Pancreatitis Flashcards
1
Q
Aetiology of acute pancreatitis
A
- Gallstones and alcoholism together account for about 80% of acute pancreatitis worldwide.
- Small gallstones may cause transient obstruction as they pass through the ampulla via the bile ducts, or larger stones may impact at the lower end of the common bile duct, resulting in pancreatic duct obstruction.
- Beyond this, the precise mechanism of gallstone pancreatitis remains obscure.
2
Q
History and investigations helpful in determining the cause of acute pancreatitis
A
History:
- Previous gallstones
- Alcohol intake
- Family history
- Drug intake
- Exposure to known viral causes or prodromal symptoms
Initial investigations (acute phase)
- Pancreatic enzymes in plasma
- Liver function tests
- Ultrasound of gall bladder
Follow-up investigations (recovery phase)
- Fasting plasma lipids
- Fasting plasma calcium
- Viral antibody titres
- Repeat biliary ultrasound
- MRCP
- CT (helical or multislice with pancreas protocol)
3
Q
Pathophysiology of acute pancreatitis (1)
A
- Acute pancreatitis is characterised by the sudden onset of diffuse inflammation of the pancreas.
- A range of diverse factors initiate disturbances of cellular metabolism, chiefly concerned with membrane stability.
- This leads to inappropriate activation of zymogens (pre-enzymes) within the pancreas.
- Activation of trypsin is probably the key initiating event and this overwhelms intrinsic antitrypsin activity, leading to interstitial oedematous pancreatitis.
- Fortunately, the extent and severity of inflammation remain mild and self-limiting in most patients and systemic effects are mild.
- In the least severe cases, there is minimal peritoneal exudation and no pancreatic changes detectable on contrast-enhanced CT scanning.
- In more severe disease, the pancreas becomes swollen and oedematous but remains viable.
- If laparotomy is inadvertently performed at this stage, clear, non-infected peritoneal fluid is found, with whitish patches on great omentum and mesentery representing areas of fat saponification (‘fat necrosis’).
- If it is extensive, calcium becomes sequestered in these areas and this is incriminated in the drop in blood calcium characteristic of severe acute pancreatitis.
4
Q
Pathophysiology of acute pancreatitis (2)
A
- As severity increases, trypsin and other enzymes cause increasingly extensive local damage as well as activation of complement and cytokine systems leading on to systemic inflammatory response syndrome (SIRS) and organ failure.
- Manifestations include shock, acute respiratory distress syndrome (ARDS), renal failure and disseminated intravascular coagulation
5
Q
Pathophysiology of acute pancreatitis (3)
A
- A substantial proportion of these patients develop infection of the necrotic pancreas, usually with Gram-negative organisms translocated from bowel.
- This occurs within 2 weeks of the onset and greatly increases mortality.
- Pancreatic abscess formation is a different phenomenon, developing later and having a somewhat better prognosis.
- In patients dying of acute necrotising pancreatitis, the peritoneal cavity becomes filled with dark, blood-stained inflammatory exudate containing fine lipid droplets.
- This is known as acute haemorrhagic pancreatitis.
- The peritoneal surface is grossly inflamed and semi-digested, and the pancreas is a necrotic mass.
6
Q
Clinical features of acute pancreatitis
A
Mild attack
- Acute abdominal pain
- Minimal or rapidly resolving abdominal signs, e.g. abdominal distension, some abdominal tenderness and guarding, absent bowel sounds
- Minimal systemic illness
- Moderate tachycardia
Severe attack
- Severe acute abdominal pain
- Severe toxaemia and shock
- Generalised peritonitis (diffuse abdominal tenderness, guarding, rigidity, absent bowel sounds)
- Acute respiratory distress syndrome (may develop during the first few days)
7
Q
Investigation of suspected pancreatitis
A
- Plasma amylase: A level above 1000 i.u. /ml is usually regarded as diagnostic of acute pancreatitis
- Plasma lipase
- elevated alanine aminotransferase (ALT) levels are highly specific for gallstone pancreatitis
- X Ray
- USS
- CT/Contrast CT - demonstrates necrosis
- Endoscopy
8
Q
Clinical classification
A
Categorisation is based on thoroughly tested scoring systems originally developed by
- Ranson in USA and
- modified by Imrie
9
Q
Glasgow scoring system of severity prediction in acute pancreatitis
A
Ranson’s Criteria
10
Q
Mild acute pancreatitis
A
- Mild attacks are common. The patient looks generally well with minimal systemic features.
- Nevertheless, there is often considerable pain. The abdomen is usually distended and diffusely tender but with little guarding.
- Bowel sounds are absent as a result of inflammatory ileus.
- The patient may be mildly jaundiced from periampullary oedema.
- The differential diagnosis includes biliary colic, acute cholecystitis, an acute exacerbation of a peptic ulcer or even a perforation of a peptic ulcer.
- Lower lobe pneumonia or an inferior myocardial infarction may sometimes present like this.
- Sometimes the pancreatitis diagnosis is made after plasma amylase is unexpectedly found to be elevated.
11
Q
Severe acute pancreatitis
A
- In a severe attack the patient looks apathetic, grey and shocked and there are typical abdominal signs of generalised peritonitis, i.e. extreme tenderness, guarding and rigidity.
- In this case, the differential diagnosis includes other major abdominal catastrophes, especially faecal peritonitis from perforated large bowel and concealed haemorrhage from a leaking aortic aneurysm or ruptured ectopic pregnancy.
- Massive bowel infarction due to arterial occlusion may present like this but abdominal signs are less marked.
- An important early and dangerous complication of severe acute pancreatitis is acute respiratory distress syndrome (ARDS).
12
Q
Management of acute pancreatitis
Mild
A
Mild attacks:
- Mild attacks require no further emergency investigation once diagnosed on plasma amylase, and are managed by fluid resuscitation and analgesia: recovery is usually rapid. These patients need no dietary restriction.
- Later management is aimed at treating predisposing factors.
- Gallstones should be sought by ultrasonography; if present, cholecystectomy is the definitive treatment and is ideally performed on the same admission or at worst 2–4 weeks after recovery.
- Ductal stones should be removed endoscopically before discharge from hospital. Alcohol abuse must be discouraged.
13
Q
Management of acute pancreatitis
Severe (1)
A
Specified list of criteria which should be evaluated on admission:
- Haemoglobin estimation and white cell count
- Arterial blood gas estimations
- Blood sugar
- Plasma electrolytes, creatinine and urea
- ‘Liver function tests’ (i.e. bilirubin, alkaline phosphatase, lactate dehydrogenase (LDH), transaminases, plasma proteins)
- Plasma calcium and phosphate
- C-reactive protein
systemic toxaemia (SIRS)(Systemic Inflammatory Response Syndrome), shock and multiple organ dysfunction syndrome (MODS); ARDS(Acute Respiratory Distress Syndrome) develops rapidly with little warning but a deteriorating arterial PO2 may herald its onset.
14
Q
Management of acute pancreatitis
Severe (2)
A
- Supportive measures are still the mainstay of treatment.
- These include oxygen supplementation and carefully planned intravenous fluid resuscitation.
- A nasogastric tube is passed to aspirate the stomach only if gastroparesis causes troublesome vomiting.
- Enteral nasogastric or nasojejunal feeding has been reported to significantly decrease morbidity.
- If enteral feeding is not tolerated because of ileus, then total parenteral nutrition may be necessary.
- Gross fluid and electrolyte disturbances as well as hypocalcaemia are also likely to occur.
15
Q
Complications of acute pancreatitis
Mortality
A
- 15% of patients admitted to hospital with acute pancreatitis have severe disease, which carries a high risk of potential complications
- further 10% initially diagnosed with mild pancreatitis deteriorate markedly during admission and become severe
- mortality is 10–30%, i.e. 2–5% of all cases, and obese patients have a higher mortality.
- About half of those that die, do so within the first week, usually of ARDS and pulmonary failure
- Other early life-threatening complications are associated with multiple organ dysfunction (MODS)
16
Q
Complications of acute pancreatitis
Pancreatic necrosis and infection
A
- pancreatic and peripancreatic necrosis may manifest during the first 2 weeks of the attack
- identified using intravenous contrast-enhanced CT scanning in which necrotic pancreas does not opacify, having lost its blood supply
- Infection of devitalised pancreatic and peripancreatic tissues occurs in about one-third of patients with severe pancreatitis
- Infection may be suspected on CT by gas bubbles in pancreatic fluid collections but can only be confirmed by percutaneous aspiration (with microscopy and culture of the aspirate), usually performed under CT guidance.
17
Q
Complications of acute pancreatitis
Fluid collections around the pancreas
A
- acute peripancreatic fluid collections may develop
- CT-guided percutaneous drainage is valuable
- Fluid collections persisting for longer than 6 weeks are termed pancreatic pseudocysts
- pancreatic abscess may appear. This is a well-localised collection of pus within the gland, and contrasts with infected necrotising pancreatitis which appears earlier and is not localised.
18
Q
Chronic pancreatitis
A
- patients suffer persistent and severe upper abdominal pain
- These patients do not develop the other features of acute pancreatitis and may not have elevated amylase levels
- Carcinoma of the pancreas and chronic pancreatic inflammation should both be considered in patients with this pattern of pain
- Inflammatory swelling of the pancreatic head occasionally causes obstructive jaundice but carcinoma in this position is a far more common cause of jaundice.
- usually no abnormal abdominal signs
