FRCA Notes

Acute Pancreatitis

A previous ICM SAQ on pancreatitis (54% pass rate) offered half of the total marks avaiable for knowing the management in a critical care setting.

The remainder were for knowing the aetiology, diagnostic criteria and classifications of severity.

Resources

  • Acute pancreatitis is an acute inflammatory disorder of the pancreas
  • The incidence of acute pancreatitis is rising, typically 10-30/100,000
  • It accounts for 2.4% of ICU bed occupation
  • In-hospital mortality is as high as 40%

Classification

  • Interstitial oedematous pancreatitis (80%)
    • Typically a milder disease course
    • Resolution of inflammation without lasting local or systemic effects

  • Necrotising pancreatitis (20%)
    • Necrosis of the pancreas and/or peri-pancreatic tissue
    • Far greater propensity for systemic complications

  • The acronym 'I-GET-SMASHED' is the classical way of remembering the causes of acute pancreatitis
  • Gallstones and alcohol account for 2/3rds of cases

    • I GET SMASHED

  • Idiopathic or Ischaemic (e.g. shock, CPB, vasculitides)

  • Gallstones
    • Lifetime risk of acute pancreatitis <2%
    • When gallstones migrate into biliary tree, transient obstruction of the pancreatic duct occurs
    • There is premature intracellular activation of digestive enzymes
    • 'Autodigestion' of pancreatic cells occurs, leading to an intense inflammatory response
  • Ethanol
    • Lifetime risk among chronic, heavy drinkers <5%
    • Via a direct toxic effect on pancreatic cells
    • Sustained, high alcohol intake a greater risk than binge drinking
  • Trauma - be it blunt, penetrating or surgical in nature

  • Steroids
  • Mumps, EBV, CMV, coxsackie virus
  • Autoimmune
  • Scorpion venom
  • Hypercalcaemia (e.g. from hyperparathyroidism), hyperlipidaemia, hypothermia
  • ERCP - due to obstruction of biliary tree by contrast media injection
  • Drugs including NSAIDs, diuretics, azathioprine and sulfonamides

  • Genetic causes include cystic fibrosis and ɑ1-antitrypsin deficiency
  • Malignant pancreatitis e.g. from carcinoma

Additional risk factors

  • T2DM
  • Obesity
  • Smoking
  • Social deprivation

Early Phase

  • Host response to pancreatic injury causes systemic inflammatory response
  • May cause precipitous multi-organ failure and death
  • Local complications may be present (see below)
  • For the majority, the inflammation resolves
  • A minority progress to a late phase

Late Phase

  • There is evolution of local complications ± organ failure
  • As with early phase, it is the degree of accompanying organ failure that determines mortality

Revised Atlanta criteria for acute pancreatitis

  • Need at least two from:
    1. Epigastric or generalised abdominal pain consistent with disease
    2. Raised serum amylase (or serum lipase) >3x upper limit of normal
    3. Characteristic imaging results from ultrasound, contrast-enhanced CT or MRI

Other features

  • Abdominal distension ± peritonism
  • Vomiting
  • Pyrexia
  • Retroperitoneal haemorrhage:
    • Grey-Turner's sign (flanks)
    • Cullen's sign (umbilicus)
    • Fox's sign (inguinal ligament)

Severity stratification

  • Mild disease is characterised by the absence of local complications or organ failure
  • Moderate disease is defined by:
    • 'Transient' organ failure (<48hrs)
    • Local/systemic complications without persistence
  • Those with organ failure persisting beyond 48hrs are deemed to have severe disease

  • Scoring systems (e.g. the Glasgow-Imrie Score) do not robustly predict outcome in a clinically meaningful timeframe

    • Factors indicating high risk of critical care admission
    Age >70yrs
    BMI >30kg/m2
    Not responsive to initial fluid resuscitation
    >30% pancreatic necrosis
    CRP >150mg/L at 48hrs
    Pleural effusions
    ≥3 Ranson's criteria

  • Treatment of acute pancreatitis is entirely supportive
  • The initial aims of medical management are:
    • (Goal-directed) fluid therapy
    • Analgesia
    • Supplemental oxygen

Intravenous fluids

  • There is frequently significant intravascular volume depletion, owing to a combination of:
    • Decreased oral intake
    • Vomiting
    • Capillary leak
    • High insensible losses (fever, tachypnoea)
    • Vasodilation causing 'relative' hypovolaemia
  • This leads to pancreatic hypoperfusion

  • Therefore fluid therapy should occur early, with some suggestion the benefit is limited beyond 24hrs
  • No strong evidence-based recommendations for fluid type/volume/rate of administration
    • As such practice is extrapolated from sepsis management i.e. balanced crystalloids to maintain organ perfusion as evidenced by normal lactate and UO >0.5ml/kg/hr
    • There's a growing suggestion that aggressive fluid therapy:
  • Early vasopressor therapy may help limit harmful effects of high-volume fluid resuscitation

Analgesia

  • Effective analgesia has positive sequelae beyond the patient experience, such as:
    • Reducing the stress response
    • Minimising pulmonary complications such as atelectasis, lobar collapse, LRTI

  • A typical analgesic regimen includes:
    • Paracetamol (but avoidance of NSAIDs)
    • Parenteral opioids ± PCA

  • The recent EPIPAN study (2023) has cast doubt on the role of the thoracic epidural in these patients
    • Patients were randomised to TEA + standard care or standard care alone
    • No significant difference in ventilator-free days at 30 days
    • TEA use was associated with a longer duration of mechanical ventilation

Oxygenation

  • Early effective analgesia to reduce hypoventilation
  • HFNO increasingly used to avoid mechanical ventilation
  • SpO2 >94% unless otherwise indicated
  • Production and excretion of inflammatory mediators leads to damage of the alveolo-capillary membrane, leading to ARDS

Nutrition

  • Enteral nutrition should be commenced within 72hrs if inadequate normal diet
    • No evidence to support 'resting' the pancreas
    • No evidence to support earlier enteral nutrition support
    • Nasogastric route preferred; NJ tube only if NG feeding isn't tolerated e.g gastric outlet obstruction from local complications

  • Enteral nutrition is preferred over PN due to:
    • Maintaining gut integrity and reducing risk of translocation
    • Reduces (line) infection associated with PN
    • Cheaper
    • Avoids need for central line
    • Associated with improved morbidity/mortality due to less pancreatic necrosis and organ failure

  • Hyperglycaemia often accompanies pancreatitis due to stress-mediated counter-regulatory hormone secretion and loss of functioning pancreatic islet cells
  • No evidence to support anything other than 'conventional' glycaemic control (<10mmol/L)

Antibiotics

  • Not routinely recommended as inflammation is often sterile
  • There may be concomitant infection (cholangitis, pneumonia) or developing infection (infected necrosis)
  • Should use antibiotics in those with proven or suspected bacterial infections

Care bundle

  • VTE prophylaxis
  • Stress ulcer prophylaxis
  • Maintain UO >0.5ml/kg/hr - avoid nephrotoxic drugs

Interventional

  • Identification and definitive management of gallstones to prevent recurrent disease (e.g. cholecystectomy, ERCP ± endoscopic biliary sphincterotomy)
  • Removal of infected intra- and extra-pancreatic necrosis

Specialist centre referral indications

  • Necrotic, infective, haemorrhagic or systemic complications of acute pancreatitis
  • Acute pancreatitis in children
  • Tertiary referral if hospital stay >2 weeks after onset of symptoms

Local collections

  • Acute peri-pancreatic fluid collection

  • Pancreatic necrosis
    • May be either an acute necrotic collection or walled - off necrosis
    • No role for prophylactic antbiotics
    • Sterile necrosis rarely requires intervention
    • Infected necrosis may require intervention; this should be delayed at least two weeks and until 'walled-off' necrosis has occurred
    • Intervention includes percutaneous drainage and minimally invasive necrosectomy (high mortality)

  • Pancreatic pseudocyst formation
    • An encapsulated collection of fluid with minimal necrosis
    • Typically sterile, enzyme-rich fluid
    • Typically resolve spontaneously without any intervention

Local vascular complications

  • Splenic, mesenteric or portal vein thrombosis
    • Due to intensive inflammation adjacent to major venous structures
    • May require anticoagulation

  • Arterial pseudoaneurysm of the splenic or hepatic artery branches
    • High risk of bleeding and mortality >30%
    • Recommended to undergo prophylactic transcatheter arterial embolisation

  • Intra - abdominal haemorrhage

Regional complications

Systemic complications

  • Exocrine insufficiency
  • Endocrine insufficiency ('type 3c diabetes')
  • ARDS
  • MODS