Severe pancreatitis, evidence of ductal stones, cholangitis, no response to treatment within 48 hours.
Normal pancreatic juice is a colorless, bicarbonate-rich fluid (pH ~8.0) that contains around 15 g of protein and approximately ~2.5 liters are secreted per day.
Haemorrhagic spots and ecchymosis in the flanks (Grey-Turner's sign) and discolouration around the umbilicus (Cullen's sign) due to enzymes seeping across the retroperitoneum.
Avoid alcohol, stop all offending medication, and control hyperlipidemia.
They activate pancreatic enzymes, leading to acute pancreatitis.
Hypovolemia due to diffuse capillary leak and vomiting causing raised haematocrit, blood urea, serum creatinine levels, and hypoalbuminaemia revealed after fluid correction.
40% within 6 weeks.
Pancreatic calcification, steatorrhoea, and diabetes mellitus.
The main intestinal phase is mediated by the release of secretin due to duodenal acidification, and by the release of bile and cholecystokinin following the entry of fat and proteins in the duodenum.
Approximately 33% of patients with gallstone pancreatitis will experience a recurrence within 8 weeks.
An acute pseudocyst is a collection of fluid with pancreatic juice in or near the pancreas localized by a thin fibrin wall or granulation tissue. It usually resolves spontaneously.
P isoenzyme estimation is more relevant because it is more specific to the pancreas and is estimated with urinary amylase and serum lipase for better sensitivity.
IV ranitidine 50 mg 6th hourly, IV omeprazole 40 mg BD, or IV pantoprazole 80 mg BD.
It utilizes platelets and causes disseminated intravascular coagulation (DIC).
Intra-abdominal hemorrhage and pseudocyst.
Diarrhea, asthenia, loss of weight and appetite, steatorrhoea, and malabsorption.
The most common congenital anomaly of the pancreas (3-10%) due to the absence of fusion between the dorsal and ventral duct systems during the 6th week of development.
Open surgery is the gold standard for infected pancreatic necrosis.
End stage with pancreatic fibrosis leading to loss of clinical exocrine and/or endocrine function, such as steatorrhoea and/or diabetes mellitus. Complications may or may not be present.
It is used for Ranson and Glasgow scoring systems.
Pancreatic pseudocysts usually form 4 weeks after an attack of acute pancreatitis.
100%.
Pain is due to irritation of retro pancreatic nerves, ductal dilatation and stasis, or chronic inflammation.
Stone in the biliary tree, autoimmune pancreatitis, idiopathic causes (20%), metabolic conditions (hypercalcaemia, hypertriglyceridemia, hyperparathyroidism), drugs (steroids, azathioprine), trauma, genetic factors (cystic fibrosis), hereditary factors (familial hereditary pancreatitis), and congenital anomalies (sphincter of Oddi dysfunction, pancreas divisum).
The cephalic phase is triggered by the sight, smell, or thought of food and is mediated by acetylcholine.
Serum calcium
Criteria include cardiac (hypotension, pulse >130/minute, arrhythmias, ECG changes), pulmonary (PaO2 >60 mm Hg, ARDS), renal (urine output <40 ml/hour, increase in blood urea and serum creatinine), metabolic (falling serum calcium, magnesium, and albumin), haematologic (fall in haematocrit, DIC), gastrointestinal (severe ileus, sequestration of fluid), and neurologic (irritability, confusion, localising features).
It is associated with a worse prognosis.
Surgery can be open, laparoscopic, endoscopic, or percutaneous (radiologically guided).
It is important to assess pulmonary insufficiency or ARDS.
Walled-off necrosis (WON) is confirmed by CT scan and CT-guided aspiration, with collected fluid sent for culture.
Pain is typically in the epigastric region, persistent and severe, radiating to the back.
Alcohol abuse (80%) and smoking.
Amylase and lipase are secreted in their active forms.
MRI / MR cholangiopancreatography (MRCP)
Gallstone pancreatitis
Respiratory complications include distension of abdomen, diaphragmatic elevation, pleural effusion, reduced surfactant activity in alveoli due to lecithinase, severe pain, pleural effusion (left), intravascular coagulation in lungs, and ARDS. Arterial blood gas analysis should be done and often needs ventilator support.
It indicates that the pancreatitis is more likely to be severe.
Oral feeding with fluids may be started early if tolerated.
NSAIDs can worsen pancreatitis and cause renal failure due to already decreased renal perfusion.
NG tube insertion and anti-emetics.
A pancreatic pseudoaneurysm is diagnosed by CT angiogram.
Every 6-8 hours initially.
ACR is calculated by urinary amylase × serum creatinine divided by serum amylase × urinary creatinine × 100.
More than 40%.
Acute pancreatitis is primarily caused by the unregulated activation of trypsin within pancreatic acinar cells, leading to auto-digestion and an inflammatory cascade.
Persistent elevation of amylase suggests complications like pseudocyst, ascites, and abscess formation.
Hyperbilirubinaemia may be due to biliary stone/obstruction, cholangitis, or non-obstructive cholectasis.
Pain relief or reduction by leaning forward in patients with acute pancreatitis.
Chronic relapsing pancreatitis, chronic persistent pancreatitis, non-calcifying pancreatitis, and calcifying pancreatitis.
Inactive proenzymes like trypsinogen are activated by trypsin in the duodenum.
Chronic pancreatitis
Emphysematous pancreatitis is the presence of gas in the pancreatic parenchyma, a dangerous type, and can be diagnosed by CT scan.
Haematocrit levels higher than 44% are associated with a worse prognosis.
Pancreatic pseudocysts are commonly located in the peripancreatic region, in the lesser sac (between the colon and stomach), but can also occur in relation to the duodenum, jejunum, colon, and splenic hilum.
The TAP assay in serum and urine reveals the severity of acute pancreatitis.
Nasojejunal tube placement and feeding should be started as early as possible once ileus subsides to reduce infection rates and improve nutritional status.
Calcium gluconate 10 ml 10% IV 8th hourly is given to treat hypocalcaemia.
Surgical intervention is indicated if the patient's condition deteriorates despite good conservative treatment.
50 ml hourly or 0.5ml/kg/hr.
Less than 10%.
Infection occurs by bacterial translocation across the gut due to an altered mucosal barrier.
Amylase may not rise in chronic pancreatitis due to significant destruction and loss of acinar cells.
Hypochloraemic metabolic alkalosis is common due to repeated vomiting.
Normal amylase levels do not exclude pancreatitis, especially in late presentations or chronic alcoholics.
CECT is useful in confirming the diagnosis of pancreatitis if hematological results are inconclusive. It assesses the severity and detects local complications. Non-enhancement finding is typical of pancreatic necrosis.
It indicates that one can wait for spontaneous resolution.
They cause activation of digestive enzymes and blockage of pancreatic microcirculation, leading to pancreatic ischaemia.
Calcium is utilized for saponification.
Lavage and drainage procedure.
Long-standing inflammation of the pancreas with diffuse scarring and structuring in the pancreatic duct leading to irreversible destruction of the exocrine and, in the late stage, the endocrine parenchyma.
Erect CXR & Supine AXR
Early stage with no complications, preserved clinical exocrine and endocrine function, but subclinical signs like impaired glucose tolerance and reduced exocrine function may be present.
The protein part of the juice is secreted by acinar cells.
α cells secrete glucagon, which raises blood glucose levels.
A pancreatic pseudocyst is a collection of fluid in a false cavity lined by granulation tissue but not true epithelium, with an organized thick fibrous covering. It is not a true cyst as there is no epithelial lining.
Gastric decompression with NGT is used if there is persistent vomiting, significant gastroparesis, or intestinal obstruction (ileus).
Hyperglycaemia is often seen and can indicate the severity of the condition.
Unconventional approaches include continuous lavage, antibiotics with percutaneous drainage, surgical drainage without debridement, or minimally invasive debridement.
Early phase (lasts for 2 weeks with oedematous pancreatitis or sterile necrosis) and late phase (after 2-3 weeks with pancreatic abscess or infective necrosis).
Less than 1%.
The colocalisation hypothesis suggests that trypsinogen within the cytoplasmic vacuoles of acinar cells gets colocalised with lysosomal hydrolases, commonly cathepsin B, to activate into trypsin, leading to intrapancreatic inflammation and pancreatitis.
Organ failure that resolves in 48 hours (transient organ failure) and/or local/systemic complications without persistent organ failure.
The common pathway involves either causing spasm of the sphincter of Oddi or increased secretion of pancreatic enzymes, leading to the activation of trypsinogen into trypsin, which then activates other enzymes.
Hypertriglyceridaemia is common especially in hyperlipidaemic patients.
A Ryle’s tube passed will be felt per abdominally because the stomach is stretched towards the abdominal wall.
Bacterial growth in fluid culture along with CT showing necrosis indicates infected necrosis, which needs early pancreatic necrosectomy.
Formation of a fistula (20%).
Within the first 48-72 hours.
To allow for demarcation/organization of necrotic areas, as repeated surgeries may be required.
The primary function of pancreatic juice is to aid in the digestion of proteins, carbohydrates, and fats, and to alkalize duodenal content.
Air under the diaphragm, air-fluid level in the duodenum, pleural effusion, renal halo sign, obliteration of psoas shadow, localized ground glass appearance, elevated hemidiaphragm, pulmonary infiltrates, complete whiteout (ARDS)
Pancreatic fistula can be confirmed by biochemical analysis, ERCP, and CT fistulogram.
β cells secrete insulin, which lowers blood glucose levels.
Serum amylase hydrolyzes starch, glycogen, and polysaccharides into simple sugars.
Hypocalcaemia is a common finding and can indicate the severity of the condition.
Endoscopic internal drainage can be done via a cystogastrostomy, cystoduodenostomy, or cystojejunostomy.
First confirm the diagnosis (amylase/CT) and assess severity (Ranson’s/Apache II).
Signs of infected pancreatic necrosis on a CT scan include gas bubbles.
The duration of antibiotic therapy is 14 days.
Aim for urine output >0.5ml/kg/hr.
The Ampulla of Vater is located on the posteromedial wall of the second part of the duodenum, at the level of the spine of the 2nd lumbar vertebra. It contains a sphincteric complex (Sphincter of Oddi).
The uncinate process is a lower posterior extension of the head of the pancreas, passing behind the superior mesenteric vessels and anterior to the IVC and aorta. It usually does not extend beyond the right renal hilum. An anomalous right hepatic artery may pass through the uncinate process.
Idiopathic pancreatitis can be controlled or prevented by cholecystectomy and sphincterotomy.
No organ failure, no local or systemic complications.
Alcohol causes direct toxicity, hypersecretion of gastric and pancreatic juices, reflux, plugging of pancreatic proteins, injury by release of free radicals, spasm of Oddi, and stimulates trypsinogen.
Reduced insulin secretion, increased glucagon and catecholamine secretion cause hyperglycaemia, more so in diabetic patients.
Encapsulated fluid collection with a well-defined inflammatory wall with minimal or no necrosis.
Infection, rupture, pancreatic ascites, pancreaticopleural fistula, haemorrhage, abscess, bleeding from splenic vessels, cholangitis, duodenal obstruction, portal/splenic vein thrombosis, segmental portal hypertension, cholestasis due to CBD block.
Amylase will be high with normal CEA in pseudocyst; amylase will be normal/low with high CEA >400 ng/ml in mucinous neoplasm.
To differentiate between sterile and infected necrosis.
Type A pain involves short relapsing episodes lasting days to weeks with pain-free intervals. Type B pain is prolonged, severe, and unrelenting.
Because the patient may develop complications that require surgical intervention, and it is better to do all surgery in the same operation instead of opening the patient twice.
Pancreatic fistula occurs due to ductal wall disruption and necrosis or after surgical intervention for acute pancreatitis (necrosectomy).
A cholecystectomy should be performed as soon as the patient recovers from the acute attack, preferably during the same admission (3 to 5 days after pancreatic inflammation resolves).
Acute fluid collections are local complications of acute pancreatitis that commonly occur in the peripancreatic area, occasionally intrapancreatic.
It indicates an increased risk of developing necrotizing pancreatitis.
Serum lactescence is most specific in hereditary hyperlipidaemia or alcohol pancreatitis.
Prolonged NBM results in poorer recovery due to nutritional debilitation.
Tramadol and pethidine are recommended, but not morphine as it increases the tone of the sphincter of Oddi.
The pancreas develops from the dorsal and ventral buds.
Third generation cephalosporins, imipenem, meropenem, cefuroxime.
An acute inflammation of the prior normal gland parenchyma leading to reversible pancreatic parenchymal damage of varying severity with raised pancreatic enzyme levels in blood and urine.
To assess oxygenation and acid-base status.
An ACR greater than 5% suggests acute pancreatitis; it can also increase in diabetic ketoacidosis and renal diseases.
The pancreas is supplied by the celiac artery via the splenic artery (pancreatic branches for the tail) and the superior pancreaticoduodenal artery (for the head). The superior mesenteric artery supplies the inferior pancreaticoduodenal artery (for the head).
Amylase levels may be low in cystic fibrosis, liver damage, pancreatic cancer, and pregnancy with toxaemia.
Peripancreatic fluid collection with interstitial pancreatitis, no necrosis, no wall formation, occurs within 4 weeks.
Methemalbuminemia, when it occurs in acute pancreatitis, indicates poor prognosis.
Serum lipase levels rise within 4-8 hours and stay elevated for 8-14 days, making it more sensitive and specific for diagnosing acute pancreatitis, especially in patients with delayed presentation.
Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps and other infections, Autoimmune, Scorpion toxin and other toxins, Hypercalcaemia, Hypertriglyceridemia, ERCP, Drugs.
Autoimmune pancreatitis is associated with primary sclerosing cholangitis, Sjögren’s syndrome, and biliary cirrhosis, and is characterized by high levels of circulating IgG4, pancreatitis, bile and pancreatic ductal strictures, and pancreatic head mass.
Sudden onset of upper abdominal pain referred to the back, vomiting, high fever, tachypnoea with cyanosis, tenderness, rebound tenderness, guarding, rigidity, abdominal distension, mild jaundice, features of shock and dehydration, oliguria, hypoxia, acidosis, Grey-Turner's sign, Cullen's sign, Fox sign, haematemesis/malaena, hiccough, ascites, paralytic ileus, pleural effusion, pulmonary oedema, consolidation, rapid onset ARDS, and neurological derangements.
They should be done in the acute setting (within 72 hours).
Diabetes mellitus, often brittle due to concomitant glucagon deficiency, requiring insulin.
Lack of fusion leads to a short duct of Wirsung, causing the majority of pancreatic secretion to drain through the minor pancreatic duct (duct of Santorini), which terminates at the minor duodenal papilla. This can lead to stenosis or inadequate patency of the minor papilla, preventing normal drainage and increasing intra-ductal pressure.
Intermediate stage with complications but preserved clinical exocrine and endocrine function. Complications may include cholestasis, pseudocyst, and sinistral portal hypertension.
Impacted stone in the ampulla of Vater
Systemic complications include peritoneal sepsis, pancreatic ascites, pancreatic pleural effusion, intra-abdominal hemorrhage, multiple organ failure, hypocalcemia, and hyper/hypoglycemia.
Acid suppression does not change the course of the disease but protects against stress ulcer formation.
Sterile pancreatic necrosis is a focal or diffuse area of non-viable pancreatic parenchyma with peripancreatic fat necrosis, initially sterile but eventually gets infected.
Aggressive early hydration in the first 24 hours using 400 ml/hour crystalloids (Ringer lactate, normal saline).
Antibiotics are used prophylactically in severe acute pancreatitis to prevent infection of necrosis and therapeutically in cholangitis and infection of pancreatic necrosis/pseudocyst.
The majority of the main pancreatic duct (duct of Wirsung) is formed from the ventral bud, and the accessory duct (duct of Santorini) is formed from the dorsal bud.
To monitor for rapid fluid therapy and for Total Parenteral Nutrition (TPN) using carbohydrates, amino acids, vitamins, essential elements.
40%, which needs drainage.
Anterior relations of the body of the pancreas include the stomach, posterior wall of the omental bursa, transverse colon, and middle colic artery. Posterior relations include the aorta, origin of the superior mesenteric artery, left crus of the diaphragm, left suprarenal gland, left kidney, and splenic vein.
A rise in amylase level is common in acute pancreatitis, pseudocyst of the pancreas, pancreatic trauma, and after ERCP.
Persistent organ failure (>48 hours), which can be single or multiple organ failure.
Systemic effects include the release of lecithinase, amylase, prostaglandins, bradykinins, and platelet activation factor, leading to local and systemic inflammation, bacteraemia, septicaemia, hypovolemic shock, acute renal failure, pulmonary insufficiency, ARDS, and respiratory failure.
Hemispherical, smooth, soft, not moving with respiration, not mobile, upper margin diffuse, lower margin well defined, resonant or impaired resonant on percussion, with transmitted pulsation confirmed by knee-elbow position.
Very high (>5000 units/mL).
38%.
The 'sentinel loop sign' indicates a dilated proximal jejunal loop near the pancreas, and the 'colon cut-off sign' indicates distension of the transverse colon with collapse of the descending colon due to localized ileus from inflammation around the pancreas.
If a pancreatic fistula persists for 6 months, treatment options include sphincterotomy, resection of the fistula with pancreatic resection, and pancreaticojejunostomy.
The late sequelae of chronic pancreatitis include pancreatic endocrine (15%) and exocrine (20%) insufficiency.
The normal value of serum amylase is 200 – 250 Somogyi units (40 – 140 IU/L).
APACHE II is used to monitor a patient’s response to therapy and takes into account 12 continuous variables, age, pre-morbid conditions, and the GCS.
Roux-en-Y cystojejunostomy has a lower recurrence rate than cystogastrostomy.
The prevention of pancreatic stimulation (keep patient NBM).
Supportive measures include ventilation with PEEP if hypoxemic, dialysis and CVP monitoring if in ARF, and fluid resuscitation and inotropes if hypotensive.
The pancreas is located deep in the abdomen, retroperitoneal, behind the stomach, between the duodenum and spleen, at the level of the 2nd and 3rd lumbar vertebrae.
The neck of the pancreas measures 1.5 cm in length and is located between the celiac trunk (above) and superior mesenteric vessels (below). The anterior superior gastroduodenal artery arises near the upper neck at the junction with the head. Posteriorly, the superior mesenteric vein joins the splenic vein to form the portal vein behind the neck.
Serum amylase is considered elevated if the level is more than three times the upper limit of normal.
The parasympathetic supply to the pancreas is from the vagus nerve, and the sympathetic innervation is from the splanchnic nerves.
Total count is raised with neutrophilia. Thrombocytopaenia, raised FDP, decreased fibrinogen, prolonged partial thromboplastin time and PT are common. DIC can develop later.
No, lipase or amylase level estimation has no role in identifying the etiology of acute pancreatitis.
A collection containing variable amounts of both fluid and necrosis associated with necrotizing pancreatitis.
Pseudocyst following biliary pancreatitis has four times more mortality than that of alcoholic pancreatitis.
Hereditary pancreatitis is caused by a genetic mutation leading to defective trypsin inhibitors, resulting in high concentrations of intrapancreatic active trypsin which activates other enzymes, leading to pancreatitis.
Serum bilirubin, albumin, prothrombin time, and alkaline phosphatase are commonly assessed.
It is a very useful method for diagnosing acute pancreatitis.
The ventral bud rotates around the 2nd part of the duodenum, bringing the bile duct over to the left side of the 2nd part of the duodenum.
Biliary tract disease.
Acute interstitial oedematous pancreatitis and acute necrotizing pancreatitis.
The tail of the pancreas is the distal part related to the spleen. It is enveloped by the splenorenal ligament along with splenic vessels, making it vulnerable to damage during splenectomy. It is anterior to the left adrenal gland and contacts the hilum of the spleen, and may be mobile.
Other conditions include salivary gland diseases like parotitis, mesenteric ischemia, ruptured aortic aneurysm, intestinal obstruction, duodenal ulcer perforation, ectopic gestation, salpingitis, ectopic amylase production in cancers, and renal failure.
Two of the following three features: abdominal pain consistent with epigastric pain, serum lipase/amylase activity of at least 3x greater than the upper limit of normal, and characteristic findings of acute pancreatitis on CECT, MRI, or trans-abdominal ultrasound.
The half-life of lipase is 10 hours, which is much longer than amylase, so it remains longer in the serum and is mainly used in diagnosing acute pancreatitis.
It will be a tender mass, and the patient will be toxic with fever and chills.
Spiral CT (CECT) is considered the gold standard after 72 hours to look for edema, altered fat and fascial planes, fluid collections, necrosis, bowel distension, mesenteric edema, and hemorrhage.
Hypercalcaemia and hypertriglyceridemia.
Walled-off necrosis (WON) may form a pseudocyst, abscess, or be replaced by fibrous tissue during healing.
Fresh frozen plasma and platelet concentrate may be required in anticipation of DIC and haemorrhage.
The conventional treatment for infected pancreatic necrosis is laparotomy with debridement and adequate drainage.
The main pancreatic duct begins at the tail of the pancreas, runs through the body and head, and joins the bile duct in the wall of the second part of the duodenum to form the hepatopancreatic ampulla (Ampulla of Vater), opening at the major duodenal papilla (~8-10 cm from the pylorus).
Treatment options include critical care, blood transfusion, emergency angiographic embolization, or open surgery and ligation of the involved vessel.
100%.
An ACR less than 1% indicates macroamylasemia, where amylase binds with large abnormal circulating proteins, causing a false raise in serum amylase levels.
Venous drainage of the pancreas is achieved via the pancreaticoduodenal veins, which drain into the portal vein.
Hypocalcaemia is either due to decreased albumin level or specific loss of ionized calcium. Hypocalcaemia due to reduced ionized calcium carries poor prognosis.
Lipase is increased in acute and chronic pancreatitis, pseudocyst, cystic fibrosis, pancreatic cancer, bowel ischemia, renal failure, liver diseases, alcoholism, and after ERCP.
20% of patients.
Mumps, VZV, CMV, mycoplasma, parasitic infections.
Pethidine and other analgesics. Morphine and NSAIDs are not used as they cause spasm of the sphincter of Oddi.
A pancreatic pseudoaneurysm is caused by enzymatic digestion (elastase) of the vessel wall, leading to weakening and aneurysmal dilatation.
The accessory pancreatic duct begins in the lower part of the head of the pancreas and opens into the minor duodenal papilla (~6-8 cm from the pylorus).
The posterior relations of the head of the pancreas include the hilum of the right kidney, right renal vessels, IVC, left renal vein, right crus of diaphragm, posterior pancreaticoduodenal arcade, right gonadal vein, and distal common bile duct (CBD).
Idiopathic pancreatitis is likely caused by gallbladder sludge or microcrystals, and can also be due to malfunction of the sphincter of Oddi.
Mild AP, Moderately severe AP, and Severe AP.
Etiological factors for pancreatic duct obstruction include biliary tract stones, duodenal ulcer, duodenal Crohn’s, periampullary diverticulum/tumor, trauma, pancreatic duct stricture, pancreatic divisum, ascariasis, and Clonorchis sinensis.
The normal value range for serum lipase is 0 – 50 units/L, depending on the method and laboratory.
Serum amylase is moderately sensitive for acute pancreatitis. Levels rise within 6-12 hours, peak at 24 hours, and normalize in 3-7 days. Elevation for more than 10 days indicates complications such as pseudocysts formation.
A mature, encapsulated collection of pancreatic and/or peripancreatic necrosis with a well-defined wall.
CT scan.
If the cyst is >6 cm, infected, persisting after 6 weeks, progressive, multiple, due to trauma, communicating, causing severe pain, or if the chance of spontaneous resolution is low and the risk of complications is high.
The amylase creatinine clearance ratio is increased in acute pancreatitis. A value more than 6% signifies acute pancreatitis.
Mortality rates can be as high as 40% - 100%.
When the cyst is infected, haemorrhagic, or ruptured.
