How much alchohol is safe for your liver??

The festive season is nearly here – that means parties, catching up with friends and family, TV, food and drink. But exactly how harmful is over indulging on alcohol at Christmas for your liver and your health generally? And is the damage permanent?

Counting the Alchohol  units

The amount of alcohol in drinks can vary quite widely, and it’s worth looking for versions of your favourite drinks that have less alcohol, which can also be cheaper and often have less calories.

Check the alchohol units from below figures:

Safe daily limits of Alchohol use:

•    Men should drink no more than 21 units of alcohol per week, no more than four units in any one day, and have at least two alcohol-free days a week.

•    Women should drink no more than 14 units of alcohol per week, no more than three units in any one day, and have at least two alcohol-free days a week.

Pregnant women. Advice from the Department of Health states that ... "pregnant women or women trying to conceive should not drink alcohol at all. If they do choose to drink, to minimise the risk to the baby, they should not drink more than 1-2 units of alcohol once or twice a week and should not get drunk". 

Liver turns glucose into fat and store it to use it when needed. Alcohol affects the way the liver handles fat, so your liver cells just get stuffed full of it. This is fatty liver. If it happens, you may feel a vague discomfort in your abdomen because your liver is swollen. You might also feel sick and lose your appetite.

Fortunately, your liver is likely to recover. Fatty liver will go away again in someone who isn’t a heavy drinker because the liver will repair itself.

How alcohol affects the liver

1) When our liver tries to break down alcohol, the resulting chemical reaction can damage its cells. This damage can lead to inflammation and scarring as the liver tries to repair itself.

2). Alcohol can damage our intestine which lets toxins from our gut’s bacteria get into the liver. These toxins can also lead to inflammation and scarring. 

The problem is, you won’t know all this is happening. “People can spend 20 years damaging their liver and feel fine until it gets serious,” says Day. “But two or three heavy sessions a week for a year will increase the chance of liver damage.”

Other health effects of Festival Drinking

Other temporary effects you might have from infrequent heavy drinking sessions include:

•    Damage to your stomach lining which results in diarrhoea or sickness

•    Feeling shaky or anxious because of alcohol’s withdrawal effect on the brain

•    Negative effects on your mood, skin, weight and sleep.

You can usually address these with a return to a healthier lifestyle.  Some health consequences of heavy sessions however can be more severe. People who have had 15 units (about seven and a half pints of 4% beer) or more in one session are vulnerable to something called Holiday Heart Syndrome. This is when high levels of alcohol causes the heart to beat irregularly, which results in shortness of breath, changes in blood pressure and an increase in the risk of a heart attack, and even sudden death.

Longer-term heavy drinking sessions pose serious health problems. Your chances of getting liver, chronic pancreatitis increase.

If you are planning to drink this Christmas and New Year:

•    Stick to the daily unit guidelines and you’ll reduce the chances of negative consequences for your health.

•    Avoid drinking everyday over the Christmas period.

•    Limit the amount of time you spend at certain events that you know will involve heavy drinking.

Be aware of how much you’re drinking if you’re feeling hurt or upset because you could easily damage the relationships you should be celebrating at Christmas time.

If you drink most days of the week, you will increase your risk of developing liver disease.

Evidence about how much and how often you need to drink to increase your chances of developing liver disease is unclear. But all the research shows that the more alcohol you drink, the more likely you are to develop liver disease.

•    Men who drink more than 35 units of alcohol a week for 10 years or more

•    Women who drink more than 28 units of alcohol a week for 10 years or more (4)

Evidence suggests that other factors that increase your risk of developing liver disease include:

•    being dependent on alcohol – around seven in 10 people with alcoholic liver disease have an alcohol dependency problem (5)

•    being female – this could be because women develop higher levels of alcohol in the blood than men even if they’ve drunk the same amount of alcohol (6)

•    being overweight – excess weight can exacerbate many of the mechanisms of liver damage caused by excessive drinking (7)

•    genetics – certain genetic factors, including those affecting the liver’s handling of fat, influence the risk of a heavy drinker developing liver disease.

Excessive drinking can make your liver get fat – reducing your consumption can help it return to its normal size

Drink more than eight units a day (four pints of 4% lager) if you’re a man and over five units a day (a couple of 175ml glasses of wine) if you’re a woman, for two or three weeks and you’re likely to develop something called 'fatty liver’.

The liver turns glucose into fat which it sends round the body to store for use when we need it. Alcohol affects the way the liver handles fat so your liver cells get stuffed full of it.

If this happens, you may feel a vague discomfort in your abdomen because your liver is swollen. You might also feel sick and lose your appetite. A blood test may be able to show if you have fatty liver.

The good news: your liver will start shedding the excess fat if you stop drinking for two weeks and don’t exceed the lower risk guidelines after that. If you don’t change your drinking pattern, the bad news is that fatty liver is the first stage of liver disease.

The four stages of liver disease: Identifying the symptoms

People can spend 20 years damaging their liver and not feel any of the effects this is doing to them. This is because the liver has enormous reserves so that you can damage an awful lot of it and it can still do all of its jobs.

Early symptoms of liver disease can include:

•    fatigue

•    nausea

•    vomiting

•    diarrhoea

•    abdominal pains 

Later stage liver damage symptoms are more serious – and you’ll know about them.

They can include:

•    jaundice (yellow skin)

•    vomiting blood

•    fatigue

•    weakness, loss of appetite

•    itching

•    easy bruising

•    swelling of the legs ankles, or abdomen

•    liver cancer

•    bleeding in the gut

•    increased sensitivity to alcohol and drugs, both medical and recreational (because the liver cannot process them) (9) (10)

When you develop cirrhosis, cutting out alcohol is essential to prevent you from dying from liver failure which is when your liver stops working completely. In the most serious cases of cirrhosis, you will only be considered for a liver transplant if you do not drink alcohol for at least three months.

Are you suffering from recurrent attacks of pancreatitis?? What are the rare causes?? And what is Repeated attacks of pancreatitis without any cause ? (IDIOPATHIC RECURRENT PANCREATITIS)

Recurrent Attack of Pancreatitis from Unknown cause :

Acute pancreatitis is an inflammatory process of the pancreas that can affect peripancreatic tissues and distant sites. An cause can be found in most patients after an attack of acute pancreatitis, with gallstone disease and alcohol abuse most often implicated. When patients have more than one clinical episode of acute pancreatitis they are given the diagnosis of acute recurrent pancreatitis (ARP). Most causes of acute pancreatitis can lead to recurrent disease if the underlying factor remains uncorrected.

The cause of recurrent pancreatitis is found in 70–90% of patients after an initial evaluation, which includes a thorough history, physical exam, routine labs, and transabdominal ultrasound or CT. In the 10–30% of patients in whom the initial evaluation fails to reveal an etiology, the diagnosis of idiopathic ARP (IARP) is applied. The extent of the evaluation impacts the frequency with which an etiology can be found, and in turn how often the label idiopathic can be applied. Evaluation and therapy is important because >50% of untreated patients experience recurrent episodes that may lead to chronic pancreatitis.

Initital evaluation of acute recurrent pancreatitis:

Acute pancreatitis is diagnosed in the proper clinical setting with the aid of laboratory values and imaging studies. Patients may present with acute epigastric pain, nausea, vomiting, fever, and tachycardia. Laboratory analysis usually reveals elevated pancreatic enzymes and leukocytosis. Abdominal ultrasound and CT help support the diagnosis and exclude other causes. After confirmation of the presence of acute pancreatitis, the focus shifts to determining the etiology. The initial evaluation includes a search for evidence of alcohol abuse, drug-induced pancreatitis, and a family history of pancreatitis, and other clues that may suggest the origin.

The serum amylase level is used to help establish the diagnosis of pancreatitis and may be predictive of the underlying pathology. Pancreatitis resulting from gallstones, microlithiasis (small stones), or drugs is typically associated with a greater elevation in amylase than lipase . The amylase level, as compared to lipase, tends to be lower in alcoholic pancreatitis, hypertriglyceridemia-induced pancreatitis, neoplasia, and chronic pancreatitis . Lipase elevation is more specific for pancreatitis than amylase, and the level remains elevated longer, but the level is not predictive of the etiology. The ratio of lipase to amylase may help distinguish alcoholic from nonalcoholic pancreatitis, with an increased ratio suggesting alcohol-induced disease. Of note, the amylase and lipase levels do not correlate with disease severity and they are not useful for determining prognosis.

Liver function tests are routinely measured and may be elevated because of biliary obstruction resulting from gallstones, microlithiasis, a choledochocele, neoplasia of the ampulla or pancreas, or sphincter of Oddi dysfunction (SOD). Liver function tests may also increase as a result of pancreatic head edema, inflammation, or pseudocyst formation. A 3-fold or greater increase in the Liver enzyme level is generally regarded as the best indicator of gallstone-induced pancreatitis. One study, however, noted that the best indicator of bile duct stones is a serum total bilirubin > 1.35 mg/dl on the second day of hospitalization . Although it is unclear which laboratory parameter is the most predictive, both may be used to help assess the presence of gallstone-induced pancreatitis in an individual patient. Metabolic causes of pancreatitis should be excluded by checking the serum calcium and triglyceride levels. These values should be measured soon after admission, or well after resolution of the pancreatitis, because of the drop in calcium and triglyceride levels that can occur during hospitalization.

Transabdominal ultrasound is a simple, inexpensive, and highly sensitive procedure for evaluating the biliary tract . CT more accurately delineates the pancreas and may also help identify the cause, assess the severity, and detect complications of pancreatitis . Some recommend performing CT only when the first attack is severe, when the course is complicated, or in the elderly. Patients not scanned during the first episode are generally scanned with their second attack regardless of age or disease severity. However, I believe that the yield is great enough to justify a CT in all patients during their first episode.

The extent of evaluation required before conferring the diagnosis of Idiopathic Acute Recurrent Pancreatitis varies among studies. The purist would demand a complete and exhaustive workup before diagnosis. However, most use this diagnosis when a more limited evaluation, as detailed above, fails to reveal an etiology. A more extensive evaluation may include specialized labs, ERCP, endoscopic ultrasound (EUS), and magnetic resonance cholangiopancreatography (MRCP). This additional workup usually leads to the diagnosis of microlithiasis, SOD, or pancreas divisum . Other causes such as hereditary pancreatitis , cystic fibrosis , a choledochocele , annular pancreas , an anomalous pancreatobiliary junction , pancreatobiliary tumors , and chronic pancreatitis may be found as well. When this more extensive evaluation fails to reveal an etiology, then the diagnosis of "true" Idiopathic (without any cause) recurrent pancreatitis may be assigned.

Rare causes of Recurrent Pancreatitis:

1.Microlethiasis:

Although technically different, the terms microlithiasis and biliary sludge are often used interchangeably. Microlithiasis refers to stones of <3 mm in diameter, whereas biliary sludge is a suspension of crystals, mucin, glycoproteins, cellular debris, and proteinaceous material.

The optimum method of detecting microlithiasis is yet to be established. Transabdominal ultrasound is a noninvasive study with a sensitivity of about 50%. However, repeat examination may improve the yield. Duodenal bile aspiration is an invasive procedure that has a sensitivity of about 66%. ERCP is more invasive, but has a sensitivity of about 85%. During ERCP, the common bile duct is directly aspirated for bile. Cholecystokinin is commonly administered before duodenal drainage or ERCP, to enhance gallbladder contractility and improve the yield. In most centers, collected bile is centrifuged at 2000 revolutions/min for 10 min; the sediment is warmed to 37°C and then examined by polarized microscopy. The quantity of crystals needed to define a positive result differs among institutions, but most believe that the presence of even a small number of crystals is abnormal. EUS is increasingly being used because it offers the greatest diagnostic sensitivity. The presence of microlithiasis may also be noted at the time of MRCP.

Therapy for microlithiasis can significantly reduce the risk of recurrent pancreatitis. Several therapeutic options exist for microlithiasis. Laparoscopic cholecystectomy is nearly always curative and generally considered the procedure of choice . ERCP with sphincterotomy (incision of the bile duct sphincter) is indicated in high operative risk patients. A low-fat diet and ursodeoxycholic acid are acceptable alternatives in high surgical risk patients; however, long term therapy is required.

Sphincter of oddi dysfunction:(SOD)

The sphincter of Oddi is a 5- to 15-mm-long fibromuscular sheath that encircles the terminal common bile duct, pancreatic duct, and common channel. This sphincter regulates the flow of bile and pancreatic juice into the Intestine.

SOD is a frequent and treatable cause of IARP and is seen in roughly one third of these patients.

Patients with SOD are classified as having either biliary type or pancreatic type disease.

Sphincter of Oddi manometry (SOM) is the gold standard for diagnosing SOD. SOM employs a water-perfused catheter system, which is inserted endoscopically into the common bile duct or pancreatic duct, to measure the sphincter pressure.

Noninvasive therapies for SOD include a low-fat diet, analgesics, anticholinergics, calcium channel blockers, and nitrates. Although these noninvasive therapies may help a minority of patients, most believe them to be of limited utility in the management of SOD. Invasive therapies include endoscopic sphincterotomy, pancreatic duct stent placement, and surgical sphincteroplasty. Intrasphincteric botulinum toxin or nitric oxide injection and balloon dilation are no longer performed because they have a limited efficacy and frequent, often severe complications.

The use of pancreatic duct stenting for SOD has not been well studied, and available results have been disappointing. Stent placement may offer short term relief of symptoms and help to predict those most likely to benefit from endoscopic sphincterotomy. However, because of its lack of long-term efficacy and high rate of complications, pancreatic duct stent therapy is not recommended for these patients.

Endoscopic sphincterotomy is the therapy of choice and is believed to decrease the risk of recurrent pancreatitis. Biliary sphincterotomy effectively reduces the pancreatic sphincter pressure and leads to clinical improvement in roughly 80% of patients.

Pancreas divisum:

Pancreas divisum is the most common congenital malformation of the pancreas, effecting 5–8% of the population.

Although it is controversial, most hold the belief that pancreas divisum is a common cause of IARP and is implicated in about 20% of patients. The diagnosis is suspected during ERCP, when injection of contrast media into the major papilla reveals an absent or small ventral pancreatic duct . The diagnosis is confirmed by minor papilla injection, which usually demonstrates a lack of communication between the dorsal and ventral ducts. However, at times the ventral and dorsal ducts do communicate via a thin filamentous channel (incomplete pancreas divisum). The clinical presentation and response to therapy for "incomplete" and "complete" pancreas divisum are identical. EUS or MRCP may also make the diagnosis.

Endoscopic and surgical therapies decrease the rate of recurrent pancreatitis in 70–90% of patients with pancreas divisum and IARP when followed for up to 5 yr. Treatment is directed toward relieving outflow obstruction at the level of the minor papilla. Endoscopic therapy is generally favored, with surgery reserved for those in whom endoscopic approaches fail.

Hereditary (familial) pancreatitis:

Hereditary pancreatitis is a genetic disorder with an autosomal dominant means of transmission and an estimated 80% penetrance . There is no gender predominance, and symptoms typically arise in childhood but may be delayed until the mid-30s.

Hereditary (familial) pancreatitis

Hereditary pancreatitis is a genetic disorder with an autosomal dominant means of transmission and an estimated 80% penetrance. There is no gender predominance, and symptoms typically arise in childhood but may be delayed until the mid-30s.

Therapy does not differ from other causes of acute and chronic pancreatitis, nor does the management of complications. Endoscopic clearance of pancreatic duct stones and surgical pancreatic decompression (pancreaticojejunostomy with anastomosis of the pancreatic duct to the jejunum) may be beneficial.

Cystic fibrosis

Cystic fibrosis is a genetic disease with an autosomal recessive means of transmission and is the most common disorder affecting the exocrine pancreas.

Therapy does not differ from that for other causes of acute and chronic pancreatitis.

Choledochocele

Cystic dilation may occur throughout the biliary system and can involve the extrahepatic and/or intrahepatic bile ducts. Todani et al. , based on the location, first classified these cysts into five types. A type III cyst, or choledochocele, is a rare congenital or acquired condition in which the intramural segment of the distal pancreatobiliary ductal system is dilated and herniates into the duodenal lumen. They vary in size from a few millimeters to several centimeters.

Although abnormal laboratory values, transabdominal ultrasound, CT, or MRCP may suggest a choledochocele, the diagnosis is usually confirmed by ERCP.

Anomalous pancreatobiliary junction

The sphincter does not separate the bile and pancreatic ducts, and therefore pancreatic and bile juices may freely flow between ducts and lead to pancreatitis.

ERCP and injection of the major papilla reveal the long common channel and simultaneous filling of the bile duct and pancreatic duct. EUS or MRCP may also establish the diagnosis. Sphincter ablation by endoscopic sphincterotomy encourages normal flow of bile and pancreatic juice and may decrease the risk of recurrent pancreatitis.

Annular pancreas

Annular pancreas is a congenital anomaly that manifests as a band of pancreatic tissue partially or completely encircling the duodenum, usually at the level of or just proximal to the major papilla.

ERCP typically identifies the duct of the pancreatic annulus encircling the duodenum

Gastrojejunostomy (resection of the lesion with anastomosis of the jejunum and stomach) may be required to bypass the segment of obstructed bowel.

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Pancreatobiliary tumors

Five to seven percent of patients with pancreatobiliary tumors, benign or malignant, present with IARP. The presence of a neoplasia may be suggested by significant weight loss, steatorrhea, radiological evidence of a solid or cystic pancreatic mass or ductal dilation, and increased age. Although younger patients less commonly have a neoplasia, they are frequently affected by lesions such as islet cell tumors that are often amenable to curative resection. Even the elderly may have potential curable lesions such as cystic neoplasms. Although pancreatic adenocarcinoma is most often implicated, these other tumors must be considered as well.

CT, magnetic resonance imaging (MRI), ERCP, and EUS are all useful for identifying pancreatobiliary neoplasms. CT imaging may be adequate to evaluate patients <40 yr of age with IARP. ERCP is usually performed, in addition to CT, in patients over 40 yr because of the increased risk of malignancy. EUS is quickly becoming a favored procedure because of the ability to diagnose, stage, and biopsy pancreatobiliary tumors. In fact, most studies have found EUS to have the highest sensitivity for identifying pancreatic neoplasm relative to other imaging modalities, especially for tumors < 2–3 cm in diameter. The diagnosis may be confirmed by CT-guided biopsy, ERCP-directed brush cytology, or EUS-guided fine needle aspiration.

rent pancreatitis

All patients with ARP should undergo an initial evaluation, which includes a thorough history, routine labs, and imaging studies. When this workup fails to reveal an etiology, then a patient can be given the diagnosis of IARP and a more extensive evaluation is indicated.

Advanced laboratory analysis for patients < 40 yr of age may include an -1-antitrypsin phenotype, CFTR gene analysis, a sweat chloride test, trypsin gene studies, and duodenal aspiration for microcrystals. The level of the tumor marker, CA 19-9, should be measured in patients > 40 yr of age. The role of genetic testing for hereditary pancreatitis and cystic fibrosis, outside of a research setting, is unclear. One can argue a need for testing because of the comfort a patient receives in knowing the diagnosis and because of the potential impact on family planning. Diagnosing hereditary pancreatitis may also be important because of the potential influence on pancreatic cancer screening. However, the need for an ideal method of screening these patients are disputed. Others may argue that it is currently premature to recommend routine genetic testing because of inadequacies in genetic analysis and the absence of established guidelines for genetic counseling. Also, there are no unique endoscopic or surgical approaches for the management of hereditary pancreatitis or cystic fibrosis versus other forms of acute and chronic pancreatitis. Therefore, genetic testing currently has negligible influence on clinical management. We recommend that when genetic testing is not employed, a physician keep a registry of patients suspected of having either disorder, so that they may benefit from newly discovered medications and gene therapy.

ERCP reveals a diagnosis in about 70% of patients with IARP after a negative initial evaluation. Because the initial episode of pancreatitis may be an isolated event and because of the risk of ERCP, most agree that this procedure is not justified after the first episode of pancreatitis. Many believe, however, that ERCP is indicated when the first episode is severe or when a patient has two or more episodes. However, there are some who advocate performing an ERCP after the first episode regardless of the patient's age or disease severity. At the time of the ERCP, bile is aspirated and examined for microcrystals, SOM is performed when SOD is suspected, and the minor papilla is cannulated when pancreas divisum is suspected.

Management:

Episodes of acute pancreatitis are treated similarly regardless of the etiology. Intravenous fluids are given, oral intake is withheld, metabolic and electrolyte disturbances are corrected, analgesics are administered, and respiratory, renal, and vascular complications are treated as necessary. Specific therapy for given disorders, when available, should be managed as outlined earlier.

Therapeutic options for patients with TIARP are limited, and little information exists regarding their care. Several centers have reported favorable results with the use of pancreatic duct stents or endoscopic sphincterotomy (biliary or pancreatic) in patients with TIARP.

Conclusion :

ARP may be caused by a number of disorders. Often, our greatest challenge is to establish the correct diagnosis in those patients without a history of gallstone disease or alcohol abuse. In the 10–30% of patients with "idiopathic" acute recurrent pancreatitis, the use of specialized laboratory analysis, ERCP, EUS (ENDOSCOPIC ULTRASOUND), and MRCP may lead to the diagnosis. These procedures may be used not only to establish the correct diagnosis, but also to direct therapy and often improve a patient's long term prognosis.

HOW TO DIAGNOSE AND MANAGE ACUTE PANCREATITIS: GUIDELINES BY International Association of Pancreatology, and American Pancreatic Association.

HOW TO DIAGNOSE AND MANAGE ACUTE PANCREATITIS: GUIDELINES BY International Association of Pancreatology, and American Pancreatic Association.

Summary of recommendations

A. Diagnosis of acute pancreatitis and etiology

1. The definition of acute pancreatitis is based on the fulfillment of ‘2 out of 3’ of the following criteria: clinical (upper abdominal pain), laboratory (serum amylase or lipase

>3x upper limit of normal) and/or imaging (CT, MRI, ultrasonography) criteria.(GRADE 1B, strong agreement)

2. On admission, the etiology of acute pancreatitis should be determined using detailed personal (i.e. previous acute pancreatitis, known gallstone disease, alcohol intake,

medication and drug intake, known hyperlipidemia, trauma, recent invasive procedures such as ERCP) and family history of pancreatic disease, physical examination,

laboratory serum tests (i.e. liver enzymes, calcium, triglycerides), and imaging (i.e. right upper quadrant ultrasonography).(GRADE 1B, strong agreement)

3. In patients considered to have idiopathic acute pancreatitis, after negative routine work-up for biliary etiology, endoscopic ultrasonography (EUS) is recommended as

the first step to assess for occult microlithiasis, neoplasms and chronic pancreatitis. If EUS is negative, (secretin-stimulated) MRCP is advised as a second step to identify

rare morphologic abnormalities. CT of the abdomen should be performed. If etiology remains unidentified, especially after a second attack of idiopathic pancreatitis,

genetic counseling (not necessarily genetic testing) should be considered.(GRADE 2C, weak agreement)

B. Prognostication/prediction of severity

4. Systemic inflammatory response syndrome (SIRS) is advised to predict severe acute pancreatitis at admission and persistent SIRS at 48 hours.(GRADE 2B, weak

agreement)

5. During admission, a 3-dimension approach is advised to predict outcome of acute pancreatitis combining host risk factors (e.g. age, co-morbidity, body mass index),

clinical risk stratification (e.g. persistent SIRS) and monitoring response to initial therapy (e.g. persistent SIRS, blood urea nitrogen, creatinine).(GRADE 2B, strong

agreement)

C. Imaging

6. The indication for initial CT assessment in acute pancreatitis can be: 1) diagnostic uncertainty, 2) confirmation of severity based on clinical predictors of severe acute

pancreatitis, or 3) failure to respond to conservative treatment or in the setting of clinical deterioration. Optimal timing for initial CT assessment is at least 72e96 hours

after onset of symptoms.(GRADE 1C, strong agreement)

7. Follow up CT or MR in acute pancreatitis is indicated when there is a lack of clinical improvement, clinical deterioration, or especially when invasive intervention is

considered.(GRADE 1C, strong agreement)

8. It is recommended to perform multidetector CT with thin collimation and slice thickness (i.e. 5mm or less), 100e150 ml of non-ionic intra-venous contrast material at a

rate of 3mL/s, during the pancreatic and/or portal venous phase (i.e. 50e70 seconds delay). During follow up only a portal venous phase (monophasic) is generally

sufficient. For MR, the recommendation is to perform axial FS-T2 and FS-T1 scanning before and after intravenous gadolinium contrast administration.(GRADE 1C,

strong agreement)

D. Fluid therapy

9. Ringer’s lactate is recommended for initial fluid resuscitation in acute pancreatitis.(GRADE 1B, strong agreement)

10a. Goal directed intravenous fluid therapy with 5e10 ml/kg/h should be used initially until resuscitation goals (see Q10b) are reached.(GRADE 1B, weak agreement)

10b. The preferred approach to assessing the response to fluid resuscitation should be based on one or more of the following: 1) non-invasive clinical targets of heart rate <

120/min, mean arterial pressure between 65-85 mmHg (8.7e11.3 kPa), and urinary output > 0.5e1ml/kg/h, 2) invasive clinical targets of stroke volume variation, and

intrathoracic blood volume determination, and 3) biochemical targets of hematocrit 35-44%.(GRADE 2B, weak agreement)

E. Intensive care management

11. Patients diagnosed with acute pancreatitis and one or more of the parameters identified at admission as defined by the guidelines of the Society of Critical Care

Medicine (SCCM). Furthermore, patients with severe acute pancreatitis as defined by the revised Atlanta Classification (i.e. persistent organ failure) should be treated in

an intensive care setting.(GRADE 1C, strong agreement)

12. Management in, or referral to, a specialist center is necessary for patients with severe acute pancreatitis and for those who may need interventional radiologic,

endoscopic, or surgical intervention.(GRADE 1C, strong agreement)

13. A specialist center in the management of acute pancreatitis is defined as a high volume center with up-to-date intensive care facilities including options for organ

replacement therapy, and with daily (i.e. 7 days per week) access to interventional radiology, interventional endoscopy with EUS and ERCP assistance as well as surgical

expertise in managing necrotizing pancreatitis. Patients should be enrolled in prospective audits for quality control issues and into clinical trials whenever

possible.(GRADE 2C, weak agreement)

14. Early fluid resuscitation within the first 24 hours of admission for acute pancreatitis is associated with decreased rates of persistent SIRS and organ failure.(GRADE 1C,

strong agreement)

15. Abdominal compartment syndrome (ACS) is defined as a sustained intra-abdominal pressure > 20 mmHg that is associated with new onset organ failure.(GRADE 2B,

strong agreement)

16. Medical treatment of ACS should target 1) hollow-viscera volume, 2) intra/extra vascular fluid and 3) abdominal wall expansion. Invasive treatment should only be

used after multidisciplinary discussion in patients with a sustained intra-abdominal pressure >25mmHg with new onset organ failure refractory to medical therapy and

nasogastric/ rectal decompression. Invasive treatment options include percutaneous catheter drainage of ascites, midline laparostomy, bilateral subcostal laparostomy,

or subcutaneous linea alba fasciotomy. In case of surgical decompression, the retroperitoneal cavity and the omental bursa should be left intact to reduce the risk of

infecting peripancreatic and pancreatic necrosis.(GRADE 2C, strong agreement)

F. Preventing infectious complications

17. Intravenous antibiotic prophylaxis is not recommended for the prevention of infectious complications in acute pancreatitis.(GRADE 1B, strong agreement)

18. Selective gut decontamination has shown some benefits in preventing infectious complications in acute pancreatitis, but further studies are needed.(GRADE 2B, weak

agreement)

19. Probiotic prophylaxis is not recommended for the prevention of infectious complications in acute pancreatitis.(GRADE 1B, strong agreement)

G. Nutritional support

20. Oral feeding in predicted mild pancreatitis can be restarted once abdominal pain is decreasing and inflammatory markers are improving.(GRADE 2B, strong agreement)

21. Enteral tube feeding should be the primary therapy in patients with predicted severe acute pancreatitis who require nutritional support.(GRADE 1B, strong agreement)

22. Either elemental or polymeric enteral nutrition formulations can be used in acute pancreatitis.(GRADE 2B, strong agreement)

23. Enteral nutrition in acute pancreatitis can be administered via either the nasojejunal or nasogastric route.(GRADE 2A, strong agreement)

24. Parenteral nutrition can be administered in acute pancreatitis as second-line therapy if nasojejunal tube feeding is not tolerated and nutritional support is

required.(GRADE 2C, strong agreement)

H. Biliary tract management

25. ERCP is not indicated in predicted mild biliary pancreatitis without cholangitis.(GRADE 1A, strong agreement). ERCP is probably not indicated in predicted severe

biliary pancreatitis without cholangitis (GRADE 1B, strong agreement). ERCP is probably indicated in biliary pancreatitis with common bile duct obstruction (GRADE 1C,

strong agreement) ERCP is indicated in patients with biliary pancreatitis and cholangitis (GRADE 1B, strong agreement)

26. Urgent ERCP (<24 hrs) is required in patients with acute cholangitis. Currently, there is no evidence regarding the optimal timing of ERCP in patients with biliary

pancreatitis without cholangitis.(GRADE 2C, strong agreement)

27. MRCP and EUS may prevent a proportion of ERCPs that would otherwise be performed for suspected common bile duct stones in patients with biliary pancreatitis who

do not have cholangitis, without influencing the clinical course. EUS is superior to MRCP in excluding the presence of small (<5mm) gallstones. MRCP is less invasive,

less operator-dependent and probably more widely available than EUS. Therefore, in clinical practice there is no clear superiority for either MRCP or EUS.(GRADE 2C,

strong agreement)

I. Indications for intervention in necrotizing pancreatitis

28. Common indications for intervention (either radiological, endoscopical or surgical) in necrotizing pancreatitis are: 1) Clinical suspicion of, or documented infected

necrotizing pancreatitis with clinical deterioration, preferably when the necrosis has become walled-off, 2) In the absence of documented infected necrotizing

pancreatitis, ongoing organ failure for several weeks after the onset of acute pancreatitis, preferably when the necrosis has become walled-off.(GRADE 1C, strong

agreement)

29. Routine percutaneous fine needle aspiration of peripancreatic collections to detect bacteria is not indicated, because clinical signs (i.e. persistent fever, increasing

inflammatory markers) and imaging signs (i.e. gas in peripancreatic collections) are accurate predictors of infected necrosis in the majority of patients. Although the

diagnosis of infection can be confirmed by fine needle aspiration (FNA), there is a risk of false-negative results.(GRADE 1C, strong agreement)

30. Indications for intervention (either radiological, endoscopical or surgical) in sterile necrotizing pancreatitis are: 1) Ongoing gastric outlet, intestinal, or biliary

obstruction due to mass effect of walled-off necrosis (i.e. arbitrarily >4-8 weeks after onset of acute pancreatitis), 2) Persistent symptoms (e.g. pain, ‘persistent

unwellness’) in patients with walled-off necrosis without signs of infection (i.e. arbitrarily >8 weeks after onset of acute pancreatitis), 3) Disconnected duct syndrome

(i.e. full transection of the pancreatic duct in the presence of pancreatic necrosis) with persisting symptomatic (e.g. pain, obstruction) collection(s) with necrosis without

signs of infections (i.e. arbitrarily >8 weeks after onset of acute pancreatitis).(GRADE 2C, strong agreement)

J. Timing of intervention in necrotizing pancreatitis

31. For patients with proven or suspected infected necrotizing pancreatitis, invasive intervention (i.e. percutaneous catheter drainage, endoscopic transluminal drainage/

necrosectomy, minimally invasive or open necrosectomy) should be delayed where possible until at least 4 weeks after initial presentation to allow the collection to

become ‘walled-off’.(GRADE 1C, strong agreement)

32. The best available evidence suggests that surgical necrosectomy should ideally be delayed until collections have become walled-off, typically 4 weeks after the onset of

pancreatitis, in all patients with complications of necrosis. No subgroups have been identified that might benefit from earlier or delayed intervention.(GRADE 1C, strong

agreement)

K. Intervention strategies in necrotizing pancreatitis

33. The optimal interventional strategy for patients with suspected or confirmed infected necrotizing pancreatitis is initial image-guided percutaneous (retroperitoneal)

catheter drainage or endoscopic transluminal drainage, followed, if necessary, by endoscopic or surgical necrosectomy.(GRADE 1A, strong agreement)

34. Percutaneous catheter or endoscopic transmural drainage should be the first step in the treatment of patients with suspected or confirmed (walled-off) infected

necrotizing pancreatitis.(GRADE 1A, strong agreement)

35. There are insufficient data to define subgroups of patients with suspected or confirmed infected necrotizing pancreatitis who would benefit from a different treatment

strategy.(GRADE 2C, strong agreement)

L. Timing of cholecystectomy (or endoscopic sphincterotomy)

36. Cholecystectomy during index admission for mild biliary pancreatitis appears safe and is recommended. Interval cholecystectomy after mild biliary pancreatitis is

associated with a substantial risk of readmission for recurrent biliary events, especially recurrent biliary pancreatitis.(GRADE 1C, strong agreement)

37. Cholecystectomy should be delayed in patients with peripancreatic collections until the collections either resolve or if they persist beyond 6 weeks, at which time

cholecystectomy can be performed safely.(GRADE 2C, strong agreement)

38. In patients with biliary pancreatitis who have undergone sphincterotomy and are fit for surgery, cholecystectomy is advised, because ERCP and sphincterotomy

prevent recurrence of biliary pancreatitis but not gallstone related gallbladder disease, i.e. biliary colic and cholecystitis.(GRADE 2B, strong agreement)