Gastroenterology - Diseases of the pancreas Flashcards
What are the different types of pancreatitis?
Pancreatitis is divided into acute and chronic. Acute pancreatitis occurs on the background of a previously normal pancreas and the pancreas returns to functionally and structurally back to normal after the episode. It occurs as isolated or recurrent attacks.
In chronic pancreatitis, there is continuing inflammation with irreversible structural changes. In practice it is not always possible to separate acute from chronic forms because the acute causes (if untreated) may eventually lead to chronic pancreatitis and there may be relapses of the chronic condition - “acute on chronic pancreatitis”
What is the prognosis in acute pancreatitis?
Most patients will recover from the attack with only general supportive care, but 25% will develop severe acute pancreatitis with multiorgan failure and about 20% of these patients die.
Name some causes of acute pancreatitis
"I GET SMASHED" Idiopathic Gallstones Ethanol Trauma (e.g. post ERCP, post surgical)
Steroids
Mumps
Autoimmune
Scorpion bites
Hypercalcaemia/ hypertriglyceridaemia (metabolic conditions)
ERCP
Drugs (azothioprine, oestrogens, didanosine)
What is the pathogenesis of acute pancreatitis?
Whatever the cause, the final common pathway is marked elevation of intracellular calcium leading to activation of intracellular proteases and the release of pancreatic enzymes. Acinar cell injury and necrosis follows, which promotes migration of inflammatory cells from the microcirculation into the interstitium.
Release of a variety of mediators and cytokines leads to a local inflammatory response and sometimes a systemic inflammatory response that can result in single or multiple organ failure.
What are the clinical features of acute pancreatitis?
Usually epigastric or upper abdominal pain radiating through to the back, associated with nausea and vomiting.
On examination:
- epigastric or general abdominal tenderness
- guarding
- rigidity
- be wary of other symptoms (e.g. coma, multiorgan failure) that may dominate the clinical picture
- Ecchymoses around the umbilicus (Cullen’s sign) or in the flanks (Grey-Turner’s sign) indicate severe necrotizing pancreatitis
What blood tests should be performed in pancreatitis?
- Raised serum lipase or amylase in conjunction with an appropriate history and clinical signs, strongly indicates a diagnosis of acute pancreatitis. Normal levels of amylase occur if the patient presents late when urinary amylase or serum lipase levels may still be raised
- FBC, CRP, U&E, LFT, Ca++, and ABG are also measured on admission and at 24 and 48 hours and used to assess the severity of pancreatitis
NB - amylase can also be raised in acute cholecystitis, perforated peptic ulcer and intestinal ischaemia, but very high levels (i.e. >3 times normal) are diagnostic
What is the Glasgow criteria?
Glasgow criteria for pancreatitis grades severity and predicts the likelihood of a poor prognosis. Three or more factors present during the first 48 hours predict a severe episode. These include: “PANCREAS”
PaO2 <8.0kPA Age >55 Neutrophilia >15 Calcium <2 uRea >16 Enzymes - LDH, aminostransferase Albumin <30 g/L Sugars (BM >10)
What imaging should be requested in cases of suspected pancreatitis?
An erect CXR is performed to exclude perforated peptic ulcer as the cause of the pain and raised amylase.
Abdominal US is performed as a screening test to look for gallstones as a cause of pancreatitis and may show swelling of the inflamed pancreas.
Contrast enhanced spiral CT scanning or MRI is performed in all but the mildest attack of pancreatitis to confirm the diagnosis, identify the presence and extent of pancreatic necrosis (associated with organ failure and higher mortality) and identify peripancreatic fluid collections. It is performed after 72 days as early CT may underestimate the severity of pancreatitis.
How should patients with pancreatitis be managed?
Risk stratification is essential as management depends on severity. Glasgow criteria, Ranson’s criteria and the acute physiology and chronic health evaluation score (APACHE) are acceptable tools. Obesity and a CRP >200 mg/L in the first 4 days are also associated with a worse outcome.
If predicted severe disease:
- medical therapy
- HDU or ITU
- prophylactic antibiotics
- nasogastric feeding
- ERCP within 48 hours if gallstone pancreatitis and/or cholangitis
- contrast enhanced CT/ MRI within 3-7 days
- monitor for complications
If predicted mild disease:
- medical therapy (pain control, NBM, IV fluid, NG tube)
- monitor for complications
What general supportive care should be offered to patients with acute pancreatitis?
Early fluid replacement is essential and in severe pancreatitis 5L or more of crystalloid daily may be required to maintain adequate urine output (>0.5ml/kg body weight/ hour).
Supplemental oxygen is given and requirements are guided by pulse oximetry and ABGs.
LMWH is given to prevent DVT.
Electrolyte and metabolic abnormalities are corrected and a sliding scale (variable rate) insulin infusion may be necessary for control of blood glucose.
Pain is controlled by pethidine and tramadol and a patient controlled system is necessary if persistent. Morphine is avoided because it increases sphincter of Oddi pressure and may aggravate pancreatitis.
In patients with predicted severe attacks, there is a likelihood of oral nutrition for a number of weeks. Nutrition is provided by a nasogastric tube or nasojejunal tube (placed endoscopically) for patients who are intolerant of nasogastric feeding due to exaccerbation of pain or nausea and vomiting.
What therapies can be given in acute pancreatitis to reduce the severity or frequency of complications?
Broad spectrum antibiotics - e.g. cefuroxime or aztreonam, reduce the risk of infection of the necrotic pancreas and are given from the outset. Early ERCP (within 48-72 hours) and sphincterotomy improves the outcome in patients with biliary pancreatitis and evidence of cholangitis or a high suspicion of CBDstone (dilated CBD or CBD stone seen on US or jaundice) or when pancreatitis is predicted to be severe.
Surgical treatment is sometimes required for very severe necrotising pancreatitis, particularly if it is infected or if complications such as pancreatic abscesses or pseudocysts appear.
What are the complications of acute pancreatitis?
Hyperglycaemia
Hypocalcaemia
Renal failure
Shock
What causes hypovolaemic shock in pancreatitis?
Third space extravasation. Third space fluid is sequestered fluid that is unavailable for maintaining volume in the vascular compartment. In acute pancreatitis, it refers to the peripancreatic collection of fluid that commonly occurs as the pancreas autodigests itself. If conditions improve, the third space fluid gains entry back into the vascular compartment and may cause fluid overload.
What causes hypoxaemia in pancreatitis?
Circulating pancreatic phospholipase destroys surfactant.
Loss of surfactant induces atelectasis and intrapulmonary shunting, which produces a V/Q mismatch.
ARDS may also occur.
What is a pancreatic pseudocyst?
This is a complication of pancreatitis in 20% of cases. It is a collection of digested pancreatic tissue around the pancreas. It presents as an abdominal mass with a persistence of serum amylase >10 days (amount of amylase in the fluid surpasses the renal clearance).
Treatment depends on the size, if <5cm, observe and follow with CT scan. Most resolve without surgical intervention. If >5cm, treat with CT or US guided drainage.
