Acute pancreatitis Flashcards
What is acute pancreatitis?
Autodigestion of pancreatic tissue by the pancreatic enzymes, leading to necrosis
What is the pathophysiology of acute pancreatitis?
- A disorder of the exocrine pancreas (part of the pancreas responsible for digestive enzyme secretion), and is associated with acinar cell injury with local and systemic inflammatory responses.
- Inflammatory condition of the pancreas → damage to pancreas causes release of digestive proteolytic enzymes that autodigest pancreatic tissue. This leads to necrosis, inflammation etc
What are the causes of acute pancreatitis?
I GET SMASHED: Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune/Ascaris infection, Scorpion venom, Hypertriglyceridaemia, ERCP, Drugs.
What drugs can cause acute pancreatitis?
- Mesalazine
- Azathioprine
- Sodium valproate
- ## Furosemide
Are gallstones more common in males or females?
Females
Are alcoholic causes of acute pancreatitis more common in males or females?
Males
How can acute pancreatitis be classified?
- Mild- no organ failure, no complications
- Moderate- no/transient (<48 hours) organ failure, possible complications
- Severe- persistent (>48 hours) organ failure, possible complications
What are the clinical features of acute pancreatitis?
- Constant severe epigastric pain that radiates to the back- sudden onset (stabbing pain), worse with movement and may improve when leaning forward
- Abdominal distension
- Nausea and vomiting
- Fever
- Decreased appetite (anorexia)
- Signs of pleural effusion due to diaphragm irritation
- Signs of Shock (severe AP) → hypovolaemia (dry mucous membranes, decreased skin turgor, sweating), hypotension, tachycardia
What do we see in severe pancreatitis?
Haemorrhagic pancreatitis is a severe form of pancreatitis due to extensive bleeding and necrosis within the pancreas and surrounding tissues.
You see:
- Cullen’s sign - peri umbilical bruising
- Grey-Turner - flank bruising
What can nausea and vomiting lead to?
- Dehydration ( can lead to hypovolemic shock)
- electrolyte abnormalities
- hypokalaemic metabolic alkalosis ( vomiting leds to loss of H+ and CL- and loss of H+ causes K+ to leave cells -> excretion)
What is the Glasgow score (PANCREAS) for severity?
≥3 means severe pancreatitis.
- PaO2 <7.9kPa
- Age >55
- Neutrophilia
- Calcium <2mmol - hypocalcaemia is indicator of severity
- Renal function (urea >16 mmol)
- Enzymes → (LDH >600 (tissue damage) or AST >200 (liver))
- Albumin <32 g/L
- Sugar (glucose >10 mmol)
What other scoring systems can you use for severity of pancreatitis?
Ranson score or APACHE II.
What bedside investigations for acute pancreatitis?
Abdominal exam,
basic observations,
ECG
capillary blood glucose,
What are the common blood tests for acute pancreatitis?
- High serum amylase or lipase - amylase will rise in the first 3 days then drop
- FBC:
- Leukocytosis with **left shift - increase in number of immature neutrophils in the blood due an acute inflammatory response.
- Elevated Haematocrit (>44%) is predictor of poor prognosis due to increased risk of developing necrotising pancreatitis as it indicates severe fluid loss and inadequate perfusion.
- Urea/Creatinine (elevated means dehydration/hypovolaemia)
- LFTs → elevated ALT (Alanine aminotransferase) from hepatocytes suggests gallstones as the cause.
- Also check for coagulation screen to show if the liver is working properly
- May cause Hypocalcaemia (indicator of severity)
- CRP → if >200 units/L there is high risk of developing pancreatic necrosis
Which is more useful - amylase or lipase?
Lipase is more sensitive and specific than serum amylase.
Has longer half life than amylase and can be useful for late presentations (>24 hours)
Does amylase correlate with disease severity?
No, it does not indicate severity.
What imaging is done in acute pancreatitis and why?
Early US imaging to assess aetiology, contrast-enhanced CT for complications such as pseudocysts or necrotising pancreatitis.
When can diagnosis of acute pancreatitis be made without imaging?
Characteristic pain + amylase/lipase 3x normal.
What are the key aspects of management for acute pancreatitis?
- Fluid resuscitation- Aggressive early hydration with crystalloids with a urine output aim of >0.5mls/kg/hr
- Analgesia with IV opioids
- Enteral nutrition normally offered for anyone with moderately severe or severe acute pancreatitis within 72 hours of presentation - it can also help improve outcomes if oral nutrition is not tolerated due to nausea + vomiting
- Avoid NBM unless necessary - parental nutrition inly if enteral nutrition fails.
When can we do ERCP for acute pancreatitis?
For gallstone pancreatitis.
When is debridement done in acute pancreatitis?
For patients with infected necrosis AND worsening organ dysfunction.
What complications are there of acute pancreatitis?
ARDS, peripancreatic fluid collections, pseudocysts (can occur 4 weeks after, persistently raised amylasE), pancreatic necrosis, abscess, haemorrhage, sepsis, acute renal failure, hypocalcaemia.
What is the prognosis like of acute pancreatitis?
Majority improve in 3-7 days; mortality increases in severe cases.
What causes chronic pancreatitis?
Alcohol abuse most of the time.
When is pain worse in chronic pancreatitis?
15-30 mins after meals.
What is a main symptom of chronic pancreatitis?
Steatorrhoea due to pancreatic insufficiency. (foul smelling, greasy stool)
Other symptoms include: epigastric pain, weight loss etc.
What other condition develops in most patients with chronic pancreatitis?
Diabetes mellitus (>20 years after symptoms begin) due to loss of endocrine function due to progressive pancreatic destruction
Therefore they need HbA1c monitoring every 6 months.
What investigations are the main ones for chronic pancreatitis?
- CT pancreas with IV contrast most sensitive at detecting pancreatic calcification
- Faecal elastase (will be low) - used to assess exocrine function as it assesses pancreatic enzyme production
- Normal amylase/lipase in chronic pancreatitis
Management of chronic pancreatitis?
Pancreatic enzyme supplements (creon - mixture of digestive enzymes) and analgesia.
