general surgery & transplant

Terms in this set (151)

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.
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.
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.
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.
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.
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]
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
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.
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 composition

Gallbladder 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.
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)

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.
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
No lab study is specific for cholelithiasis
Leukocytosis and elevated C-reactive protein level are associated with acute calculus cholecystitis

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
Gallbladder cancer
Gallbladder polyps
Acalculous cholecystitis
Biliary dyskinesia
Biliary tree stricture
Coronary artery disease
Esophageal motility disorders
Renal stones
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.
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 imaging

Cholangiogram 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.
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.
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.
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.
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
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
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"
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.
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.
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.
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
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 antibiotics

Always 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