Related Subjects:
Acute Cholecystitis
|Acute Appendicitis
|Chronic Peritonitis
|Abdominal Aortic Aneurysm
|Ectopic Pregnancy
|Acute Cholangitis
|Acute Abdominal Pain/Peritonitis
|Assessing Abdominal Pain
|Penetrating Abdominal Trauma
|Acute Pancreatitis
|Acute Diverticulitis
Lipase is more useful than amylase as it is equally sensitive but more specific and is high for longer. Higher lipase does not always correlate with worse pancreatitis
Initial Management of Acute Pancreatitis |
- ABC, IV Fluids 3L+/day fluid resuscitation, Catheter
- Effective Analgesia Morphine 5-10 mg IV and antiemetics
- FBC, CRP, U&E, LFT, Amylase, Lipase, Ca, Lactate
- ABG, CXR, AXR, blood and urine cultures
- Consider Antibiotics if septic
- NG tube if vomiting. Enteral feeding following assessment
- Consider ITU/HDU for those with severe disease
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About
- Poor correlation between amylase level and severity of pancreatitis.
- Acute inflammation of the pancreas release of amylase and lipase
- Significant morbidity and mortality
- May be associated with systemic inflammatory syndrome
- Increasing incidence - improved detection and increased alcohol abuse
Causes
- Gallstones, Alcoholism
- Pancreatic cancer, Post ERCP complication
- Hereditary predisposition
- Hypertriglyceridaemia - look at fundi for lipaemia retinalis
- Hyperparathyroidism - check calcium
- Trauma, Snake bite, Infections - HIV, CMV, EBV
- Drugs - steroids, thiazides, azathioprine, sulphonamides
- ART drugs - ritonavir, didanosine
- Azathioprine, Steroids, Asparaginase
- Fibrates, Statins, Omega 3 fish oils
- Thiazide diuretics, Furosemide (US Lasix), enalapril,
- Valproic acid, Carbamazepine, Cisplatin, Erythromycin
- Pentavalent antimonials, pentamidine,octreotide, rifampicin
- Scorpion stings
Diagnosis: needs at least 2 of 3 of
- Abdominal pain
- ↑↑ amylase or lipase or equivalent (>3 times upper limit of normal).
- Imaging suggesting pancreatitis USS/CT/MRI
Aetiology
- The release of activated proteases and autodigestion of the pancreas such as trypsin, lipase and amylase causes local tissue injury and a marked inflammatory response. This can lead to a systemic inflammatory response
Differential
- Perforated peptic ulcer, Acute cholecystitis
- Biliary colic, Ischaemic bowel, Ruptured aortic aneurysm.
- Myocardial infarction - always check ECG +/- Troponin if concerned
Types
- Acute/mild/oedematous pancreatitis which settles
- Acute/severe/haemorrhagic with longer course and complications
- Pancreatic phlegmon - inflammatory mass seen by radiology/surgery
- Sterile pancreatic necrosis - pseudocyst with fluid in the lesser sac
- Pancreatic abscess - contains pus and may be drained percutaneously
- Infected pseudocyst can develop later
Clinical
- Epigastric pain through to back eased with sitting up and forwards
- The Pain may come on after a large meal
- Tachycardia, tachypnea, low BP, pyrexia
- Peritonitis with guarding, Signs of gallstones, alcoholism
- Abdominal signs may be mild but can more usually be more severe with peritonitis
- Shocked, sepsis, Bruising in flanks - Grey Turner's sign
- Periumbilical bruising - Cullen's sign (haemorrhagic pancreatitis)
Prognosis - Ranson's criteria: At admission or diagnosis
- ↑ Age > 55
- ↑ WCC > 16,000/mm3
- ↑ Glucose > 11 mmol/L [US 200 mg/dl]
- ↑ LDH > 350 iu/L
- ↑ AST > 600 iu/L
First 48 hours
- ↑ Hct fall > 10%
- ↓ Calcium < 2 mmol/L [US Ca < 8 mg/dl ]
- ↓ PaO2 < 8 Kpa
- ↑ BE > -4 mmol/L
- ↑ Urea increase > 1.8 mmol/L [US BUN increase > 5 mg/dl]
- ↑ Fluid needs > 6 L
Prognosis
- 0-2 criteria < 5% mortality
- 3-4 criteria 20% mortality
- 5-6 criteria 40% mortality
- 7-8 criteria 100% mortality
Investigations
- FBC (Hb falls with haemorrhage), U&E (Urea may rise), Calcium (falls)
- Lipids - increased Triglycerides (can cause falsely low amylase)
- Amylase - A raised Amylase > 200 Somogyi units are not unique to Pancreatitis but may also be seen in abdominal pain due to perforation of a viscus, small bowel obstruction, Leaking abdominal aortic aneurysm, Ectopic pregnancy. A level of > 1000 is more diagnostic but there is not a close correlation between amylase level and clinical severity. Raised amylase but no symptoms - macroamylasaemia is a genetically determined condition where amylase molecules polymerise and are not removed by the kidneys, but functionally normal. The result is high levels of amylase activity in the blood, with a normal pancreas. Check urinary to plasma amylase which is diagnostic.
- LFT: An ALT > 150 is a strong indicator of gallstones [1]
- Lipase - has a higher sensitivity and specificity than amylase
- Erect CXR/AXR - exclude perforation/ileus
- USS Abdomen should be done within 24 hrs to primarily look for gallstones as well as other masses, liver cirrhosis, ascites, malignancy or pseudocyst
- Blood gases - metabolic acidosis, hypoxia in severe cases
- Contrast-enhanced computed tomography (CECT) and/or magnetic resonance imaging (MRI) of the pancreas should be reserved for patients in whom the diagnosis is unclear or who fail to improve clinically. CT abdomen or more commonly now MRI can help determine how much of the pancreas is necrosed and the presence of any fluid. Fluid may be aspirated to detect infection. MRCP may be required in rare cases to exclude rare anatomical causes and may require administration of secretin. [1]
Abdominal CT showing severe pancreatic necrosis
Complications
- Pancreatic necrosis
- Pseudocyst
- Collections of pancreatic enzymes secondary to ruptured pancreatic duct. They can rupture, haemorrhage, & become infected. Manage conservatively for 4–6 wk w/ abdominal CT. Drain if growing or symptomatic or signs
of infection, or hemorrhage. Drainage can be performed by endoscopy, interventional radiology, or surgery
- Pancreatic abscess
- Ascites
- Sepsis, ARDS
- Hypovolaemic shock
- Renal failure, Hyperglycaemia, Hypocalcaemia
- Chronic pancreatitis (pain, diabetes and malabsorption)
Mortality
- Early (< 2 weeks) : SIRS and Multiorgan failure
- Late (> 2 weeks) : Complications such as infected necroses
Management
- ABCs with IV fluid replacement. Keep an accurate record of fluid balance is necessary in all but the mildest cases with CVP monitoring if needed, urinary catheter and clinical assessments of hydration, oxygenation etc. Patients who are vomiting require an NG tube. Aggressive hydration should be provided to all patients unless cardiovascular and/or renal comorbidities preclude it. Aim for urine output 30-60 mls/hr. VTE assessment. Watch Capillary blood glucose 4 hourly.
- Patients with organ failure and/or the systemic inflammatory response syndrome (SIRS) should be admitted to an intensive care unit or intermediary care setting whenever possible
- Analgesia: Any opioid usually Morphine 2.5-5 mg may be used. Traditionally Pethidene was preferred but there is no firm evidence base for this. There has been some concern over the sphincter of Oddi spasm with morphine, but recently this has been shown to be clinically irrelevant.
- Feeding: In mild cases, oral feedings can be started immediately if there is no nausea and vomiting. In severe cases, enteral nutrition is recommended to prevent infectious complications, whereas parenteral nutrition should be avoided.
- Routine use of prophylactic antibiotics in patients with severe AP and/or sterile necrosis is not recommended. Broad-spectrum antibiotics are given where sepsis is suspected. Current practice is to give IV antibiotics with good pancreatic penetration, such as meropenem, in the presence of organ failure or shock.
- ERCP and sphincterotomy should be considered usually within 72 hours where there are gallstones and cholangitis or jaundice and a common duct stone that requires removal. Cholecystectomy may be delayed and done later.
- Asymptomatic pancreatic and/or extrapancreatic necrosis and/or pseudocysts do not warrant intervention regardless of size, location, and/or extension. Surgery may be required where there is severe necrotizing pancreatitis or if there is an abscess or pseudocyst. A necrosectomy involves removing dead pancreatic tissue which may be done by laparoscopy. Infection increases the indication for necrosectomy. Necrosectomy can be done through a variety of approaches. In stable patients with infected necrosis, surgical, radiologic, and/or endoscopic drainage should be delayed, preferably for 4 weeks, to allow the development of a wall around the necrosis.
Further reading
- Working IAP/APA acute pancreatitis guidelines. IAP/APA evidence-based guidelines for the management of acute pancreatitis. Pancreatology, 2013;13 (4 suppl 2): e1-15
References