History

Fact Explanation
Pattern of presentation Acute pancreatitis, inflammation of the pancreatic parenchyma is a common cause of emergency admission with acute abdomen. There is premature activation of pancreatic enzymes within the pancreatic ducts resulting auto-digestion of the gland. The initial cellular injury is followed by an inflammatory reaction. Patient presentation varies according to the severity which ranges from mild to severe.[1]
Abdominal pain Abdominal pain is a cardinal symptom of acute pancreatitis. The pain is acute in onset, severe and reaches a peak within minutes. Pain is usually felt in the epigastric region and characteristically radiates to the back. The patient experiences comfort when bending or leaning forwards.
Nausea and vomiting Nausea and vomiting is a constant feature of pancreatitis.
Fever Fever is not a common symptom of acute pancreatitis. Swinging pyrexia with rigors may be due to acute cholangitis.
Anorexia Due to the systemic inflammatory response.
Presentation with localized complications Common local complications include pancreatic necrosis with secondary infection, pancreatic abscess, pseudocyst formation and pseudoaneurysm. The onset is usually after the acute attack and carries an increased morbidity and mortality. Pancreatic pseudocysts develop 4 weeks after the acute attack and present with abdominal pain and epigastric mass. Abscess formation and secondary infection present with fever, abdominal pain and tender abdominal mass following recovery of initial attack.
Presentation with systemic complications Acute pancreatitis is known cause of systemic inflammatory response syndrome (SIRS). Chemical mediators generated as part of the inflammatory reaction within the pancreas are released into the circulation. The resulting systemic inflammatory response may lead to multiple organ failure. Patients with severe acute pancreatitis may present with acute renal failure, disseminated intravascular coagulation, acute lung injury, haemodynamic instability etc.[2]
Risk factors/ Aetiology The two most important causes of acute pancreatitis are alcohol consumption and gallstone disease. The pathogenesis of alcohol induced pancreatitis is multi-factorial - Direct pancreatic injury, poor nutrition, hypersecretion of pancreatic enzymes and hyperlipidaemia. Gallstones located within the gallbladder or bile ducts may pass downwards and get obstructed at the common bile and pancreatic duct opening. The patient may complain of a past history of chronic upper abdominal pain, dyspeptic symptoms and fatty food intolerance. Evaluate the current drugs the patient is on, corticosteroids, sodium valproate, azathioprine and oestrogens may precipitate an attack. Abdominal trauma, surgery, ERCP may rarely be the cause. A positive family history for pancreatitis may suggest hereditary pancreatitis or auto-immune pancreatitis.[3]
References
  1. JHA RK, MA Q, SHA H, PALIKHE M. Acute pancreatitis: a literature review. Med Sci Monit [online] 2009 Jul, 15(7):RA147-56 [viewed 31 August 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/19564840
  2. PITCHUMONI CS, AGARWAL N, JAIN NK. Systemic complications of acute pancreatitis. Am J Gastroenterol [online] 1988 Jun, 83(6):597-606 [viewed 31 August 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/3287900
  3. BIRGISSON H, MöLLER PH, BIRGISSON S, THORODDSEN A, ASGEIRSSON KS, SIGURJóNSSON SV, MAGNúSSON J. Acute pancreatitis: a prospective study of its incidence, aetiology, severity, and mortality in Iceland. Eur J Surg [online] 2002, 168(5):278-82 [viewed 31 August 2014] Available from: doi:10.1002/ejs.46

Examination

Fact Explanation
General examination : Reduced conscious level Confusion may be multi-factorial. Metabolic derangement, hypovolaemic shock, toxiaemia and hypoxaemia may contribute to central nervous system dysfunction.
General examination : Fever Fever is rare in the early stages but may develop with time. Infection of the necrotic pancreas and acute cholangitis may present with fever. Some patients may experience hypothermia in the initial stages.
General examination : Icterus In gallstone pancreatitis bile flow may be obstructed by the presence of a stone at the ampulla.
General examination : Features of dehydration Due to poor intake and fluid loss. The mucous membranes and skin appears dry. The eyes may be sunken. Skin elasticity is reduced. The capillary refill time will be prolonged.
General examination : Hemorrhage into the skin layers In severe hemorrhagic acute pancreatitis there may be bleeding into the fascial planes of the abdomen. Presence of a hematoma in the flank region (Grey Turner’s sign) and surrounding the umbilicus (Cullen’s sign) are rare features.[1]
Skin nodules on the abdomen and lower limbs Due to fat necrosis. Pancreatic lipase released as a result of pancreatitis leads to auto-digestion of fat tissues of the skin and subcutaneous tissue. The nodules are small tender and erythematous.[2]
Cardiovascular system : Hypotension and tachycardia Features of severe acute pancreatitis.
Abdominal examination – Tenderness in the epigastrium Due to the underlying inflamed pancreas. Guarding will be present due to contraction of the overlying abdominal wall muscles.
Abdominal examination : Distension Due to intestinal ileus.
Abdominal examination : Epigastric mass An inflammatory mass may be palpable in the epigastium. It would be tender, with diffuse margins and may be difficult to further define due to tenderness within the region.
References
  1. MEYERS MA, FELDBERG MA, OLIPHANT M. Grey Turner's sign and Cullen's sign in acute pancreatitis. Gastrointest Radiol [online] 1989 Winter, 14(1):31-7 [viewed 31 August 2014] Available from: doi:10.1007/BF01889150
  2. LEE WS, KIM MY, KIM SW, PAIK CN, KIM HO, PARK YM. Fatal pancreatic panniculitis associated with acute pancreatitis: a case report. J Korean Med Sci [online] 2007 Oct, 22(5):914-7 [viewed 31 August 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/17982246

Differential Diagnoses

Fact Explanation
Biliary colic/ Acute cholecystitis Gallstone formation is the commonest disease affecting the gallbladder. Gallstones are categorized into cholesterol, bile pigment and mixed stones. The risk factors for gallstone formation depends on the type of stone. Cholesterol stones are formed in lithogenic bile formed as a result of impaired gallbladder emptying, increased cholesterol content in bile and reduced bile acids in bile. Black pigment stones are characteristically seen in chronic hemolytic conditions. Brown pigment stones are associated with bacterial or parasitic infection of bile and with hepatic cirrhosis. Majority of stones are asymptomatic. The common presentations of gallstone disease are biliary colic, acute cholecystitis and chronic cholecystitis. Obstruction of the gallbladder neck by a stone leads to intermittent spasms of the gallbladder. This leads to a colicky pain in the epigastrium or right hypochondrium with is severe, acute in onset and characteristically radiates to the inferior scapular region. The pain usually lasts 2h and may be prolonged if complications occur. Nausea and vomiting in less compared to pancreatitis. Secondary infection of the gallbladder leads to acute cholecystitis. The character of the pain changes into a continuous pain, patient will be febrile and jaundice may be present. The patients is in pain but is not as toxic or ill as in pancreatitis. On examination tenderness is present in the right hypochondrium and an inflammatory mass may be felt. Diagnosis of the condition is by abdominal USS and X-ray.[1]
Perforated peptic ulcer Perforation is a known complication of peptic ulcer disease (PUD). Perforation is common in duodenal ulcers than in gastric ulcers. Most patients have a previous history of chronic abdominal pain, nausea & vomiting, dyspeptic symptoms and gastrointestinal bleeding or perforation can be the first presentation of PUD. The patient presents with severe, sudden onset abdominal pain usually starting in the left upper quadrant. The patient may be in shock. As the gastric or duodenal contents spread within the peritoneal cavity, the pain gradually becomes generalized. Shoulder tip pain is caused by irritation of the under surface of the diaphragm. The intestinal contents precipitate peritonitis which may progress to generalized peritonitis. The abdominal examination reveals board like rigidity and is held immobile by the patient. Bowel sounds are absent due to generalized peritonitis. The liver dulness on percussion is diminished and displaced downwards due to the presence of gas within the peritoneum. Diagnosis is based on clinical presentation and erect chest X-ray showing gas underneath the diaphragm. If the diagnosis is doubtful a contrast swallow can be used to identify the leak. Prompt surgical closure of the perforation is indicated after initial resuscitation.[2]
Pneumonia of the basal lobe Acute pancreatitis can be confused with extra-abdominal conditions causing abdominal pain.[3] The pain from inflammation of the pancreas may radiate to the chest and mimic pneumonia or myocardial infarction. Pneumonia of the basal lung lobes present with pleuritic type chest pain, productive cough, dyspnea and systemic symptoms. Cough is a prominent symptom with yellow color sputum production. Spread of inflammation the adjacent pleura can cause chest pain which is precipitated by coughing or breathing movements. The patient may be febrile. Examination of the chest will reveal features of consolidation - reduced chest movement, increased tactile vocal fremitus, dull percussion note, bronchial breathing and reduced breath sounds on the affected side. Abdominal examination is usually normal. Chest Xray, sputum analysis for microbial agents usually confirm the diagnosis.
Myocardial infarction Myocardial infarction is another condition which should be considered when pain is in the epigastric region and radiates to the chest. This picture together with prominent vomiting is characteristically seen in inferior myocardial infarction. Myocardial infarction usually presents with central constricting type severe chest pain which radiates to the left arm, jaw and neck. The onset of the pain is acute and may be precipitated by exercise, emotion or cold environment. The patient is anxious and distressed. Dizziness and syncope may be present. Examination of the chest is usually normal. Massive infarction or complicated infarction may present with features of heart failure, cardiogenic shock or mitral regurgitation/ ventricular septal defect. The patent usually has a history of risk factors for atherosclerosis - hypertension, diabetes, hyperlipidaemia, smoking etc. The diagnosis can be confirmed by ECG - ST elevation/ depression or my cardiac bio-markers - Troponin level.
References
  1. STRASBERG STEVEN M.. Acute Calculous Cholecystitis. N Engl J Med [online] 2008 June, 358(26):2804-2811 [viewed 31 August 2014] Available from: doi:10.1056/NEJMcp0800929
  2. SVANES C. Trends in perforated peptic ulcer: incidence, etiology, treatment, and prognosis. World J Surg [online] 2000 Mar, 24(3):277-83 [viewed 31 August 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/10658061
  3. VENDARGON S, WONG PS, TAN KK. Pneumonia presenting as acute abdomen in children: a report of three cases. Med J Malaysia [online] 2000 Dec, 55(4):520-3 [viewed 31 August 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/11221169

Investigations - for Diagnosis

Fact Explanation
Diagnosis of acute pancreatitis Diagnosis is often based on clinical presentation which is confirmed by laboratory investigations. Further investigations are required to determine the severity, identify the aetiology and exclude any complications.
Serum amylase A three to four fold rise in the serum amylase levels is diagnostic of acute pancreatitis.
Serum lipase Elevation of lipase levels lasts longer than amylase levels. It can be used in patients who present late, 2-4 days after the acute attack. Serum lipase is considered a more sensitive and specific investigation than serum amylase.[1] [2]
Ultrasound scan – Abdomen Apart from edema around the pancreas USS does not show other specific features for diagnosing acute pancreatitis. Gallstones within the biliary system and dilatation of the proximal bile duct help establish the aetiology for pancreatitis. It can be used to exclude other differential diagnosis such as acute cholecystitis and acute appendicitis.
Contrast-enhanced CT This is considered the single best imaging modality for diagnosis of acute pancreatitis. Necrosis of pancreatic tissue, edema of surrounding tissue and fat necrosis can be identified by CT scan. The severity of the attack can be assessed and can be staged according to the Balthazar criteria. The grade of pancreatitis and the extent of pancreatic necrosis are assessed in this criteria. The accuracy of determining the severity of the attack by this method is considered higher than in Ranson and APACHE 2 score.[3] Local complications such as pseudocyst formation, pseudoaneurysm and pancreatic abscess can be screened for.[4]
Magnetic resonance imaging (MRI) Even though MRI can be used instead of CT to obtain similar results, the lack of facilities and availability limits its use.
Abdominal X-ray Plain radiography has limited value as a diagnostic test. Calcified gallstones can be identified near the region of the ampulla. Calcification within the pancreatitis may indicate a hereditary type of pancreatitis. Presence of hemoperitoneum can be used to differentiate perforated peptic ulcer.
ERCP/ EUS These investigations can be used to exclude the presence of gallstones at the ampulla. ERCP can be used as a therapeutic option to remove the obstruction gallstone by sphincterotomy. Patients with biliary obstruction and acute cholangitis require urgent ERCP.
References
  1. TREACY J, WILLIAMS A, BAIS R, WILLSON K, WORTHLEY C, REECE J, BESSELL J, THOMAS D. Evaluation of amylase and lipase in the diagnosis of acute pancreatitis. ANZ J Surg [online] 2001 Oct, 71(10):577-82 [viewed 31 August 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/11552931
  2. SMITH RC, SOUTHWELL-KEELY J, CHESHER D. Should serum pancreatic lipase replace serum amylase as a biomarker of acute pancreatitis? ANZ J Surg [online] 2005 Jun, 75(6):399-404 [viewed 31 August 2014] Available from: doi:10.1111/j.1445-2197.2005.03391.x
  3. LEUNG TK, LEE CM, LIN SY, CHEN HC, WANG HJ, SHEN LK, CHEN YY. Balthazar computed tomography severity index is superior to Ranson criteria and APACHE II scoring system in predicting acute pancreatitis outcome. World J Gastroenterol [online] 2005 Oct 14, 11(38):6049-52 [viewed 31 August 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/16273623
  4. MCMENAMIN DA, GATES LK JR. A retrospective analysis of the effect of contrast-enhanced CT on the outcome of acute pancreatitis. Am J Gastroenterol [online] 1996 Jul, 91(7):1384-7 [viewed 31 August 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/8678000

Investigations - Fitness for Management

Fact Explanation
Full blood count To screen for secondary infection. White blood cell count is also used in determining the severity.
Blood urea, Serum creatinine To assess renal functions.
Serum electrolytes Electrolyte imbalances are common among patients with severe acute pancreatitis. Serum calcium less than 2.0mmol l–1 is suggestive of severe pancreatitis.
Liver function tests : AST/ALT/Serum albumin To screen for disturbances in hepatic function.
Arterial blood gas To identify acid-base and electrolyte imbalances. Respiratory failure may be present in severe acute pancreatitis.
Blood glucose level To screen for hyper/ hypoglycaemia.
References

Investigations - Screening/Staging

Fact Explanation
Severity stratification Severity stratification is important to identify patients presenting with severe acute pancreatitis who are at higher risk of developing complications. Various scoring systems are used for this purpose. Ranson score, Glasgow score and the APACHE II scoring system can be used. Both the Ranson and Glasgow score assess parameters both at presentation and after 48 hours. As per Ranson score - Age more than 55yr, White blood cell count > 16*109, Blood glucose > 10 mmol l–1, LDH > 700 units l–1 & AST > 250 at admission and arterial oxygen saturation < 8 kPa, Serum calcium < 2.0 mmol l–1, Base deficit > 4mmol l–1, Fluid sequestration > 6 litres and Blood urea nitrogen rise > 5 mg% after 48h is considered severe acute pancreatitis. Ranson score is considered an accurate measure of the severity compared to APACHE 2 and the more recent APACHE 3 score.[1]
Chest X-ray Pleural effusions and features of acute respiratory distress syndrome may be seen in severe acute pancreatitis.
Clotting profile To identify coagulations abnormalities in systemic disease.
References
  1. CHATZICOSTAS C, ROUSSOMOUSTAKAKI M, VLACHONIKOLIS IG, NOTAS G, MOUZAS I, SAMONAKIS D, KOUROUMALIS EA. Comparison of Ranson, APACHE II and APACHE III scoring systems in acute pancreatitis. Pancreas [online] 2002 Nov, 25(4):331-5 [viewed 31 August 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/12409825

Management - Specific Treatments

Fact Explanation
Management of acute pancreatitis There is no specific treatment for acute pancreatitis patients. Management consists of symptomatic relief, monitoring and management of complications. Patients presenting with mild acute pancreatitis can be conservatively managed with observation and symptomatic treatment (fluid management & analgesia) alone. Management of severe acute pancreatitis requires more intense monitoring and aggressive fluid resuscitation, pain relief, anti-emetic therapy, nutritional support and prophylaxis antibiotics.[1] If a definitive cause such as gallstone disease is identified specific treatment options can be taken.
Management setting Patients with mild pancreatitis can be managed in the ward setting. Patients with features of severe pancreatitis as predicted by scoring systems require admission to an intensive care unit or high dependency unit.[2]
Oxygen supplementation Monitor arterial blood saturation. Oxygen is administered if failure for adequate saturation is present. Respiratory support via ventilation may be required if acute respiratory distress syndrome develops.
Analgesics For pain relief. Analgesics should be administered according to the analgesic ladder introduced by the WHO. Certain opioids such as morphine are avoided due to the risk of pancreatic duct constriction and further deterioration.[3] Pethidine is preferred in these patients.
Anti-emetic drugs For relief of nausea and vomiting.
Fluid management Monitor fluid intake and output. Fluid resuscitation should be guided by cardiovascular parameters, urine output and central venous pressure. Pancreatic ascites is due to a persistent leak via an opened up pancreatic duct. These patients may present with abdominal distention and shock. Manage hypovolaemic shock with intravenous crystolloids and colloids.
Nutrition Enteral nutrition is preferred to parenteral nutrition in severe acute pancreatitis. A nasogastric tube can be used for gastric emptying in the acute setting and can also be used as a feeding method. Avoid prolonged fasting.[4]
Prophylactic antibiotics Intravenous antibiotics can be used in severe pancreatitis to reduce the risk of infective complications. Combination of antibiotics to provide broad spectrum cover – Cefuroxime, metronidazole and ciprofloxacin is used. Mild attacks of pancreatitis usually do not require prophylactic antibiotics.[5]
Management of gallstone pancreatitis If gallstone disease is suspected by the presence of jaundice, cholangitis or a previous history of gallstone related symptoms, these patients require urgent ERCP to remove the obstructing stone by sphincterotomy. Imaging with EUS, MRCP can be used visualize the biliary tree. Dilatation of the common bile duct is a feature of gallstone pancreatitis. Further evaluation is required to determine the suitable time for ERCP intervension in these patients.[6]
Management of organ failure These patients require management within an intensive care unit. Acute respiratory distress syndrome requires intubation and ventilation. Hemodynamic instability is managed with intravenous fluids initially with the support of inotropes. DIC is managed with conservatively with blood product transfusion. Acute renal failure is managed with correction of electrolyte imbalances and fluid management.
Management of local complications In most instances these are managed conservatively while surgery is reserved for resistant patients. Repeat CT scan is required if the patient worsens after recovery of the acute attack. Pancreatic abscesses are drained under antibiotic cover. Percutaneous drainage with image guidance is preferred. Open drainage is needed if the above mentioned methods fail. Pancreatic pseudocysts can be managed by endoscopic and surgical measures. Endoscopic drainage of the cyst into the stomach or duodenum is the preferred option. Endoscopic ultrasound is used to puncture the cyst through the stomach or duodenum and a draining tube is placed in situ. Surgical drainage is used if endoscopic methods fail or if the cyst is complicated. Percutaneous drainage is avoided.[7]
References
  1. HEINRICH S, SCHäFER M, ROUSSON V, CLAVIEN PA. Evidence-based treatment of acute pancreatitis: a look at established paradigms. Ann Surg [online] 2006 Feb, 243(2):154-68 [viewed 31 August 2014] Available from: doi:10.1097/01.sla.0000197334.58374.70
  2. TENNER S, BAILLIE J, DEWITT J, VEGE SS, AMERICAN COLLEGE OF GASTROENTEROLOGY. American College of Gastroenterology guideline: management of acute pancreatitis. Am J Gastroenterol [online] 2013 Sep, 108(9):1400-15; 1416 [viewed 31 August 2014] Available from: doi:10.1038/ajg.2013.218
  3. THOMPSON DR. Narcotic analgesic effects on the sphincter of Oddi: a review of the data and therapeutic implications in treating pancreatitis. Am J Gastroenterol [online] 2001 Apr, 96(4):1266-72 [viewed 31 August 2014] Available from: doi:10.1111/j.1572-0241.2001.03536.x
  4. MCCLAVE SA, CHANG WK, DHALIWAL R, HEYLAND DK. Nutrition support in acute pancreatitis: a systematic review of the literature. JPEN J Parenter Enteral Nutr [online] 2006 Mar-Apr, 30(2):143-56 [viewed 31 August 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/16517959
  5. ISENMANN R, RüNZI M, KRON M, KAHL S, KRAUS D, JUNG N, MAIER L, MALFERTHEINER P, GOEBELL H, BEGER HG, GERMAN ANTIBIOTICS IN SEVERE ACUTE PANCREATITIS STUDY GROUP. Prophylactic antibiotic treatment in patients with predicted severe acute pancreatitis: a placebo-controlled, double-blind trial. Gastroenterology [online] 2004 Apr, 126(4):997-1004 [viewed 31 August 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/15057739
  6. VITALE GC. Early Management of Acute Gallstone Pancreatitis Ann Surg [online] 2007 Jan, 245(1):18-19 [viewed 31 August 2014] Available from: doi:10.1097/01.sla.0000250967.32581.c9
  7. WILSON C. Management of the later complications of severe acute pancreatitis - pseudocyst, abscess and fistula. Eur J Gastroenterol Hepatol [online] 1997 Feb, 9(2):117-21 [viewed 31 August 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/9058620