An inflammatory disorder of the parenchyma of the pancreas can present as either acute or chronic pancreatitis (Banks et al., 2010). This paper aims to discuss the pathology of pancreatitis.

Aetiology

Gall stone obstruction and high alcohol consumption are among the commonest causes (Bhattacharya, 2013). Other causes include mechanical obstruction or injury from Trauma, post ERCP, periampullary neoplasms, parasites such as Ascaris lumbricoides, hereditary conditions like pancreas divisum, medications (corticosteroids, azathioprine), ischaemic conditions (artheroembolism, shock, polyarteritis nodosa), mumps, coxsackievirus, scorpion bite, hypertriglyceridemia, and hyperparathyroidism or other hypercalcaemic states. With the exclusion of the above causes, autoimmune pancreatitis and hereditary pancreatitis the cause may be considered to be idiopathic (Bhattacharya, 2013; Cotran et al., 2014; Mohy-ud-din and Morrissey, 2020).

Pathophysiology

Tissue injury results from inappropriate activation of pancreatic enzymes and subsequent autodigestion (Shah et al., 2019). Three mechanisms have been proposed and all lead to the primary endpoint of acinar cell injury (Cotran et al., 2014): (1) pancreatic duct obstruction, where external compression or internal blockage of pancreatic duct results in accumulation of pancreatic fluid, subsequent activation of lipase, interstitial fat necrosis, recruitment of inflammatory cells, the release of inflammatory cytokines within the parenchyma, increased vascular permeability, interstitial Edema, further vascular compromise and finally acinar cell injury (Cotran et al., 2014; Shah et al., 2019). (2) Primary acinar cell injury, where there is direct damage to the acinar cell from substances like alcohol or ischaemic states. (3) defective intracellular transport, where misplaced packaging of digestive enzymes with hydrolytic enzymes within the cell leads to aberrant activation of lysosomal enzymes and acinar cell injury (Cotran et al., 2014).

Following injury, there is an activation of pancreatic enzymes, usually, trypsin and digestion of parenchymal components setting up focal tissue injury and inflammation. In mild pancreatitis there is usually only Edema and inflammation with focal fat necrosis; while severe forms involve widespread proteolysis of acinar duct cells and blood vessels causing necrotising pancreatitis with haemorrhage and fat necrosis (Bhattacharya, 2013; Gapp and Chandra, 2020; Mohy-ud-din and Morrissey, 2020.  There can be a release of activated pancreatic enzymes in circulation leading to systemic manifestations (Cotran et al., 2014)

Clinical presentation

The patient usually presents with sudden onset epigastric pain that is severe, continuous, and radiating to the back (Bhattacharya, 2013; Cotran et al., 2014; Shah et al., 2019). The pain may sometimes localise to the right or left upper quadrant and radiate to the chest. The patient may feel some relief when sitting up but the pain is generally refractory to most pain killers. It is associated with nausea and vomiting with retching (Bhattacharya, 2013).

Certain systemic manifestations may arise and include shock (breakdown of gastrointestinal barrier with flora), acute respiratory distress syndrome (widespread alveolar destruction by enzymes), DIC (from widespread activation of coagulation factors by trypsin), renal failure, neurologic disturbances, subcutaneous fat necrosis (action of lipases) and arthralgia (Banks et al., 2010, Chatila et al., 2019; Cotran et al., 2014). A rare syndrome of pancreatic panniculitis and polyarthritis may also develop.

On physical examination, the patient is relatively well in mild pancreatitis. With severe illness, the patient may have signs of shock (tachypnoea, tachycardia, hypotension, confusion); fever and jaundice suggesting a gall stone aetiology; epigastric tenderness, absence of bowel sounds, and sometimes grey turner’s or Cullen’s sign from haemorrhage into the fascial planes (Bhattacharya, 2013; Cotran et al., 2014; Gapp and Chandra, 2020).

Laboratory findings

Elevated serum amylase to 3 times above reference range within 24 hours of presentation. Additional elevated lipases within 96 hours. Elevated CRP and procalcitonin, raised white cell count and hypocalcaemia are equally useful (Bhattacharya, 2013; Shah et al., 2019).

Concerning imaging modalities, contrast-enhanced CT is the gold standard for diagnosis. Transabdominal Ultrasound may be beneficial in gall stone pancreatitis. Plain abdominal radiography may only be used to rule out other causes such as calcified gall stones; MRI is also very informative with the added benefit of non-ionizing radiation (Bhattacharya, 2013; Shah et al., 2019).

Severity scores

To identify patients with severe pancreatitis that may need an intensified level of care and monitoring, certain severity scores are available to the clinician.

Patients are classified as severe and in need of urgent care in the following:

APACHE (Acute Physiology and Chronic Health Examination) II score ≥8 on admission

Evidence of organ dysfunction on admission

CRP ≥ 150mg/L at 48 hours post-admission

Glasgow score >3 at 48 hours post-admission

Ranson score >3 at 48 hours post-admission

Evidence of necrosis on contrast-enhanced CT (using Balthazar criteria)

Procalcitonin >1.8 ng/mL19,24

(Balthazar, 1990; Bhattacharya, 2013; Chatila et al., 2019; Matull et al., 2006; Shah et al., 2019)