Acute pancreatitis lq

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Acute Pancreatitis - High-Yield Questions (LQ)


ETIOLOGY & PATHOPHYSIOLOGY

Q1. What are the two most common causes of acute pancreatitis (AP)?
Gallstones (40-70%) and alcohol abuse (25-35%). Gallstones are the leading cause in women; alcohol is more common in men (though this demographic is changing).
  • Swanson's Family Medicine Review; Yamada's Textbook of Gastroenterology
Q2. List other important causes of AP (mnemonic: I GET SMASHED).
LetterCause
IIdiopathic
GGallstones
EEthanol
TTrauma
SSteroids
MMumps/infections (also Mycoplasma, coxsackievirus, EBV, HIV)
AAutoimmune
SScorpion sting / ERCP (post-procedural)
HHypercalcemia / Hypertriglyceridemia (>1000 mg/dL)
EERCP / Emboli (ischemia)
DDrugs (valproate, L-asparaginase, steroids, azathioprine, 6-MP)
Also: Pancreas divisum, hereditary (PRSS1, SPINK1, CFTR mutations), neoplasm.
  • Current Surgical Therapy 14e; Sleisenger & Fordtran's GI and Liver Disease
Q3. What serum triglyceride level is considered diagnostic for hypertriglyceridemia-related AP?
>1000 mg/dL with no other clear cause. Note: serum triglycerides can be secondarily elevated by pancreatitis itself, so persistent elevation after resolution supports this diagnosis.
  • Rosen's Emergency Medicine

DIAGNOSIS

Q4. What are the diagnostic criteria for acute pancreatitis? (Atlanta Classification) Two of the following three must be present:
  1. Acute-onset epigastric pain, often radiating to the back
  2. Serum lipase or amylase > 3x upper limit of normal
  3. Imaging (CT/MRI/US) showing pancreatic inflammation
  • Current Surgical Therapy 14e; Sabiston Textbook of Surgery
Q5. Which enzyme - lipase or amylase - is preferred for diagnosing AP, and why?
Lipase is preferred - it is more sensitive and specific for AP than amylase, has a longer elevation window (stays elevated for 7-14 days vs. amylase 3-5 days), and is not elevated by salivary gland disease or macroamylasemia.
Q6. What is the first-line imaging investigation for AP?
Abdominal ultrasound - performed to evaluate for a biliary (gallstone) etiology. CT is reserved for: diagnostic uncertainty, atypical presentations, hemodynamically unstable patients (to rule out other diagnoses), or to assess for complications (necrosis).
  • Rosen's Emergency Medicine
Q7. When should CT abdomen be obtained in AP?
  • Diagnostic uncertainty (atypical symptoms or non-elevated enzymes)
  • Hemodynamically unstable patients (to rule out mesenteric ischemia, perforation)
  • Suspected pancreatic necrosis or failure to improve after 48-72 hours
  • Recurrent AP (CT in all cases)
  • Current Surgical Therapy 14e
Q8. What are Grey-Turner's sign and Cullen's sign? What do they indicate?
  • Grey-Turner's sign: reddish-brown/ecchymotic discoloration of the flanks - retroperitoneal hemorrhage
  • Cullen's sign: bluish periumbilical ecchymosis - hemoperitoneum
Both are rare but indicate severe necrotizing pancreatitis with hemorrhage into surrounding spaces. They appear late in the disease course.
  • Tintinalli's Emergency Medicine; Yamada's Textbook of Gastroenterology; Bailey & Love's Surgery

SEVERITY SCORING

Q9. What are Ranson's criteria for NON-gallstone pancreatitis? (Classic - frequently examined)
At AdmissionAt 48 Hours
Age >55 yearsHematocrit decrease >10%
Blood glucose >200 mg/dLSerum calcium <8 mg/dL
WBC >16,000 cells/mm³Base deficit >4 mEq/L
LDH >350 IU/LBUN increase >5 mg/dL
AST >250 IU/LFluid requirement >6 L
PaO₂ <60 mmHg
Score ≥3 = Severe pancreatitis
  • PPV: ~50%, NPV: ~90% (mainly used to rule OUT severe pancreatitis)
  • Sabiston Textbook of Surgery
Q10. What are the differences in Ranson's criteria for GALLSTONE pancreatitis?
ParameterNon-GallstoneGallstone
Age>55 yr>70 yr
Glucose>200 mg/dL>220 mg/dL
WBC>16,000>18,000
LDH>350 IU/L>400 IU/L
AST>250 IU/LSame
Base deficit (48h)>4 mEq/L>5 mEq/L
BUN rise (48h)>5 mg/dL>2 mg/dL
Fluid req. (48h)>6 L>4 L
PaO₂ (48h)<60 mmHgNot used
  • Sabiston Textbook of Surgery
Q11. What is the BISAP score? What does it stand for? Five parameters assessed within 24 hours of admission:
  • B - BUN >25 mg/dL
  • I - Impaired mental status (GCS <15)
  • S - SIRS criteria (≥2 present)
  • A - Age >60 years
  • P - Pleural effusion on imaging
Score 0 = <1% mortality; Score 5 = >20% mortality. Easy to compute at bedside.
  • Sabiston Textbook of Surgery
Q12. What APACHE II score defines severe pancreatitis?
≥8. Advantage: can be used at admission and repeated serially. Disadvantage: complex, not specific for AP, age-dependent.
  • Sabiston Textbook of Surgery
Q13. What CRP level and timing defines severe pancreatitis?
CRP ≥150 mg/mL, but peaks at 48-72 hours after onset - cannot be used reliably at admission. Sensitivity decreases if measured <48 hours.
  • Sabiston Textbook of Surgery
Q14. What is the CT Severity Index (CTSI / Balthazar Score)?
Pancreatic InflammationPointsNecrosisPoints
Normal pancreas0None0
Focal/diffuse enlargement1<30%2
Intrinsic changes + peripancreatic fat changes230-50%4
Single fluid collection / phlegmon3>50%6
Two or more fluid collections / gas4
Total CTSI = Inflammation score + Necrosis score (max 10). Higher scores correlate with increased morbidity and mortality.
  • Sabiston Textbook of Surgery

SEVERITY CLASSIFICATION (2012 Atlanta)

Q15. What are the three grades of AP severity by the revised Atlanta Classification (2012)?
GradeDefinitionMortality
MildNo organ failure, no local/systemic complicationsVery rare (<5%)
Moderately SevereTransient organ failure (<48h), local/systemic complications without persistent organ failureIntermediate
SeverePersistent organ failure (>48 hours), single or multi-organ36-50%; up to very high with infected necrosis
  • Current Surgical Therapy 14e
Q16. What is persistent SIRS and why is it important in AP?
SIRS lasting >48 hours carries a 25% mortality vs. 8% for SIRS that resolves within 48 hours. SIRS is currently the recommended system for evaluating severity at presentation and at 48 hours.
  • Current Surgical Therapy 14e

COMPLICATIONS

Q17. Classify local complications of acute pancreatitis.
Setting<4 weeks>4 weeks
Interstitial edematous pancreatitisAcute Peripancreatic Fluid Collection (APFC) - non-encapsulatedPseudocyst - encapsulated, well-defined wall
Necrotizing pancreatitisAcute Necrotic Collection (ANC)Walled-Off Necrosis (WON) - encapsulated solid/liquid
Most APFCs and pseudocysts resolve spontaneously.
  • Current Surgical Therapy 14e; Sleisenger & Fordtran's
Q18. What CT finding is diagnostic for infected pancreatic necrosis?
Gas bubbles within a peripancreatic collection on CT - pathognomonic for infected necrosis.
  • Current Surgical Therapy 14e
Q19. What systemic complications can occur in severe AP?
  • ARDS / pleural effusion (most common pulmonary complication)
  • Acute kidney injury / renal failure
  • Shock / hypotension
  • DIC
  • Hyperglycemia
  • Hypocalcemia (saponification of fat - calcium binds to fatty acids released by lipase)
  • Hemorrhage (erosion into vessels)
Q20. Why does hypocalcemia occur in AP?
Pancreatic lipase causes fat saponification - free fatty acids released by lipolysis bind calcium, depositing calcium soaps in peripancreatic fat, leading to hypocalcemia. This is a poor prognostic sign.

MANAGEMENT

Q21. What is the preferred IV fluid for resuscitation in AP, and what is the recommended starting rate?
Lactated Ringer's (LR) is preferred over normal saline (NS reduces inflammatory cascade). Goal-directed resuscitation starting at 5-10 mL/kg/hour. Most patients need 2500-4000 mL in the first 24 hours.
  • Avoid over-resuscitation (risk: ARDS, abdominal compartment syndrome)
  • Avoid under-resuscitation (risk: end-organ damage, pancreatic necrosis)
  • Current Surgical Therapy 14e
Q22. What are the current guidelines on feeding in AP?
Early oral feeding within 24 hours of admission is recommended, even if lipase has not normalized.
  • Mild-moderate AP: low-fat or normal solid diet (skip liquid/soft diet step)
  • Severe AP / intolerant: nasogastric or nasojejunal feeds once hemodynamically stable
  • Parenteral nutrition: reserved for those who don't tolerate enteral feeding within 5-7 days (associated with increased infected necrosis and MOF compared to enteral feeds)
  • Current Surgical Therapy 14e
Q23. When are antibiotics indicated in AP?
NOT for prophylaxis. Antibiotics should be used only for confirmed or suspected infected pancreatic necrosis or in septic patients with no other source.
  • Preferred: carbapenems (achieve high concentrations in necrotic pancreatic tissue)
  • Infections are often polymicrobial with enteric organisms; E. coli is most common isolate
  • Add antifungal coverage empirically
  • Current Surgical Therapy 14e
Q24. What is the role of ERCP in gallstone pancreatitis?
  • NOT routine for all gallstone pancreatitis (most stones pass spontaneously)
  • Urgent ERCP indicated for acute cholangitis (as soon as possible)
  • Choledocholithiasis without cholangitis: wait 24-48 hours; ERCP if obstruction doesn't resolve
  • Mild biliary pancreatitis: cholecystectomy during index admission to reduce recurrence, readmission, and mortality
  • Current Surgical Therapy 14e
Q25. What are indications for intervention (drainage/debridement) in necrotizing pancreatitis?
  • Infected pancreatic necrosis (main indication)
  • Symptomatic walled-off necrosis (WON) not resolving
  • Preferred approach: step-up strategy (percutaneous drain first → endoscopic/minimally invasive necrosectomy if needed → open surgery as last resort)
  • Intervention for sterile necrosis is avoided unless clinically deteriorating

QUICK HIGH-YIELD FACTS (Exam Favourites)

FactAnswer
Most common cause of AP overallGallstones
Most common cause in menAlcohol
Most common cause of AP in childrenSystemic disease (33%) / Trauma (10-40%)
Drug most commonly causing AP in childrenValproate
Enzyme more specific for APLipase
First imaging to orderAbdominal ultrasound (for biliary etiology)
Ranson ≥3 = ?Severe pancreatitis
APACHE II ≥8 = ?Severe pancreatitis
CRP threshold for severity≥150 mg/mL at 48-72h
Preferred resuscitation fluidLactated Ringer's
Hypocalcemia in AP mechanismFat saponification
Grey-Turner signFlank ecchymosis (retroperitoneal hemorrhage)
Cullen's signPeriumbilical ecchymosis (hemoperitoneum)
Both signs indicateSevere/hemorrhagic AP (late finding)
APFC (within 4 wks, no necrosis) matures intoPseudocyst (>4 wks, encapsulated)
Gas in peripancreatic collection on CTInfected necrosis (pathognomonic)
Antibiotic of choice in infected necrosisCarbapenem
Surgery in AP (first-line for infected necrosis)Step-up approach (drain → necrosectomy)
Mortality in severe AP36-50% (up to higher with infected necrosis)

Sources: Sabiston Textbook of Surgery 21e; Current Surgical Therapy 14e; Sleisenger & Fordtran's GI & Liver Disease; Rosen's Emergency Medicine; Yamada's Textbook of Gastroenterology 7e; Tintinalli's Emergency Medicine; Bailey & Love's Surgery 28e

History taking for a intestine volvolus

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History Taking for Intestinal Volvulus

A volvulus is a twist of a bowel segment around its mesentery, causing luminal obstruction (>180°) and, if tight enough, vascular occlusion (>360°) leading to ischaemia. History taking should be systematic, covering presenting complaints, context, risk factors, and red flag features for strangulation.

1. PATIENT DEMOGRAPHICS (ask first - they guide everything)

QuestionRationale
Age?Sigmoid volvulus: typically elderly (>60 yrs); Caecal volvulus: younger adults; Neonatal/midgut volvulus: newborns/infants
Sex?No strong sex predilection overall, but caecal volvulus is slightly more common in women
Institutionalised or long-term care?Strong association with sigmoid volvulus
Geographic origin?Sigmoid volvulus is the most common cause of large bowel obstruction in indigenous black African populations and eastern Europe; less common in Western countries

2. PRESENTING COMPLAINT - CARDINAL SYMPTOMS

Ask specifically about each of the four classic features of intestinal obstruction:

A. Abdominal Pain

  • Onset: Sudden or gradual? (Fulminant = sudden, severe onset; indolent = insidious, slow)
  • Character: Colicky (cramping, comes in waves) or constant?
    • Colicky pain = peristalsis fighting obstruction
    • Constant/severe unremitting pain = strangulation / ischaemia (RED FLAG)
  • Location: Periumbilical (small bowel) or lower abdomen (large bowel/sigmoid)?
  • Radiation: Any radiation to back or pelvis?
  • Severity: Scale 0-10. Beware: the patient whose pain is not controlled with IV opiates - suggests ischaemia
  • Progression: Has it changed in character? (Colicky pain that becomes constant = evolving strangulation)

B. Abdominal Distension

  • When did the abdomen start swelling?
  • How rapidly did it develop? (Massive, rapid distension is the hallmark of sigmoid volvulus)
  • Is it localised or generalised?
  • Any visible movement of the abdomen? (Visible peristalsis = mechanical obstruction)

C. Vomiting

  • When did vomiting start relative to pain? (Earlier onset in high/small bowel; later in large bowel)
  • Frequency and volume?
  • Character of vomitus:
    • Undigested food / bile (early, high obstruction)
    • Green/bilious (mid-small bowel)
    • Faeculent/faecal-smelling (late feature - bacterial overgrowth, low obstruction)
  • Bilious vomiting in a neonate = midgut volvulus until proven otherwise (EMERGENCY)

D. Constipation / Change in Bowel Habit

  • Last time flatus was passed? (Absolute constipation = no flatus or stool = complete obstruction)
  • Last bowel motion?
  • Has there been any diarrhoea? (Partial obstruction can cause overflow diarrhoea)
  • Note: Some patients may pass stool/flatus early because the bowel distal to the obstruction empties - this does not exclude obstruction

3. ASSOCIATED SYMPTOMS

SymptomSignificance
Fever / rigorsSuggests ischaemia, bowel perforation, or sepsis - RED FLAG
Passage of blood per rectumMucosal ischaemia; haemorrhagic infarction
Loss of appetite / anorexiaGeneral sign of obstruction
Dehydration symptoms (thirst, reduced urine output, dry mouth)Especially prominent in small bowel volvulus with repeated vomiting
Syncope or collapseSevere systemic compromise - perforation or septic shock
Urinary symptomsMay indicate pelvic mass causing extrinsic compression

4. ONSET & PROGRESSION PATTERN

Classify the presentation:
  • Fulminant - sudden onset, severe pain, early profuse vomiting, rapidly deteriorating course (common in caecal volvulus, midgut volvulus, strangulation)
  • Indolent - insidious onset, slow progression, less pain, late vomiting (more common in sigmoid volvulus in elderly)
Ask:
  • "How did it start - suddenly or slowly?"
  • "Has it been getting worse continuously or does it come and go?"
  • "Have you had similar episodes before that resolved on their own?" (Recurrent episodes suggest intermittent/partial volvulus)

5. PAST HISTORY - RISK FACTORS

Risk FactorType of Volvulus
Chronic constipationSigmoid volvulus (elongated colon)
High-residue / high-fibre dietSigmoid volvulus (African populations)
Previous abdominal surgery (adhesions)Secondary volvulus (small bowel)
Previous stomaSecondary volvulus around stoma
Congenital malrotation (known or suspected)Midgut volvulus (neonates/children)
Pelvic masses (fibroids, ovarian cysts)Sigmoid volvulus
PregnancyCaecal or sigmoid volvulus
Previous episodes of volvulusHigh recurrence rate - especially sigmoid
Hirschsprung's disease / megacolonSigmoid volvulus (idiopathic megacolon in African patients)
Neurological disorders (Parkinson's, MS, spinal cord injury)Sigmoid volvulus (impaired colonic motility)
Psychiatric illness / institutionalisationSigmoid volvulus (chronic psychotropic drug use, immobility)
Gastric bandingSigmoid/caecal volvulus

6. DRUG HISTORY

Drug ClassRelevance
Psychotropic medications (antipsychotics, anticholinergics)Slow colonic transit, predispose to sigmoid volvulus
Opioids / constipating medicationsChronic constipation
LaxativesNote regular use - suggests chronic constipation
AnticoagulantsImportant if surgery/intervention is planned

7. FAMILY & SOCIAL HISTORY

  • Family history of colorectal cancer, IBD, or congenital bowel disorders?
  • Dietary history: High-fibre/high-residue diet? Long periods of fasting?
  • Mobility and activity level: Bedridden / institutionalised?
  • Alcohol use (associated with nutritional deficiencies and dysmotility)
  • Occupation and living conditions (care home, prison, psychiatric facility)

8. SPECIAL POPULATIONS - TARGETED HISTORY

Neonates / Infants (Midgut Volvulus)

  • Bilious (green) vomiting - the most important feature; any bilious vomiting in a neonate is a surgical emergency
  • Abdominal distension (may be minimal early on)
  • Bloody stools (late sign - ischaemia)
  • Feeding refusal / lethargy
  • Maternal history of polyhydramnios (associated with gut obstruction in utero)
  • Antenatal scans showing bowel dilation?

Elderly / Institutionalised (Sigmoid Volvulus)

  • History may be unreliable - patient may not communicate symptoms clearly
  • Carers' account: Increasing abdominal size, not opening bowels, not eating
  • Massive distension is key; pain is unusual - if pain is present, suspect ischaemia
  • Background history of repeated similar episodes

Younger Adults (Caecal Volvulus)

  • More acute presentation, more pain
  • Ask about previous right-sided abdominal surgery
  • Pregnancy in women of reproductive age

9. RED FLAGS - STRANGULATION / ISCHAEMIA

Elicit these specifically as they demand urgent surgical intervention:
Red FlagImplication
Constant, severe, unrelenting pain (not colicky)Strangulation/ischaemia
Fever (>38°C) with obstructionIschaemia or perforation
Peritoneal signs (rigidity, guarding, rebound) on examinationPeritonitis / perforation
Bloody rectal dischargeMucosal/transmural ischaemia
Rapid deterioration / haemodynamic instabilitySeptic shock from perforation
Pain NOT controlled with IV opiatesStrangulated bowel

10. SYSTEMATIC SUMMARY - SUGGESTED SEQUENCE IN CLERKING

1. Chief complaint: pain / distension / vomiting / constipation - which came first?
2. Onset, duration, progression
3. Character and location of pain
4. Vomiting: onset, character (bilious? faeculent?)
5. Bowel habit: last flatus and stool
6. Associated: fever, rectal bleeding, urinary symptoms
7. Previous episodes? Self-resolution?
8. Past surgical history (adhesions, stoma, prior bowel surgery)
9. Medical history: constipation, neurological disorders, psychiatric illness, malrotation
10. Drugs: psychotropics, opioids, laxatives
11. Social: institutionalised? Diet? Mobility? Pregnancy?
12. Family history
13. Review of systems: dehydration, syncope, anorexia

Sources: Bailey & Love's Short Practice of Surgery 28e; Rosen's Emergency Medicine; Sleisenger & Fordtran's GI & Liver Disease; Fischer's Mastery of Surgery 8e
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