SPOT QUESTIONS 6

1. SPOT QUESTIONS 6

2. Q1 Finding at gastroscopy 1. Describe this lesion 2. Diagnosis 3. Treatment

3. An ulcerated polypoid gastric lesion, appears to arise from submucosa with overlying normal mucosa • GIST. Differential: atypical adenocarcinoma, MALT lymphoma, other lymphoma, other benign tumour • Biopsy (“inkwell”, or in ulcerated region) – HISTO diagnosis by c-KIT staining. EUS if available. Staging CT SCAN ABDO (direct spread, METS to liver and peritoneal cavity, lymph node spread is rare). Assessment of patient comorbidities. Discussion in UGI MDT meeting. Complete excision (R0 resection). Imatinib for metastatic or unresectable disease (over 80% will respond). Discuss mutational testing for exon domain mutation (predicts reponse to Imatinib) and availability for adjuvant therapy with local Novartis drug rep. 3 monthly follow-up with 3-6mthly CT imaging.

4. Q2 This patient was injured in a motor vehicle crash two hours earlier when his motorbike hit a stationary car. [Compound wound actually in proximal 1/3rd lower leg] 1. Describe the changes shown in the photograph. 2. What is the immediate problem? 3. Full EMST assessment reveals that the patient has no other injuries. Describe how the patient should be managed.

5. Compound # right proximal tibia/fibula with apparent neurovascular compromise to distal limb (compressed vs severed deep popliteal artery and nerves from displaced tibial plateau #)‏ • Restoration of vascular supply to the distal limb by reduction of # deformity then assessment of neurovascular status. Need to exclude other coexistant life-threatening injuries. • Realignment and xray lower limb # (if position not held with splint, maintain manually). Clinical examination +/- Doppler assessment of distal vessels. Tetanus prophylaxis, analgesia, antibiotics and sterile dressing for compound wound. Prompt operative management (Orthopaedic, Vascular +/- Plastics) to salvage limb and restore distal vascular supply as matter of priority. Tissue debridement, thorough lavage, likely external fixation #, and wound ? left open. Consider intra-operative angiography to confirm vascular patency/exclude intimal tear. May require fasciotomy to treat or prevent compartment syndrome. Planned re-look operation at 48hrs. Early amputation may give best functional outcome in some scenarios. Document findings and treatments accurately.

6. Q 1. What is this radiological investigation? 2. What does the radiological investigation show? 3. How do you classify this condition? What is the treatment for this condition?

7. MRCP vs THC/PTC vs ERCP • Choledochal cyst Todani Type I • Todani classification (1977) according to site and shape: • Type 1; fusiform or saccular extra-hepatic • Type 2; isolated protrusion or diverticular outpouching CBD • Type 3; choledochocele with wide-mouth dilation CBD at confluence with the duodenum • Type 4; intra- and extra-hepatic ducts. 4a multiple intra-hepatic, 4b multiple extra-hepatic. • Type 5; multiple intra-hepatic with hepatic fibrosis (Caroli's) • Treatment: • Complete excision with roux-en-Y hepaticojejunostomy and simultaneous cholecystectomy • Type III consider ERCP/Sx, Type II consider diverticulectomy • LFTS & CA19-9 six monthly, MRCP annually

8. Q This is a CT scan demonstrating a mass in the head of the pancreas. The patient had originally presented 12 months earlier with vague abdominal pain. There has been only a modest increase in size of the mass during this time and the patient hasn't become jaundiced. 1. What is the differential diagnosis of a mass in the head of the pancreas and what is the most likely diagnosis in this case? 2. How is operability determined? 3. What other examination and/or investigations (if any) would you perform? 4. What are the arguments for and against biopsy?

9. Benign, pre-malignant, malignant (primary, secondary - rare). Cystic vs solid. • Effacement or invasion of portal vein or superior mesenteric vessels. Absence of liver, nodal and peritoneal metastases. • Tumour markers CA 19-9, CEA, αFP. Amylase and pancreatic lipase. Review imaging with experienced HPB radiologist and discuss indication for MRI. • For: 10% resections have resultant benign pathology despite highly morbid operation. Oncological guidance of treatments and prognostication. Against: tumour spread/seeding, sclerotic nature of tumour may give a false -ve result, imaging/tumour markers +/- EUS, ERCP brushings for cytology and clinical presentation usually give definitive diagnosis.

10. This patient presents with hypertension. 1. What is the diagnosis of this adrenal medullary tumour? 2. What other symptoms may occur? 3. What pre-operative investigations are required and why? 4. What is the recommended treatment?

11. Phaeochromocytoma – likely functional • May be asymptomatic. Episodic episodes in spells (paroxysms) which are variable in presentation but may typically include forceful heartbeat, pallor, tremor, headache, and diaphoresis; may be spontaneous or precipitated by postural change, anxiety, medications (eg Maxolon, anaesthetics), and manouvers that increase intra-ABDO pressure (eg change in position, lifting, defecation, exercise, colonoscopy, pregnancy and trauma). • 24hr urinary metanephrines and catechoalmaines. Contrast-enhanced MDCT ABDO. Consider radio-labelled iodine MIBG scintigraphy and MRI. 10% bilateral, 10% malignant. • Medical management initially followed by adrenalectomy.

12. Q2 This 33 year old woman has recently undergone a right axillary dissection and lattisimus dorsi musculo-cutaneous flap reconstruction as part of her treatment for breast cancer. 1. What deformity does the photograph demonstrate? 2. Describe the attachments and the action of the muscle involved. 3. Briefly describe the origin and course of the nerve that may have been damaged.

13. Winged scapula • Arises: upper 8 ribs & ant intercostal membranes from MCL. Lower 4 interdigitating with external oblique. Inserts: inner medial border scapula. 1&2 upper angle; 3&4 length of costal surface; 5-8 inferior angle. Action: laterally rotates and protracts scapula • Long thoracic nerve arises from roots of brachial plexus (C5-7). Branches from C5&6 join in scalenus medius muscle and emerge from lateral border as a single trunk to enter axilla by passing over first digitation of serratus anterior. C7 branch passes over 1st dig. also to join nerve on muscle surface in medial wall of axilla to form nerve to serratus anterior. Nerve emerges from behind 1st part of the axillary vein and lies behind MAL behind lateral branches of intercostal arteries, on the muscle initially outside then deep to the muscle fascia.

14. This patient presents with severe epigastric pain. 1. What is the diagnosis? 2. How do you grade severity? 3. What are potential vascular complications? 4. What is the recommended treatment?

15. Acute pancreatitis – Balthazar Grade D with non-enhancing pancreatic body anterior to the splenic vein • Severe disease: APACHE II score >8 or CRP >150mg in first 24hours, or persisting organ failure after 48 hours. APACHE II is 12 routinely available physiological and biochemical measurements, coupled with a score for age and pre-existing health. • Arterial (10%): erosion or pseudoaneurysm (splenic 40%, GDA 30%, pancreaticoduodenal 20%, L gastric/SMA/hepatic less commonly) → haemorrhage, ischaemic COMPs (local or remote) Venous (common, up to 45%): splanchnic venous thrombosis and associated varices, DVT/PE, fat emboli Microvascular: SIRS → sepsis → (septic shock) → MODS, ARDS with pulmonary oedema & pulm. vasc. HT Vascular access COMPs during management: infection, thrombosis, arteriovenous fistula, pneumothorax

16. Unstable haemorrhage, embolization not feasible or failed → operative, pseudoaneurysm stable → percutaneous transcatheter angiographic embolization, venous thrombosis → consider therapeutic clexane, consider decompression pseudocyst obstructing splanchnic vein, but usually no intervention

17. Pelvic #

18. Closed or compound, stable or unstable, force lateral/A-P/vertical shear/combination. Tile classification: Type A – isolated # iliac wing or pubic rami by direct compression (stable, conservative management); Type B1 – lateral compression, # of pelvic ring with post displacement over sacrum and mostly # of pubic arch (bladder, urogenital, rectal, soft tissue injury → unstable); Type B2 - “open book” (most common type) arising from anterior force. Causes pubic symphysis disruption +/- # sup & inf pubic rami, combined with post disruption of ant or post ligaments of SI joint (severe soft tissue damage, lower urogenital, vagina & rectal injury, requires ant comprsn + external fixation): Type C – complete horizontal & vertical instability resulting from ant and post # and/or disruptions with complete sacral disruption and displaced vertical sacral #). Causes: fall from height, AP shearing force in a dashboard impact (major bld loss & assoc injuries to bladder, urethra, rectum, vagina, sciatic & femoral nerve, iliac vessels. Requires immediate reduction + fixation)‏

19. Latissimus dorsi

20. Spine T7 →all L & S vertebrae, post iliac crest. Slips from lower 4 ribs, fuses with lumbar fascia→ intertubercular groove • Nerve supply → thoracodorsal nerve. Off posterior cord brachial plexus (C6-8), arising between upper and lower subscapular nerves, passes downwards behind axillary artery and vein to lie on subscapularis. Within posterior aspect of axilla it approaches the descending thoracodorsal vascular bundle (comprising large subscapular art. then smaller thoracodorsal art. more distally) from a postero-medial direction. • Lattisimus dorsi: • Arises from all thoracic spines & supraspinous ligaments from T7 downwards & lumbar & sacral spines via lumbar fascia, post 1/3rd iliac crest, last 4 ribs (interdigitating with ext oblique) & inf angle of scapula • Inserts to floor of bicipital groove of humerus after spiralling around teres major • Action – extends, adducts & med rotates arm. Costal attachments help with deep inspiration and forced expiration.

21. CREST syndrome

22. A form of systemic scleroderma associated with antibodies against centromeres. Calcinosis (subcutaneous tissues), Raynaud’s (white-blue-red in stress & cold), oEsophageal (hypo-motility, increased incidence Barrett’s) and gut dysmotility, Sclerodactyly, and Telangiectasia. Skin involvement limited to face, hands and feet. Arthralgias in 90%. • Aetiology: primary trigger for CREST syndrome is not known, some cite borrelia infection, others a vascular endothelial autoimmune process. • Medical treatment: No cure currently. Multidisciplinary – dermatologist, rheumatolgist, gastroenterologist, psychiatrist, OT & PHYSIO. Immunosuppressants (eg cylclophosphamide). Raynaud’s: hand warmers, calcium antagonists, ACE-i, intermittent prostacyclin.

23. Surgical treatments: Calcinosis: excise localized painful large deposits to relieve symptoms; recurrence is rare. Raynaud’s: Cervical sympathectomy is less beneficial for scleroderma patients than for patients with Raynaud phenomenon secondary to peripheral vascular disease. Sometimes digital sympathectomy. Esophageal: Screen for reflux oesophagitis & Barrett’s. Dilate benign strictures. Avoid surgery for reflux in scleroderma patients except in the most severe refractory cases. Sclerodactyly: for extensive contractures only. Telangiectasia: Bowel resection for uncontrollable GI bleeding from telangiectasia is rarely necessary.

24. Internal hernia Diagrammatic illustration showing various types of internal hernias: A = paraduodenal (4 “mouths” all facing each other: inferior, superior, retroduodenal, paraduodenal proper (NB: thromobosis/operative trauma IMV), B = foramen of Winslow, C = intersigmoid, D = pericaecal, E = transmesenteric, and F = retroanastomotic. Also post-surgical – defect in mesentery or omentum or peritoneum. Note named henias: hiatal/para-oesophageal, lumbar, obturator, diaphragmatic, sciatic

25. Radiation enteritis

26. Acute radiation enteritis: Due to the direct effects of radiation on the bowel mucosa. Is exceedingly common; virtually every patient has some manifestation of acute radiation-induced injury of the GI tract in the form of abdominal cramping, tenesmus, urgency, bleeding, diarrhoea, and incontinence. • Risk factors: Patient related – thin build, HT, adhesions from previous PID or surgery fixing SB in RTx field, advanced age, DM, collagen vascular disease. Treatment related: concomitant CTx, the total radiation dose, the fractionation, and the distribution. • Typically, these patients are managed symptomatically and supportively. Use antispasmodics, analgesics, and anti-diarrhoeal agents combined with IVF replacement if necessary. The symptoms of most patients resolve within weeks of radiation therapy cessation.

27. Chronic radiation enteritis: An indolent but relentlessly progressive disease. Occurs in 5-15%, although chronic diarrhoea in 30-40%. May present with symptoms within months or decades after radiation therapy. • HISTO: transmural bowel damage with associated obliterative endarteritis of the small vessels. Associated lymphoid atrophy, lymphatic dilation, and fibrosis of the sub-mucosal tissue also observed. The progressive vascular sclerosis leads to chronic ischemia of the overlying tissue, ultimately resulting in mucosal atrophy. Scar tissue replaces the submucosal tissue, resulting in further decrease in vascularity and contracture of the intestinal wall. Chronic mucosal ulceration may result in fistula formation and hemorrhage. • Treatment is extremely challenging. Initial non-operative modalities include diet modification, nutritional support, and control of symptoms with medications (including loperamide, sulfasalazine, sucralfate enemas). Argon Plasma Coagulation for bleeding controls 90%. Alternative is heater probe or formalin (dilute 50ml 4% in 400ml saline, apply drops or soaked gauze for 30sec then wash off). Severe, progressive disease may require surgical intervention, especially for complications, such as obstruction, fistula formation, perforation, and haemorrhage.