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acute pancreatitis

Written by Chin Ming Huay

Last Reviewed: April 2019

Review Due: April 2020

 

DEFINITION

' a new-onset inflammatory disorder of the pancreas with the severity of the disease ranging from mild oedema to pancreatic necrosis and multiple organ failure'

 

AETIOLOGY

I GET SMASHED

Idiopathic

Gallstones

Ethanol

Trauma

Steroid

Malignancy/Mumps

Autoimmune

Scorpion Sting

Hypertriglyceridaemia/Hypercalcaemia

ERCP

Drugs (e.g. diuretics, NSAIDs and azathioprine)

N.B. Gallstones, excessive alcohol intake and post-ERCP are the most common causes of acute pancreatitis

SIGNS AND SYMPTOMS

Pain

Site: Epigastric

Onset: Rapid onset, gradually worsening over several hours

Character: Tight, ‘band-like’

Radiation: Radiates to the back

Associated symptoms: As below

Timing: Hours

Exacerbating Factors: Worse on moving

Relieving Factors: Lying down, not moving

Severity: Moderate to very severe

Nausea & Vomiting

Loss of appetite (mostly due to pain)

Steatorrhoea (pale stools) and darker urine may be present

 

In severe pancreatitis:

Grey Turner’s Sign (bruising of the flanks)

Cullen’s Sign (periumbilical bruising)

Signs of hypovolaemia or hypovolaemic shock (including tachycardia, dry mucous membranes, cool peripheries and sweaty/clammy skin)​

 

PATHOPHYSIOLOGY

The pancreas becomes inflamed in response to autodigestion of the pancreatic cells which occurs when the digestive enzymes in pancreatic secretions become activated. This triggers a systemic inflammatory response and significant movement of fluid into the peritoneal cavity (third space losses) due to leaky capillaries therefore leading to hypovolaemia and hypovolaemic shock.

 

Gallstone pancreatitis is caused by obstruction of the flow of pancreatic enzymes into the duodenum by a gallstone. Trypsinogen is cleaved into trypsin, leading to damage of the pancreatic acinar cells. Increased intracellular calcium may also potentiate activation of trypsinogen.

 

There are a few different mechanisms involved in alcohol-induced pancreatitis. Alcohol may directly affect the pancreatic acinar cells, causing inflammation and damage to the cell membranes. It may also interfere with calcium homeostasis which may potentiate activation of trypsinogen.

 

Investigations

Serum Amylase

Diagnostic if raised more than 3 times the upper limit of normal, within 24 hours of onset of pain. Levels start to fall back to normal after 3-5 days, so delayed serum amylase testing may show a false negative.

FBC

Raised WCC

U&Es

Raised Urea

LFTs

Evidence of gallstone disease

 

Bone Profile

Low Calcium

 

Erect CXR

To exclude duodenal perforation which may be another cause of epigastric pain and raised serum amylase, also to exclude ARDS which may be a complication of pancreatitis

 

Abdominal Ultrasound

To investigate for gallstone disease

 

CT/MRCP

To assess pancreatic damage

 

TREATMENT

Treatment for acute pancreatitis is largely supportive. If there is a clear reversible underlying cause, such as gallstones, this should be treated appropriately.

Analgesia

IV Fluids

Fluid losses in pancreatitis can be significant. Ensure haemodynamic stability and measure urine output.

Thrombroprophylaxis

Subcutaneous LMWH for prevention of DVT and PE

Feeding

Early enteral nutrition is preferred however this may be through an NG tube if patient cannot tolerate normal diet

Specific Causes:

Alcohol - Counselling, referral to addiction services if required and vitamin replacement

Gallstones - ERCP or Cholecystectomy may be indicated

EPIDEMIOLOGY

Incidence in the UK ranges from 150 to 420 cases per 1,000,000 people.

 

 
 

COMPLICATIONS

Systemic Inflammatory Response

Multiorgan Failure

Pancreatic Pseduocysts

Pancreatic Necrosis

Pleural Effusion

Pneumonia

Acute Kidney Injury

Paralytic Ileus

Jaundice

Portal Vein Thrombosis

Hypo/Hyperglycaemia

Hypocalcaemia

 

PROGNOSIS

The Glasgow PANCREAS scoring system for pancreatitis indicates severity and predicts mortality.

 

PaO2 <8.0 kPa

Age >55 years
Neutrophils (Total white cell count) >15 x109/L

Calcium <2mmol/L

Renal (Increase in urea) >1.8mmol/L
Enzymes – Serum LDH >600U/L and serum AST >250U/L
Albumin <30g/L
Sugar (Blood glucose) >10 mmol/L

A score >3 suggests severe pancreatitis

Mortality:

0-2 of the above: Mortality <1%

>6 of the above: Mortality can go up to 100%

 

REFERENCES

NICE Guideline 104 Pancreatitis 2018 https://www.nice.org.uk/guidance/ng104
 

Zyromski NJ. Acute Pancreatitis. BMJ Best Pract. 2019 https://bestpractice.bmj.com/topics/en-gb/66/guidelines


Kumar & Clark. Kumar and Clark’s Clinical Medicine, 8th Edition | Parveen Kumar, Michael Clark. Saunders Ltd. 2012.