Armando Hasudungan
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Acute Pancreatitis

Acute Pancreatitis

Summary of acute pancreatitis This is a relatively common serious cause of abdominal pain in the middle aged and elderly. Often due to gallstone and alcohol. Clinical presentation is often severe constant epigastric pain radiating to the back. Serum amylase and lipase are one of the most important tests for suspicion of acute pancreatitis. Treatment is conservative and nil by mouth.

Video: Acute Pancreatitis Overview

 

Overview

Overview Acute pancreatitis is a relatively common condition presenting with severe, acute, constant epigastric pain. Incidence of ~5 per 100,000/year. Acute pancreatitis has a significant mortality. Early complications include acute renal failure, DIC, hypocalcemia and ARDS.

Definition
Acute Pancreatitis: An inflammatory process in which pancreatic enzymes are activated and cause autodigestion of the gland.
Chronic Pancreatitis: Irreversible damage causing fibrosis and scarring to the pancreas, resulting in exocrine and endocrine dysfunction
Pancreatic pseudocyst: Cystic space within the pancreas not lined by epithelial cells, often associated with chronic pancreatitis.
Presentation

Patient with severe epigastric pain

Pancreas Anatomy and Physiology

Pancreatic anatomy Pancreas extends retroperitoneally across posterior abdominal wall. It means “All (pan) Flesh (Kreas)”. The pancreas consists of the following parts:

  • Head
  • Neck
  • Body
  • Tail

The head is encircled by duodenum and tail in contact with spleen. Pancreas has a poorly developed capsule & therefore adjacent structures (common bile duct, duodenum, splenic vein, transverse colon) are commonly involved in inflammatory process.

Blood Supply

  • Pancreatic branches of the splenic artery
  • Superior pancreaticoduodenal artery
  • Inferior pancreaticoduodenal artery

Venous drainage

  • Drains with the splenic vein → Superior Mesenteric → Portal vein

Nerve invervation

  • Parasympathetic → Vagus nerve → Stimulates pancreatic juice secretion
  • Sympathetic

Lymphatic drainage

  • Head and Neck → Pancreticoduodenal nodes →
  • Body and Tail → Pancreaticosplenic nodes →

Embryology

  • Fusion of the ventral and doral outpounchings of forgut

Normal Phys

Pancreatic physiology exocrine (98%) & endocrine (2%) functions

Exocrine: Pancreatic acinar cells produce digestive enzymes, which are stored in secretory granules. The Pancreatic exocrine secretion is regulated by cephalic, gastric & intestinal stimuli. Acinar cells secrete pancreatic juice made up the enzymes:

  • Amylase → Carbohydrate digestion
  • Lipase → Lipid digestion after bile has emulsified the fat
  • Proteases (MANY!) → Protein digestion

Exocrine section is stimulated by:

  • Vagus nerve
  • Secretin (hormone)
  • Cholecystokinin

Endocrine: Islets of Langerhans – clusters of hormone-producing cells secreted directly into circulation. Endocrine cells of the pancreas:

  • Beta cells → Insulin
  • Alpha cells → Glucagon
  • D cells → Somatostatin.
Cells of the Pancreas Secretion Function
Acinar cells secrete enzymes
into the duodenum
Nucleases Breaksdown nucleotides
Proteases Digests Proteins
Lipases Digests lipids
B-amylase Digests carbohydrates
Islets of Lagerhan secrete hormones
into the bloodstream
Glucagon Stimulates glucose release into the bloodstream from glucose stores
Insulin Increases cell uptake and storage of glucose

Risk Factors

Risk Factors
Middle aged
Gallstones
Alcohol
Hypertriglyceridaemia
Medications

  • Azathioprine
  • Thiazide diuretics
  • Furosemide
HIV/AIDS
Endoscopic retrograde cholangiopancreatography
Trauma
SLE
Sjogren’s syndrome

Signs and Symptoms

Sands

Clinical Presentation Severe constant epigastric pain radiating to the centre of the back, with associated nausea and vomiting. The patient may be distressed, sweating and mildy pyrexial. Signs of guarding, tripod position seems of relieve pain. Signs of shock is severe acute pancreatitis. The oftiquoted, but uncommon bluish discolouration in the loins (Grey Turner’s sign) only develops after several days

Investigations

Investigations

Investigations Serum amylase and lipase are diagnostic. Serum lipase remains elevated for longer then serum amylase and is more specific, but less sensitive. Other investigations include CRP (elevated), FBC, LFT (show abnormality), EUC and serum glucose. Abdominal x-ray can be performed but often show un-specific findings. CT may be required (shows pancreatic oedema, haemorrhage and necrosis). Ultrasound scan must be done within 48hours of admission to identify gallstone in the bile duct.

Remember Amylase is not specific to the pancreas. It can be elevated in gastrointestinal ischemia with infarction or perforation, vomiting associated with pancreatitis can cause elevated amylase of salivary origin. Elevated serum lipase level is more specific than is amylase to pancreatic origin and remains elevated longer than does amylase

Diagnosis Should be suspected in a patient with acute onset of a persistent, severe, epigastric pain with tenderness on palpation. Requires the presence of 2 of the following 3 criteria:

  • Acute onset of persistent, severe, epigastric pain often radiating to the back.
  • Elevation in serum lipase or amylase to 3 times or greater than the upper limit of normal.
  • Characteristic findings of AP on imaging (CT, MRI, transabdominal ultrasound).

Severity

Glasgow Imrie criteria (PANCREAS)

  • PaO2 <8kPa
  • Age >55y – Poorer Prognosis
  • Neutrophils/WCC >15000
  • Corrected Calcium – Increased protease in serum chelates serum calcium
  • Raised blood urea – Increased protease in serum leads to increase in protein breakdown leading to ureamia
  • Elevated Enzymes – LFT dysfunction (specifically in gall stone causes)
  • Albumin – Increased protease leads to albumin breakdown and shift of albumin to interstitium cause of increased in permeabiliy.
  • Sugar, blood glucose >10mmol/L – beta cell damage

Grades of severity

  • Mild acute pancreatitis
    • No organ failure
    • No local or systemic complications
  • Moderately severe acute pancreatitis
    • Organ failure that resolves within 48 h (transient organ failure) and/or
    • Local or systemic complications without persistent organ failure
  • Severe acute pancreatitis
    • Persistent organ failure (>48 h)
      • Single organ failure
      • Multiple organ failure

Aetiology

Aetiology

Aetiology The most common cause of acute pancreatitis is gallstones (60%) and alcohol (30%). Many are idopathic. Good acronym to remember is GETSMASHED

Pathophysiology

Pathology2

Pathophysiology Inflammation of pancreas results in cell death. The pancreatic cells release its enzymes everywhere resulting in further pancreatic inflammation. The enzymes self-digests the pancreatic tissue. Lipase and amylase levels are increased in the blood.


Difference between acute pancreatitis and chronic pancreatitis

difference between acute and chronic

Management

Treatment of pancreatitis is mainly supportive and includes “pancreatic rest”. Withholding food or liquids by mouth until symptoms subside, and adequate narcotic analgesia, usually with meperidine.

management

Management Conservative treatment involves oxygen, obtaining IV access for IV fluids and collecting bloods. IV analgesia + antiemetic. Nil-by-mouth and provide and nasogastric tube. Insert urinary catheter and monitor urine output hourly. Also monitor blood pressure and heart rate. Consider early insertion of a central venous line to monitor central venous pressure and guide IV fluid therapy in the seriously ill particularly the elderly.

Complications

Complications

Complications Acute pancreatitis has a significant mortality. Early complication include acute renal failure, disseminated intravascular coagulation (DIC), hypocalcemia, respiratory distress. late complications include pancreatic abscess or pseudo abscess and fat necrosis. Necrosis may be sterile or infected. Haemorrhage may occur and result in Cullen’s sign (periumbilical eccymosis) on 5% of cases. If risk factors for pancreatitis is not changed, chronic pancreatitis may result long-term.

Continuous pancreatic inflammation may develop into full blown MODS or SIRS.


Signs of systemic inflammatory response syndrome (SIRS)

SIRS—defined by presence of two or more criteria:

  • Heart rate >90 beats/min
  • Core temperature <36°C or >38°C
  • White blood count <4000 or >12000/mm3
  • Respirations >20/min or PCO2 <32 mm Hg

Prognosis Mortality is associated with pancreatic necrosis and the presence of sepsis.

Difference between acute and chronic pancreatitis

difference between acute and chronic

References

UpToDate
Best Practice