What is the hydrogen breath test?

The hydrogen breath test is a test that uses the measurement of hydrogen in the breath to diagnose several conditions that cause gastrointestinal symptoms. In humans, only bacteria – specifically, anaerobic bacteria in the colon – are capable of producing hydrogen. The bacteria produce hydrogen when they are exposed to unabsorbed food, particularly sugars and carbohydrates, not proteins or fats. Although limited hydrogen is produced from the small amounts of unabsorbed food that normally reach the colon, large amounts of hydrogen may be produced when there is a problem with the digestion or absorption of food in the small intestine, that allows more unabsorbed food to reach the colon.

Large amounts of hydrogen also may be produced when the colon bacteria move back into the small intestine, a condition called bacterial overgrowth of the small bowel. In this latter instance, the bacteria are exposed to unabsorbed food that has not had a chance to completely traverse the small intestine to be fully digested and absorbed. Some of the hydrogen produced by the bacteria, whether in the small intestine or the colon, is absorbed into the blood flowing through the wall of the small intestine and colon. The hydrogen-containing blood travels to the lungs where the hydrogen is released and exhaled in the breath where it can be measured.

When is hydrogen breath testing used?

Hydrogen breath testing is used in the diagnosis of three conditions.

• The first is a condition in which dietary sugars are not digested normally. The most common sugar that is poorly digested is lactose, the sugar in milk. Individuals who are unable to properly digest lactose are referred to as lactose intolerant. Testing also may be used to diagnose problems with the digestion of other sugars such as sucrose, fructose and sorbitol.
• The second condition for which hydrogen breath testing is used is for diagnosing bacterial overgrowth of the small bowel, a condition in which larger-than-normal numbers of colonic bacteria are present in the small intestine.
• The third condition for which hydrogen breath testing is used is for diagnosing rapid passage of food through the small intestine. All three of these conditions may cause abdominal pain, abdominal bloating and distention, flatulence (passing gas in large amounts), and diarrhea.

The sphincter of Oddi is a muscular valve that controls the flow of digestive juices (bile and pancreatic juice) through ducts from the liver and pancreas into the first part of the small intestine (duodenum). Sphincter of Oddi dysfunction (SOD) describes the situation when the sphincter does not relax at the appropriate time (due to scarring or spasm). The back-up of juices causes episodes of severe abdominal pain.

The sphincter of Oddi is a muscular valve that controls the flow of digestive juices (bile and pancreatic juice) through ducts from the liver and pancreas into the first part of the small intestine (duodenum). Sphincter of Oddi dysfunction (SOD) describes the situation when the sphincter does not relax at the appropriate time (due to scarring or spasm). The back-up of juices causes episodes of severe abdominal pain.

Doctors often consider SOD in patients who experience recurrent attacks of pain after surgical removal of the gallbladder (cholecystectomy). More than half a million of these surgeries are performed annually in the United States, and 10–20% of these patients present afterwards with continuing or recurrent pains. SOD is also considered in some patients who suffer from recurrent attacks of unexplained inflammation of the pancreas (pancreatitis).

About half of these patients will have findings on laboratory studies or imaging (blood test, ultrasound, CT scan, or MRCP) to suggest a definite abnormality, such as a stone in the bile duct. MRCP (magnetic resonance cholangiopancreatography) is nowadays a good non-invasive test for checking on the biliary and pancreatic drainage systems.

Based on patients histories, physical examinations, and other clinical data, doctors can categorize these patients as having SOD Types I and II. The categories help guide treatment of the disease. They are based on a system called the Milwaukee criteria.

When symptoms are severe, standard treatment is to perform an endoscopic procedure called ERCP (endoscopic retrograde cholangiopancreatography). ERCP is a procedure for the examination or treatment of the bile duct and pancreatic duct. The procedure carries a risk of serious complications and is done under sedation by experts trained in the technique. It combines the use of x-rays and an endoscope that is passed down to the duodenum, where the bile duct and pancreatic ducts drain, and a dye that is injected into the ducts.

An additional procedure, sphincter of Oddi manometry (SOM), involves passing a catheter into the bile and/or pancreatic duct during ERCP to measure the pressure of the biliary and/or pancreatic sphincter. It is considered the gold standard diagnostic modality for SOD.

Treatment depends on what is found. It may often involve cutting the muscular sphincter (sphincterotomy) to remove any stones or to relieve any scarring or spasm of the sphincter.

As noted above, a very important problem in this context is that these ERCP procedures carry a significant risk of complications. In particular, ERCP (with or without sphincter of Oddi manometry) can cause an attack of pancreatitis in 5–10% of cases. While most of these result in a few days in the hospital, about 1% of patients suffer a major attack, with weeks or months in the hospital. Sphincterotomy also carries a small risk of other severe complications such as bleeding and perforation, and the possibility of delayed narrowing of a duct (stenosis) due to scarring.

Functional SOD

Patients with a similar pain problem, but who have little or no abnormalities on blood tests and standard scans (including MRCP), are categorized as having SOD Type III. The episodes of pain are assumed due to intermittent spasm of the sphincter. It is very difficult to effectively evaluate and manage patients with Type III SOD. Some physicians are skeptical of its existence, or assume that it is a part of a broader problem of a functional digestive disturbance such as irritable bowel syndrome.

Because of the risks of ERCP, patients with suspected SOD III are usually advised to try medical treatments first. Some respond to the use of antispasmodic drugs and/or antidepressants that may help decrease pain.  There have been studies of other medical therapies, such as calcium channel blocking drugs. Despite a few encouraging reports, these methods have not proven to be effective generally, and are not widely used.

Patients who fail these approaches (at least those with severe symptoms) are usually advised to see specialists at referral centers. Further evaluation may involve additional or more specialized tests to help guide treatment options.

Clinical Research Study

The uncertainties in how best to diagnose and to treat “suspected” sphincter of Oddi dysfunction (and the risks involved) mandate further scientific investigation. The National Institutes of Health has recently funded an important study called “EPISOD” in 6 major Gastroenterology centers in USA.

The studies are being conducted at centers located in:

• Johns Hopkins Hospital, Baltimore, MD
• University of Alabama at Birmingham, Birmingham, AL
• Medical University of South Carolina Digestive Disease Center, Charleston, SC
• Indiana University, Indianapolis, IN
• Hennepin County Medical Center, Minneapolis, MN
• Virginia Mason Medical Center, Seattle, WA

Additional details are available at the NIH website at http://clinicaltrials.gov/ by searching: sphincter of Oddi dysfunction III.

Adapted from IFFGD publication #260 by: Peter B. Cotton, MD, Professor of Medicine, Digestive Disease Center, Medical University of South Carolina, Charleston, SC

Is inflammatory bowel disease (IBD) the same thing as Irritable Bowel Syndrome (IBS)?

No. Inflammatory bowel disease, including UC and CD, is different from irritable bowel syndrome (IBS). Unlike IBD, IBS does not cause inflammation, ulcers or other damage to the bowel. Instead, IBS is a much less serious problem called a functional disorder. This means that the digestive system looks normal but doesn’t work as it should. Symptoms of IBS may include crampy pain, bloating, gas, mucus in the stool, diarrhea and constipation. IBS has also been called spastic colon or spastic bowel

Source: http://www.webmd.com/ibd-crohns-disease/crohns-disease/ibd-versus-ibs

Bloating is a very common and subjective ailment which can effect patients of all ages. It can be associated with any of the causes of abdominal distension but it is most commonly associated with irritable bowel syndrome. Bloating can have a major impact both socially and psychologically. It is incompletely understood and inadequately treated.

For further information see related separate article Irritable Bowel Syndrome.

Ursofalk (Orphan Australia)
250 mg capsules
Approved indication: chronic cholestasis
Australian Medicines Handbook Section 12

In primary biliary cirrhosis, there is chronic inflammation which destroys the intrahepatic bile ductules. At first, patients may be asymptomatic, but the reduced excretion of bile can cause steatorrhoea. The disease slowly progresses and death can result from hepatic failure or the complications of cirrhosis. Primary biliary cirrhosis is now a common indication for a liver transplant. Although there is no effective drug treatment, some patients will benefit from ursodeoxycholic acid.

Ursodeoxycholic acid is a bile acid which is synthesised from its precursor by intestinal bacteria. Its mechanism of action in primary biliary cirrhosis is uncertain. Ursodeoxycholic acid may have an effect by increasing the flow and altering the composition of bile. It has also been used in the treatment of gallstones.

In clinical trials with at least two years of follow up, patients who took ursodeoxycholic acid had improved liver function tests. This may not always improve the patient’s symptoms or the histology of the liver.

Ursodeoxycholic acid has few known adverse effects. Diarrhoea is the main adverse reaction. Patients can complain of an increase in itching when they begin treatment. This may respond to a reduction in the dose. Ursodeoxycholic acid is contraindicated if there is acute inflammation of the gall bladder or obstruction of the common bile duct.

Ursodeoxycholic acid will probably have a role in delaying the need for liver transplantation. A placebo-controlled study of 145 patients with primary biliary cirrhosis found that the disease progressed more slowly in patients given ursodeoxycholic acid. This group also had a significantly lower probability of transplantation or death during the two-year study.¹

Reference

1 . Poupon RE, Poupon R, Balkau B. Ursodiol for the long-term treatment of primary biliary cirrhosis. The UDCA-PBC Study Group. N Engl J Med 1994;330:1342-7.

Celebrex (Searle)
100 mg and 200 mg capsules
Approved indication: arthritis
Australian Medicines Handbook Section 15.1

Non-steroidal anti-inflammatory drugs act by inhibiting the enzyme cyclo-oxygenase(COX).¹ This enzyme is required for the synthesis of prostaglandins and its activity increases in inflammation. It has two isoforms, COX-1 andCOX-2, both of which are blocked to varying degrees by non-steroidal anti-inflammatory drugs. As COX-1 may produce protective prostaglandins in the stomach, its inhibition could be responsible for some of the adverse effects of the drugs. Celecoxib is much more selective for COX-2, so it may cause fewer adverse effects than the older drugs.

Patients with symptoms of rheumatoid arthritis take celecoxib in two divided doses. A single daily dose may be used in osteoarthritis. The drug is quickly absorbed. Although taking the capsules with food delays absorption, the bioavailability is increased. Celecoxib is metabolised in the liver by cytochrome P450 CYP2C9so there is a potential for interactions with drugs such as fluconazole.

In studies lasting up to 12 weeks, celecoxib has reduced the pain of osteoarthritis more effectively than placebo. Trials, of up to 24 weeks, in patients with rheumatoid arthritis have found the efficacy of celecoxib to be similar to that of naproxen 500 mg twice daily.

The effect of celecoxib on the gut has been assessed by endoscopy. Gastric ulcers were seen significantly less frequently during treatment with celecoxib, than they were in patients taking naproxen or diclofenac. Celecoxib, however, is not free of gastrointestinal adverse effects. Dyspepsia, abdominal pain and diarrhoea occur more frequently than with placebo. In animal studies, COX-2inhibitors retard ulcer healing.¹

Most of the enzyme activity in platelets is COX-1, so celecoxib should have little effect on bleeding time. The potential of COX-2 inhibitors to cause fluid retention, renal impairment or hypertension is unknown. In clinical trials peripheral oedema occurred with equal frequency (2.1%) in patients taking celecoxib or naproxen. Celecoxib is not recommended for patients with aspirin-sensitive asthma.

The COX-2 inhibitors have the potential to replace non-steroidal anti-inflammatory drugs for the relief of arthritic symptoms. Whether or not they fulfill this potential will depend on their long-term safety. For example, will they cause fewer gastrointestinal haemorrhages than the non-steroidal anti-inflammatory drugs?

Reference

1. Hawkey CJ. COX-2 inhibitors. Lancet 1999;353:307-14.

The laparoscopic cholecystectomy is considered the “gold standard” in chronic calculous cholecystitis treatment. After the gallbladder removal the physiology of gallbladder bile formation is changed.

Absence of the gallbladder leads to development of functional biliary hypertension and dilatation of common bile duct and the common hepatic duct. The dilatation of right and left hepatic ducts may be formed within 3-5 years after cholecystectomy. Functional hypertension in the common bile duct leads to development of functional hypertension in Wirsung’s pancreatic duct accompanied by chronic pancreatitis symptoms.

During this period in some patients this is accompanied by chronic pancreatitis progression, dysfunction of the sphincter of Oddi and duodeno-gastral reflux. Duodeno-gastral reflux causes the development of atrophic (bile-acid-depen­dent) antral gastritis . After cholecystectomy 40% to 60% of patients suffer from dyspeptic disorders, 5% to 40% from pains of different localizations. Up to 70% of patients show symptoms of chronic “bland” intrahepatic cholestasis, chronic cholestatic hepatitis and compensatory bile-acid-dependent apoptosis of hepatocytes. In some of cholecystectomized patients with high concentration of hydrophobic hepatotoxic co-cancerogenic deoxycholic bile acid in serum and/or feces high risk of the colon cancer is found.

Therefore, depending on dysfunction (hyper tonus) or relaxation (hypo tonus) of the sphincter of Oddi, pathology in hepato-biliary-pancreato-duodenal-gastral zone will form after cholecystectomy.

Postcholecystectomy syndrome is a dysfunction of the sphincter of Oddi, caused by noncalculous obstructive disorder, which decrease bile passage and pancreatic juice outflow into the duodenum.

More reading

Simply put, Small Intestine Bacterial Overgrowth is a chronic bacterial infection of the small intestine.  The infection is of bacteria that normally live in the gastrointestinal tract but have abnormally overgrown in a location not meant for so many bacteria.  

The Problem
The bacteria interfere with our normal digestion and absorption of food and are associated with damage to the lining or membrane of the SI (leaky gut syndrome, which I prefer to call leaky SI in this case). 

• They consume some of our food which over time leads to deficiencies in their favorite nutrients such as iron and B12, causing anemia.

• They consume food unable to be absorbed due to SI lining damage, which creates more bacterial overgrowth (a vicious cycle).

• After eating our food, they produce gas/ expel flatus, within our SI.  The gas causes abdominal bloating, abdominal pain, constipation, diarrhea or both (the symptoms of IBS).  Excess gas can also cause belching and flatulence.

• They decrease proper fat absorption by deconjugating bile leading to deficiencies of vitamins A & D and fatty stools.

• Through the damaged lining, larger food particles not able to be fully digested, enter into the body which the immune system reacts to.  This causes food allergies/ sensitivities.

• Bacteria themselves can also enter the body/bloodstream.  Immune system reaction to bacteria and their cell walls (endotoxin) causes chronic fatigue and body pain and burdens the liver.

• Finally, the bacteria excrete acids which in high amounts can cause neurological and cognitive symptoms.

 

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Reviewed and Approved by a member of the DoveMed Editorial Board
First uploaded: May 28, 2015
Last updated: Aug. 4, 2016

Source: https://www.dovemed.com/diseases-conditions/choledocholithiasis/

Gallstones are marble-like deposits that form in the gallbladder, due to changes in the concentration of various components of bile. Bile is a fluid that is made by the liver and stored in the gallbladder.

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Reviewed and Approved by a member of the DoveMed Editorial Board
First uploaded: Aug. 2, 2015
Last updated: April 8, 2016

Source: https://www.dovemed.com/diseases-conditions/gallstones/

Description

Lithotripsy uses the technique of focused shock waves to fragment a stone in the kidney or the ureter. The affected person is placed in a tub of water or in contact with a water-filled cushion. A sophisticated machine called Lithotripter produces the focused shock waves. A high-voltage electrical discharge is passed through a spark gap under water. The shock waves thus produced are focused on the stone inside the person’s body. The shock waves are created and focused on the stone with the help of a machine called C-Arm Image Intensifier. The wave shatters and fragments the stone. The resulting debris, called gravel, can then pass through the remainder of the ureter, through the bladder, and through the urethra during urination. There is minimal chance of damage to skin or internal organs because biologic tissues are resilient, not brittle, and because the shock waves are not focused on them.

The shock wave is characterized by a very rapid pressure increase in the transmission medium and is quite different from ultrasound. The shock waves are transmitted through a person’s skin and pass harmlessly through soft tissues. The shock wave passes through the

Kidney stones that are too big to pass through the ureter become very painful (B). During lithotripsy, the patient is put in a tub of water, or on a water-filled blanket. Shock waves are used to break up the stone (C). These smaller pieces are able to pass out of the body (D). (

Illustration by GGS Inc.

)

kidney and strikes the stone. At the edge of the stone, energy is transferred into the stone, causing small cracks to form on the edge of the stone. The same effect occurs when the shock wave exits the stone. With successive shock waves, the cracks open up. As more cracks form, the size of the stone is reduced. Eventually, the stone is reduced to small particles, which are then flushed out of the kidneys or ureter naturally during urination.

Source Read more: http://www.surgeryencyclopedia.com/La-Pa/Lithotripsy.html#ixzz53XzP0D6h

Cystic duct

The cystic duct connects the top of the gallbladder’s neck to the common hepatic duct. It then joins the common bile duct, which meets pancreatic duct before it empties into the duodenum. In the average adult, the cystic duct measures four centimeters in length.

Role of Bile Acids In Digestion
Bile is a complex fluid containing water, electrolytes and a battery of organic molecules including bile acids, cholesterol, phospholipids and bilirubin that flows through the biliary tract into the small intestine. There are two fundamentally important functions of bile in all species:

Bile contains bile acids, which are critical for digestion and absorption of fats and fat-soluble vitamins in the small intestine.
Many waste products, including bilirubin, are eliminated from the body by secretion into bile and elimination in feces.
Adult humans produce 400 to 800 ml of bile daily, and other animals proportionately similar amounts. The secretion of bile can be considered to occur in two stages:

Initially, hepatocytes secrete bile into canaliculi, from which it flows into bile ducts. This hepatic bile contains large quantities of bile acids, cholesterol and other organic molecules.
As bile flows through the bile ducts it is modified by addition of a watery, bicarbonate-rich secretion from ductal epithelial cells.
In species with a gallbladder (man and most domestic animals except horses and rats), further modification of bile occurs in that organ. The gall bladder stores and concentrates bile during the fasting state. Typically, bile is concentrated five-fold in the gall bladder by absorption of water and small electrolytes – virtually all of the organic molecules are retained.

Secretion into bile is a major route for eliminating cholesterol. Free cholesterol is virtually insoluble in aqueous solutions, but in bile, it is made soluble by bile acids and lipids like lecithin. Gallstones, most of which are composed predominantly of cholesterol, result from processes that allow cholesterol to precipitate from solution in bile.

Role of Bile Acids in Fat Digestion and Absorption
Bile acids are derivatives of cholesterol synthesized in the hepatocyte. Cholesterol, ingested as part of the diet or derived from hepatic synthesis is converted into the bile acids cholic and chenodeoxycholic acids, which are then conjugated to an amino acid (glycine or taurine) to yield the conjugated form that is actively secreted into cannaliculi.
Bile acids are facial amphipathic, that is, they contain both hydrophobic (lipid soluble) and polar (hydrophilic) faces. The cholesterol-derived portion of a bile acid has one face that is hydrophobic (that with methyl groups) and one that is hydrophilic (that with the hydroxyl groups); the amino acid conjugate is polar and hydrophilic.

Their amphipathic nature enables bile acids to carry out two important functions:

Emulsification of lipid aggregates: Bile acids have detergent action on particles of dietary fat which causes fat globules to break down or be emulsified into minute, microscopic droplets. Emulsification is not digestion per se, but is of importance because it greatly increases the surface area of fat, making it available for digestion by lipases, which cannot access the inside of lipid droplets.
Solubilization and transport of lipids in an aqueous environment: Bile acids are lipid carriers and are able to solubilize many lipids by forming micelles – aggregates of lipids such as fatty acids, cholesterol and monoglycerides – that remain suspended in water. Bile acids are also critical for transport and absorption of the fat-soluble vitamins.
Role of Bile Acids in Cholesterol Homeostasis
Hepatic synthesis of bile acids accounts for the majority of cholesterol breakdown in the body. In humans, roughly 500 mg of cholesterol are converted to bile acids and eliminated in bile every day. This route for elimination of excess cholesterol is probably important in all animals, but particularly in situations of massive cholesterol ingestion.

Interestingly, it has recently been demonstrated that bile acids participate in cholesterol metabolism by functioning as hormones that alter the transcription of the rate-limiting enzyme in cholesterol biosynthesis.

Enterohepatic Recirculation
Large amounts of bile acids are secreted into the intestine every day, but only relatively small quantities are lost from the body. This is because approximately 95% of the bile acids delivered to the duodenum are absorbed back into blood within the ileum.

Venous blood from the ileum goes straight into the portal vein, and hence through the sinusoids of the liver. Hepatocytes extract bile acids very efficiently from sinusoidal blood, and little escapes the healthy liver into systemic circulation. Bile acids are then transported across the hepatocytes to be resecreted into canaliculi. The net effect of this enterohepatic recirculation is that each bile salt molecule is reused about 20 times, often two or three times during a single digestive phase.

It should be noted that liver disease can dramatically alter this pattern of recirculation – for instance, sick hepatocytes have decreased ability to extract bile acids from portal blood and damage to the canalicular system can result in escape of bile acids into the systemic circulation. Assay of systemic levels of bile acids is used clinically as a sensitive indicator of hepatic disease.

Pattern and Control of Bile Secretion
The flow of bile is lowest during fasting, and a majority of that is diverted into the gallbladder for concentration. When chyme from an ingested meal enters the small intestine, acid and partially digested fats and proteins stimulate secretion of cholecystokinin and secretin. As discussed previously, these enteric hormones have important effects on pancreatic exocrine secretion. They are both also important for secretion and flow of bile:

Cholecystokinin: The name of this hormone describes its effect on the biliary system – cholecysto = gallbladder and kinin = movement. The most potent stimulus for release of cholecystokinin is the presence of fat in the duodenum. Once released, it stimulates contractions of the gallbladder and common bile duct, resulting in delivery of bile into the gut.
Secretin: This hormone is secreted in response to acid in the duodenum. Its effect on the biliary system is very similar to what was seen in the pancreas – it simulates biliary duct cells to secrete bicarbonate and water, which expands the volume of bile and increases its flow out into the intestine.

Source:  http://www.vivo.colostate.edu/hbooks/pathphys/digestion/liver/bile.html

Author:

Salam F Zakko, MD, FACP, AGAF

Section Editor:

Sanjiv Chopra, MD, MACP

Deputy Editor:

Shilpa Grover, MD, MPH, AGAF

Contributor Disclosures

Author:

Salam F Zakko, MD, FACP, AGAF

Section Editor:

Sanjiv Chopra, MD, MACP

Deputy Editor:

Shilpa Grover, MD, MPH, AGAF

Also found in: Dictionary, Thesaurus, Encyclopedia, Wikipedia.

The Postcholecystectomy Syndrome (PCS): is a heterogeneous group of diseases and symptoms presenting following gallbladder removal. Symptoms occur in about 5 to 40 percent of patients who undergo cholecystectomy, and can be transient, persistent or lifelong. The chronic condition is diagnosed in approximately 10% of postcholecystectomy cases.

Post-cholecystectomy Syndrome may include: 

• Diarrhoea as a troublesome problem range from 9 to 12% of which bile acid malabsorption (BAM) , 65% of these patients. [1]
• Depression disorders occurring in 0.9%-3.0% of patients[2]
• Bile (duodenogastric) reflux occurring in 20%-30% of patients[3,4,5].  Likely damage attributable to chronic bile exposure post-cholecystectomy includes:
  • cellular damage to esophagogastric junction
  • bile induced Gastroesophageal Mucosal Injury (Protective barrier that constrains the acidic reflux)
  • increase the incidence of gastric and esophageal cancer
• Sphincter of Oddi dysfunction (SOD) is seen in 1% of patients after cholecystectomy, but in 14%-23% of patients with the post-cholecystectomy syndrome [6]
• increased Body Mass Index (weight gain) with metabolic syndrome, gastritis, liposoluble vitamin deficiency. Cholecystectomy can have nutritional and metabolic consequences and in the long-term[7]

The onset of symptoms may range from 2 days to 25 years.  There may also be gender-specific risk factors for developing symptoms after cholecystectomy. In one study, the incidence of recurrent symptoms among female patients was 43%, compared to 28% of male patients.”

Patients with cholecystectomy had more comorbidities, particularly chronic fatigue syndrome, fibromyalgia, depression, and anxiety. Postcholecystectomy gastroparesis patients had increased health care utilization and had a worse quality of life.

Postcholecystectomy Syndrome in more detail

Absence of the gallbladder leads to development of functional biliary hypertension and dilatation of common bile duct and the common hepatic duct. The dilatation of right and left hepatic ducts may be formed within 3-5 years after cholecystectomy. Functional hypertension in the common bile duct leads to development of functional hypertension in Wirsung’s pancreatic duct accompanied by chronic pancreatitis symptoms.

During this period in some patients this is accompanied by chronic pancreatitis progression, dysfunction of the sphincter of Oddi and duodeno-gastral reflux. Duodeno-gastral reflux causes the development of atrophic (bile-acid-depen­dent) antral gastritis . After cholecystectomy 40% to 60% of patients suffer from dyspeptic disorders, 5% to 40% from pains of different localizations. Up to 70% of patients show symptoms of chronic “bland” intrahepatic cholestasis, chronic cholestatic hepatitis and compensatory bile-acid-dependent apoptosis of hepatocytes. In some of cholecystectomized patients with high concentration of hydrophobic hepatotoxic co-cancerogenic deoxycholic bile acid in serum and/or feces high risk of the colon cancer is found.

Not disclosed to patients, specialist medical opinion and studies list the following expected risks, side effects, diseases, syndromes and conditions after the removal of the gallbladder and its function. The majority of these problems are not accepted by the HDC as a risk and are blocked from disclosure to patients during the informed consent process, or advised during post-operative follow-ups.

They are but not exclusive to:

Evidence based medical studies confirming statistically significant increased risk of cancer following cholecystectomy, required by law but never disclosed by doctors during the informed consent process listed as:

Source references:

1. M. Farahmandfar, M. Chabok, M. Alade, A. Bouhelal and B. Patel, Post Cholecystectomy Diarrhoea—A Systematic Review, Surgical Science, Vol. 3 No. 6, 2012, pp. 332-338. http://dx.doi.org/10.4236/ss.2012.36065
2. Tsai M-C, Chen C-H, Lee H-C, Lin H-C, Lee C-Z (2015) Increased Risk of Depressive Disorder following Cholecystectomy for Gallstones. PLoS ONE 10(6): e0129962. https://doi.org/10.1371/journal.pone.0129962
3. Nudo R, Pasta V, Monti M, Vergine M, Picardi N. Correlation between post-cholecystectomy syndrome and biliary reflux gastritis. Endoscopic study. https://www.ncbi.nlm.nih.gov/pubmed/2699712
4. Lorusso D1, Pezzolla F, Montesani C, Giorgio P, Caruso ML, Cavallini A, Guerra V, Misciagna G. Duodenogastric reflux and gastric histology after cholecystectomy with or without sphincteroplasty https://www.ncbi.nlm.nih.gov/pubmed/2253017
5. Shah Gilani SN1, Bass GA1, Kharytaniuk N2, Downes MR3, Caffrey EF3, Tobbia I3, Walsh TN4. Gastroesophageal Mucosal Injury after Cholecystectomy: An Indication for Surveillance? https://doi.org/10.1016/j.jamcollsurg.2016.12.003
6. Bistritz, L., & Bain, V. G. (2006). Sphincter of Oddi dysfunction: Managing the patient with chronic biliary pain. World Journal of Gastroenterology?: WJG, 12(24), 3793–3802. http://doi.org/10.3748/wjg.v12.i24.3793
7. Donato F. Altomare, Maria T. Rotelli, Nicola Palasciano. Diet After Cholecystectomy http://www.eurekaselect.com/node/152535/article
8. Wikipedia,  Postcholecystectomy syndrome.  https://en.wikipedia.org/wiki/Postcholecystectomy_syndrome
9. Steen W Jensen, MD; Chief Editor: John Geibel, MD, DSc, MSc, AGAF Postcholecystectomy Syndrome [medscape.com]
10. S.S.JaunooS MohandasL.M.Almond. Postcholecystectomy syndrome (PCS) [ScienceDirect]
11. Sureka B, Mukund A. Review of imaging in post-laparoscopy cholecystectomy complications. Indian J Radiol Imaging 2017;27:470-81  [Indian Journal of Radiology and Imaging]
12. Murshid KR. The postcholecystectomy syndrome: A review. Saudi J Gastroenterol [serial online] 1996 [cited 2018 Jan 15];2:124-37. Available from:  http://www.saudijgastro.com/text.asp?1996/2/3/124/34017
13. Girometti, R., Brondani, G., Cereser, L., Como, G., Del Pin, M., Bazzocchi, M., & Zuiani, C. (2010). Post-cholecystectomy syndrome: spectrum of biliary findings at magnetic resonance cholangiopancreatography. [The British Journal of Radiology, 83(988), 351–361]
14. Jacob L. Turumin, Victor A. Shanturov, Helena E. Turumina. Irkutsk Institute of Surgery, Irkutsk Regional Hospital, Irkutsk 664079. The role of the gallbladder in human [ScienceDirect]
15. Dr. Jacob L. Turumin, MD, PhD, DMSci Biliary Diseases Laparoscopic Cholecystectomy. Postcholecystectomy Syndrome. http://www.drturumin.com/en/index.html#sthash.Y35Uey8C.dpuf
16. Martin, Walton. “RECENT CONTROVERSIAL QUESTIONS IN GALL-BLADDER SURGERY.” Annals of Surgery 79.3 (1924): 424–443. Print. [PMC]
17. The NIDDK Gastroparesis Clinical Research Consortium (GpCRC). “Cholecystectomy and Clinical Presentations of Gastroparesis.” Digestive diseases and sciences 58.4 (2013): 1062–1073. [PMC]
18. Yong Zhang , Hao Liu , Li Li , Min Ai , Zheng Gong, Yong He, Yunlong Dong, Shuanglan Xu, Jun Wang , Bo Jin, Jianping Liu, Zhaowei Teng Cholecystectomy can increase the risk of colorectal cancer: A meta-analysis of 10 cohort studies Published: August 3, 2017 https://doi.org/10.1371/journal.pone.0181852
19. Mearin, F., De Ribot, X., Balboa, A. Duodenogastric bile reflux and gastrointestinal motility in pathogenesis of functional dyspepsia. Role of cholecystectomy.  Digest Dis Sci (1995) 40: 1703. https://doi.org/10.1007/BF02212691
20. Simona Manea, Georgeta & Carol, Stanciu. (2008). DUODENOGASTROESOPHAGEAL REFLUX AFTER CHOLECYSTECTOMY. Jurnalul de Chirurgie. 4 [Researchgate]

Another opinion not accepted by NZ Laparoscopic Surgeons or heath consumer watch dog Health and Disability Commissioner and as such never presented to patients when legally obtaining informed consent for gallbladder surgery (Cholecystectomy)

The body is permanently damaged and cannot be healthy without a gallbladder and its function. You can live, but in many cases you will be miserable. Some common side effects of gallbladder removal are an upset stomach, nausea, and vomiting. Gas, bloating, and diarrhoea. Persistent pain in the upper right abdomen.

It is gross medical negligence to send a patient home after surgery and pretend there are no side effects and can lead a perfectly normal life without a gallbladder and its purpose. Due to the considerable numbers of affected New Zealand patients, under United Nations Universal Declaration of Human Rights, Article 5 and 25 an ongoing crime is occurring.

Article 5: No one shall be subjected to cruel, inhuman or degrading treatment

Article 25: Everyone has the right to a standard of living adequate for the health and well-being of himself and of his family, including food, clothing, housing and medical care and necessary social services, and the right to security in the event of unemployment, sickness, disability, or other lack of livelihood in circumstances beyond his control.

Most patients suffer permanent impairments of the digestive system as a consequence of cholecystectomy, and develop various disorders as a result of poor digestion. The gall bladder is a vital organ with a crucial role in the absorption of fat and fat-soluble vitamins A, D, E and K and in essential fatty acids (omega-3 and omega-6), and poor cholesterol metabolism. In the long run, this may contribute to fatty liver. The absence of the gall bladder affects not only the process of food digestion but a wide range of other internal processes as well. In time, patients who have suffered cholecystectomy are also exposed to a high risk of developing heart disease, diabetes and disorders of the nervous system. This is due to inappropriate synthesis and assimilation of vital nutrients, vitamins and minerals.

Source references:

1. National Research Council. 1989. Diet and Health: Implications for Reducing Chronic Disease Risk. Washington, DC: The National Academies Press. https://doi.org/10.17226/1222. https://www.nap.edu/read/1222/chapter/14#317
2. Mike Adams. What conventional medicine won’t dare tell you about gall bladder removal surgery. http://www.naturalnews.com/007733_gall_bladder_surgery.html
3. Barbara Bolen, PhD. Emmy Ludwig, MD. What to Do About IBS After Gallbladder Removal. http://ibs.about.com/od/relatedconditions/a/IBS-After-Gallbladder-Removal.htm

Alternative opinions not accepted continued

The postcholecystectomy syndrome may occur in two weeks or two decades following gallbladder surgery. The symptoms can be mild and just diminish of person’s quality of life. For some patients, PCS makes life miserable. Mostly, it does not depend on upon the surgical techniques, equipment, or experience of the surgeon. Just absence of gallbladder causes this problem.

The typical symptoms of the postcholecystectomy syndrome include

• Intolerance of some foods, mostly fatty foods
• Upper abdominal pain
• Constant gas, bloating, flatulence
• Nausea, vomiting
• Stubborn heartburn
• Constipation
• Chronic diarrhea
• Symptoms, which are very far from stomach such as depression, anxiety, low memory, skin dryness or itchiness, yellowish skin, blurred vision, bruises, tingling and numbness, often colds and more

The problem is that there is no conventional treatment of the PCS. The patients are under the care of the variety of doctors and medical practitioners with different skills, knowledge, and viewpoint on the postcholecystectomy syndrome. There are three kinds of situations.

The first one is when the symptoms happen rarely, and the entire lab and visual tests are normal. Patient has symptomatic treatment with the painkillers or gets a referral to a pain management clinic, or sends to a psychiatrist for depression and anxiety. Frequently PCS misdiagnosed with gastroesophageal reflux disease, food poison or food sensitivity, gastritis, dyspepsia, IBS, dumping syndrome, etc.

The second situation, the lab, and visual tests demonstrate increases in the pancreatic or liver enzymes, presence of the dilatation of the common bile duct. Symptoms become chronic. That is followed by numerous diagnostic tests, which are often insecure, visits to the countless doctors, hospitals, and taking all sorts of medications.

The third scenario, the individual underwent many tests that revealed severe structural changes in the bile duct, pancreas, liver, duodenum, and sphincter of Oddi. At this time, patients have numerous doctor visits, medications, ER admissions, consultations of specialists, and endoscopic surgeries.

These three situations are not separate disorders; these are the different stages of the sphincter of Oddi dysfunction, chronic biliary pancreatitis, metabolic acidosis, dysbiosis, and adhesion syndrome. Biliary means connection to bile system. The health of the bile, bile ducts, sphincter of

Oddi, and gallbladder is inextricably bound to the health of the pancreas, small, large intestines, and stomach.

Like all chronic diseases, there are the functional stage, structural stage, and advanced stage of the postcholecystectomy syndrome

Source : https://www.biotherapy-clinic.com/article/postcholecystectomy-syndrome-pain-and-indigestion-after-gallbladder-surgery

“In 12 years of practice, I have rarely met any ‘cholecystectomy patient’ who didn’t have to make changes to feel better afterwards. Sooner or later their underlying nutritional deficiencies caught up to them and affected their health.”

Dr. Miranda Jorgenson, licensed Chiropractic Physician

Functions of the Gallbladder

The gallbladder stores and concentrates bile between meals. Gallbladder motor function is regulated by bile acids via the membrane bile acid receptor, TGR5, and by neurohormonal signals linked to digestion, for example, cholecystokinin and FGF15/19 intestinal hormones, which trigger gallbladder emptying and refilling, respectively. The cycle of gallbladder filling and emptying controls the flow of bile into the intestine and thereby the enterohepatic circulation of bile acids. The gallbladder also largely contributes to the regulation of bile composition by unique absorptive and secretory capacities. The gallbladder epithelium secretes bicarbonate and mucins, which both provide cytoprotection against bile acids. The reversal of fluid transport from absorption to secretion occurs together with bicarbonate secretion after feeding, predominantly in response to an adenosine 3′,5′-cyclic monophosphate (cAMP)-dependent pathway triggered by neurohormonal factors, such as vasoactive intestinal peptide. Mucin secretion in the gallbladder is stimulated predominantly by calcium-dependent pathways that are activated by ATP present in bile, and bile acids. The gallbladder epithelium has the capacity to absorb cholesterol and provides a cholecystohepatic shunt pathway for bile acids. Changes in gallbladder motor function not only can contribute to gallstone disease, but also subserve protective functions in multiple pathological settings through the sequestration of bile acids and changes in the bile acid composition. Cholecystectomy increases the enterohepatic recirculation rates of bile acids leading to metabolic effects and an increased risk of nonalcoholic fatty liver disease, cirrhosis, and small-intestine carcinoid, independently of cholelithiasis.

Housset C1,2, Chrétien Y1,2, Debray D1,3, Chignard N1. Functions of the Gallbladder. https://doi.org/10.1002/cphy.c150050

Author

Salam F Zakko, MD, FACP  Section Editor

Sanjiv Chopra, MD  Deputy Editor

Peter A L Bonis, MD

Last literature review version 17.1: January 2009 | This topic last updated: January 28, 2008 (More)

INTRODUCTION — The most significant challenge in the evaluation of patients with upper digestive symptoms who are found to have gallstones, is whether the stones are the cause of the symptoms (ie, gallstone disease) or are an incidental finding. Making this distinction is important because both gallstones and upper digestive symptoms are common in the general population but are not always related. While cholecystectomy can be curative in those whose symptoms are related to gallstones, it exposes the rest to unnecessary risk, delays definitive treatment for the actual cause of symptoms, and incurs unnecessary expense.

This topic review will provide an overview of the evaluation of patients with possible, uncomplicated gallstone-related disease. An approach to asymptomatic patients found to have gallstones is presented separately. (See “Approach to the patient with incidental gallstones”). Complications related to gallstones are discussed on their corresponding topic reviews.

CLINICAL FEATURES — When considering gallstone disease it is helpful to categorize patients into the following clinical groups: Gallstones on imaging studies but without symptoms (category 1) Typical biliary symptoms and gallstones on imaging studies (category 2) Atypical symptoms and gallstones on imaging studies (category 3) Typical biliary symptoms but without gallstones on imaging studies (category 4)

As will be discussed below, the approach to patients in category 1 and 2 is generally straightforward. Patients in category 1 should generally be left alone, while those in category 2 should undergo treatment aimed at eliminating the gallstones. By contrast, optimal approaches to patients who fall into the last two categories (3 and 4) are less clear. Management of such patients should be individualized but depends largely upon the likelihood (based upon clinical features and diagnostic testing) that the patient’s symptoms are related to the gallstones. The following discussion provides guidance to aid in this process.

Biliary type symptoms — In most patients, the first symptoms experienced from gallstones are recurrent pain attacks generated by the gallstones (biliary colic). Less frequently, the initial symptoms are those of one of the complications of gallstones (most commonly acute cholecystitis, acute biliary pancreatitis, acute cholangitis, or choledocholithiasis with extrahepatic cholestasis).

Biliary colic — Biliary colic is usually caused by the gallbladder contracting in response to hormonal or neural stimulation usually due to a fatty meal, forcing a stone (or possibly sludge or microlithiasis) against the gallbladder outlet or cystic duct opening, and leading to increased intragallbladder pressure and pain. The stones often fall back from the cystic duct as the gallbladder relaxes. As a result, the discomfort progresses in less than an hour to a steady plateau that ranges from moderate to excruciating and remains constant for more than an hour, then slowly subsides over several hours. In most patients the pain is not very severe which is why it takes several attacks before a patient seeks medical attention. The frequency of recurrent attacks is variable ranging from years to hours [1] .

Despite the term “colic”, the pain is usually constant and not colicky. The classic attack is described as an intense dull pressure-like discomfort in the right upper or mid abdomen or in the chest that may radiate to the back and the right shoulder blade [2,3] . The pain classically follows ingestion of a fatty meal (about one to two hours after) and usually does not occur during fasting. However, the pain may be unrelated to meals in a substantial proportion of patients [4] . One group suggested that the pain had a circadian pattern, peaking at 9:30 PM [4,5] . In most cases the pain has a characteristic pattern and timing for individual patients.

The pain is often associated with diaphoresis, nausea and vomiting. It is not exacerbated by movement and not relieved by squatting, bowel movements, or flatus [1] . After the attack, the physical examination is usually normal with the possible exception of residual upper abdominal tenderness.

Although many patients are not symptomatic when they are undergoing medical evaluation, some patients present during an attack of symptoms. In such cases, biliary colic must be distinguished from the more serious complication of acute cholecystitis, which is associated with gallbladder wall inflammation, fever and an elevated white cell blood count. Prolonged or recurrent cystic duct blockage can progress to total obstruction causing acute cholecystitis. An episode of prolonged right upper quadrant pain (greater than four to six hours), especially if associated with fever, should arouse suspicion for acute cholecystitis as opposed to an attack of simple biliary colic. (See “Clinical features and diagnosis of acute cholecystitis”). Other acute abdominal pain diagnoses must also be considered in such patients. (See “Differential diagnosis of abdominal pain in adults”).

PREDICTIVE VALUE OF SYMPTOMS — Multiple studies have evaluated the association of gallstones with symptoms [2,6-14] . A consistent observation has been that the most specific feature pointing toward gallstones as the cause of symptoms was biliary colic. However, up to 80 percent of patients with gallstones referred for cholecystectomy had other abdominal symptoms [8] . At least two systematic reviews have provided estimates of the strength of the association between symptoms and gallstones: One systematic review focused on a total of 24 relevant studies that evaluated the association between seven abdominal symptoms and the presence of gallstones on ultrasonography or oral cholecystography as the reference standard [8] . The presence of biliary colic (diagnostic odds ratio {OR} 2.6, 95 percent CI 2.4 to 2.9), radiating pain (OR 2.8, 95 percent CI 2.2 to 3.7) and use of analgesics (OR 2, 95 percent CI 1.6 to 2.5) were consistently related to the presence of gallstones. However, the magnitude of these associations was notably weak. Similar conclusions were reached in an earlier systematic review that included 21 controlled studies evaluating an association between gallstones and dyspeptic symptoms [7] . Upper abdominal pain was most consistently associated with the presence of gallstones (OR 2.0). A weaker association was found with nausea and vomiting (OR 1.4). In contrast, there was no significant association with other symptoms such as flatulence, heartburn, acid regurgitation, bloating and belching.

A limitation of these studies is that the reference standard chosen was the presence of gallstones on imaging tests. A more clinically relevant reference standard may be whether symptoms were relieved following cholecystectomy, a question that has also been addressed in several reports [10,11,14] .

An illustrative study focused on 92 patients who had undergone cholecystectomy for symptomatic gallstones and were followed for a mean of 31 months [10] . Abdominal pain continued to be present (or arose de novo) in 30 percent of patients. A pain-free outcome was significantly associated with a preoperative diagnosis of biliary colic, fatty food intolerance, and a thick-walled gallbladder on ultrasound.

Interestingly, several other symptoms appeared to be improved after cholecystectomy including abdominal bloating, dyspepsia, heartburn, fat intolerance, nausea and vomiting. However, these observations should not be interpreted as suggesting that gallstones are a possible cause of all these complaints. Relief of symptoms may have been due to the natural history of some of these disorders, a placebo response, or other nonspecific effect of the procedure. Furthermore, it is notable that abdominal symptoms continued or developed in one-third of patients, despite this being a highly selected group of patients whose symptoms had implicated gallstones to an extent that warranted cholecystectomy.

Similar findings were noted in a second study that included 225 patients who had undergone laparoscopic cholecystectomy, 91 percent of whom had biliary pain [11] . Pain was relieved in 82 percent of such patients when stones were documented preoperatively. However, pain was also relieved in 52 percent of patients without gallstones preoperatively (patients thought to have acalculous cholecystitis), in 80 percent of patients with atypical pain, and in 44 percent of patients with non-pain syndromes.

A third report included 2481 patients who had undergone elective cholecystectomy at one of several centers [14] . The mean number of abdominal symptoms per patient decreased significantly. However, 27 percent of patients who had identified a symptom that was most bothersome before surgery, still had that symptom six months after surgery. Symptom persistence rates ranged for 6 percent (for vomiting) to 40 percent (for gas and flatulence). The authors concluded that symptoms categorized as dyspeptic were more likely to persist compared with the more typical biliary symptoms, although the prevalence of all symptoms decreased after cholecystectomy.

Conclusion — In aggregate, these data suggest that in patients with gallstones, no single clinical feature or combination of features confidently predicts that symptoms will be relieved following cholecystectomy. Symptom relief is most likely in patients whose principal symptom is biliary colic. Non-specific atypical symptoms like indigestion, abdominal bloating, and belching, although commonly reported by patients with gallstones, are less likely to be caused by cholelithiasis since they are least likely to disappear after cholecystectomy. As will be discussed below, additional testing has been proposed to better discriminate those with symptoms attributable to gallstones. However, none has been proven to be superior to clinical judgment.

DIAGNOSIS — The diagnosis of uncomplicated gallstone disease should be suspected based upon the clinical features described above (ie, principally biliary colic). Such patients should then undergo evaluation to diagnose the presence of gallbladder stones or sludge.

Gallstone disease is usually considered as part of the differential diagnosis of patients presenting with upper abdominal symptoms. Thus, the decision to implicate the gallbladder has to be made based upon clinical suspicion for a varied group of disorders that include peptic ulcer disease, cardiac chest pain, esophageal chest pain, gastroesophageal reflux disease, nonulcer dyspepsia, irritable bowel syndrome, sphincter of Oddi dyskinesia, hepatitis, and chronic pancreatitis.

It is important to consider that many of these diagnoses are common in the general population and thus may coexist but be unrelated to the gallstones. Thus, a hunting expedition with imaging studies to look for gallstones in patients with nonspecific or atypical symptoms is discouraged. Such patients should be considered to have dyspepsia, and undergo appropriate evaluation and/or treatment based upon the predominant symptoms and suspicion for particular diagnoses. (See “Approach to the patient with dyspepsia”).

As discussed earlier, biliary colic is the most accurate predictor of gallstone disease, but while imaging studies can detect gallstones, there is no clinical or laboratory test that can make the diagnosis of biliary colic. The diagnosis is based upon a meticulous history; questioning should focus on eliciting a history consistent with biliary colic as described above.

Physical examination — Patients with simple biliary colic are not usually ill appearing and do not have fever or tachycardia. The pain is characteristically dull and not severe enough to bring the patient to the emergency department, but, if a patient does present during a pain episode, the abdominal examination is generally benign and non-revealing. There are no peritoneal signs since the pain is purely visceral without gallbladder inflammation. However, voluntary guarding may be encountered depending upon the severity of the pain.

Physical examination can also help distinguish patients with acute cholecystitis. While biliary-type pain is present in both uncomplicated biliary colic and in acute cholecystitis, the pain in uncomplicated biliary colic is entirely visceral in origin since the gallbladder wall is not inflamed. Thus, it is generally less well localized and patients do not exhibit a positive “Murphy” sign on physical examination. A Murphy’s sign is elicited by palpating the area of the gallbladder fossa just beneath the liver edge while the patient is asked to inspire deeply, causing the gallbladder to descend toward the examining fingers. Patients with acute cholecystitis commonly experience increased discomfort and may have an associated inspiratory arrest (a positive Murphy’s sign). (See “Clinical features and diagnosis of acute cholecystitis”).

Laboratory studies — Laboratory studies should be normal in patients with uncomplicated biliary colic both during asymptomatic periods and during attacks of symptoms. However, laboratory studies can be helpful for excluding other diagnoses. Although the choice and order of testing varies depending upon the clinical presentation and suspicion for a particular diagnosis, the following are reasonable screening tests: Liver biochemical tests (serum AST, ALT, total bilirubin, alkaline phosphatase). (See “Approach to the patient with abnormal liver function tests”). Serum amylase and lipase (to evaluate for pancreatitis) Complete blood count (to evaluate for leukocytosis and anemia) Urine analysis

IMAGING STUDIES — Imaging studies are useful for confirming the presence of gallstones or sludge in a patient with a history suggestive of biliary colic. They may also be useful for excluding other diagnoses.

Ultrasonography — Ultrasonography is generally considered to be the most useful test to detect the presence of gallstones since it is non-invasive, readily available, relatively inexpensive, and does not subject the patient to ionizing radiation. As noted above, it should generally be requested in patients suspected of having gallstones based upon a history of biliary colic.

Multiple studies have evaluated test characteristics of ultrasonography in determining the presence of gallstones. A systematic review estimated that the sensitivity was 84 percent (95 percent CI 76 to 99 percent) and specificity was 99 percent (95 percent CI 97 to 100 percent) [15] .

However, it is important to recognize that precise estimates of sensitivity and specificity are difficult to determine since surgical confirmation of a negative sonogram is unlikely. In a study that compared ultrasonography with direct percutaneous mini-endoscopy in patients who had undergone topical gallstone dissolution, ultrasonography was negative in 12 of 13 patients in whom endoscopy demonstrated 1 to 3 mm stones or fragments [16] (show endoscopy 1).

Furthermore, the accuracy of ultrasonography is operator dependent. The ultrasound examination must be conducted with the patient having fasted for at least eight hours, because stones are best seen in a distended gallbladder when they are surrounded with bile. The entire gallbladder must be examined axially and sagittally. Every effort should be made to examine the outlet of the gallbladder (Hartmann’s pouch), where gallstones may be hidden. The gallbladder neck must be traced all the way into the porta hepatis to exclude stones in this region. If an out-pouching from the gallbladder (phrygian cap) is present, the redundant portion of the fundus must not be overlooked.

Even with an experienced operator, it is generally accepted that ultrasound is not highly sensitive for determining the number or size of stones in the gallbladder. This is especially true for very small stones approaching 1 or 2 mm in diameter that frequently, when present in large numbers, can appear on ultrasonography as one large stone.

Characteristics of stones on ultrasound — On ultrasonography, gallstones appear as an echogenic focus that casts an acoustic shadow (show radiograph 1) and seeks gravitational dependency [17,18] :

Two additional ultrasonographic entities that are frequently described are sludge and gravel. Gravel is the appearance of multiple small stones that are echogenic and cast a shadow. Sludge is echogenic in appearance but does not cast an acoustic shadow. It also is more viscous and does not move to the dependent portion of the gallbladder as rapidly as gravel [19,20] . If the gallbladder is totally filled with stones, or if it is contracted around many stones, it may be confused with gas in a partially collapsed duodenal bulb, emphysematous cholecystitis, porcelain gallbladder, or a calcified hepatic artery aneurysm. The ultrasonographer performing the procedure regularly uses specific maneuvers and techniques to identify and distinguish gallstones from some of these other appearances, further underscoring the degree to which ultrasonography is operator dependent.

Gallstones must be distinguished from gallbladder polyps, which can produce similar sonographic images. This is usually done by examining the patient in different positions to demonstrate the movement of stones to the dependent region of the gallbladder. Occasionally, vigorous rolling of the patient or pressure on the gallbladder in sharp jerky movements may be necessary to make the distinction. In addition, stones cast an acoustic shadow while polyps do not. (See “Gallbladder polyps and cholesterolosis”).

Plain abdominal X-ray — Plain abdominal x-rays are generally not useful in looking for gallstones in symptomatic patients. Only about 10 percent of gallstones have enough calcium in their composition to make them sufficiently radio-opaque to be visible on a plain radiograph (show radiograph 2).

Oral cholecystography — Oral cholecystography (OCG), once used commonly to diagnose gallstones and measure gallbladder function, is now used only rarely since it is less sensitive and specific compared with ultrasonography [15,21] . It is still occasionally used in patients in whom a high quality ultrasound examination cannot be obtained (such as in obese patients), to confirm the presence of adenomyomatosis of the gallbladder, and to evaluate patients who are being considered for medical dissolution therapy with ursodeoxycholic acid, in whom it is important to demonstrate stone number and size, relative density of the stones to bile, cystic duct patency and the gallbladder’s concentrating ability. (See “Patient selection for the nonsurgical treatment of gallstone disease”).

OCG is based upon an orally administered contrast agent that is absorbed through the intestine, taken up by the liver, and secreted into bile. Gallstones appear as filling defects within the contrast (show radiograph 3). Several contrast agents have been used; in the United States the most frequently used is iopanoic acid (Telepaque, Winthrop Pharmaceuticals, New York, New York). The standard dose of contrast is 3 grams (six tablets) of Telepaque. If the gallbladder shows no visualization, then a repeat dose of another six tablets is given the next evening and the x-ray examination is repeated the following morning. Other available similar agents are sodium tyropanoate (Bilopaque, Winthrop Pharmaceuticals), and calcium ipodate (Oragraffin, Squibb, Princeton, New Jersey).

False negative results can occur due to poor absorption from the intestine (due to malabsorption syndromes, inflammatory bowel disease, and ileal bypass), diminished liver function (such as in patients with hepatitis or cirrhosis, where the dye may not be adequately conjugated and excreted), or extrahepatic biliary obstruction. It is unlikely that the gallbladder will visualize when the serum bilirubin is greater than 2 to 3 mg/dL.

An approximation of gallbladder motor function can also be obtained if the patient is given a fatty meal following which the decrease in gallbladder size is estimated on serial x-rays. However, this is not recommended in patients who have known gallbladder stones since it may induce biliary colic.

Computed tomography — The sensitivity of computed tomography (CT) for gallstones is poor since most stones are isodense with bile and thus not visible on CT scanning [22,23] . CT can be useful for screening patients in whom medical dissolution therapy is being considered since the presence of calcifications within gallstones (readily apparent on CT) makes it unlikely that such therapy will be successful. (See “Patient selection for the nonsurgical treatment of gallstone disease”)

Cholescintigraphy — Cholescintigraphy has no role in the diagnosis of gallstones but is very useful in excluding acute cholecystitis in patients who present with acute biliary colic. (See “Clinical features and diagnosis of acute cholecystitis”).

APPROACH TO THE PATIENT — As noted above, the approach to the patient can be understood based upon the categorization described above.

Patients with gallstones but no symptoms (category 1) — Patients who are asymptomatic but found to have incidental gallstones on an imaging test should be left alone since the risk of developing life threatening severe complications is arguably less than the likelihood of developing such complications from prophylactic treatment. This recommendation is based upon studies showing that the rate of progression from asymptomatic to symptomatic gallstones is very low (about 1 percent per year). Furthermore, when patients do become symptomatic, the initial presenting symptoms are usually not severe. (See “Approach to the patient with incidental gallstones”).

As a result, patients with incidental gallstones can be educated about potentially concerning symptoms, allowing the uncommon patient destined to develop symptoms to seek treatment before severe complications arise. Thus, prophylactic cholecystectomy is not advised. (See “Approach to the patient with incidental gallstones”)

Patients with biliary symptoms and gallstones (category 2) — In contrast to patients with incidental gallstones, prophylactic treatment should be advised to patients of category 2 who have or had biliary type symptoms (see “Biliary colic” abovesee “Biliary colic” above) or complications (such as cholangitis, pancreatitis, cholecystitis, choledocholithiasis, gallstone ileus and Mirizzi syndrome) clearly related to gallstones, since such patients are likely to have recurrent and more severe symptoms. The National Cooperative Gallstone Study (one of the most definitive studies on the subject) showed that the risk of further symptoms and complications in such patients was approximately 70 percent within two years after initial presentation [24] .

Patients with gallstones but atypical symptoms (category 3) — Atypical symptoms in patients with gallstones (category 3) are unlikely to be caused by the gallstones. Thus, a careful search for other causes of symptoms is prudent. However, symptoms as described by patients are highly subjective and often change. As a result, it is always useful to review the symptoms on more than one occasion to see if any particular patient can be assigned to one of the other categories with the understanding that the less consistent the symptoms are, the higher the likelihood that they will not respond to treating the gallstones.

An empiric trial of oral dissolution therapy with ursodeoxycholic acid is reasonable if other serious illnesses such as cardiac disease or peptic ulcer disease have been excluded and the patient is a candidate for medical gallstone dissolution therapy. (See “Nonsurgical treatment of gallstone disease”). If the symptoms were indeed from the gallstones, ursodeoxycholic acid therapy relieves the symptoms in most patients within three months, long before the stones have dissolved [25] . Thus, a response to therapy may be helpful in guiding further management.

Patients with typical biliary symptoms but without gallstones on ultrasonography (category 4) — Patients in this category have either small stones (microlithiasis) or sludge that were missed on conventional imaging studies or other causes of biliary symptoms unrelated to gallstones such as sphincter of Oddi dysfunction. There is now increasing evidence that sludge can produce symptoms [26-28] and that it represents lithogenic bile containing cholesterol monohydrate crystals, bilirubin granules, and a mucus glycoprotein gel [29] . The conversion of ultrasonographic sludge into macroscopic gallstones has been documented in several studies [30,31] .

It is important to confirm the presence of microlithiasis or sludge in patients of this category because while symptomatic sludge and microlithiasis will respond to cholecystectomy or medical therapy, cholecystectomy may worsen the symptoms of patients with sphincter of Oddi dysfunction [32] .

As noted earlier, ultrasonography may not detect small gallstones or biliary sludge. Sensitivity for small gallstones can be improved upon by repeating the examination at a later time [33] . Further evaluation for microlithiasis can be considered in patients whose repeat ultrasonography is unrevealing.

Microlithiasis, or microcrystalline disease, can cause symptoms and complications similar to those seen with larger gallstones including biliary colic, cholecystitis, cholangitis, obstructive jaundice, and acute pancreatitis [26-28,34,35] . The diagnosis can be established by bile microscopy and endoscopic ultrasonography, which, in patients with typical biliary symptoms, considered as the next step [36] . Both these tests are done through an upper endoscopy, which also serves to exclude other conditions such as peptic ulcer disease.

Bile microscopy — Bile microscopy is regarded as the reference standard for the diagnosis of microlithiasis with an overall sensitivity of 65 to 90 percent [37-41] . The test relies upon the theory that patients with cholesterol microlithiasis have bile that is supersaturated with cholesterol and thus have cholesterol monohydrate crystals (show figure 1) in their gallbladder bile while those with bilirubinate microlithiasis have amorphous reddish-brown bilirubinate granules in their gallbladder (show figure 2) [42,43] . However, the methods of performing the test have not been well standardized leading to a great deal of confusion regarding how to collect and process the bile samples for analysis and what constitutes a positive test.

Most available studies describe the test as it pertains to the detection of microlithiasis in patients with idiopathic recurrent pancreatitis, but even then, no two reports seem to have used the same technique for bile collection, bile processing, or microscopic crystal analysis. Nevertheless, most investigators agree that microcrystals are formed in the gallbladder where bile is concentrated and they produce biliary colic or pancreatitis as they pass through the cystic duct and/or ampulla. Thus, microcrystals should ideally be sought in gallbladder bile; hepatic bile is significantly less concentrated and thus has a lower yield for the detection of microlithiasis [28,38,44] .

Gallbladder bile can be collected using one of the following techniques: Through direct percutaneous puncture of the gallbladder under ultrasound or fluoroscopic guidance During ERCP either through selective gallbladder cannulation or by aspirating bile from the common bile duct after stimulating gallbladder contraction by an infusion of the CCK analogue sincalide During endoscopy during which bile is suctioned from the duodenum around the region of the ampulla after gallbladder stimulation with intravenous cholecystokinin (sincalide), which causes the gallbladder to contract

Collection during endoscopy is the simplest and most practical method. The procedure can be combined with endoscopic ultrasonography (see below) to further increase sensitivity [36,48] . At our center, if the endoscopic ultrasound examination is negative, then while the endoscope is still in the patient sincalide (Kinevac 0.03 microg/kg body weight) is given by intravenous drip over 45 minutes; the longer infusion is safer and more effective than a short bolus technique [45] . The tip of the endoscope is positioned next to the ampulla and the bile is aspirated. Bile flow usually starts to accelerate within five minutes of the start of the CCK infusion. The first 5 to 10 minutes of bile flow is normally light in color representing common bile duct and hepatic bile. Gallbladder bile is the darker bile that starts flowing several minutes later.

The darker bile is collected in a separate collecting tube and kept for analysis. The bile is incubated at 37 degrees C for 24 hours, then centrifuged at 3,000 G for 30 minutes [46] . The supernatant is discarded and the sediment is made to mix into the liquid remaining at the bottom of the tube. A drop of that liquid is placed on a slide and examined using a polarizing microscope; a polarizing filter facilitates identification of cholesterol crystals, which exhibit birefringence (they shine against the dark background of the polarizing microscope). The test is considered positive if any cholesterol crystals or amorphous red brick bilirubinate granules are seen.

The proportion of patients found to have microcrystals has varied substantially in various reports. More recent studies seem to show a lower prevalence of microlithiasis (around 3.5 percent) [47] in patients of clinical category 4 compared to earlier reports in which the prevalence ranged from 33 to 90 percent [38,46] . This is thought to be in part due to the methods used to detect microcrystals and the definition of a positive test.

In earlier prospective studies, investigators inspected a drop of uncentrifuged bile on a slide and the test was considered positive if any cholesterol crystals or amorphous calcium bilirubinate granules were observed. These results correlated well with the presence or absence of gallstones in human subjects [38] . Subsequent studies demonstrated that the sensitivity of the test could be improved significantly if the bile was centrifuged and made to stand overnight at 37 degrees C [46] . While the presence of any cholesterol crystals is theoretically abnormal, to increase specificity, some of the newer reports considered the test to be positive only if more than three crystals were seen per high power field [47] . However, whether findings based upon this approach correlate with clinical outcomes has not been established. As a result, this methodology has not been widely accepted. Furthermore, improved sensitivity of extracorporeal ultrasonography for detection of small stones and sludge has reduced the need for microcrystal analysis, since relatively fewer patients are designated as having typical symptoms without gallstones (ie, clinical category 4).

In initial studies, for example, investigators inspected a drop of uncentrifuged bile on a slide. When any cholesterol crystals or amorphous calcium bilirubinate granules were observed, the test was considered positive; the results correlated well with the presence or absence of gallstones in human subjects [38] . Subsequent studies demonstrated that the sensitivity of the test could be improved significantly if the bile was centrifuged and made to stand overnight at 37 degrees C [46] .

While presence of any cholesterol crystals is theoretically abnormal, specificity can be increased by considering the test positive only if more than three crystals are seen per high power field [47] . This definition has been used in the relatively recent reports, which may explain why they have described a lower prevalence of microlithiasis (around 3.5 percent) in patients in clinical category 4 compared to earlier reports in which the prevalence ranged from 33 to 90 percent.

Endoscopic ultrasonography — Imaging of the gallbladder can be obtained by endoscopic ultrasound (EUS) during which an ultrasound transducer, on the tip of an endoscope, is placed into contact with the gastric antrum, which is in close proximity to the gallbladder, thereby allowing for its visualization without interference from bowel gas, subcutaneous tissue or the liver. As a result, EUS is more sensitive than extracorporeal ultrasonography for the detection of gallstones, particularly in patients who are obese or have other anatomic considerations limiting views with transabdominal ultrasonography [48,49] .

Several studies have demonstrated EUS can be useful for the detection of small stones and microcrystals as illustrated by the following examples: In a study of 45 patients in whom there was a clinical suspicion of cholelithiasis but with at least two normal US examinations, EUS detected evidence of cholelithiasis in 26 patients and was more sensitive than microscopic examination of duodenal bile [48] . In a study of 89 patients with acute pancreatitis, EUS revealed small gallbladder stones (1 to 9 mm) in 14 patients who had otherwise negative standard imaging studies including ultrasonography [49] . Subsequent ERCP and cholecystectomy confirmed the presence of stones in all 14 patients. EUS detected microcrystals in 5 of 15 patients with pancreatitis but a negative ultrasound examination [37] . The sensitivity of EUS combined with bile microscopy in detecting microcrystals was 92 percent in 66 patients with biliary type pain and a negative abdominal ultrasound [36] . Resolution of symptoms after cholecystectomy was noted in 90 of these patients.

Because it is invasive, EUS is generally reserved for patients with biliary colic or suspected complications of gallstones (such as pancreatitis) who have a negative transabdominal ultrasound [36,50] . EUS also has a role in diagnosis of patients with suspected choledocholithiasis. (See “Endoscopic ultrasonography in patients with suspected choledocholithiasis”).

MANAGEMENT — There are two general considerations in the management of uncomplicated gallstone disease. Management of biliary colic Prophylactic treatment to prevent further attacks and/or the development of complications

Biliary colic — The management of acute biliary colic mainly involves pain control. Pain control can usually be achieved with intravenous administration of meperidine, which is preferred to morphine since it has less of an effect on sphincter of Oddi motility [51-53] . Patients should be instructed to remain NPO to prevent the release of cholecystokinin. Those with prolonged attacks (especially if accompanied by vomiting) should also receive intravenous hydration.

If the diagnosis is fairly certain there is increasing evidence that the use of nonsteroidal antiinflammatory drugs (NSAIDs) can produce effective analgesia for biliary colic, and may favorably alter its natural history. The latter benefit may reflect the role of prostaglandins in the development of acute cholecystitis. (See “Clinical features and diagnosis of acute cholecystitis”, section on Pathogenesis).

We use ketorolac (30 to 60 mg adjusted for age and renal function given in a single intramuscular dose) for patients who present to the emergency department with biliary colic. Treatment usually relieves symptoms within 20 to 30 minutes. Patients are then prescribed ibuprofen 400 mg orally to be taken during subsequent attacks, until definitive treatment can be accomplished. In a study comparing ketorolac with meperidine in 324 patients, the two agents were found to be equivalent for pain control but meperidine caused more adverse events mainly in the form of nausea and dizziness [54] .

Prophylactic treatment — When the acute attack of biliary colic subsides, definitive prophylactic therapy should be considered to remove the offending stones to prevent recurrent attacks of biliary colic and the occurrence of more severe complications. Several modalities are available ranging from the surgical removal of the gallbladder to the medical dissolution of the stones while sparing the gallbladder. The choice of the management pathway is generally based upon the patient’s surgical risk and preference.

Cholecystectomy is the most commonly recommended modality. The gallbladder along with its contained stones is removed under general anesthesia. This surgical procedure may be performed through an open right upper quadrant muscle cutting incision or laparoscopically. The latter has become popular since the early 1990s since it eliminates the need to cut the rectus abdominis muscle leading to significantly shortened hospital stay and convalescence.

However, the laparoscopic procedure has been associated with an increased risk of common bile duct injury [54,55] . In addition, the laparoscopic procedure has to be converted to an open procedure in about 10 percent of cases due to a variety of technical or patient issues. Ultimately, the choice of technique is based upon the experience and preference of the surgeon performing the procedure and the medical condition of the patient. (See “Complications of laparoscopic cholecystectomy”).

While removal of the gallbladder is commonly considered to have no lasting physiologic consequences, about 50 percent of patients note more frequent and less formed stools while 10 to 15 percent of patients develop frank diarrhea for which they seek medical attention [6] . An increased risk of right sided colon cancer in patients who have undergone cholecystectomy has also been suggested [56] .

In some cases, surgical removal of the gallbladder may not be feasible, usually because of patient comorbidities. Several nonsurgical techniques for treatment of gallstones have been developed. These include principally medical dissolution therapy with oral bile acids, topical chemical dissolution using solvents to lavage the gallbladder, and extracorporeal shock wave lithotripsy. While the development of laparoscopic cholecystectomy has generally reduced enthusiasm for these approaches, they remain reasonable options in selected patients. (See “Patient selection for the nonsurgical treatment of gallstone disease”).

SUMMARY AND RECOMMENDATIONS — When considering gallstone disease it is helpful to categorize patients into the following clinical categories.

Gallstones but without symptoms — These patients are unlikely to develop symptoms and when they do occur they are generally mild. Thus, patients should be educated about symptoms potentially related to gallstones (principally biliary colic) without recommending specific therapy to address the gallstones. (See “Approach to the patient with incidental gallstones”).

Typical biliary symptoms and gallstones — Such patients should generally undergo treatment (generally cholecystectomy) since they are likely to develop recurrent symptoms, which can be severe. The National Cooperative Gallstone Study (one of the most definitive studies on the subject) showed that the risk of further symptoms and complications in such patients was approximately 70 percent within two years after initial presentation [24] .

Atypical symptoms and gallstones — Such patients should undergo a search for non-gallstone-related causes of symptoms. If investigation is unrevealing, treatment of gallstones can be considered with the understanding that the rate of persistent symptoms is high. (See “Approach to the patient with dyspepsia”).

Typical biliary symptoms but without gallstones — Clinical suspicion for gallstone disease should be maintained in such patients. A repeat extracorporeal ultrasound should be obtained. If results are unrevealing, EUS and collection of duodenal bile for microscopy should be considered. If results continue to be unrevealing, a search for other causes of biliary pain is reasonable.

INFORMATION FOR PATIENTS — Educational materials on this topic are available for patients. (See “Patient information: Gallstones”). We encourage you to print or e-mail this topic review, or to refer patients to our public web site, www.uptodate.com/patients, which includes this and other topics.

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https://somepomed.org/articulos/contents/mobipreview.htm?14/53/15185/abstract/2,3,7-14

“The absence of the gallbladder leads to functional biliary hypertension and increased hepatic and common bile duct . 3-5 years after cholecystectomy increases right and left hepatic ducts equity.

Functional hypertension in the common bile duct contributes to the appearance of functional and hypertension in Wirsung’s pancreatic duct with the development of the phenomena of chronic pancreatitis . At the same time period in some patients this is accompanied by the progression of chronic pancreatitis, sphincter of Oddi dysfunction and duodenogastric (Biliary / bile ) reflux.

Duodenogastric reflux of mixture of bile with pancreatic juice promotes atrophic gastritis in the antral part of stomach.

From 40% to 60% of patients after cholecystectomy dyspeptic suffering from various disorders, from 20% to 40% of pains of different localization .

Up to 70% of patients after cholecystectomy have chronic effects of “bland” cholestasis, chronic cholestatic hepatitis and chronic compensatory bile acid-dependent apoptosis of hepatocytes.

Patients undergoing cholecystectomy had an increased prevalence of metabolic risk factors for cardiovascular disease, including type 2 diabetes mellitus, high blood pressure, and high cholesterol levels.

Part of patients after cholecystectomy with increased concentration of hydrophobic hepatotoxic co-carcinogenic deoxicholic bile acid in serum and/or feces with increased risk of colon cancer”

 “Biliary Diseases Laparoscopic Cholecystectomy. Postcholecystectomy Syndrome Dr. Jacob L. Turumin (Iakov L. Tyuryumin), MD, PhD, DMSci”

  “The incidence of postcholecystectomy syndrome has been reported to be as high as 40% in one study, and the onset of symptoms may range from 2 days to 25 years.  There may also be gender-specific risk factors for developing symptoms after cholecystectomy. In one study, the incidence of recurrent symptoms among female patients was 43%, compared to 28% of male patients.”

 “cholecystectomy is associated with several physiological changes in the upper gastrointestinal tract which may account for the persistence of symptoms or the development of new symptoms after gallbladder removal. The cholecyst sphincter of Oddi reflex, cholecyst-antral reflex, and cholecyst-oesophagal reflexes are all disrupted and some local upper gastrointestinal hormonal changes also occur after cholecystectomy. Thus, there is an increased incidence of gastritis, alkaline duodene gastric reflux and gastro-oesophageal reflux after cholecystectomy, all of which may be the basis for postcholecystectomy symptoms.”

 Postcholecystectomy syndrome (PCS), S. Mohandas, L.M. Almond, Department of General Surgery, Worcestershire Royal Hospital, Worcester, UK

Up to 15-20 % of cholecystectomized patients, continue to have a variety of gastrointestinal symptoms such as fatty food intolerance, nausea and vomiting, heartburn, flatulence, indigestion, diarrhea, mild occasional abdominal pain attacks and severe RUQ pain with extreme post-cholecystectomy distress. The term used to describe this condition is post-cholecystectomy syndrome (PCS). The reported frequency of postcholecystectomypain ranged from 14% to 34% in the reviewed literature, but postoperative dyspepsia was a more frequent symptom that occurred in up to 54% of cholecystectomized patients

It is obvious that irritable bowel syndrome (IBS) may occur after cholecystectomy, and, therefore, dyspeptic symptoms in patients with PCS may be caused by altered gut motility.

Sphincter of Oddi dysfunction (SOD), accounts for 1.5 – 3% of PCS patients

The majority of PCS patients suffered from dyspepsia with mild and occasional pain attacks that caused by functional motility disturbances of the upper gut and the sphincter of Oddi (SO). 2-5% of the PCS patients with continuous severe distress, intense right upper quadrant pain and recurrent cholangitis accounted from all cholecystectomized adults.

PCS symptoms could have several pathophysiological origins. The minority of PCS is caused by an organic disease of the gastrointestinal tract. In a substantial number of patients, no organic disease can be found as a cause of biliary type pain after cholecystectomy. Many patients in whom no organic abnormality can be found suffer from motility disorders of the biliary tract and the upper gut.

 Madacsy L, Dubravcsik Z, Szepes A (2015) Postcholecystectomy Syndrome: From Pathophysiology to Differential Diagnosis – A Critical Review. Pancreat Disord Ther 5:162. doi:10.4172/2165-7092.1000162 https://www.omicsonline.org/open-access/postcholecystectomy-syndrome-from-pathophysiology-to-differentialdiagnosis–a-critical-review-2165-7092-1000162.php?aid=63731

 Patients with cholecystectomy had more comorbidities, particularly chronic fatigue syndrome, fibromyalgia, depression, and anxiety. Postcholecystectomy gastroparesis patients had increased health care utilization and had a worse quality of life.

Cholecystectomy and Clinical Presentations of Gastroparesis, the NIDDK Gastroparesis Clinical Research Consortium (GpCRC)*

 “Cholecystectomy can have nutritional and metabolic consequences in the short-term (diarrhea, abdominal pain and bloating) and in the long-term (increased Body Mass Index with metabolic syndrome, gastritis, liposoluble vitamin deficiency). Pathogenic mechanisms behind these disturbances are reviewed and the need for an early post-operative nutritional intervention based on low-lipid, high-fibers diet, is highlighted. [7]

Altomare DF, Rotelli MT, Palasciano N. Diet after cholecystectomy.  https://doi.org/10.2174/0929867324666170518100053

Cholecystectomy itself is associated with many physiological changes in the upper gastrointestinal tract that may account for the persistence of the symptoms or the development of new symptoms after gallbladder removal. The cholecystosphincter of the Oddi reflex, cholecysto-antral reflex, and cholecyst-esophageal reflexes are all disrupted, and some local upper gastrointestinal hormonal changes often occur after cholecystectomy. Therefore, there is an increased incidence of gastritis, alkaline duodenogastric reflux, and gastro-esophageal reflux after cholecystectomy, which may be the basis for postcholecystectomy symptoms.^18,19,20

Shirah, B. H., Shirah, H. A., Zafar, S. H., & Albeladi, K. B. (2018). Clinical patterns of postcholecystectomy syndrome. Annals of hepato-biliary-pancreatic surgery, 22(1), 52-57. https://dx.doi.org/10.14701%2Fahbps.2018.22.1.52

Source references:

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2. Tsai M-C, Chen C-H, Lee H-C, Lin H-C, Lee C-Z (2015) Increased Risk of Depressive Disorder following Cholecystectomy for Gallstones. PLoS ONE 10(6): e0129962. https://doi.org/10.1371/journal.pone.0129962
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5. Shah Gilani SN1, Bass GA1, Kharytaniuk N2, Downes MR3, Caffrey EF3, Tobbia I3, Walsh TN4. Gastroesophageal Mucosal Injury after Cholecystectomy: An Indication for Surveillance? https://doi.org/10.1016/j.jamcollsurg.2016.12.003
6. Bistritz, L., & Bain, V. G. (2006). Sphincter of Oddi dysfunction: Managing the patient with chronic biliary pain. World Journal of Gastroenterology?: WJG, 12(24), 3793–3802. http://doi.org/10.3748/wjg.v12.i24.3793
7. Donato F. Altomare, Maria T. Rotelli, Nicola Palasciano. Diet After Cholecystectomyhttp://www.eurekaselect.com/node/152535/article
8. Wikipedia, Postcholecystectomy syndrome.  https://en.wikipedia.org/wiki/Postcholecystectomy_syndrome
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13. Girometti, R., Brondani, G., Cereser, L., Como, G., Del Pin, M., Bazzocchi, M., & Zuiani, C. (2010). Post-cholecystectomy syndrome: spectrum of biliary findings at magnetic resonance cholangiopancreatography. [The British Journal of Radiology, 83(988), 351–361]
14. Jacob L. Turumin, Victor A. Shanturov, Helena E. Turumina. Irkutsk Institute of Surgery, Irkutsk Regional Hospital, Irkutsk 664079. The role of the gallbladder in human[ScienceDirect]
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16. Martin, Walton. “RECENT CONTROVERSIAL QUESTIONS IN GALL-BLADDER SURGERY.” Annals of Surgery 79.3 (1924): 424–443. Print. [PMC]
17. The NIDDK Gastroparesis Clinical Research Consortium (GpCRC). “Cholecystectomy and Clinical Presentations of Gastroparesis.” Digestive diseases and sciences 58.4 (2013): 1062–1073. [PMC]
18. Yong Zhang , Hao Liu , Li Li , Min Ai , Zheng Gong, Yong He, Yunlong Dong, Shuanglan Xu, Jun Wang , Bo Jin, Jianping Liu, Zhaowei Teng Cholecystectomy can increase the risk of colorectal cancer: A meta-analysis of 10 cohort studies Published: August 3, 2017 https://doi.org/10.1371/journal.pone.0181852
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