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109 Cards in this Set
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Symptoms
Dysphagia (often with liquids), regurgitation of undigested food and aspiration while recumbent, minimal pain. |
Achalasia
Description Motility disorder characterized by a triad of: primary esophageal aperistalsis and atony; megaesophagus; failure of lower esophageal sphincter (LES) relaxation. The LES fails to relax with swallowing. Circular muscle of the LES is thickened. Auerbach’s plexus absent. |
Diagnosis
Esophagram—Marked dilation above constricted distal esophagus. Abnormal peristalsis. Endoscopy—Excludes an esophageal stricture whether benign or malignant. Esophageal Manometry—Uncoordinated peristalsis, primary peristal- sis absent, gastroesophageal (GE) sphincter has above-normal resting pressure and does not relax with swallowing. Complications of untreated achalasia: megaesophagus, increased risk of squamous cell carcinoma. Treatment Steps 1. Pneumatic dilatation. 2. Botulinum toxin injected in LES. 3. Longitudinal esophageal myotomy (open or laparoscopic) is sur- gical procedure of choice. Usually, antireflux procedure (e.g., Nissen or Toupet fundoplication) added to myotomy. |
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Symptoms
Most hiatal hernias are asymptomatic. Symptoms of gastroe- sophageal reflux disease (GERD) can occur, including retrosternal burning pain especially lying supine, lifting, or straining; regurgita- tion of bitter fluid; nocturnal cough, recurrent pneumonia from as- piration; dysphagia. Bleeding rare. |
Sliding Hiatal Hernia
Description Esophagogastric junction and proximal stomach displaced into me- diastinum. Ninety-five percent of hiatal hernias are sliding. Symp- toms caused by accompanying esophageal reflux. There is no true hernia sac |
Diagnosis
Chest x-ray (CXR): Air–fluid level in mediastinum. GE reflux may be evident on esophagram. Esophagoscopy to rule out other lesions and document esophagitis. Distal esophagus pH monitoring most sensitive test. Treatment Steps 1. No treatment if asymptomatic. 2. Treat GERD symmptoms medically (see Chapter 4). 3. Surgical antireflux procedures—Nissen fundoplication, Hill repair, Belsey fundoplication |
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Symptoms
Fullness after meals, epigastric postprandial pain (69%), bowel sounds in chest, early postprandial vomiting (50%), breathlessness while eating. Chronic blood loss in up to one-third of patients due to recurrent bleeding from the gastric mucosa. |
Paraesophageal Hiatal Hernia
Description Esophageal junction in normal anatomic position. Stomach herni- ates through hiatus usually to left of esophagus. May strangulate or volvulize leading to rapid death (20–30%). |
Diagnosis
CXR: air–fluid level in mediastinum. Esophagram establishes the di- agnosis. Esophagoscopy to rule out Barrett’s esophagus. Treatment Steps Because of high rate of complications, all paraesophageal hiatal her- nias should be surgically repaired (abdominal and/or thoracic ap- proach) with or without an accompanying antireflux procedure. Good to excellent surgical results in 80–90% of patients. |
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Symptoms
Progressive dysphagia, odynophagia, chest pain, weight loss. |
Esophageal Cancer
Description Squamous carcinoma most common cell type: distal third (30%), middle third (50%), upper third (20%). Spreads by lymphatics, vas- cular invasion, and direct extension. Adenocarcinoma 5–10% of pri- mary carcinomas of esophagus. Frequency of adenocarcinoma has increased and currently accounts for > 50% all esophageal tumors. Extraesophageal extension present in high percentage of patients at time of diagnosis. Highly aggressive. Five-year survival rate only 3% when lymph nodes are involved. |
Diagnosis
Esophagram—Irregular mass narrowing lumen of esophagus, mini- mal proximal dilatation. Esophagoscopy—Biopsy for tissue diagnosis, tumor length. Rule out gastric involvement. Bronchoscopy—For upper- and middle-third lesions to rule out tra- cheobronchial involvement. Computed tomographic (CT) scan and endoscopic ultrasonography (EUS) helps with staging. Other imaging studies used for staging are: magnetic resonance imaging (MRI), positron-emission to- mography (PET), and video-assisted thoracoscopic surgery (VATS). Treatment Steps 1. Surgery; only 30% resectable. Esophagectomy (transhiatal blunt esophagectomy or Ivor Lewis procedure), total or partial, de- pending on tumor location and size. Stomach or the left-sided colon are used to reestablish gastrointestinal (GI) tract continu- ity. Resection may also provide palliation in low-risk patients. 2. Radiation therapy preoperative may shrink tumor mass allowing resection. Combined with chemotherapy may be effective adju- vant therapy. However, no definitive survival advantage to either chemo- or radiation therapy has been demonstrated. 3. Endoscopic laser therapy used to establish esophageal patency in unresectable obstructing tumors. |
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Symptoms
Dysphagia, pain, fever, neck tenderness and crepitus (with cervical perforations), chest pain, dyspnea, shock, mediastinal air (Hamman’s sign). |
Esophageal Perforation
1. Instrumental Perforation Causes The most common cause of esophageal perforation is iatrogenic disrup- tion, which includes endoscopy, dilation, paraesophageal surgery, Seng- staken–Blakemore (SB) tube, intubation, sclerotherapy. Description Susceptible at areas of narrowing: cricopharyngeal area, midportion near aortic arch and mainstem bronchi, diaphragmatic hiatus. |
Diagnosis
X-rays: soft tissue air, mediastinal air (takes 1 hour to be seen), pleural effusion, pneumothorax, mediastinal widening. Esophagram shows site of perforation (usually into left pleural cavity). Treatment Steps 1. Antibiotics for all patients. 2. Observation for those patients with small localized perforation with minimal symptoms and no sepsis. 3. Surgical repair required in almost all cases. a. Early diagnosis (< 24 hours)—primary repair. b. Late diagnosis—primary reinforced repair, drainage alone (cervical perforation), esophageal exclusion and diversion, or esophagectomy (if underlying significant esophageal pathol- ogy, e.g., cancer is present). Criteria for Nonoperative Therapy Contained mediastinal leak, free drainage back into esophagus, min- imal symptoms, no sign of sepsis. Surgical repair possible within 24 hours of perforation. After 24 hours, resection combined with diverting procedures may be necessary (“spit fistula”). |
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Symptoms
Sudden, severe pain in lower chest and upper abdomen; shock; rigid abdomen. |
Esophageal Perforation Spontaneous Perforation
Description Postemetic transmural perforation usually following an alcoholic binge (Boerhaave syndrome). Patients generally present with medi- astinitis. Posterior, distal esophagus most usual site. Fifty percent with concomitant GERD. Differential Diagnosis Pancreatitis, myocardial infarction, perforated peptic ulcer, dissecting aortic aneurysm. |
Diagnosis
X-rays: soft tissue air, mediastinal air (takes 1 hour to be seen), pleural effusion, pneumothorax, mediastinal widening. Esophagram shows site of perforation (usually into left pleural cavity). Treatment Steps 1. Antibiotics for all patients. 2. Observation for those patients with small localized perforation with minimal symptoms and no sepsis. 3. Surgical repair required in almost all cases. a. Early diagnosis (< 24 hours)—primary repair. b. Late diagnosis—primary reinforced repair, drainage alone (cervical perforation), esophageal exclusion and diversion, or esophagectomy (if underlying significant esophageal pathol- ogy, e.g., cancer is present). Criteria for Nonoperative Therapy Contained mediastinal leak, free drainage back into esophagus, min- imal symptoms, no sign of sepsis. Surgical repair possible within 24 hours of perforation. After 24 hours, resection combined with diverting procedures may be necessary (“spit fistula”). |
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Symptoms
Epigastric pain, pain relieved by food and/or antacids, nocturnal awakenings, nausea, vomiting, and anorexia. Approximately one- third are asymptomatic. |
Duodenal Ulcer
Description Associated with acid hypersecretion. Increased number of parietal cells. Peak incidence between the ages of 20 and 60. Typically, peri- ods of remission and exacerbation. Ninety-five percent occur in duodenal bulb (posterior wall within 2 cm of the pylorus). Risk fac- tors include: Helicobactor pylori (almost 100%), tobacco use, nonsteroidal anti-inflammatory drugs (NSAIDs), and Zollinger–Ellison syndrome. |
Diagnosis
Endoscopy is 95% accurate and is diagnostic procedure of choice. Upper GI series 75–80% accurate, showing an ulcer crater or scar- ring of the duodenal bulb. The saline load test can be used to determine gastric outlet obstruction. Treatment Steps Medical—See Chapter 4. Surgical—Indications for surgery are hemorrhage, perforation (Fig. 18–1), obstruction, and intractability. Surgical procedures: 1. Perforated duodenal ulcer—vagotomy and pyloroplasty, vago- tomy and antrectomy, highly selective vagotomy (laparoscopic or open), omentopexy (Graham patch) with vagotomy. 2. Bleeding duodenal ulcer—oversew the bleeder with pyloro- plasty and truncal vagotomy. 3. Obstructing duodenal ulcer—truncal vagotomy with gastrojejunostomy |
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Symptoms
Similar to duodenal ulcer. Pain localizes to left of midline, mostly postprandial |
Gastric Ulcer
Description Appear later in life. Peak incidence in fifth decade. More common in men. Usually no acid hypersecretion. Cause factor is mucosal in- jury or defect in “mucosal defense” that renders mucosa susceptible to gastric acid. Majority occur on lesser curve of stomach. Malignant potential (10%). Ninety percent have H. pylori. Types 1. Ulcer located at incisura angularis on the lesser curvature (low acid output, associated with blood group A). 2. Ulcers located in stomach and duodenum (high acid output, as- sociated with blood group O). 3. Ulcer located in pylorus or prepyloric area (high acid output, as- sociated with blood group O). 4. Ulcer located high in stomach (juxtacardia, low acid output). 5. Ulcer located anywhere in stomach (associated with NSAIDs). |
Diagnosis
Upper GI series can localize (90% sensitive). Endoscopy (97% sensi- tive) important. Must biopsy ulcer 8–12 times to rule out malig- nancy. Treatment Steps 1. Principles of medical treatment are similar to those of treatment of duodenal ulcer. (See Chapter 4.) 2. Because recurrence rate is higher after medical therapy, surgical therapy should be considered earlier. Procedure of choice is antrectomy with Billroth I anastomosis. No vagotomy with type I gastric ulcers. • Type 1: distal gastrectomy (use Billroth I). • Types 2, 3: antrectomy with truncal vagotomy. • Type 4: extended distal gastrectomy or 90% near total gastrec- tomy with Roux-en-Y esophagogastrojejunostomy |
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Symptoms
• Early—vague, nondescript symptoms. • Late—indigestion, postprandial fullness, eructation, loss of ap- petite, heartburn, vomiting. Pain pattern is similar to peptic ulcer disease. |
Gastric Carcinoma
Description Adenocarcinoma is the most common (95%); classified into ulcer- ating (25%), polypoid (25%), superficial spreading (15%, best prognosis), linnitus plastica or “leather bottle” (10%), and ad- vanced (35%). Risk factors include: dietary (nitrosamines, smoked/salted or pickled foodstuffs), tobacco use, alcohol, and en- vironmental factors. Almost all have H. pylori. Adenomatous polyps and atypical gastritis are premalignant lesions. Most have adenocar- cinoma and are located in the antrum. Cancer at the gastroe- sophageal junction is associated with Barrett’s esophagus and GERD. Major factors influencing survival are level of spread through gastric wall and lymph node involvement. Seventy-five per- cent have metastasis at the time of diagnosis. Age range: 50–70 years; male-to-female ratio is 2:1. |
Diagnosis
Barium Meal Upper GI Series (Double Contrast)—polypoid mass, ulcer crater not extending outside boundary of gastric wall, nondisten- sible stomach. Endoscopy—With biopsy, 90% accurate. Endoscopic ultrasound may be of value in determining depth of tumor and presence of enlarged lymph nodes. CT Scan—Evaluation of metastatic spread. Treatment Steps 1. Radical subtotal gastrectomy for cure, distal lesions. 2. Radical total gastrectomy for proximal lesions. Half of those oper- ated on are resectable. 3. Chemotherapy reserved for unresectable or recurrent disease (no impact on survival). 4. Gastrojejunostomy for palliative bypass in unresectable disease. 5. Radiotherapy to control pain and bleeding in unresectable cases. |
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Symptoms
Crampy abdominal pain, vomiting, obstipation, distention, failure to pass flatus. |
SMALL INTESTINE
A. Obstruction Description Can be classified into: • Simple—no vascular compromise. • Strangulating—vascular obstruction. • Paralytic ileus—impairment of muscle function, closed-loop block- age at two points. Can be caused by adhesions (70%), hernia (8%), tumor (9%), inflammatory disease (4%), volvulus, or intussusception. SMALL BOWEL OBSTRUCTION • Adhesions • Malignancy • External hernia • Volvulus • Crohn’s disease • Intra-abdominal abscess • Intussusception • Radiation stricture • Foreign body • Gallstone ileus |
Diagnosis
High-pitched bowel sounds on physical examination. Peritoneal signs signify peritonitis secondary to strangulation and/or perfora- tion. X-ray: distended small-bowel loops in stepladder pattern, air–fluid levels. Small bowel follow-through and CT scan may delineate the point of obstruction. Treatment Steps 1. Nonsurgical management for partial small bowel obstruction (SBO), which includes replacing electrolyte losses, intravenous fluids, nothing by mouth (NPO), and often nasogastric tube de- compression. 2. Consider trial of long-tube decompression. Uncommonly used secondary to risk of perforation or intussusception. 3. Complete SBO––surgery as needed. 4. Operative therapy: exploratory laparotomy with lysis of adhesions and small bowel resection if indicated. 5. Septrafilms (hyaluronic acid) can be used to reduce adhesions (by 50%). Results Morbidity—30% (60% with strangulated bowel, 20% with neoplasia, 20% with adhesion and hernia). |
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Symptoms
Bleeding and obstruction. Weight loss in nearly all malignant tu- mors. Carcinoid syndrome (flushing, pain, diarrhea, bronchocon- striction, valvular disease) from release of vasoactive substances from metastatic carcinoid tumors. |
SMALL INTESTINE
Neoplasms Description Jejunum and ileum, 5% of all tumors of GI tract. Benign are more common. Most are asymptomatic; 10% become symptomatic. Benign Tumors—Leiomyomas (18–20%), lipomas (15%), neurofi- bromas (10%), adenomas (15%), polyps (15%), hemangiomas (13%), fibromas (10%). Malignant Tumors—Adenocarcinomas (30–50%), lymphomas (15%), leiomyosarcomas (20%), carcinoids (30–50%). Less than 5% metastatic tumors (melanoma, gastric carcinoma). |
Diagnosis
Often made at time of laparotomy. Bowel obstruction with no previ- ous surgery is suspicious for neoplasm. Small-bowel series (entero- clysis is most sensitive). Endoscopy (procedure of choice with duo- denal neoplasms). Arteriography (useful with vascular neoplasms: hemangiomas). CT/MRI may complement staging. Biochemical analysis of urine samples (5-hydroxyindoleacetic acid in carcinoid tumors). Treatment Steps 1. Wide resection. 2. Bypass for palliation. |
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Symptoms
Obstruction due to stricture, bleeding from ulcerated mucosa, necrosis with perforation, fistula formation, abscess formation |
SMALL INTESTINE
Radiation Injury Description Pathogenesis involves progressive obliterative vasculitis. May be diag- nosed many years remote from time of radiation therapy. |
Treatment Steps
1. Avoid surgery if possible. (Total parenteral nutrition [TPN] used with severe symptomatic disease, poor nutritional status.) Mini- mal dissection. 2. Resection or bypass with wide margins. May need to exteriorize if bowel viability is in question. |
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Symptoms
May mimic appendicitis if Meckel’s diverticulitis is present. Bleeding (more common in children). Intestinal obstruction from intussusception (more common in adults). |
Meckel’s Diverticulum
Description Congenital anomaly, persistent omphalomesenteric duct. A true di- verticulum found on the antimesenteric border. Found in 2% of the population. Two feet from ileocecal valve; 2 inches long. May con- tain heterotopic tissue (pancreas, gastric mucosa, other types). Four percent symptomatic, usually in childhood MECKEL’S DIVERTICULUM “RULE OF TWOS” • 2% of population • 2 feet from ileocecal valve • 2 inches long • 2 types of heterotopic tissue (pancreas, gastric mucosa) • Shaped like a 2 • 2x more common in males • 2% symptomatic |
Diagnosis
X-ray and small-bowel series unreliable. Technetium scan will local- ize heterotopic gastric mucosa, if present (accuracy, 90%). Treatment Steps 1. Surgical resection (with GI bleeding, excise diverticulum with suf- ficient margin of ileum to encompass ulceration). The contralat- eral ileal wall is usually the source of the bleeding and therefore, a wedge resection is not appropriate. 2. Incidental finding at laparotomy: leave alone. |
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Symptoms
Crampy abdominal pain, diarrhea, nausea and vomiting, fear of eating, weight loss. Diagnosis Physical Examination—Abdominal mass right lower quadrant. Check for other sites of disease (e.g., perianal area for fistula). Endoscopy—Reddened mucosa, skip lesions. Biopsy. Small Bowel Series—String sign, fistulas. Thickened bowel wall. |
Crohn’s Disease
Description Chronic inflammatory disease of the GI tract. There are three types: inflammatory, fibrostenotic, and fistulizing. Unknown cause. Peak age of onset is between second and fourth decades. Transmural in- volvement of bowel wall, noncaseating granulomas, aphthous ulcers, malignant potential, extraintestinal manifestations are common. Ob- struction and perforation with abscess and fistula formation. Skip le- sions. Seventy percent progress to operation for complications of the disease. Anal manifestations of the disease are common. |
Treatment Steps
Medical Therapy—Antibiotics, steroids, sulfasalazine, 5-aminosali- cyclic acid (ASA), immunosuppressive agents (6-mercapto- purine, azathioprine), bowel rest, central hyperalimentation. Surgical Therapy—(Use eventually required in 75%). Indications: failure of medical therapy or complications of the disease. Surgery: excision, bypass, stricturoplasty. Contraindications to stricturoplasty are fistula, open perforation, abscess, associated inflammatory mass. Recurrence—(40% within 5 years, 60% within 10 years, 75% within 15 years). The major problem in surgical treatment. |
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Symptoms
Right-Sided Lesions—Dull abdominal pain, occult bleeding. Left-Sided Lesions—Change in bowel habits, visible blood, change in stool caliber. Rectal Lesions—Tenesmus, incomplete evacuation, blood-streaked stool. |
Carcinoma of the Colon and Rectum
Description Second most common malignancy. Pathogenesis unclear. Likely en- vironmental influence. Diets high in fat, low in fiber: higher inci- dence. Other risk factors (25%): first-degree relatives, inherited ge- netic syndrome, prior colorectal cancer or adenomatous polyp, inflammatory bowel disease, hereditary nonpolyposis colorectal can- cer (HNPCC) or Lynch syndrome, familial polyposis coli. Seventy- five percent have no specific risk factors. The sigmoid colon in the most common primary site and the liver, the most common site of metastasis. Screening: digital examination, stool for occult blood, sigmoidoscopy, colonoscopy. |
Diagnosis
Digital examination, barium enema, colonoscopy, CT scan, endorec- tal ultrasound, liver function tests, CXR. Carcinoembryonic antigen level (provides a baseline level for future comparison). Screen 50 years or older annually for fecal occult blood and every 5 years with flexible sigmoidoscopy, or colonoscopy every 10 years. Treatment Steps Operative excision with adequate margins. Rectal carcinoma: level of resection depends on location of tumor. Lesions < 8 cm from anal verge may need abdominoperineal resection; > 8 cm, low anterior resection. Adjuvant therapy in colorectal cancer: (1) for stage 2 and 3 rectal cancer, 5-fluorouracil (5-FU) and postoperative radiation therapy; (2) no role for radiation therapy in colon cancer. Addi- tional chemotherapy is appropriate for stage 3 and 4 colon cancer. |
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Symptoms
Blood per rectum, minimal pain. |
Diverticulosis
Description Colonic outpouching from bowel wall. Males and females equal inci- dence. Sixty-five percent of population by age 85. Bleeding occurs in 15%. Hemorrhage arises in right colon in 70–90%. Seventy percent stop bleeding spontaneously; 30% have recurrent bleeding. |
Diagnosis
Endoscopy, bleeding scan, arteriography. Treatment Steps (Lower GI Bleed or Diverticulosis) 1. Selective infusion of vasopressin or rarely angioembolization. 2. Segmental colonic resection if bleeding site is localized. 3. Subtotal colectomy if bleeding not localized. |
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Symptoms
Left lower quadrant (LLQ) pain, anorexia, nausea and vomiting, fever, abdominal mass. |
Diverticulitis
Description Inflammation of diverticulae. Limited to sigmoid colon in 90%. Inflammation is usually contained by pericolic fat and mesentery. |
Diagnosis
Clinical presentation, CT scan. Barium enema and colonoscopy only after acute inflammation lessened (usually > 1 week following acute episode). Treatment Steps 1. Bowel rest, antibiotics, intravenous fluids, analgesia. 2. If there is an abscess, CT-guided drainage. 3. Elective surgical resection in young, diabetic, immunocompro- mised, or one prior episode of diverticulitis. Surgical resection when inflammation has subsided (approximately 8 weeks follow- ing recent attack). 4. Operations for diverticular disease: One-Stage Procedure—Resection and primary anastomosis. Two-Stage Procedure—Hartman operation (sigmoid resection, and decending colostomy, mucous fistula or leaving a rectal stump as a “Hartman’s pouch”). Operating room sigmoid resection, pri- mary anastomosis, and proximal diverting colostomy. Three-Stage Procedure—Colostomy and drainage. Subsequent resec- tion as a second procedure. Subsequent takedown of colostomy and primary ananstomosis. This series of procedures is uncom- monly done secondary to prolonged hospital stay, increased morbidity and mortality. |
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Symptoms
Bloody diarrhea, fever, crampy abdominal pain, tenesmus, urgency, incontinence. |
Ulcerative Colitis
Description Mucosal inflammation, crypt abscesses, mucosa sloughs, colon becomes shortened. Two peaks in incidence: second and sixth decades Can involve rectum alone or entire colon. Malignant potential in- creases with time (2–5% at 10 years, then 1% 1 year thereafter). Ex- traintestinal manifestations (arthralgias, ankylosing spondylitis, sclerosing cholangitis, and liver dysfunction, uveitis, nephrolithiasis). |
Diagnosis
Endoscopy—Friable, erythematous mucosa. Barium Enema—Loss of haustral markings, stricture, stovepipe colon. Treatment Steps Medical—Intravenous fluids, NPO, steroid enemas, correct elec- trolyte abnormalities, sulfasalazine. Surgery—Reserved for treatment of complications (hemorrhage, perforation, toxic megacolon, carcinoma, intractability). Total proctocolectomy with ileostomy. Proctocolectomy with ileoanal anastomosis (ileal J pouch). |
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Symptoms
Bleeding, pruritus ani, pain (secondary to thrombosis). |
Hemorrhoids
Description Internal hemorrhoids above dentate line. External below dentate line. Location of internal hemorrhoids: right anterior, right posterior, left lateral. Causes: Hereditary, straining, portal hypertension,and pregnancy. |
Diagnosis
Physical examination, anoscopy. Treatment Steps 1. Medical symptomatic relief (high-fiber diet, stool softeners, bulk agents [psyllium]). 2. Rubber band ligation. Contraindication to banding—presence of foreign material (e.g., breast or penile implant, or pacemaker). 3. Surgical excision. Indication for surgical hemorrhoidectomy— SURGICAL PRINCIPLES Colon, Rectum, Anus 502 ULCERATIVE COLITIS VS. CROHN’S DISEASE OF THE COLON Ulcerative Colitis Crohn’s Disease Rectum Involved Spared in 25% Colon Begins in rectum with proximal Neocolonic pattern frequent spread Ileum Rarely involved Commonly involved as “skip lesions” Mucosal involvement Circumferential Patchy, segmental cram facts Ustage 4 hemorrhoids that fail conservative therapy. Contraindica- tion to surgical hemorrhoidectomy—inflammatory bowel disease, suspicion of neoplasm. 4. Anal dilatation. Uncommonly done secondary to incontinence issue |
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Symptoms
Exquisite pain, painful defecation, blood on toilet paper. Diagnosis Sentinel pile, painful digital examination, endoscopy when acute episode resolved. |
Anal Fissure
Description Superficial linear ulceration in the posterior midline. Sentinel pile (skin tag), seen in chronic fissures. Ulceration occurs in the squa- mous epithelium; therefore, very painful. Straining at stool. Consti- pation. Condition is cyclic. Secondary anal fissures occur secondary to inflammatory bowel disease, malignancy, acquired immune deficiency syndrome (AIDS), syphilis, tuberculosis |
Treatment Steps
1. Acute fissure is treated nonsurgically. Chronic fissure is treated operatively with consideration for biopsy. 2. Local cleansing agents. 3. Sitz baths. 4. Topical ointments. 5. Stool softeners. 6. Anal dilatation. 7. Lateral internal sphincterotomy (open or closed). |
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Symptoms
Pain, anorexia, vomiting, diarrhea, cutaneous hyperesthesia, guarding and rebound at McBurney’s point, Rovsing’s sign, psoas sign, obturator sign, Blumberg’s sign. |
APPENDIX––APPENDICITIS
Description Appendix: variable location in relation to the cecum. Teniae con- verge on appendix. Closed-loop obstruction of lumen, vascular con- gestion, serosal inflammation, perforation. |
Diagnosis
Physical examination. Fecalith in right lower quadrant (RLQ) is di- agnostic, altered right psoas shadow. Leukocytosis (may be absent). Ultrasound and CT scan useful in equivocal cases. However, use clin- ical judgment. If appendicitis is still clinically suspected despite negative lab or radiologic workup, seek surgical opinion. Treatment Steps 1. Intravenous fluids and antibiotic therapy. 2. Appendectomy (open or laparoscopic). Normal appendix is re- moved as an incidental finding of malrotation or if an explo- ration is done for possible appendicitis (to avoid future confusion over the diagnosis). |
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Symptoms
Right upper quadrant (RUQ) or epigastric pain. Pain radiates to tip of scapula. Nausea and vomiting. |
Acute Cholecystitis
Description Bacterial or chemical inflammation of the gallbladder. Cystic duct obstruction and altered bile chemistry are two conditions necessary to cause acute cholecystitis. Occurs in the 4th to 8th decade. Inci- dence higher in females. Obstruction of the cystic duct. Bacteria in 50–75% (Escherichia coli, Klebsiella, Enterobacter). |
Diagnosis
Physical examination: Murphy’s sign. Mild jaundice. Ultrasound is the most sensitive and specific diagnostic test to detect stones and surrounding inflammation, and can provide other anatomic infor- mation in the hepatobiliary system. Hepatoiminodiacetic acid (HIDA) scan 90% accurate (normal HIDA, gallbladder fills in 30 minutes). Treatment Steps Antibiotics. Cholecystectomy, delayed or immediate. Percutaneous cholecystostomy in poor-risk patients. Not to be performed in the presence of gallbladder gangrene or perforation (Fig. 18–2). Variant forms: empyema of gallbladder, gangrene, acalculous cholecystitis |
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Signs and Symptoms
Pain in RUQ and epigastric pain. May radiate to tip of scapula. Nausea and vomiting. Attacks often follow large meals. |
Chronic Cholecystitis
Description Repeated attacks of acute cholecystitis. Stones almost always present. |
Diagnosis
Physical examination. Ultrasound to identify stones. Oral cholecys- tography if symptoms are typical but ultrasound negative. Endo- scopic retrograde cholangiopancreatography (ERCP) to identify cholesterol crystals if other tests negative and symptoms persist Treatment Steps Laparoscopic cholecystectomy for routine management. An open cholecystectomy is indicated in cases of cirrhosis, bleeding disorders, pregnancy, gallbladder cancer, and severe cardiopulmonary disor- ders. |
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Symptoms
Fever and chills, jaundice, biliary colic (Charcot’s triad). Severe: additional hypotension and mental confusion (Reynolds’ pentad). |
Cholangitis
Description Infection in the biliary tree. Bacteria (commonly E. coli, Klebsiella, Enterococcus), obstruction, increased pressure. Most commonly associated with choledocholithiasis. |
Diagnosis
Clinical presentation. RUQ tenderness. Elevated white blood cell count, bilirubin, and alkaline phosphatase. Ultrasound of RUQ to document gallstones. CT scan to rule out periampullary malignancies or liver abscesses. Treatment Steps Antibiotics. Triple antibiotics if severe (60% of cases with multiple organisms). Endoscopic sphincterotomy with stone extraction. Ex- ploratory laparotomy, cholecystectomy with common bile duct exploration and T-tube drainage. |
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Symptoms
Pain in RUQ. Distention. Nausea. Vomiting. Colicky abdominal pain. |
Gallstone Ileus
Description Antecedent cholecystointestinal or choledochointestinal fistula. Gallstone obstructs at intestinal narrowing (usually in distal ileum). Occurs more likely in the elderly (70s) and is four times more com- mon in women. Less commonly Bouveret’s syndrome (stone enters and obstructs the duodenum). Gallbladder carcinoma occurs in 15% of those with gallstone ileus. |
Diagnosis
Air in biliary tree (pneumobilia) occurs in 40%. Dilated small-bowel loops. Opaque stone in the intestinal tract (15–20%). Nonopaque stone in intestinal tract identified by ultrasound. Treatment Steps 1. Fluid resuscitation, correction of electrolyte abnomalities, naso- gastric decompression, antibiotic prophylaxis. 2. Exploratory laparotomy, enterotomy proximal to the impacted stone with removal of the stone. Repair of biliary–enteric fistula. 3. Cholecystectomy if medically stable. |
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BILIARY OBSTRUCTION
differential diagnosis |
• Gallstones
• Benign strictures • Malignant strictures • Pancreatitis • Extrinsic compression • Obstructed biliary stents |
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Symptoms
Nonspecific. Pain. Weight loss. Jaundice. Anorexia. RUQ mass. |
Gallbladder Carcinoma
Description Most common malignancy of biliary tract. Association with gall- stones (95%, particularly larger ones), porcelain gallbladder (calci- fied wall, should have cholecystectomy even if asymptomatic), biliary adenoma, biliary infection with Salmonella. Adenocarcinoma in 82%. More common in females. One to two percent undergo cholecystec- tomy. Tends to be diagnosed in advanced stage. Seventy percent have liver metastases at the time of diagnosis. |
Diagnosis
Advanced disease: CT scan. Curable, localized disease found at time of cholecystectomy. Treatment Steps If tumor localized to mucosa and submucosa, cholecystectomy. Serosal or lymph node involvement: cholecystectomy with node re- section and hepatic wedge resection. If N2 nodes (peripancreatic, duodenal, portal, celiac, or superior mesenteric artery [SMA]) are present, do not proced with resection. Results: overall 5-year survival rate, 2–5%. |
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Symptoms
Pain, distention, weight loss, fatigue, anorexia, fever, jaundice, ascites. Diagnosis The tumor marker, α-fetoprotein (AFP) is elevated (although fibro- lamellar type seen in younger patients, it is not associated with AFP elevation). CT scan with or without percutaneous biopsy. Arteriogra- phy. Intraoperative ultrasound. |
Hepatocellular Carcinoma
Description More common in Africa and Asia. Risk factors include: cirrhosis, hepatitis B, hemochromatosis, schistosomiasis, aflatoxin, and α1- antitrypsin deficiency. Eighty percent of primary liver tumors. Very often presents in advanced stage. |
Treatment Steps
1. Only 25% are resectable (5-year survival rate: 18–36%). Can re- move up to 80% of liver. 2. Transplantation. 3. Palliation: intra-arterial chemotherapy, hepatic artery ligation. 4. Cryoablation developing as alternative to resection. |
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Symptoms
Fever, malaise, chills, anorexia, weight loss, abdominal pain, RUQ tenderness, jaundice, hepatomegaly Diagnosis Leukocytosis (very high); CXR: atelectasis, pneumonia, effusion (all right-sided), CT scan, ultrasound, arteriography. |
Pyogenic Liver Abscess
Description Follows an acute abdominal infection. Routes: portal system, ascen- sion from the biliary tree, hepatic artery, direct extension, trauma. Untreated, 100% mortality rate; treated, 20% mortality rate. Right lobe more common. Solitary or multiple. Bacteria: E. coli, Klebsiella, enterococcus, bacteroides. May rupture into adjacent peritoneal, pericardial, or thoracic cavities. |
Treatment Steps
1. Eliminate abscess and underlying cause. 2. Percutaneous drainage if single. 3. Operative drainage if multiple or multilocated abscess. 4. Long-term antibiotics, especially for multiple small hepatic ab- scesses. |
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Symptoms
Recent diarrheal syndrome in minority. Similar to pyogenic abscess. |
Amebic Liver Abscess
Description Prevalence higher in tropical zones, travelers to tropical countries. More common in males, peak incidence fourth decade. Spread by fecal–oral route of E. histolytica. Typically reaches the liver by way of the portal vein from intestinal amebiasis. Only 5% of people in- fected with amebiasis develop liver abscess. Ninety percent in right lobe. May grow to large size. History to separate from hydatid cyst. Amebic abscess fluid looks like anchovy paste. |
Diagnosis
Serum antibody for E. histolytica (indirect hemagglutinin test). Only one-third have positive amebic stool cultures. Treatment Steps 1. Metronidazole 750 mg by mouth, three times a day for 10 days. 2. Operative treatment reserved for rupture. 3. Percutanous drainage may be considered. In cases of abscess re- fractory to Flagyl, large left liver lobe abscess, bacterial contami- nation (10–15%). There is danger of anaphylaxis from spillage with open drainage of cyst. |
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Symptoms
Ascites. Hepatic encephalopathy, hypersplenism, hemorrhoids, ca- put medusa, esophageal variceal bleed. Stigmata of cirrhosis: spider angiomata, palmar erythema, testicular atrophy, gynecomastia, hepatomegaly. Jaundice. |
PORTAL HYPERTENSION/ESOPHAGEAL
VARICEAL BLEEDING Description Present when portal venous pressure exceeds 15 mm Hg. Collaterals between portal and systemic venous circulations lead to splenic varices, hemorrhoids, and esophageal varices. Commonly associated with cirrhosis (United States) and schistosomiasis (worldwide). |
Diagnosis
Liver function tests, liver biopsy, hepatitis profile, endoscopy if bleeding. Treatment Steps Acute variceal bleed (50% mortality): 1. Injection sclerotherapy by way of esophagogastroduodeno- scopy (EGD); 90% initial success. 2. Vasopressin infusion or octreotide (somatostatin) infusion. 3. Balloon tamponade (Sengstaken–Blakemore tube). 4. Transjugular intrahepatic portosystemic shunt (TIPS). 5. Emergency portosystemic shunt. Shunt procedures: 1. End-to-side and side-to-side shunts are nonselective and are as- sociated with encephalopathy. 2. Selective shunts (e.g., distal splenorenal Warren shunt) is asso- ciated with cirrhosis. Prophylactic treatment: β-blocker (propranolol) long-term prophy- lactic medication in portal hypertension (HTN) to prevent esophageal varices from bleeding. |
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Symptoms
Epigastric and back pain, fever, tachycardia, hypotension, nausea, vomiting, epigastric tenderness, flank ecchymosis (Grey–Turner’s sign), periumbilical ecchymosis (Cullen’s sign). |
Acute Pancreatitis
Description Inflammation from escape of active pancreatic enzymes. Eighty per- cent due to alcohol and biliary disease (predominantly gallstones). Trauma, hyperlipidemia, hypercalcemia, pancreas divisum. Also caused by scorpion, Ascaris, or Clonorchis sinensis. Drugs causing pan- creatitis: azithioprine, furosemide, Tylenol/flagyl/Zantac, ery- thromycin/tetracycline. Ninety percent mild cases; 10% life-threatening. RANSON’S CRITERIA (PREDICTING THE SEVERITY OF ACUTE PANCREATITIS) On Admission W WBC > 16,000/mm3 A Age > 55 yr G Glucose > 200 mg/dL A AST > 250 IU/dL L LDH > 350 IU/L At 48 Hours B Base deficit > 4 mEq/L E Estimated fluid gain > 6 L C Calcium < 8 mg/dL H Hct fall > 10% U Urea rise > 5 mg/dL P PaO2 < 60 mm Hg |
Diagnosis
Serum amylase and lipase, hypocalcemia, hyperbilirubinemia, leuko- cytosis, CT scan (dynamic angio-CT also measures amount of pan- creatic necrosis). CT-guided fine-needle aspiration (FNA) differenti- ates infected compared to sterile pancreatic necrosis. Upper gastrointestinal (UGI) series, sentinal loop on plain film abdomen, ultrasound of biliary tree. Treatment Steps 1. Bowel rest, NPO, intravenous fluids, analgesia, nasogastric tube, antibiotics. Antibiotics especially if pancreatic necrosis is present. 2. TPN for prolonged cases. 3. ERCP and endoscopic sphincterotomy to treat gallstone pancre- atitis. 4. Surgery: correct biliary disease (e.g., cholecystectomy for gall- stone pancreatitis); reserved for complications of pancreatitis (abscess, ascites, hemorrhagic, pseudocyst). Pancreatic debride- ment and open packing/closed lavage for pancreatic necrosis; 50% develop infection and mostly with gram-negative rod bacteria. |
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Symptoms
Epigastric and back pain, anorexia and weight loss, pancreatic insuf- ficiency with malabsorption, steatorrhea, possibly diabetes. |
Chronic Pancreatitis
Description Recurrent abdominal pain of pancreatic origin. Irreversible damage. Exocrine and endocrine insufficiency. Most often alcohol related (70%). Ten-year survival rate only 43%. |
Diagnosis
Clinical findings: Plain Films—Pancreatic calcifications. CT Scan—Calcifications, size of pancreas. ERCP—Identify ductal abnormalities (“chain of lakes”). SMA and Celiac Arteriogram—Pseudo-aneurysm with or without splenic/portal vein thrombosis. Treatment Steps 1. Analgesia, correct exocrine and endocrine function. 2. Surgery: indications: intractable abdominal pain, local complica- tions, main duct stenosis, pancreas divisum, rule out malignancy. Ampullary procedures; transduodenal sphincteroplasty. 3. Ductal drainage procedures: side-to-side pancreaticojejunostomy (Puestow procedure). |
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Symptoms
Jaundice, weight loss, abdominal pain, pain in epigastrium and back, palpable gallbladder (Courvoisier’s sign). Diagnosis Liver function tests (LFTs) reflect ductal obstruction. Elevated carci- noembryonic antigen (CEA), CA 19–9, occult blood in stool. CT scan to evaluate size of tumor and relation to surrounding structures (Fig. 18–3), ERCP or percutaneous transhepatic cholangiography, arteriog- raphy (define anatomy/resectability), percutaneous biopsy. Prognos- tic factors in pancreatic carcinoma include lymph node status, margin involvement, vascular invasion, and need for blood transfusion. |
Pancreatic Carcinoma
Description Ninety percent duct cell adenocarcinoma (remainder are cystade- noma and acinar cell carcinoma); 65% arise in pancreatic head. Pre- sent in advanced stage. Fifth leading cancer-related death. Other risk factors include advanced age, smoking, diabetes, alcohol abuse, exposure to benzidine, naphthylamine, and partial gastrectomy. |
Treatment Steps
Resection for cure, if possible: pancreaticoduodenectomy. Five-year survival rate, 15–35%. Bypass for palliation: choledochojejunostomy, gastrojejunostomy. Adjuvant chemo- and radiation therapy improve survival. CONTRAINDICATIONS FOR PANCREATIC RESECTION • Liver or peritoneum involvement • Periaortic lymph node metastasis • Celiac lymph node metastasis • SMA and superior mesenteric vein (SMV) tumor involvement |
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Whipple’s
triad. Fasting hypoglycemia (insulin:glucose ratio > 0.3). Elevated C- peptide and proinsulin. |
Insulinoma
Most common. β-cell origin. Equal distribution throughout the pan- creas. Eighty percent solitary benign; 10% malignant. Whipple’s triad. Fasting hypoglycemia (insulin:glucose ratio > 0.3). Elevated C- peptide and proinsulin. |
Preoperative localization: CT scan localizes tu-
mors > 1 cm. Arteriography. Intraoperative ultrasound used in local- ization. Resection is curative for large lesions, and enucleation also adequate for small lesions. Debulk for palliation. Medical therapy: diazoxide. |
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Hypergastrinemia and PUD (especially in
unusual locations). Zollinger–Ellison syndrome. Elevated fasting gas- trin and secretin stimulation test. |
Gastrinoma
Second most common. Hypergastrinemia and PUD (especially in unusual locations). Zollinger–Ellison syndrome. Elevated fasting gas- trin and secretin stimulation test. Fifty percent malignant. |
Resection
for cure. Preoperative localization. Explore if localization attempts fail. Eighty percent of lesions found in the gastrinoma triangle (boundaries are: cystic–common bile duct, second to third part of duodenum, and neck–body junction of the pancreas). Somatostatin and high-dose omeprazole for treatment |
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Elevated plasmin glucagon is diagnostic. Hyperglycemia. Necrolytic migratory erythema.
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Glucagonoma
From α cells. Mainly in the body and the tail of the pancreas. Ele- vated plasmin glucagon is diagnostic. Hyperglycemia. Majority are malignant. Necrolytic migratory erythema. |
Present in advanced
stage. Resect for cure. Debulk for relief of symptoms. |
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Watery Diarrhea,
Hypokalemia, Achlorhydria, or Verner–Morrison |
VIPoma (Vasoactive Intestinal Polypeptide
Tumors) or WDHA Syndrome (Watery Diarrhea, Hypokalemia, Achlorhydria, or Verner–Morrison Syndrome) |
Fifty percent have metastasis at presentation, and treatment is subto-
tal pancreatectomy if no tumor found in the presence of the syndrome. |
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Symptoms
Nonspecific abdominal pain. Left upper quadrant (LUQ) pain. Pain referred to left shoulder (Kehr’s sign). |
SPLEEN
A. Trauma Description Most commonly injured organ in blunt trauma. Associated with left chest rib fractures. |
Diagnosis
Clinical suspicion (e.g., multiple left-sided rib fractures). Gross blood on diagnostic peritoneal lavage. Focused abdominal sonogra- phy for trauma (FAST) is frequently the first study done on a trauma patient with a suspected splenic injury. CT scan findings in stable pa- tients. Treatment Steps Splenectomy. Splenic salvage in appropriate cases. Nonoperative therapy in children. Vaccinate the splenectomy patient against Haemophilus influenzae B, pneumococcus, and meningococcus (en- capsulated organism). |
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Symptoms
Spontaneous bleeding. Spleen normal size or small. |
Immune Thrombocytopenic Purpura
Description Persistently low platelet count. Antiplatelet factor (circulating im- munoglobulin G [IgG]) directed against a platelet antigen. Majority are young women. Childhood cases typically occur after a viral ill- ness under age 6. Also associated with human immunodefieciency virus (HIV). |
Diagnosis
Thrombocytopenia, bone marrow aspirate megakaryocytes. Treatment Steps 1. Steroids, response in 3–7 days. Complete remission with steroids is rare. 2. IV gamma globulin (1–2 g/kg), plasmapheresis. 3. Elective splenectomy, when refractory to medical management (75% of cases), i.e., persistent thrombocytopenia (platelets < 80,000) or recurrence after tapering or discontinuation of steroids. 4. Emergent splenectomy with central nervous system (CNS) bleeding. 5. Laparoscopic splenectomy is an option. |
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Symptoms
Asymptomatic lymphadenopathy, night sweats, weight loss, pruritus, malaise. |
Hodgkin’s Disease
Description Malignant lymphoma; Reed–Sternberg cells; asymptomatic lym- phadenopathy: cervical (70%), axillary, inguinal. Four pathologic subtypes: lymphocyte predominance (best prognosis), nodular scle- rosis (most common), mixed cellularity, lymphocyte depletion (worst prognosis). Metastasize in predictable patterns (spread via lymphatics). |
Diagnosis
Hematologic tests, bone marrow aspirate, LFTs, CT scan abdomen and chest, CXR, lymph node biopsy, lymphangiogram. Staging lap- arotomy: splenectomy, liver biopsy (bilateral), lymph node sampling, oophoropexy. Bilateral bone marrow biopsy from the iliac crest. In women of childbearing years, fix ovary to the pelvic wall or behind uterus to protect it from radiation. Treatment Steps 1. Radiation (all stages). 2. Chemotherapy (stage III A or above). 3. Staging laparotomy: when result may change therapy. It is contro- versial and mainly for stages I and II. Improved imaging and liberal use of chemotherapy has made staging laparotomy less common. |
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Two-thirds have asymptomatic lymphadenopathy.
Onset may be in extranodal site (e.g., gastric non-Hodgkin’s lym- phoma). May appear as asymptomatic splenomegaly. Constitutional symptoms commonly present. |
Non-Hodgkin’s Lymphoma (NHL)
Clinical course and natural history more diverse than Hodgkin’s. Usu- ally older patients are more common than with Hodgkin’s disease. Pattern of spread is variable; two grades: high-grade (diffuse) or low- grade (nodular). |
Chemotherapy and radiation therapy. It
is spread via the bloodstream and can present as a superior vena cava (SVC) syndrome, acute spinal cord compression syndrome, central obstruction or meningeal involvement. Indications for splenectomy in NHL are hypersplenism, pancytopenia, symptomatic splenomegaly, and recurrent splenic infarcts. |
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Symptoms
Preceded by upper respiratory infection (URI). Followed by nausea, vomiting, headache, confusion, shock, coma, death within 24 hours. |
Postsplenectomy Sepsis
Description Risk highest for splenectomy for thalassemia and reticuloendothelial (RE) diseases like Hodgkin’s, lowest for trauma and idiopathic thrombocytopenic purpura (ITP). Risk may be as high as 1% per year. Risk greatest for children younger than 4 years, and within 2 years of splenectomy. Fifty percent mortality rate |
Diagnosis
Clinical suspicion. Blood cultures positive for Streptococcus pneumo- niae in 50%. Encapsulated organisms predominate (pneumococci, H. influenzae). Treatment Steps 1. Broad-spectrum antibiotics. 2. Supportive care. 3. Prophylaxis: Pneumovax, prophylactic antibiotics. |
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Symptoms
Pulselessness, pain, pallor, paresthesias, paralysis, and poikilother- mia. |
Arterial Embolism
Description Heart is the source of arterial emboli in 90% (see Cram Facts). Left atrial myxoma (histology of its embolus is diagnostic). Symptoms are acute in onset and occur at bifurcations (femoral bifurcation most common). CARDIAC SOURCES OF EMBOLI • Left ventricular thrombus (post-MI patients) • Left atrium clot (atrial fibrillation) • Valvular disease (prosthetic valve, endocarditis, rheumatic heart disease) with or without right-to-left cardiac shunt • Left atrial myxoma (primary cardiac tumor, no risk factors) |
Diagnosis
Physical examination, duplex scan, arteriography. Treatment Steps 1. Heparinization. 2. Consider thrombolytic therapy (tPA). 3. Embolectomy (does not treat the embolus but prevents further emboli or propagation of thrombosis) can restore flow to tissues. |
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Symptoms
Claudication, rest pain, tissue loss. Leriche syndrome: buttock clau- dication, impotence, diminished femoral pulses, bruit, thrill, eleva- tion pallor, dependent rubor. |
Aortoiliac Occlusive Disease
Description Arteriosclerosis involves arteries singly or in combination. Slow progression of occlusive disease allows for collateral formation. ATHEROSCLEROSIS RISK FACTORS • Cigarette smoking • Diabetes • Hypertension • Hyperlipidemia • Genetics |
Diagnosis
History and physical. Noninvasive tests: ankle–brachial index (Fig. 18–4), pulse volume recording, duplex scan, arteriography. Treatment Steps Medical—Control risk factors, control hypertension, lower choles- terol, stop smoking, cilastozol (Pletal), exercise program. Surgical—Bypass, endarterectomy, angioplasty with or without stent (consider patient’s comorbid factors and location and extent of the lesion in deciding for stent or open procedure). |
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Symptoms
Intact aneurysms are asymptomatic. Expanding or leaking causes back pain and abdominal pain. Pulsatile abdominal mass. |
Abdominal Aortic Aneurysm
Description Typically involve infrarenal aorta, but may extend above renals. Most are fusiform. More degenerative than atherosclerosis. More common in males. (See Fig. 18–5.) ATHEROSCLEROSIS RISK FACTORS • Cigarette smoking • Diabetes • Hypertension • Hyperlipidemia • Genetics |
Diagnosis
Physical examination, calcific outline on plain x-ray, ultrasound, CT scan (Fig. 18–6), arteriography. Treatment Steps 1. Asymptomatic less than 5 cm: observe. 2. Greater than 5 cm: Elective aneurysmectomy with aortobifemoral graft or tube graft. 3. Endovascular repair (stent grafts) undergoing clinical trials. En- dovascular abdominal aortic aneurysm (AAA) repair has more limitations based on anatomic issues. |
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Symptoms
Claudication, rest pain, tissue loss. |
Femoropopliteal Occlusive Disease
Description Arteries involved singly or in combination. |
Diagnosis
Physical examination, noninvasive tests, arteriography Treatment Steps 1. Control risk factors, cilastozol (Pletal), pentoxifylline (Trental), exercise programs. 2. Surgery for disabling claudication, rest pain, or tissue loss. |
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Symptoms
Transient ischemic attacks (amaurosis fugax), stroke, vertebral–basi- lar insufficiency (ataxia, vertigo, diplopia), diminished pulses, bruits. |
Cerebrovascular Disease
Description Lesions of the extracranial cerebral vessels. Decreased cerebral per- fusion from occlusive lesions, thrombosis, or embolization. Majority due to thromboembolic etiologies. |
Diagnosis
Duplex scan, arteriography (Fig. 18–7). Angiogram can be done as an intervention, but CT or magnetic resonance angiography is possi- ble without the risks of an invasive procedure. Treatment Steps 1. Medical therapy. Antiplatelet agents (aspirin, persantine, ticlopide). 2. Endarterectomy. 3. Carotid balloon angioplasty with stenting undergoing clinical trials. |
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Symptoms
Asymptomatic in 50%, swelling, tenderness, Homan’s sign (calf pain with dorsiflexion of foot). Phlegmasia alba dolens: milk leg. Phlegmasia cerulea dolens: venous gangrene |
Deep Vein Thrombosis (DVT)
Description Those at risk: elderly, bedridden, hip replacement and other ortho- pedic procedures, pelvic and abdominal procedures, trauma, malig- nancy, and estrogen therapy. Virchow’s triad: stasis, intimal damage, hypercoagulability. |
Diagnosis
Duplex scan, venography, impedance plethysmography, fibrinogen scan (best study for calf DVT). Prophylactic Measures 1. Early ambulation postoperatively. 2. Low-dose subcutaneous heparin or enoxaparin/low-molecular- weight heparin. 3. Elastic compression stocking or intermittent pneumatic compres- sion device. Treatment Steps 1. Bed rest (for iliofemoral DVT or extensive clot burden). 2. Thrombolytic therapy with iliofemoral DVT. 3. Gradient compressive hose. 4. Inferior vena cava (IVC) filter if failure of anticoagulation or con- traindications or complications from anticoagulation. 5. Venous thrombectomy (and fasciotomies for compartment syndrome in cases of severe compromise). Very uncommon. MEDICATIONS FOR DVT • Unfractionated heparin (maintain partial thromboplastin time 1.5 × control) or • Low-molecular-weight heparin (once or twice daily subcutaneous injection) and • Warfarin (Coumadin) orally for long-term treatment |
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Symptoms
Dull ache, feeling of leg heaviness relieved by elevation. Dilated veins along anatomic distribution of greater and lesser saphenous veins. May be accompanied by signs of chronic deep venous disease. |
Varicose Veins
Description Dilated, tortuous veins in the leg. Primary—Normal deep system. Secondary—Diseased deep system. |
Diagnosis
Clinical examination, Trendelenburg test, duplex scan, Perthes’ test. Treatment Steps 1. Support hose. 2. Sclerotherapy. 3. Ligation and stripping. |
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Description
Inflammation and thrombosis of vein, pain, swelling, warmth. |
Superficial Thrombophlebitis
Mondor disease is superficial thrombophlebitis of the thoracoepigastric veins of the anterior chest wall or breast. Migratory thrombophlebitis is associated with pancre- atic carcinoma. |
Treat
with hot compresses, leg elevation, analgesics, excision of vein if pu- rulent, systemic anticoagulation if process extends to deep venous system, or ascending superficial thigh. |
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Symptoms
Pain, groin mass. |
Indirect Hernia
Description Fifty percent of all hernias. Congenital defect. Patent processus vagi- nalis. Lateral to inferior epigastric vessels. Chronic intra-abdominal pressure elevation. Rule out colon disease, prostate (strain to void), or pulmonary (chronic cough). |
Diagnosis
Physical examination. Reducible or irreducible; incarcerated or strangulated. Treatment Steps 1. High ligation of sac. Close defect in transversalis fascia. 2. Laparoscopic hernia repair also an option. 3. If incarcerated or strangulated, open abdomen (midline inci- sion) |
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Description
Weakness in the inguinal floor (Hesselbach’s triangle). Most com- mon in elderly or young heavy lifters. |
Direct Hernia
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Treatment Steps
1. Cooper’s ligament repair. 2. Mesh repair (open versus laparoscopic) also an option. |
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Symptoms
Fever, pain, erythema, drainage, swelling. |
WOUND INFECTIONS
Description Usually caused by break in sterile technique, carrier in operating room, ruptured viscus, large wound inoculum. Local factors: devital- ized tissue, foreign body, hematoma, seroma. Systemic risk factors: age, steroids, immunosuppression, diabetes, obesity, length of operation, and blood transfusion |
Diagnosis
Physical examination, cultures. Treatment Steps 1. Drainage. 2. Debridement. 3. Antibiotics. |
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Symptoms
Heat intolerance, sweating, insomnia, muscle weakness, weight loss, nervousness, irritability, staring appearance, fine hair or alopecia, exophthalmos, vitiligo, onycholysis. |
Hyperthyroidism
Description Increased levels of thyroid hormone. Loss of normal feedback. Graves’ disease, autoimmune. Thyroid-stimulating immunoglobulins in 90% with Graves’ disease. |
Diagnosis
T4 and T3 levels high. Thyroid-stimulating hormone (TSH) is low. Elevated radioactive iodine uptake. Treatment Steps 1. Antithyroid drugs—propylthiouracil or tapazole, radioiodine (131I). 2. Subtotal thyroidectomy. |
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Symptoms
Compression of neck structures, cough, fullness in neck, neck mass. |
Nontoxic Nodular Goiter
Description Compensatory response to decreased production of thyroid hor- mone, inadequate intake of iodine, medications that impair hor- mone production, enzyme deficiency. |
Diagnosis
Exam, ultrasound of thyroid gland. Increased TSH. Decreased levels of thyroid hormone. Treatment Steps 1. Thyroid hormone replacement. 2. Surgery reserved for compressive symptoms, cosmesis, threat of malignancy |
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Signs & Symptoms
Solitary neck mass most common. Lymphadenopathy. |
Thyroid Carcinoma
Description Low overall mortality. Favorable prognosis for most cell types. Papil- lary, 60–70%. Follicular, 15–20%. Medullary. Anaplastic aggressive. Previous neck irradiation. Best prognosis is papillary. RISK FACTORS FOR THYROID CARCINOMA • Extremes of age • Rapid growth • Local invasion (hoarseness and fixation) • External radiation • Cold hypofunctional nodule + family history (medullary and papillary) |
Diagnosis
Thyroid function tests, thyroid scan, ultrasound, fine-needle aspira- tion, neck exploration. Treatment Steps 1. Surgery: thyroid lobectomy and isthmusectomy, subtotal thy- roidectomy, total thyroidectomy. Procedure depends on cell type and size of tumor. 2. Postoperative thyroid suppression. 3. Radioactive iodine for metastatic disease. |
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Signs and Symptoms
Weakness, anorexia, nausea, constipation, renal colic, renal stones, osteoporosis, osteitis fibrosa cystica, subperiosteal resorption, pancreatitis, gallstones, depression, anxiety. |
PARATHYROID—PRIMARY
HYPERPARATHYROIDISM Description Increase in serum parathyroid hormone. Single or multiple parathyroid adenomas or hyperplasia. |
Diagnosis
Increased serum calcium, decreased serum phosphate. Increased serum parathyroid hormone: carboxyterminal fragment longer half- life, biologically inactive. Chloride-to-phosphate ratio > 33. Localization: CT scan, venous catheterization, and sampling. Thallium-tech- netium subtraction scan. Treatment Steps 1. Surgery: One enlarged gland, remove. 2. Generalized hyperplasia: Remove 3.5 glands or total parathyroidectomy with reimplantation. |
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Symptoms
Hypertension, headache, weakness, polydipsia, edema. |
Primary Hyperaldosteronism
Description Excess aldosterone secretion. No adrenocorticotropic hormone (ACTH) regulation. One percent of all cases of hypertension. More common in women. Adenoma in 75%, hyperplasia in 25%. The most common adrenal tumor is incidental. Surgical resection for any functional tumor or any adreanal tumor ≥ 5 cm. |
Diagnosis
Elevated serum aldosterone levels, decreased serum renin level. Hy- pernatremia, hypokalemia, hypochloremia, alkalosis. Localization: CT scan, MRI, venous catheterization, and sampling. Treatment Steps Adenoma—Surgical removal, adrenalectomy. Hyperplasia—Medical therapy, spironolactone. |
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Symptoms
Change in menstrual cycle, virilization, weight gain, lassitude, mus- cle weakness, psychiatric disturbance, hypertension, edema, purple striae, buffalo hump. |
Hypercortisolism
Description Cushing’s Disease—Pituitary ACTH excess usually from a pituitary adenoma that leads to adrenal hyperplasia. Cushing Syndrome—If due to an adrenal source of cortisol, low ACTH. More common in women, young age. Seventy-five per- cent of adrenal tumors are benign, 98% unilateral. |
Diagnosis
Plasma cortisol levels, low-dose dexamethasone suppression test, uri- nary-free cortisol excretion, ACTH assay, high-dose dexamethasone suppression test, metapyrone test, CT scan. Treatment Steps Cushing’s Disease—Transsphenoidal hypophysectomy. Cushing Syndrome (if caused by adrenal neoplasm)—Adrenalectomy |
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Symptoms
Sustained or paroxysmal hypertension, perspiration, pallor, flushing, palpitation, trembling, weakness, anxiety. |
Pheochromocytoma
Description Catecholamine-producing tumors for amine precursor uptake and decarboxylation (APUD) cells. Neural crest origin. Adrenal medulla or sympathetic system. Of all patients with hypertension, 0.1%. Ma- lignant, 10%; bilateral, 10%; in adrenal or periadrenal area, 90%. |
Diagnosis
Urine for catecholamine metabolites: Vanillylmandelic acid (VMA), normetanephrine, metanephrine. Urinary-free epinephrine and nor- epinephrine. Localization: metaiodobenzylguanidine (MIBG) scan, CT scan. Treatment Steps 1. Surgery: Preparation with α-blocking agent phenoxybenzamine, followed by β blockade (propranolol hydrochloride [Inderal]). 2. Adrenalectomy with careful intraoperative monitoring. |
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Symptoms
Cough, dyspnea, chest or shoulder pain, hoarseness, weight loss, clubbing, hemoptysis. May be asymptomatic |
Lung Cancer
Description Peak incidence 50–70 years. Cigarette smoking, exposure to asbestos, other toxic agents. Cell types: squamous (40–70%), adenocarcinoma (15%), bronchoalveolar (5%), undifferentiated (20–30%). Most common malignancy in males. |
Diagnosis
CXR (Fig. 18–8), sputum cytology, CT scan, bronchoscopy, transpleural needle biopsy, mediastinoscopy, open-lung biopsy. Treatment Steps 1. Thoracotomy with wedge resection. 2. Lobectomy. 3. Pneumonectomy. 4. Radiation. 5. Chemotherapy. |
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Symptoms
Painless lump, nipple discharge, erythema, asymmetry, nipple inver- sion, bone pain, weight loss. Edema of overlying skin (peau d’or- ange); hard, irregular, fixed mass in advanced cases. |
Breast Cancer
Description Most common cancer in females; can occur in males. Risk factors: previous cancer, heredity, early menarche, late menopause. Ductal or lobular accounts for 85%; spreads by lymphatic and hematogenous routes. |
Diagnosis
Liver function tests may be elevated in advanced cases, hypercal- cemia with bone metastasis, CXR, CT scan of abdomen, mammogra- phy (Fig. 18–9), breast biopsy, fine-needle aspiration. Treatment Steps 1. Breast conservation: lumpectomy with axillary dissection, radia- tion therapy; stage I and stage II. 2. Mastectomy. 3. Adjuvant chemotherapy (cylophosphamide, methotrexate, 5-FU). Antiestrogen therapy (tamoxifen). Note: Equivalent survival with modified radical mastectomy (MRM) versus lumpectomy, axillary node dissection, and radiation. |
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Symptoms
Breast pain varying with menstrual cycle. Breast masses may appear in cyclic manner. Tender mass; thickened, nodular areas. |
Mammary Dysplasia
Description Incidence peaks age 35–40. Most common breast complaint. Common cause of breast mass. Atypical hyperplasia premalignant. |
Diagnosis
Physical examination, mammography. Treatment Steps 1. Biopsy dominant masses to rule out carcinoma. 2. Avoid caffeine. 3. Danazol in severe cases. 4. Simple mastectomy with breast reconstruction in severe cases. |
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Symptoms
Asymptomatic mass, found incidentally. Firm, freely movable. |
Fibroadenoma
Description Common cause of breast mass in young women, peak age to 25. May grow to large size. Unusual to find cancer invading fibroadenoma. |
Diagnosis
Physical examination, needle biopsy. Treatment Steps 1. Observation. 2. Excisional biopsy. |
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Symptoms
Nipple discharge. May be too small to feel on physical examination. Description Benign; may degenerate if allowed to enlarge. Grows within ducts. Nipple discharge, bloody |
Intraductal Papilloma
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Diagnosis
Physical examination. Note area of discharge on nipple and areolar palpation. Treatment Steps Excision. |
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Description
Most associated with lactation. Signs and Symptoms Fever, erythema, tender mass. |
Breast Abscess
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Diagnosis
Physical examination. Treatment Steps 1. Antibiotics. 2. Operative drainage. 3. Biopsy wall of abscess and skin to rule out inflammatory carcinoma. |
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Symptoms
Change in existing nevus: bleeding, ulceration, irregular border, size change. |
Melanoma
Description Increasing incidence (1/75, eighth most common cancer in the world), ultraviolet irradiation. Genetic predisposition: fair skin, blonde hair, blue eyes higher risk. Majority originate de novo 10–50% from preexisting nevi. Ninety percent in skin, rest in eye, anus, viscera. Distant metastasis occur in lungs and liver. Four types: lentigo maligna, superficial spreading, acral lentiginous, nodular. Prognosis depends on level of invasion, thickness, and ulceration. RISK FACTORS FOR MELANOMA • Sun exposure • Dyplastic nevus syndrome • Xeroderma pigmentosum • Family history of other skin cancer (nonmelanoma) • High socioeconomic status • Family history of melanoma |
Diagnosis
Biopsy: full thickness. Breslow thickness best prognosis factor. Treatment Steps 1. Wide local excision. 2. Amputation. 3. Lymph node dissection. 4. Isolated limb perfusion. 5. Immunotherapy. |
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Symptoms
Painless mass, enlarging. May become painful and interfere with function. Most often in lower extremities. |
Soft Tissue Sarcomas
Description Uncommon. One percent of malignant tumors. Liposarcomas, ma- lignant fibrous histiocytomas, leiomyosarcomas, fibrosarcomas, rhab- domyosarcomas are most common. Hematogenous spread to lung. The most common site is the extremities. Adult: most common types are malignant fibrous histiocytoma and liposarcoma. Children: most common types are rhabdomyosarcoma and fibrosarcoma. Stewart–Treves syndrome—angiosarcoma in edematous extremity post modified radical mastectomy for breast cancer |
Diagnosis
Biopsy along longitudinal axis of extremity (do not cross fascial com- partments). CT scan or MRI of area. CXR. Treatment Steps 1. Surgical resection: avoid simple enucleation. 2. Irradiation, surgery, and chemotherapy in combination (limb sparing). |
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2 months
Developmental Milestones During Childhood Social/Cognitive Gross Motor Fine Motor Language |
Social smile
Lifts head 45° Eyes follow object to midline Coos |
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Developmental Milestones During Childhood
4 months Social/Cognitive Gross Motor Fine Motor Language |
Laughs/Aware of caregiver/Localizes sound )
Lifts head 90° Eyes follow object past midline |
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6 months
Developmental Milestones During Childhood Social/Cognitive Gross Motor Fine Motor Language |
Differentiates parents from others/Separation anxiety
Rolls over/Holds self up with hands/Sits Grasps/rakes/Attempts to feed self Babbles |
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9 months
Developmental Milestones During Childhood Social/Cognitive Gross Motor Fine Motor Language |
Interactive games
Crawls Grasps with thumb First words |
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12 months
Developmental Milestones During Childhood Social/Cognitive Gross Motor Fine Motor Language |
Pulls to stand/Walks with help
Pincer grasp/Makes tower of 2 blocks ~5- to 10-word vocabulary |
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18 months
Developmental Milestones During Childhood Social/Cognitive Gross Motor Fine Motor Language |
Parallel play
Walks well/Walks backward Makes tower of 4 blocks/Uses cup or spoon 10- to 50-word vocabulary 2-word sentences |
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Developmental Milestones During Childhood
2 yr Social/Cognitive Gross Motor Fine Motor Language |
Dresses self with help
Runs/Climbs stairs (initially 2 feet/step, then 1 foot/step) Makes tower of 6 blocks 50- to 75-word vocabulary/3-word sentences |
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3 yr
Developmental Milestones During Childhood Social/Cognitive Gross Motor Fine Motor Language |
Magical thinking
Climbs/descends stairs Makes tower of 9 blocks/Able to draw circle (O) |
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4 yr
Developmental Milestones During Childhood Social/Cognitive Gross Motor Fine Motor Language |
Plays with others
Hops on 1 foot Able to draw line image (+); later able to draw closed line drawing (Δ) 250+ word vocabulary/4-word sentences |
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6 yr
Developmental Milestones During Childhood Social/Cognitive Gross Motor Fine Motor Language |
Able to distinguish fantasy from reality
Skips Draws a person Fluent speech |
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Extension of head causes extension and flexion of limbs; startle reflex
Childhood Reflexes Time of Disappearance Area of CNS Associated with Abnormal Persistence or Disappearance |
Moro
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3 months
Medulla, vestibular nuclei |
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Placing finger in palm causes grasping
Childhood Reflexes Time of Disappearance Area of CNS Associated with Abnormal Persistence or Disappearance |
Grasp
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3 months
Medulla, vestibular nuclei |
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Rubbing cheek causes turning of mouth to stimuli
Childhood Reflexes Time of Disappearance Area of CNS Associated with Abnormal Persistence or Disappearance |
Rooting
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3 months
Medulla, vestibular nuclei |
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When head turned, arm on faced side extends and arm on opposite side flexes (fencer's position)
Childhood Reflexes Time of Disappearance Area of CNS Associated with Abnormal Persistence or Disappearance |
Tonic neck
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3 months
Medulla, vestibular nuclei |
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Rubbing foot dorsum causes foot to step up
Childhood Reflexes Time of Disappearance Area of CNS Associated with Abnormal Persistence or Disappearance |
Placing
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2 months
Cortex |
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Newborn/1 wk
Screening Nutrition Daily Care Accident Prevention Behavioral Issues |
Phenylketonuria,hypothyroidism, genetic metabolic disorders (maple syrup urine disease, cystic fibrosis, etc.) in high-risk patients; hearing; visual mobility and reflexes
Breast or bottle feeding |
Crying, sleep position, bathing
Smoke detectors, baby furniture, car seats Parent–child interaction |
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1 month
Screening Nutrition Daily Care Accident Prevention Behavioral Issues |
Visual mobility and reflexes
Breast or bottle feeding, fluoride supplements |
Sleep, bowel and bladder habits
Sun exposure Importance of close contact |
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2 months
Screening Nutrition Daily Care Accident Prevention Behavioral Issues |
Visual mobility and reflexes
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Sleep, bowel habits
Close supervision, risks with ability to roll over |
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4 months
Screening Nutrition Daily Care Accident Prevention Behavioral Issues |
Visual mobility and reflexes
Solid foods, fruits and vegetables |
Teething
Keeping small objects out of reach Vocal interaction |
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6 months
Screening Nutrition Daily Care Accident Prevention Behavioral Issues |
Visual mobility and reflexes
Cup training, daily caloric needs, finger foods, avoidance of milk or juice at bedtime |
Shoes
Preparation for increased mobility (“child-proofing” the house), electrical socket covers, stair and door gates Stranger anxiety, separation anxiety |
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9 months
Screening Nutrition Daily Care Accident Prevention Behavioral Issues |
Hgb/Hct; visual mobility and reflexes
Iron supplementation, self-feeding, spoon training |
Tooth care, favorite toys
Aspiration risks Communication, discipline |
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Screening
12 months Nutrition Daily Care Accident Prevention Behavioral Issues |
Visual mobility and reflexes; lead exposure; PPD in high-risk areas
Bottle weaning, eating at table, whole cow's milk |
Poisoning risks, stair safety, burns
Speech, rules, positive reinforcement |
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15 months
Screening Nutrition Daily Care Accident Prevention Behavioral Issues |
Hgb/Hct; visual mobility and reflexes
Family meals |
Toilet training, temper tantrums, punishment, listening to parent read
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18 months
Screening Nutrition Daily Care Accident Prevention Behavioral Issues |
Visual mobility and reflexes
Reinforcement of utensil use |
Nightmares, bedtime regimens
Supervised play, dangerous toys Discipline, “terrible 2s”, toilet training, games |
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2 yr
Screening Nutrition Daily Care Accident Prevention Behavioral Issues |
Lead exposure; visual mobility and reflexes
Avoiding unhealthy snacks, encouraging eating during meals |
Transition from crib to bed, toothbrush training
Toddler independence, explanation of body parts, early play with other children |
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3 yr
Screening Nutrition Daily Care Accident Prevention Behavioral Issues |
Visual acuity; cholesterol (if family history of high cholesterol or CAD)
Healthy diet |
Regular sleep schedule, television limitation
Water safety, animal safety Day care or babysitters (earlier if both parents work), play with other children, reinforce consistent toileting, conversation |
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4 yr
Screening Nutrition Daily Care Accident Prevention Behavioral Issues |
Hearing; lead exposure; visual acuity; PPD (if high-risk group); urinalysis
Meals as time for family bonding |
Self-dental care
Pedestrian and bicycle safety, car seat or seat belt, dangers of strangers, guns, fires, poisons, teach phone number Chores, interactions at day care or preschool, school preparation |
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6 yr
Screening Nutrition Daily Care Accident Prevention Behavioral Issues |
Lead exposure; visual acuity
Avoidance of excess weight; obesity prevention counseling |
Exercise, hygiene, school activities
Swimming Allowance, encourage learning and development, reading |
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10 yr
Screening Nutrition Daily Care Accident Prevention Behavioral Issues |
Hearing; visual acuity
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Hazardous activities, drug use (including alcohol and tobacco)
Friends, sexual education, puberty, responsibility |
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12 yr
Screening Nutrition Daily Care Accident Prevention Behavioral Issues |
Hearing; visual acuity; PPD (if high-risk group); Pap smear only if sexually active (girls)
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Adequate sleep, school and extracurricular activities
Sexual responsibility Body image, privacy issues |
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14 yr and older
Screening Nutrition Daily Care Accident Prevention Behavioral Issues |
Hearing; Hgb/Hct (girls); visual acuity; STD screening (if sexually active)
Weight maintenance |
School and activities
Risk-taking behavior, driving, sexual responsibility Dating, sexuality, goals, careers, independence issues |
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Vaccination Schedule
Birth |
HepB
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Vaccination Schedule
2 mo |
HepB
Rota DTaP Hib PCV IPV |
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Vaccination Schedule
4 mo |
Rota
DTaP Hib PCV IPV |
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Vaccination Schedule
6 mo |
Rota
DTaP Hib PCV |
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Vaccination Schedule
12-15mo |
HepB
Hib PCV IPV MMR VZV |
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Vaccination Schedule
15-18 |
DTaP
HepA × 2 |
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Vaccination Schedule
4-6 yr |
DTaP
IPV MMR VZV |
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Vaccination Schedule
11-12yr |
Td
MCV4 HPV × 3 |
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Vaccination Schedule
13-18yr |
MCV4
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