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SPOT QUESTIONS 4 (Sept 2004) ‏

SPOT QUESTIONS 4 (Sept 2004) ‏. Q1 Specimen of large resected thyroid. 1. Diagnosis 2. Pathology 3. Complications of disease 4. 5 specific complications of total thyroidectomy. Q2 Cut section of thyroid gland with nodule – history of young girl with family history of thyroid cancer

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SPOT QUESTIONS 4 (Sept 2004) ‏

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  1. SPOT QUESTIONS 4 (Sept 2004)‏

  2. Q1 Specimen of large resected thyroid. 1. Diagnosis 2. Pathology 3. Complications of disease 4. 5 specific complications of total thyroidectomy

  3. Q2 Cut section of thyroid gland with nodule – history of young girl with family history of thyroid cancer 1. Diagnosis 2. What would congo red stain show? 3. Pre-operative investigations

  4. Q3 • Ascending colon cut specimen • 1. Diagnosis • 2. Symptoms • 3. Prognosis according to specimen findings

  5. Q4 Cut section of adrenal gland – history of HT and adrenal medullary tumour 1. Diagnosis 2. Symptoms 3. Pre-operative work-up

  6. Q5 Hand with wasted thenar eminence muscles 1. Diagnosis 2. Typical symptoms 3. Treatment options

  7. Q6 History of multiple colonic polyps 1. Diagnosis 2. Classification 3. Two specific complications of resection 4. Other treatments

  8. Specimen of large resected thyroid. 1. Diagnosis 2. Pathology 3. Complications of disease 4. 5 specific complications of total thyroidectomy

  9. Multinodular goitre. May be non-toxic or with thyrotoxicosis (toxic MNG or Plummer disease). May contain foci of thyroid carcinoma (eg papillary cell or follicular cell)‏ • MACRO: asymmetrically enlarged, irregular cystic nodularity of gland associated with focal haemorrhage MICRO: variable degree of colloid accumulation, follicular epithelial hyperplasia, and follicular involution with focal intervening areas of fibrosis, calcification and haemorrhage. PATHOGENESIS: Repeated episodes of hyperplasia, nodule formation, degeneration (involution) and fibrosis. It occurs either in response to iodine deficiency or else, in iodine-replete areas, as the result of intrinsic heterogeneity of TSH receptors. MNG has a high familial incidence. • Pressure effects: oesophageal compression with dysphagia, tracheal compression, obstruction of superior vena cava, recurrent laryngeal nerve palsy. Cosmetic deformity. Bleed into nodule may cause pain or more importantly acute tracheal compression (especially retrosternal). Functional effects: thyrotoxicosis [tachycardia, CHF, AF], rarely hypothyroidism. May harbour malignancy.

  10. Complications of surgery: • Recurrent laryngeal nerve injury (<1% permanent, up to 5% temporary)‏ • External laryngeal nerve injury • Hypoparathyroidism ie hypocalcaemia (1-3% permanent, 5-10% temporary)‏ • Bleeding (5%)‏ • Wound infection, dehiscience, suture granuloma, keloid/unsightly scar • Laryngeal oedema, tracheal malacia, need for tracheostomy • Recurrent MNG or hyperthyroidism (5% in Graves' disease)‏ • Need for life-long thyroxine medication

  11. Cut section of thyroid gland with nodule – history of young girl with family history of thyroid cancer 1. Diagnosis 2. What would congo red stain show? 3. Pre-operative investigations

  12. Familial Medullary thyroid cancer. Arise from parafollicular C cells ultimobranchial body origin. RET proto-oncogene mutation (Chr10q). Rearrangement gene after irradiation → papillary thyroid Ca • Medullary thyroid carcinomas contain amyloid depositis, derived from altered calcitonin molecules. This amyloid turns salmon-red with Congo red, and there is yellow-green birefringence in polarized light. • FNA cytology thyroid lesion under USS guidance. Serum calcitonin levels +/- CEA. Staging USS or CT SCAN of neck and chest x-ray. In MEN need to exclude phaeochromocytoma (50%) and parathyroid hyperplasia (80%, but <20% have hypercalcaemia). Familial medullary carcinoma may be isolated or occur with phaeochromocytoma – often bilateral – and hyperparathyroidism (MEN IIA). It may also occur with or without marfanoid habitus, multiple neuromas, and ganglioneuromatosis (MEN IIB). Hirschsprung's disease and lichen planus amyloidosis also occur in patients with familial medullary cancer.

  13. Ascending colon cut specimen 1. Diagnosis 2. Symptoms 3. Prognosis according to specimen findings

  14. Ascending colon carcinoma (likely adenocarcinoma)‏. ? Involving ileocaecal valve. • Asymptomatic, lethargy, fatigue, weakness, weight loss, abdominal pain/discomfort (persistent, sometimes postprandial), abdominal mass, altered bowel function (rarely), obstruction (involving IC valve), appendicitis. Iron deficiency anaemia and positive faecal occult blood often first indication. • Tumour extending beyond muscularis propria. ? LN status. • Prognosis according to clinicopathological stage (TNM stage). Overall 50% 5yr survival. • TNM Stage I 80-95%; Stage II 60-90%; Stage III 30-55%; Stage IV 0-10% • Dukes Stage A 90%; B 60%; C 30%; Distant METS 10% • Poor prognostic markers: +ve margins, apical LN involvement, perforation, obstruction, mucinous, poorly differentiated, vascular invasion, associated adenomas

  15. Colonic TNM • T1 – invades, no through, submucosa • T2 – invades not through, muscularis propria • T3 – invades not through, serosa, or through into non-peritonealized pericolic tissue • T4 – perforated peritoneum or invades adjacent structure • N1 – 3 or less nodes • N2 – 4 or more nodes • N3 – nodes along named vascular trunk • M1 – distant METS

  16. Cut section of adrenal gland – history of HT, palpitations and tremor 1. Diagnosis 2. Other symptoms 3. Pre-operative work-up

  17. Phaeochromocytoma – benign or mailgnant • Asymptomatic. Classically, episodic hypertension associated with triad of palpitations, headache and sweating. May also complain of anxiety (‘impending doom’ sensation), tremors, weight loss, dizziness, nausea and vomiting, abdominal discomfort, constipation, psychosis and visual blurring. Some patients have diarrhoea (due to VIP). Crisis precipitated by trauma or surgery. • Diagnostic: the best (and usually only test) is to measure fractionated 24hr urinary catecholamines and metanephrines. Measuring plasma free metanephrines is 97-100% sensitive and 85-95% specific. (Provocative tests – using glucagon, histamine, or tyramine – are not accurate and are potentially dangerous. Clonidine suppression tests are rarely used). Localisation: Contrast-enhanced MDCT ABDO scan. MRI avoids radiation exposure and has characteristic bright appearance on T2 phase. MIBG may be helpful for localising extra-adrenal pheochromocytomas. Routine bloods (include Ca & PO4), CXR, ECG.

  18. Malignant HISTO features – none, diagnosis is based on presence of metastases. METS to regional LN, liver, lung, bone. • Familial syndromes with phaeochromocytomas: • MEN IIA and IIB • Von Hippel-Lindau • Von Recklinghausen • Sturge-Weber

  19. Hand with wasted thenar eminence muscles 1. Diagnosis 2. Typical symptoms 3. Treatment options

  20. Wasting of thenar eminence muscles from prolonged median nerve compression (carpal tunnel, supracondylar entrapment, cubital fossa entrapment, anterior interosseus nerve entrapment)‏ • Principle clinical features are pain (burning or aching), numbness and tingling in median nerve distribution of hand (sparing palmar branch given off higher up). Symptoms are particularly worse after repetitious movement and at night, and on awakening the patient has to shake the hand to obtain relief. Patient often states hand feels “clumsy”, but with no specific weakness. • Treatment: conservative and operative (indicated here with thenar atrophy)‏ • Non-surgical (includes treat underlying causes): • Splint, wrist support for keyboard operators, modify activity, night splints, physiotherapy, anti-inflammatories, hydrocortisone injection, diuretics

  21. Surgical: • Indications: • Persistent and progressive signs and symptoms • Thenar atrophy • Non-operative therapy failure • Inability to perform job/daily activity • Perform complete carpal tunnel release (open or laparoscopic)‏ under regional or general anaesthesia. Post-operative splinting then rehabilitation programme.

  22. Causes (ARMPIT NAD): • Acromegaly • Rheumatoid arthritis • Myxoedema • Pregnancy • Idiopathic • Trauma (occupational)‏ • Neoplasia • Amyloidosis • Diabetes • Clinical assessment: Symptoms, dysfunction. LOOK, sensory – 2 point & vibration, motor, provocative tests – Tinel (pressing/tapping nerve), Phalen (prolonged wrist flexion), Carpal compression.

  23. History of multiple colonic polyps 1. Diagnosis 2. Classification 3. Two specific complications of resection 4. Other treatments

  24. Large retroperitoneal tumour obliterating mesocolon. Likely desmoid tumour given probable FAP background. Differential: malignant fibrous histiocytoma, liposarcoma, leiomyosarcoma, rhabdomyosarcoma, myxofibrosarcoma • May behave benignly or aggressively. Divided into extra-abdominal, abdominal and intra-abdominal. Extra-abdominal occur principally in muscles of shoulder, chest wall, back and thigh. Abdominal desmoids generally in anterior ABDO musculoaponeurotic structures in women during or after pregnancy. Intra-ABDO desmoids tend to occur in mesentery or pelvic walls, often in patients with FAP (Gardner syndrome). A locally invasive non-metastasizing tumour that occurs in the mesentery or abdominal wall. These deep-seated fibromatoses lie in interface between exuberant fibrous proliferations and low-grade fibrosarcomas. Occur at any age, most frequently in teens to thirties. • Local recurrence frequent and persistent when incompletely excised, anastomotic leak, ischaemic intestine • Tamoxifen, NSAIDs, chemotherapy, radiotherapy

  25. Q7 1. Differential diagnosis 2. What features on examination would you want to know? 3. How would you manage?

  26. Q8 1. Diagnosis 2. Differential 3. Key points on operation to remove

  27. Q9 Blunt ABDO trauma. 1. Diagnosis 2. Classification of severity 3. Treatment options

  28. Q10 Intra-op photo of pancreatico-jejunal anastomosis 1. What does this photo show? 2. How else can you anastomose pancreas? 3. How can you prevent the anastomosis shown from leaking?

  29. Q11 IOC finding 1. Diagnosis 2. Classification 3. Treatment

  30. Q12 • Previously healthy 12-year-old boy 1. Diagnosis 2. Natural history 3. Complications 4. Surveillance

  31. Photo of hand with ulcer on it 1. Differential diagnosis 2. What features on examination would you want to know? 3. How would you manage?

  32. Benign: inflammatory - ulcerated psoriasis, pyoderma gangrenosum; infective – fungal; vascular – ischaemic, vasculitic; traumatic – burn, infected graze Malignant: SCC, in-situ SCC, Paget's disease, superficial multicentric BCC, amelanotic melanoma, Merkel cell. • Painful/painless, size, depth, fixed/mobile/adherent to underlying tendons, distal nerve function and limb pulses, margins for excision/proximity to joint creases, associated infection & cellulitis, lymphadenopathy, other possible neoplastic lesions. • Malignant (likely): Punch biopsy to confirm histological diagnosis. Treat infection. Will then require complete excision with minimum 1cm margins. Full-thickness skin graft if overlying joint crease (from radial aspect distal forearm or retro-auricular or sternal depending on size), otherwise SSG from upper inner arm or thigh. Benign: debride, dressings, antibiotics, anti-fungals, steroids

  33. Photo of mid-line neck lump 1. Diagnosis 2. Differential 3. Key points on operation to remove

  34. Thyroglossal duct cyst. • Differential: lipoma, dermoid cyst, epidermal cyst, lymphadenitis, enlarged Delphic node with thyroid malignancy, enlargement of or neoplasia within thyroid pyramidal lobe, ectopic thyroid gland, thyroglossal duct carcinoma (arising within aberrant thyroid tissue, rare <1%)‏ • Exclude lingual thyroid or thyroid pyramidal neoplasia. Resection with total excision of the cyst, the central hyoid bone and the entire fistulous tract extending to the foramen cecum, is mandatory for cure. This Sistrunk procedure has low recurrence rates (5%). Avoid perforation of cyst. Meticulous haemostasis as wound haemorrhage may result in airway compromise.

  35. Transverse incision over cyst. Dissect cyst from surronding structures. Divide sternohyoid + thryohyoid muscles at their insertion to expose hyoid bone. Encircle hyoid bone with right angle clamp 1cm from mid-point & then divide with bone cutter or cautery. Traction on divided hyoid to help division of opposite side. Dissection proceeds cephalad to the foramen caecum where the tract and investing tissues are suture-ligated.

  36. Blunt ABDO trauma. 1. Diagnosis 2. Classification of severity 3. Treatment options

  37. Grade Description I <10% subcapsular haematoma, <1cm laceration II 10-50% subcapsular haematoma, <5cm intraparenchymal, lac 1-3cm III >50% subcapsular or >5cm intraparenchymal, or lac >3cm IV Laceration involving segmental or hilar vessels with >25% devascularisation V Shattered spleen, hilar devascularisation • Splenic injury (Grade IV with devascularization, & query contrast leakage posteromedially)‏ • AAST Classification

  38. Management: • Unstable or laparotomy for associated injuries → splenic preservation where feasible, low threshold for splenectomy • Interventional radiology with embolization • Stable → conservative, close observation • 60% adults managed non-operatively with 80% success (90% with children)‏ • Most failure occur in 72 hrs but may occur at 2 weeks. Risk of delayed re-bleed after NOM is 1-8%. • Failure factors (increase grade (IV), contrast leak, age > 55 yrs, degree of haemoperitoneum)‏

  39. Criteria for Non-op Management of Splenic Injury • No indications for laparotomy (e.g. perforated viscous)‏ • Hemodynamically normal after resus with crystalloid • No injuries that preclude physical examination of the abdomen (e.g. significant brain injury, spinal cord injury)‏ • Transfusion requirement <3-4units/24 hour (PRBC)‏ • Constant availability of surgical and critical care resources • Advantages of NOM: • Avoidance of non-therapeutic laparotomies (with assoc cost & morbidity)‏ • Fewer intra-ABDO complications • Reduced transfusion risk

  40. Criteria for Failure of Non-op Management (from DSTC)‏ • Haemodynamic instability • Evidence of continued splenic haemorrhage • Associated intra-abdominal injury requiring surgery • Replacement of > 50% patient’s blood volume • Other • Failed angio embolization of A-V fistulae/pseudoaneurysm • Peritoneal signs/rebound tenderness

  41. Intra-op photo of pancreatico-jejunal anastomosis (end to side)‏ 1. What does this photo show? 2. How else can you anastomose pancreas? 3. How can you prevent the anastomosis shown from leaking? A two-layer, end-to-side, duct-to-mucosa retrocolic pancreaticojejunostomy

  42. Pancreatico-jejunal end-to-side anastomosis likely post Whipples resection. A hand-sewn, two-layer, end-to-side, duct-to-mucosa retrocolic pancreaticojejunostomy. • Pancreaticojejunostomy either end-to-side (including capsule to mucosa), end-to-end (two-layer invaginating, “binding” sleeve), end-to-end separate Roux loop to hepaticojejunostomy; pancreaticogastrostomy end-to-side. With or without stent. Longitudinal panreaticojejunostomy +/- limited pancreatic resection – modified Puestow or Frey procedure or Beger procedure • Well vascularized, tension free, technically secure anastomosis. Anastomosis by experienced pancreatic surgeon. Trans-anastomotic stent and a separate Roux loop. Meticulous haemostasis around anastomosis. Post-operative octreotide 100mcg Q8H iv will reduce consequence of minor leakage. Peri-anastomotic drain. No significant difference leak rate with fast-track reinstitution of enteral feeding.

  43. IOC showing choledochal cyst 1. Diagnosis 2. Classification 3. Treatment

  44. 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- and extra-hepatic, 4b multiple extra-hepatic. • Type 5; multiple intra-hepatic with hepatic fibrosis (Caroli's) • 85% are either types 1 or 4. • 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

  45. 1. Diagnosis 2. Natural history 3. Complications 4. Surveillance

  46. Peutz-Jeghers syndrome with jejuno-jejunal intussusception • An autosomal dominant disorder with high degree of penetrance. Tumour suppressor gene STK11 (Chr19) is implicated in many. Characterized by the development of multiple hamartomatous gastrointestinal polyps, mucocutaneous pigmented lesions on the lips or buccal mucosa, and an increased risk of cancer within (gastric, intestinal, rectal) and outside the gastrointestinal tract (pancreatic, biliary, lung, breast, cervix & fallopian tube, ovary/testis). • [Hamartoma = A tumour-like, non-neoplastic disordered proliferation of mature tissues that are native to the site of origin] • Hamartomatous GI polyps may cause GI obstruction or intussusception as in this case. GI bleeding – occult or overt. Adenomatous change occurs in 3-6% of hamartomas. 20% life-time risk CRC, 5% gastric.

  47. - Annual upper and biannual lower endoscopy. Remove all polyps >15mm size. • Small bowel imaging every 2-3 years (? MRI)‏ • Cervical smears. Breast screening. Testicular self + annual physician examination.

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