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SPOT QUESTIONS

~ May 2006. SPOT QUESTIONS. 1.What is the diagnosis? 2. What determines the prognosis? 3. Further management?. Acral lentiginous melanoma on the sole of the left foot

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SPOT QUESTIONS

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  1. ~ May 2006 SPOT QUESTIONS

  2. 1.What is the diagnosis? 2. What determines the prognosis? 3. Further management?

  3. Acral lentiginous melanoma on the sole of the left foot • Breslow thickness, Clark's level, ulceration, nodal metastases (size, number, extra-nodal extension), in-transit metastases, distant METS, mitotic rate, lymphocytic reaction, tumour regression status, incomplete or inadequate excision, sex, site, within naevus better, raised LDH level. • Punch biopsy, contrast enhanced MDCT scan ABDO/PELVIS (incl groin LN's), CXR or CHEST CT, routine bloods – FBC, LFTs, RENL, LDH. Discuss MDTM with above. Options - forefoot amputation, groin dissection for palpable or radiologically pathological lymph nodes (for staging and local control of disease), otherwise SLNBx for staging. Palliative for widespread METS.

  4. 16 y old boy. 1. Diagnosis 2. Treatment 3. Surgical options 4. What advice would you give

  5. Ingrown toenail lateral aspect left great toe. (Nail = densely keratinised stratum corneum). • Topical and oral antibiotics, hygiene instructions, cessation of smoking -> reassess at 2/52 and/or advise operative management under LA • Resection of overlying skin and granulation tissue only and releasing of ingrown nail, or lateral resection of granulation tissue, lateral nail and nail bed up to and including proximal nail germinal matrix. Alternative to nail bed excision is ablate nail bed with phenol, then wash with methylated spirits. • High likelihood of recurrence without resection of nail bed germinal matrix; smoking cessation; hygiene advice; operative risk (including infection & osteomyelitis, non-healing wound, bleeding, repeat procedures)‏

  6. Recent ETOH related pancreatitis (8 weeks ago), now septic. 1. Describe CT 2. Describe management

  7. Oral and iv contrast enhanced CT showing an approx 10cm rim-enhancing fluid collection in the lesser sac, arising from the body of the pancreas and consistent with being a pancreatic pseudocyst. No gas contained within collection. • Unlikely to resolve spontaneously (8 weeks post pancreatitis, big cyst, likely big communication) hence needs drainage with options being percutaneous (into stomach or to skin), endoscopic, or operative (open or laparoscopic) via anastomosis with stomach or small bowel. Prior to above need imaging of pancreatic duct via MRCP or ERCP to define anatomy and exclude strictures preventing resolution. Management would be discussed with specialist pancreatic surgeon.

  8. Right colon of a 34 year old woman 1. Describe specimen 2. What to look for on pathology 3. Other organs to examine

  9. Ascending colon containing ulcerating malignant lesion and a fungating villous-like polyp • Young person with right sided colonic cancer and prob pre-malignant polyp consistent with HNPCC. Pathology in adenoma: number, size, type, dysplasia, invasion. In malignant ulcer: poorly diff adenoCa, signet ring or mucinous type, depth of invasion, lymphovascular invasion, nodal metastases, margins, tumour infiltrating lymphocytes & Crohn's-like lymphocytic reaction. Immunohistochemistry for loss of mis-match repair proteins. If loss of protein expression MLH1-> b-RAF. If +ve = sporadic, if -ve test for germline mutation for MSI in HNPCC • Staging of colonic cancer: liver and lung imaging (CT SCAN). Other organs at risk carcinoma in HNPCC: endometrial (40-60%), ovarian, gastric, hepatobiliary, pancreatic, small bowel, ureteric & renal pelvis, brain.

  10. Modified Amsterdam criteria – clinical: • 3 relatives with CRC or HNPCC associated cancer • 2 successive generations • 1 diagnosed before age 50 • 1 first degree relative • FAP excluded in CRC • Bethesda criteria – clinico-pathological • CRC in one or more 1st degree relative with HNPCC-related cancer, with one diagnosed before age 60 • 2 or more 1st or 2nd degree relatives regardless of age • CRC in patient before age 50 • Adenomas before age 40 • Synchronous, metachronous or other HNPCC-associated tumour regardless of age • CRC with MSI-H histology in patient before age 60 (tumour infiltrating lymphocytes, Crohn's-like lymphocytic reaction, mucinous/signet ring differentiation, or medullary growth pattern)‏

  11. 80 female with perianal lump 1. Diagnosis 2. What 2 pieces of further information would you like 3. Investigations 4. Operative options

  12. Full-thickness rectal prolapse • Patient comorbidities (eg dementia, psychiatric illness), pelvic floor function, previous surgery for prolapse • Flexible sigmoidoscopy to exclude lesion as lead-point. Consider anorectal physiology and colonic transit studies in some patients. Routine pre-op investigations (anaesthetic fitness)‏

  13. Perineal and abdominal (laparoscopic or open)‏ • Perineal - DeLorme's procedure (mucosa 'sleeve' excision and muscle coat plication) - Altemeier perineal rectosigmoidectomy - Perineal rectopexy - Thierch procedure (anal encirclement) • Abdominal (laparoscopic or open) - Rectopexy +/- sigmoid resection (Frykman-Goldberg operation) +/- stoma - mesh or non-mesh

  14. ABDO rectopexy. ADV: low recurrence rate. DISADV: GA required, ABDO operation, anastomotic risk if sigmoid resection, infection of prosthetic material, intractable constipation, sexual & urinary dysfunction. • PERINEAL. ADV: no ABDO operation, can be done under regional anaesthesia, low mortality, short hospital stay, minimal post-op pain, no constipation, repeatable. DISADV: higher recurrence rate, anastomotic risk if performed, urgency of defecation. • Awaiting international multicentre randomised trial (PROSPER – PROlapse Surgery PErineal or Rectopexy) comparing ABDO vs PERINEAL and resection vs non-resection techniques.

  15. Oesophagogastrectomy specimen with Barrett's and cancer. 1. Describe specimen 2. Incidence 3. Aetiology / list pathological features

  16. Distal oesophagus with irregular Z-line between normal squamous epithelium and probable Barrett's type epithelium. Multiple ulcerations present. • 1% adult population, up to 12% patients with GORD. • Metaplastic intestinal columnar epithelialisation of the distal oesophageal epithelium in response to chronic gastric refluxate. At risk of ulceration, and increasing grades of dysplasia leading to invasive adenocarcinoma. Duration and frequency of GOR and other genetic & environmental factors (eg smoking, EtOH, obesity – especially central obesity) are also involved. Both NSAIDs (by non-selectively blocking COX receptors) and H. pylori appear to be protective and associated with a lower risk of developing oesophageal adenocarcinoma.

  17. GORD 20% population, Barrett's in 10% of these. Predominantly caucasians, M:F 2:1 ratio. • Most oesophageal adenoCa (EAC) arises within Barrett oesophagus. Incidence development EAC from Barrett oesophagus = 0.3 – 1.0% yearly. Factors ↑ risk dysplasia & Ca: length of Barrett's segment, duration of Barrett's, smoking, obesity, poor diet. • Obesity and EAC: 5kg/m2 increase (15kg in male, 13kg in woman) has RR 1.5 for EAC • Nearly 80% of Barrett's patients are overweight, obese, or centrally obese. Prevalence of metabolic syndrome among these patients is nearly 50% (c.f. 21% in the normal community). In patients with long segment Barrett's, some report higher rates of central obesity or enlarged waist circumference, plasma insulin levels, and serum IL-6 levels.

  18. 70 y female 5 yrs post mastectomy. 1. Describe appearance 2. Management options

  19. Chest wall recurrence of RIGHT breast cancer with dermal satellite metastases and lymphoedema. LR after mastectomy may be a marker of associated systemic disease. • Biopsy taken for confirmation of recurrence and for hormone sensitivity analysis with treatment as indicated from pathology. Staging with imaging - CXR/ABDO USS or CT CHEST ABDO/bone scan. Discussion in a BREAST MDT meeting. (Consider local resection as may be an option for symptom control, to enhance quality of remaining life, and to improve effectiveness of radiotherapy. Reconstruction is often difficult as relies on poor-quality tissue. Resurfacing with non-irradiated flap tissues may enable further RTx or brachytherapy). Usually mainstay of treatment is radiotherapy and palliative chemotherapy together with endocrine treatments, switching to alternative therapy eg tamoxifen -> exemestane or anastrozole/letrozole.

  20. Diarrhoea, nausea, fever and ABDO pain 2 weeks post R hemicolectomy 1. Diagnosis 2. Pathophysiology 3. How to confirm diagnosis

  21. Pseudomembranous colitis with characteristic creamy fibrinous plaques of colonic mucosa. • Clostridium difficile (anaerobic, G +ve, spore-forming bacillus) is gut resident in 3% population and 10% patients admitted to hospital. Certain broad-spectrum antibiotics allow the organism to proliferate by killing off other competing gut organisms. Cl difficile elaborates at least 4 toxins, including toxin A (an enterotoxin) and toxin B (a cytotoxin) [mediate colonic tissue damage by disruption of the actin-based cytoskeleton of enterocytes]. Colitis may commence from 2 days to many weeks after antibiotic use. • Stool cultures and Cl difficile toxin assays (NB: significant false -ve rate hence often need multiple stool samples to diagnose). If performed, biopsy at colonoscopy/rigid sigmoidoscopy. Stop broad-spectrum antibiotic therapy and commence either oral metronidazole or oral vancomycin (NB: up to 20% recurrence as failed initial clearance, but bacterial resistance is rare).

  22. Causative antibiotics: potent – clindamycin, 3rd generation cephalosporins (ceftriaxone, cefotaxime), fluoroquinolones (ciprofloxacin). Single dose peri-op cephalosporin has 1.5% incidence CDI. • Increased incidence with: age, severity and duration of underlying disease, duration and number of antibiotic treatments, length of hospital stay. • New aggressive strain of CDI is ribotype 027 or NAP1. Causes more severe disease and mortality rate 17%. • Clinically: colicky ABDO pain and diarrhoea. NB: diarrhoea absent in 20%, especially if post-op ileus. • Probiotics have no beneficial effect in meta-analysis. Intravenous immunoglobulin has been used. Faecal transplants via NG tube show promise. • Colectomy + ileostomy in peritonitis, anticipated perforation, persistent sepsis, older patient and immunocompromised

  23. 50 yr old female 1. What does the CT show? 2. Likely causes? 3. Management options

  24. RIF phlegmonous mass containing likely purulent material and gas • Perforated appendicitis, perforated diverticulitis (caecal, possibly sigmoidal), leaking anastomosis after ileocolic resection, traumatic perforation (eg blunt or penetrating ABDO injury, colonoscopic perforation especially post caecal polyp excision/biopsy), tubo-ovarian abscess • Management influenced by cause and clinical status of patient. Options include percutaneous drainage under radiological guidance, open drainage via RIF/flank dissection and drainage, or (most likely operative approach) laparotomy, drainage +/- resection and stoma formation as necessary

  25. 60 y old women, present for 2 years, 1. Likely diagnosis 2. How to confirm and treat 3. Complications of surgery

  26. Submandibular mass in this age group most likely (>50%) malignant, either primary submandibular or lymph node MET from cancer of oral cavity (anterior 2/3rds tongue, floor of mouth, gums, mucosa or cheek)‏. Benign differential: chronic sialoadenitis, pleomorphic adenoma. NB: carcinoma ex pleomorphic adenoma • Thorough examination of oral cavity, fine-needle aspiration cytology, and contrast-enhanced CT scan of neck +/- chest (if no recent CXR). Sub-specialist (ENT) consultation for endoscopy as necessary. Treatment based on histology and stage. • Complications of submandibular gland resection include marginal mandibular nerve palsy (depressor anguli oris paralysis with dribbling from corner of mouth), lingual nerve palsy (lose sensation anterior 2/3rds of tongue), hypoglossal nerve palsy (paralysis of all intrinsic and extrinsic muscles of tongue except palatoglossus), bleeding, recurrence

  27. Benign Salivary Gland Tumours: • Pleomorphic adenoma (50%)‏ • Warthin tumour (5-10%)‏ • Oncocytoma (1%)‏ • Other adenomas (eg basal cell, canalicular) (5-10%)‏ • Ductal papillomas • Malignant Salivary Gland Tumours: • Mucoepidermoid carcinoma (15%)‏ • Adenocarcinoma NOS (10%)‏ • Acinic cell carcinoma (5%)‏ • Adenoid cystic carcinoma (5%)‏ • Malignant mixed tumour (3-5%)‏ • Squamous cell carcinoma (1%)‏ • Other carcinomas (2%)‏

  28. 54 yo Greek farmer 1. What does CT show 2. Other investigations to confirm diagnosis 3. Lifecycle of the condition

  29. Hydatid liver cyst in left lobe of liver. Multiple peripheral daughter cysts within the main cyst cavity. Peripheral calcification around lateral aspect of main cystic lesion. • Diagnosis is suggested from history and radiological features. Confirm ecchinococcus infection with serology (indirect haemoglutination test) [false -ves 10-20%] +/- immunoelectrophoresis (more sensitive, best test). Others – Casoni cell mediated hypersensitivity test (rarely used), complement fixation (lots false -ves). May have eosinophilia on FBC and abnormal LFTs. • Definitive host = dogs. Infected by eating infective offal. Have adult tapeworms (3-6mm) in intestines and pass ova in faeces → ingested by intermediate hosts. Adult tapeworms only develop in definitive host. Intermediate hosts = sheep, cattle, rodents, & humans (accidental). Infected by faecal oral route or eating infected animal. Ova hatch, then larvae penetrate intestine and pass to liver (75%), lung (15%) or other sites. Develop into cyst filled with clear fluid and brood capsules that bud into the cyst lumen & contain scoleces.

  30. Treatment Hydatids disease:Medical • Pre- and post-operative albendazole, total 6 month therapy • Inoperable cases can be treated with albendazole or mebendazole. An overall response rate of 55-79% has been documented, with cure in 29% of cases. Albendazole is the drug of choice because of its greater absorption from the GI tract with higher plasma levels. Mebendazole is poorly absorbed and must be taken at higher doses for several months for a therapeutic effect. Albendazole is administered in 3 or more cycles of 400-800 mg twice daily for 4 weeks (adult dose), followed by a 2-week period of rest. If response to 3 cycles is not evident, subsequent courses are unlikely to be beneficial. Response to therapy is best monitored by serial imaging studies.

  31. Treatment Hydatids disease:Surgical • Treatment of choice for most. • Alveolar less amenable to surgery. Liver options include: partial hepatectomy, cystectomy, pericystectomy. In 20% of cases, disease recurs despite surgery. • May inactivate fertile cyst with 30% saline. • An alternative to surgery is the PAIR method (ie, puncture the cyst, aspirate fluid, introduce a protoscolicidal agent, then reaspirate), which requires ultrasonographic guidance. Extreme care needed to avoid anaphylactic shock. Albendazole therapy may be combined with PAIR. • Some severe cases of alveolar hydatid disease have led to liver transplantation.

  32. 1. What is the diagnosis 2. 5 pathological complications 3. Complications of resection

  33. Multinodular goitre in female • Pathological complications: • Superior vena caval compression syndrome • Tracheal compression -> stridor, dyspnoea • Sudden airway obstruction from bleed into retrosternal nodule • Oesophageal compression -> dysphagia • Vocal cord palsy from pressure effect on RLN • Thyrotoxicosis • Harbouring of malignancy • Severe cosmetic morbidity

  34. 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)‏ • Recurrent MNG or hyperthyroidism (5% in Graves' disease)‏ • Bleeding (5%)‏ • Wound infection, dehiscience, suture granuloma, keloid/unsightly scar • Laryngeal oedema, tracheal malacia, need for tracheostomy • NB: need for life-long thyroxine medication, possible need for calcium replacement

  35. Scrotal swelling left side 1. Differential 2. Clinical features to differentiate 3. Investigations to confirm

  36. Differential (acute versus chronic)‏ • Testicular torsion • Torsion testicular appendices • Torsion epididymal appendices • Epididymo-orchitis • Trauma • Inguinoscrotal hernia • Inflammatory unilateral hydrocoele • Inflammatory neoplasia, sperm granuloma • Clinical features to differentiate • History: Age of patient, onset of pain + swelling, voiding symptoms, pyuria, STD risk, FHx • Examination: Fever, relief of pain with scrotal elevation, position of testicle, point tenderness/'blue dot' on transillumination, absence of cremasteric reflex, groin nodes

  37. Investigations: • Best “test” = operative exploration • USS +/- Doppler • LAB tests: • urine specimen (first catch) – M/C/S • Urethral swabs for gonococci and chlamydia • FBC • Tumour markers • Radionucleotide scanning (↑ uptake epididymitis, ↓ uptake testicular torsion)‏

  38. Seat belt bruising post MVA 1. Significance, associated injuries 2. CT findings you would look for

  39. Lap seat belt trauma • Compressive: • Rupture of SB or colon • Tear or avulsion of mesentery • Solid organ injury involving spleen, liver, kidneys • Duodenal and pancreatic injury • Thrombosis or intimal tear of iliac artery or abdominal aorta • ABDO wall contusion, haematoma • Hyperflexion: • Chance # of lumbar vertebrae (espec L1/2)‏ • CT findings suggestive of above • Free air/fluid/blood • Solid organ injury and grade of injury • Mesenteric stranding, bowel wall disruption, any subtle signs of intestinal injury, non-perfusion or thrombosis • Lumbar # • Minimal abnormality possible

  40. 1. Diagnosis 2. Aetiology 3. Treatment 4. How would you consent

  41. Perianal abscess at 11 O'clock position • Cryptoglandular theory favoured (blocked anal gland that subsequently becomes infected). Usually no predisposing factors, but more common in diabetes, immunocompromised, previous perianal abscess/fistula, perianal Crohn's disease, male and smoker. • EUA rectum and anus, Incision & Drainage of abscess (under GA). Course of oral antibiotics peri-operatively. • Explain aetiology and likely natural course without intervention. Operative risks include: trauma to anal sphincter (flatus/faecal incontinence, temporary/permanent), bleeding, recurrence (30-50% fistula rate), wound healing complications, insertion of seton, possible need for repeat procedures. Other: expected time off work, expected time in hospital.

  42. 1. Diagnosis from colonoscopy photo 2. Aetiology 3. Treatment

  43. Melanosis coli • A benign and reversible condition with deposition of lipofuscin brown pigment (not melanin as name implies) into the colon mucosa. The most common cause of melanosis coli is the abuse of laxatives, and commonly anthraquinone containing laxatives such as Senna and other plant glycosides. • Can confirm with biopsy which shows characteristic pigment-laden macrophages within the submucosa on PAS staining. No adverse effects or consequences of melanosis coli have been identified. Advise stopping laxatives.

  44. Tumor attached to the small bowel, antimesenteric side 1. Diagnosis 2. Presentation 3. Pathology for prognosis

  45. Gastrointestinal stromal tumour of small bowel (GIST)‏. Arise from interstitial cells of Cajal. • Presentation • Pain (dull, crampy)‏ • 50% as emergency admissions for obstruction or bleeding • Obstruction • Uncommon cause of SBO in general (<5%)‏ • Stenosis • Volvulus • Intussusception • Bleeding • Occult • Overt • Massive (leiomyosarcoma, angioma)‏ • Incidental on ABDO imaging or operation

  46. Pathology for diagnosis: • Cell type (spindle, epithelioid)‏ • Immunohistochemistry (positive: c-kit [CD117], CD34, ± actin) (negative: Desmin, S100)‏ • Pathology for prognosis (all have malignant potential): • Size >2cm SB, >5cm gastric • Mitotic rate >5 per 10hpf • Infiltration and metastases • Tumour necrosis • Vascular invasion (NOT lymphatics)‏ • Nuclear pleomorphism • C-kit mutations (predicts response to Glivec medication)‏

  47. Carcinoid (APUDoma arising from enterochromaffin cells throughout the gut). • May be associated with MEN types 1 & 2 (usually foregut carcinoid) with neoplasms in other organs in 15% (colon, lung, stomach, breast). 88% are midgut, appendix > ileum > jejunum. Multiple tumours in 40%. Midgut tumours produce serotonin and substance P, gastrin, somatostatin, motilin, secretin, neurotensin, pancreatic polypeptide. Foregut and hindgut carcinoids do not produce serotonin. • Grossly carcinoids are firm, yellowish submucosal nodules. Special stains may demonstrate argentaffin or argyrophil reactions. • Regarded as “a malignant neoplasm in slow motion”. At diagnosis, 40% invade muscularis and 45% metastasised to lymph nodes or liver. 80% tumours >2cm have spread at time of diagnosis.

  48. Usually asymptomatic. 30% SB carcinoids cause obstruction, pain, bleeding or the carcinoid syndrome. Obstruction due to sclerosis and kinking due to vascoactive substances from METS in mesentery. 10% have carcinoid syndrome at diagnosis, others develop later. Consists of cutaneous flushing, diarrhoea, bronchoconstriction, and right-sided cardiac valvular disease due to collagen deposition. APUD peptides inactivated by liver, hence syndrome if liver METS, primary ovarian or bronchial caricinoid, rectal or oesophageal. Syndrome due to serotonin, but also other vasoactive substances, including amines (histamine, dopamine), tachykinins (substance P, kallikrein, neuropeptide K), peptides (pancreatic polypeptide, chromogranins, neurotensin, motilin) and prostaglandins.

  49. Some detected by imaging, others incidentally at surgery. Elevated urinary levels of 5-hydroxyindoleacetic acid (5-HIAA) or of serum chromogranin A. A provocation test with injection of pentagastrin to cause carcinoid symptoms and raised levels of serum serotonin and substance P. • R0 resection of disease, in presence of incurable disease still resect obstructing disease as tumour growth slow, resect liver METS or palliate with hepatic artery embolization or infusional chemotherapy. Octreotide to suppress tumour growth and control symptoms of carcinoid syndrome. • After resection of SB carcinoid 5yr survival = 70%. 40% with inoperable METS and 20% with liver METS survive 5yrs or longer. Median survival; from HISTO diagnosis 14yrs, from onset of carcinoid syn 8yrs.

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