Pancreatitis pt.1 Flashcards
What is pancreatitis?
Inflammation of the pancreas
Mortality rate of pancreatitis
Most cases are mild (mortality <1%) but patients can deteriorate quickly, severe cases have a high mortality rate (~15%)
Causes of acute pancreatitis
- Most common causes in the UK are gallstones and alcohol
- The most common causes can be remembered with the mnemonic ‘I GET SMASHED’. The first 4 letters represent the most common causes of pancreatitis.
I – Idiopathic
G – Gallstones/Genetic (Cystic Fibrosis)
E – Ethanol
T – Trauma
S – Steroids
M – Mumps (and other infections)/Malignancy
A – Autoimmune
S – Scorpion sting
H – Hypercalcaemia/Hypertriglyceridemia
E – ERCP
D – Drugs (Medication)
What are risk factors for pancreatitis
male gender, increasing age, obesity, smoking
Etiology of acute pancreatitis
Typically caused by hypersecretion or backflow (due to obstruction) of exocrine digestive enzymes, which results in autodigestion of the pancreas
Signs and symptoms of acute pancreatitis
- Upper abdominal pain, typically severe and sudden in onset (usually described as radiating to the back)
- Pain that gets worse after eating
- Nausea and vomiting
- Decreased appetite
- Fever
- Tachycardia
History taking in acute pancreatitis
- Past medical: history of gallstones, biliary disease, or previous pancreatitis.
- Past surgical: recent procedures (e.g., ERCP).
- Drug history: regular and over-the-counter medications.
- Social history: alcohol intake, smoking.
- Family history: hereditary pancreatitis.
Clinical examination findings in acute pancreatitis
- Epigastric tenderness, abdominal distention (due to local reactive ileus or retroperitoneal fluid), reduced bowel sounds (if an ileus has developed).
- Signs of systemic inflammatory response (indicative of more severe pancreatitis): fever, hypotension, tachycardia (this one is less helpful since it can be an adrenergic response to pain and stress).
= Specific signs: Cullen’s sign (periumbilical bruising), Grey-Turner’s sign (flank bruising).
Complications of acute pancreatitis
Local:
Ongoing inflammation can lead to ischaemic infarction of the tissue which could cause pancreatic necrosis. This can be suspected in patients with:
severe acute pancreatitis
signs of sepsis/prolonged raised inflammatory markers
clinical deterioration (after 72h usually)
Necrotic tissue is prone to infection and may require specialist management (e.g. drainage) hence the need to escalate your concerns to seniors.
Pancreatic pseudocysts can also occur
Systemic:
Pancreatitis can also lead to systemic complications. These include pulmonary complications such as ARDS or pulmonary oedema. Inflammatory changes may also extend to the kidneys, stomach, colon which can lead to related complications.
- Early: necrotising pancreatitis, infected pancreatic necrosis, pancreatic abscess, acute respiratory distress syndrome (ARDS).
- Late: pancreatic pseudocysts, portal vein/splenic thrombosis, chronic pancreatitis, pancreatic insufficiency (more commonly affects exocrine function).
Assessing severity of pancreatitis
- The level of serum amylase does not have any bearing onto the severity of pancreatitis itself.
- Severity can be calculated using several scores, and are used for prognostication of acute pancreatitis.
- These include the modified Glasgow criteria, APACHE II and the Ranson criteria
Where is the pancreas found?
Sits in the upper part of the retroperitoneal space of the abdomen
What can the pancreas be divided into and where are they found?
The pancreas has four parts:
- A head,which sits in the C-shaped cavity created by the duodenum, and usually has a small uncinate process which hooks upwards behind the superior mesenteric artery and superior mesenteric vein
- The constricted neck connects the head to the body, behind this the portal vein forms from the union of the splenic and superior mesenteric veins
the body runs upwards and to the left across the midline - The tail travels with the splenic vessels between the layers of the splenorenal ligament, to reach the hilum of the spleen
Function of the pancreas
The pancreas functions as both an exocrine and an endocrine gland:
- The exocrine pancreas consists of acinar and ductal cells which produce 750-1000ml of pancreatic juice per day. This is secreted into the duodenum via the pancreatic duct and aids the processes of digestion and absorption of food.
- The endocrine pancreas consists of tiny clusters of endocrine cells called the islets of Langerhans which are embedded throughout the pancreatic tissue. There are several different cell types which release specific hormones into the bloodstream via capillaries and play an essential role in regulating glucose homeostasis and gut function.
What can pancreatic damage be divided into? Which is more common and which is more severe?
Pancreatic damage can be classified into two major categories:
- Interstitial oedematous pancreatitis: most common, better prognosis
- Necrotising pancreatitis: less common, around 5-10%, more severe
Is damage reversible in pancreatitis?
The damage that occurs during acute pancreatitis is potentially reversible (to varying degrees), whereas chronic pancreatitis involves ongoing inflammation of the pancreas that results in irreversible damage.
What is chronic pancreatitis associated with?
Chronic pancreatitis is associated with endocrine and exocrine dysfunction, as well as chronic abdominal pain
Diagnosis of acute pancreatitis
he International Association of Pancreatology criteria state that two of three criteria must be satisfied for a diagnosis of acute pancreatitis to be made:
- Abdominal pain plus a history suggestive of acute pancreatitis
- Serum amylase/lipase of over three times the upper limit of normal
- Imaging findings characteristic of acute pancreatitis
What can acute pancreatitis be classified into clinically?
Classification of acute pancreatitis is governed by the Atlanta Criteria:
- Mild: most common, no organ dysfunction/complications, resolves normally within a week
- Moderate: initially some evidence of organ failure which improves within 48 hours
- Severe: persistent organ dysfunction for greater than 48 hours, together with local or systemic complications
Differential diagnosis of severe sudden onset upper abdominal pain/epigastric pain
Severe, sudden onset epigastric pain has several other serious causes. These include:
Leaking abdominal aortic aneurysm
Aortic dissection
Myocardial infarction
Perforated gastric/duodenal ulcer
Esophageal rupture
Imaging (e.g. CT) is often required to rule out alternate pathology.
Diverticula vs diverticulitis
- Diverticula are small pouches that form in the wall of the colon, usually without causing sympting
- Diverticulitis occurs when diverticula become inflamed or infected (e.g. from blockage), leading to symptoms like abdominal pain, fever, and changes in bowel habits
Laboratory investigations for pancreatitis
Routine bloods including LFTs and lactate are warranted as well as serum amylase and serum lipase. Serum lipase is being a preferred diagnostic marker due to its accuracy. Bone profile i.e. calcium, triglycerides, alcohol level on admission can all further assist on identifying the underlying cause (to subsequently guide management).
- CRP and FBC
- U/Es
Bedside investigation in pancreatitis
ECG: a baseline investigation that should be performed for all patients presenting with epigastric pain (to avoid missing the myocardial infarction masquerading as epigastric pain)
Urinalysis: a routine investigation in acute abdominal pain (however, the urological system is unlikely to be the cause of sudden onset epigastric pain)
Laboratory investigations
Imaging in pancreatitis
As mentioned previously, the diagnosis of acute pancreatitis can and should be made clinically, however, imaging is sometimes used to support the diagnosis or rule out other pathology.
Relevant imaging investigations include:
- Erect chest X-ray: used to look for free gas under the diaphragm (pneumoperitoneum) in patients who present with epigastric tenderness.
- Abdominal ultrasound (USS)
- CT abdomen and pelvis (CT-AP)
Abdominal ultrasound in pancreatitis
- A useful investigation to assess the biliary tree for evidence of obstruction (e.g. biliary dilatation).
- The pancreas can sometimes be assessed using abdominal USS (e.g. evidence of oedema may be noted), however, the presence of bowel gas often obscures the pancreas, making assessment difficult or impossible.
- It is not to look for pancreatitis specifically. This can then inform whether there is a risk of an obstructing stone that may need an ERCP to remove it.
CTAP in acute pancreatitis
- Used to exclude other causes of severe abdominal pain and assess for complications of pancreatitis (e.g. pseudocyst formation).
- CT-AP provides optimum imaging of the pancreas and is typically performed at 48-72 hours after the initial presentation if patients do not clinically improve (to assess for evidence of pancreatic necrosis or other complications)
- not routinely used to diagnose pancreatitis. The findings of necrosis usually become clearer after 48-72 hours and that is when CT imaging could be considered. It could be considered if the clinical assessment & blood tests prove inconclusive with pancreatitis.
Management of acute pancreatitis
- No curative management, supportive treatment is the mainstay
- Attempt to treat the underlying cause, particularly if gallstones are present
- Immediate supportive management includes: Agress IV fluids resuscitation (5-10 ml/kg/hr or 3-5L per day), correction of electrolyte disturbances, analgesia (condition is severely painful, paracetamol and opiates are needed), nil by mouth until pain improves, control of blood glucose
- If oral diet is not tolerated, consider whether patients need NJ feeding in patients with severe disease as this is unlikely to resolve within a few days. If enteral feeding is not possible, total parenteral nutrition (TPN) should be considered in people with ongoing lack of nutrition, though enteral feeding is associated with better outcomes. Oral feeding can be built up as the patient tolerates (unless there’s ileus or too much pain to allow this
Antibiotics in pancreatitis
Current evidence suggests that routine antibiotic use for acute pancreatitis does not provide any benefit to patients and therefore should be avoided. In the context of pancreatic necrosis, antibiotics are often used prophylactically due to the increased risk of infection
What is done during sphincterotomy in ERCP?
Dilation of the sphincter of oddi (a muscular valve surrounding the major duodenal papilla in your digestive tract that controls the flow of bile and pancreatic juice out of the gallbladder and pancreas respectively through the ampulla of Vater into the second part of the duodenum
What controls the sphincter of oddi?
The sphincter of Oddi is relaxed by the hormone cholecystokinin via vasoactive intestinal peptide when eating
Gallstone pancreatitis management
Specific management of gallstone pancreatitis may include:
- Endoscopic retrograde cholangiopancreatography (ERCP): to relieve biliary obstruction, with or without sphincterotomy to dilate the sphincter of Oddi. This allows ductal stones to be removed, biliary sludge to be cleared, and relief of the obstructed biliary tree driving pancreatitis.
- Cholecystectomy: should be performed on all patients with gallstone pancreatitis during the same admission as the acute episode. Delay is associated with a high chance of disease recurrence and readmission. The bile duct should be explored during this procedure to rule out ductal stones.
When does Pancreatic abscess occur and management
occurs when peripancreatic collections of fluid become infected, urgent drainage is required
When does infected pancreatic necrosis happen and management
occurs when necrosing pancreatic tissue becomes infected, patients require antibiotics and necrosectomy
Lipase vs amylase for pancreatitis
- Both are digestive enzymes released from acinar cells of the exocrine pancreas
- While amylase is cleared in the urine, lipase is reabsorbed back into the circulation.
- In cases of acute pancreatitis, serum activity for both enzymes is greatly increased. Serum lipase is now the preferred test due to its improved sensitivity, particularly in alcohol-induced pancreatitis.
- Lipase is also thought to be more specific for the pancreas than amylase due to its relative but not exclusive organ specificity.
- Its prolonged elevation creates a wider diagnostic window than amylase. In acute pancreatitis, amylase can rise rapidly within three to six hours of the onset of symptoms and may remain elevated for up to five days. Lipase, however, usually peaks at 24 hours with serum concentrations remaining elevated for eight to 14 days. This means it is far more useful than amylase when the clinical presentation or testing has been delayed for more than 24 hours.
- Current guidelines and recommendations indicate that lipase should be preferred over total and pancreatic amylase for the initial diagnosis of acute pancreatitis and that the assessment should not be repeated over time to monitor disease prognosis. Repeat testing should be considered only when the patient has signs and symptoms of persisting pancreatic or peripancreatic inflammation, blockage of the pancreatic duct, or development of a pseudocyst.
- Testing both amylase and lipase is generally discouraged because it increases costs while only marginally improving diagnostic efficiency compared to either marker alone.
What are pancreatic pseudocysts?
This a collection of fluid containing enzymes, blood and necrotic tissue. These are often managed conservatively as the majority will respond however they are also prone to haemorrhage/rupture/infection and a sudden deterioration must raise concern
