Complications of pancreatitis

Section: Hepatobiliary Sub-section: Pancreas Curriculum: Curriculum, page 89

Definition

Complications of Acute Pancreatitis

Key concepts:

1. Patient physiology determines need for intervention. Serial review identifies trend in patient trajectory
2. If intervention necessary, should be delayed as long as possible, best avoided in first 2 weeks following index episode
3. Each intervention carries risk and benefit. Gain maximised when intervention limited (step-up approach)

Local complications: collections

Defined by time < or > 4 weeks, presence or absence of necrosis

• Interstitial oedematous pancreatitis
  • Acute peripancreatic fluid collection (<4 weeks)
    • 25%
    • Ill defined, homogenous, may be multiple.
    • No necrotic material.
    • Usually sterile, resolve without intervention.
    • Small number may persist and develop into pseudocyst.
  • Pancreatic pseudocyst
    • Fluid collection with no solid component persisting beyond 4 weeks of presentation.
    • Can be symptomatic (biliary or gastric outlet obstruction, bleeding or become secondarily infected)
    • Thought to result from disruption of duct.
      • Disruption of duct only occurs following necrosis of duct or parenchyma (pancreatic necrosis must be present by definition).
      • Therefore, pancreatic pseudocysts are rare; most persistent collections should be thought of and managed as walled of necrotic collections.
      • Asymptomatic or small pseudocysts do not require treatment, resolve spontaneously.
• Necrotising pancreatitis
  • Acute necrotic collection (ANC)
    • Fluid collection with solid necrotic component within 4 weeks.
  • Walled-off necrosis (WON) – > 4 weeks.
    • CT – well defined, mature, enhancing wall, containing fluid and solid necrotic material.
  • Infected necrosis
    • Daignosis
      • Suspect in clinical deterioration
      • CT shows gas
      • Uncertainty consider FNA and gram stain
    • Treatment
      • Broad spectrum antiobtiocs
      • Minimally invasive techniques
        • Percutaneous, endoscopic and laparoscopic drainage
        • Step-up strategy

Complications

Organ failure

• Respiratory – non-invasive support, may need mechanical ventilation
• Cardiovascular – aggressive fluid resuscitation to optimise tissue perfusion. Acid-base balance, lactate, mixed venous O2 sats useful in assessing adequacy of volume restoration. Vasoactive support often required.
• Renal – volume resus, fluid balance. May need dialysis for fluid overload, hyperkalaemia or acidosis.
• Gastrointestinal dysfunction – compromised by splanchnic vasoconstriction (shock or secondary exogenous vasoconstrictor support).
  • Intolerance of enteral feeding
  • Breakdown of intestinal barrier, causing bacterial translocation and infection of pre-existing necrosis

Gastric outlet obstruction

• Secondary to local complicaiton e.g fluid/cysts/collections
• Casuing mechanical outlet obssutrction
• Can also be caused by delayed gastric emptying in globally sick patient

 Abdominal compartment syndrome

• Intra-abdominal hypertension present in 60-80% of patient with severe panc
• Contributed to organ dysfunction
• Eventually can elad to compartment syndrome
• Once suspected regular urinary bladder pressure measurement is advised
• Non-surgical interventions mainstay of treatment
  • Nasogastric decompression
  • Short-term use of neuromuscular blockers - deep sedation and paralysis
  • Percutaneous drainage of fluid collections.
• Decompressive laparotomy
  • Poor outcomes
  • Last resort but likely futile

Biliary obstruction

• Role of ERCP:
  • Mild disease – no role, unless after complete resolution, definitive management where cholecystectomy precluded by comorbidity.
  • Severe disease
    • If biliary sepsis (pain, jaundice, fever, within 12 hours + organ dysfunction)
    • If resolving jaundice – observe
    • Persistent jaundice but clinically improving – biliary imaging MRCP or EUS
    • Persistent jaundice and clinical deterioration – ERCP and biliary decompression
• Large collection can cause extrinsic compression of extrahepatic biliary system.

Haemorrhage

• Rare in absence of intervention.
• Relatively common into walled off collection or following necrosectomy.
• Enzymes cause erosion of major vessels with or without pseudoaneurysm formation, which may rupture and result in significant haemorrhage
• Consequence of:
  • Large raw surface
  • Partly controlled sepsis
  • Exposed major vessels
• Urgent CTA and embolization is treatment of choice
• Normal CTA may suggest venous source, with bleeding due to venous congestion maybe from portal venous thrombosis.

Venous thrombosis

• Should be on prophylactic clexane
• Splenic vein thrombosis
  • Frequently identified – combination of local inflammation, extrinsic compression and low flow state.
• SMV or portal vein thrombosis should be on therapeutic
  • LMWH for 6 months to attempt to maintain patency and avoid cavernous transformation of portal vein.

Colonic ischaemia

• Mesenteric vascular compromise common in severe acute pancreatitis.
• Part of global systemic hypoperfusion.
• Full thickness intestinal ischaemia is rare. Patchy full thickness ischaemia may lead to fistulation with secondary sepsis. Defunctioning ileostomy may be required for sepsis control.

Enteric fistula

• Abscess formation +/- focal enteric ischaemia can lead to fistulation between acute necrotic or walled off collection and lumen of the bowel.
• Foregut fistula often leads to clinical improvement; hindgut fistulas usually result in marked clinical deterioration.
• May need defunctioning ileostomy

Malnutrition

• Cochrane review including 8 RCT demonstrated reduction in mortality, systemic complications and surgical interventions in patients given enteral nutrition
• Reasonable to attempt NG prior to NJ feeding.
• TPN indicated for failure to meet nutritional needs with enteral, complex fistulas, high output losses e.g. diarrhoea

Pancreatic duct fistula

• Most commonly following drainage of a collection
  • Continue high put which is positive for amylase/lipase
• Most small volume will spontaneously heal
• If persistent
  • Endoscopic transpapillary stenting initially
    • Endoscopic drainage may be beneficial to allow gastric drainage of fistula
  • If fails may require distal pancreatectomy

Pancreatic necrosis

• Necrotising pancreatitis
  • Acute necrotic collection (ANC)
    • Fluid collection with solid necrotic component within 4 weeks.
  • Walled-off necrosis (WON) – > 4 weeks.
    • CT – well defined, mature, enhancing wall, containing fluid and solid necrotic material.

Evolution of pancreatic necrosis/collections:

1. True pancreatic necrosis – minimal separation of devitalised tissue
2. Transitional pancreatic necrosis – partial but incomplete separation
3. Walled-off necrosis (WON) – good separation of devitalised tissue within fluid-filled cavity and formation of fibrous wall lined with granulation tissue
4. Pseudocyst – almost complete resolution of solid component, well formed fibrous wall lined with granulation tissue

Management

• Not-infected

  • Observe
    • May take >12 weeks
  • May require intervention for symptoms but treatment should be delayed till after 4 weeks

• Infected

  • Diagnosis
    • Suspect in clinical deterioration
    • CT shows gas
    • Uncertainty consider FNA and gram stain
  • Treatment
    • Broad spectrum antibiotics
    • If unresolving sepsis then may require intervention
      • Minimally invasive techniques
        • Percutaneous, endoscopic and laparoscopic drainage
        • Step-up strategy

• See Surgical management of pancreatic necrosis

Late complications (> 4 weeks)

Pancreatic duct stricture

• Can result from local tissue damage and fibrotic repair.
• Can cause recurrent attacks of abdominal pain, raised lipase and dilatation of distal duct system
• Management:
  • Dilatation and temporary stenting at ERCP
  • Surgical resection of stricture along with pancreatic tail
  • Surgical drainage of pancreatic duct system into Roux loop

Disconnected duct syndrome

• Complication of necrotising pancreatitis
• Necrosis or pseudocyst may develop in former pancreatic bed following mucosal closure of cutaneous or gastric end of pancreatic fistula.
• This is preceded by necrosis, fibrosis and atrophy of the middle of the gland, leading to disconnected duct syndrome.
• EUS transgastric drainage may be useful
• Transpapillary options likely limited due to fibrotic occlusion at pancreatic neck
• Surgical resection or drainage procedures are often required, however surgery is challenging if large venous collaterals from splenic vein thrombosis
• Salvage distal pancreatectomy and splenectomy is frequently required

Late extrahepatic biliary stricture

• Result of focal fibrosis and scarring within pancreatic head.
• Debris and stones may form above stricture causing episodes of cholangitis
• Endoscopic stenting at ERCP can alleviate acute attack
• Remodelling of fibrotic segment using a fully covered self-expanding metal stent (SEMS) can results in prolonged relief, but high rate of recurrence on stent removal.
• Failure of endoscopic remodelling is an indication for a formal hepatico-jejunostomy

Portal and splenic vein thrombosis and cavernous transformation

• Associated with up 15% of patients dying with acute pancreatitis
• Venous drainage diverted to short gastric, gastroepiploic and cardinal veins causing large venous collaterals
• Late haemorrhage due to gastric varices is rare
• If surgery required, consider preoperative embolization of splenic artery to decompress system
• Right sided or SMV and portal venous occlusion with cavernous transformation of pancreatic head, duodenum and hepatico-duodenal ligament is a more significant problem as it may preclude intermediate surgical intervention (e.g. hepatico-jejunostomy).
• Recurrent low-grade sepsis in presence of cavernous transformation may be challenging to manage.
• Rarely, multivisceral transplant may be the only option