surgical scars
ED VITALS AND LABS
Na: 134 L
K: 3.2 L
Cl: 99
CO2: 24
BUN: 36 H
Crt: 1.7 H
BUN/Crt: 21.2
Glu: 129 H

Ca: 7.9 L
Corr. Ca: 9.6
Mg: 2
WBC: 12.5 H

Neut: 79% H

Lymp: 13.5% L
Mono: 6%
Eos: 1.3%
Baso: 0.2%
Hgb: 5.6 CL
Hct: 20 CL
Plt: 817 H
RDW: 25.5% H
MCV: 89.7
AST: 106 H
ALT: 88 H
AlkP: 621 H
T Bili: 2.87 H
Direct Bili: 2.66 H
T Prot: 6.7
Alb: 1.8 L

Amylase: 79
Lipase: 338 H
Temp: 98.2 F
HR: 118
BP: 155/79
RR: 18
O2 sat: 98% room air
PTT: 31.2
PT: 11.6
INR: 1.11

Retic. Count: 6.49 H
TIBC: 232 L
Iron: 47
Ferritin: 557.8 H

FS Glu: 87
URINALYSIS
Dark yellow, cloudy
Glucose: negative
Bilirubin: small
Ketones: negative
Specific Gravity: 1.014
Blood: large
pH: 5.5
Protein: 30
Urobilinogen: 1
Nitrates: negative
Leukocyte Esterase: small
WBCs: 2 - 5
RBCs: 15 - 30
Epithelial Cells: 1 - 10
Bacteria: few
EMBRYOLOGY
PATHOLOGY OF THE GALLBLADDER
GALLSTONES
Epidemiology and Risk Factors
and Related Disorders
REVIEW OF LITERATURE
Thank you!
AMPULLARY ADENOMAS
Chronic Cholecystitis with Cholelithiasis (Cholesterol stones)
- One of the most common and costly of all digestive diseases

- Large variation in overall prevalence between different ethnic populations

- Higher rates of cholelithiasis in western Caucasian, Hispanic, and Native American populations

- Native Americans have highest prevalence of gallstones in North America; 73 percent of female Pima Indians over the age of 25 years have gallstones (***testable material)

- Lower rates in eastern European, African American, and Japanese populations

- African Americans have 40% lower risk of hospitalization due to gallstones as compared to Caucasians
RISK FACTORS
"Forty, Female, Fertile, Fat"
AGE: Major risk factor; Age 40 is the cut-off between relatively low and high rates of cholecystectomies. Incidence is 4 times higher after 40. Very rare in children if not found in the setting of hemolytic state

GENDER: Higher prevalence in women (striking difference in young adult populations)

PREGNANCY: Major risk factor for cholesterol stones and biliary sludging

SEX HORMONES: Cause bile to become supersaturated with cholesterol which promotes gallstone formation

OCPs and ERT: Estrogen therapy associated with higher rates of gallstones. Risk of gallstone formation is higher with ERT than OCPs

OBESITY: Increased risk due to enhanced cholesterol synthesis and secretion; 3-fold increased risk in young adults who are morbidly obese compared to general population
ADDITIONAL RISK FACTORS
FAMILY HX and GENETICS: Family history studies have demonstrated higher risk of gallstones if first degree relative with gallstones as compared to matched controls

RAPID WEIGHT LOSS: Associated with increased risk due to 18-fold increase in bile mucin content and 40 percent bile calcium concentration during rapid weight loss; Gallstones are a known complication of bariatric surgery

DISEASE STATES: Diabetes mellitus, cirrhosis, Crohn’s disease, hemolytic disease

MEDICATIONS: Clofibrate, a lipid-lowering agent, reduces bile-secretion. This results in cholesterol supersaturated bile and stone precipitation. Ceftriaxone is a major cause of biliary sludge formation in hospitalized patients.

DECREASED PHYSICAL ACTIVITY: Physician’s Health Study demonstrated that physical activity is a protective factor against symptomatic gallstones

SERUM LIPIDS: Positive association between gallstones and apolipoprotein E4 phenotype and elevated serum triglycerides. HDL is negatively correlated with incidence of gallstones. ***There is no conclusive evidence linking elevated serum cholesterol and gallstones
Presentation Outline
- Benign neoplasms of the ampulla of Vater are rare, (less than 10 percent of periampullary neoplasms). Most common benign lesions are villous and tubulovillous adenomas

- Potential to undergo malignant transformation to ampullary carcinomas - clinical significance extends beyond the need to treat associated symptoms

- Can occur sporadically, or in the setting of familial polyposis syndromes such as familial adenomatous polyposis (FAP) and its related conditions. Many patients with ampullary adenomas have numerous duodenal adenomatous polyps. Sporadic ampullary adenomas are usually diagnosed in patients who are older than 40 years of age, most commonly in patients who are in their seventies.

- Although still rare, ampullary adenomas are being increasingly recognized with the extensive availability of flexible endoscopy and the widespread application of screening and surveillance programs for high-risk patients such as those with FAP
AMPULLARY ADENOMAS (cont.)
- Presenting symptoms (if any) are usually non-specific, reflecting ampullary (biliary or pancreatic) obstruction resulting from the mass-effect of the adenoma compressing and impeding biliary or pancreatic outflow.

- The most common presentation is with jaundice (present in 50 to 75 percent of patients). It is usually painless or accompanied only by a vague or dull ache in the epigastrium. Other symptoms may include biliary colic, nausea, vomiting, and weight loss. Less commonly, patients may present with acute pancreatitis, iron deficiency anemia, and overt upper gastrointestinal bleeding. ***Up to 25 percent of patients have associated common bile duct stones secondary to cholestasis***

-
Diagnostic Studies:
transabdominal ultrasound, abdominal CT scan, endoscopic retrograde cholangiopancreatography (ERCP) including biopsy, MR cholangiopancreatography (MRCP), and endoscopic ultrasound (EUS).

- Management Options: pancreaticoduodenectomy, surgical local excision, or endoscopic ampullectomy. Patients also have the option to forego excision and undergo close endoscopic surveillance.
EMBRYONIC WEEK 7
ANATOMIC VARIATIONS
MIRIZZI'S SYNDROME
- Common hepatic duct obstruction caused by an extrinsic compression from an impacted stone in the cystic duct or Hartmann's pouch of the gallbladder

- It has been estimated to occur in 0.7 to 1.8 percent of all cholecystectomies

- Often not recognized preoperatively, which can lead to significant morbidity and biliary injury, particularly with laparoscopic surgery

- Two Mechanisms: mechanical obstruction of the hepatic duct because of the proximity of the cystic duct and the common hepatic duct, and secondary inflammation with frequent episodes of cholangitis
VARIANTS:
McSherry Type 1: Compression of the common hepatic duct or common bile duct by a stone impacted in the cystic duct or Hartmann's pouch

McSherry Type 2: Erosion of the calculus from the cystic duct into the common hepatic duct or common bile duct, producing a cholecystocholedochal fistula

- Mirizzi's syndrome presents a difficult challenge for laparoscopic surgery because the dense adhesions and edematous inflammatory tissue cause distortion of the normal anatomy and increase the risk for biliary injury. Thus, the use of laparoscopic surgery as the primary treatment of Mirizzi syndrome is controversial.

- Open cholecystectomy remains the standard of care for Mirizzi syndrome with compression of the common duct. For patients with a fistula, or erosion into the common duct, the choice of repair depends on the extent of the damage to the common duct.
MIRIZZI'S SYNDROME (cont.)
- Refers to stones in the gallbladder (gallstones)

- 3 Types of Stones:
- Cholesterol stones (yellow to green); associated with obesity, diabetes, hyperlipidemia, multiple pregnancies, OCPs, Crohn’s disease, advanced age, Native American ancestry, cirrhosis, and cystic fibrosis
- Pigment stones – black stones associated with hemolytic disease (sickle cell disease, thalassemia, hereditary spherocytosis, artificial cardiac valves) and alcoholic cirrhosis; Brown stones found in bile ducts are associated with biliary tract infection
- Mixed stones – components of both cholesterol and pigment stones; account for the majority of gallstones
CHOLELITHIASIS
- Gallstones are mostly asymptomatic

- Biliary colic occurs due to temporary obstruction of the cystic duct by a gallstone. Pain is caused by the gallbladder contracting against this obstruction

- Pain typically located in RUQ or epigastrium; pain typically occurs after eating and at night; only lasts a few hours

- Boas’ sign: referred right subscapular pain during episode of biliary colic

- Complications of gallstones include cholecystitis (acute or chronic), choledocholithiasis, gallstone ileus, and malignancy

- Diagnosed by RUQ ultrasound – high sensitivity and specificity (>95%) for stones >2mm
May use CT scan and MRI as alternatives

- Treatment is elective cholecystectomy for patients with recurrent bouts of biliary colic
ACUTE CHOLECYSTITIS
- Obstruction of the cystic duct (NOT infection) induces acute inflammation of the gallbladder wall

- Pain is always present; located in RUQ or epigastrium; may radiate to right scapula or shoulder; accompanied by nausea, vomiting, anorexia

- Physical exam: RUQ tenderness with rebound tenderness, hypoactive bowel sounds
Murphy’s sign: pathognomonic; inspiratory arrest during deep palpation of RUQ (not present in many cases)

- Diagnosis by RUQ ultrasound (test of choice) – high sensitivity and specificity; findings include thickened gallbladder wall, pericholecystic fluid, distended gallbladder, and presence of stone(s)

- CT scan has same accuracy but better at identifying complications (perforation, abscess, pancreatitis)

- Can use radionuclide scan (hepatoiminodiacetic acid; HIDA) – equal accuracy; can rule out acute cholecystitis if normal HIDA scan; Positive HIDA – gallbladder is not visualized after injection; if still not visualized 4 hours after injection, diagnosis of acute cholecystitis can be made
- Treatment is conservative: hydration with IV fluids, bowel rest, IV antibiotics, analgesics

- Cholecystectomy is indicated in most patients with symptomatic gallstones, preferably first 24 – 48 hours
ACALCULOUS CHOLECYSTITIS
- Cholecystitis without stones obstruction the cystic duct

- Usually idiopathic; seen in patients with severe underlying illness, possibly associated with dehydration, ischemia, burns, severe trauma, and post-operative state

- Same signs and symptoms of acute cholecystitis

- Diagnosis is often difficult because patients are typically severely ill and have other medical problems; clinical features often less pronounced

- Treatment is emergent cholecystectomy; if patient is too ill for surgery, performing percutaneous drainage of the gallbladder with cholecystostomy is indicated
- Refers to gallstones in the common bile duct (CBD)
Primary vs Secondary: primary stones (5%)
originate in the CBD (typically pigment stones),
whereas secondary stones (95%) originate in the
gallbladder and then pass into the CBD (typically cholesterol or mixed)

- Patients may be asymptomatic for years. When symptomatic, patients have RUQ or epigastric pain and jaundice

- Diagnosis: elevated total and direct bilirubin levels and ALK-P; RUQ ultrasound is the initial study, but is not sensitive for choledocholithiasis; ERCP is gold standard (diagnostic and therapeutic). Percutaneous transhepatic cholangiography (PTC) is alternative

- Treatment: ERCP with sphincterotomy and stone extraction with stent placement (90% successful)
In select cases, a laparoscopic choledocholithotomy can be preformed
CHOLEDOCHOLITHIASIS
- Infection of the biliary tract secondary to
obstruction; obstruction causes biliary stasis
and bacterial overgrowth

- Choledocholithiasis accounts for 60% of cases;
other causes include pancreatic and biliary
neoplasm, post-operative strictures, invasive
procedures (ERCP, PTC), and choledochal cysts

***Cholangitis is potentially life-threatening and
may require emergency surgery***

- Charcot’s Triad: RUQ pain, jaundice, fever (present in 50-70% of cases)

- Reynold’s Pentad: Charcot’s Triad with septic shock and altered mental status
(CNS depression)
CHOLANGITIS
- Mostly adenocarcinoma occurring in the elderly

- Usually associated with gallstones; also associated with porcelain gallbladder and cholecystenteric fistula

- Nonspecific clinical features that suggest extrahepatic bile duct obstruction such as jaundice, biliary colic, weight loss, anorexia, RUQ mass, or palpable gallbladder (sign of advanced disease)

- Difficult to remove with surgery; depending on depth of invasion, cholecystectomy vs radical cholecystectomy (including wedge resection of liver and lymph node dissection)

- Prognosis is dismal; 90% of patients die of advanced disease within 1 year of diagnosis; disease often goes undetected until advanced stages
CARCINOMA OF THE GALLBLADDER
DIFFERENTIAL - PAINLESS JAUNDICE
Classically associated with neoplastic etiologies of extrahepatic or obstructive jaundice
Adenoma of the Ampulla of Vater
Carcinoma of Ampulla of Vater
Extrahepatic Cholangiocarcinoma
Ductal Adenocarcinoma of the Pancreatic Head
Choledocholithiasis
Cholecystitis
Mirizzi's Syndrome
Common Bile Duct Stricture
DIFFERENTIAL - POSTMENOPAUSAL BLEEDING
Atrophic Endometrium
Hormone Replacement Therapy (unopposed estrogen)
Endometrial Cancer
Endometrial Hyperplasia
Endometrial/Cervical Polyps
Uterine Leiomyomas (Fibroids)
Cervicitis
Atrophic Vaginitis
- Univariate and multivariate logical regression analysis was used to evaluate positive predictive factors for adenocarcinoma

- Age, sex, presence of symptoms, tissue type, degrees of dysplasia on endoscopic biopsy, papilla enlargement on CT (>1cm), and ductal dilation (>7mm)

- Histologic sections were examined by pathologists according to the Vienna classification of gastrointestinal neoplasia
DISCUSSION
- Complete removal is essential to cure ampullary adenomas because of the potential for malignancy

- Endoscopic resection of ampullary adenoma is successful in 75-90% of patients (15% recurrence rate and 20% complication rate)

- Pancreaticoduodenectomy is considered the standard treatment for ampullary cancer

- A biopsy performed during endoscopy is the best method by which to obstain accurate diagnostic information, however an initial finding of adenoma cannot exclude the presence of a focus of carcinoma in an unsampled part of a lesion (leading to 20-30% false negative rates)

- The study observed a correlation between the probability a that a diagnosis of adenoma would be upgraded to carcinoma and the presence of ductal dilation or high-grade dysplasia
Transduodenal Ampullectomy
with Common Bile Duct Exploration
and Possible Cholecystectomy
- On initial inspection of the right upper quadrant, the gallbladder was noted to be thickened and edematous.

- There was an adhesion between the fundus of the gallbladder and what was presumed to be the common bile duct; the hepatoduodenal ligament was noted to be edematous; the inflammation extended to the first and second portions of the duodenum.

- Anatomical planes were severely blurred due to extensive, likely chronic, inflammation and edema; tissue was friable; possible Mirizzi's syndrome

- The decision was made to place a cholecystostomy tube in anticipation of a later transduodenal ampullectomy with cholecystectomy approximately three months later to allow time for inflammation to resolve

- The gallbladder was drained and bile was sent for culture; intraoperatively, the uterus was palpated and felt to be myomatous; additionally, an infraumbilical hernia was noted, and was excised and repaired
Post-Operative Care
Post-operatively, she received subcutaneous heparin, and oxycodone and morphine as needed for pain control

Bile culture results on 5/7/2013 returned positive for vancomycin-resistant enterococcus and candida sp.; She was then placed on linezolid and fluconazole

She was discharged home with cholecystostomy tube after receiving proper education of
cholecystostomy tube care
SICU
ABDOMINAL ULTRASOUND
4/21/2013
CT ABDOMEN AND PELVIS
4/21/2013
ERCP
PATHOLOGY - AMPULLA OF VATER BIOPSY
4/22/2013
MRCP
4/27/2013
Tubulovillous Adenoma
Height: 168 cm
Weight: 92.4 kg
BMI: 32.7 (obesity)
FINAL DIAGNOSES
Chronic cholecystitis secondary to ampullary adenoma, choledocholithiasis, and Mirizzi’s syndrome

Severe anemia due to dysfunctional uterine bleeding secondary to uterine fibroids

Inflammatory cloacogenic anal polyp

Tubular adenoma of ascending colon

Prerenal azotemia
REFERENCES
Antoniou SA, Antoniou GA, Makridis C. Laparoscopic treatment of Mirizzi syndrome: a systematic review. Surg Endosc 2010; 24:33.

Beltran MA, Csendes A, Cruces KS. The relationship of Mirizzi syndrome and cholecystoenteric fistula: validation of a modified classification. World J Surg 2008; 32:2237.

Cirillo DJ, Wallace RB, Rodabough RJ, et al. Effect of estrogen therapy on gallbladder disease. JAMA 2005; 293:330.
Erben Y, Benavente-Chenhalls LA, Donohue JM, et al. Diagnosis and treatment of Mirizzi syndrome: 23-year Mayo Clinic experience. J Am Coll Surg 2011; 213:114.

Everhart JE, Yeh F, Lee ET, et al. Prevalence of gallbladder disease in American Indian populations: findings from the Strong Heart Study. Hepatology 2002; 35:1507.

Greco S, Cassinotti A, Massari A, et al. Isolated ampullary adenoma causing biliary obstruction. J Gastrointestin Liver Dis 2008; 17:329.

Halldestam I, Kullman E, Borch K. Incidence of and potential risk factors for gallstone disease in a general population sample. Br J Surg 2009; 96:1315.

Irani S, Arai A, Ayub K, et al. Papillectomy for ampullary neoplasm: results of a single referral center over a 10-year period. Gastrointest Endosc 2009; 70:923.

Lawrence PF, Bell RM, Dayton MT, eds. Essentials of Surgical Specialities. 3rd ed. Lippincott Williams & Wilkins, 2007

Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL, eds. Harrison’s Principles of Internal Medicine. 17th ed. New York, NY: McGraw-Hill; 2005:946.

Patel R, Davitte J, Varadarajulu S, Wilcox CM. Endoscopic resection of ampullary adenomas: complications and outcomes. Dig Dis Sci 2011; 56:3235.

Winter JM, Cameron JL, Olino K, et al. Clinicopathologic analysis of ampullary neoplasms in 450 patients: implications for surgical strategy and long-term prognosis. J Gastrointest Surg 2010; 14:379.
- Preautions should be taken in the management of patients with ampullary adenoma, especially when the risk factors of ductal dilation and high-grade dysplasia are present

- Surgical resection is strongly recommended when a lesion has 2 risk factors even if result of endoscopic biopsy is benign

- If 1 risk factor is present, additional study using endoscopic ultrasound, intraductal ultrasound, or careful papillectomy can be considered for diagnostic and therapeutic purpose
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