So, today I was on a consultant ward round, with one of those consultants that loves to cross-examine their medical students. I actually don’t mind the questioning. I know some students hate it and find it intimidating but I find it really helpful and it lets me engage with the ward round. Famous last words…
But, yep. So there was a patient with pancreatitis of unknown cause. And the consultant asks us students, what are the causes of pancreatitis? And because I was halfway through this blog post I could give him a few, without having to be the one that said scorpion bite. Yay me! SMASHED it 😉
The patient had no evidence of gallstones on ultrasound and didn’t drink excessively. So, consultant gets started on the F1s- what about other causes? Have you checked for viruses? Calcium? Any medications? Come on guys, go through your sieve. And I think to myself- wow, being an F1 is kind of like being a medical student but with more responsibility. Still get cross-examined by consultants. Still need to use mnemonics.
Definition: inflammation of the pancreas. May be acute, with variable involvement of other regional tissues or remote organ systems or chronic, characterised by irreversible parenchymal atrophy and fibrosis leading to impaired endocrine and exocrine function.
Aetiology/ risk factors:
-There is self-perpetuating pancreatic inflammation by enzyme-mediated autodigestion (e.g. pancreatic enzyme juice back pressure due to gallstones blocking bile duct = activation of pancreatic pro-enzymes within pancreatic ducts/acini), oedema and fluid shifts causing hypovolaemia as extracellular fluid is trapped in the gut, peritoneum and retroperitoneum (worsened by vomiting).
-Progression may be rapid from mild oedema to necrotizing pancreatitis. 50% of cases that advance to necrosis are further complicated by infection.
–Causes of acute pancreatitis: Get Smashed (I don’t think there is a single doctor or med student that doesn’t use this mnemonic. If you’re a non-medic, just pull this one out if you’re ever in A&E for jokes. Make up the context.)
Ethanol (second most common-35%)
Mumps (other infection: EBV, CMV, Coxsackie B, mycoplasma)
Scorpion venom (according to the lecturer that first introduced us to this mnemonic, students always remember this one for some reason…)
Hyperlipidaemia, Hypercalcaemia (e.g. from Hyperparathyroidism), Hypothermia
ERCP (& other abdo surgery) & Emboli
Drugs e.g. Azathioprine, oestrogens, thiazides, isoniazid, NSAIDs, valproate
Also- pregnancy, neoplasia, idiopathic
Chronic Pancreatitis: alcohol (70%), idiopathic (20%), familial (rarely), cystic fibrosis (=thick exocrine secretions, plugged up pancreatic duct), haemochromatosis (iron overload), pancreatic duct obstruction (stone, tumour), recurrent acute pancreatitis, hyperparathyroidism (raises Ca), hypertriglyceridaemia, autoimmune, congenital (pancreas divisum- single pancreatic duct is not formed, but remains as two distinct dorsal and ventral ducts)
–Acute pancreatitis is common: annual UK incidence ~1/1000
-Peak age is 60yrs. Males = alcohol Female = gallstones
–Chronic pancreatitis: annual UK incidence ~1/100,o00
-Mean age is 40-50yrs in alcohol associated disease
-gradual or sudden severe epigastric or central abdominal pain radiating to the back
–sitting forward may relieve pain, aggravated by movement
-vomiting prominent, nausea, anorexia
-Recurrent severe epigastric pain that ‘bores’ through to back, relieved by sitting forward or hot water bottles. Can be exacerbated by eating or drinking alcohol.
–Steatorrhoea- fatty stool = pale, floats, hard to flush, foul smelling
–Symptoms relapse and worsen
–rigid abdomen +/- local/ general tenderness
–shock– low BP, cold peripheries, pale, clammy skin, low urine output
–ileus (function bowel obstruction from reduced motility)- absent bowel sounds
–jaundice (e.g. from gallstones or alcoholic liver pathology)
–Cullen’s (periumbilical bruising) and Grey Turner’s (flank bruising) signs if severe and haemorrhagic
–Erythema ab igne (a.k.a hot water bottle rash- mottled, dusky greyness) from hot water bottle use
-signs of complications e.g. malnutrition, weight loss
-brittle (uncontrollable) diabetes- swings in blood glucose levels
–Serum amylase: raised (> 1000 U/mL or ~3x upper limit of normal). Level not related to disease severity. May be normal even if severe disease as levels start to fall within 24-48h. (Cholecystitis, mesenteric infarction & GI perforation can cause small rises in amylase. Excreted renally, so renal failure raises levels.)
–Serum lipase: raised. More sensitive & specific test than amylase, but more expensive, so no prize for guessing which one is used in hospital…
–FBC: raised WCC
–U&Es, Glucose: high, Calcium high
–CRP: elevated inflammatory marker. > 150 mg/L at 36h after admission is a predictor of severe pancreatitis.
–LFTs: may be deranged if gallstone or alcoholic pancreatitis
–ABG: monitor oxygenation and acid base status, for hypoxia and metabolic acidosis
–Abdominal X-ray: absence of psoas (muscle) shadow suggesting retroperitoneal fluid, sentinel loop of proximal jejenum.
A sentinel loop is a dilation of an isolated segment of small intestine near the site of an inflamed organ, indicating localised ileus due to the inflammation leading to local muscle paralysis, distention and gas accumulation. In acute pancreatitis the sentinel loop is usually seen in left hypochondrium. (Acute cholecystitis = right hypochondrium. Acute appendicitis = right iliac fossa).
–Erect chest X-ray: exclude other causes e.g. perforation (would show air under diaphragm). There may also be pleural effusion.
–CT: standard choice of imaging if diagnosis uncertain or to assess severity and complications- e.g. necrosis, deterioration
–MRI: may be better than CT, but more expensive, less available. See where this is going…
–U/S: look for gallstones or biliary dilation
-ERCP: if liver function tests worsen (but ERCP is also a cause of pancreatitis so take care)
–Glucose: serum glucose elevated (endocrine function of pancreas affected- essentially diabetes). May do a glucose tolerance test.
–Amylase & Lipase: usually normal
–Immunoglobulins: may be raised, especially IgG4 in autoimmune pancreatitis.
–U/S +/- CT: pancreatic calcifications confirms diagnosis. U/S can show hyperechoic foci with post-acoustic shadowing (U/S terms for ‘not normal’, something to do with an increase in the U/S waves being echoed because of a change in density compared to surrounding structures, which also causes a signal void behind the abnormal structure). May see pancreatic cysts on CT.
–MRCP + ERCP– careful as this may precipitate acute attack (get smashEd). Early changes: main duct dilatation and stumping of branches. Late changes: duct strictures with alternating dilatation.
–Abdominal X-ray: will show speckled calcification
–Faecal elastase: reduced levels in chronic pancreatitis indicating pancreatic exocrine insufficiency
–Breath tests e.g. 13C-holien: assess pancreatic exocrine function
Acute Pancreatitis :
Modified Glasgow Criteria for Predicting Severity of Pancreatitis:
PaO2 < 8 kPa
Age > 55
Neutrophilia -WBC > 15 x 109/L
Calcium < 2 mmol/L
Renal function- Urea > 16 mmol/L
Enzymes- LDH > 600 iu/L or AST > 200 iu/L
Albumin < 32 g/L (serum)
Sugar- blood glucose > 10 mmol/L
–3 + positive factors detected within 48h of onset suggests severe pancreatitis, and should prompt transfer to ITU/HDU.
–Nil by mouth & likely to need NG tube (suck out fluid from stomach, to decrease pancreatic stimulation) = ‘drip and suck’.
-Fluid & electrolyte resuscitation: IV fluids, lots of 0.9% saline to counteract interstitial fluid accumulation until vital signs are adequate and urine output >30ml/h. Insert a urinary catheter to measure output and consider CVP (central venous pressure) monitoring.
-Consider nutrition (enteral or parenteral)
–Analgesia: pethidine (75-100mg/4h IM) or morphine
-Hourly pulse, BP, and urine output; daily FBC, U&E, Ca, glucose, amylase, ABG. If worsening → ITU. Give O2 if their PaO2 is falling. Blood sugar control if needed.
-If suspected abscess formation or pancreatic necrosis (CT)- consider parenteral nutrition +/- laparotomy and debridement (necrosectomy- i.e. take out all the dead pancreas). Antibiotics may help in severe specific disease (e.g. imipenem if > 30% necrosis).
–ERCP + gallstone removal (+sphincterotomy) may be needed if progressive jaundice
-Repeat imaging (CT) to monitor progress
–Analgesia for exacerbations of pain. May do a coeliac plexus block to help with pain = kill the sensory nerves innervating the pancreas.
–Lipase e.g Creon (= enzyme replacement)
–Fat-soluble vitamins e.g. Multivate (as fat digestion affected)
–Insulin needs vary
–Diet: no alcohol, low fat may help. May try Medium Chain Triglycerides which don’t need lipase, but this could worsen diarrhoea.
–Endoscopic therapy (ERCP): may consider. Sphincterotomy, stone extraction, dilation or stenting of strictures.
–Surgery: if unremitting pain or weight loss e.g. pancreatectomy (take the thing out) or pancreaticojejunostomy (a.k.a Puestow procedure-make connection between pancreatic duct and jejunum so pancreatic juice can enter jejunum) or resection (pancreaticoduodenectomy/ Whipple’s procedure), or limited resection of the pancreatic head (Beger procedure) or combined opening of the pancreatic duct and excavation of the pancreatic head (Frey Procedure).
Acute Pancreatitis :
–Early complications: shock, ARDS (Acute Respiratory Distress Syndrome), renal failure (due to hypovolaemia so give lots of fluid), DIC (Disseminated Intravascular Coagulation), sepsis, hypocalcaemia (digested fatty acids + calcium = human soap), hyperglycaemia (transient, 5% need glucose)
–Late complications (> 1wk):
–Pancreatic necrosis and pseudocyst (fluid in lesser sac of the abdomen- space behind stomach) with fever, a mass +/- persistent elevated amylase/LFTs. May resolve or need drainage
–Abscess (collection of pus)- drain it
–Bleeding from elastase eroding a major vessel (e.g. splenic artery)- embolisation can save their life
–Thrombosis in splenic/ gastroduodenal arteries or colic branches of SMA (superior mesenteric artery), causing bowel necrosis.
–Fistulae– normally close spontaneously
–Recurrent oedematous pancreatitis- so often that near-total pancreatectomy (take the thing out) is contemplated
Chronic Pancreatitis: pseudocyst, diabetes, biliary duct obstruction/ stricture, duodenal obstruction, local arterial aneurysm, splenic vein thrombosis, gastric varices, pancreatic ascites, pancreatic carcinoma.
-Acute pancreatitis is mild in 80% (5% mortality). 20% develop severe complicated and life-threatening disease (70% mortality with infected pancreatic necrosis).
-Prognosis of chronic pancreatitis is difficult to predict as pain may improve, stabilise or worsen. Surgery improves symptoms in 60-70% but results often not sustained. Life expectancy can be reduced by 10-20 years.
References: Cheese & Onion, Rapid Surgery