A 55-year-old man was admitted with severe upper abdominal pain and nausea. He had a history of alcohol abuse. O/E the epigastrium was tender with guarding. ^[1]

Acute pancreatitis ^[1]

Why? The triad of (1) severe epigastric pain (often radiating to the back), (2) history of alcohol abuse (one of the two most common aetiologies alongside gallstones), and (3) epigastric tenderness with guarding is classic.

Differential diagnoses presented on the slide: acute pancreatitis vs. gastroenteritis vs. renal colic. The combination of severe epigastric pain with guarding in an alcohol abuser makes acute pancreatitis the most likely working diagnosis ^[1].

Serum amylase/lipase ^[1]

• Amylase or lipase ≥ 3× the upper limit of normal fulfils the biochemical criterion, but acute pancreatitis is diagnosed when two of three are present: typical pain, enzyme elevation, or characteristic imaging. Enzyme elevation alone is not the whole diagnosis.
• Lipase is generally preferred because it is more pancreas-specific and stays elevated longer.
• Why these first? Because pancreatitis is fundamentally a clinical + biochemical diagnosis — imaging is NOT needed to make the initial diagnosis if symptoms and enzymes are concordant.

Inflammation of the pancreatic tissue → obstruction of small pancreatic ducts → leak of pancreatic juices to surrounding tissues → swollen oedematous pancreas with areas of haemorrhage and necrosis → peripancreatic fluid collection ^[1]

First-principles explanation: The pancreas produces powerful proteolytic enzymes (trypsin, elastase, phospholipase A2) that are normally activated only in the duodenum. In pancreatitis, premature intracellular activation of trypsinogen to trypsin triggers autodigestion. The inflammatory cascade causes:

1. Oedema → the gland swells (interstitial oedematous pancreatitis)
2. Necrosis → if blood supply is compromised or inflammation is severe, portions of parenchyma die (necrotizing pancreatitis)
3. Peripancreatic fluid → enzyme-rich juice leaks into the retroperitoneal space and lesser sac
4. Systemic response → cytokine storm can cause SIRS, organ failure

Interstitial oedematous vs. Necrotizing pancreatitis ^[1]

He developed fever a few days later, with increasing abdominal pain, abdominal distension, and deranged LFT. ^[1]

This clinical deterioration is the trigger to reassess and consider cross-sectional imaging. Fever after only a few days does not by itself diagnose infected necrosis; it may reflect SIRS or another infection, while infected pancreatic necrosis more often becomes a concern later in the course (typically after about 10–14 days). Increasing pain and distension suggest a local complication, and deranged LFTs should prompt assessment for a biliary cause or obstruction ^[9].

Role of imaging:

• Confirm diagnosis if symptoms are atypical or serum amylase/lipase levels are less than expected
• Determine the cause of pancreatitis; exclude neoplasm or confirm presence of cholelithiasis
• Patient's condition does not improve (disease severity)
• Monitor evolution and complications ^[1]

This is extremely high-yield. Do not routinely order CT on day 1 for a straightforward clinical/biochemical presentation. Current ACG guidance reserves CT for an uncertain diagnosis or failure to improve after 48–72 hours; ACR likewise considers contrast CT usually appropriate in a critically ill patient after this interval. Early CT remains appropriate when an important alternative diagnosis must be excluded ^[9][10].

Extrapancreatic spread of inflammation — fluid collection, obliteration of peripancreatic soft tissue & fascial thickening. Look for necrosis — non-enhancement (necrotising pancreatitis) with acute necrotic collections (ANC). ^[1]

Other complications: Walled off necrosis (WON), ascites, mesenteric involvement ^[1]

How to read the lecture images:

• Slide 12: the swollen, heterogeneous pancreas has areas that fail to enhance after IV contrast—this is the visual basis for calling pancreatic necrosis. The surrounding fat is no longer crisp: inflammatory stranding, fluid and fascial thickening extend beyond the gland and obliterate normal peripancreatic tissue planes.
• Slide 13: the peripancreatic collection is heterogeneous rather than simple fluid, consistent with fluid mixed with necrotic debris. In the early phase this is an acute necrotic collection (ANC). Call it walled-off necrosis (WON) only when a mature, enhancing capsule has formed—usually at least 4 weeks after onset ^[11].
• Necrosis may involve pancreatic parenchyma, peripancreatic tissue, or both; do not require an arbitrary percentage of non-enhancing gland before recognising it.

• 2019 SAQ Q5: 55-year-old lady, epigastric pain, amylase 1250 → Diagnosis = acute pancreatitis. Investigations to guide management = USS abdomen (gallstones?), CT abdomen (if deteriorating/complications), FBC, CRP, Ca²⁺, glucose, LDH (severity scoring). Common causes = gallstones, alcohol, idiopathic ^[4].

A 44-year-old lady was referred to the OP department after a routine PA CXR showed an abnormality. She never smoked in her life but was treated for TB 10 years previously. ^[1]

Haziness in left lung → specifically LUL (left upper lobe) collapse ^[1]

Image walkthrough (slides 16 and 20): on the PA radiograph, the left upper zone has a subtle veil-like opacity rather than a rounded mass. The accompanying volume-loss signs—not opacity alone—make collapse the diagnosis. On the lateral view, the collapsed upper lobe becomes an abnormal anterior/retrosternal density. Reading both projections prevents the subtle PA-film haziness from being dismissed.

Hazy or veil-like appearance "Tented" left hemidiaphragm Increase retrosternal density on lateral CXR Look for proximal obstructing lesion ^[1]

Why does this happen? When the LUL bronchus is obstructed, air distal to the obstruction is reabsorbed by the blood → the lobe deflates → it loses volume → surrounding structures shift toward the collapsed lobe:

• Elevated hemidiaphragm (or "tented")
• Mediastinal shift toward the side of collapse
• The collapsed lobe appears as a veil-like opacity because it is now a thin sheet of airless tissue draped over the mediastinum

A contrast CT scan of the thorax was performed. Bronchoscopy showed narrowing of the LUL bronchus without endobronchial lesion. BAL and sputum analysis revealed no cells or growth. TB culture was pending. ^[1]

CT: LUL collapse with narrowed LUL bronchus. No mediastinal masses or nodes. Rest of lungs are normal. ^[1]

CT correlation (slide 23): the mediastinal- and lung-window axial images show the collapsed LUL displaced anteriorly and a narrowed LUL bronchus. There is no hilar/mediastinal mass or lymphadenopathy to explain the obstruction, supporting the bronchoscopic diagnosis of a benign post-TB stricture in this case.

LUL collapse secondary to TB stricture ^[1]

TB can cause bronchial stenosis through:

1. Endobronchial TB → granulomatous inflammation of bronchial wall
2. Healing with fibrosis → cicatricial stricture
3. Extrinsic compression by calcified lymph nodes (less common)

In adults, lobar collapse on CXR should be [investigated] to exclude neoplastic lesion ^[1]

RUL collapse — Golden S-sign ^[1]

• 2016 SAQ Q5: 60-year-old man with mass in left upper zone → lung malignancy with hypercalcaemia (SCC → PTHrP), raised ALP (bone mets), raised creatinine (myeloma vs renal impairment) ^[5].
• 2021 MCQ Q82: CXR with bilateral perihilar consolidation, blunted costophrenic angles, cardiomegaly, Kerley B lines, upper lobe venous diversion → heart failure (not pneumonia or metastatic disease) ^[6].

A 25-year-old law student was admitted with a few days of right lower abdominal pain. She was nauseous and feverish. O/E tender RLQ with guarding and febrile. ^[1]

Appendicitis ^[1]

Differential diagnoses presented on the slide: appendicitis vs. mesenteric adenitis vs. ovarian torsion. In this 25-year-old woman, the lecture chooses ultrasound because it can assess both the appendix and ovaries without ionising radiation. That case-based choice should not be memorised as a universal adult rule: current ACR guidance rates CT abdomen/pelvis with IV contrast as usually appropriate for a non-pregnant adult with RLQ pain and suspected appendicitis, whereas US-first pathways remain especially useful in children, pregnancy and centres with appropriate expertise ^[12][13].

Faecolith or scarring that occludes neck of appendix → closed-loop obstruction → bacterial infection and ulceration of wall which perforates → abscess formation or generalised peritonitis ^[1]

Most frequent condition requiring emergency surgery (80%). Produced by luminal obstruction, secondary distention, engorgement, edema and bacterial overgrowth. Peak frequency in children: 12–15 years of age. ^[1]

The slide's isolated “80%” statement is historical lecture wording without a defined denominator; do not use it as a current epidemiological statistic. The clinically useful sequence is obstruction → distension/venous congestion → ischaemia and bacterial invasion → gangrene/perforation.

First-principles explanation: The appendix is a blind-ended tube. When the lumen is obstructed (by faecolith, lymphoid hyperplasia in children, rarely neoplasm in elderly), the mucosa continues to secrete mucus → intraluminal pressure rises → venous drainage is impaired → wall becomes ischaemic → bacteria translocate → inflammation (appendicitis). If untreated, the wall becomes gangrenous and perforates → either localized abscess (if omentum walls it off) or generalized peritonitis.

USG showed thickened appendix and normal right ovary ^[1]

Image walkthrough (slide 31): graded-compression US shows an enlarged, blind-ending tubular structure in the RLQ—the abnormal appendix—while the separate ovarian image shows a normal-sized right ovary with follicles. The paired images answer both parts of the clinical question: confirm appendicitis and check the major gynaecological alternative.

Why USG in this lecture case? In a young female patient, you also need to exclude ovarian pathology (torsion, ruptured cyst, ectopic pregnancy). USG is:

• No radiation (important in young/female of reproductive age)
• Can visualize both appendix and ovaries
• Real-time and can assess for graded-compression tenderness

Graded-compression technique Focal tenderness Lack of compressibility Transverse diameter ≥ 6mm Appendicolith Peri-caecal or peri-appendiceal fluid ^[1]

Increased flow (on Doppler) ^[1] Echogenic periappendiceal fat (inflamed mesentery) ^[1] Appendicolith and soft tissue mass — on USG the appendicolith appears as an echogenic structure with posterior acoustic shadowing, surrounded by a soft-tissue mass; on plain AXR it may be seen as a radiopaque focus in the RLQ ^[1]

What the montage adds: slide 35 demonstrates the appendix in both long and short axes, with echogenic inflamed periappendiceal fat and mural hyperaemia on Doppler. Slide 36 correlates a small RLQ radiopaque focus on AXR with an echogenic, shadowing appendicolith on US and an adjacent inflammatory mass. Slide 37 shows an ill-defined phlegmon rather than a neatly outlined appendix—an important visual clue to perforation.

Appendix may be difficult to identify, mucosa disrupted. Phlegmon: inflammatory mass ^[1]

Why is the appendix hard to see after perforation? Because the wall has lost its integrity and the appendix "dissolves" into the surrounding inflammatory mass (phlegmon). The phlegmon is a mass of inflamed omentum, bowel loops, and mesentery walling off the perforation.

CT Advantages:

• Less operator dependent
• Higher sensitivity than US
• Pooled sensitivity 94% (US 88%)
• Pooled specificity 95% (US 94%)
• Indications: Obese patients, delineate disease extent in perforated appendicitis, guide abscess drainage
• Non-visualisation of the appendix on CT has a high negative predictive value of 98.7% ^[1]

Dilated, fluid-filled appendix ^[1]

Appendix abscess: Peri-caecal mass with fluid, infiltration of mesenteric fat ^[1]

Image walkthrough: slide 39 shows the enlarged fluid-filled appendix on both coronal and axial contrast CT, with wall enhancement and surrounding inflammatory fat stranding. Slide 40 shows complicated disease: a rim-enhancing pericaecal fluid collection (abscess) with marked adjacent mesenteric-fat infiltration.

• 2016 SAQ Q9: 7-year-old boy, fever, RLQ tenderness → (a) Appendicitis; (b) USG — reasons: no radiation (child), can assess appendix and exclude other causes, can show specific signs (thickened appendix, non-compressible, ≥ 6mm); (c) Thickened non-compressible appendix ≥ 6mm, appendicolith, periappendiceal fluid; (d) CT — especially useful in obese child ^[5].

An 18-month-old baby girl was admitted with 1 day history of crying and being off her food. Her mother described episodes where she draws up her legs and cries. ^[1]

Dilated small bowel. A "tumour" or intussusceptum in the RUQ ^[1]

Image walkthrough: the abdominal radiograph shows dilated small-bowel loops and a rounded soft-tissue opacity in the RUQ (arrows on slide 43), representing the intussusceptum. It demonstrates obstruction but is not the definitive test. A normal AXR cannot exclude intussusception; current paediatric guidance reserves AXR mainly for suspected obstruction or perforation ^[15].

Classic clinical triad: acute abdominal colic, currant-jelly stools, a palpable abdominal mass (the slide notes the mass in less than 50% of patients). Age: 6 months – 2 years. Mostly ileo-colic. ^[1]

Invagination or prolapse of a segment of bowel (intussusceptum) into the lumen of adjacent bowel (intussuscipiens) due to peristalsis. Major cause of SBO in children, less common in adults. The slide states that 80% of adult cases are due to a polypoid tumour. Children — commonly near the ileocaecal valve. ^[1]

Treat that adult “80% polypoid tumour” line as a lecture-era simplification: the durable point is that adult intussusception is much more likely than childhood disease to have a structural lead point and therefore usually requires cross-sectional evaluation and surgical input.

Why the ileocaecal region? The ileocaecal valve is a natural anatomical transition point where the narrow ileum meets the wider caecum. Enlarged Peyer's patches (from viral illness, e.g., adenovirus, rotavirus) act as a lead point, and normal peristalsis telescopes the ileum into the caecum.

Why currant-jelly stools? As the bowel is telescoped, the mesenteric vessels are compressed → venous congestion → mucosal ischaemia → bloody mucus mixed with stool = "currant jelly" appearance. This is a late sign indicating significant vascular compromise.

USG: Primary imaging modality for initial diagnosis. Sensitivity: 98–100%, Negative predictive value: 100%, Specificity: 88–100%, Alternative diagnosis. ^[1]

Why USG?

1. No radiation in a paediatric patient
2. Very high sensitivity and specificity when performed by an experienced paediatric ultrasonographer
3. Can identify the classic signs AND can be used to guide therapeutic reduction

The target/doughnut sign (transverse view) and pseudokidney sign (longitudinal view):

Three-ring structure:

• Central ring: lumen and wall of intussusceptum
• Middle ring: mesenteric fat
• Outer ring: bowel wall of intussusceptum and intussuscipiens ^[1]

How the diagram maps to the ultrasound: on slide 49, the central ring contains the lumen and wall of the intussusceptum, the middle echogenic ring is dragged-in mesenteric fat, and the outer ring contains the apposed bowel walls of intussusceptum and intussuscipiens. The live US image beside the diagram is the transverse doughnut/target counterpart of that anatomy.

The intussusception was reduced with water under ultrasound control ^[1]

Post-reduction — fluid filled bowel ^[1]

Image sequence (slide 45): before reduction, the longitudinal image shows the pseudokidney sign and the transverse image shows the doughnut sign. After water reduction, the prior target mass is gone and fluid now fills the reduced bowel—an imaging endpoint of successful passage.

How does this work? After resuscitation and with paediatric surgical/radiology support, liquid (water/saline) or air is introduced per rectum under ultrasound or fluoroscopic guidance. Hydrostatic or pneumatic pressure pushes the intussusceptum back out of the intussuscipiens; current paediatric guidance reports success in more than 80% of appropriately selected cases ^[15].

Contraindications to enema reduction:

• Peritonitis (perforation)
• Free intraperitoneal air
• Hemodynamic instability / shock
• Signs of bowel necrosis

In these cases → surgical reduction (manual or resection if gangrenous bowel).

When reading any CXR, use the ABCDE approach:

• A — Airway: tracheal deviation, main bronchi
• B — Bones: ribs, clavicles, scapulae, spine (fractures, lytic lesions)
• C — Cardiac: heart size (CT ratio < 0.5 on PA film), mediastinal contour
• D — Diaphragm: costophrenic angles blunted (effusion), free air under diaphragm
• E — Everything else: lung fields (consolidation, masses, collapse), soft tissues, lines/tubes

Bilateral perihilar consolidation, blunting of costophrenic angles, cardiomegaly, Kerley B lines, upper lobe venous diversion → Heart failure ^[6]

Mnemonic: ABCDE of heart failure CXR:

• A — Alveolar oedema (bat-wing pattern)
• B — Kerley B lines (interstitial oedema, interlobular septal thickening)
• C — Cardiomegaly (CT ratio > 0.5)
• D — Upper lobe Diversion (cephalization of vessels)
• E — Pleural Effusion (blunted costophrenic angles)

Percutaneous transhepatic biliary drainage (PTBD) for malignant biliary obstruction, abscess drainage (e.g., appendix abscess), embolization for bleeding ^[8]

From 2021 MCQ Q2: 50-year-old man with painless jaundice, pruritus, weight loss, pancreatic head mass on USG → PTBD to relieve biliary obstruction ^[6].