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General Surgery > Acute Pancreatitis > Flashcards

Acute Pancreatitis Flashcards

1
Q

What is the defn of “Acute Pancreatitis”?

A

reversible pancreatic parenchymal damage of varying severity owing to an acute inflammatory ds of the pancreas

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2
Q

What clinical features are necessary for a dx of acute pancreatitis to be made?

A

At least 2 of the following 3 features:

1) Abd pain consistent w/ epigastric pain (acute onset of persistent, sev, epigastric pain often radiating to the back)
2) serum lipase/amylase activity of at least 3x greater than the upper limit of normal
3) characteristic findings of acute pancreatitis on CECT or MRI or trans-abd U/S

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3
Q

Discuss the epidemiology of acute pancreatitis

A

in 80% pts = mild + resolves w/out serious morbidity
remaining 20% -> sev form w/ local + systemic complications assoc w/ mortality rates as high as 40% - most late death d/t multi-organ dysfxn 2ndary to infected pancreatic necrosis

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4
Q

What are the causes of acute pancreatitis?

A 
(I GET SMASHED)
Idiopathic (15-25%)
Gall stones (38%)
Ethanol (36%)
Trauma
Steroids
Mumps + other infxns (VZV, CMV, mycoplasma, parasitic)
Autoimmune - SLE, Sjorgren's
Scorpion toxin + other toxins
Hypercalcaemia, hypertriglycerodemia (metabolic causes)
ERCP
Drugs (SAND)
Rare causes: neoplasm, congenital, genetics
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5
Q

Discuss the general pathophysiology of acute pancreatitis

A

Caused by unregulated activation of trypsin w/in pancreatic acinar cells, activating pro-enzymes => auto-digestion & an inflamm cascade that both amplifies local inflammatory response => progression to SIRS

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6
Q

How do gallstones cause acute pancreatitis?

A

d/t obstruction of pancreatic duct => interstitial oedema => impairs blood flow to the pancreatic cells => ischaemic cellular injury => activation of pro-enzymes => destruction of pancreatic acinar cells

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7
Q

How does alcohol cause acute pancreatitis?

A

via its direct toxic effects and/or metabolites on acinar cells => predisposes gland to autodigestive injury

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8
Q

How does a pt w/ acute pancreatitis present clinically?

A

acute + constant pain in epigastric area - boring sensation that radiates to back
pt unable to get comfortable when lying supine - pain alleviated by sitting up & leaning forward
pain might last several days
N & V

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9
Q

Apart from hx of presenting complaint, what other information is NB to the pt’s entire hx?

A

rule out other DDx - gastric/hepatobiliary/medical/emergencies

NB ascertain etiology

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10
Q

What are some important things to note on PE in a pt presenting w/ suspected acute pancreatitis?

A

General Appearance: lying motionless (diffuse peritonitis); sitting up/leaning forward (pancreatitis); small red tender nodules on skin + legs - subcutaneous fat necrosis

Vital signs: tachycardia, hypotension, low grade fever, tachypnoea

Abd exam:
distention, focal epigastric tenderness, palpable mass?
signs of peritonism - rebound tenderness, guarding, board-like rigidity
signs of haemorrhagic pancreatitis - Grey-Turner Sign (flank ecchymosis), Cullen’s sign (periumbilical ecchymosis), Fox’s sign (inguinal ecchymosis)
Auscultation - diminished/absent bowel signs?

*Resp Exam

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11
Q

Which investigations are NB for a dx of acute pancreatitis?

A

Elevated serum amylase
Elevated serum lipase
Urinary diastase - used when serum amylase is equivocally raised or normal

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12
Q

What are some other causes of an elevated serum amylase?

A

GI - PUD, I/O, perforated bowel, ischaemic bowel, cholecystitis, cholangitis, appendicitis
Non-GI - Renal failure, ARDS, ruptured ectopic pregnancy/ovarian cysts/PID, salivary gland injury/inflammation, macroamylasemia, DKA or any acidosis, neoplasms

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13
Q

which factors/investigations are considered by the Ranson/Glasgow Criteria to assess the sev & prognosticate acute pancreatitis?

A 
LDH
LFT - AST + albumin
Glucose
FBC - WCC, Hb
Renal Panel + Ca2+
ABG
CRP
ECG/Cardiac enz
Erect CXR + Supine AXR
CECT
MRI
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14
Q

What investigations are done in order to determine the underlying pathology?

A

LFT - >ALT = gallstone pancreatitis; >Br for 6-12hrs = impacted stone in ampulla of Vater; >AST = for Ranson/Glasgow scoring sys
U/S Abd
Ca2+/Mg2+/PO4 w/ alb -> hypercalcaemia
Fasting lipids -> hyperlipidaemia

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15
Q

What is considered “mild acute pancreatitis” based on the Atlanta Classification for severity?

A

No organ failure
No local or sys complications
Usually resolves in the first week
Mortality is rare

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16
Q

What is considered “moderate acute pancreatitis” based on Atlanta Classification for severity?

A

Transient organ failure (resolves w/in 48hrs)

Local complications/exacerbation of comorbid ds

17
Q

What is considered “sev acute pancreatitis” based on the Atlanta Classification for severity?

A

Persistent organ failure (>48hrs), single or multiple organ failure
local complications are peripancreatic fluid collections, pancreatic + peripancreatic necrosis (sterile/infected), pseudocyst + walled-off necrosis (sterile/infected)
Mortality range from 36-50%

18
Q

What are some danger signs to look out for in the first few hours?

A 
Encephalopathy
Hypoxemia, tachypnoea
Tachycardia, hypotension, haematocrit
Presence of Grey Turner's/Cullen's sign
Oliguria, Azotaemia
19
Q

Describe the fx considered in the Glasgow (Imrie’s) criteria

A 
(PANCREAS)
PaO2 <60mmHg
Age >55yrs
Neutrophil/WCC >15x10^9/dL
Ca2+ <2mmol/L
Renal (urea) >16mmol/L
Enz LDH >600IU/L or AST/ALT >200IU/L
Albumin <32g/L
Sugar (glucose) >10mmol/L

> /= 3 criteria -> severe

20
Q

Describe the fx considered in the Ranson criteria

A 
On admission:
Serum LDH >350IU/L
Serum AST >250IU/L
Blood Glucose >10mmol/L
Age >55yo
WBC >16 000 cells/mm^3
Initial 48hr:
Serum Ca2+ <2mmol/L
Hct >10%
PaO2 <60mmHg
BUN >/= 1.8mmol/L
Base deficit (-ve base excess) >4mEq/L
Sequestration of Fluids >6L
21
Q

Describe the course of acute pancreatitis

A

most episodes = mild + self-limiting, needing only brief hospitalization
20-25% pts develop a sev ds w/local + extra-pancreatic complications -> early development + persistence of hypovolemia + multiple organ dysfxn
Death = bimodally distributed:
Early - w/in 1/52; d/t sev organ failure, SIRS. V little can be done in terms of tx
Late - most common cause = infxn w/ resultant sepsis. Multi-organ failure can be course of death

22
Q

What is the mgmt/tx strategy for acute pancreatitis?

A

1) Dx -> severity stratification

2) Assess for aetiology then: supportive tx; monotor + manage complications; tx aetiology + prevent future recurrence

23
Q

What does supportive tx for acute pancreatitis entail?

A

Cornerstone = prevention of pancreatic stimulation (NBM)
Aggressive IV fluid resuscitation
Tx of fluid + electrolyte abns
Pain mgmt
Prevent vomiting
antibiotic mgmt
+/- definitive tx + support for organ failure

24
Q

What are some of the local complications of acute pancreatitis?

A

Acute fluid collections (30-50%)
Pseudocysts (10-20%)
Sterile pancreatic necrosis (20%)
Infxn (5%) - usually 2ndary enteric GNR -> pancreatic abscess; infected pancreatic necrosis
Chr pancreatitis, exocrine insufficiency & endocrine insufficiency

25
Q

What are some systemic complications of acute pancreatitis?

A 
Peritoneal sepsis
Pancreatic ascites -> abd compartment syndrome
Pleural Effusion
Intra-abd haemorrhage -> shock
Multiple organ failure
Hypocalcaemia, hyper/hypoglycaemia

General Surgery (15 decks)

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