Acute Severe Pancreatitis: Causes

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Acute severe pancreatitis

Acute infl ammation of the pancreas may cause local tissue destruction and
a generalized infl ammatory response causing distal organ failure.

Causes

P ost-procedure (e.g. after ERCP or biliary surgery).


A lcohol (up to 40% of cases).
N eoplasms (pancreatic).
C ystic fi brosis, or C old (hypothermia).
R heology (e.g. vasculitis/SLE, hypoperfusion, ischaemia).
E ndocrine (hypercalcaemia).
A natomical/functions abnormalities.
T riglycerides/hyperlipidaemia.
I diopathic.
T rauma (especially blunt abdominal trauma).
I nfections (especially mumps, rubella, EBV, HIV, CMV).
S tones/gall stones (up to 35% of cases).
Toxins (e.g. steroids, azathioprine, didanosine, pentamidine,
envenomation).

Presentation and assessment

General: pyrexia, marked third-space loss (i.e. oedema, ascites, pleural


effusions).
Abdominal/GI: abdominal pain (often radiating to the back):
Nausea and vomiting, diarrhoea may also occur
Cullens sign (umbilical bruising)
Grey Turners sign (fl ank bruising)
Cardiovascular: tachycardia, hypotension.
Respiratory: tachypnoea/dyspnoea due to pain or metabolic acidosis.
Respiratory distress and/or hypoxia may occur due to abdominal
splinting or pleural effusion
Renal: oliguria (<0.5 ml/kg/hour), AKI, metabolic acidosis.
Other:
Super-added infection/sepsis (typically respiratory or abdominal)
Hypocalcaemia
Hyperglycaemia
Multiple organ failure

Investigations

ABGs (metabolic acidosis is common; hypoxia).


FBC (raised WCC; thrombocytopaenia in DIC).
Coagulation screen ( i PT/APTT, d fi brinogen in DIC).
U&Es, (raised urea/creatinine if AKI develops).
LFTs (jaundice or liver dysfunction, especially with gall stone disease or
malignancy).
Serum amylase and lipase (raised in pancreatitis, but moderate rises
may be non-specifi c).
Serum glucose (hyperglycaemia is common).
Serum calcium (hypocalcaemia is common).

Serum magnesium and phosphate, and serum CRP.


Blood, urine and sputum culture (if infection is suspected).
CXR, AXR (raised hemidiaphragm, pleural effusions, basal atelectasis,
or pulmonary infi ltrates may be present).
US abdomen (to evaluate the biliary tract or identify gall stones).
CT abdomen, contrast-enhanced (to confi rm the diagnosis and assess
severity); indications for CT include:
Hyperamylasaemia, clinically severe disease, temperature >39
Ranson score >3, APACHE II score >8
Failure to improve after 72 hours of conservative treatment
Acute deterioration
CT abdomen should be repeated after 4872 hours to identify and
delineate any complications/necrosis which may have developed.

Differential diagnoses

Bowel obstruction/perforation, or bowel ischaemia.


Cholecystitis/cholangitis.
Renal colic.
MI.
Pneumonia.

DKA.

Immediate management

Give O 2 as required, support airway, breathing, and circulation.


In severe cases respiratory support may be required using NIV or
mechanical ventilation:
Drainage of massive pleural effusions may improve lung function
Drainage of severe ascites to improve ventilation has been
described
Aggressive fl uid resuscitation is likely to be necessary, with inotropic/
vasopressor support as required:
Urinary catheterization and fl uid balance monitoring is required
Invasive monitoring of CVP may be required
CO monitoring may be helpful if CVS instability is present
Analgesia (e.g. morphine PCA or infusion) and antiemetics should be
prescribed.
Correct coagulopathy/electrolyte disturbance:
Hypocalcaemia may be corrected with calcium chloride 10% IV
(10 ml)
Hyperglycaemia is likely to require an IV insulin sliding scale
The severity of the pancreatitis should be assessed using a scoring
system ( b p.279).

Further management
Regular reassessment of oxygenation/fl uid balance is required.
Maintain glycaemic control (serum glucose 610 mmol/L).
Intra-abdominal pressure monitoring should be commenced in patients
with severe abdominal distension and/or oliguria unresponsive to
blood pressure and fl uid status correction.
Renal replacement therapy may become necessary.
NGT enteral feeding is possible in most patients (80%) but an NJ tube
may be needed:
PN may be used in patients in whom a 7-day trial of enteral feeding
has failed
If gallstone obstruction is suspected ERCP should be performed
(ideally within 2472 hours of onset):
Early cholecystectomy may be indicated
Be vigilant for complications, including:
Pancreatic necrosis, abscess or pseudocyst formation
Diabetes mellitus; hypocalcaemia
Pancreatic encephalopathy
Sepsis
Early sepsis is likely to be extra-pancreatic in origin (e.g. pneumonia).
Pancreatic necrosis may result in super-added pancreatic infection:
Routine antimicrobial prophylaxis is not generally recommended
(although the evidence is inconclusive, and some centres still use
prophylaxis)
Where infection is suspected (e.g. by the presence of gas on
radiological imaging) radiologically-guided fi ne-needle aspiration
should be attempted
Where infection or abscess is confi rmed, antibiotics (e.g.
meropenem 1 g IV 8-hourly) and radiologically guided drainage
should be undertaken
In severe cases surgical pancreatic necrosectomy may become
necessary, but it should be noted that delayed surgery is associated
with better survival than surgery undertaken early
Indications for surgical referral include infected pancreatic necrosis or
pancreatic abscess, persistent biliary peritonitis.

Pitfalls/diffi cult situations


An APACHE II score >8 is associated with a severe attack; identifying
severe cases early enables rapid aggressive intervention.
CT scanning within 48 hours may underestimate necrosis but initial
scan may help with differential diagnosis.
Timing of surgical intervention can be diffi cult, early intervention is
associated with higher mortality.
Pseudocyst formation is common (10% of cases), but rarely needs
urgent treatment.
There is little evidence at present that drug therapy such as octreotide
is of any benefi t.
Pancreatitis complicated by Candida infections is associated with worse
outcomes, and empiric antifungal cover may be needed in severe

infections (e.g. using an echinocandin such as caspofungin).


Other factors associated with severity/worse outcome include:
Pleural effusion present on admission
CRP >150 mg/L within fi rst 48 hours of symptoms
Obesity (BMI >30)
Proven necrosis >30%
Persistent organ failure

Pancreatitis severity scoring


Ranson criteria (score 1 for each of the following): 1
At presentation:
Age >55
Blood glucose > 11 mmol/L
White cell count >16 x 10 9 /L
Lactate dehydrogenase (LDH) >400 iu/L
AST >250 iu/L
Within 48 hours after presentation:
Haematocrit fall by >10%
Serum calcium <2 mmol/L
Base defi cit >4 mmol/L
Blood urea rise >1 mmol/L
Fluid sequestration >6 L
PaO 2 <8 kPa.
Score 02 < 1% mortality Score 34 15% mortality
Score 56 40% mortality Score >6 ~100% mortality
Modifi ed Glasgow scale ( _ 3 in 48 hours predicts severe disease) 2
Age >55.
PaO 2 <8 kPa.
WCC >15 x 10 9 /L.
Serum calcium <2 mmol/L.
ALT >100iu/L.
Lactate dehydrogenase (LDH) >600 iu/L.
Blood glucose >10 mmol/L.
Serum albumin <32 g/L.
Blood urea >16 mmol/L.
Computed tomography grading
A radiological grading system is also used ranging from A (normal) to D (thmost severe grade, associated
severe infl ammation, necrosis or infection).
Reprinted with permission from the Journal of the American College of Surgeons, formerly
Surgery Gynaecology & Obstetrics. Prognostic signs and the role of operative management
in acute pancreatitis. Randon JHC, Rifkind KM, Roses DF, et al., Surg Gynecol Obstet
1974;139:6981.
2 Reproduced from Gut , S.L. Blamey et al ., Prognostic factors in acute pancreatitis, 25, 12,
pp.13401346, copyright 1984, with permission from BMJ Publishing Group Ltd.
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