general surgery & transplant

fluid maint calc
Calculate Fluid Maintenance: (0-10 kg= 4cc/kg/h)+( 11-20kg=2cc/kg/hr)+(>20kg=1cc/kg/hr) [Lecture]
Sigmoid colon of people of Western Europe and United States with lower-fiber diet
1. True diverticula: through all layers of wall; uncommon, in cecum and ascending colon
2. Acquired ( false diverticula): prevelant in Western countries: 95% in sigmoid colon. Penetration point of marginal artery entry -high intraluminal pressures in sigmoid > diverticula
3. Diverticulosis= multiple false diverticula in the colon.
3. Asymptomatic diverticula are found when a barium enema is performed for some other purpose
Diverticulitis and diverticulosis SX
Sx include
1. abd pain, often LLQ
2. change in bowel habis, including bleeding, constipation, diarrhea or alternating constipation and diarrhea
3. Physcial examis often unremarkable or mild tenderness in LLQ
4. Fever and leukocytosis are absent
5. Xray findings: segmental spasm and luminal narrowing
6. Endoscopic eval of lumen doesn’t show anything but openings of the diverticula
Diverticulitis and diverticulosis TX
Patients are encouraged to consume fruits and vegis, whole grain breads and bran products.
o 10% bleed – usually stops on its own; If can’t be localized, bleeding > take whole colon out; BUT massive GI bleeds ( req. > 4 units of blood in 24 hr) are are most commonly caused by diverticula
Diverticulitis df
Define Diverticulitis (312-314)
Limited infection of one or more diverticula, including extension into adjacent tissue.
Initiated by obstruction of the neck of the diverticulm by a fecalith > microperforation
Clinical Presentation the same as diverticulosis but there is FEVER , sometimes a palpable mass
SIGNS of obstruction: distention, high pitched bowel sounds; sever constipation or obstipation; upright abd radiographs: pneumoperotoneum.
1. initially medical: ( 85 % cases):
a. admitting to hospital
b. IV hyfration
c. Npo
d. IV abx: broad spectrum of G(-) coliforms and anaerobes ( B. fragilis) for 5-7 d
diverticular disease indications
Identify and recognize the indications for surgery of diverticular disease. (313 table 16-1)
Polyps are small mucosal excrescences that grow into the lumen of the colon and rectum ( 50% -rectosigmoid region; 50% multiple) Found in barium enema ( 5% show polyps)
Identify and recognize frequency and malignancy potential of the following colonic polyp( 16-2)
A. Type B. Frequency C. Location
D. Malignancy potential E. TX
1. A) Tubular B) Common10%adults C) Rectosigmoid-20% D) 7% malignant E) Endoscopic excision
2. A) Tubulo-villous D) 20% malignancy
3. A) Villous B) Common elderly C) Rectosigmoid 80% D) 33 % malignant E) Surgical removal
4. A) Villous>3 cm diam. D) > 33% malignant
5. A) Inflammatory B) Uncommon (IBD) C) Colon & rectum D) None E) observation
Dukes-Astler-Coller System
Stage: Description: 5yr surv:
A = confined to mucosa, 85-90% survival
B1 =Extension to muscularis propia; negative nodes. 5 yr-survival= 70-75%
B2 =Extention through muscularis propia; negative nodes. 5 yr survival= 60-65%
C1 =B1 penetration, pos. nodes. 5yr survival = 30-35%
C2 =B2 penetration, pos. nodes. 5 yr survival = 25%
D =Distant metastiase. 5yr survival = < 5%
Adenomas polyp
Adenomas are pre-malignant>vigilance!: tubular, tubulovillous, villous adenoma
Most polyps sessile ( flat, intimately attached) or pedunculated ( rnd, attached to mucosa by a long thin neck
colon cancer predispose
Evidence of malignant potenial:
1. high incidence of cancer associated w polyps in:
a. familial polyposis syndrome or Gardners syndrome
2. Simultaneous occurance of cancer and polyps in same spec.
3. Carcinogens that produce both adenomas and cancer in same model
4. Lower Ca risk with removal of polyps.
5. See chart for histological type risk for Ca
colon &rectum CA Associated factors:
a. cancer family syndrome ( hereditary nonpolyposis colon cancer or HNPCC )
b. intraluminal chemical carcinogenesis: from ingestion or intraluminal biochem rx? -controversial
c. diet factors: (high fiber, low fat> low incidence)
d. carotenoids and other antioxidant consumption : decrease incidence
e. prostaglandin inhibitors ( ASA, sulindac ) decrease incidence
f. ulcerative colitis
g. Crohns colitis
h. Lymphogranuloma venereum ( L1, L2, L3 of Chlamydia trachomatous)
i. Villous and tubulovillous polyps
j. Age > 70 y ( starts to increase at 40 y)
k. Men ( ^ colon ca); women ( ^ rectal Ca
ulcerative colitis & Crohn’s
Identify and recognize the characteristics and clinical manifestation of ulcerative colitis and Crohn’s disease:
• Ulcerative colitis is an idiopathic inflammatory boel disordr that involves the mucosa and submucosa of the large bowel and rectum
• Bimodal age distribution: 2/3 at 15-30 yrs; then 1/3 at age 55y- FHx 20 % cases- 10/100000
Ulcerative colitis
Diarrhea= severe and bloody, perianal fistula = rare, Strictures/obstruction = uncommon, Perforation = Free, uncommon.
Pattern of Development:
Rectum = Always, Terminal ileum = normal, distribution = continuous, megacolon = frequent
Gross = Friable, bleeding granular exudates, pseudopolps, isolated, ulcers.
Microscopic = Inflamed submucosa, mucosa, crypt abscesses; fibrosis uncommon
Radiologic = Lead-pipe, foreshortening, continuous, concentric
Natural HX: Exacerbations, remissions, dramatic flare-ups
Med Hx: Initial response high ( >80%)
Surgical Tx: curative
Recurrence: No
Crohn’s Colitis:
Diarrhea = less severe, infrequent bleeding. Perianal fistula = Common. Strictures/obstruction = common. Perforation = localized & common
Pattern of Development:
Rectum= often normal. Terminal ileum = diseased in majority. Distribution = skip lesions. Megacolon = less common
Gross: Linear ulcers, transverse fissures, cobblestoning, thickening, strictures
Microscopic: Transmural inflammation, granulomas, fibrosis
Radiologic: String sign in small bowel; segmental, asymmetric internal fistulae.
Natural Hx: Exacerbations, remissions chronic indolent
Med Tx: Response less predictable
Surgical Tx: Palliative
Recurrence: Common
intestine obstruction common sites
Most common site: sigmoid colon
3 most common causes:
adenocarcinoma, (65%)
scarring assoc with diverticulitis (20%)
volvulus (5%)
inflammatory disorders, benign tumors, foreign bodies, fecal impaction and other misc. problems account for the remainder.
Hemorrhoids Grading
Graded according to level of prolapse:
1st: bulge in anal canal lumen
2nd: protrudes w defacation, reduces spontaneously
3rd: protrudes w hefacation, manually reduced
4th: protrudes permanently incarcerated
External : either present or absent
Mixed: internal and externalAnoscope must be used to visualize
Painless unless thrombosis, ulceration, or gangrene
Bleeding minimal or major enough to cause anemia

Hemorrhoid TX
Bulk forming agents (psyllium) and avoidance of constipation
2nd, 3rd degree treated w banding
4th degree : surgical hemorroidectomy
external: few problems, unless perianal hygiene is poor> pruritis
-Thrombosed external hemorrhid: self limited
Excise thrombus with local anesthesia in first 24-48 hrs
Peri-anal abcess
Believed to start with obstruction of the perianal gland
Located between the internal and external sphincters
Discharge at level of anal crypts “cryptoglandular origin”
Intersphincteric may become peri-anal > complex ischiorectal and supralevator abcessess
a. Perianal and ischiorectal abscesses are the most common. (70% of perirectal abscesses)
Clinical Presentation
Perianal swelling ar readily apparent in perirectal abscesses,
Spontaneous draining of pus
Cardinal signs of infection:
Fever, pain, redness, swelling, loss of function
Peri-anal abscess TX
Tx: Complete and thorough drainage
e. Failure to drain> ongoing pain, sepsis, overall tx failure
f. ABX alone no effect. May be used in conjunction with surgical incision and drainage immunocompromised pts
Anal Fissure
Anal fissure (331): Most common cause of severe localized anorectal pain
Severe pain, unlike hemorrhoids which cause pressure and discomfort
Anal fissures are painful linear tears in lining of the anal canal below the level of the dentate canal.
Clinical Manifestations:
-They are secondary to local trauma ( constipation or excessive diarrhea)
-Pain starts w defecation, persists for minutes to hours
-Minimal bleeding, bright red
Anal fissure TX
For mild sx:
-Avoidance of diarrhea or constipation
-Bulk laxitives
-Mild non-narcotic analgesic
-Sitz baths
If tx fails or Chronic: surgery indicated
gallstones, most common type?
most common types of gallstones = cholelithiasis
Choledocholithitasis DF
common bile duct
Biliary colic
Describe biliary colic (338) = colic due to passage of gallstones along the bile duct.
-A person with biliary colic has pain in the right upper abdomen that is caused by the blockage of bile from the gallbladder. The most common cause for biliary colic is gallstones.
-What are the symptoms of biliary colic?
Biliary colic pain is often severe and located in the right upper abdomen. Pain may be triggered by eating a meal that is high in fat.
-How does the doctor treat biliary colic?
Treatment for biliary colic is usually surgical to remove the obstructing gallstones and gallbladder.
-common SX of biliary colic include:
Severe abdominal pain, Upper abdominal pain, Right upper abdominal pain, Abdominal tenderness:, Right upper abdominal tenderness, Upper abdominal tenderness, Nausea, Indigestion, Vomiting, Anorexia.Less common symptoms of biliary colic include:
Back pain , Urine color change:, Brown urine , Fever , Chills, Jaundice: , Yellow skin, Yellow eyes

acute cholecystitis (cystic duct) signs and SX
Sx of gallstones: Most people with gallstones do not have any sx. sx develop when a gallstone become stuck in a bile duct. When this happens it can cause right upper abdominal pain that may travel to the back. Other symptoms include nausea, vomiting, fever, jaundice, brown urine, and clay-colored stools.
-Signs and symptoms
Gallstones may be asymptomatic, even for years. These gallstones are called “silent stones” and do not require treatment. Symptoms commonly begin to appear once the stones reach a certain size (>8 mm). A characteristic symptom of gallstones is a “gallstone attack”, in which a person may experience intense pain in the upper-right side of the abdomen, often accompanied by nausea and vomiting, that steadily increases for approximately 30 minutes to several hours. A patient may also experience referred pain between the shoulder blades or below the right shoulder. These symptoms may resemble those of a “kidney stone attack”. Often, attacks occur after a particularly fatty meal and almost always happen at night. Other symptoms include abdominal bloating, intolerance of fatty foods, belching, gas, and indigestion.-A positive Murphy’s sign is a common finding on physical examination.
-Causes:Gallstone risk factors include overweight, age near or above 40, female, and pre-menopausal the condition is more prevalent in caucasians than in people of other races. A lack of melatonin could significantly contribute to gallbladder stones, as melatonin both inhibits cholesterol secretion from the gallbladder, enhances the conversion of cholesterol to bile, and is an antioxidant, capable of reducing oxidative stress to the gallbladder. Researchers believe that gallstones may be caused by a combination of factors, including inherited body chemistry, body weight, gallbladder motility (movement), and perhaps diet. The absence of such risk factors does not, however, preclude the formation of gallstones.
No clear relationship has been proven between diet and gallstone formation; however, low-fiber, high-cholesterol diets and diets high in starchy foods have been suggested as contributing to gallstone formation. Other nutritional factors that may increase risk of gallstones include rapid weight loss, constipation, eating fewer meals per day, eating less fish, and low intakes of the nutrients folate, magnesium, calcium, and vitamin C. On the other hand, wine and whole-grain bread may decrease the risk of gallstones. Pigment gallstones are most commonly seen in the developing world. Risk factors for pigment stones include hemolytic anemias (such as sickle-cell disease and hereditary spherocytosis), cirrhosis, and biliary tract infections. People with erythropoietic protoporphyria (EPP) are at increased risk to develop gallstones.
-Pathophysiology: Cholesterol gallstones develop when bile contains too much cholesterol and not enough bile salts. Besides a high concentration of cholesterol, two other factors are important in causing gallstones. The first is how often and how well the gallbladder contracts; incomplete and infrequent emptying of the gallbladder may cause the bile to become overconcentrated and contribute to gallstone formation. The second factor is the presence of proteins in the liver and bile that either promote or inhibit cholesterol crystallization into gallstones. In addition, increased levels of the hormone estrogen as a result of pregnancy, hormone therapy, or the use of combined (estrogen-containing) forms of hormonal contraception, may increase cholesterol levels in bile and also decrease gallbladder movement, resulting in gallstone formation.
-Diagnosis:A 1.9 cm gallstone impacted in the neck of the gallbladder and leading to cholecystitis as seen on ultrasound. Note the 4 mm gall bladder wall thickening.Gallstones as seen on plain Xray.
-Treatment:Medical. Cholesterol gallstones can sometimes be dissolved by oral ursodeoxycholic acid, but it may be required that the patient takes this medication for up to two years.Gallstones may recur, however, once the drug is stopped. Obstruction of the common bile duct with gallstones can sometimes be relieved by endoscopic retrograde sphincterotomy (ERS) following endoscopic retrograde cholangiopancreatography (ERCP). Gallstones can be broken up using a procedure called lithotripsy (extracorporeal shock wave lithotripsy),which is a method of concentrating ultrasonic shock waves onto the stones to break them into tiny pieces. They are then passed safely in the feces. However, this form of treatment is suitable only when there is a small number of gallstones.
-Surgical: Cholecystectomy (gallbladder removal) has a 99% chance of eliminating the recurrence of cholelithiasis. Only symptomatic patients must be indicated to surgery. The lack of a gallbladder may have no negative consequences in many people. However, there is a portion of the population — between 10 and 15% — who develop a condition called postcholecystectomy syndrome which may cause gastrointestinal distress and persistent pain in the upper-right abdomen, as well as a 10% chance of developing chronic diarrhea.
There are two surgical options for cholecystectomy:
Open cholecystectomy: This procedure is performed via an incision into the abdomen (laparotomy) below the right lower ribs. Recovery typically consists of 3-5 days of hospitalization, with a return to normal diet a week after release and normal activity several weeks after release.
-Laparoscopic cholecystectomy: This procedure, introduced in the 1980s,is performed via three to four small puncture holes for a camera and instruments. Post-operative care typically includes a same-day release or a one night hospital stay, followed by a few days of home rest and pain medication. Laparoscopic cholecystectomy patients can, in general, resume normal diet and light activity a week after release, with some decreased energy level and minor residual pain continuing for a month or two. Studies have shown that this procedure is as effective as the more invasive open cholecystectomy, provided the stones are accurately located by cholangiogram prior to the procedure so that they can all be removed.
2 types biliary colic
here are two main types of biliary colic:
Gallstone becomes trapped in the common bile duct
Gallstone becomes trapped in the cystic duct
gallstones become trapped in the cystic duct
gallstones= Bile is made by the liver, and stored in the gallbladder. The gallbladder pushes bile into the intestine through the bile duct. In the intestine, the bile helps digest food. Gallstones start to form when cholesterol, calcium and phosphate crystallize in the bile. These crystals continue to grow to form stones.What are the symptoms of gallstones?
Most people with gallstones do not have any symptoms. Symptoms develop when a gallstone become stuck in a bile duct. When this happens it can cause right upper abdominal pain that may travel to the back. Other symptoms include nausea, vomiting, fever, jaundice, brown urine, and clay-colored stools.

How does the doctor treat gallstones?
Gallstones that are causing no symptoms may not require treatment. Treatment for gallstones that are causing recurrent symptoms includes medications to dissolve the gallstones, lithotripsy, and endoscopic procedures to remove them from the bile duct. In some cases, it may be recommended to remove the gallbladder.

gallstone sx

In some cases, gallstones may cause few, if any, symptoms.

Symptoms of gallbladder disease due to gallstones include:
Abdominal pain:
Upper abdominal pain
Right upper abdominal pain
Pain may travel to the back
Back pain on the right side
Flank pain on the right side
Abdominal tenderness:
Right upper abdominal tenderness
Yellow skin
Yellow eyes
Urine color change:
Brown urine
Abnormal appearing stool:
Clay colored stool

gallstone evaluation

he evaluation of gallstones begins with a history and physical examination.

Physical findings in someone with gallstones may include:
Abdominal tenderness in the right-upper quadrant of the abdomen.
Jaundice may be present if there is blockage of the bile duct.

Testing is usually required to confirm the diagnosis of gallstones.

Tests that may be used to evaluate gallstones include:
Serum amylase
Serum lipase
Serum bilirubin
Complete blood count
Liver profile
Kidney profile
Blood cultures

Gallbladder imaging tests that may be used to evaluate gallstones include:
Abdominal x-rays
A special x-ray the highlights the course of the common bile duct.
Ultrasound of the abdomen
CT scanning of the abdomen
MRI scan of the abdomen
Nuclear scanning of the gallbladder (HIDA scan)
Offers the additional benefit of allowing for the removal of gallstones from the common bile duct thus avoiding the need for emergency surgery.

Gallstone TX

Gallstones that are causing no symptoms may not require treatment. Treatment for gallstones that are causing recurrent symptoms includes medications to dissolve the gallstones, lithotripsy, and endoscopic procedures to remove them from the bile duct.

In some cases, it may be recommended to remove the gallbladder. Those with gallstones and a history for cirrhosis, portal hypertension, sickle cell anemia, or diabetes, may benefit from the removal of the gallbladder.

Treatment for gallstones that are causing symptoms includes:
Oral bile salt therapy:
Used to dissolve the gallstones
Ursodeoxycholic acid (Ursodiol)
Endoscopic retrograde sphincterotomy:
A flexible, lighted scope reaches the intestine via the esophagus and stomach.
Gallstones are removed from the gallbladder through the bile duct.
Lithotripsy for gallstones:
Gallstones are broken into smaller pieces by subjecting them to high frequency sound waves.
Laparoscopic cholecystectomy:
Usually the treatment of choice for those with gallstones who are experiencing symptoms
The gallbladder is removed through a small incision in the abdomen, using a flexible, lighted scope.
General cholecystectomy:
The gallbladder is removed through an incision in the abdomen, without the use of endoscopy.
Less commonly used due to the advent of laparoscopic gallbladder removal.

cholelithiasis – Causes, Symptoms And Treatment
Diseases of the gallbladder and biliary tract are common and, in many cases, painful conditions that may be life threatening and usually require surgery. They are generally associated with deposition of calculi and inflammation.
-Cholelithiasis is the fifth leading cause of hospitalization among adults and accounts for 90% of all gallbladder and duct diseases. Women have two to three times the incidence as men of developing cholelithiasis. The disease may also be more prevalent in persons who are obese, who have high cholesterol, or who are on cholesterol lowering drugs. The prognosis is usually good with treatment unless infection occurs, in which case prognosis depends on its severity and response to antibiotics.In most cases, gallbladder and bile duct diseases occur during middle age. Between ages 20 and 50, they’re six times more common in women, but incidence in men and women becomes equal after age 50. Incidence rises with each succeeding decade.

Causes of Cholelithiasis

Cholelithiasis stones or calculi (gallstones) in the gallbladder. results from changes in bile components. Gallstones are made of cholesterol, caldurn bilirubinate, or a mixture of cholesterol and bilirubin pigment. They arise during periods of sluggishness in the gallbladder due to pregnancy. hormonal contraceptives. diabetes mellitus. celiac disease, cirrhosis of the liver, and pancreatitis.

One out of every 10 patients with gallstones develops Cholelithiasis, or gallstones in the common bile duct (sometimes called common duct stones). This condition occurs when stones pass out of the gallbladder and lodge in the hepatic and common bile ducts. obstructing the flow of bile into the duodenum. Prognosis is good unless infection occurs.

Cholangitis, infection of the bile duct, is commonly associated with choledocholithiasis and may follow percutaneous transhepatic cholangiography or occlusion of endoscopicstents. Predisposing factors may include bacterial or metabolic alteration of bile acids. Widespread inflammation may cause fibrosis and stenosis of the common bile duct. The prognosis for this rare condition is poor without stenting or surgery.
Cholecystitis. acute or chronic inflammation of the gallbladder. is usually associated with a gallstone impacted in the cystic duct, causing painful distention of the gallbladder. Cholecystitis accounts for 10% to 25% of all patients requiring gallbladder surgery. The acute form is most common during middle age; the chronic form occurs most commonly among the elderly. The prognosis is good with treatment.
Cholesterolosis. polyps or crystal deposits of cholesterol in the gallbladder’s submucosa, may result from bile secretions containing high concentrations of cholesterol and insufficient bile salts. The polyps may be localized or speckle the entire gallbladder. Cholesterolosis the most common pseudotumor. isn’t related to widespread inflammation of the mucosa or lining of the gallbladder. The prognosis is good with surgery.
Biliary cirrhosis-?source
Biliary cirrhosis. ascending infection of the biliary system, sometimes follows viral destruction of liver and duct cells. but the primary cause is unknown. This condition usually leads to obstructive jaundice and involves the portal and periportal spaces of the liver. It’s nine times more common among women ages 40 to 60 than among men. The prognosis is poor without liver transplantation.
Gallstone terminal ilieum
Gallstone ileus results from a gallstone lodging at the terminal ileum; it’s more common in the elderly. The prognosis is good with surgery.
Postcholecystectomy syndrome-?source
Postcholecystectomy syndrome commonly results from residual gal1stones or stricture of the common bile duct. It occurs in 1 % to 5 % of all patients whose gallbladders have been surgical1y removed and may produce right upper quadrant abdominal pain, biliary colic, fatty food intolerance, dyspepsia. and indigestion. The prognosis is good with selected radiologic
procedures, endoscopic procedures, or surgery.
Acalculous cholecystitis
Acalculous cholecystitis is more common in critical1y ill patients, accounting for about 5% of cholecystitis cases. It may result from primary infection with such organisms as Salmollella typhi. Escherichia coli, or Clostridium or from obstruction of the cystic duct due to lymphadenopathy or a tumor. It appears that ischemia usually related to a low cardiac output. also has a role in the pathophysiology of this disease. Signs and symptoms of acalculous cholecystitis include unexplained sepsis, right upper quadrant pain, fever, leukocytosis, and a palpable gallbladder.
acute cholocystitis
Cholecystitis is often caused by cholelithiasis (the presence of choleliths, or gallstones, in the gallbladder), with choleliths most commonly blocking the cystic duct directly. This leads to inspissation (thickening) of bile, bile stasis, and secondary infection by gut organisms, predominantly E. coli and Bacteroides species. The gallbladder’s wall becomes inflamed. Extreme cases may result in necrosis and rupture. Inflammation often spreads to its outer covering, thus irritating surrounding structures such as the diaphragm and bowel. Less commonly, in debilitated and trauma patients, the gallbladder may become inflamed and infected in the absence of cholelithiasis, and is known as acute acalculous cholecystitis. Stones in the gallbladder may cause obstruction and the accompanying acute attack. The patient might develop a chronic, low-level inflammation which leads to a chronic cholecystitis, where the gallbladder is fibrotic and calcified.
-Cholecystitis usually presents as a pain in the right upper quadrant. This is usually a constant, severe pain. During the initial stages, the pain may be felt in an area totally separate from the site of pathology, known as referred pain. In cholecystitis the referred pain may occur in the right scapula region.This may also present with the above mentioned pain after eating greasy or fatty foods such as pastries, pies, and fried foods.
This is usually accompanied by a low-grade fever, diarrhea, vomiting, nausea and granulocytosis. The gallbladder may be tender and distended. More severe symptoms such as high fever, shock and jaundice indicate the development of complications such as abscess formation, perforation or ascending cholangitis. Another complication, gallstone ileus, occurs if the gallbladder perforates and forms a fistula with the nearby small bowel, leading to symptoms of intestinal obstruction.
-Chronic cholecystitis manifests with non-specific symptoms such as nausea, vague abdominal pain, belching, and diarrhea.
Cholecystitis is usually diagnosed by a history of the above symptoms, as well examination findings:
fever (usually low grade in uncomplicated cases)
tender right upper quadrant +/- Murphy’s sign
Ortner’s sign – tenderness when hand taps the edge of right costal arch.
Georgievskiy – Myussi’s sign (phrenic nerve sign) – pain when press between edges of sternocleidomastoid
Boas’ sign – Increased sensitivity below the right scapula (also due to phrenic nerve irritation).
Subsequent laboratory and imaging tests are used to confirm the diagnosis and exclude other possible causes.
Ultrasound can assist in the differential.[1][2]
[Differential diagnosis
[edit]Acute cholecystitis
This should be suspected whenever there is acute right upper quadrant or epigastric pain, other possible causes include:
Perforated peptic ulcer
Acute peptic ulcer exacerbation
Amoebic liver abscess
Acute amoebic liver colitis
Acute pancreatitis
Acute intestinal obstruction
Renal colic
Acute retro-colic appendicitis
[edit]Chronic cholecystitis
The symptoms of chronic cholecystitis are non-specific, thus chronic cholecystitis may be mistaken for other common disorders:
Peptic ulcer
Hiatus hernia
Functional bowel syndrome, it is defined pathologically by the columnar epithelium has reached down the muscular layer.
[edit]Quick Differential
Biliary colic – Caused by obstruction of the cystic duct. It is associated with sharp and constant epigastric pain in the absence of fever and usually there is a negative Murphy’s sign. Liver function tests are within normal limits since the obstruction does not necessarily cause blockage in the common hepatic duct, thereby allowing normal bile excretion from the liver. An ultrasound scan is used to visualise the gallbladder and associated ducts, and also to determine the size and precise position of the obstruction.
Cholecystitis – Caused by blockage of the cystic duct with surrounding inflammation, usually due to infection. Typically, the pain is initially ‘colicky’ (intermittent), and becomes constant and severe, mostly in the right upper quadrant. Infectious agents that cause cholecystitis include E. coli, Klebsiella, Pseudomonas, B. fragilis and Enterococcus. Murphy’s sign is positive, particularly because of increased irritation of the gallbladder lining, and similarly this pain radiates (spreads) to the shoulder, flank or in a band like pattern around the lower abdomen. Laboratory tests frequently show raised hepatocellular liver enzymes (AST, ALT) with a high white cell count (WBC). Ultrasound is used to visualise the gallbladder and ducts.
Choledocholithiasis – This refers to blockage of the common bile duct where a gallstone has left the gallbladder or has formed in the common bile duct (primary cholelithiasis). As with other biliary tree obstructions it is usually associated with ‘colicky’ pain, and because there is direct obstruction of biliary output, obstructive jaundice. Liver function tests will therefore show increased serum bilirubin, with high conjugated bilirubin. Liver enzymes will also be raised, predominately GGT and ALP, which are associated with biliary epithelium. The diagnosis is made using endoscopic retrograde cholangiopancreatography (ERCP), or the nuclear alternative (MRCP). One of the more serious complications of choledocholithiasis is acute pancreatitis, which may result in significant permanent pancreatic damage and brittle diabetes.
Cholangitis – An infection of entire biliary tract, and may also be known as ‘ascending cholangitis’, which refers to the presence of pathogens that typically inhabit more distal regions of the bowel[3]
Cholangitis is a medical emergency as it may be life threatening and patients can rapidly succumb to acute liver failure or bacterial sepsis. The classical sign of cholangitis is Charcot’s triad, which is right upper quadrant pain, fever and jaundice. Liver function tests will likely show increases across all enzymes (AST, ALT, ALP, GGT) with raised bilirubin. As with choledocholithiasis, diagnosis is confirmed using cholangiopancreatography.
It is worth noting that bile is an extremely favourable growth medium for bacteria, and infections in this space develop rapidly and may become quite severe.
choleocystitis eval
Laboratory values may be notable for an elevated alkaline phosphatase, possibly an elevated bilirubin (although this may indicate choledocholithiasis), and possibly an elevation of the WBC count. CRP (C-reactive protein) is often elevated. The degree of elevation of these laboratory values may depend on the degree of inflammation of the gallbladder. Patients with acute cholecystitis are much more likely to manifest abnormal laboratory values, while in chronic cholecystitis the laboratory values are frequently normal.
Sonography is a sensitive and specific modality for diagnosis of acute cholecystitis; adjusted sensitivity and specificity for diagnosis of acute cholecystitis are 88% and 80%, respectively. The 2 major diagnostic criteria are cholelithiasis and sonographic Murphy’s sign. Minor criteria include gallbladder wall thickening greater than 3mm, pericholecystic fluid, and gallbladder dilatation.
The reported sensitivity and specificity of CT scan findings are in the range of 90-95%. CT is more sensitive than ultrasonography in the depiction of pericholecystic inflammatory response and in localizing pericholecystic abscesses, pericholecystic gas, and calculi outside the lumen of the gallbladder. CT cannot see noncalcified gallbladder calculi, and cannot assess for a Murphy’s sign.
Hepatobiliary scintigraphy with technetium-99m DISIDA (bilirubin) analog is also sensitive and accurate for diagnosis of chronic and acute cholecystitis. It can also assess the ability of the gall bladder to expel bile (gall bladder ejection fraction), and low gall bladder ejection fraction has been linked to chronic cholecystitis. However, since most patients with right upper quadrant pain do not have cholecystitis, primary evaluation is usually accomplished with a modality that can diagnose other causes, as well.
choleocystitis tx
For most patients, in most centres, the definitive treatment is surgical removal of the gallbladder. Supportive measures are instituted in the meantime and to prepare the patient for surgery. These measures include fluid resuscitation and antibiotics. Antibiotic regimens usually consist of a broad spectrum antibiotic such as piperacillin-tazobactam (Zosyn), ampicillin-sulbactam (Unasyn), ticarcillin-clavulanate (Timentin), or a cephalosporin (e.g.ceftriaxone) and an antibacterial with good coverage (fluoroquinolone such as ciprofloxacin) and anaerobic bacteria coverage, such as metronidazole. For penicillin allergic patients, aztreonam and clindamycin may be used.
Gallbladder removal, cholecystectomy, can be accomplished via open surgery or a laparoscopic procedure. Laparoscopic procedures can have less morbidity and a shorter recovery stay. Open procedures are usually done if complications have developed or the patient has had prior surgery to the area, making laparoscopic surgery technically difficult. A laparoscopic procedure may also be ‘converted’ to an open procedure during the operation if the surgeon feels that further attempts at laparoscopic removal might harm the patient. Open procedure may also be done if the surgeon does not know how to perform a laparoscopic cholecystectomy.
In cases of severe inflammation, shock, or if the patient has higher risk for general anesthesia (required for cholecystectomy), the managing physician may elect to have an interventional radiologist insert a percutaneous drainage catheter into the gallbladder (‘percutaneous cholecystostomy tube’) and treat the patient with antibiotics until the acute inflammation resolves. A cholecystectomy may then be warranted if the patient’s condition improves.
choleocystitis complications
Perforation or rupture
Ascending cholangitis
Rokitansky-Aschoff sinuses
[edit]Complications of cholecystectomy
bile leak (“biloma”)
bile duct injury (about 5-7 out of 1000 operations. Open and laparoscopic surgeries have essentially equal rate of injuries, but the recent trend is towards fewer injuries with laparoscopy. It may be that the open cases often result because the gallbladder is too difficult or risky to remove with laparoscopy)
wound infection
bleeding (liver surface and cystic artery are most common sites)
organ injury (intestine and liver are at highest risk, especially if the gallbladder has become adherent/scarred to other organs due to inflammation (e.g. transverse colon)
deep vein thrombosis/pulmonary embolism (unusual- risk can be decreased through use of sequential compression devices on legs during surgery)
fatty acid and fat-soluble vitamin malabsorption
[edit]Gall bladder perforation
Gall bladder perforation (GBP) is a rare but life-threatening complication of acute cholecystitis. The early diagnosis and treatment of GBP are crucial to decrease patient morbidity and mortality.
Approaches to this complication will vary based on the condition of an individual patient, the evaluation of the treating surgeon or physician, and the facilities’ capability. Perforation can happen at the neck from pressure necrosis due to the impacted calculus, or at the fundus. It can result in a local abscess, or perforation into the general peritoneal cavity. If the bile is infected, diffuse peritonitis may occur readily and rapidly and may result in death A retrospective study looked at 332 patients who received medical and/or surgical treatment with the diagnosis of acute cholecystitis. Patients were treated with analgesics and antibiotics within the first 36 hours after admission (with a mean of 9 hours), and proceeded to surgery for a cholecystectomy. Two patients died and 6 patients had further complications. The morbidity and mortality rates were 37.5% and 12.5%, respectively in the present study. The authors of this study suggests that early diagnosis and emergency surgical treatment of gallbladder perforation are of crucial importance.[4]
BOAS sign
Boas’ or Boas’s sign is hyperaesthesia (increased or altered sensitivity) below the right scapula can be a symptom in acute cholecystitis (inflammation of the gallbladder) [1] It is one of many symptoms a medical provider may look for during an abdominal examination[2] It is less than 7% sensitive[citation needed]. It’s namesake is Ismar Isidor Boas (1858-1938), German physician and first licensed GI specialist in his country.
Charots triad

Charcot’s cholangitis triad is the combination of jaundice; fever, usually with rigors; and right upper quadrant abdominal pain. Occurs as a result of ascending cholangitis. When the presentation also includes hypotension and mental status changes, it is known as Reynolds’ pentad.[1] It is named for Jean-Martin Charcot.[2]

-Charcot’s neurologic triad is the combination of nystagmus, intention tremor, and scanning or staccato speech. This triad is associated with multiple sclerosis, where it was first described;[1] however, it is not considered pathognomonic for it. It is named for Jean-Martin Charcot.[2]

Reynolds pentad
Reynolds’ pentad is a collection of signs and symptoms suggesting the diagnosis of septic or ascending cholangitis, a serious infection of the biliary system. It is a combination of Charcot’s triad 2 (jaundice, fever, abdominal pain) with hypotension (low blood pressure) and an altered mental state.
Rovsing’s sign
Rovsing’s sign, named after the Danish surgeon Niels Thorkild Rovsing,[1] is a sign of appendicitis. If palpation of the left lower quadrant of a person’s abdomen results in more pain in the right lower quadrant, the patient is said to have a positive Rovsing’s sign and may have appendicitis.
In acute appendicitis, palpation in the left iliac fossa may produce pain in the right iliac fossa.
-referral pain: This anomaly occurs because the pain nerves deep in the intestines do not localize well to an exact spot on the abdominal wall, unlike pain nerves in muscles. Pain from a stomach ulcer or gallstone can be interpreted by the brain as pain from the stomach, liver, gall bladder, duodenum, or first part of the small intestine. It will “refer” pain often to the mid upper abdomen. Because the appendix is a piece of intestine, it follows a similar referral pattern. An appendix with some early inflammation may give a non-specific irritation somewhere near the umbilicus (belly button). Should the inflammation become severe, it may actually irritate the inner lining of the abdominal cavity called the peritoneum. This thin layer lies under or behind the abdominal wall muscles. Now the pain is “localized”. If pressure is applied to the muscles of the right lower abdomen (or iliac fossa) near a very irritated appendix, then the muscle fibers in that area will be stretched and will hurt.
A Rovsing’s sign is elicited by pushing on the abdomen far away from the appendix in the left lower quadrant as in most people the appendix is in the right lower quadrant. While this maneuver stretches the entire peritoneal lining, it only causes pain in any location where the peritoneum is irritating the muscle. In the case of appendicitis, the pain is felt in the right lower quadrant despite pressure being placed elsewhere.
Most practitioners push on the left lower quadrant to see where the patient complains of pain. If pain is felt in the right lower quadrant, then there may be an inflamed organ or piece of tissue in the right lower quadrant. The appendix is generally the prime suspect, although other pathology can also give a “positive” Rovsing’s sign. If left lower quadrant pressure by the examiner leads only to left-sided pain or pain on both the left and right sides, then there may be some other pathologic etiology. This may include causes relating to the bladder, uterus, ascending (right) colon, fallopian tubes, ovaries, or other structures.
The eponym Rovsing sign is also used in patients with horse-shoe kidney, consisting of abdominal pain, nausea, and vomiting with hyperextension of the spine
Mc Burney’s Point
McBurney’s point is the name given to the point over the right side of the abdomen that is one-third of the distance from the ASIS (anterior superior iliac spine) to the umbilicus (the belly button). This point roughly corresponds to the most common location of the base of the appendix where it is attached to the cecum.
The anterior cutaneous branch of iliohypogastric nerve is found near McBurney’s point.
-Deep tenderness at McBurney’s point, known as McBurney’s sign, is a sign of acute appendicitis.[2] The clinical sign of referred pain in the epigastrium when pressure is applied is also known as Aaron’s sign.
Specific localization of tenderness to McBurney’s point indicates that inflammation is no longer limited to the lumen of the bowel (which localizes pain poorly), and is irritating the lining of the peritoneum at the place where the peritoneum comes into contact with the appendix. Tenderness at McBurney’s point suggests the evolution of acute appendicitis to a later stage, and thus, the increased likelihood of rupture. Other abdominal processes can also sometimes cause tenderness at McBurney’s point. Thus, this sign is highly useful but neither necessary nor sufficient to make a diagnosis of acute appendicitis. Also, the anatomical position of the appendix is highly variable (for example in retrocaecal appendix, an appendix behind the caecum), which also limits the use of this sign as many cases of appendicitis do not cause point tenderness at McBurney’s point. For most open appendectomy incisions (as opposed to laparoscopic appendectomies), the McBurney’s point is the guide for surgeons as to where to place the skin incision.
Psoas Sign
The psoas sign is a medical sign that indicates irritation to the iliopsoas group of hip flexors in the abdomen, and consequently indicates that the inflamed appendix is retrocaecal in orientation (as the iliopsoas muscle is retroperitoneal). It is elicited by performing the psoas test by passively extending the thigh of a patient lying on his side with knees extended, or asking the patient to actively flex his thigh at the hip.[1] If abdominal pain results, it is a “positive psoas sign”. The pain results because the psoas borders the peritoneal cavity, so stretching (by hyperextension at the hip) or contraction (by flexion of the hip) of the muscles causes friction against nearby inflamed tissues. In particular, the right iliopsoas muscle lies under the appendix when the patient is supine, so a positive psoas sign on the right may suggest appendicitis. A positive psoas sign may also be present in a patient with a psoas abscess.
Obturator sign
The obturator sign, also known as the Cope sign, is an indicator of irritation to the obturator internus muscle.
The technique is carried out on each leg in succession. First the patient lies on his back with the right hip flexed at 90 degrees. The examiner then holds the patient’s right ankle in his right hand. With his left hand, the examiner rotates the hip by moving the right knee inward. This is flexion and internal rotation of the hip.
In the clinical context, it is performed when acute appendicitis is suspected. In this condition, the appendix becomes inflamed and enlarged. The appendix may come into physical contact with the obturator internus muscle, which will be stretched when this maneuver is performed on the right leg. This causes pain and is an evidence in support of an inflamed appendix.
The principles of the obturator sign in the diagnosis of appendicitis are similar to that of the psoas sign.
Choledocholithiasis is the presence of gallstones in the common bile duct. This condition causes jaundice and liver cell damage, and requires treatment by cholecystectomy and/or ERCP.
Signs and SX:-A positive Murphy’s sign is a common finding on physical examination. Jaundice of the skin or eyes is an important physical finding in biliary obstruction. Jaundice and/or clay-colored stool may raise suspicion of choledocholithiasis or even gallstone pancreatitis.[3] If the above symptoms coincide with fever and chills, the diagnosis of ascending cholangitis may also be considered.
-Causes: While stones can frequently pass through the common bile duct (CBD) into the duodenum, some stones may be too large to pass through the CBD and may cause an obstruction. One risk factor for this is duodenal diverticulum.
-Pathophysiology: This obstruction may lead to jaundice, elevation in alkaline phosphatase, increase in conjugated bilirubin in the blood and increase in cholesterol in the blood. It can also cause acute pancreatitis and ascending cholangitis.
-Diagnosis: Common bile duct stone impacted at ampulla of Vater seen at time of ERCP
Choledocholithiasis (stones in common bile duct) is one of the complications of cholelithiasis (gallstones), so the initial step is to confirm the diagnosis of cholelithiasis. Patients with cholelithiasis typically present with pain in the right-upper quadrant of the abdomen with the associated symptoms of nausea and vomiting, especially after a fatty meal. The physician can confirm the diagnosis of cholelithiasis with an abdominal ultrasound that shows the ultrasonic shadows of the stones in the gallbladder.
The diagnosis of choledocholithiasis is suggested when the liver function blood test shows an elevation in bilirubin. The diagnosis is confirmed with either an Magnetic resonance cholangiopancreatography (MRCP), an ERCP, or an intraoperative cholangiogram. If the patient must have the gallbladder removed for gallstones, the surgeon may choose to proceed with the surgery, and obtain a cholangiogram during the surgery. If the cholangiogram shows a stone in the bile duct, the surgeon may attempt to treat the problem by flushing the stone into the intestine or retrieve the stone back through the cystic duct.
On a different pathway, the physician may choose to proceed with ERCP before surgery. The benefit of ERCP is that it can be utilized not just to diagnose, but also to treat the problem. During ERCP the endoscopist may surgically widen the opening into the bile duct and remove the stone through that opening. ERCP, however, is an invasive procedure and has its own potential complications. Thus, if the suspicion is low, the physician may choose to confirm the diagnosis with MRCP, a non-invasive imaging technique, before proceeding with ERCP or surgery.
-Treatment: Fluoroscopic image taken during ERCP and duodenoscope assisted cholangiopancreatoscopy (DACP). Multiple gallstones are present in the gallbladder and cystic duct. The common bile duct and pancreatic duct appear to be patent.
Treatment involves removing the stone using ERCP. Typically, the gallbladder is then removed, an operation called cholecystectomy, to prevent a future occurrence of common bile duct obstruction or other complications.
A gallstone is a crystalline concretion formed within the gallbladder by accretion of bile components. These calculi are formed in the gallbladder, but may pass distally into other parts of the biliary tract such as the cystic duct, common bile duct, pancreatic duct, or the ampulla of Vater.
Presence of gallstones in the gallbladder may lead to acute cholecystitis, an inflammatory condition characterized by retention of bile in the gallbladder and often secondary infection by intestinal microorganisms, predominantly Escherichia coli and Bacteroides species. Presence of gallstones in other parts of the biliary tract can cause obstruction of the bile ducts, which can lead to serious conditions such as ascending cholangitis or pancreatitis. Either of these two conditions can be life-threatening, and are therefore considered to be medical emergencies.
-Presence of stones in the gallbladder is referred to as cholelithiasis (from the Greek: chol-, “bile” + lith-, “stone” + iasis-, “process”). If gallstones migrate into the ducts of the biliary tract, the condition is referred to as choledocholithiasis (from the Greek: chol-, “bile” + docho-, “duct” + lith-, “stone” + iasis-, “process”). Choledocholithiasis is frequently associated with obstruction of the biliary tree, which in turn can lead to acute ascending cholangitis (from the Greek: chol-, “bile + ang-, “vessel” + itis-, “inflammation”), a serious infection of the bile ducts. Gallstones within the ampulla of Vater can obstruct the exocrine system of the pancreas, which in turn can result in pancreatitis.
[edit]Characteristics and compositionGallbladder opened to show numerous gallstones. The large, yellowish calculus is probably composed largely of cholesterol, while the greenish to brownish color of the other stones suggests these are composed of bile pigments such as biliverdin and stercobilin.

Images of a CT of gallstones

Gallstones can vary in size from as small as a grain of sand to as large as a golf ball.[citation needed] The gallbladder may contain a single large stone or many smaller ones. Pseudoliths, sometime referred to as sludge, are thick secretions that may be present within the gallbladder, either alone or in conjunction with fully formed gallstones. The clinical presentation is similar to that of cholelithiasis.[citation needed] The composition of gallstones is affected by age, diet and ethnicity.[1] On the basis of their composition, gallstones can be divided into the following types:
Cholesterol stones
Cholesterol stones vary in color from light-yellow to dark-green or brown and are oval 2 to 3 cm in length, often having a tiny dark central spot. To be classified as such, they must be at least 80% cholesterol by weight (or 70%, according to the Japanese classification system).[2]
Pigment stones
Pigment stones are small, dark stones made of bilirubin and calcium salts that are found in bile. They contain less than 20% of cholesterol (or 30%, according to the Japanese classification system).[2]
Mixed stones
Mixed gallstones typically contain 20-80% cholesterol (or 30-70%, according to the Japanese classification system).[2] Other common constituents are calcium carbonate, palmitate phosphate, bilirubin, and other bile pigments. Because of their calcium content, they are often radiographically visible.

Choleolithiasis 5min clinical
Description:Cholelithiasis manifests in cholesterol, pigment, or mixed stones formed and contained in the gallbladder.Synonym=Gallstones
Pediatric Considerations=Uncommon at < 10yrs, Associated with blood dyscrasia, Most gallstones in pediatric population are pigment stones. Epidemiology: Incidence-Increased in Native Americans and Hispanics. Increases with age by 1-3% per year; peaks at 7th decade 2% of the US population develops gallstones annually. Prevalence: Population: 8-10% of US, Predominant sex: Female > Male (2-3:1)
Risk Factors:Age (peak in 60-70s), female, Caucasian, Hispanic, or Native American descent
Hereditary (such as patients carrying the p.D19H variant for the hepato-canalicular cholesterol transporter ABCG5/ABG8 have an increased risk for
Metabolic syndrome (i.e., obesity, dyslipidemia, hypertension, and type 2 diabetes)
Pregnancy and multiparity
Cholestasis in association with prolonged fasting and long-term total parenteral nutrition
Rapid weight loss following bariatric surgery
Metabolic changes in association with short gut syndrome, terminal ileal resection, and inflammatory bowel disease
Hemolytic disorders (e.g., hereditary spherocytosis and sickle cell anemia) and cirrhosis (for black or pigment stones)
Medications (such as early use of birth control pills; estrogen replacement therapy at high doses)
Biliary tract infection (such as liver flukes) and stricture (for intraductal formation of brown pigment stones)Genetics
Animal studies indicate that gallstone formation is a dominant trait determined by at least 2 genes; susceptible strains fail to down-regulate cholesterol synthesis during cholesterol feeding.
General Prevention
Ursodiol (Actigall) taken during rapid weight loss prevents gallstone formation (1)[A]
Regular exercise and dietary modification may reduce the incidence of gallstone formation.
Gallstone formation is a complex process mediated by genetic, metabolic, immune, and environmental factors.
Production of bile supersaturated with cholesterol (cholesterol stones)
Decrease in bile content of either phospholipid (lecithin) or bile salts
Biliary stasis or impaired gallbladder motility
Generation of excess unconjugated bilirubin in patients with hemolytic diseases; passage of excess bile salt into the colon with subsequent absorption of excess unconjugated bilirubin in patients with IBD or after distal ileal resection (black or pigment stones)
Hydrolysis of conjugated bilirubin or phospholipid by bacteria in patients with biliary tract infection or stricture (brown stones or primary bile duct stones, rare in the Western world and common in Asia )
Commonly Associated Conditions
90% of people with gallbladder carcinoma have gallstones.
Signs and Symptoms
Mostly asymptomatic (80%):
5-10% become symptomatic each year.
Over their lifetime, < 1/2 of the patients with gallstones develop symptoms. Episodic right upper quadrant or epigastric pain lasting longer than 15 minutes and sometimes radiating to the back (biliary colic), usually postprandially; the majority of patients will develop recurrent symptoms after the first episode. Nausea Vomiting Fatty food intolerance (not proven) Indigestion or bloating sensation Physical Exam Physical exam is usually normal in patients with cholelithiasis. Epigastric and/or right upper quadrant tenderness (Murphy’s sign) when in association with cholecystitis Fever and jaundice in patients with choledocholithiasis and cholangitis; jaundice can also be caused by extrinsic compression of the bile duct by a stone in the gallbladder or cystic duct (Mirizzi syndrome). Flank and periumbilical ecchymoses (Cullen sign and Grey-Turner sign) in patients with acute hemorrhagic pancreatitis In patients with concomitant acute calculus cholecystitis and gallbladder cancer, a mass in the right upper quadrant may be palpated. Diagnostic Tests and Interpretation Lab No lab study is specific for cholelithiasis Leukocytosis and elevated C-reactive protein level are associated with acute calculus cholecystitis Imaging Ultrasound (best technique to diagnose gallstones and differentiate from cholecystitis). Ultrasound can detect gallstones in 97-98% of patients. Thickening of the gallbladder wall (5 mm or greater), pericholecystic fluid, and direct tenderness when the probe is pushed against the gallbladder (sonographic Murphy sign) are all radiographic signs of acute calculus cholecystitis. CT scan (no advantage over ultrasound except in detecting distal common bile duct stones) MRCP is reserved for cases of suspected common bile duct stones due to high cost Endoscopic ultrasound (EUS) has been shown to be as sensitive as endoscopic retrograde cholangiopancreatography (ERCP) for detection of common bile duct stones in patients with gallstone pancreatitis. HIDA scan is useful in differentiating acalculous cholecystitis from other causes of abdominal pain. False-positive results can arise from fasting status or insufficient resistance of the sphincter of Oddi. 10-30% of gallstones are radiopaque calcium or pigment-containing gallstones and are more likely to be visible on plain x-ray. A “porcelain gallbladder” is a calcified gallbladder, visible by x-ray; associated with gallbladder cancer (25%). Pathological Findings Pure cholesterol stones have a white or slightly yellow color. Pigment stones may be black or brown. Black stones contain polymerized calcium bilirubinate, most often secondary to cirrhosis or hemolysis, and almost always form in the gallbladder. Brown stones are associated with biliary tract infection, caused by bile stasis, and as such may form either in the bile ducts or gallbladder. Differential Diagnosis Peptic ulcer diseases Gastritis Hepatitis Pancreatitis Cholangitis Gallbladder cancer Gallbladder polyps Acalculous cholecystitis Biliary dyskinesia Biliary tree stricture Choledocholithiasis Choledochocyst Coronary artery disease Esophageal motility disorders Appendicitis Pneumonia Renal stones ALERT Geriatric Considerations Age alone should not alter the therapy plan. Medication (Drugs) First Line Analgesics for pain relief Oral dissolution therapy is rarely used today Antibiotics is indicated in patients with signs of acute cholecystitis Prophylactic antibiotics in low-risk patients do not prevent infections for laparoscopic cholecystectomies (2)[A] Second Line NSAIDs may have a role in pain relief, given that prostaglandins are important in the development of pain. Additional Treatment General Measures Treat only symptomatic gallstones and observe asymptomatic stones Attempt conservative therapy during pregnancy. If necessary, perform surgery preferentially in the 2nd trimester. Prophylactic cholecystectomy for patients with large gallstones (>2-3 cm), calcified (porcelain) gallbladder (risk for gallbladder cancer), and patients with recurrent pancreatitis due to microlithiasis
In morbidly obese patients, simultaneous cholecystectomy may be performed in combination with bariatric procedures in effort to reduce later stone-related complications.

Issue for Referral
Patients with retained or recurrent bile duct stones following cholecystectomy should be refered to gastroenterology for ERCP.
Surgery/Other Procedures
Surgical intervention should be considered for patients who have symptomatic cholelithiasis or gallstone-related complications such as cholecystitis (3)[B].
Laparoscopic cholecystectomy is currently the standard of care for most cases (4)[B]. In well-selected patients, transumbilical single-port laparoscopic cholecystectomy (TUSPLC) is a novel and promising method for the treatment of symptomatic cholelithiasis. Natural orifice transluminal endoscopic surgery (NOTES) may become an alternative in the near future:
Surgery-related complications include common bile duct injury (0.5%), right hepatic duct/artery injury, cystic duct or duct of Luschka leak, biloma formation, or bile duct stricture in the long term.
Conversion to open procedure based on the judgment of the operating surgeon
Intraoperative cholangiogram (IOC) may help delineate bile duct anatomy when dissection proves difficult. Selective or routine use of IOC is a topic of debate, but may be associated with earlier recognition and decreased incidence of bile duct injury (5)[B].
Open cholecystectomy is indicated for gallbladder cancer diagnosed preoperatively.
Percutaneous cholecystostomy (PC) in high-risk patients with cholecystitis or gallbladder empyema. PC may also be used in patients with symptoms of cholecystitis for >72 hrs in which altered anatomy might significantly increase the surgical risk. Interval cholecystectomy is usually advisable after the resolution of cholecystitis and optimization of associated medical conditions to prevent recurrent cholecystitis.
In-Patient Consideratons
For patients with symptomatic cholelithiasis, laparoscopic cholecystectomy has become an outpatient procedure; for patients who developed gallstone-related complications (i.e., cholecystitis, cholangitis, and pancreatitis), inpatient care is necessary.

Initial Stabilization
Patients are treated during the acute phase with nothing by mouth (NPO), intravenous fluids, and antibiotics.
Adequate pain control with narcotics and/or nonsteroidal anti-inflammatory drugs (NSAIDs) are also needed.
Follow-Up Recommendations
Patient Monitoring
Medical attention if asymptomatic stones become symptomatic
Patients on oral dissolution agents should be followed up with liver enzyme, serum cholesterol, and imaging studies.
A low-fat diet may be helpful.
Patient Education
Change in lifestyle (e.g., regular exercise) and dietary modification (low-fat diet and reduction of total calorie intake) may reduce gallstone-related hospitalizations.
Patients with asymptomatic gallstones should be educated about the typical symptoms of biliary colic and gallstone-related complications.
<1/2 of patients with gallstones become symptomatic.
Cholecystectomy: Mortality <0.5% elective, 3-5% emergency; morbidity <10% elective, 30-40% emergency
~10-15% of the patients will have associated choledocholithiasis.
After cholecystectomy, stones may recur in the bile duct.
Acute cholecystitis (90-95% secondary to gallstones)
Gallbladder empyema
Gallstone pancreatitis
Acute cholangitis
Common bile duct stones with obstructive jaundice
Biliary-enteric fistula
Gallstone ileus
Gallbladder perforation
Peritonitis and sepsis
Liver abscess
Gallbladder cancer
Mirizzi syndrome (bile duct obstruction caused by gallstones lodged in gallbladder or cystic duct)
Lammert F, Miquel JF. Gallstone disease: From genes to evidence-based therapy. J Hepatol. 2008. [PMID:18308417]

See Also
Cholangitis (acute); Cholecystitis; Choledocholithiasis
574.00 Calculus of gallbladder with acute cholecystitis, without mention of obstruction
574.10 Calculus of gallbladder with other cholecystitis, without mention of obstruction
574.20 Calculus of gallbladder without mention of cholecystitis, without mention of obstruction
266474003 Calculus in biliary tract (disorder)
Laparoscopic cholecystectomy has become the most frequently used procedure; lithotripsy and oral dissolution therapy may be considered in rare circumstances.
Acute acalculous cholecystitis is associated with bile stasis and gallbladder ischemia.
Prophylactic cholecystectomy is not indicated in patients with diabetes and asymptomatic gallstones. There is no evidence that asymptomatic diabetics are at increased risk of developing complications of gallstone disease.
The best imaging modality for the diagnosis of gallstones is transabdominal ultrasound (sensitivity of 97% and specificity of 95%); not sensitive for occult gallstones or microlithiasis (stones smaller than 5 mm).
Think of gallstones in the post-bariatric surgery patient complaining of “gas pains” as they are adjusting to their new diet.

Ascending cholangitis or acute cholangitis
Ascending cholangitis or acute cholangitis (or sometimes cholangitis without a modifier – from Greek chol-, bile + ang-, vessel + itis-, inflammation) is an infection of the bile duct (cholangitis), usually caused by bacteria ascending from its junction with the duodenum (first part of the small intestine). It tends to occur if the bile duct is already partially obstructed by gallstones. Cholangitis can be life-threatening, and is regarded as a medical emergency. Characteristic symptoms include jaundice, fever, abdominal pain, and in severe cases, low blood pressure and confusion. Initial treatment is with intravenous fluids and antibiotics, but there is often an underlying problem (such as gallstones or narrowing in the bile duct) for which further tests and treatments may be necessary, usually in the form of endoscopy to relieve obstruction of the bile duct.
SX:Ascending cholangitis or acute cholangitis
A person with cholangitis may complain of abdominal pain (particularly in the right upper quadrant of the abdomen), fever, rigors (uncontrollable shaking) and a feeling of uneasiness (malaise). Some may report jaundice (yellow discoloration of the skin and the whites of the eyes).
-Physical examination findings typically include jaundice and right upper quadrant tenderness. Charcot’s triad is a set of three common findings in cholangitis: abdominal pain, jaundice, and fever.This was assumed in the past to be present in 50-70% of cases, although more recently the frequency has been reported as 15-20%. Reynolds’ pentad includes the findings of Charcot’s triad with the presence of septic shock and mental confusion. This combination of symptoms indicates worsening of the condition and the development of septicemia, and is seen less commonly still.
-In the elderly, the presentation may be atypical; they may directly collapse due to septicemia without first showing typical features.Those with an indwelling stent in the bile duct may not develop jaundice.
coleoangitis DX
Blood tests: Routine blood tests show features of acute inflammation (raised white blood cell count and elevated C-reactive protein level), and usually abnormal liver function tests (LFTs). In most cases the LFTs will be consistent with obstruction: raised bilirubin, alkaline phosphatase and γ-glutamyl transpeptidase. In the early stages, however, pressure on the liver cells may be the main feature and the tests will resemble those in hepatitis, with elevations in alanine transaminase and aspartate transaminase.
Blood cultures are often performed in people with fever and evidence of acute infection. These yield the bacteria causing the infection in 36% of cases,usually after 24-48 hours of incubation. Bile, too, may be sent for culture during ERCP. The most common bacteria linked to ascending cholangitis are gram-negative bacilli: Escherichia coli (25-50%), Klebsiella (15-20%) and Enterobacter (5-10%). Of the gram-positive cocci, Enterococcus causes 10-20%. A small proportion of cases, especially in the elderly and those who have undergone previous surgery of the biliary system, is due to anaerobic organisms such as Clostridium and Bacteroides. In the developing world, cholangitis may also be caused by parasites such as Ascaris lumbricoides and Clonorchis sinensis. In people with AIDS, a large number of opportunistic organisms has been known to cause AIDS cholangiopathy, but the risk has rapidly diminished since the introduction of effective AIDS treatment.[1]
[edit]Medical imagingCholangiogram through a nasobiliary drain showing the common bile duct in black (diagonally from top left to bottom right in the center) with an interruption in the contour due to a large gallstone.
Given that ascending cholangitis usually occurs in the setting of bile duct obstruction, various forms of medical imaging may be employed to identify the site and nature of this obstruction. The first investigation is usually ultrasound, as this is the most easily available.[1] Ultrasound may show dilation of the bile duct and identifies 38% of bile duct stones; it is relatively poor at identifying stones further down the bile duct. Ultrasound can help distinguish between cholangitis and cholecystitis (inflammation of the gallbladder), which has similar symptoms to cholangitis but appears differently on ultrasound.[7] A better test is magnetic resonance cholangiopancreatography (MRCP), which uses magnetic resonance imaging (MRI); this has a comparable sensitivity to ERCP.[7] Smaller stones, however, can still be missed on MRCP depending on the quality of the hospital’s facilities.[1]
The gold standard (best possible) test for biliary obstruction is still endoscopic retrograde cholangiopancreatography (ERCP). This involves the use of endoscopy (passing a tube through the mouth into the esophagus, stomach and thence to the duodenum) to pass a small cannula into the bile duct. At that point, radiocontrast is injected to opacify the duct, and X-rays are taken to get a visual impression of the biliary system. On the endoscopic image of the ampulla, one can sometimes see a protuberant ampulla from an impacted gallstone in the common bile duct, or the frank extrusion of pus from the common bile duct orifice. On the X-ray images (known as cholangiograms), gallstones are visible as nonopacified areas in the contour of the duct. For diagnostic purposes, ERCP has now generally been replaced by MRCP. ERCP is only used first-line in critically ill patients in whom delay for diagnostic tests is not acceptable; however, if the index of suspicion for cholangitis is high, an ERCP is typically done to achieve drainage of the obstructed common bile duct.[1]
If other causes rather than gallstones are suspected (such as a tumor), computed tomography and endoscopic ultrasound (EUS) may be performed to identify the nature of the obstruction. EUS may be used to obtain biopsy (tissue sample) of suspicious masses.[1] EUS may also replace diagnostic ERCP for stone disease, although this depends on local availability.

Cholangitis causes
Bile duct obstruction, which is usually present in acute cholangitis, is generally due to gallstones. 10-30% of cases, however, are due to other causes such as benign stricturing (narrowing of the bile duct without an underlying tumor), postoperative damage or an altered structure of the bile ducts such as narrowing at the site of an anastomosis (surgical connection) and various tumors (cancer of the bile duct, gallbladder cancer, cancer of the ampulla of Vater, pancreatic cancer or cancer of the duodenum).[8] Cholangitis may also complicate medical procedures involving the bile duct, especially ERCP. To prevent this, it is recommended that those undergoing ERCP for any indication receive prophylactic (preventative) antibiotics.[3]
The presence of a permanent biliary stent (e.g. in pancreatic cancer) slightly increases the risk of cholangitis, but stents of this type are often needed to keep the bile duct patent under outside pressure.
cholangitis pathogenisis
Bile is produced by the liver, and serves to eliminate cholesterol and bilirubin from the body, as well as emulsifying of fats to make them more soluble in water and aid in their digestion. Bile is formed in the liver by hepatocytes (liver cells) and excreted into the common hepatic duct. Part of the bile is stored in the gall bladder because of back pressure (exerted by the sphincter of Oddi), and may be released at time of digestion. The gall bladder also concentrates the bile by absorbing water and dissolved salts from it. All bile reaches the duodenum (first part of the small intestine) through the common bile duct and the ampulla of Vater. The sphincter of Oddi, located at the junction of the ampulla of Vater and the duodenum, is a circular muscle that controls the release of both bile and pancreatic secretions into the digestive tract.[1]
The biliary tree is normally relatively free of bacteria because of certain protective mechanisms. The sphincter of Oddi acts as a mechanical barrier. The biliary system normally has low pressure (8 to 12 cmH2O)[9] and allows bile to flow freely through. The continuous forward flow of the bile in the duct flushes bacteria, if present, into the duodenum, and does not allow establishment of an infection. The constitution of bile—bile salts[1] and immunoglobulin[2] secreted by the epithelium of the bile duct also has a protective role.
Bacterial contamination alone in absence of obstruction does not usually result in cholangitis.[2] However increased pressure within the biliary system (above 20 cmH2O)[10] resulting from obstruction in the bile duct widens spaces between the cells lining the duct, bringing bacterially contaminated bile in contact with the blood stream. It also adversely affects the function of Kupffer cells, which are specialized macrophage cells that assist in preventing bacteria from entering the biliary system. Finally, increased biliary pressure decreases production of IgA immunoglobulins in the bile.[11] This results in bacteremia (bacteria in the blood stream) and gives rise to the systemic inflammatory response syndrome (SIRS) comprising fever (often with rigors), tachycardia, increased respiratory rate and increased white blood cell count; SIRS in the presence of suspected or confirmed infection is called sepsis.[1] Biliary obstruction itself disadvantages the immune system and impairs its capability to fight infection, by impairing the function of certain immune system cells (neutrophil granulocytes) and modifying the levels of immune hormones (cytokines).[1]
In ascending cholangitis, it is assumed that organisms migrate backwards up the bile duct as a result of partial obstruction and decreased function of the sphincter of Oddi.[1] Other theories about the origin of the bacteria, such as through the portal vein or transmigration from the colon, are considered less likely.
Cholangitis TX
Fluids and antibiotics:Cholangitis requires admission to hospital. Intravenous fluids are administered, especially if the blood pressure is low, and antibiotics are commenced. Empirical treatment with broad-spectrum antibiotics is usually necessary until it is known for certain which pathogen is causing the infection, and to which antibiotics it is sensitive. Combinations of penicillins and aminoglycosides are widely used, although ciprofloxacin has been shown to be effective in most cases, and may be preferred to aminoglycosides because of fewer side effects. Metronidazole is often added to specifically treat the anaerobic pathogens, especially in those who are very ill or at risk of anaerobic infections.
-Antibiotics are continued for 7-10 days.Drugs that increase the blood pressure (vasopressors) may also be required to counter the low blood pressure.Endoscopy
The definitive treatment for cholangitis is relief of the underlying biliary obstruction. This is usually deferred until 24-48 hours after admission, when the patient is stable and has shown some improvement with antibiotics, but may need to happen as an emergency in case of ongoing deterioration despite adequate treatment,[1] or if antibiotics are not effective in reducing the signs of infection (which happens in 15% of cases).[2][3]
Endoscopic retrograde cholangiopancreatography (ERCP) is the most common approach in unblocking the bile duct. This involves endoscopy (passing a fiberoptic tube through the stomach into the duodenum), identification of the ampulla of Vater and insertion of a small tube into the bile duct. A sphincterotomy (making a cut in the sphincter of Oddi) is typically done to ease the flow of bile from the duct and to allow insertion of instruments to extract gallstones that are obstructing the common bile duct; alternatively or additionally, the common bile duct orifice can be dilated with a balloon.[12] Stones may be removed either by direct suction or by using various instruments, including balloons and baskets to trawl the bile duct in order to pull stones into the duodenum. Obstructions that are caused by larger stones may require the use of an instrument known as a mechanical lithotriptor in order to crush the stone prior to removal.[13] Obstructing stones that are too large to be removed or broken mechanically by ERCP may be managed by extracorporeal shock wave lithotripsy. This technique uses acoustic shock waves administered outside the body to break down the stones.[14] An alternative technique to remove very large obstructing stones is electrohydraulic lithotripsy, where a small endoscope known as a cholangioscope is inserted by ERCP to directly visualize the stone. A probe uses electricity to generate shock waves that break down the obstructing stone.[15] Rarely, surgical exploration of the common bile duct (termed choledochotomy), which can be performed with laparoscopy, is required to remove the stone.[16]
Narrowed areas may be bridged by a stent, a hollow tube that keeps the duct open. Removable plastic stents are used in uncomplicated gallstone disease, while permanent self-expanding metal stents with a longer lifespan are used if the obstruction is due to pressure from a tumor such as pancreatic cancer. A nasobiliary drain may be left behind; this is a plastic tube that passes from the bile duct through the stomach and the nose and allows continuous drainage of bile into a receptible. It is similar to a nasogastric tube, but passes into the common bile duct directly, and allows for serial x-ray cholangiograms to be done to identify the improvement of the obstruction. The decision on which of the aforementioned treatments to apply is generally based on the severity of the obstruction, findings on other imaging studies, and whether the patient has improved with antibiotic treatment.[1] Certain treatments may be unsafe if blood clotting is impaired, as the risk of bleeding (especially from sphincterotomy) is increased in the use of medication such as clopidogrel (which inhibits platelet aggregation) or if the prothrombin time is significantly prolonged. For a prolonged prothrombin time, vitamin K or fresh frozen plasma may be administered to reduce bleeding risk.[1]
It may be difficult to obtain endoscopic access to the obstruction located higher (proximal) up in the biliary system, or when it is due to a stricture in the priorly performed anastomosis between the bile duct (surgically joining) with the duodenum or jejunum.[2] When this happens, percutaneous transhepatic cholangiography (PTC) may be needed to relieve pressure. This involves identifying the bile duct by ultrasound and then passing a tube through the skin (percutaneous).[3] PTC is generally performed by radiologists. PTC has potential complications, so occasionally further attempts at ERCP by more experienced doctors are preferred.[1]
Continual contamination of bile duct by indwelling stents (as may occur in chronic conditions like tumor of the head of pancreas) requires monitoring by repeated radiologic tests and changing of the stents.[2]
Not all gallstones implicated in ascending cholangitis actually originate from the gallbladder, but cholecystectomy (surgical removal of the gallbladder) is generally recommended in people who have been treated for cholangitis due to gallstone disease. This is typically delayed until all symptoms have resolved and ERCP or MRCP have confirmed that the bile duct is clear of gallstones.[1][2][3] Those who do not undergo cholecystectomy have an increased risk of recurrent biliary pain, jaundice, further episodes of cholangitis, and need for further ERCP or related procedures; the risk of death is also significantly increased.
Acute cholangitis prognosis
Acute cholangitis carries a significant risk of death, the leading cause being irreversible shock with multiple organ failure (a possible complication of severe infections).[8] Improvements in diagnosis and treatment have led to a reduction in mortality: before 1980, the mortality rate was greater than 50%, but after 1980 it was 10-30%.[8] Patients with signs of multiple organ failure are likely to die unless they undergo early biliary drainage and treatment with systemic antibiotics. Other causes of death following severe cholangitis include heart failure and pneumonia.[18]
Risk factors indicating an increased risk of death include older age, female gender, a history of liver cirrhosis, biliary narrowing due to cancer, acute renal failure and the presence of liver abscesses.[19] Complications following severe cholangitis include renal failure, respiratory failure (inability of the respiratory system to oxygenate blood and/or eliminate carbon dioxide), cardiac arrythmia, wound infection, pneumonia, gastrointestinal bleeding and myocardial ischemia (lack of blood flow to the heart, leading to heart attacks)
Acute Pancreatitis
Acute pancreatitis or acute pancreatic necrosis[1] is a sudden inflammation of the pancreas. Depending on its severity, it can have severe complications and high mortality despite treatment. While mild cases are often successfully treated with conservative measures, such as NPO (nil per os or nothing by mouth (NBM)) and IV fluid rehydration, severe cases may require admission to the ICU or even surgery (often requiring more than one intervention) to deal with complications of the disease process.
Acute Pancreatitis:Sx
he most common symptoms and signs include:
Severe epigastric pain radiating to the back
Nausea, vomiting, diarrhea and loss of appetite
Hemodynamic instability, which include shock
Signs which are less common, and indicate severe disease, include:
Grey-Turner’s sign (hemorrhagic discoloration of the flanks)
Cullen’s sign (hemorrhagic discoloration of the umbilicus)
Grünwald sign (appearance of ecchymosis around the umbilicus due to local toxic lesion of the vessels)
Körte’s sign (pain or resistance in the zone where the head of pancreas is located (in epigastrium, 6-7 cm above the umbilicus)
Kamenchik’s sign (pain with pressure under the xiphoid process)
Mayo-Robson’s sign (pain while pressing at the top of the angle lateral to the Erector spinae muscles and below the left 12th rib (left costovertebral angle (CVA))[2]
Other conditions to consider are:
Pancreatic pseudocyst
Pancreatic dysfunction (diabetes mellitus; malabsorption due to exocrine failure)
Pancreatic cancer
Although these are common symptoms, they are not always present. Simple abdominal pain may be the sole symptom.
Grey Turners sign
Grey Turner’s sign refers to bruising of the flanks.
This sign takes 24-48 hours. It can predict a severe attack of acute pancreatitis,[1] with mortality rising from 8-10% to 40%.[citation needed]It is a sign of retroperitoneal hemorrhage.
It may be accompanied by Cullen’s sign, which may then be indicative of pancreatic necrosis with retroperitoneal or intraabdominal bleeding.
It is named for British surgeon George Grey Turner.
Causes include:
acute pancreatitis, whereby methaemalbumin formed from digested blood tracks subcutaneously around the abdomen from the inflamed pancreas
blunt abdominal trauma
ruptured abdominal aortic aneurysm.
Ruptured/ hemorrhagic ectopic pregnancy.
spontaneous bleeding secondary to coagulopathy (congenital or acquired)
Cullen’s sign
Cullen’s sign is superficial edema and bruising in the subcutaneous fatty tissue around the umbilicus.
It is named for Thomas S. Cullen (1869-1953),an obstetrician who first described the sign in ruptured ectopic pregnancy in 1916.
This sign takes 24-48 hours to appear and can predict acute pancreatitis, with mortality rising from 8-10% to 40%. It may be accompanied by Grey Turner’s sign[3] (bruising of the flank), which may then be indicative of pancreatic necrosis with retroperitoneal or intraabdominal bleeding.
Causes include:
acute pancreatitis, where methemalbumin formed from digested blood tracks around the abdomen from the inflamed pancreas
bleeding from blunt abdominal trauma
bleeding from ruptured abdominal aortic aneurysm
bleeding from ruptured ectopic pregnancy
Importance of the sign is on a decline since better diagnostic modalities are now available
Pancreatitc pseudocyst
A pancreatic pseudocyst is a circumscribed collection of fluid rich in pancreatic enzymes, blood, and necrotic tissue, typically located in the lesser sac of the abdomen.
Pancreatic pseudocysts are usually complications of pancreatitis, although in children they frequently occur following abdominal trauma. Pancreatic pseudocysts account for approximately 75% of all pancreatic masses. The prefix pseudo- (Greek for “false”) distinguishes them from true cysts, which are lined by epithelium; pseudocysts are lined with granulation tissue.
Pathophys:Acute pancreatitis results amongst other things in the disruption of pancreatic parenchyma and the ductal system. This results in extravasation of pancreatic enzymes which in turn digest the adjoining tissues. This results in a collection of fluid containing pancreatic enzymes, hemolysed blood and necrotic debris around the pancreas. The lesser sac being a potential space, the fluid collects here preferentially. This is called an acute pancreatic collection. Some of these collections resolve on their own as the patient recovers from the acute episode. However, others become more organized and get walled-off within a thick wall of granulation tissue and fibrosis. This takes several weeks to occur and results in a pancreatic pseudocyst.
-the questions that need to be answered are:
where, how big and how many?
is there a communication with the pancreatic ductal system? Draining such a pseudocyst carries an increased risk of pancreatic fistula.
The most useful imaging tools are
Ultrasonography[- The role of ultrasonography in imaging the pancreas is limited by patient habitus, operator experience and the fact that the pancreas lies behind the stomach (and so a gas-filled stomach will obscure the pancreas).
Computerized tomography[- This is the gold standard for initial assessment and follow-up
Magnetic resonance cholangiopancreatography (MRCP) – to establish the relationship of the pseudocyst to the pancreatic ducts
Treatment: A small pseudocyst that is not causing any symptoms may be managed conservatively. However, a large proportion of them will need some form of treatment, The interventions available are:
Endoscopic trans-gastric drainage
Imaging guided percutaneous drainage
Laparoscopic/open cystogastrostomy or cystojejunostomy
Complications of pseudocyst:f pancreatic pseudocyst include infection, hemorrhage, obstruction and rupture. For obstruction, it can cause compression in the GI tract from the stomach to colon, compression in urinary system, biliary system, and arteriovenous system.
Pancreatitis causes
A common mnemonic for the causes of pancreatitis spells “I get smashed”, an allusion to heavy drinking (one of the many causes):
I – idiopathic. Thought to be hypertensive sphincter or microlithiasis.
G – gallstone. Gallstones that travel down the common bile duct and which subsequently get stuck in the Ampulla of Vater can cause obstruction in the outflow of pancreatic juices from the pancreas into the duodenum. The backflow of these digestive juices causes lysis (dissolving) of pancreatic cells and subsequent pancreatitis.
E – ethanol (alcohol)
T – trauma
S – steroids
M – mumps (paramyxovirus) and other viruses (Epstein-Barr virus, Cytomegalovirus)
A – autoimmune disease (Polyarteritis nodosa, Systemic lupus erythematosus)
S – scorpion sting (e.g. Tityus trinitatis), and also snake bites
H – hypercalcemia, hyperlipidemia/hypertriglyceridemia and hypothermia
E – ERCP (Endoscopic Retrograde Cholangio-Pancreatography – a procedure that combines endoscopy and fluoroscopy)
D – drugs (SAND – steroids & sulfonamides, azathioprine, NSAIDS, diuretics such as furosemide and thiazides, & didanosine) and duodenal ulcers. As an example, the U.S. Food and Drug Administration (FDA) reported in August 2008 six cases of hemorrhagic or necrotizing pancreatitis in patients taking Byetta, a diabetes medicine approved in 2005. Two patients died. The FDA previously reported 30 other cases of pancreatitis. Patients taking Byetta should promptly seek medical care if they experience unexplained severe abdominal pain with or without nausea and vomiting.[3]
This mnemonic is also roughly arranged according to the frequency of its causes. Thus: Gallstone pancreatitis is more common than pancreatitis caused by alcohol, trauma, or steroids.
[edit]Less common causes
pancreas divisum
long common duct
carcinoma of the head of pancreas, and other cancer
ascaris blocking pancreatic outflow
chinese liver fluke
ischemia from bypass surgery
fatty necrosis
infections other than mumps, including varicella zoster
repeated marathon running.
cystic fibrosis
valproic acid
Anorexia or bulimia
Codeine reaction[4][5]
[edit]Causes by demographic
The most common causes of pancreatitis, are as follows :
Western countries – chronic alcoholism and gallstones accounting for more than 85% of all cases
Eastern countries – gallstones
Children – trauma
Adolescents and young adults – mumps
Pancreatitis pathogenisis
The exocrine pancreas produces a variety of enzymes, such as proteases, lipases, and saccharidases. These enzymes contribute to food digestion by breaking down food tissues. In acute pancreatitis, the worst offender among these enzymes may well be the protease trypsinogen which converts to the active trypsin. Trypsin is most responsible for auto-digestion of the pancreas which in turn causes the pain and complications of pancreatitis.
The acute pancreatitis (acute hemorrhagic pancreatic necrosis) is characterized by acute inflammation and necrosis of pancreas parenchyma, focal enzymic necrosis of pancreatic fat and vessel necrosis – hemorrhage. These are produced by intrapancreatic activation of pancreatic enzymes. Lipase activation produces the necrosis of fat tissue in pancreatic interstitium and peripancreatic spaces. Necrotic fat cells appear as shadows, contours of cells, lacking the nucleus, pink, finely granular cytoplasm. It is possible to find calcium precipitates (hematoxylinophilic). Digestion of vascular walls results in thrombosis and hemorrhage. Inflammatory infiltrate is rich in neutrophils.
pancreatitis Eval
Blood Investigations – Full blood count, Renal function tests, Liver Function, serum calcium, serum amylase and lipase, Arterial blood gas, Trypsin-Selective Test
Imaging – Chest Xray (for exclusion of perforated viscus), Abdominal Xrays (for detection of “sentinel loop” dilated duodenum sign, and gallstones which are radioopaque in 10%) and CT abdomen
[edit]Amylase and lipase, serum calcium, glycosuria
Elevated serum AMYLASE and LIPASE levels, in combination with severe abdominal pain, often trigger the initial diagnosis of acute pancreatitis.
Serum lipase rises 4 to 8 hours from the onset of symptoms and normalizes within 7 to 14 days after treatment.-Serum amylase may be normal (in 10% of cases) for cases of acute or chronic pancreatitis (depleted acinar cell mass) and hypertriglyceridemia.
Reasons for false positive elevated serum amylase include salivary gland disease (elevated salivary amylase) and macroamylasemia.
If the lipase level is about 2.5 to 3 times that of amylase, it is an indication of pancreatitis due to alcohol.–DECREASED serum Calcium
Glycosuria-Regarding selection on these tests, two practice guidelines state:
“It is usually not necessary to measure both serum amylase and lipase. Serum lipase may be preferable because it remains normal in some nonpancreatic conditions that increase serum amylase including macroamylasemia, parotitis, and some carcinomas. In general, serum lipase is thought to be more sensitive and specific than serum amylase in the diagnosis of acute pancreatitis”
“Although amylase is widely available and provides acceptable accuracy of diagnosis, where lipase is available it is preferred for the diagnosis of acute pancreatitis (recommendation grade A)”[8]
Most (PMID 15943725, PMID 11552931, PMID 2580467, PMID 2466075, PMID 9436862), but not all (PMID 11156345, PMID 8945483) individual studies support the superiority of the lipase. In one large study, there were no patients with pancreatitis who had an elevated amylase with a normal lipase.[9] Another study found that the amylase could add diagnostic value to the lipase, but only if the results of the two tests were combined with a discriminant function equation.[10]
[edit]Computed tomography
Regarding the need for computed tomography, practice guidelines state:
2006: “Many patients with acute pancreatitis do not require a CT scan at admission or at any time during the hospitalization. For example,a CT scan is usually not essential in patients with recurrent mild pancreatitis caused by alcohol. A reasonable indication for a CT scan at admission (but not necessarily a CT with IV contrast) is to distinguish acute pancreatitis from another serious intra-abdominal condition, such as a perforated ulcer.”
2005: “Patients with persisting organ failure, signs of sepsis, or deterioration in clinical status 6-10 days after admission will require CT (recommendation grade B).”[8]
CT abdomen should not be performed before the 1st 48 hours of onset of symptoms as early CT (<48 h) may result in equivocal or normal findings.
CT Findings can be classified into the following categories for easy recall :
Intrapancreatic – diffuse or segmental enlargement, edema, gas bubbles, pancreatic pseudocysts and phlegmons/abscesses (which present 4 to 6 wks after initial onset)
Peripancreatic / extrapancreatic – irregular pancreatic outline, obliterated peripancreatic fat, retroperitoneal edema, fluid in the lessar sac, fluid in the left anterior pararenal space
Locoregional – Gerota’s fascia sign (thickening of inflamed Gerota’s fascia, which becomes visible), pancreatic ascites, pleural effusion (seen on basal cuts of the pleural cavity), adynamic ileus, etc.
[edit]Magnetic resonance imaging
While computed tomography is considered the gold standard in diagnostic imaging for acute pancreatitis,[11] magnetic resonance imaging (MRI) has become increasingly valuable as a tool for the visualization of the pancreas, particularly of pancreatic fluid collections and necrotized debris.[12] Additional utility of MRI includes its indication for imaging of patients with an allergy to CT’s contrast material, and an overall greater sensitivity to hemorrhage, vascular complications, pseudoaneurysms, and venous thrombosis.[13]
Another advantage of MRI is its utilization of magnetic resonance cholangiopancreatography (MRCP) sequences. MRCP provides useful information regarding the etiology of acute pancreatitis, i.e., the presence of tiny biliary stones (choledocholithiasis or cholelithiasis) and duct anomalies.[12] Clinical trials indicate that MRCP can be as effective a diagnostic tool for acute pancreatitis with biliary etiology as endoscopic retrograde cholangiopancreatography, but with the benefits of being less invasive and causing fewer complications.
[edit]Endoscopic ultrasound
pancreatitis progression/pathophys
Progression of pathophysiology
Acute pancreatitis patients recover in maximum cases Some may develop abscess, pseudocyst or duodenal obstruction. In 5 percent cases, it may result in ARDS(acute respiratory distress syndrome), DIC(disseminated intravascular coagulation), etc Acute pancreatitis can be further divided into mild and severe pancreatitis. Mostly the Atlanta classification (1992) is used. In severe pancreatitis serious amount of necrosis determine the further clinical outcome. About 20% of the acute pancreatitis are severe with a mortality of about 20%. This is an important classification as severe pancreatitis will need intensive care therapy whereas mild pancreatitis can be treated on the common ward.
Necrosis will be followed by a systemic inflammatory response syndrome (SIRS) and will determine the immediate clinical course. The further clinical course is then determined by bacterial infection. SIRS is the cause of bacterial (Gram negative) translocation from the patients colon.
There are several ways to help distinguish between these two forms. One is the above mentioned Ranson Score.
Pancreatitis Prognosis
In predicting the prognosis, there are several scoring indices that have been used as predictors of survival. Two such scoring systems are the Ranson criteria and APACHE II (Acute Physiology and Chronic Health Evaluation) indices. Most,[16][17] but not all [18] studies report that the Apache score may be more accurate. In the negative study of the Apache II,[18] the Apache II 24 hr score was used rather than the 48 hour score. In addition, all patients in the study received an ultrasound twice which may have influenced allocation of co-interventions. Regardless, only the Apache II can be fully calculated upon admission. As the Apache II is more cumbersome to calculate, presumably patients whose only laboratory abnormality is an elevated lipase or amylase do not need prognostication with the Apache II; however, this approach is not studied. The Apache II score can be calculated at
Practice guidelines state:
2006: “The two tests that are most helpful at admission in distinguishing mild from severe acute pancreatitis are APACHE-II score and serum hematocrit. It is recommended that APACHE-II scores be generated during the first 3 days of hospitalization and thereafter as needed to help in this distinction. It is also recommended that serum hematocrit be obtained at admission, 12 h after admission, and 24 h after admission to help gauge adequacy of fluid resuscitation.”[7]
2005: “Immediate assessment should include clinical evaluation, particularly of any cardiovascular, respiratory, and renal compromise, body mass index, chest x ray, and APACHE II score”
Ranson criteria is a clinical prediction rule for predicting the severity of acute pancreatitis. It was introduced in 1974.
-At admission: age in years > 55 years, wbc > 16000 cells/mm3, blood glucose > 10 mmol/L (> 200 mg/dL)
serum AST > 250 IU/L, serum LDH > 350 IU/L
-At 48 hours:serum calcium < 2.0 mmol/L (< 8.0 mg/dL), Hematocrit fall > 10%, Oxygen (hypoxemia PO2 < 60 mmHg), BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration -negative base excess > 4 mEq/L, Sequestration of fluids > 6 L
-The criteria for point assignment is that a certain breakpoint be met at anytime during that 48 hour period, so that in some situations it can be calculated shortly after admission. It is applicable to both gallstone and alcoholic pancreatitis.
Alternatively, pancreatitis can be diagnosed by meeting any of the following:[2]
[edit]Ranson’s score
Ranson’s score of ≥ 8 Organ failure Substantial pancreatic necrosis (at least 30% glandular necrosis according to contrast-enhanced CT)
Interpretation If the score ≥ 3, severe pancreatitis likely. If the score < 3, severe pancreatitis is unlikely Or, Score 0 to 2 : 2% mortality Score 3 to 4 : 15% mortality Score 5 to 6 : 40% mortality Score 7 to 8 : 100% mortality
Mnemonic for memorizing Ranson’s criteria At admission: “GA LAW” (glucose, age, LDH, AST, WBC count) At 48 hours: “C Hobbs” (i.e. Calvin and Hobbes): (calcium, hematocrit, O2, BUN, Base deficit, sequestration (of fluid) greater than 6 L (see: fluid balance)
APACHE: Main article: APACHE II
“Acute Physiology And Chronic Health Evaluation” (APACHE II) score > 8 points predicts 11% to 18% mortality Online calculator
Hemorrhagic peritoneal fluid
Indicators of organ failure
Hypotension (SBP <90 mmHG) or tachycardia > 130 beat/min
PO2 <60 mmHg
Oliguria (<50 mL/h) or increasing BUN and creatinine
Serum calcium < 1.90 mmol/L (<8.0 mg/dL) or serum albumin <33 g/L (<3.2.g/dL)>
Balthazar & necrosis scores
Computed Tomography Severity Index (CTSI) is a grading system used to determine the severity of acute pancreatitis. The numerical CTSI has a maximum of ten points, and is the sum of the Balthazar grade points and pancreatic necrosis grade points:
Balthazar Grade
A=Normal CT= 0pts
B=focal or diffuse enlargement of the pancreas = 1pt
C=Pancreatic gland abnormalities and peripancreatic inflammation. = 2pts
D=Fluid collection in a single location = 3pts
E= 2or more fluid collections and / or gas bubbles in or adjacent to pancreas = 4pts
no necrosis=0pts
0-30% necrosis = 2pts.
30-50% necrosis= 4 pts
>50% necrosis = 6pts
-CTSI’s staging of acute pancreatitis severity has been shown by a number of studies to provide more accurate assessment than APACHE II, Ranson, and C-reactive protein (CRP) level.[20][21][22][23] However, a few studies indicate that CTSI is not significantly associated with the prognosis of hospitalization in patients with pancreatic necrosis, nor is it an accurate predictor of AP severity
pancreatitis TX
Pain control
Originally it was thought that analgesia should not be provided by morphine because it may cause spasm of the sphincter of Oddi and worsen the pain, so the drug of choice was meperidine. However, due to lack of efficacy and risk of toxicity of meperidine, more recent studies have found morphine the analgesic of choice.[citation needed] Meperidine may still be used by some practitioners in more minor cases, or where morphine is contraindicated.
[edit]Bowel rest
In the management of acute pancreatitis, the treatment is to stop feeding the patient, giving him or her nothing by mouth, giving intravenous fluids to prevent dehydration, and sufficient pain control. As the pancreas is stimulated to secrete enzymes by the presence of food in the stomach, having no food pass through the system allows the pancreas to rest. Approximately 20% of patients have a relapse of pain during acute pancreatitis.[26] Approximately 75% of relapses occur within 48 hours of oral refeeding.
The incidence of relapse after oral refeeding may be reduced by post-pyloric enteral rather than parenteral feeding prior to oral refeeding.[26] IMRIE scoring is also useful.
[edit]Nutritional support
Recently, there has been a shift in the management paradigm from TPN (total parenteral nutrition) to early, post-pyloric enteral feeding (in which a feeding tube is endoscopically or radiographically introduced to the third portion of the duodenum). The advantage of enteral feeding is that it is more physiological, prevents gut mucosal atrophy, and is free from the side effects of TPN (such as fungemia). The additional advantages of post-pyloric feeding are the inverse relationship of pancreatic exocrine secretions and distance of nutrient delivery from the pylorus, as well as reduced risk of aspiration.
Disadvantages of a naso-enteric feeding tube include increased risk of sinusitis (especially if the tube remains in place greater than two weeks) and a still-present risk of accidentally intubating the trachea even in intubated patients (contrary to popular belief, the endotracheal tube cuff alone is not always sufficient to prevent NG tube entry into the trachea).
A meta-analysis by the Cochrane Collaboration concluded that antibiotics help with a number needed to treat of 11 patients to reduce mortality.[27] However, the one study in the meta-analysis that used a quinolone, and a subsequent randomized controlled trial that studied ciprofloxacin were both negative.[28]
An early randomized controlled trial of imipenem 0.5 gram intravenously every eight hours for two weeks showed a reduction in from pancreatic sepsis from 30% to 12%.[29]
Another randomized controlled trial with patients who had at least 50% pancreatic necrosis found a benefit from imipenem compared to pefloxacin with a reduction in infected necrosis from 34% to 20%[30]
A subsequent randomized controlled trial that used meropenem 1 gram intravenously every 8 hours for 7 to 21 days stated no benefit; however, 28% of patients in the group subsequently required open antibiotic treatment vs. 46% in the placebo group. In addition, the control group had only 18% incidence of peripancreatic infections and less biliary pancreatitis that the treatment group (44% versus 24%).[31]
In summary, the role of antibiotics is controversial. One recent expert opinion (prior to the last negative trial of meropenem[31]) suggested the use of imipenem if CT scan showed more than 30% necrosis of the pancreas.[32]
Early ERCP (endoscopic retrograde cholangiopancreatography), performed within 24 to 72 hours of presentation, is known to reduce morbidity and mortality.[33] The indications for early ERCP are as follows :
Clinical deterioration or lack of improvement after 24 hours
Detection of common bile duct stones or dilated intrahepatic or extrahepatic ducts on CT abdomen
The disadvantages of ERCP are as follows :
ERCP precipitates pancreatitis, and can introduce infection to sterile pancreatitis
The inherent risks of ERCP i.e. bleeding
It is worth noting that ERCP itself can be a cause of pancreatitis.
Surgery is indicated for (i) infected pancreatic necrosis and (ii) diagnostic uncertainty and (iii) complications. The most common cause of death in acute pancreatitis is secondary infection. Infection is diagnosed based on 2 criteria
Gas bubbles on CT scan (present in 20 to 50% of infected necrosis)
Positive bacterial culture on FNA (fine needle aspiration, usually CT or US guided) of the pancreas.
Surgical options for infected necrosis include:
Minimally invasive management – necrosectomy through small incision in skin (left flank) or stomach
Conventional management – necrosectomy with simple drainage
Closed management – necrosectomy with closed continuous postoperative lavage
Open management – necrosectomy with planned staged reoperations at definite intervals (up to 20+ reoperations in some cases)
[edit]Other measures
Pancreatic enzyme inhibitors are not proven to work.[34]
The use of octreotide has not been shown to improve outcome.
pancreatitis compications
Complications can be systemic or locoregional.
Systemic complications include ARDS, multiple organ dysfunction syndrome, DIC, hypocalcemia (from fat saponification), hyperglycemia and insulin dependent diabetes mellitus (from pancreatic insulin producing beta cell damage)
Locoregional complications include pancreatic pseudocyst and phlegmon / abscess formation, splenic artery pseudoaneurysms, hemorrhage from erosions into splenic artery and vein, thrombosis of the splenic vein, superior mesenteric vein and portal veins (in descending order of frequency), duodenal obstruction, common bile duct obstruction, progression to chronic pancreatitis
Pancreatitic ducts
The pancreatic duct, or duct of Wirsung (also, the Major pancreatic duct due to the existence of an accessory pancreatic duct), is a duct joining the pancreas to the common bile duct to supply pancreatic juices which aid in digestion provided by the “exocrine pancreas”. The pancreatic duct joins the common bile duct just prior to the ampulla of Vater, after which both ducts perforate the medial side of the second portion of the duodenum at the major duodenal papilla.
-Most people have just one pancreatic duct. However, some have an additional accessory pancreatic duct, called the Duct of Santorini.
-Compression, obstruction or inflammation of the pancreatic duct may lead to acute pancreatitis. The most common cause for obstruction is choledocholithiasis, or gallstones in the common bile duct. Obstruction can also be due to Duodenal Inflammation in Crohn’s Disease [1]. A gallstone may get lodged in the constricted distal end of the ampulla of Vater, where it blocks the flow of both bile and pancreatic juice into the duodenum. Bile backing up into the pancreatic duct may initiate pancreatitis.[2]
Pancreatic ductal carcinoma is a common form of pancreatic cancer.
-Accessory panc duct: Most people have just one pancreatic duct. However, some have an additional accessory pancreatic duct also called the Duct of Santorini, which connects straight to the duodenum at the minor duodenal papilla. Both these ducts connect to the second part (the vertical one) of the duodenum.
However, the Duct of Santorini, which bypasses the Ampulla of Vater, is non-functional whereas the Duct of Wirsung is functional and carries the digestive enzymes released by the pancreas.
In some cases, the main pancreatic duct is smaller than the accessory pancreatic duct and the two may not be connected. In such people, the accessory duct carries most of the pancreatic juice.
Pancreatic divisum
Pancreas or Pancreatic divisum is a congenital anomaly in the anatomy of the ducts of the pancreas in which a single pancreatic duct is not formed, but rather remains as two distinct dorsal and ventral ducts.
-human embryo begins life with two ducts in the pancreas, these are the ventral duct and the dorsal duct. Normally, the two ducts will fuse together to form one main pancreatic duct; this occurs in more than 90% of embryos. In approximately 10% of embryos the ventral and dorsal ducts fail to fuse together, resulting in pancreas divisum. In utero, the majority of the pancreas is drained by the dorsal duct which opens up into the minor papilla. The ventral duct drains the minority of the pancreas and opens into the major papilla. In adults however, this situation is reversed whereby 70% of the pancreas is drained by the ventral duct. Therefore in pancreas divisum, where fusion of the ducts does not occur, the major drainage of the pancreas is done by the dorsal duct which opens up into the minor papilla.
– Sx, TX, DX:A majority of individuals born with pancreas divisum will never have symptoms for their entire life. In most cases, pancreas divisum is only detected during an autopsy of a person that is deceased. However, approximately 1% of those with pancreas divisum will develop symptoms during their lifetime[citation needed]. Symptoms commonly include abdominal pain, nausea and/or vomiting, and pancreatitis. A small number of individuals may develop chronic pancreatitis.
Diagnosis: MRCP image of pancreas divisum.
The most common and accurate way of diagnosing an individual with this anomaly is by an ERCP. This test can demonstrate the presence of two separately draining ducts within the pancreas. Other tests can assist doctors with diagnosis, such as a CT scan and an MRI.
Treatment: Pancreas divisum in individuals with no symptoms does not require treatment. Treatment of those with symptoms varies and has not been well established. A surgeon may attempt a sphincterotomy by cutting the minor papilla to enlarge the opening and allow pancreatic enzymes to flow normally. During surgery, a stent may be inserted into the duct to ensure that the duct will not close causing a blockage. This surgery can cause pancreatitis in patients, or in rare cases, kidney failure and death.
An association with adenoma of the minor papilla has been reported.
Courvoisier’s sign
severe jaundice with a palpable, nontender gallbladder, indicating obstruction of biliary passages from something other than a gallstone, possibly a tumor.
pathophysiology1) development of solid tumor originating from ductal system 2) metastases are most common to liver and regional lymph nodes
Signs and Symptoms
1) abdominal pain (gnawing or burning nature typically) 2) jaundice 3) enlarged, palpable gallbladder in 40% of patients (Courvoisier’s sign) 4) light-colored stools 5) dark urine 6) pruritus 7) weight loss 8) splenomegaly 9) venous thrombosis 10) migratory thrombophlebitis (Trousseau’s sign)
Breast risks
Identify and recognize major risk factors for breast cancer (CA):
o Age, genetic mutations, ≥2 1° relatives, past Hx, high breast tissue density, biopsy confirmed atypical hyperplasia
dentify and recognize the complete list of breast cancer risk factors
o Age, ETOH consumption, birth control pills, genetic (BRCA genes), early menarche, FHx breast/ovarian CA, HRT, late first-term preg, late menopause, LCIS, multiple previous biopsies, no term preg, PMHx of breast CA, atypical hyperplasia biopsy, race, radiation exposure, sex, weight
Mammo guidelines & screening
ACA (also table 20-3 in book)
• Every year ≥40 y.o.
• Every 1-2 years age 40-49; Every year there after
• Biennial between 50-74 years
-Identify and recognize the recommendations for Breast cancer Detection/Screening American cancer in asymptomatic women per the American Cancer Society (ACS). (Book) I have checked table 20-3 and it represents the current recommendation set forth by the ACS.20-39yrs: CBE: q 3 years BSE:Monthly (optional). MAMMO: N/A
>40yrs: CBE: Yearly. BSE: monthly optional. MAMMO: yearly

lymph drainage order

Identify and recognize the “basics” as it relates to the order of lymphatic drainage of the breast and how this in turn relates to a sentinel lymph node biopsy:

-75% of drainage occurs into the axillary nodes (rest to internal mammary nodes)
• Central, lateral, subscapular, pectoral
• Central modes are the most commonly palpable nodes
• Any node >1cm is concerning (drains low to high)

mammo masses
o Benign= Round or oval smooth masses; lrg round calcifications
o Malignant= Masses that have irregular or spiculated margins; linear/branching microcalcifications
Ultrasound in evaluating breast masses

Strengths: Characterize palpable lesions or suspicious areas found physically or on mammography, especially in <30. Easily distinguish solid from cyst & simple from complex cysts.

Weaknesses: Operator/equipment dependent. Hard to assess whether whole breast was imaged

• Usually late teens – early 30’s
• Palpated freely movable/discrete/firm/rounded mass; typically 1-3 cm
• Fine-needle aspiration or core biopsy
• Fibrous stromal tissue & tissue clefts lined with normal epithelium
• Observation preferred to excision
Breast Cyst
Solitary or multiple firm/mobile/slightly tender masses
• Less well defined borders than Fibroadenoma
• Mammography or US
• Aspiration of large cysts
• Fluid will be straw-colored or greenish (cytology not necessary)
• Identify and recognize the most common cause of breast mass of women in their 4th and 5th decade
Nipple discharge
Identify and recognize the most common cause of nipple discharge
• Duct ectasia
• Discharge may be clear, milky, or green-brown
• Apply to occult blood test paper
• Identify and recognize nipple discharge that is considered to be pathologic
• Spontaneous discharge from a single duct w/ bloody discharge
• 10-15% malignant in unilateral/bloody discharge
• Mammography for diagnostic work up
Breast Cancer
Lobular carcinoma in situ (LCIS):Pre-cancer, all cells contained w/in basement membrane.
•Does not metastasize
•More broad spectrum/global
•Greater risk for invasive CA development
Ductal carcinoma in situ (DCIS):
•Pre-cancer, found in the duct, usually at the same spot
Infiltrating ductal carcinoma:
•90% of invasive CA; firm irregular mass; better defined on mammography
Infiltrating lobular carcinoma:
•10% of invasive CA; difficult to detect w/ mammography
•Characterized by multi-centricity & presence in contralateral breast; indistinct borders.
Inflammatory carcinoma: (Associated skin findings)
•Skin edema (peau d’orange); erythema
•2° to dermal lympatics congested w/ malignant cells generally of ductal origin. (Poor prognosis)
breast cancer staging guide
Primary tumor (T):
•Tis – carcinoma in situ
•T1 – ≤ 2cm
•T2 – >2, ≤5 cm
•T3 – >5 cm
•T4 – tumor of any size w/ extension to chest wall or skin
Regional lymph nodes (N):
•N0 – no lymph node metastasis
•N1 – 1-3 axillary lymph nodes
•N2 – 4-9 axillary lymph nodes
•N3 – ≥10 axillary lymph nodes
Distant metastasis (M):
•M0 – no distant metastasis
•M1 – distant metastasis
Breast cancer stages
Stage 0: Tis N0 M0
Stage 1: T1 N0 M0
Stage IIA: T0 T1 T2
T1 N1 N0
Stage IIB: T2 N1 MD
Stage IIIA: T0 N2 MD
T1 N2 MD
T2 N2 MD
T3 N1 MD
T3 N2 MD
Stage IIIB: T4 N0 MD
T4 N1 MD
T4 N2 MD
Stage IIIC: AnyT-N3-M0
Stage IV: Any T Any N M1
Paget’s disease of the nipple.
o Cutaneous nipple abnormality, which may be moist & exudative, dry & scaly, erosive, or just a thickened area.
Itching, burning, sticking pain in the nipple
breast cancer 5-year survival rates for TX based on stage of cancer
Stage 1= 96%
Stage 2= 82%
Stage 3= 53%
Stage 4= 18%
Axillary lymph node dissection complications
o Lymphedema & decreased ROM in the shoulder
o If injury to the long thoracic or thoracodorsal nerve
• “Winged scapula” & latissimus dorsi paralysis
o Loss of sensation to the skin of the upper arm
***Calculate Fluid Maintenance: [Lecture]
• (0-10 kg= 4cc/kg/hr) +
• (11-20kg=2cc/kg/hr) +
• (>20kg=1cc/kg/hr
-asymptomatic diverticula=80% asymptomatic
-Identify and recognize the most common location of acquired/ false diverticula: 1) Sigmoid colon=95%.
-Define Diverticulosis:Presence of multiple false diverticula in the colon.
-Define Diverticulitis: Limited infection of 1+ diverticula (may extend into adjacent tissue)
clinical manifestation and treatment of Diverticulitis:
•LLQ pain, alteration of bowel habits (diarrhea), occasionally a palpable mass & fever
•Sx directed Tx •Admission, IV hydration, NPO, IV Abx for 5-7d
Diverticulosis:•Recurrent Abd pain (LLQ), change in bowel habits (bleeding/ constipation/diarrhea), ? mild tenderness LLQ•Increase fiber intake•Any other management is controversial
-Indications for surgery of diverticular disease: Perforation, obstruction, intractability, bleeding, fistula
colonic polyps
Tubular•Common (10% of adults); 7% malignancy
Villous•Fairy common in elderly; 33% malignancy
Inflammatory•Uncommon, except in IBD; no malignancy potential
Duke’s classification
o Staging for lrg bowel CA
o A (confined) – D (distant metastases)
colon cancer risks
disease and hereditary/genetic conditions that predispose one to colon cancer.
oDisease•Ulcerative colitis, Crohn’s, lymphogranuloma venerum, certain polyps
oGenetic•Familial polyposis syndrome, Gardner’s syndrome, cancer family syndrome (HNPCC)
UC Vs. Crohns
oUlcerative colitis•Severe bloody diarrhea, freq megacolon, rectum involvement
oCrohn’s disease•Less severe diarrhea w/ infrequent bleeding, perianal fistulas, strictures & obstructions common, perforations, ileum diseased in most pt’s
large intestine obstruction
the most common site for Large intestine obstruction. -Sigmoid colon
o 3 most common causes
•Scarring associated w/ diverticulitis
Hemrrhoids/peri-anal abcesss/ anal fissure
Identify and recognize the clinical manifestation of:
oHemorrhoids (328) (know a grading system exists)
•Painless bleeding (bright red & coats stool), blood vessel protrusion
•Graded as 1-4 depending on level of protrusion
Peri-anal abcess (330)
•Perianal pain & swelling, pus drainage, fever, redness, loss of function
Anal fissure (331)
•Pain w/ defecation (mins-hours), minimal bleeding, gentle retraction of buttocks will reveal a tear at the anal verge
cholelithiasis/gallbladders common tyoes
most common types of gallstones (cholelithiasis) in the U.S (337)
o Cholesterol
common bile duct
define Choledocholithiasis (common bile duct)
oGallstone out of BG & into the common bile duct
epigastric RUQ pain,
=Describe biliary colic
oEpigastric/RUQ visceral pain that usually radiates to the back at the same level
oUsually steady & severe, may last 1-4 hours
acute cholecystitis (cystic duct):manage
Identify and recognize the signs and symptoms and management of acute cholecystitis (cystic duct):
o Associated w/ bacteria
o Fever present (>101°F
o N/V, pain (biliary colic), dyspepsia
•Pts often doubled up in pain
o Abd soft, bowel sounds present, + Murphy’s sign
•Pain on inspiration with pressure in RUQ & up under ribs
o—US or HIDA scan
oAnalgesic, lithotripsy, Abx
oCholecystectomy indicated
•W/in 3 days
Charots triad and Reynolds pentab
➢ Identify and recognize the clinical manifestation of acute cholangitis.
o Charcot’s triad
• Jaundice, RUQ pain, fever w/ chills
o Reynolds Pentad (acute suppurative cholangitis)
• Triad + hypotension & mental confusion
Imaging of choice for suspected biliary tract disease?
-• Sensitivity & specificity = 95%
gallstone risks
Identify and recognize factors that predispose one to gallstone formation. (338)
oGenetics & environment
•Age, race, obesity, gender, multiparity, high-dose estrogen oral contraceptives, some cholesterol lowering agents, rapid weight loss, prolonged TPN
dentify and recognize when ERCP is utilized. (351)
oTo clear common bile duct stones
pancreatic duct and papilla
PANCREAS-Identify and recognize the main pancreatic duct and papilla. (Names)
oAmpulla of Vater, & Santorini duct (main duct)
pancreatic divisium characteristics
Identify and recognize the characteristic s of pancreas divisum, its prevalence and its clinical significance.
oWhen the common bile duct & main pancreatic do not fuse during fetal development (ventral & dorsal ducts)
oCreates separate entrances into the duodenum
oIdiopathic recurrent pancreatitis
etiology, clinical manifestation, DX, work up & TX Acute pancreatitis: •Usually associated w/ ETOH abuse
•60% of non-EOTH abusers w/ pancreatitis have gallstone obstruction•Non-cramping epigastric pain
•Often radiates to LUQ/RUQ/ or back
•Usually relieved sitting or standing •Fever, tachycardia, upper abdominal tenderness w/ guarding, BS usually absent
DX/Labs: •Leukocytosis, elevated serum amylase & lipase o Lipase better single test than amylase
•NPO until pain/tenderness has subsided, monitor fluid level, electrolytes & resp rate. May req IV isotonic fluids & O2
•Surgery not usually indicated, but removal of obstruction may be necessary
Pancreatic Pseudocysts–
Pancreatic Pseudocysts
• A collection of peripancreatic fluid in a cyst-like structure that has no epithelial lining
• Epigastric pain, N/V, early satiety
• Clinical presentation
• Pain for >1 week after episode of pancreatitis, palpable abdominal mass, persistent elevation of lipase & amylase
• US &/or CT
• Maintain TPN & avoiding oral intake that would stimulate pancreatic activity
• Usually resolve on their own
• Drainage if sudden onset of fever occurs or symptoms do not resolve w/in 4-6 weeks
Cullen,Grey turner, Courvoirsier’s, ransons
➢Define Cullen’s sign=Periumbilical ecchymosis
➢Define Grey Turner’s sign=Flank hematoma
➢Define Courvoirsier’s sign=A palpable NT GB in a jaundiced pt•Commonly associated w/ malignancy
➢Identify and recognize the components of the Ranson’s criteria (at admission):3+ criteria at admission •Age >55•WBC >16,000•Glucose >200mg/100mL•LDH >350•AST >250
–ID& recognize the most common complication of pancreatitis:PSEUDOCYSTS-oParalytic ileus o Sterile peripancreatic fluid collections
Thyroid nodule work-up
➢Identify and recognize the work up and management of a Thyroid nodule (Fig. 21-5)
oPalpable nodule > neck ultrasound > fine needle aspiration
oIf benign…Synthroid for 6 months and re-assess
•Still residual nodule…re-aspirate
oIf malignant or indeterminate…surgical resection
Thyroid Fine needle aspiration
Importance of fine needle aspiration
• Extremely accurate & is considered the single most important study in eval of thyroid mass
• Only 3% w/ benign diagnoses have thyroid CA
• 85% ID’d as malignant are CA at resection
papillary carcinoma
o MC thyroid malignancy
o Concentric layers of calcium found in the stalk formations
o Grow slowly, good prognosis
o Lobectomy/isthmectomy or
o Total thyroidectomy w/ radioiodine ablation
thyroid CA-3 most common
o Papillary > Follicular > Medullary
hyperparathyroidism-ca lab findings
➢Identify and recognize the clinical presentation and lab findings (calcium) in primary hyperparathyroidism.
o “Stones, bones, groans, moans, & psych overtones”
• Stones = urolithiasis
• Bones = bone resorption cyst or brown tumor formation
• Groans = diffuse joint/muscle pain, fatigue, lethargy
• Moans = abdominal pain from peptic ulcers & pancreatitis
• Psych overtones = depression or worsening psychosis
o Hypercalcemia (confirmed w/ 2nd test)
MEN- classifications
o Autosomal dominant familial endocrine tumor syndromes
o MEN-1
• Combines parathyroid hyperplasia w/ other endocrine neoplasms
• Usually pancreatic islet cells or anterior pituitary tumors
o MEN-2
• Occurs with medullary thyroid CA, pheochromocytoma & 1° hyperparathyroidism
o MEN-2B
• Occurs with medullary thyroid CA, pheochromocytoma & a characteristic phenotype (replaces hyperparathyroidism)
• Phenotype presents as: Marfanoid habitus, prognathism, puffy lips, bumpy tongue, hyperflexible joints, corneal nerve hypertrophy (seen w/ slit lamp)
transplant rejection: signs SX manage heart lung kidney
➢Identify and recognize the acute signs, symptoms and management of transplant rejection
Heart•Fever, abdominal pain, new arrhythmia (, syncope (or near syncope), worsening CHF
•IV diuretic, broad spectrum Abx, IV steroids if directed by transplant center, arrange for immediate transportation to tertiary care institution
Lung:•Dyspnea, wheezing, strider, deteriorating PFT’s, post-obstructive PNA
•IV steroids & transfer to tertiary hospital w/ staff skilled at handling difficult airways
Kidney:•Decreased urine output, increased BP, pyuria, worsening proteinuria
• Expedited renal biopsy, IV steroids, Tx other co-existing Sx, & transfer to tertiary hospital
heart transplant rejection ECG
ECG findings of heart transplant rejection.
o Reduction in QRS voltage
transplant heart baseline rate
baseline resting heart rate in a transplanted heart.
o 100-110 bpm
valvar abnormalities heart transplant
➢Identify and recognize common valvular abnormalities in the transplanted heart.
oTricuspid is the MC due to repeated surveillance endomyocardial biopsies
vasoactive agents: heart transplant unresponsive to
vasoactive agents that a transplanted heart is unresponsive to.
o Atropine or direct sympathetic/parasympathetic stimuli
lung transplant: airway complication, delayed
➢Identify and recognize the most common site of delayed airway complications in a transplanted lung.
oBronchus-bronchus anastomosis
➢Identify and recognize the DELAYED airway anastomosis complications following a lung transplant.
oExcess granulation tissue
oBronchial stenosis
oFistula formation
➢Indentify and recognize the most common delayed complication following Lung transplantation and how these patients present
oBronchial stenosis
•Dyspnea, wheezing, strider, deteriorating PFT’s, post-obstructive PNA
acute renal allograft rejection: signs SX
Identify and recognize the signs and symptoms of acute renal allograft rejection.
oDecreased urine output, increased BP, pyuria, worsening proteinuria
All of the following are clues that a patient may be rejecting her transplanted heart except…
Low ECG voltage
Abdominal pain
Worsening angina
New arrhythmia
Worsening angina
Which cardiac valve is commonly incompetent in the transplanted heart?
Because the pericardium is not included with the transplanted heart, recipients will not develop cardiac tomponade. T or F?
True or False? The transplanted heart is responsive to direct sympathetic/parasympathetic stimuli, but unresponsive to administered vasoactive agents such as epinephrine.
The baseline resting heart rate is typically 100 to 110 in the transplanted heart. T or F?
transplant case 1
-You are working a clinical shift in
a small, rural ED.-You are presented with
an 67 yo man who has developed
increasing shortness of breath and
poorly described upper abdominal pain. -He also has documented a mild fever of 101°F earlier today.
HPI:He underwent a successful heart transplant
8 months earlier secondary to end stage
congestive cardiomyopathy. His post-transplantation course has been uneventful.He is visiting from “away” in order to attend his favorite niece’s high school graduation.-On close questioning, he describes….
PND for the previous weekA near syncopal episode yesterday No chest pain Concerns that he’ll miss
the graduation ceremony.
-Pertinent RX’s:= Cyclosporine, Prednisone,Furosemide
PE: VS: •T 38.5°C •BP 105/75 •P 105
•RR 22 •RA-O2 Sat 90%
Patient is anxious, but alert
Neck vein distention at 45 degrees
Persistent crackles at his lug bases
A tender liver edge
++++++worried about…..?????Do you have to be concerned about possible acute cardiac allograft rejection? YES!!!!
Although he remains quite stable, you are appropriately concerned about the possibility of acute allograft rejection, so you….
Administer additional parenteral furosemide
Initiate broad spectrum antibiotics after drawing blood cultures
Call the patient’s transplant center and, on their advice, administer IV steroids
Arrange immediate patient transfer to the nearest tertiary care institution
– No safe time, 1st 6 months these pts are close to home
Heart transplant
The only option for patients with end-stage heart disease…
other than long-term permanent mechanical assistance
Nearly 2,500 in the USA annually
The surgical approach hasn’t changed much…
but immunosuppressive therapy has, with much better outcomes
-Transplantation outcomes are impressive
1-year survival approached 85%
5-year survival >70%
>90% of patients have normal and unrestricted function
-Unrestricted = 90% of survivors of heart transplant
-The heart is denervated, so….
Unresponsive to direct sympathetic or parasympathetic stimuli
Responsive to endogenous circulating catecholamines
Responsive to administered vasoactive drugs
E.g. epinephrine, norepinephrine
But, atropine is ineffective
– Atropine does not work b/c the vagus nerve does not work. Lost vagal tone = baseline tachycardia. They won’t have angina, not heart pain will come in with heartfailure. V-tach suggests rejection.
-The heart is denervated, so….Baseline tachycardia is usual
Loss of vagal influence
100-110 BPM typical

Patients don’t experience angina
Even with occlusive disease


Post-transplant arrhythmias
Post-transplant arrhythmias
PAC’c and PVC’s common
Sinus node dysfunction common
May require a pacemaker
Atrial fib and flutter, if sustained, increases the risk of rejection
Sustained VT suggests…
Acute rejection
Advanced transplant atherosclerosis
—Piggyback heart, nbative and doner, has 2 rythms— 1 lead 2 hearts beating 2 p waves. Av node working but not conduction from the native heart. 2 complexes
Unique post-transplantation issues
Despite the absence of a pericardium, scarring and adhesions can result in tamponade
Portions of the native atria are retained, so the ECG can demonstrate two P-wave rhythms
With only one pacing the ventricles
“Piggy Back” transplants can produce challenging ECGs
-Advanced coronary disease, diffuse, have angina equivalents but NO ANGINA! Diastolic murmer
-Immunologic injury can lead to accelerated coronary artery disease
Diffuse, concentric and longitudinal
Multiple surveillance endomyocardial biopsies routine
Tricuspid valve regurgitation is common
Usually well tolerated
May require valve replacement
acute allograft rejection
Always think acute allograft rejection for patients with…
Worsening CHF*
Syncope and near syncope*
GI symptoms*
Secondary to hepatic congestion
Unexplained fever*
New arrhythmias
Reduction in QRS voltage*
heart trans: febrile, inflammation
Additional tasks
For febrile patients, full cultures and broad spectrum antibiotics
Always contact the LVAD center for recommendations re: immunosuppressive Rx
– Another thing to remember…
The inflammatory response to infection is impaired by immunosuppressive therapy
This diminishes symptoms, signs and test/radiological results
Infections are often advanced at the time of clinical presentation
-Wc rie doesn’t happen, muted inflammation have a low threshold for starting abx, broad spectrum call the transplant facility and give them some steroids too usually. Furosimide is a good abx.

When a delayed airway complication develops in a transplanted lung, it most often will involve the…

The trachea at the anastomosis
The right and/or left main bronchi
The bronchioles

The trachea at the anastomosis
All of the following are delayed complications at the transplanted lung bronchial anastomosis site except…
Excessive granulation tissue
Bronchial necrosis and dehiscence
Bronchial stenosis
Bronchial necrosis and dehiscence
tranplant case 2 lung
You are working a clinical shift in
a small, rural ED.
You are presented with
an 32 yo woman who has developed
slowly progressive shortness of breath and, more recently, strider with exertion.
During a coughing episode just prior to presentation, she experienced a prolonged episode of strider that frightened her.
-Stridor w/ exertion most concerning factor
HX:Pertinent Historical Facts
She underwent a successful bilateral lung transplant
12 months earlier secondary to end stage
alpha-1-antitrypsin deficiency syndrome.
Her post-transplantation course has been uneventful.
She is visiting from “away” in order to hike within the beautiful nearby national park.

On close questioning, she….
Feels well except for her chief complaint
Denies fever, pleurisy, hemoptysis, sputum production
Has had no chest pain
Is concerned that she’ll miss
her hiking friends at the top of Old Baldy
– RX: Cyclosporine
Albuterol MDI with spacer prn
-PE:VS: •T 37°C •BP 110/80 •P 80
•RR 16 •RA-O2 Sat 97%
– Just as you are about to leave the exam room, she has a single coughing episode with associated inspiratory strider.
She quickly recovers.
Her monitor indicators, including oxygen saturation measurements, remain normal.
Patient is calm & in no distress
Trachea is midline, non-tender
Lungs are clear
Heart sounds are normal
-You appropriately suspect this patient has an upper airway disorder related to her lung transplant.
-Although your patient remains totally stable
under your observation, you are appropriately concerned about the possibility of progressive bronchial stenosis, granulation tissue or tracheobronchomalacia
(it doesn’t matter to you which )You call the patient’s transplant center and, on their advice, administer IV steroids

You arrange urgent patient transfer to the nearest tertiary care institution with personnel who are skilled at handling difficult airway

LT facts
Most common conditions requiring lung transplant
Idiopathic pulmonary fibrosis
Cystic fibrosis
Alpha-1- antitrypsin deficiency
Idiopathic pulmonary hypertension
-Lung transplant outcomes…
5 year median survival
80% of survivors have no activity restrictions
40% of 5-year survivors are gainfully employed in some capacity
– During the lung transplant procedure…
The airway anastomosis is typically bronchus-to-bronchus
This anatomosis is the most vulnerable site for complications
This is due to tenuous blood supply, with revascularization taking up to 4 wks
-Airway anastomotic complications after lung transplant (in up to 33% of patients)
Focal infection ∆
Bronchial necrosis and dehiscence ∆
Excess granulation tissue Ω
Tracheobronchomalacia Ω
Bronchial stenosis Ω
Fistula formation Ω
-Acute complications (develop in the peri-operative period
-Won’t bronchoscope these people
Bronchial stenosis-LT

Most common delayed complication

Clinical presentation is progressive
Deteriorating PFTs
Post-obstructive pneumonia
-Stenosis = most common problem. Can do CT, really need bronchoscopy
-Diagnostic tests
CT scan
Flow-volume curves

Bronchoscopic balloon dilation
Laser or cryo-surgery
Endobronchial stent
Sleeve resection

Granulation tissue-LT
Symptomatic when the airway narrows by 25+%
Clinical presentation is progressive
Deteriorating PFTs
Post-obstructive pneumonia
-Diagnostic tests
CT scan
Flow-volume curves
Bronchoscopic debridement
Loss of cartilage integrity
Severe when the airway narrows by 75+% during expiration
Clinical presentation is progressive
Deteriorating PFTs
Post-obstructive pneumonia
-Diagnostic tests
Inspiratory/expiratory CT scan
Fiberoptic bronchoscopy
Flow-volume curves
Nocturnal noninvasive ventilation
Endoscopic stenting
LT comps

Other chronic LT complications include…

Bronchiolitis obliterans
50% incidence at 5-year survival

Bacterial, viral, fungal

Stay tuned

True or False

Fever, graft pain and graft tenderness are common signs of acute renal allograft rejection.


All of the following suggest acute renal allograft rejection except…

Decreased urine output
Increased blood pressure
Recurrent UTI’s
Worsening proteinuria

Recurrent UTI’s
case # trans
You are working a clinical shift in
a small, rural ED.You are presented with
a 28 yo man who complains of
general malaise, headache, and
decreased urine output .

He underwent a successful kidney transplant
2 years earlier secondary to severe and poorly controlled Type 1 diabetes mellitus and hypertension.

He reluctantly admits that he stopped his immunosuppressive drugs
(prednisone and cyclosporine)
2 months previously because
“I just want to get it over with”.

Cyclosporine (not taking)
Prednisone (not taking)
Furosemide (poorly compliant)
Diltiazem (poorly compliant)
Insulin (poorly compliant)
– PE:VS: •T 37°C •BP 190/110 •P 80
•RR 16 •RA-O2 Sat 95%

Patient appears depressed, but in no obvious distress
Lungs are clear
Heart sounds are normal
Abdomen soft and non-tender
-nWBC: 14,500
Hb / Hct: 12 / 36
BUN / Creatinine: 64 / 3.2
Blood Glucose: 255
Na: 132 K 4: Cl: 98 HCO3: 23
UA: 20 WBC/HPF 3+ Proteinuria

-You contact the patient’s PCP
(who practices in the bordering state)
and learn that 5 months previously the patient’s tests revealed…

BUN / Creatinine: 24 / 1.3

UA: 0 WBC/HPF Trace Proteinuria
You appropriately suspect this patient has acute renal allograft rejection. What are your management decisions?
-Your provide IV hydration,
insulin therapy to manage his hyperglycemia,
and parenteral ciprofloxacin
(after sending a urine culture).

You arrange immediate patient transfer
to his transplantation center
for emergent renal biopsy.

RF facts

Most patients experiencing renal allograft rejection are asymptomatic

Fever, graft pain, graft tenderness and graft swelling are uncommon

Clinical manifestations include…
Decreased urine output*
Increased blood pressure*
Worsening prote
-Noncompliance with the immunosuppressive therapeutic regimen is not an uncommon cause of renal allograft rejection

Due to…
Intolerable side effects
Financial constraints
Depression & hopelessness
-The treatment plans vary, depending on histological characteristics

Therefore, an expedited renal biopsy is recommended prior to therapy if at all possible

If the biopsy does indeed demonstrate acute rejection, pulsatile steroid injections are typically immediately initiated

Solid Organ Transplant Quiz

Chronic immunosuppressive therapy in patients with solid organ transplants increases the risk for secondary malignancy. Which of the following is most likely to develop?

Epithelial cancers
Kaposi’s Sarcoma
Ano-genital cancersEpithelial cancers

basic trans facts
Chronic immunosuppressive therapy has been a miracle for patients requiring solid organ transplants, but…
This significantly increases the long-term risk of developing malignancyAverage age
at diagnosis:
40 years
3-5 yearsThe Transplanted Heart is Denervated
Unresponsive to direct sympathetic or parasympathetic stimuli
Responsive to endogenous circulating catecholamines
Responsive to administered vasoactive drugs
E.g. epinephrine, norepinephrine
But, atropine is ineffectiveThe Transplanted Heart is Denervated
Baseline tachycardia is usual
Loss of vagal influence
100-110 BPM typical
Patients don’t experience angina
Even with occlusive dis-
-The Transplanted Heart
Always think acute allograft rejection for patients with…
Worsening CHF
Syncope and near syncope
GI symptoms
Secondary to hepatic congestion
Unexplained fever
New arrhythmias
Reduction in QRS voltage
-For febrile patients, full cultures and broad spectrum antibioticsAlways contact the LVAD center for recommendations re: immunosuppressive -Airway anastomotic complications after lung transplant occur in up to 33% of patients
Focal infection ∆
Bronchial necrosis and dehiscence ∆
Excess granulation tissue Ω
Tracheobronchomalacia Ω
Bronchial stenosis Ω
Fistula formation Ω
-Most patients experiencing renal allograft rejection are asymptomatic

Fever, graft pain, graft tenderness and graft swelling are uncommon

Clinical manifestations include…
Decreased urine output
Increased blood pressure
Worsening proteinuria
-Chronic immunosuppressive therapy has been a miracle for patients requiring solid organ transplants, but…

This significantly increases the long-term risk of developing malignancy
-The risks for developing skin cancers are significantly increased

Squamous cell: up to 250-fold
Kaposi’s Sarcoma: 20-fold
Basal cell: 10-fold
Melanoma: 4-fold

skin CA

The risks are significantly increased

Squamous cell: up to 250-fold
Kaposi’s Sarcoma: 20-fold
Basal cell: 10-fold
Melanoma: 4-fold

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