Pancreatitis 

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.


Pancreatitis

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.)

Image result for scorpionGallstones (most common-38%) (R/Fs: Female, fat, forty)

Ethanol (second most common-35%)

Trauma

Steroids

Mumps (other infection: EBV, CMV, Coxsackie B, mycoplasma)

Autoimmune

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, autoimmunecongenital (pancreas divisum- single pancreatic duct is not formed, but remains as two distinct dorsal and ventral ducts)

Epidemiology:

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

Symptoms:

Acute Pancreatitis:

-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

Chronic Pancreatitis:

-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

Weight loss

Bloating

Symptoms relapse and worsen

 

Signs:

Acute Pancreatitis:

rigid abdomen +/- local/ general tenderness

pyrexia

tachycardia, tachypnoea

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

Image result for grey turner's sign

 

Chronic Pancreatitis:

Epigastric tenderness

Erythema ab igne (a.k.a hot water bottle rash- mottled, dusky greyness) from hot water bottle use

Image result for erythema ab igne

-signs of complications e.g. malnutrition, weight loss

-brittle (uncontrollable) diabetes- swings in blood glucose levels

Investigations:

Acute Pancreatitis:

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)

 

Chronic Pancreatitis:

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

Image result for pancreatic calcification
a) AXR and b) CT in chronic alcoholic pancreatitis

Faecal elastase: reduced levels in chronic pancreatitis indicating pancreatic exocrine insufficiency

Breath tests e.g. 13C-holien: assess pancreatic exocrine function

Management:

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

Chronic Pancreatitis:

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).

 Image result for whipple's procedure

 

Complications:

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.

Prognosis:

-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

 

Advertisements

3 thoughts on “Pancreatitis 

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s