here are no sensory fibers above the dentate line (squamomucosal junction), hemorrhoids are not painful unless they thrombose when protruded. Fissures and hemorrhoids commonly occur together. Exam \212 \212 \212 \212 to R/O other diseases Abdominal examination Rectal examination: Proctoscopy Sigmoidoscopy higher up than the rect osigmoid junction). Prolapsing hemorrhoids are obvious. to see the internal hemorrhoids to identify rectal pathology higher up (you can get no Classification and treatment All patients should be instructed in the use of a high-fiber d iet and refraining from straining and long trips to the bathroom (see Table 13.24). Infrare d coagulation: Applied for 1.5 \200\2232 sec, 3 \200\2238 times to localized areas works by coagulating vessels and tethering mucosa to subcutaneous tissue. Sclerosants: (2 mL of 5% phenol in oil injected above the dentate line) SE : Impotence; prostatitis. Rubber band lig ation: Do fewer than three band-treatments per session; a cheap treatment, but needs skill. Banding produces an ulcer to anchor the mucosa (see: Pain, bleeding, infection). Conventio nal hemorrhoidectomy: Excision and ligation of vascular pedicles. Done as day-case surgery, needing 2 wks off work. SE: Hemorrhage or stenosis. Stapled hemorrhoidectomy: Results in a quicker return to normal activity than conventional surgery because of less pain. Will no t remove large pro- truding anal tags (fourth-degree). 491 Table 13.24 Hemorrhoidal classification and treatment Stage I Definition Enlarged with bleeding Treatment Fiber Suppositories Sclerotherapy Fiber Suppositories Banding Fiber Banding Conve ntional or stapled hemorrhoidectomy II Protrusion with spontane- ous reduction III Protrusion requiring manual reduction IV Irreducible protrusion Fiber Stapled hemorrhoidectomy in selected cases Conventional hemorrhoidectomy Treatment of prolapsed, thrombosed hemorrhoid is with excision if <72 h, otherwise analgesi a, sitz baths, and bed rest. Pain usually resolves in 2 wks. Anal fissure Anal fissure is a midline longitudinal split in the squamous lining of the low er anus, often, if chronic, with a mucosal tag at the external aspect \200\224the \200\234 sentinel pile. \200\235 90% are posterior (anterior ones follow parturition) and are perpet uated by internal sphincter spasm. Defecation is very painful and spasm may constrict the r ectal artery, making healing difficult. Causes Primary cause: Diarrhea or hard stools, acqu ired disorder. Rare causes: Syphilis, herpes, trauma, Crohn \200\231s, anal cancer, psorias is; more common in the lateral location. Exam Examine with a bright light. Do a digital rec tal exam sigmoidoscopy. Groin nodes suggest a complicating factor (e.g., immunosuppressi on from HIV). Treatment Try 2% lidocaine ointment, extra dietary roughage + good anal toile t, sitz baths. Glyceryl trinitrate ointment (0.2 \200\2230.3%) or 0.2% nifedipine ointment relieves pain and ischemia caused by chronic fissures and spasm and can prevent need for su rgery, but may cause headache. If conservative measures fail, consider day-case lateral par tial internal sphincterotomy . Manual anal dilatation (under general anesthesia) is also us ed but has fallen out of favor due to increased risk of postop anal incontinence (24.3% vs. 4.8% for lateral sphincterotomy). Pilonidal sinus/cyst Obstruction of natal cleft hair fol licles 6 cm above the anus, with ingrowing of hair; excites a foreign-body reaction and ma y cause secondary tracts that open laterally abscesses, with foul-smelling discharge. Tr eatment is excision of the sinus tract primary closure, but is unsatis- factory in 10% o f patients. Complex tracts can be laid open and packed individually, or skin flaps can be u sed to cover the defect. 492 Anal ulcers are rare. Consider Crohn \200\231s disease, anal cancer, TB, syphilis. Skin tag s seldom cause trouble but are easily excised. Anorectal abscess/fistula is usually caused by enteric organisms (rarely S . aureus or tuberculosis [TB]). Location: Perianal ( 45%), i schiorectal (30%), intersphincteric (>20%), supralevator ( 5%). Redness and swelling may sp read well into the buttock. Do incision and drainage, usually under GA unless small periana l (+ fistulotomy if needed, e.g., in Crohn \200\231s disease). Associations: DM, Crohn \200 \231s, malignancy. Don \200\231t rely on antibiotics. Anal cancer Increased risk: Syphilis, anal warts (herpesvirus [HPV] 16, 6, 11, and 18 implicated), anoreceptive homosexuals (oft en young). Histology: Squamous cell (80%); rarely, basaloid, melanoma, or adenocarcinoma. T he patient may present with bleeding, pain, bowel habit change, pruritus ani, masses, and s tricture. Differential diagnosis: Condyloma acuminata, leucoplakia, lichen sclerosus, Bowen \200\231s, Paget \200\231s, or Crohn \200\231s disease. Treatment: Radiotherapy + 5-FU + m itomycin/cisplatin is usually preferred to anorectal excision and colostomy, and 75% of pat ients retain normal anal function. y r e g r u S Gastric and duodenal ulcer disease Ulcerative disease of the stomach and duodenum has decli ned in incidence sharply from levels seen in 1960. Risk factors include smoking, NSAID use, Helicobacter pylori , and increased acid production or a defect in mucosal defense. Sympto ms Cardinal feature is epigastric pain described as burning, stabbing, or gnawing relieved by eating or antacids. Other associated symptoms include nausea, vomiting, bleeding, weight loss. Differential diagnosis includes cholelithiasis, pancreatitis, pancreatic cancer, MI, and gastric neoplasia. Evaluation \212 Barium swallow and upper GI study H. pylori \212 EGD: Biopsy for neoplasia and Recurrent peptic ulceration in unusual places; think of Zolli nger \200\223Ellison \212 syndrome (gastrinoma). Do secretin stimulation test. Medical management \212 Treat H. pylori \212 Antihistamines \212 Proton pump inhibitors \212 Prostaglandin analogs \212 Sucralfate \212 Antacids Surgical management Operative i ntervention is reserved for the treatment of complicated ulcer disease (intractability, hem orrhage, perforation, obstruction). Operations for benign gastric ulceration Elective opera tion for gastric fundus ulceration is rarely needed as ulcers respond well to medical treat ment, stopping smoking, and avoidance of NSAIDs. Emergency surgery is sometimes needed for hemorrhage or per- foration. Hemorrhage is usually treated by underrunning the bleeding ulc er base or excision of the ulcer. If the former is done, then a biopsy should be taken to e xclude malignancy. Perforation is usually managed by excision of the hole for histology, th en closure. Prepyloric ulceration is considered peptic disease and an anti-acid procedure s hould be considered, especially if the patient has been on acid suppression therapy. 493 Gastric carcinoma Curative surgical options include D 1 resection (removal of tumor and per i- gastric lymph nodes) and D 2 resection (removal of the D 1 tier of lymph nodes and the n ext tier out, along the celiac axis). There is considerable controversy as to which should be performed, as some studies have shown worse morbidity and mortality for D 2 resections p erformed in Western countries. It is likely that the results reflect the lack of dedicated specialists, such as those in Japan, where gastric carcinoma is particularly common. D 2 re sections should therefore only be performed in specialist centers. Partial gastrectomy (the Billroth operations) Billroth I: Partial gastrectomy with simple re-anastomosis (rejoining ). Billroth II (Polya gastrectomy): Partial gastrectomy. The duodenal stump is oversewn (le aving a blind loop), and anastomosis is achieved between the proximal jejunum and the stoma ch remnant (Figure 13.10). Physical complications of gastrectomy and peptic ulcer surgery S ee Table 13.25. Recurrent ulceration: Symptoms are similar to those experienced preopera- t ively but complications are more common and response to medical treat- ment is poor. Furthe r surgery with a total gastrectomy may be necessary. Consider Zollinger \200\223Ellison syn drome. Abdominal fullness: Feeling of early satiety (perhaps with discomfort and dis- tensi on) improving with time. Advise patient to take small, frequent meals. Dumping syndrome: Fa inting and sweating after eating due to food of high osmotic potential being dumped into th e jejunum; causes rapid fluid shifts. \200\234Late dumping \200\235 is due to rebound hypo glycemia and occurs 1 \200\2233 h after meals. Both tend to improve with time but may be he lped by eating less sugar and more guar and pectin (slows glucose absorption). Acarbose may also help to reduce the early hyperglycemic stimulus to insulin secretion. Bilious vomitin g: This is difficult to treat but often improves with time. Diarrhea: May be disabling afte r vagotomy. Codeine phosphate may help. Gastric tumor: A rare complication of any surgery t hat affects acid production. Amylase elevation: If associated with abdominal pain, this may indicate affer- ent loop obstruction after Billroth II surgery (requires emergency surgery ). Metabolic complications Weight loss: Often due to poor calorie intake. Bacterial overgro wth malabsorption (the blind loop syndrome) may occur. Anemia: Usually from lack of iron hypochlorhydria and stomach resection. B 12 levels are frequently low but megaloblastic an emia is rare. Osteomalacia: There may be pseudofractures that look like metastases. 494 Table 13.25 Complications of peptic ulcer surgery Recurrence (%) 2 7 Dumping (%) 20 14 Diarrhea (%) 1 4 Metabolic Partial gastrectomy Vagotomy and pyloroplasty Highly selective vagotomy ++++ ++ >7 6 <1 0 (These values are approximate based on the literature) y r e g r u S Figure 13.10 tomach uodenum Surgery for duodenal ulcer Peptic ulcers usually present as epigastric pain and dyspepsia ( p. 208). There is no reliable method of distinguishing clinically between gastric and duo- denal ulcers. Although management of both is usually medical in the first instance (with H. pylori eradication [p. 208]), surgery still has a role. Surgery is usually only required f or complications such as hemorrhage, per- foration , and pyloric stenosis , although it may be considered for the few patients who are not responsive/tolerant to medical therapy. Sev eral types of operation have been tried but, as with any operation, one must consider effic acy, side effects, and mortality. Elective surgery may be undertaken for patients who are i ntolerant of or fail to respond to medical treatment: \212 May be useful in patients unable to tolerate Highly selective vagotomy: medical treatment. The vagus supply is denervated only where it supplies the lower esophagus and stomach. The nerve of Latarjet to the pylorus is left intact; thus, gastric emptying is unaffected. A va gotomy reduces acid production from Vagotomy and pyloroplasty: the stomach body and fundus and reduces gastrin production from the antrum. However, it interferes with emptying of the pyloric sphincter and so a drainage procedure (e.g., pyloroplasty) must be added. This ope ration is now almost obsolete and is only performed in exceptional circumstances. Gastrecto my disease. \212 \212 is rarely required in the modern management of peptic ulcer Emergency surgery may be required for the following complications: may be controlled endosc opically by adrenaline injection, \212 Hemorrhage cautery, laser coagulation, or heat prob e. Operation should be consid- ered for severe hemorrhage or rebleeding, especially in the elderly. At surgery, the bleeding ulcer base is underrun or oversewn. Occasionally, the gas troduodenal artery must be ligated. Most patients undergo surgery, although some advocate a n Perforation: initial conservative approach (NPO, NG tube, IV antibiotics) in patients wit hout generalized peritonitis. This can prevent surgery in up to 50% of such cases. If emerg ency surgery is required, laparoscopic repair of the hole will usually suffice. H. pylori e radication should be commenced postop. This is a late complication, presenting with vomitin g of Pyloric stenosis: large amounts of food some hours after meals. (Adult pyloric stenosi s is a complication of duodenal ulcers and has nothing to do with congenital hypertrophic p yloric stenosis.) 495 \212 \212 Treatment: Endoscopic balloon dilatation, followed by maximal acid sup- pression, may be tr ied in the first instance (NB: 5% risk of perforation). If this is unsuccessful, a drainage procedure (e.g., gastroenterostomy or pyloroplasty) highly selective vagotomy may be pe rformed, often laparo- scopically. The operation should be done after correction of the met abolic defect (hypochloremic, hypokalemic metabolic alkalosis). Surgery for gastroesophageal reflux disease Fundoplication for gerd The goal of surgery for GERD is to reestablish lower esophageal sphincter tone and prevent continued esophageal in flammation. Indications \212 \212 \212 \212 Evaluations \212 \212 \212 Multivariant analysis has shown that three factors are significant predictors of an excellent to good ou tcome for antireflux surgery: (1) an abnormal 24 h pH score, (2) the presence of symptoms o f heartburn and regurgitation, (3) a clinical response to acid suppression therapy. Large h iatal hernias and long-term chronic disease maybe associated with a shortened esophagus. Fa ilure of laparoscopic fundoplication is higher in patients with a shortened esophagus. Proc edure Gastric fundoplication involves wrapping the gastric fundus around the lower esophagu s, closing the hiatus, and securing the wrap in the abdomen. There are various types of pro cedure: Nissen (360-degree wrap), Toupet (270-degree posterior wrap), Watson (anterior hemi fundoplication). Now usually performed laparoscopically which, when performed in specialist centers, is at least as effective at controlling reflux as open surgery but with lower res ulting morbidity. Wound infections and respiratory complications are also more common in op en surgery, and the incidence of dysphagia is similar for the two procedures. Failure of medical therapy Barrett \200\231s esophagus without dysplasia Recurrent pneumoni a secondary to aspiration Mechanically defective sphincter Videoesophagram Upper GI endoscopy Esophageal manometry and 24 h pH monitoring. Obesity surgery Patients are eligible for surgical management of morbid obesity if their BM I is >40 without a comorbidity and \211 35 with comorbidity. Surgical treatment can resul t in one-half to one-third of weight being lost within the first 1 \200\2231.5 years follow ing surgery. This requires a great deal of patient education and cooperation. Many comorbid ities will reverse. Comorbidity of obesity \212 \212 \212 \212 496 Cardiovascular dysfunction Non-insulin dependent diabetes Respiratory insufficiency Increas ed intra-abdominal pressure leading to GERD, urinary inconti- nence, venous stasis Nephroti c syndrome Pseudotumor cerebri Degenerative osteoarthritis Cholelithiasis Infectious compli cations \212 \212 \212 \212 \212 \212 \212 \212 Indications for bariatric surgery for morbid obesity \212 \212 \212 \212 \212 Surgical procedures include: \212 Sexual hormone dysfunction Colon cancer Psychosocial impairment y r e g r u S 2 BMI 40 kg/m BMI 35 \200\22340 kg/m 2 with significant comorbidities Unsuccessful attem pt at weight loss by nonoperative means Clearance by a dietician and mental health expert N o medical contraindications to surgery Gastric procedures \200\224restrictive: \212 \212 Gastroplasty: Horizontal stapling, vertical banded gastroplasty (VBGP) Gastric bypass: Form ation of a small gastric pouch that is drained via a gastrojejunostomy Laparoscopic vertica l sleeve gastrectomy \212 Small bowel bypass \200\224malabsorptive: \212 \212 Jejunoileal bypass: Obligatory malabsorption associated with numerous complications (cirrho sis) and now avoided. Partial biliopancreatic bypass: Both restrictive and malabsorptive wi th small gastric pouch emptying into small bowel without pancreatic and biliary secretions (because contents empty into terminal ileum, thus minimizing absorption). \212 Complications associated with obesity surgery (<15%) \212 \212 \212 \212 Pulmonary emboli Anastomotic leak Bowel obstruction from internal hernia Vitamin B 12 , calcium, iron, vitamin D, protein deficiencies Breast lumps and breast cancer Incidence and Mortality (2011) Most common non-skin cancer i n women in the United States; estimated new cases 230,480. Second leading cause of cancer d eath, with estimated death of 40,000. Risk of death is on the decline since 1990 due to scr eening. History The presenting complaint is a mass, bloody nipple discharge, pain, change i n the skin of the breast, or abnormal mammogram (most common). Risk factors Age; obesity; c onsuming more than one acholic beverage per day. Menstrual history: Parity; age of first ch ildbirth; use of hormone replacement therapy, birth control pills, or tamoxifen. Family his tory of breast or ovarian cancer. Examination Inspect the breast (arms both up and down) no ting contour of the breast, nipple/areolar complex, skin overlying the breast (specifically for redness or dimpling), and symmetry. For abnormalities identified, note symmetry, fixat ion to the skin or chest wall, and characteristics of the lump. Nodal evaluation of the axi llary, supraclavicular, and cervical basins. Investigations Annual mammography is recommend ed for all women beginning at age 40 and for high- risk women beginning at age 30, consider MRI. Clinical examination is crucial and all suspicious of abnormalities, whether suspicio us by imaging or physical examination, must undergo biopsy, preferably by core needle biops y Imaging includes: Mammography, US, MRI; many breast cancers are identi- fied by breast im aging and have no symptoms. Abnormalities of the breast Causes of lumps: Fibroadenoma, cyst , cancer, fibroadenosis, mastitis, galactocele, abscess, fibrocystic change; 497 non-breast lumps; lipoma, fat necrosis, and sebaceous cyst. Causes of nipple discharge: Duc t ectasia (green/red, often multiple ducts and bilateral), intraductal papilloma/adenoma/ca rcinoma (bloody/brown, often single duct and unilateral), lactation. Abnormal mammogram \201 ndings: Microcalcification, architectural distortion of density, asymmetric density. M ammograms are classified by birad levels (see Table 13.26). Causes of abnormal mammogram: F ibroadenoma, cyst, cancer, ductal carcinoma in-situ, atypical hyperplasia, radial scar, col umnar cell hyperplasia. Management Core needle biopsy is used to diagnose most abnormalitie s identified on either mammogram or physical examination. If there are discordances between the abnormal finding and the pathology, excisional biopsy is performed. If there is concor dance and the pathology is benign, no further investigation is necessary with the following exceptions. For mastitis, continue breast-feeding if lactating and treat with antibiotics. Abscesses must be drained and wound care initiated. If the finding is atypical hyperplasia , excisional biopsy is recommended and consider of the use of tamoxifen for prevention. For nipple discharge, microdochectomy/ total duct excision. See Figure 13.11. Breast cancer Ge netic factors: Brac1, brac2 are responsible for 5 \200\22310% of breast cancer; widespread testing is not recommended unless strong family history of breast or ovarian cancer. TNM St aging: \212 TIS or/and inflammatory breast cancer. N0 negative nodes; N1 1 \200\2233 positive nodes; N2 4 \200\22310 positive nodes; N3 >10 positive nodes. M0 no metastases; M1 metastases presen t. in situ ; T1 <2 cm; T2 2 \200\2235 cm; T3 >5 cm; T4 fixed to chest wall or skin \212 \212 Early breast cancer including DCIS: Wide local excision (WLE) with radiation therapy (RT) or mastectomy plus or minus reconstruction, with sentinel lymph node biopsy or axillar y lymph node dissection. WLE plus RT has equal survival but higher local recurrence rates c ompared to mastectomy. Consider endocrine therapy. Staging Assess liver function test and c alcium levels; CT scan of the chest and abdo- men and bone scan. A positron emission tomogr aphy (PET) scan may be used. Staging reserved for high-risk patients or those with symptoms . 498 Table 13.26 Mammogram birad levels Birads Level 0 Finding Needs additional imaging and/or comparison to prior studies Negative Benign finding Probable benign finding <2% risk of cancer, 1 2 3 short-term follow-up recommended 4 Suspicious abnormality for cancer 2 \200\22395%. Should be seen right away 5 Highly suspicious abnormality >95% likely for cancer. Appropriate action should be taken Known biopsy-proven adenocarcinoma 6 y r e g r u S Figure 13.11 + \206\222 \206\222 \206\222 \206\222 \206\222 \206\222 \206\222 Adjuvant therapy Radiation therapy for all patients with WLE; post- mastectomy RT to the ch est wall for T3 or T4 and N2 or N3 tumors. RT results in reduced local regional recurrence. Chemotherapy improves survival, with the most common combination being doxorubicin-based, with taxanes added for high-risk patients. Herceptin is used for HER-2 neu -positive diseas e. Endocrine therapy for those patients who are estrogen or progesterone receptor-positive. Tamoxifen is most commonly used for 5 yrs postoperatively. Aromatase inhibitors may also b e used in postmenopausal women with possibly fewer side affects. In premenopausal women wit h estrogen receptor-positive tumors, ovarian ablation/suppression can be considered. Treatm ent of metastatic disease: RT can be used for metastatic lesions at high risk for functiona l deficit; hormonal therapy is effective in many patients with estrogen receptor-positive d isease; after failure of one hor- monal therapy, switching to another may be effective. Pre venting breast cancer deaths Promoting breast awareness: Mammography: The detection rates o f mam- mography are 6.4 cancers per 1,000 healthy women >50. Breast cancer screening with m ammography decreases deaths in women >50 by 25%. Prevention with the use of tamoxifen is po ssible for high-risk women (equal to the risk of a women of 60), resulting in a 50% risk re duction. Sentinel lymph node biopsy is used in staging breast cancer patients. For those pa tients who are sentinel lymph node-negative, no addition surgery is completed in the axilla ; for those who are positive, a completion axillary dissection is performed. Sentinel lymph node biopsy has a 2% risk of lym- phedema with minimal risk of functional deficit of the a rm. Axillary lymph node dissection has a risk of lymphedema of 10 \200\22320%, with 20% of patients having functional deficit of the arm. The sentinel lymph node procedure is complet ed as follows: A vital blue dye and/or radiocolloid is injected either peri-tumorally or in the retroareolar area; an incision is made in the axilla and a -probe or visual inspect ion is used to identify and remove the sentinel lymph node for pathologic assessment. Multi center trials report identification rates >90% and false-negative rates <12%. 499 Colorectal adenocarcinoma Incidence and mortality (2011) Third most common cancer diagnosed and second most common cause of cancer deaths in the United States, with 141,000 estimated cases and 49,000 deaths annually. familial Predisposing adenomatous polyposis, previous ca ncer, low-fiber diet. NSAIDs may be protective. Genetics: No close relative affected: Color ectal cancer risk is 1:50. One first-degree relative affected: Risk = 1:17; if two are affe cted, 1:10 (refer when 10 yrs younger than the youngest affected relative). Polyps are lump s that appear above the mucosa. There are two types: \212 Neoplastic polyps, UC, Crohn \200\231s, factors Hyperplastic, inflammatory, lymphoid aggregate, hamar- Non-neoplastic: toma (juvenile polyps, Peutz \200\223Jeghers \200\231 syndrome) Neoplastic: if >2 cm. \212 Tubular or villous adenomas: Malignant potential, especially Symptoms of polyps: Asymptomatic, passage of blood/mucus per rectum. They should be biopsie d and removed. Most can be reached by the flexible colonoscope to avoid the morbidity of co lectomy. Check resection margins are clear of tumor. Presentation of cancer Left-sided: Ble eding per rectum, altered bowel habit, tenesmus, mass (60%). Right-sided : Weight loss, ane mia, abdominal pain. Either : Abdominal mass, obstruction, perforation, hemorrhage, fistula . See Figure 13.12 and Table 13.27. Tests CBC (microcytic anemia); fecal occult blood (FOB) ; proctoscopy, sigmoidoscopy, barium enema, or colonoscopy (can be done virtually by CT); L FT, CT/MRI; liver US. Carcino-embryonic antigen (CEA) levels may be used to monitor disease and effectiveness of treatment (p. 680). If polyposis in family or strong family history, consider genetic testing. Spread transcoelomic. Surgical treatment Surgery is considered cu rative for Stage I and II disease. Attention to technique may reduce local recurrence rates . Hemicolectomies: Right is for cecal tumors, ascending or proximal trans- verse colon (ext ended right including the middle colic artery). Left is for tumors in the distal transverse colon, descending colon, and proximal sig- moid colon. Anterior resection is for distal si gmoid or high rectal tumors. Abdomino-perineal (a-p) resection is for tumors low in the rec tum that are abutting or invading the sphincter muscles: Permanent colostomy and re- moval of rectum and anus. Low anterior resection for tumors of the mid and low rectum. Stapling d evices are helpful. Radiotherapy and chemotherapy (neoadjuvant) is used preop in stage II o r III rectal cancer to reduce local recurrence and increase sphincter preservation rates. A djuvant therapy is reserved generally for stage III and IV colon cancer and in stage II-IV rectal cancer. Chemotherapy: Usually 5-FU-based chemotherapy folinic acid and newer agen ts (e.g., irinotecan, oxaliplatin) for 6 months postop; increases survival in patients with stage III or IV colorectal cancer. Adjuvant chemo- therapy in stage II (T3N0) colon tumors is beneficial in young patients with more aggressive histology (see Table 13.28). Patients with resectable hepatic metastases (<4), >1-yr disease-free interval, and no extrahepatic spread will have improved survival following hepatic metastectomy. Screening guidelines are listed in Table 13.29. Local, lymphatic, hematogenous (liver, lung, bone), or 500 y r e g r u S Table 13.27 Signs and symptoms of colorectal cancer \212 \212 Persistent change in bowel habit for >6 wks Persistent rectal bleeding any age, with no obv ious external evidence of benign anal disease Iron-deficiency anemia without an obvious cau se and Hb <10 g/dL An easily palpable abdominal or rectal mass \212 \212 Figure 13.12 Location of cancers of the large bowel NB: These are averages: Black females tend to have more proximal neoplasms, whereas white m ales tend to have more distal neoplasms. Table 13.28 Survival for colon and rectal cancer (SEER data 1988 \200\2232000) Stage I (T1-T2, N0,MO) IIA (T3, N0,M0) IIB (T4a, N0, M0) IIC (T4b, N0, M0) IIIA (T1 \200 \2232, N1, MO) (T1, N2a, M0) IIIB (T3 \200\2234a, N1,M0) (T2-T3, N2a,M0) Colon, 5 yr (%) 74 67 59 37 73 Rectal, 5 yr (%) 74 65 52 32 74 501 46 45 (T1 \200\2232, N2b,M0) IIIC (T4a, N2a, M0) (T3 \200\2234a, N2b, M0) 28 33 (T4b, N1 \200\2232,M0) IV (Tx, Nx, M1) 6 6 Table 13.29 Universal adult screening for colorectal cancer \212 The American Cancer Society guidelines for the early detection of col- orectal cancer inclu de the following screening methods for average-risk individuals beginning at age 50 until 7 5 yrs: Colonoscopy every 10 yrs Flexible sigmoidoscopy every 5 yrs High-sensitivity fecal o ccult blood test (FOBT) every 1 year \212 \212 \212 Pancreatic cancer Pancreatic cancer is divided into neoplasms of the exocrine pancreas and endocrine pancreas (Table 13.30). Exocrine pancreatic cancer is more com- mon. Pancreatic d uctal adenocarcinoma is the tenth leading new cancer diagnosis and the fourth leading cause of cancer death in the United States. In 2012, it is estimated that there will be 43,920 n ew cases, and 37,390 will die from pancreatic cancer. Neoplasms of the exocrine pancreas Pa ncreatic ductal cancer is more common in men, African Americans, and individuals >70. The o nly known risk factor is smoking. Other factors that suggest an association are family hist ory, chronic pancreatitis, and previous gastric surgery. 70% of pancreatic ductal cancers o ccur in the head (periampullary), 15% occur in the body, 10% occur in the tail, and 5% are diffuse. The most common presentation for periampullary tumors is painless jaundice. Other associated symptoms include weight loss, epigastric pain, nausea, and vomiting. Tests Bilir ubin, alk phos, CA 19 \200\2239. Contrast enhanced spiral CT, endoscopic US, ERCP, staging laparoscopy. Treatment Surgical resection, when possible, provides the greatest survival be nefit. For tumors of the head, a pancreaticoduodenectomy ( Whipple procedure ) is done. Sma ll resectable tumors (<2 cm) of the head of the pancreas result in a 18 \200\22324% 5-yr su rvival. For tumors of the tail, a distal pancreatectomy splenectomy is performed. These tumors tend to be much larger at the time of diagnosis because patients are largely asympto matic. Palliation for periampullary cancer can be achieved with gastrojejunostomy and hepat icojejunostomy at the time or attempted resection, or with transhepatic stents. Adjuvant ch emotherapy with 5-FU-based regimens and radiation has been shown to improve survival follow ing curative resection for pancreatic can- cer. For unresectable cancer, neoadjuvant chemor adiation may convert the tumor to a resectable lesion. The primary treatment of endocrine t umors of the pancreas is excision. If disease is unresectable, systemically active therapy can be directed at the products of the tumors (e.g., H 2 receptor blockers in Zollinger \200\223Ellison syn- drome, diazoxide in insulinomas, somatostatin analogs). 502 Table 13.30 Neoplasms of the endocrine pancreas Islet cell type Hormone \227 cell Syndrome Glucagonoma Clinical features Migratory rash, diabetes, diarrhea Hypoglycemia, mental confusion Dyspeps ia, diabetes, gallstones, Diagnostic test \206\221 Glucagon after tolbutamide \206\221Insulin \206\221Glucose with out % Malignant Nearly 100 Glucagon \222 cell cell Insulin Somatostatin Insulinoma Somatostatinoma 10 Nearly 100 steatorrhea \206\221Ketones 2 cell G cell VIP Gastrin VIPoma Gastrinoma Diarrhea? (Zollinger \200\223Ellison) \200\224 Severe peptic ulcer disease (PUD), diarrhea 40 \206\221gastrin after secre- tin 70 5 0 3 Surgery Thyroid nodules and cancer The single thyroid nodule is a common problem; 10% will be mali gnant. Causes malignancy. Examination Watch the neck during swallowing water. Stand behind and feel thyroid for size, shape, tenderness, and mobility. Percuss for retrosternal extens ion. Any nodes? Bruits? If the thyroid is enlarged, is the thyroid smooth or nodular? Is th e patient euthyroid, thyrotoxic (p. 298), or hypothyroid (p. 302)? Check TSH,T3, and T4 lev els. \212 Cyst, adenoma, discrete nodule in multinodular goiter, Endemic (iodine deficiency); congenital; goitro- Smooth, nontoxic goiter: gens; thyroiditis; physiological; Hashimoto \200\231s thyroiditis Graves \200\231 disease Smooth, toxic goiter: If >4 cm across, malignancy is more likely. M ultinodular goiter: Hypothyroidism and malignancy are rare. \212 \212 \212 Usually euthyroid but hyperthyroidism may develop. Tests US, to see if nodule is solid, cystic, calcified, or part of a group of nodules. Radi onucleotide scans may show malignant lesions as hypofunctioning or \200\234cold, \200\235 whereas a hyperfunctioning \200\234hot \200\235 lesion suggests adenoma. Fine-needle aspir ate (FNA) Can be done in the office or by US guid- ance (most common). 70 \200\22390% will be diagnostic. No clinical/lab test is good enough to tell without doubt if follicular neop lasms found on FNA are benign, so such patients are referred for surgery. Thyroid neoplasia Uncommon malignancy but the most common endocrine cancer. Affects women more than men, age s 25 \200\22365. Most common presentation is a cold nodule on US. Risk of cancer in nodule is 12 \200\22315%. Increased risk in those <40 yrs and with calcifications of the nodule no ted on US. Known risk factors (1) History of radiation (2) History of goiter. (3) Family hi story of thyroid disease (multiple endocrine neoplasia [MEN]-2a, -2b). (4) Female. (5) Asia n. Five types: 25%. Middle-aged; spreads early via blood (bone, lungs). \212 Follicular: W ell-differentiated. Treat by total thyroidectomy, T4 suppression, and radioiodine ( 131 I) ablation. Anaplastic: absence of unresectable disease, excision + radiotherapy may be tried . 5%. Sporadic (75%) or part of MEN syndrome (p. 304). May Medullary: produce calcitonin. T hey do not concentrate iodine. Do thyroidectomy + node clearance (do pheochromocytoma scree n preop). External beam radiotherapy should be considered to prevent regional recurrence. 6 0%. Often seen in the young; spread to nodes and lung. Total Papillary: thyroidectomy (to r emove nonobvious tumor) node excision + radio- iodine to ablate residual cells may all b e needed. Give T4 to suppress TSH. Prognosis is better if young and female. 5%. : \211\210 3:1. May present with stridor or dysphagia. Do Lymphoma: full staging pretreatment (chemoradiotherapy). Assess histology for mucosa-associated lymphoid tissue (MALT) origin (associated with a good prognosis). \212 Rare. : \211\210 3:1. Elderly; poor response to any treatment. In the \212 504 \212 \212 Thyroid surgery indications Pressure symptoms, hyperthyroidism, carcinoma, cosmetic reasons . Render euthyroid preop, by antithyroid drugs and/or propranolol. Check vocal cords by ind irect laryngoscopy pre- and postop. Early complications Recurrent laryngeal nerve palsy, he morrhage (if compresses airway, instantly remove sutures for evacuation of clot), hypoparathyroidism (check plasma Ca 2+ daily, usually transient), thyroid storm (symptoms of severe hyperthyr oidism; treat by propranolol PO or IV, antithyroid drugs, and iodine [p. 782]). Late compli cations Hypothyroidism. y r e g r u S Esophageal cancer Benign tumors make up 1%; most are common leiomyoma or GIST. The incidenc e of esophageal cancer is on the rise, especially in Western coun- tries. The types of esop hageal cancer include squamous cell, adenocarci- noma, and small cell cancer. The most comm on presenting symptoms are dysphagia and weight loss. Squamous cell cancer of the esophagus \212 \212 \212 Adenocarcinoma \212 \212 More common worldwide Associated with cigarette use and alcohol More common in the proximal one-third of the esophagus More common in the United States Associated with Plummer \200\223Vinson syndrome, obesity, reflux esophagitis Barrett \200\231s esophagus (there is a 44-fold increased risk of ade nocarcinoma if severe reflux for >10 yrs). Evaluation \212 \212 \212 \212 \212 Treatment Resection: \212 Barium swallow EGD with biopsy Endoscopic US CT scan Staging laparoscopy (see Table 13.31) Transthoracic (radical) resection with en-bloc lymphadenectomy; three incisions Transhiatal resection; easier to perform \212 Reconstruction: \212 \212 Adjuvant therapy: \212 Gastric pull-up with pyloroplasty based on the right gastric artery Colonic interposition Given preoperatively (neoadjuvant) or postoperatively for stage II or III tumors Cisplatin, 5-FU Radiation Palliation with metal stents for stage IV disease 505 \212 \212 \212 Table 13.31 Staging for esophageal cancer and 5-yr survival TNM TisN0M0 T1N0M0 T2N0M0, T3N0M0 T1N1M0, T2N1M0 T3-T4N1 \200\2232M0 Any T, Any N M1 Stage 0 I IIA IIB III IV 5-yr survival 100 85 45 20 10 <4 Gastric cancer The incidence of gastric cancer, unlike esophageal, has dropped dramati- cal ly in the past 70 yrs ( 70%). Risk factors include lower economic status; smoking; consumpt ion of salted, smoked foods; atrophic gastritis; genetic factors (HNPCC), H. pylori . Adeno carcinoma accounts for >90%; others include squamous cell, carci- noid, GIST, lymphoma. Pat hology The adenocarcinoma may be polypoid, ulcerating, or leather bottle-type (linitis plas tica). Some are confined to mucosa and submucosa, so-called early gastric carcinoma. Presen tation symptoms Often nonspecific. Dyspepsia (p. 208) lasting >1 month in patients aged 40 \200\22350 yrs demands GI investigation. Others: Weight loss, vomiting, dysphagia, anemia. Signs suggesting incurable disease: Epigastric mass, hepatomegaly, jaundice, ascites (p. 22 7), large left supraclavicular (Virchow \200\231s) node (Troisier \200\231s sign), acanthos is nigricans. Spread is local, lymphatic, blood-borne, and transcoelomic; e.g., to ovaries (Krukenberg tumor). Evaluation \212 \212 \212 Treatment \212 EGD with multiple biopsies; always biopsy ulcers Endoscopic US CT scan/MRI to evaluate for metastatic disease (see Table 13.32) Endoscopic mucosal resection may remove early cancers limited to the mucosa. Surgical resec tion with gross negative margins of 6 cm Need at least 15 lymph nodes harvested to determin e the nodal status of the disease Adjacent organs should be resected en-bloc only if involv ed with tumor and only one organ is involved. Stage II and IIIA may benefit from a more ext ensive nodal dissection D 2 (12 lymph node stations) versus D 1 (6 lymph node stations) wit h an improved 5-yr survival, 80% versus 55%, respectively. Reconstruction esophagojejunosto my. Adjuvant therapy includes radiation and 5-FU-based chemotherapy. \212 \212 \212 \212 \212 is performed with a Roux-en-Y end-to-side \212 Table 13.32 Staging for gastric cancer 506 TNM TisN0M0 T1N0M0 T1N1MO, T2N0M0 T1N2M0, T2N1M0, T3N0M0 T2N2M0, T3N1M0, T4N0M0 T3N2M0 T4N1 \200\2233M0, T1 \200\2233N3M0, or M1 Stage 0 IA IB II IIIA IIIB IV Cutaneous neoplasms Cutaneous neoplasms are the most commonly diagnosed tumor in the United States, with 600,000 new cases annually. The most common cutane- ous neoplasms include: \212 Basal cell cancer \212 Squamous cell cancer Melanoma: \212 \212 y r e g r u S Accounts for 5% of all skin cancers but leads to 65% of all skin cancer-related deaths The evaluation and treatment of cutaneous neoplasms is based on whether the lesion is melan oma or nonmelanoma skin cancer. Melanoma Risk factors: \212 \212 \212 \212 \212 \212 Types of melanoma: \212 \212 \212 \212 Fair complexion Sun exposure Previous history of melanoma Dysplastic nevi syndrome Large co ngenital nevi have a 5 \200\22320% lifetime risk of developing melanoma Xeroderma pigmentos um Lentigo maligna ( 10 \200\22315%), least aggressive Superficial spreading ( 70%) Nodular me lanoma ( 15 \200\22330%), most aggressive Acryl lentiginous melanoma ( 2 \200\2238%), seen in greater percentage of darker-skinned individuals (African Americans, Asians, Hispanics) Most common sites: \212 Women: Legs \212 Men: Back of body Depths of invasion <0.75 mm 0. 76 \200\2231.5 mm 1.5 \200\2234 mm >4 mm Any depth + 1 nodal station Any depth + >1 nodal s tation Or disseminated disease *Dependent on site as well Staging: JCC 5-yr survival* (%) 99 Stage IA 90 Stage IB 75 Stage IIA 65 Stage IIB 40 Stage III 0 Stage IV 507