Acute pancreatitis

Acute pancreatitis

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Introduction

Acute pancreatitis is a process that occurs on the background of a previously normal pancreas and can return to normal after resolution of the episode.

Etiology
  1. Gallstones
  2. Alcohol
  3. Infections (e.g. mumps, Coxsackie B)
  4. Pancreatic tumours
  5. Drugs (e.g. azathioprine, oestrogens, corticosteroids, didanosine)
  6. Iatrogenic (e.g. post-surgical, post-ERCP)
  7. Hyperlipidaemias
  8. Miscellaneous

  • Trauma
  • Scorpion bite
  • Cardiac surgery

  1. Idiopathic
Epidemiology

3% of all cases of abdominal pain admitted to hospital.
Incidence: 2–28 per 100 000.

Pathophysiology
  • Premature and exaggerated activation of digestive enzymes within the pancreas itself.
  • Then pancreatic inflammatory response.
  • An acute rise in intracellular calcium may be the initiating mechanism.
  • Pancreatic proteolytic enzymes become activated.
  • Activated enzymes which are responsible for cellular necrosis.
  • In the case of gallstone related pancreatitis it is believed that stones occlude the pancreatic drainage at the level of the ampulla leading to pancreatic ductular hypertension.
  • A collection of fluid and debris may develop in the lesser sac, following inflammatory rupture of the pancreatic duct; this is known as a pancreatic fluid collection.
  • Such ‘pseudocysts’ are common and usually asymptomatic, resolving as the pancreatitis recovers.
  • Pseudocysts greater than 6 cm in diameter seldom disappear spontaneously and can cause constant abdominal pain and compress or erode surrounding structures, including blood vessels, to form pseudoaneurysms.
  • Pancreatic ascites occurs when fluid leaks from a disrupted pancreatic duct into the peritoneal cavity.
  • Leakage into the thoracic cavity can result in a pleural effusion or a pleuro-pancreatic fistula. 
Clinical features
  1. The typical presentation is with severe, constant upper abdominal pain, of increasing intensity over 15–60 minutes, pain radiates to the back.
  2. Nausea and vomiting are common.
  3. There is marked epigastric tenderness, but guarding and rebound tenderness are absent.
  4. Bowel sounds absent.
  5. In severe cases, the patient becomes hypoxic and develops hypovolaemic shock with oliguria.
  6. Discoloration of the flanks (Grey Turner’s sign) or the periumbilical region (Cullen’s sign) is a feature of severe pancreatitis with haemorrhage.
  7. Presentation with complications (see below)
Investigations
Blood tests
  1. Baseline investigations
    1. CBC; WBC ↑,
    2. Urea ↑ and electrolytes,
    3. blood glucose; ↑
    4. LFT ; SGPT ↑,
    5. Plasma calcium; ↓ and
    6. Arterial blood gases; pO2 ↓,
  2. Serum amylase is an extremely sensitive test (if 3x normal within 24 h). Amylase levels gradually fall back towards normal over the next 3–5 days. A persistently elevated serum amylase concentration suggests pseudocyst formation.
Caution: With a late presentation the serum amylase level may give a false-negative result.
  1. Urinary amylase levels may be diagnostic as these remain elevated over a longer period of time.
  2. Serum lipase levels are also raised for a longer time. But overall accuracy is not significantly greater than amylase.
  3. C-reactive protein level is useful in assessing disease severity and prognosis. 
These are documented at presentation and then repeated at 24 and 48 hours and provide a basis for assessing the severity of an attack.
Radiology 
  1. An erect chest X-ray to exclude gastroduodenal perforation, which also raises the serum amylase 
  2. Plain X Ray Abdomen- may show gallstones or pancreatic calcification.
  3. An abdominal ultrasound scan: to identify a possible biliary (gallstone) cause of pancreatitis. Stones within the gall bladder are not sufficient to justify but dilated intrahepatic ducts is suggestive of bile duct obstruction.
The ultrasound may also demonstrate pancreatic swelling and necrosis, peripancreatic fluid collections  In severe pancreatitis the pancreas may be difficult to visualize because of gas-filled loops of bowel.
  1. Contrast-enhanced CT scanning: It should be performed after 72 h to assess the extent of pancreatic necrosis. CT provides very valuable prognostic information. Later, repeated CT scans can detect other complications including fluid collections, abscess formation and pseudocyst development.
  2. MRI (MRCP) assesses the degree of pancreatic damage and identifies gallstones within the biliary tree. MRI is particularly useful to differentiate between fluid and solid inflammatory masses.
  3. ERCP is used as a treatment measure to remove bile duct stones in selected cases of gallstone-related pancreatitis.
Features that predict severe pancreatitis
 [The APACHE = Acute Physiology and Chronic Health Evaluation) II scoring system] 

Initial assessment
  • Clinical impression of severity
  • Body mass index > 30
  • Pleural effusion on chest X-ray
  • APACHE II score > 8
24 hrs after admission
  • Clinical impression of severity
  • APACHE II score > 8
  • Glasgow score > 3
  • Persisting organ failure, especially if multiple
  • CRP > 150 mg/L
48 hrs after admission
  • Clinical impression of severity
  • Glasgow score > 3
  • CRP > 150 mg/L
  • Persisting organ failure for 48 hrs
  • Multiple or progressive organ failure
D/D
  1. Perforated viscus,
  2. Acute cholecystitis and
  3. Myocardial infarction.
Management

Assessment of severity at presentation, 24 hours and 48 hours is important. It allows identification of the 25% of patients with a predicted severe attack.
Patients who are predicted to have severe pancreatitis and those with necrosis or other complications should be managed in a specialist centre with an intensive therapy unit and multidisciplinary hepatobiliary specialists. 
  1. Intravenous access to manage early fluid losses.
  2. Central line and urinary catheter to monitor circulating volume and renal function.
  3. Nasogastric suction prevents abdominal distension and vomitus and hence the risk of aspiration pneumonia.
  4. Baseline arterial blood gases are a key predictive factor for severity of an episode and determine the need for continuous oxygen administration.
  5. Prophylactic antibiotics. There is evidence that the beta lactam Imipenem-cilastatin reduces the incidence of infected pancreatic necrosis.
  6. Analgesia requirements. Tramadol or other opiates are the drugs of choice for immediate post-presentation pain control. has been used as a patient-controlled system continuous and adequate pain relief.
Caution: There is a theoretical risk that morphine and diamorphine  can cause sphincter of Oddi contraction and so best avoided in acute pancreatitis.
  1. Feeding. In patients with a severe episode there is little likelihood of oral nutrition for a number of weeks. Total parenteral nutrition has been associated with a high risk of infection and has been replaced by enteral nutrition.
In the absence of gastroparesis: nasogastric administration of feed without exacerbation of pain.
Postpyloric feeding should be instituted by the endoscopic placement of a nasojejunal tube (In gastroparesis or poorly tolerated nasogastric feeding (exacerbation of pain or precipitation of nausea and vomitus), postpyloric feeding should be instituted by the endoscopic placement of a nasojejunal tube).
  1. Anticoagulation with a low molecular weight heparin for DVT prophylaxis.
  2. In a small proportion of patients, multiorgan failure will develop in the first few days after presentation, reflecting the extent of pancreatic necrosis. Such patients will require positive-pressure ventilation and often renal support. The mortality in this group is extremely high (in excess of 80%).
Gallstone-related pancreatitis
  1. Endoscopic intervention with sphincterotomy and stone extraction is the treatment of choice.
  2. In the absence of bile duct obstruction, sphincterotomy and stone extraction is only of proven benefit when the episode of pancreatitis is predicted as severe.
  3. In less severe cases: the bile duct stones can be removed later by ERCP to prevent recurrent episode of pancreatitis.
  4. Cholecystectomy should be carried out as soon as feasible after the acute episode has resolved.
Complication
Systemic
  • Systemic inflammatory response syndrome (SIRS)
  • Hypoxia
  • Hyperglycaemia
  • Hypocalcaemia
  • Reduced serum albumin concentration
Pancreatic
  • Necrosis
  • Abscess
  • Pseudocyst
  • Pancreatic ascites or pleural effusion
Gastrointestinal
  • Upper gastrointestinal bleeding
  • Variceal haemorrhage
  • Erosion into colon
  • Duodenal obstruction
  • Obstructive jaundice
Prognosis
  • About 80% of all cases are mild and have a favourable outcome.
  • Overall mortality of 10%.
  • About 98% of deaths from pancreatitis occur in the 20% of patients with severe disease and about one-third of these occur within the first week, usually from multi-organ failure.
  • After this time, the majority of deaths result from sepsis.
Glasgow criteria is used to find bad prognosis.
(More than three implies severe disease.)
  1. Age > 55 yrs
  2. PO2 < 8 kPa (60 mmHg)
  3. White blood cell count (WBC) > 15 × 109/L
  4. Albumin < 32 g/L (3.2 g/dL)
  5. Serum calcium < 2 mmol/L (8 mg/dL) (corrected)
  6. Glucose > 10 mmol/L (180 mg/dL)
  7. Urea > 16 mmol/L (45 mg/dL) (after rehydration)
  8. SGPT > 200 U/L
  9. Lactate dehydrogenase (LDH) > 600 U/L
Further reading
  1. Davidson’s Principles & Practice of Medicine 22nd
  2. Kumar & Clark’s Clinical Medicine 8th
  3. Harrison’s Principles of Internal Medicine 18th

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