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Surgery Study Guide Abdominal Hernia Hernia – abnormal protrusion of abdominal contents through a defect in the abdominal wall; definitive tx of hernia is early operative repair Anatomy o Internal (deep) inguinal ring (lateral) – opening in the transversalis fascia halfway between the ASIS and pubic tubercle o Inguinal ligament – between pubic tubercle and anterior iliac spine formed by external oblique aponeurosis o Lacunar ligament – deep and parallel to inguinal ligament inserts into pubic ramus and responsible for strangling femoral hernia o Hesselbach’s triangle – inguinal ligament (inf), epigastric vessels (lateral), and lateral border of rectus abdominus (medially) o Nerves of inguinal region Iliohypogastric, Ilioinguinal – T12, L1 IH – suprapubic skin, II – lateral scrotum, medial thigh o Ilioinguinal – most injured anterior open inguinal repair Genitofemoral, lateral femoral cutaneous Scrotum, anteromedial and lateral thigh May be injured during laparoscopic repair Femoral Types o Incarcerated – an “irreducible” hernia whose contents cannot be returned to the abdomen o Strangulated – compromise to the blood supply of the contents of the sac o Reducible – contents can be returned to abdomen o Complete – hernia passes fully into scrotum o Processus vaginalis – peritoneal extension of accompanying the testis in its descent into the scrotum o Inguinal hernia Direct – formed by defect in the floor of Hesselbach’s triangle Indirect – abdominal contents through inguinal ring through patent processus vaginalis; internal inguinal ring, superior to inguinal ligament o Richter hernia – part of bowel wall through defect in anterior abdominal wall o Obturator hernia – through the obturator canal alongside the obturator vessels; “HowshipRomberg” sign (pain mid-anterior thigh w/ abduction and internal rotation of knee) o Femoral hernia – highest risk of incarceration and strangulation; inferior to inguinal ligament and medial to femoral vessels o Umbilical hernia – improper healing of umbilical scar; simple transverse repair of fascial defect; females 10x o Spigelian hernia – lateral to rectus sheath at semilunar line at lower limit of sheath; along semilunar line (lateral edge rectus @ arcuate line) o Sliding hernia – one wall of hernia is made up of an intra-adbominal organ, usually sigmoid o Pantaloon hernia – combination of direct and indirect hernias o Epigastic hernia – defect in linea alba above umbilicus o Incisional – most common ventral hernia o Perineal hernia – pelvic floor o Peristomal – adjacent to ostomy Causes o Indirect inguinal – congenital internal inguinal ring, goes into scrotum, firm on palpation o Direct – acquired as result of developing weakness in transversalis fascia in Hesselbach’s triangle, symmetric, circular at ring while erect, palpation – posterior wall, soft o Femoral – acquired protrusion of peritoneal sac through femoral ring Clinical findings – mostly no symptoms, usually notice a lump, dragging sensation, pain in scrotum, aching; o Direct herniae produce fewer symptoms and less likely to incarcerate or strangulate Treatment o Operative Indirect Direct – reinforce floor Femoral – pectineal (Cooper’s) ligament repair Bilateral repairs can be done w/ low risk of recurrence Recurrent hernia – early inadequate repair; years later weakening of fascia; repeat recurrence collagen disorder Marcy repair – simple high ligation of the sac w/ tightening of the internal ring. Useful in infants and children Types Bassini – conjoined tendon approximated to Poupart’s ligament. Spermatic cord remains in normal position under external oblique aponeurosis Halsted – external oblique placed beneath cord Lotheisson-McVay – femoral hernia repair; Cooper’s ligament sutured to transversus abdominis aponeurosis/conjoint tendon Shouldice – transversalis fascia divided. Imbricated to Poupart’s ligament. Not widely used Laparoscopic repair – higher complications and recurrence rate but pt will return to work sooner; indicated for bilateral hernias, recurring hernias, and need to resume full activity as soon as possible o Pre-operative Treat prostatic hyperplasia first since urinary retention and UTI are common after repair o Incarcerated – attempt reduction, operation, use tension-free reapproximation o Inguinal – transversus abdominus sutured to Cooper’s ligament or inguinal ligament Prognosis o Adults – indirect hernia repair recur in 5-10%; direct 1-18%; use of mesh decreases recurrence by 50-75% Gallbladder Disease Anatomy o Triangle of Calot – common hepatic duct, cystic duct, and cystic artery (or liver) o Extrahepatic biliary tree Structure L and R hepatic ducts common hepatic duct Common hepatic duct + cystic duct common bile duct Common bile duct joins pancreatic duct and enters ampulla of Vater Sphincter of Oddi controls bile flow o Gallbladder – fundus, body, infundibulum, neck Cystic artery from right hepatic 75% of time Cystic vein portal veins Lymphatic – both to the liver and hilar nodes Gallbladder innervation Motor – vagal postganglionic celiac ganglia Sensory – sympathetic fibers from celiac plexus Valves of Heister – mucosal folds in cystic duct Functions – store bile, concentration (absorbs water and secretes mucus), and releases bile (GB contracts, Sphinter of Oddi relaxes) Gallstones o Cholesterol – 75% of gallstones in western countries; 75% of American Indian women over 40 y/o o Pigment – chronic hemolysis o 30% of patients w/ cholelithiasis end up with surgery o Prophylactic surgery if large stone >2cm or calcified gallbladder (increased incidence of cancer) Radiologic diagnosis o Plain abdominal films demonstrates 15% of stones that are opaque and may show porcelain gallbladder o Ultrasound – best for evaluating gallstones in GB and intrahepatic ductal dilatation o HIDA or DISIDA – Cholescintigraphy; best for evaluating cholecystitis, also used for common bile duct obstruction or leak o Chalangiagraphy – best for intra- or extrahepatic ductal obstruction; can be done fluroscopically by ERCP or by MRCP o CT/MRI – best for hepatic parenchyma History and Physical o Most pts w/ cholelithiasis are asymptomatic o Biliary colic – pain RUQ radiating to scapula, postprandial, associated w/ nausea or vomiting o Cholecystitis – implies infection, usually w/ stones, constant pain, fever, and chills o Choledocholithiasis – stones in CBD, RUQ pain, fever, chills, dark urine, light stools o Murphy’s sign – arrest of inspiration on deep RUQ palpation as pressure from the examiner’s hand contacts inflamed gallbladder o Charcot triad – fever, RUQ pain, jaundice o Reynold’s pentad – fever, RUQ pain, jaundice, hypotension, mental status change o Courvoisier’s law – a nontender, palpable gallbladder in a jaundiced patient indicates malignant common duct obstruction Cholecystitis – majority of cases result from calculi, bile stasis, and bacteria o Chronic – RUQ pain which may radiate to back/scapula, N&V; dx w/ ultrasound; tx surgically w/ elective lap cholecystectomy or medically w/ bile salt therapy (15% of patients are candidates, takes 2 years, and 50% of stones recur) o Acute – most causes due to stone in neck or cystic duct; women 30-80 y/o, dx w/ US, CBC, amylase, liver profile, ECG, CXR, HIDA/DISIDA; tx – immediate surgery w/in 72 hours or IV’s and antibiotics then sx after 6 weeks o TX Open – right subcostal incision, GB dissected off liver starting at top, cystic duct and artery divided Laparoscopic – place 10-mm and 5-mm ports, fill abdominal cavity w/ CO2; GB dissected form the bottom after cystic duct and artery are divided; conversion rates = 10% in good hands CBD Cholangiogram – suspect CBD stones, biliary tract anatomy unclear Lap cholecystectomy o Advantages – cosmetic, short hospital stay, rapid return to activity o Contraindications – cirrhosis, portal hypertension, pregnancy, generalized peritonitis, prior surgery, severe cardiopulmonary disease, hypotension esp. d/t hypovolemia Acalculous cholecystitis – acute or chronic cholecystitis w/o stones; develops as complications of burns, sepsis, trauma, collagen vascular disease; chronic form is referred to as biliary dyskinesia; causes – kinking of GB, thrombosis of cystic artery, sphincter spasm, prolonged fasting, dehydration, generalized sepsis; tx: lap cholecystectomy Gallstone Ileus – mechanical intestinal obstruction cause by gallstone lodged in lumen; signs- small bowel obstruction signs, distended abdomen, dx: plain films may help if examiner is aware, pneumobilia is helpful sign; tx emergency laporotomy and removal of the obstructing stone through a small enterotomy, examine proximal intestine for second stone, leave GB alone, usually fistulae close spontaneously, elective cholecystecomy Bacterial cholangitis – flow is disturbed by partial to complete obstruction which sets up bacterial infection of the biliary ducts; caused by choledocholitihiasis, biliary stricture, neoplasm; symptoms – Charcot’s triad; labs: leukocytosis, elevated serum bilirubin and alkaline phosphatase, E. coli most common; US is helpful and cholangiography is dangerous in this setting; most cases controlled w/ antibiotics, endoscopic sphincerterotomy may be needed Choledocholithiasis – calculi within the bile ducts; 50% of pts are asymptomatic; CBD may dilate to 2-3 cm proximal to the lesion; fluctuating jaundice; tx w/ lap choly w/ laparoscopic operative cholangiogram Carcinoma of the gallbladder – most common malignancy of biliary tract, 3x more common in females; risk factors: gallstones, porcelain gallbladder, adenoma; adenocarcima most common; pts present late w/ weight loss, anorexia; RUQ mass may be felt w/ ascites in advanced cases; tx cholecystecomy w/ hepatic resection; 5 year survival is 4% o Staging I – mucosa/submucosa II – muscle layer of GB III – + lymph node or liver extension (<2 cm) IV – liver extension (>2cm) Carcinoma of bile duct – rare; risk factors ulcerative colitis, sclerosing cholangitis, and infection w/ Clonorchis sinensis; RUQ pain, juanice, and pruritis; Couvosier’s sign Remember o Cholelithiasis – asymptomatic gallstones w/in the GB o Biliary colic – symptomatic gallstones causing transient RUQ pain w/o inflammation or infection o Cholecystitis – inflammation, often infection of the GB o Choledocholithiasis – stones in common bile duct o Cholangiitis – infection in the bile ducts extending to the liver o Courvoisier’s sign – jaundiced patient w/ a palpable nontender GB indicates distal common bile duct obstruction (Courvoisier’s law) GI Hemorrhage Anatomy o Portions of stomach Cardia – most proximal, gastroesophageal junction Fundus – most superior extension, Angle of His Body – largest portion, incisura angularis marks beginning of antrum Antrum – distal 25% o Sphincter of the stomach Lower esophageal sphincter – physiologic sphincter, high pressure zone of muscular activity in distal esophagus Pylorus – controls flow of food into duodenum o Blood supply of stomach – complex o Nervous innervation Vagus (parasympathetic) Branches (LARP) – left/anterior and right/posterior o Right first branch – criminal nerve of Grassi which causes recurrent ulcers when left undivided Sympathetic via greater sphlancnic (T5-T10) o Lympatics – superior/pancreaticolienal/suprapyloric/subpyloric Types of GI bleeding o Hematemesis – vomiting of bright red or “coffee-ground” blood; source is proximal to the ligament of Treitz o Hematochezia – passage of bright red blood by rectum, not specific to level o Melena – passage of black, tarry stools, does not guarantee it is from upper GI Identifying source of bleeding o Fiberoptic endoscopy – only safe w/ stable vital signs o Upper GI series o Passage of nasogastric tube o Angiography and radionuclide scanning Pathogenesis of Upper GI – acid-peptic erosion into the submucosal or extraluminal vessels o Posterior duodenal ulcers dangerous d/t proximity to gastroduodenal and superior pancreaticoduodenal o H. pylori – causative agent of duodenal, gastric ulcers and gastritis in 80% of pts not taking NSAIDs Types of Gastric ulcers o Type 1 – most common, located w/in 2cm of the boundary between parietal cells gastric mucosa, 95% are on the lesser curvature; H. pylori o Type 2 – duodenal ulcers o Type 3 – w/in 3cm of pyloris o Type 4 – adjacent to esophagus o Type 5 – anywhere due to NSAIDs Upper GI – treatment o Endoscopic therapy Bipolar and heater probe therapy – decrease rebleeding rates by 50% Lasers generally not used Majority of rebleeding occurs within 2-3 days o Indications for surgery Exsanguinating hemorrhage Profuse bleeding Continued hemorrhage – mortality increases Recurrent bleeding Pathologic features of bleeding site, e.g. posterior duodenal ulcer, giant gastric ulcer o Gastric ulcer Type 1 – hemigastrectomy, excision of distal 50% of the stomach w/ excision, Billroth I (stomach duodenum) or II (stomach jejunum) Type 2 and 3 – vagotomy w/ antrectomy and extension to include excision of ulcer Type 4 – antrectomy w/ extension of resection to include ulcer Type 5 – stop NSAIDs, primary closure, omental patch, or wedge resection o Duodenal ulcer – most d/t acid hypersecretion; goal of surgery is to reduce acid via vagotomy w/ antrectomy Lower GI Bleeding o Anorectal disease – anal fissure o Diverticular disease o Angiodysplasia of colon o Polyps o Colon carcinoma o Inflammatory bowel disease o Ischemic colitis o Mechel’s diverticulum Lung Nodules Benign lung disease o Pulmonary tuberculosis Mycobacterium tuberculosis Most common path organism seen in lungs Spread by aerosolization Present w/ necrotizing pneumonia which may go to hilar nodes caseating granulomas Tx: isoniazid, rifampin, ethmabutol, pyrazinamide Indications for surgery include: + sputum and cavitary lesion after > 5 months of tx, severe hemoptysis, bronchopleural fistula, empyema, lung mass w/ TB, disease from drug-resistant strain o Bronchiectasis Abnormal dilatation of bronchi from chronic smoldering infection; usually in more distal bronchial tree Presents w/ persistent productive cough, hemoptysis, recurrent pulmonary infections o Lung abscess Etiologies – aspiration, infection distal to occluded bronchi, septic emboli Typically resolve w/ medical therapy Sx: cavity >2 cm lasting >8 weeks, persistent bacteremia or hemoptysis, or malignancy suspected o Massive hemotysis >500cc/24hrs Mortality >10% resulting from asphyxia rather than exsanguination Diagnose and treated w/ bronchoscope Balloon catheter or angiographic embolization may be required Angio embolization may cause quadriplegia (posterior branch of posterior intercostal arteries divides into spinal and muscular branches) o Benign lung tumors Hamartoma – most common, usually found incidentally on chest x-ray Other – hemangiopericytoma, sclerosing hemangioma, granular cell tumor, fibroma, lipoma Lung Cancer – most common cause of cancer-related deaths in both sexes; etiology: tobacco, hereditary, environmental (asbestos, radon chromium), genetic (K-ras –NSCLC) o NSCLC – 80%, most common type is adenocarcinoma; TNM staging o SCLC – 20%, 2/3 pts present initially w/ disseminated and thus inoperable disease; most common presentation is pt w/ asymptomatic pulmonary nodule noted incidentally on chest x-ray – assumed malignant o Staging (both listed are surgical candidates) T1 - <3cm; T1a – no nodes involved T2a - <3cm w/ nodes involved o Mid tracheal lymph nodes important for resection considerations o Treatment – complex and depends on physical condition of pt, tumor size, lymph node status, metastases; surgical resection – stage I and II NSCLC’s o Medical and surgical contraindications to pulmonary resection Absolute: MI w/in 3 months, SVC syndrome d/t mets, bilateral endobronchial tumor, contralateral lymph node metastases, malignant pleural effusion, scalene node mets, FEV1 <0.8 L, Relative – MI w/in 6 months, Horner’s syndrome, small cell histology, main pulmonary artery involvement, pericardial involvement, recurrent laryngeal nerve paralysis d/t primary tumor in aorticopulmonary window, FEV1 <50% <0.8L, issuffienct pulmonary reserve Chemotherapy and radiation therapy – not indicated for stage IA dz, all other stages should be referred to oncologist The pathological stage of a patient’s tumor is the best predictor of survival with lymph node status have the greatest effect on long-term survival o Small cell lung cancers (SCLC) Present on imaging as bulky mediastinal lymphadenopathy and are assumed metastatic Tx w/ chemo; 80% recurrence o Carcinoid tumor Presents w/ hemoptysis, dyspnea, or recurrent pulmonary infections Tx resection o Others: bronchial adenomas, adenoid cystic carcinomas, mucoepidermoid carcinomas o If preop FEV1 > 50% of predicted, pt can tolerate pulmonary resection w/ little risk of postop pulmonary complication Pulmonary nodule o Review prior films if available o CT scan w/ contrast helps determine location of mass o PET differentiates between benign and malignant masses o Common sites for mets – brain, adrenals, bone Solitary pulmonary nodule o Definition: round lesion <3 cm in diameter surrounded by lung parenchyma o Size is important predictor of the likelihood of malignancy. Nodule <4cm have an extremely small risk of cancer o In some cases benign lesion can be diagnosed by CT b/c of distinct pattern of calcification (e.g. hamartoma or granuloma) o 1st step – establish if nodule is new or not and whether it is stable or increasing. CT should be done if there are no previous images o 2nd step Nodules with low to intermediate risk for cancer <4 mm; >1% 4-8 mm; 6% >8 mm; 50% Nodules suspicious for malignancy >8mm in pt w/ hx of cancer or in a case in which a nodule is increasing in size, has speculated margins or mixed solid/ground glass attenuation Pts w/ hx of cancer should have close follow up intervals o Diagnostic intervention can include: percutaneous needle aspiration biopsy, FDG-PET scans, VATS PNAB – provide definitive diagnosis w accuracy of about 90% for malignant lesion and 60-80% for specific benign lesions If not possible to perform PNAB, the choices are to surgically remove the nodule using video assisted thoracoscopic surgery (CATS), or perform followup CT scan FDG-PET scans (fluorodeoxyglucose-positron emission tomography) – identifies metabolically active nodules Follow up is not necessary once a nodule has been demonstrated to be stable for 24 months, with the exception of nodules that have ground glass features on CT Longer follow up is warranted b/c these features can be indicative of indolent cancers that can be stable or very slowly growing over several years o Guidelines Solitary pulmonary nodule found on X-ray Compare w/ old study o If growth, consider diagnostic intervention o If solid or no growth after >2 years, no action If no previous studies, do CT o If calcification or fat, no action o Nodule of any size needs to be investigated If CT shows nodule of any size With no hx of malignancy or =/- smoking o <4 mm Age >35 follow up CT as 12 and 24 mos Age 18-35 follow up CT after 12 mos All ages use longer follow up for ground glass nodules If growth occurs, consider PNAB or VATS o >4-8 mm Age >35 follow up CT after 3, 9, and 24 mos Age 18-35 follow up CT after 6-12 and 24 mos All ages use longer follow up for ground glass nodules If growth occurs, consider PNAB or VATS o >8 mm Consider PNAB, VATS, FDG-PET. Attention to part solid/ground glass nodule If co-morbitiies and PET neg, then consider follow up CT after 3, 9, and 24 mos If not growth, no action With Hx of malignancy – follow up CT after 3, 6, 12 mos w/ nodule of any size o If growth occurs, consider PNAB, VATS o If no growth, no action In immunocompromised pt or pt w/ fever o Follow up in <4-6 weeks and then to resolution OR o Consider PNAB, bronchoscopy, or VATS Neck Masses Cervical regions o Anterior cervical region (anterior triangle) o Lateral cervical (posterior triangle) – sternocleidomastoid, trapezius, Great auricular nerve near external jugular vein Spinal accessory nerve – damaged w/ thyroid surgery Lateral spinalclavicular nerve o Carotid triangle o Occipital triangle Thyroid anatomy o Innervation of the thyroid gland Derived from superior, middle, and inferior cervical ganglia They reach the gland through plexuses that accompany the thyroid arteries o Innervation of larynx Extrinsic – inferior laryngeal nerve off of the recurrent laryngeal nerve from CN X Intrinsic – external laryngeal nerve off of the superior laryngeal nerve from CN X Muscles of the larynx o Cricothyroid – external laryngeal nerve (only this muscle), stretches and tenses vocal ligament; damage causes bowing of larynx o Thyroartenoid – relaxes vocal ligament, inferior laryngeal nerve (from recurrent laryngeal nerve) o Posterior cricoarytenoid – abducts vocal folds o Lateral cricoarytenoid – adducts vocal folds o Transverse and oblique arytenoids Examination o Ascultation Bruit over both subclavian and common carotid aortic stenosis Bruit over single artery localized stenosis o Enlarged nodes Enlarged LN or normal structure – greater cornua of hyoid moves w/ swallowing (most lymph nodes do not move) Physical characteristics Metastatic – discrete, nontender, unilateral, firm/hard Hodgkin’s – discrete, nontender, large, firm/rubbery Tuberculosis – conglomeration, fluctuation, nontender Acute pyogenic – enlarged, tender, discrete Primary lesion Posterior triangle – scalp Thyroid mets – either to superficial or deep cervical nodes Mirror exam of nasopharynx and tonsils may be helpful Lesions in children o Cervical lymphadenopathy Don’t worry if it’s small, mobile, rubbery, in anterior cervical triangle Worry if its >2cm, nontender, fixed supraclavicular region, hard; hx of weight loss, night sweats If need for Bx is questionable – do CXR and/or CT first to R/O airway obstruction during induction o Branchiogenic anomalies Mature structures of head and neck are derived from six pairs of branchial arches, their intervening clefts externally, and pouches internally. The lesions are a result of failure of these structures to regress Second brachial cyst remnants – most common, anterior border of SCM, step-ladder incision needed to completely excise o Thyroglossal duct cysts One of the most common midline masses most commonly presenting in pre-school age children o o o o o o Thyroglossal remnants are involved with the embryogenesis of the thyroid gland Most cysts are found at or below the hyoid bone Sistrunk procedure: excise cyst and tract, excise central portion of hyoid bone extending to base of tongue Torticollis “Twisted neck”; tilted towards, rotated away; mass can be palpated, birth trauma +/-, tx conservatively Cystic hygroma Mal-developed lymphatic network which fails to connect or drain into venous system. Complete surgical excision is treatment of choice Lymphoma – most common malignant neck mass in children Malignancies FNA biopsy for definitive diagnosis CT of head and neck – choice for advanced squamous carcinoma Modified radical neck dissection-preserves spinal accessory nerve, SCM, and internal jugular vein Post op radiation if: More than two nodes contain mets Cervical nodes at more than two levels contain mets Extracapsular spread of cervical node mets Prophylactic radiation of all cancers is not recommended Thyroid nodules Thyroid moves cephalad w/ deglutition, nodes do not Isthmus of thyroid is caudad to cricoid cartilage Acute thyroiditis (low TSH and low radioactive Iodine uptake) Hyperthyroidism (Grave’s disease) Nervousness, sweating, infertility Goiter, tachycardia, warm most skin, gynecomastia, exopthalmus Tx propylthiouracil (PTU) Pts over 40, poor surgical risks, or recurrent hyperthyroidism tx w/ Radioiodine – 100% of young pts will become hypothyroid Surgery indications – very large goiter, malignant tissue, opthalmopathy, pregnancy/children, pt taking Amiodarone, psychologically impaired o Remove all but 5 gms sparing parathyroid and recurrent laryngeal nv Thyroid malignancies Types of thyroid cancer Papillary adenocarcinoma – 75% 10 year survival o Appears early in adult life as a solitary nodule o May metastasize to lungs or bones o Rate of growth may be stimulate by TSH Follicular adenocarcinoma – 65% o Greater tendency to metastasize to lungs, bone, and liver Medullary carcinoma – 35% o Screen all pts w/ medullary carcinoma for a RET point mutation on chromosome 10 Undifferentiated (anaplastic) carcinoma – 5% o Cervical lymphadenopathy and pulmonary metastases Wide range of growth and malignant behavior Anaplastic – local recurrence or pulmonary mets in 6 mos Papillary – slow growth, long life Surgery – preserve SCM, spinal accessory nerve, and sensory nerve Medullary – high incidence of nodal involvement; post-surgery if calcitonin or CEA are elevated then order US or MRI of neck and MRI mediatstinum All pts w/ thyroid cancer should be maintained on suppressive doses of thyroid hormone For follow up, it is helpful to measure serum thyroglobulin Perianal Problems Anatomy o Anal borders Posterior – coccyx Bilaterally – ischiorectal fossa Anterior – perineal body and vagina in women; urethra in men o External anal sphincter o Levator ani muscles o Anal valves, anal (Morgagnian) columns, longitudinal muscle, internal pudental artery o Venous drainage for rectal – common iliacs, superior rectal veins o Vessels and nerves superior to the pectinate line are visceral; those inferior to the pectinate line are parietal or somatic. This orientation reflects the embryological development of the anorectum Above pectinate line: arteries from inferior mesenteric artery; veins to portal venous system Below pectinate line: arteries from internal iliac artery; vein to caval venous system H&P o Anorectal exam – left lateral decubitus; inspection, palpation, anoscopy, proctosigmoidoscopy Pelvic floor disorders o Incontinence Causes Obstetric trauma – 3rd degree perineal tears, multiple deliveries, infection of episiotomy repairs Neurogenic cause – pudendal nerve injury d/t delivery or straining at stool Iatrogenic – division of external sphincter in fistula surgery Other – DM, MS, scleroderma, dermatomyositis, sever diarrhea, fecal impaction w/ over flow phenomenon, radiation proctitis Physical signs of incontinence – patulous anus, loss corrugation anal verge, flattening and maceration perineal floor, decreased sphincter tone, diminished voluntary squeeze pressures, and loss of anal sensation Work up – anorectal manometry, transrectal US (evaluates internal and external sphincter abnormalities), pudendal nerve latency studies Treatment – biofeedback (1st line tx), anal encircling procedures o Obstructed defecation Anal stenosis Causes – circumferential hemorrhoidectomy, trauma, radiation Tx – repeated dilatation Nonrelaxation of the puborectalis Functional disorder Symptoms – need for digital maneuver to eliminated stool, pelvic pain, incomplete emptying, severe straining during evacuation Diagnosis – inability to expel 60 cc balloon Tx - biofeedback Internal intusseseption (internal prolapse of the rectum) Cause – solitary rectal ulcer Tx – increase dietary fiber, stool softeners, glycerin suppositories Indications for surgery – debilitating symptoms, impending anal incontinence, chronic bleeding Low anterior resection of sigmoid and proximal rectum w/ anorectal anastomosis and rectal fixation o Rectal prolapse – protrusion of the full thickness of rectum through the anus Epidemiology & etiology Long-term internal intussusception, women in mental institutions, elderly women, hx hysterectomy Symptoms – mucosa-lined bowel protruding through anus, bleeding, anal pain, mucous discharge, anal incontinence of varying degrees o o o Tx surgically Pts in fair health w/ good continence – low anterior resection w/ rectopexy or fix rectum to sacrum w/ synthetic sling (Ripman’s procedure) Pts in poor health (perineal proctectomy w/ low colorectal or coloanal anastomosis of anal encircling procedure Pts w/ total incontinence – anterior resection of rectum and colostomy (low Hartman’s procedure) Hemorrhoids Internal – located above dentate line, rectal mucosa; symptoms – bleeding, mucous discharge, prolapse, pruritus, anal pain should not be attributed to thrombosed internal hemorrhoids Classification o 1st degree – bleed o 2nd – bleed and prolapse o 3rd – manual reduction o 4th – non-reducible External – below anal verge, covered w/ squamous epithelium Diagnose w/ anoscope Treatment depends on symptoms Thrombosed external – most resolve w/in 2 weeks 1st degree – medical therapy 2nd and 3rd – internal – rubber band ligation 3rd and 4th – surgical excision No more than two should be excised-anal stenosis Anal fissure Linear ulcer of the lower half of the anal canal usually locate in the posterior commissure in the midline Best seen by inspecting the anal verge w/ gentle separation of the gluteal cleft Associated findings include sentinel pile or tag externally and an enlarged anal papilla internally Involves squamous epithelium thus condition is painful Diagnosis is made by history – pain/bleeding w/ defecation, digital exam may be too painful, delay 4-6 weeks until pain managed medically then scope Uncertain etiology – may be due to large hard stools, diet, previous anal sx, childbirth, laxative abuse, etc Tx – warm sitz baths w/ bran or bulking agents, add nitroglycerin and diltiazime (reversible chemical sphincterotomy) for chronic cases, surgery Reversible chemical sphincterotomy – botox transiently caused striated muscle denervation leading to muscle paralysis and relaxation Anorectal suppuration – abscess/fistula Involves anal glands Spreads in intersphincteric plane Infection may extend upwards, downwards, horizontally, or circumferentially (horseshoe abscess) An anal fistula may result from the spread of an anal infection and cryptitis. One end of this abnormal canal opens into the anal canal, and the other end opens into an abscess in the ischioanal fossa or into the perianal skin Pain constant but no associated w/ defecation Fever and leukocytosis may be present Tx – drain when diagnosed Goodsall’s rule – external openings posterior to a transverse line that bisects the anus will connect to the posterior midline crypt; external openings anterior to this line will communicate to an anterior crypt by a short direct route Exception – anterior, >3cm from anal margin o o Pilonidal disease – hair from the skin of the postsacral superior gluteal cleft that drills below the skin level causing foreign body reaction and localized inflammation Tx w/ drainage, extract hair Tumors of the anal area Squamous cell carcinoma – large, central ulceration w/ rolled edges, <4cm – wide local excision Basal cell carcinoma – tx w/ wide excision Bowen’s disease – indolent in situ squamous cell carcinoma w/ anal verge, appearance usually plaque-like, presents w/ burning and pruritus, tx w/ wide local excision Paget’s disease – shallow intraepithelial tumor presenting as a plaque Condyloma acuminata – HPV, most common perianal sexually transmitted disease, tx fulguration w/ electrcautery and direct excision may be required The Acute Abdomen History and physical o Pain is the most common presenting symptom o Visceral pain – abdominal viscera innervated by autonomic nerve fibers C and respond mainly to the sensations of distention and muscular contraction – not to cutting, tearing, or local irritation; most often felt in midline, slow in onset, dull, poorly localized, and protracted o Sensory levels (structures – nervous system pathway; sensory level Liver, spleen, central diaphragm – phrenic; C3-5 Peripheral diaphragm, stomach, pancreas, GB, small bowel – celiac plexus, greater splanchnic, T6-9 Appendix, colon, pelvic viscera – mesenteric plexus, lesser splanchnic, T10-11 Sigmoid, rectum, kidney, ureters, testes – lowest splanchnic, T11-L1 Bladder, rectosigmoid – hypogastric, S2-4 o Parietal pain – afferent C and A delta fibers elicited by direct irritation; pain is localized b/c somatic afferent fibers directed to only one side of nervous system, cutaneous distribution corresponds to T6-L2, conveniently describe –RUQ, LLQ, epigastric, ect. o Referred pain – pain perceived distant from its source and results from convergence of nerve fibers at the spinal cord Subdiaphragm – goes to shoulder C4 phrenic Biliary – often perceived in R scapula; can mimic anginal pain Retrocecal appendicitis – posterolateral right flank o Location of pain – spreading or shifting pain (parallels the course of the underlying condition), location serves as “rough guide” only, “typical” descriptions of pain in only 2/3rd of causes o Character of pain – steadying pain (most common), biliary pain, colicky pain Colic – pain free intervals that reflect intermittent smooth muscle contraction Sharp, constant worsened by movement (peritonitis) Tearing pain (dissecting aneurysm) Dull pain (appendicitis, diverticulitis, pyelonephritis) o Other symptoms – vomiting (1st then pain), constipation/obstipation, diarrhea o Physical exam Palpation – guarding – place both hands on abdomen and gently depressing fingers have patient inhale deeply and gently Rectus rigidity – peritoneal inflammation Ipsilateral rigidity – renal colic Carnett’s test – raise head, muscles tense (relief of pain indicates intraperatoneal) Punch tenderness – costal area, costovertebral Murphy’s sign – palpate right subcostal, have patient breath deeply and inspiration will be stopped abruptly, indicates gallbladder disease Iliopsoas sign – pain w/ passive hip extension or active hip flexion against resistance; indicates psoas abscess, Crohn’s disease Obturator sign – internal and external rotation of flexed thigh may exert pressure on entrapped small bowel – obturator hernia Costovertebral angle tenderness may indicate pylonephritis Investigative studies – lab o 2/3 of diagnoses of acute abdomen are made w/ history and physical o Immediate – CBC, BUN, Creat, ABG, UA w/ micro, check stool for blood, chest/abdominal X-ray o Same day – clotting, amylase, liver fx, stool culture, ultrasound/CT proctosigmoid, upper endoscopy, paracentesis, culdocentesis o Next day – specific tests, ERCP, colonoscopy, Lap o X-ray – plain films are indicated w/ appreciable tenderness/distention, abnormal BS, hx of abdominal surgery, decreased sensorium, and/or Chest x-ray is essential in all acute abdomen cases Look for gas patterns, outline of solid organs, outline of fat lines, radiopaque objects; free gas under diaphragm 80% of time is perforated ulcer Angiography or MRA – ischemia/hemorrhage GI contrast – if no clinical evidence of bowel perforation, BE large bowel obstruction; only if no likelihood of large bowel obstruction o US – 80 % sensitive in appendicitis, pregnancy o CT scans – for pts w/o clear indications for laparoscopy o Proctosigmoidoscopy – large bowel obstruction, bloody stools, rectal bleed o Colonoscopy – lower GI bleed o Gastroduodenoscopy and ERCP – gastritis or PUD Laparoscopy – therapeutic and diagnostic; esp useful for young women, elderly, and critically ill Differential diagnosis o Young children – mesenteric adenitis o Young woman – tubo-ovarian disease o Elderly – malignancy Appendicitis – most common cause of cause of ileus or intestinal obstruction; 50% children have facial flush; nonspecific abdominal pain in 1/3 of all cases; most common cause of acute abdomen in children Indications for surgery o Involuntary guarding or rigidity, severe localized tenderness, tense distention, abd/rectal mass w/ high fever/hypotension o Radiologic findings – pneumoperitoneum, bowel distention, extravsation of contrast, space occupying lesion w/ fever o Endoscopic findings – perforated or uncontrollably bleeding lesion o Paracentesis – blood, pus, urine, etc Preoperative management – give analgesics, meds for cardiac, corticosterioids, diabetes, antibiotics; place NG tube, urinary catheter, informed consent o o Fluid, Electrolyte, and Acid-Base Disorders Total body water = 60% body weight o Compartments Intercellular – 66% Extracellular – 33% Interstitial – 66% ECF Intravascular – 33% ECF o Body fluid distribution by weight T – total body weight = 60% I – intracellular = 40% E – extracellular = 20% o Blood volume: 7% of body weight; ex: 70kg x 0.07 = 5 L blood o Electrolyte composition Intracellular – K+ Extracellular – Na+ o Maintenance Sodium – 1-2 mEq/kg = 70-140 mEq/day Potassium – 0.5-1 mEq/kg = 35-70 mEq/day o Fluid requirements for 24 hours – 100/50/20 100 mL/kg for first 10 kg 50 mL/kg for second 10 kg 20 mL/kg for ever kg over 20 o Hourly rate – 4/2/1 o Maintenance rates – change w/ fever, environmental temperature, respiratory rate, urine output, age (elderly don’t produce as much urine), total parenteral nutrition – rarely need fluids o Water Hypovolemia Acute – tachycardia, hypotension, concentrated urine Gradual – skin, thirst, mental status change Treatment o Replace acute losses acutely o Replace chronic losses half 1st 8 hrs, remainder in next 24-48 hrs Hypervolemia Acute – tachycardia, tachypnea, sacral edema, JVD Chronic – peripheral edema, pulmonary edema Treatment o Mild – Na restriction o If hyponatremia – water restriction also necessary o If severe – diuretics o Sodium – close relationship to volume status Hyponatremia <130 mEq/L Hyperosmolar – dilutional hyponatremia fro hyperglycemia, mannitol infusion or other osmotically active particles Normo-osmolar – pseudohypotnatremia o Hyperglycemia, hyperlipidemia, hyperproteinemia interferes with lab measurement of Na Hypo-osmolar – true hyponatremia o Hypovolemic – total body sodium is usually ow o Hypervolemic – TBS usually high; cardiac output low, hypoalbumenia o Euvolemic – syndrome of inappropriate antidiuretic hormone (hyponatremia, concentrated urine, elevated urine Na, normal or mild elevated ECF volume) Symptoms o Acute – cerebral edema, seizures, coma o Chronic – <110 mEq/L well tolerated, irritability o Diagnosis o Hypo-osmolar, hypovolemia – urine osmolality low, urine Na low o Hypo-osmolar, hypervolemic – similar o Hypo-osmolar euvolemic – urine osmolality high; urine Na high o Lab error is #1 cause of misdiagnosis Treatment o Hyperosmolar – correct hyperglycemia or other osmotic particles o Normo-osmolar – no tx needed o Hypo-osmolar Hypovolemic – isotonic fluid infusion, consider sodium replacement if severe Hypervolemic – tx underlying cause first, then salt and free water restriction are appropriate Euvolemic – restrict water is SIADH and don’t give Na since can paradoxically ower sodium as kidney extrete sodium and conserves water Hypernatremia >150 mEq/L Types o Hypovolemia: represents a volume deficit o Hypervolemia: rare but cause by iatrogenic infusion of too much sodium Symptoms o Tachycardia, hypotension, dry mucous membranes, lethargy, confusion, and coma as water shifts form intracellular compartment in CNS Diagnosis o High serum sodium w/ obvious fluid losses d/t: Extrarenal: fever, mechanical ventilation, diarrhea, etc. Renal – osmotic diuresis from hyperglycemia, mannitol; high output dilution from acute tubular necrosis Treatment o Hypovolemic Replace volume with D5W, ¼ NS, or ½ NS slowly over days Lower Na about 12 mEq/L per day Seizures will develop if sodium is lowered too fast o Hypervolemic First decrease sodium being administered Diuretics can be used Potassium Hypokalemia <3.5 mEq/L Symptoms o Ileus, weakness, cardiac dysrhythmias o ECG – flattening or inversion T-waves, depressed ST segments, U waves, prolonged QT interval, ventricular tachycardia Treatment o Renal – diuretics o Extrarenal – diarrhea, burns o Intracellular – insulin, alkalotic state o Medical – hyperaldosteronism, Cushing syndrome o 10 mEq/hr of K should raise serum K by 0.1 nEq/L Hyperkalemia > 6mEq/L Symptoms – cardiac manifestations, peaked T waves, decreased DTR, weakness, respiratory failure, paralysis Etiology o Renal failure o o Extracellular shift – Rhadbdomyolysis o Medical disease – Addison’s Treatment o Stabilize cardiac membrane and lower serum K 1 gram calcium gluconate IV Glucose/insulin to shift K intracellularly Bicarbonate will also shift K o To lower K permanently – ion-exchange resin, lasix, dialysis Chloride Hypochloremia < 90 mEq/L Symptoms – associated with dehydration or low K, vomiting Etiology – HCL lost from stomach d/t vomiting metabolic alkalosis Treatment – replace chloride and K with IV’s Hyperchloremia >100 mEq/L Cause – too much in IV fluids Tx – decrease amount of CL in fluids o Calcium Hypocalcemia < 8mg/dL Symptoms neuromuscular irritability, PVC’s o Trousseau’s sign – carpal spasm after occlusion of blood in FA o Chvostek’s sign – facial muscle spasm with tapping facial nerve Etiology – removal parathyroid gland Treat the cause – asymptomatic – po Ca o Usually oral Ca will suffice Hypercalcemia >10.5 mg/dL Symptoms – fatigue, confusion, NV, diarrhea, dehydration, anorexia Tx the cause – primary hyperparathyroidism o Cancer o Thiazides Treatment o Severe – isotonic resuscitation leading to diuresis and excretion of Ca o If unsuccessful add Lasix Acid-Base disturbances (pH = 7.35-7.45) o Regulatory system CO2 – increased CO2 decreased pH Strong Ions – Na, Cl, K, etc Pure salt solution, ion concentration is equal, pH neutral Plasma has more cations than anions To maintain neutrality, H2O dissociates, H+ excreted, HCO3 increases and pH 7.4 instead of 7.0 Weak acids – act as buffers, proteins and phosphates o Acidosis – occurs when PCO2 increases, HCO3 decreases, concentration of strong ions increase, concentration weak acids increase Respiratory acidosis Most common cause is decreased alveolar ventilation Tx – increase alveolar ventilation Metabolic acidosis Loss of bicarbonates – diarrhea, ileus, fistula Increase in acids – lactic acidosis, ketoacidosis, renal failure Tx – correct underlying metabolic problem o Alkalosis Metabolic alkalosis Most common cause is loss of gastric contents Tx – stop Cl loss and replace with isotonic saline and potassium supplementation Respiratory alkalosis Most common cause is increased alveolar ventilation Acid-base using blood gas o <7.35 acidosis HCO3 Low – metabolic acidosis High – mixed CO2 High – respiratory acidosis Low – mixed o >7.45 alkalosis HCO3 High – metabolic acidosis Low – mixed CO2 Low – respiratory alkalosis High – mixed o pH normal – mixed or compensated Misc Shock SIRS criteria (Systemic Inflammatory Response Syndrome) – two or more of the following: o Body temperature <36 C or >38 C o Tachycardia o Tachypnea o White blood cell count <4,000, >12,000, or >10% immature neutrophils Sepsis – same criteria as for SIRS but w/ a clearly established focus of infection Severe sepsis – sepsis associated w/ organ dysfunction and hypoperfusion o Systolic blood pressure <90 mm Hg o >40 mm Hg fall from normal systolic blood pressure o Lacticacidemia o Oliguria o Acute mental status changes Septic shock – patients w/ severe sepsis who: o Are not responsive to IV fluids for resuscitation o Require inotropic or vasopressor agents to maintain systolic blood pressure Wound healing Phases (think: in every fresh cut) 1. Hemostasis 2. Inflammation – vasoconstriction followed by vasodilation, capillary permeability 3. Epithelialization – epithelial coverage of wound Sutured wound epitheliaizes in 24-48 hours (then dressing can be removed and pt can shower) Marjolin’s ulcer (aka burn scar carcinoma) – malignant ulcer 4. Fibroplasia – fibroblast and accumulation of collagen, elastin, and reticulin 5. Contraction – myofibroblasts contract wound 6. Scarring 7. Remodeling Wound closure 1. Primary intention – suture wound closed immediately 2. Secondary intention – wound is left open and heals over time without sutures; it heals by granulation, contraction, and epithelialization over weeks (leaves a huge scar) Used for dirty wounds to prevent abscess from forming 3. Delayed primary closure – suture wound close 3 to 5 days after incision Postoperative complications Fever (wind, water, wound, wonder drug, walking) o Atelectasis – first 24 to 48 hours o UTI – Anytime after POD #3 o Wound infection – usually after POD #5 (but it can be anytime!) o DVT/PE/thrombophlebitis – POD #7 to #10 o Drug fever – anytime Anesthesia Malignant hyperthermia o Inherited predisposition to an anesthetic reaction causing uncoupling of the excitation-contraction system in skeletal muscle; hypermetabolism is fatal if untreated o Causative agents – general anesthesia, succinylcholine o Signs/symptoms – increased body temperature, hypoxia, acidosis, tachycardia, increase pCO2 o Tx – IV dantrolene Trauma/burns Glasgow coma scale o Eyes (4 eyes) 1. Does not open eyes 2. Opens eyes to painful stimulus 3. Opens to voice command 4. Opens spontaneously o Motor response (6-cylinder motor) 1. No movement 2. Decerebrate posture 3. Decorticate posture 4. Withdraws from pain 5. Localizes painful stimulus 6. Obeys commands o Verbal response (Jackson 5) 1. No sounds 2. Incomprehensible sounds 3. Inappropriate words 4. Confused 5. Appropriate and oriented Breast Anatomy o Borders o Superior – axillary vein Posterior – long thoracic nerve Lateral – latissimus dorsi muscle Medial – lateral to, deep to, or medial to pectoral minor muscle, depending on level of nodes taken Nerves Long thoracic – innervates serratus anterior; “winged scapula” Thoracodorsal – innervates latissimus dorsi Medial pectoral – innervates pectoralis minor and major Lateral pectoral – innervates the pectoralis major Intercostobrachial nerve – cutaneous nerve that transverses the axilla o Lymphatic drainage Lateral – axillary lymph nodes Medial – parasternal nodes that run w/ internal mammary artery Breast cancer o History risk factors (NAACP) Nulliparity Age at menarche (<13 years) Age at menopause (>55 years) Cancer of the breast (in self or family) Pregnancy w/ first child (>30 years) o Types Infiltrating ductal carcinoma (most common) Medullary carcinoma Infiltrating lobular carcinoma Tubular carcioma Mucinous carcinoma (colloid) Inflammatory breast cancer – associated w/ Peau d’orange Ductal carcinoma in situ – cancer cells in the duct w/o invasion; microcalcifications on mammography Lobular carcinoma in situ Intraductal papilloma – bloody discharge in a young woman o Fibroadenoma – most common breast tumor in pts <30 years; well-circumscribed; surgical resection for large or growing lesions Paget’s disease of breast – scaling rash/dermatitis of the nipple caused by invasion of skin by cells from a ductal carcinoma Cystosarcoma phyllodes – typically benign, mesenchymal tumor arising from breast lobular tissue; mobile, smooth breast mass on mammogram/ultrasound Detection Self-exam – monthly Ages 20-40 years: breast exam every 2-3 years by a physician >40 years: annual breast exam by a physician Mammogram Baseline mammogram between 35-40 years Mammogram every year or every other year for ages 40-50 Mammogram yearly after age 50 Staging Stage I – tumor <2 cm w/ no nodes Stage IIA – tumor <2 cm w/ mobile axillary nodes OR 2-5 cm w/ no nodes Stage IIB – tumor 2-5 cm w/ mobile axillary nodes OR tumor >5 cm w/ no nodes Stage IIIA – Tumor >5 cm w/ mobile axillary nodes OR any size tumor w/ fixed axillary nodes, no metastases Stage IIIB – Peau d’orange, chest wall invasion/fixation, inflammatory cancer, breast skin ulceration, breast skin satellite metastases, or any tumor and + ipsilateral internal mammary lymph nodes Stage IIIC – any size tumor, no distant mets; positive: supraclavicular, infraclavicular, or internal mammary lymph nodes Stage IV – distant metastases o Treatment Stage I and II – lumpectomy and radiation Stage III A/B – modified radical mastectomy Benign breast disease o Fibrocystic disease – green, straw-colored, or brown nipple discharge o Fat necrosis – breast mass following trauma o Mondor’s disease o Prolactinoma Gastric cancer Risk factors o Diet – smoked meats, high nitrates, low fruits and vegetables o Environment – pernicious anemia, H. pylori Blummer’s shelf – sold peritoneal deposit anterior to the rectum, forming a “shelf”, palpated on rectal examination Virchow’s node – metastatic gastric cancer to the nodes in the left supraclavicular fossa Crohn’s disease/Ulcerative Colitis Crohn’s – abdominal pain, diarrhea, fever, weight loss, anal disease o Mouth to anus o Skip lesions, cobblestoning o Transmural bowel wall involvement o Anal involvement is common (fistulae, abscesses, fissures, ulcers) Ulcerative colitis – bloody diarrhea (hallmark), fever, weight loss o Colon only; lead-pipe appearance on barium enema o Begins with rectum involvement and moves proximally o Mucosa/submucosa bowel wall envolvement o Anal involvement rare; 100% rectal involvement o Crypt abscesses and psuedopolyps o Complications include cancer, toxic megacolon, perforation Extraintestinal manifestations in both o Aphthous elcers o Pyoderma gangrenosum o Iritis o Erythema nodosum o Sclerosing cholangitis o Arthritis, Ankylosing spondylitis o Clubbing of fingers o Kidney (amyloid deposits, nephritic syndrome) Diverticular disease Diverticulosis – false diverticula consisting of only mucosa and submucosa that herniated through the bowel musculature; caused by weakness in the bowel wall where nutrient blood vessels enter o Most commonly involves the sigmoid colon o Risks – low-fiber diets, chronic constipation, family hx o Symptoms – bleeding, diverticulitis, asymptomatic Diverticulitis – infection or perforation of a diverticulum o Pathophysiology – obstruction of diverticulum by a fecalith leading to inflammation and microperforation o Signs/symptoms – LLQ pain, change in bowel habits, increased WBC o Colovesical is most common fistula type o Best test – CT o Indications for elective resection – two episodes of diverticulitis; should be considered after the first episode in a young, diabetic, or immunosuppressed patient o Elective surgery for recurrent bouts – one-stage operation: resection of involved segment and primary anastomosis (with preoperative bowel prep) o Hartmann’s procedure: resection of involved segment with an end colostomy and stapled rectal stump (will need subsequent reanastomosis of colon usually after 2-3 postoperative months) Colon cancer Colonic and rectal polyps o Anatomical classification Sessile (flat) Pedunculated (on a stalk) o Classification Inflammatory (pseudopolyp) – as in Crohn’s disease or UC Hamartomatous – normal tissue in abnormal configuration Hyperplastic – benign, normal cells, no malignant potential Neoplastic Tubular adenomas – 5% cancerous Tubulovillous adenoma – 20% Villous adenoma – 40% Colorectal carcinoma – adenocarcinoma of the colon or rectum o ACS recommendations – starting at age 50, at least one of the following test regimens is recommended: Colonoscopy – q 10 years Double contrast barium enema – q 5 years Flex sigmoidoscopy – q 5 years CT colonography – q 5 years o o ACS recommendations if there is a hx of colorectal cancer in 1st degree relative less than 60 years old Colonoscopy at age 40, or 10 years before the age of diagnosis of the youngest firstdegree relative, and every 5 years thereafter Staging Stage I – invades submucosa or muscularis propria (T1-2 N0 M0) Stage II – invades through muscularis propria or surrounding structures but with negative nodes (T3-4 N0 M0) Stage III – positive nodes, no distant metastasis (any T, N1-3, MO) Stage IV – positive distant metastasis (any T, any N, M1) Pancreas Ranson’s criteria – score of 3 or more is indicative of severe pancreatitis o At presentation Age >55 WBC >16,000 Glucose >200 AST >250 LDH >350 o With first 48 hours Base deficit >4 BUN increase >5 mg/dL Fluid sequestration >6 L Serum Ca++ <8 Hct decrease >10% PO2 (ABG) <60 mm Hg o Predictor of mortality 1-2: 2% 3-4: 15% 5-6: 40% 7-8: 100% OTHER TOPICS: Splenic trauma Acute thromboembolic Venous insufficiency Metastatic liver disease Cirrhosis Thyroid Abdomen Hernias Acute Abdomen Acute gastrointestinal hemorrhage Peptic Ulcer Disease Anal conditions Biliary system Preoperative care Large bowel obstruction Benign gastric lesions – bezoars, volvulus