32. How should a patient with known esophageal varices be treated to prevent an initial variceal bleed?

Show answer
The combination of beta blocker and nitrate is used for primary prophylaxis, but endoscopic band ligation is at least equivalent to pharmacotherapy without the side effects (one third of patients cannot tolerate beta-blockers because of fatigue or bronchospasm, and 20% cannot tolerate nitrates secondary to pounding headaches). These treatments reduce the incidence of an initial bleed from 30% to < 10% and the mortality from 30% to 20%. Endoscopic band ligation was previously suggested for prophylaxis only in class C disease, but mounting evidence suggests that EBL is more effective than pharmacotherapy in all patients. The effect of combined EBL and beta blockade in primary prophylaxis remains to be established but makes great intuitive sense.

References
WEB SITE
http://www.emedicine.com/med/topic1889.htm
BIBLIOGRAPHY
1. Hayes PC: Primary prophylaxis of variceal hemorrhage: A randomized controlled trial comparing band ligation, propranolol, and isosorbide mononitrate. Gastroenterology 123:735-744, 2002. Medline Similar articles
2. Hegab AM, Luketic VA: Bleeding esophageal varices: How to treat this dreaded complication of portal hypertension. Postgrad Med 109:75-86, 2001. Medline Similar articles
3. Jensen DM: Endoscopic screening for varices in cirrhosis: Findings, implications, and outcomes; Gastroenterology 122:1620-1630, 2002.
4. Lo GH, Chen WC, Chen MH, et al: Banding ligation versus nadolol and isosorbide mononitrate for the prevention of esophageal variceal rebleeding. Gastroenterology 123:728-734, 2002. Medline Similar articles
5. Lui HF, Stanley AJ, Forrest EH, et al: Gastroesophageal variceal hemorrhage. N Engl J Med 345:669-681, 2001.
6. Tait KS, Krige J, Terblanche J: Endoscopic band ligation of oesophageal varices. Br J Surg 86:437-446, 1999. Full article
7. Tierney LM, McPhee SJ, Papadakis MA (eds): Current Medical Diagnosis and Treatment, 41st ed. New York, McGraw-Hill, 2002, pp 606-609. Full article

1. Describe the blood supply to the liver.

Show answer
Total hepatic blood flow is roughly 1500 mL/min, or 25% of cardiac output. The hepatic artery normally supplies about 30% of blood flow, and the portal vein contributes 70%. The hepatic artery and portal vein each supply 50% of the liver’s oxygen, however. With portal hypertension, portal flow decreases and the relative contribution of the hepatic artery necessarily increases.

2. How is portal hypertension defined?

Show answer
The portal venous pressure is normally 5-10 mmHg; > 20 mmHg is defined as portal hypertension. Direct measurement is risky, so the hepatic venous pressure gradient (HVPG) is used instead. This is the change in hepatic vein pressure when flow is occluded by wedging a balloon catheter into it (analogous to the estimation of left atrial pressure by wedging a pulmonary artery). A normal HVPG is 2-6 mmHg; > 12 mmHg is considered portal hypertension.

3. What is hepatopetal flow?

Show answer
Appropriate portal blood flow into the liver is termed hepatopetal flow. Reversal of flow in the portal vein can occur with greatly increased hepatic vascular resistance and is called hepatofugal flow. In this case, the hepatic artery must provide the dominant blood flow to the liver.

4. What are the most common causes of portal hypertension?

Show answer

* In the world: schistosomiasis
* In the United States: chronic hepatitis C virus infection or alcoholic cirrhosis (Laennec’s disease)
* In children: extrahepatic portal venous occlusion (as in portal vein thrombosis) or biliary atresia

5. What are schistosomiasis and Katayama fever?

Show answer
Infection by a freshwater blood fluke that causes an initial dermatitis (”swimmer’s itch”) and rash followed after 1-2 months by fever, myalgias, abdominal pain, and bloody diarrhea (Katayama fever). As these parasites mate and lay eggs in the venous system, the resulting inflammation causes chronic obstructing fibrosis of the organs and vessels, which is manifested by portal hypertension. Katayama fever lasts a few weeks and is second only to malaria as a cause of chronic tropical illness. Treat with praziquantel.
KEY POINTS: CHRONIC PANCREATITIS

1. Portal venous pressure > 20 mmHg (normal = 5-10 mmHg).
2. Most common cause in the United States is alcoholic cirrhosis.
3. Anatomic causes characterized as presinusoidal, sinusoidal, or postsinusoidal.
4. Complications include ascites, esophageal varices, encephalopathy, hypersplenism, hemorrhoids.
5. Initial management is medical; surgery is reserved for refractory cases.

6. How can the causes of portal hypertension be classified anatomically?

Show answer
Presinusoidal:

* Extrahepatic: portal or splenic vein thrombosis, congenital biliary atresia, extrinsic compression (e.g., tumor)
* Intrahepatic: primary biliary cirrhosis, schistosomiasis, hepatic metastases, polycystic disease, sarcoidosis

Sinusoidal: hepatic cirrhosis (e.g., viral infection, alcohol, hemochromatosis)
Postsinusoidal: Budd-Chiari syndrome, inferior vena cava obstruction, right heart failure

7. List the four major anatomic connections between the portal and systemic venous systems.

Show answer

1. Left gastric (coronary) vein to the esophageal vein (potential esophageal varices)
2. Inferior mesenteric vein through the superior hemorrhoidal veins to the hypogastric vein (potential rectal varices)
3. Portal vein to umbilical vein to superficial veins of the abdominal wall (potential caput medusae)
4. Mesenteric veins to perilumbar veins of Retzius into the inferior vena cava (potential retroperitoneal hemorrhage)

Note that the reason these anastomoses can shunt blood (around the liver) is that the splanchnic veins lack one-way valves.

8. Define sinistral portal hypertension.

Show answer
Derived from sinister, the Latin word for “left,” this is “left-sided” portal hypertension specifically caused by splenic vein thrombosis or obstruction. This causes shunting from the short gastric branches of the splenic vein to the left gastric vein, resulting in gastric varices. Splenectomy is the definitive treatment.

9. What are the common complications of portal venous hypertension?

Show answer

* Ascites and spontaneous bacterial peritonitis
* Hemorrhage from esophageal varices (the major cause of mortality)
* Hypersplenism
* Rectal varices (hemorrhoids)
* Portosystemic encephalopathy
* Portal hypertensive gastropathy and colopathy

10. What impact can portal hypertension have on other organ systems?

Show answer

* Hyperdynamic circulation (decreased systemic vascular resistance with increased cardiac output and low blood pressure)
* Hepatorenal syndrome
* Hepatopulmonary syndrome or portopulmonary hypertension

11. Liver function is classified according to what system?

Show answer
The modified Child-Turcott-Pugh system defines three classes of liver disease based on mortality; the points should be totalled from Table 42-1.

* Class A (5-6 points): 85% 2-year survival
* Class B (7-9 points): 60% 2-year survival
* Class C (≥ 10 points): 35% 2-year survival

12. What is MELD?

Show answer
The Mayo end-stage liver disease score is a completely objective measure of disease calculated with international normalized ratio (INR), bilirubin, and creatinine. In 2002, MELD was adopted by the United Network for Organ Sharing (UNOS) for determining liver transplantation priority.

Table 42-1. CHILD-TURCOTT-PUGH SYSTEM OF SCORING LIVER DISEASE

13. How is MELD calculated?

Show answer

MELD = 10 x [0.957 x ln (creatinine mg/dL) + 0.378 x In (bilirubin mg/dL) + 1.120 x ln (INR) + 0.643 (0 if cholestatic/alcoholic)]

Result is rounded to the nearest integer.

14. How common are esophageal varices?

Show answer
At time of diagnosis of cirrhosis, approximately 30% of patients have esophageal varices, and the incidence of new varix formation in patients with known cirrhosis is roughly 6% per year. There is a 50% point prevalence of varices in cirrhotic patients. However, bleeding occurs in only about one third of patients with varices.

15. Is upper gastrointestinal bleeding in cirrhotic patients with documented varices always variceal?

Show answer
Good test-taking skills tell you the answer must be no. Twenty percent of these patients bleed from another source (e.g., alcoholic gastric ulcerations, peptic ulcer disease). This also includes patients with ascites, spider angiomata, and asterixis.

16. Are gastric varices a common bleeding source in patients with portal hypertension?

Show answer
No. Only about 5% of variceal bleeds in cirrhotic patients are caused by gastric varices. Portal hypertension with gastric varices and no esophageal varices is usually associated with splenic vein thrombosis. Gastric varices bleed much less frequently-but more severely-than their esophageal counterparts.

17. What factors are predictive of variceal bleeding?

Show answer

* Size of varices (the most important factor), which increases vessel wall tension
* Red wale markings on the varices (longitudinal “whip marks”) from decreased wall thickness
* Severity of liver disease
* Active alcohol abuse

All told, variceal hemorrhage occurs in 30% of patients within 2 years of varix documentation.
18. Does the degree of portal hypertension predict bleeding? Show answer
Surprisingly, no. Bleeding risk correlates poorly with the magnitude of portal pressure. However, bleeding rarely occurs with HVPG <12 mmHg; this threshold pressure is considered necessary but not sufficient for bleeding.

19. An initial variceal bleed is associated with what mortality and rebleeding risk?

Show answer
Thirty percent of these patients die within 6 weeks, with one third to one half of rebleeds occurring in the first 10 days. If untreated, up to 75% of patients rebleed within the first year.

20. Should selective or nonselective beta blockers be used in the treatment of esophageal varices?

Show answer
Nonselective beta blockade best minimizes bleeding by lowering blood pressure and reducing splanchnic flow. Beta1-adrenergic antagonism causes splanchnic vasoconstriction by reflex activation of alpha receptors and decreases myocardial contractility. Beta2 blockade prevents splanchnic and peripheral vasodilation. Nadolol is the drug of choice.

21. What are the major components of acute variceal bleed management?

Show answer

* Fluid or blood product resuscitation (be careful not to worsen ascites with excess crystalloid)
* Pharmacologic agents to lower portal pressure and flow to limit bleeding)
* Endoscopy to confirm diagnosis and treat by banding or sclerotherapy
* Antibiotic prophylaxis
* Lactulose catharsis (GI bleeding increases protein load-blood is protein-and may worsen encephalopathy)
* Tamponade, surgery, or transjugular intrahepatic portosystemic shunting (TIPS) if refractory or an early recurrent bleed

22. What pharmacologic treatments are used in acute variceal bleeding?

Show answer
Vasopressin (start at 0.2 U/min intravenously [IV] and increase the level while watching the electrocardiogram) decreases splanchnic perfusion and thus portal pressure. Be careful; systemic vasoconstriction can cause myocardial or mesenteric ischemia and infarction.
Terlipressin (2 mg IV every 4 hours) is a synthetic vasopressin analog with fewer side effects and simpler dosing. This has shown clear promise in randomized controlled trials but is not yet available in the United States.
Octreotide (50 μg IV bolus, then 25 μg/h IV) is a synthetic somatostatin analog that decreases portal blood flow by selective splanchnic vasoconstriction, so side effects are limited. Octreotide acts through vasoactive peptides substance P and glucagon.

23. What endoscopic treatments are used in acute variceal bleeding?

Show answer

* Sclerotherapy: intravariceal injection of a sclerosing chemical
* Endoscopic band ligation (EBL): direct strangulation of varices with rubber bands, similar to hemorrhoid banding

Either technique typically controls acute bleeding in ≤ 90% of variceal bleeding, but although sclerotherapy can be easier in the face of a large bleed, band ligation is safer (less chance of perforation) and tends to require fewer retreatments. (See Figure 42-1.)

Figure 42-1 Endoscopic band ligation. A, The endoscope is positioned over a varix and suction is applied to draw it into the ligator. A rubber band is then ejected over the base of the lesion. B, The band strangulates the varix, which sloughs off and passes through the body in about 5-7 days.

24. Why should antibiotics be given to cirrhotic patients admitted for GI bleeding?

Show answer
These patients have almost twice the risk of developing bacterial infections while hospitalized than do cirrhotic patients admitted for other reasons (nosocomial infection rates approach 50%). Spontaneous bacterial peritonitis, bacteremia, and pneumonia are the most common infections. Short-term antibiotic prophylaxis decreases infection incidence and early rehemorrhage with a resultant increase in survival. Norfloxacin, 400 mg given orally every day for 7 days, is a proven regimen.

25. What is a Sengstaken-Blakemore tube?

Show answer
A large nasogastric tube with two inflatable balloons that can be used to tamponade both the esophagus and the gastric cardia. The gastric balloon is inflated in the stomach (insert 150 mL of saline plus 25 mL of Gastrografin so that you can confirm appropriate positioning by radiograph) and pull this inflated balloon gently up against the gastroesophageal junction. Most bleeds occur in the distal 5 cm of esophagus, so if bleeding continues, the esophageal balloon should be inflated as well. In order to prevent balloon-induced esophageal ischemia or rupture, do not inflate this balloon to > 30 mmHg (portal venous pressure) and limit use to 24 hours. Half of patients rebleed after balloon deflation, and 10-25% suffer aspiration pneumonia. (See Figure 42-2.)

Figure 42-2 Sengstaken-Blakemore tube, with two balloons and suction ports.

26. What are the options for preventing recurrent variceal bleeds?

Show answer
Without treatment, 75% of patients rebleed within 1 year. Beta-blockers reduce this to 40%; when combined with sclerotherapy, the rate is 35%, and when combined with EBL, the rate is reduced to 25%. The lowest rebleeding rates are thus accomplished with EBL and chronic nadolol. Interestingly, EBL with beta blockade has demonstrated no difference in 2-year survival when compared with beta-blocker and nitrate treatment alone. Shunt surgery and TIPS are slightly better than all these options at 15% rebleeding per year, but these invasive interventions also increase morbidity.

27. How should a patient with recurrent variceal bleeds be treated?

Show answer
Primary treatment should be EBL combined with beta blockade. Failing this treatment, the second-line option is to decompress the portal venous system by shunting blood away with a portosystemic anastomosis. The decision of open versus radiologic shunting is based on the urgency and the patient’s fitness for surgery.

28. What is TIPS?

Show answer
TIPS is a percutaneous radiologic technique for diverting portal vein blood directly into the inferior vena cava. Under fluoroscopy, a stent is placed through the hepatic parenchyma to link the hepatic and portal veins. Although TIPS relieves ascites and is superior to EBL in lowering variceal bleed risk, it also exacerbates encephalopathy without any decrease in mortality. New or worsened encephalopathy occurs in at least 25% of patients after TIPS. Stent stenosis and dysfunction occurs in 30% by 1 year and 50% by 2 years. (See Figure 42-3.)

Figure 42-3 TIPS placement. A, From a hepatic vein, a needle punctures through the liver to reach a portal vein. B, The tunnel is widened with a balloon catheter. C, A permanent stent is placed. (From McNally PR (ed): GI/Liver Secrets, 2nd ed. Philadelphia, Hanley & Belfus, 2001.)

29. Describe the basic options for surgical shunting.

Show answer
Nonselective (central) shunt: portovacal and mesocaval shunts nonselectively decompress the portal venous system, thus risking hepatofugal flow and worsening hepatic failure. Large amounts of portal blood (not detoxified in the liver) in the systemic circulation worsen encephalopathy. Creating a smaller diameter conduit (partial shunt) helps preserve some anterograde portal flow and limits this effect.
Selective splenorenal (Warren) shunt: anastomosis of the distal splenic vein to the left renal vein with ligation of the left gastric. This does not decompress as thoroughly, and, therefore, this technique enjoys a lower risk of encephalopathy.
As a rule, the more central the shunt site, the more extensive the portal decompression, but the tradeoff is the increased risk of encephalopathy (as demonstrated by TIPS).

30. How can you estimate operative mortality for elective portosystemic shunting?

Show answer
Perioperative mortality correlates well with Child-Pugh class (this was the original purpose of the classification). Classes A, B, and C demonstrate 5%, 10%, and 40% mortality, respectively, at 30 days.

31. Is there a definitive treatment for recurrent variceal bleeding?

Show answer
Liver transplantation provides portal decompression and restores hepatic function. Listing criteria are strict, and the psychological assessment of the “reformed alcoholic” is particularly arduous. Prior TIPS or shunting operations are not contraindications to transplant.

1. What are the risk factors for developing esophageal cancer?

Show answer
Both alcohol and tobacco increase the risk of carcinoma of the esophagus by a factor of 10. Additional risk factors include Barrett’s esophagus with dysplasia, carcinogen exposures (e.g., nitrosamines in the Eastern world), vitamin and trace element deficiencies, and Plummer-Vinson syndrome.

2. What is the epidemiology of carcinoma of the esophagus?

Show answer
Esophageal cancer accounts for 1% of all cancers and 2% of cancer-related deaths. Generally, it is three times more common in men and occurs most commonly in the seventh decade of life. Worldwide, 95% of all esophageal cancers are of squamous cell origin; however, in the Western world, the relative incidence of adenocarcinoma has increased dramatically over the past 20 years because of the comparable increase in the incidence of Barrett’s esophagus.

3. What is Barrett’s esophagus, and how does it relate to esophageal cancer?

Show answer
Chronic reflux of gastric contents into the esophagus may lead to Barrett’s esophagus, which is characterized by replacement of the normal squamous esophageal mucosa with a glandular columnar mucosa resembling the stomach. This is also called intestinal metaplasia. If Barrett’s esophagus progresses to high-grade dysplasia, patients have a fortyfold increased risk of esophageal adenocarcinoma. Patients with high-grade dysplasia are traditionally treated by esophagectomy; however, photodynamic therapy (PDT) may eliminate dysplastic Barrett’s mucosa, obviating surgical resection. PDT remains unapproved and experimental.

4. What are the most common presenting symptoms of esophageal cancer?

Show answer
Dysphagia occurs in 85% of patients. Others symptoms include weight loss (60%), chest or epigastric pain (25%), regurgitation of undigested food (25%), hoarseness caused by recurrent laryngeal nerve involvement (5%), cough or dyspnea (3%), and hematemesis (2%).

5. What is the diagnostic work-up for patients presenting with these symptoms?

Show answer

1. History and physical examination
2. Upper gastrointestinal series (contrast study of the upper GI tract)
3. Upper endoscopy with biopsies of all concerning luminal structures
4. Computed tomography (CT) scan of chest and abdomen to define nodal and potential metastatic disease
5. Endoscopic ultrasound (EUS) to define the T stage (i.e., size) of the primary mass and regional lymph node involvement with possible fine-needle aspiration (FNA) biopsy
6. Positron emission tomography (PET) scan to define distant metastatic spread

6. What is the anatomic distribution of esophageal cancer?

Show answer
The esophagus is divided into three anatomic segments: upper, middle, and lower thirds. Fifteen percent of esophageal cancers arise in the upper third, 50% in the middle third, and 35% in the lower third.

KEY POINTS: ESOPHAGEAL CARCINOMA

1. Most common in older patients with dysphagia (85% of cases) and weight loss (60% of cases).
2. Major causative factors are alcohol and tobacco (10-fold increase in risk).
3. Diagnosis is made by upper GI endoscopy and biopsy.
4. Most common variant is adenocarcinoma; second most common is squamous cell cancer.
5. Radiographic work-up is necessary to stage disease.

7. What is neoadjuvant chemotherapy? What are its advantages and disadvantages?

Show answer
This is chemotherapy, radiation therapy, or both to the primary lesion before surgical resection.
The advantages include:

* Potential downstaging (to shrink the tumor or treat locoregional lymph node involvement)
* Early treatment of micrometastatic disease
* Treatment is better tolerated before surgical stress
* Calibrates the patient’s ability to tolerate major surgery
* Verification of primary tumor’s sensitivity to the chemotherapy or radiation therapy

The disadvantages include:

* Delay in treatment of the primary lesion, particularly when the primary tumor progresses despite neoadjuvant therapy
* Selection for chemoresistant cell lines

8. What are the surgical options for treatment of carcinoma of the esophagus?

Show answer
Surgery alone or combined with chemoradiotherapy offers the only hope for cure. The surgical approaches include: (1) transabdominal resection of lesions located at the gastroesophageal junction; (2) resection with intrathoracic anastomosis by left thoracoabdominal (Sweet procedure) or combined midline laparotomy and right thoracotomy (Ivor-Lewis procedure); and (3) transhiatal esophagectomy with cervical anastomosis. Laser therapy, esophageal stenting procedures, and dilatation are reserved for palliation.

9. What are the risks of surgery?

Show answer

* Death
* Hemorrhage
* Anastomotic leak
* Empyema and sepsis
* Anastomotic stricture
* Local recurrence of cancer
* Dysphagia

10. What is the natural history of esophageal cancer?

Show answer
In a collected series of almost 1000 untreated patients, the 1- and 2-year survival rates were 6.0% and 0.3%, respectively. Untreated patients typically succumb to progressive malnutrition complicated by aspiration pneumonia, sepsis, and death. Formation of a fistula between the aorta or pulmonary artery and the esophagus or pulmonary tree is a somewhat more dramatic (or perhaps merciful) mode of exit. Treated or untreated, esophageal cancer is a bad disease.

11. Describe the stages of esophageal cancer and the respective 5-year survival rate after esophagectomy.

Show answer

Stage I is cancer confined to the inner layer (muscularis mucosae or submucosa), and 5-year survival is as high as 80%. Stage II describes tumors that are confined to the layers outside the submucosa with local lymph node involvement, and 5-year survival can be as high as 35%. Stage III tumors have either invaded surrounding structures (lung, aorta, or trachea) irrespective of regional lymph node involvement or go through the wall of the esophagus with nodal involvement. The 5-year survival is typically < 10%. Stage IV esophageal cancer has spread to nonregional lymph nodes (supraclavicular or celiac nodes) or distant organs (lung, liver, bone). Essentially, all patients with stage IV disease die within 2 years of diagnosis.

12. What is an “R0″ (or “R zero”) resection, and how does it impact survival?

Show answer
All gross disease is removed, and microscopically, the margins of resection are negative for tumor. Achieving an R0 resection is the surgeon’s goal and is the most robust predictor of a favorable outcome after surgery for esophageal cancer. An R1 resection represents removal of all gross disease, yet resection margins are microscopically positive for tumor. The overall 5-year survival (any stage) for patients with microscopically positive margins decreases by an order of magnitude (e.g., 30% down to 3%).

References
WEB SITES

1. http://www.emedicine.com/med/topic741.htm
2. http://www.acssurgery.com/abstracts/acs/acs0309.htm

BIBLIOGRAPHY
1. Cordero JA: Self-expanding esophageal metallic stents in the treatment of esophageal obstruction. Am Surg: 66:958-959, 2000.
2. Hofstetter W: Treatment outcomes of resected esophageal cancer. Ann Surg 236:376-384, 2002. Medline Similar articles Full article
3. Kato H: Comparison of PET and computerized tomography in the use of the assessment of esophageal carcinoma. Cancer 15:921-928, 2002. Full article
4. Kelsen DP: Chemotherapy followed by surgery compared with surgery alone for localized esophageal cancer. N Engl J Med 339:1979-1984, 1998.
5. Oesophageal Cancer Group: Surgical resection with or without preoperative chemotheraphy in oesophageal cancer. Lancet 359:1727-1733, 2002.
6. Overholt BF: Photodynamic therapy in the management of Barrett’s esophagus with dysplasia. J Gastrointest Surg 4: 129-130, 2002.
7. Reed C: Techniques of esophageal surgery. Chest Surg Clin North Am 5:379-574, 1995.
8. Salazar JD: Does cell-type influence post-esophagectomy survival in patients with esophageal cancer? Dis Esophagus 11:168-171, 1998.
9. Shumaker DA: Potential impact of preoperative EUS on esophageal cancer management and cost. Gastrointest Endosc 56:391-396, 2002. Medline Similar articles Full article
10. Swaroop VS: Re: Practice guidelines for esophageal cancer. Am J Gastroenterol 94:2319-2320, 1999. Medline Similar articles
11. Urba S: Combined modality therapy for esophageal cancer-standard of care? Surg Oncol Clin North Am 11:377-386, 2002.
12. Walsh T: A comparison of multimodal therapy and surgery for esophageal adenocarcinoma. N Engl J Med 335:462-467, 1996. Medline Similar articles Full article

1. What are tracheoesophageal fistula (TEF) and esophageal atresia (EA)?

Show answer
The trachea and esophagus appear as a ventral diverticulum arising from the primitive foregut during the third week of gestation. The trachea and esophagus undergo separation by the ingrowth of ectodermal ridges during the fourth week of gestation. Failure of separation results in anomalous connection of the trachea to the esophagus (i.e., TEF) with or without incomplete formation of the esophagus (i.e., EA).

2. Describe the three most common variants and the relative incidence of each type

. Show answer

* Proximal EA with distal TEF (”proximal pouch with distal fistula”): 85%
* Isolated EA: 10%
* TEF without EA (”H fistula”): 5%

3. What other anomalies occur with tracheoesophageal malformations?

Show answer
TEF and EA result from an insult during the critical phase of embryogenesis (3-8 weeks’ gestation). Up to 70% of infants with tracheoesophageal malformations suffer one or more concomitant anomalies. Cardiovascular anomalies are the most prevalent (35%), followed by anomalies of the gastrointestinal (24%), genitourinary (20%), skeletal (13%), and central nervous (10%) systems. Twenty-five percent of infants born with tracheoesophageal malformation have one or more components of the VACTERL association (see question 2 in chapter 84).

4. Does the presence of other anomalies alter management and outcome?

Show answer
Healthy infants without concomitant anomalies generally undergo early repair with a nearly 100% survival rate, whereas infants who are severely premature or have life-threatening anomalies typically undergo delayed repair. Infants with lethal anomalies, such as trisomy 18, receive palliative care only.

5. Describe the clinical presentation, diagnosis, and preoperative management of patients with EA with distal TEF.

Show answer
Early in the newborn period, affected infants demonstrate excessive salivation (i.e., inability to swallow secretions), choking, or regurgitation with feeding (i.e., inability to swallow feeds). Respiratory distress quickly ensues because of aspiration of secretions or feeds from the esophageal pouch and reflux of gastric acid into the airways and lungs via the distal TEF. A nasogastric tube cannot be advanced into the stomach. The radiograph demonstrates a blind-ending proximal esophageal pouch and an air-filled stomach caused by the anomalous connection of the distal esophagus to the airway. The infant is maintained in a semi-upright position with sump catheter drainage of the proximal esophageal pouch to minimize contamination of the lungs either because of aspiration or reflux.

6. Describe the clinical presentation, diagnosis, and preoperative management of isolated EA.

Show answer

Isolated EA is associated with excessive salivation, choking, and regurgitation of feeds. The inability to pass a nasogastric tube into the stomach and a gasless abdomen apparent on radiograph suggests the diagnosis. Preoperative management is directed to the identification of associated anomalies and determination of gap length. Sump catheter drainage of the proximal esophageal pouch is maintained to minimize aspiration. Gastrostomy is generally performed within the first 24 hours of life to permit feeding and assessment of the distal esophageal length. Typically, infants with EA undergo delayed repair to permit growth of the distal esophagus and reduction of gap distance.

7. Describe the clinical presentation, diagnosis, and preoperative management of TEF without EA.

Show answer
These infants demonstrate repeated choking or cyanotic spells with feeding caused by the reflux of feeds from the esophagus to the lungs via the anomalous tracheoesophageal connection. Older infants and children may present with recurrent bouts of pneumonia or unexplained reactive airway disease resulting from the intermittent contamination of the lungs via the fistula. Video esophagography and bronchoscopy are used to demonstrate the fistula.

8. How are tracheoesophageal malformations corrected surgically?

Show answer
Surgical treatment entails restoration of esophageal continuity and elimination of the pathologic connection of the esophagus to the airway. Correction of EA with or without TEF requires thoracotomy, with or without ligation of TEF, and end-to-end esophageal anastomosis. The first successful procedure was performed by Cameron Haight in 1941. At 5-7 days after surgery, an esophagogram is performed; if no leak is visualized, oral feedings are started and the pleural drain is removed.
TEF without EA is approached via a cervical incision, avoiding thoracotomy. The fistulous tract is divided and healthy tissue is interposed to prevent recurrence.

9. What are the early and late complications of surgical repair?

Early complications

Early complications are related to the basic surgical principles of wound healing. Anastomotic disruption generally results from poor blood supply and tension.
Late complications

Most strictures (50%) respond to one to three dilatations performed in the first 6 months of life. Refractory strictures require identification of associated gastroesophageal reflux (GER), which may worsen stricture formation. The frequency of GER appears related to gap length (i.e., the greater the gap distance, the greater the risk of significant GER).
KEY POINTS: TRACHEOESOPHAGEAL MALFORMATIONS

1. The three most common variants are proximal esophageal atresia (EA) with distal tracheoesophageal fistula (TEE), isolated EA, and TEF without EA.
2. Early in the newborn period, affected infants demonstrate excessive salivation, choking, or regurgitation with feeding.
3. Surgical treatment entails restoration of esophageal continuity and elimination of the pathologic connection of the esophagus to the airway.

References
BIBLIOGRAPHY
1. Brown AK, Tam PK: Measurements of gap length in esophageal atresia: A simple predictor of outcome. J Am Coll Surg 182:41-45, 1996. Medline Similar articles Full article
2. Dunn JC, Fonkalsrud EW, Atkinson JB: Simplifying the Waterston’s stratification of infants with tracheoesophageal fistula. Am Surg 65:908-910, 1999. Medline Similar articles
3. Saing H, Mya GH, Cheng W: The involvement of two or more systems and the severity of associated anomalies significantly influence mortality in esophageal atresia. J Pediatr Surg 33:1596-1598, 1998. Similar articles Full article
4. Somppi E, Tammela O, Ruuska T, et al: Outcome of patients operated on for esophageal atresia: 30 years’ experience. J Pediatr Surg 33:1341-1346, 1998.
5. Spitz L: Esophageal atresia: Past, present, and future. J Pediatr Surg 31:19-25, 1996. Medline Similar articles Full article
6. Torfs CP, Curry CJ, Bateson TF: Population-based study of tracheoesophageal fistula and esophageal atresia. Teratology 52:220-232, 1995. Medline Similar articles
7. Tovar JA, Diez Pardo JA, Murcia J, et al: Ambulatory 24-hour manometric and pH metric evidence of permanent impairment of clearance capacity in patients with esophageal atresia. J Pediatr Surg 30:1224-1231, 1995.

1. What symptoms suggest gastroesophageal reflux disease (GERD)?

Show answer
Substernal burning after meals or at night, associated occasionally with regurgitation of gastric juices, is one symptom. Discomfort is relieved by standing or sitting. Dysphagia, a late complication of GERD, is caused by mucosal edema or stricture of the distal esophagus. However, no symptom is specific for GERD, and therapeutic decisions should not be made on symptoms alone.

2. What is the difference between heartburn and GERD?

Show answer
Heartburn is a lay term for mild, intermittent reflux of gastric content into the esophagus without tissue injury. It is relatively common among adults. GERD implies esophagitis with varying degrees of erythema, edema, and friability of the distal esophageal mucosa. It occurs in 10% of the population.

3. What causes GERD?

Show answer
The underlying abnormality of GERD is functional incompetence of the lower esophageal sphincter (LES), which allows gastric acid, bile, and digestive enzymes to damage the unprotected esophageal mucosa. Achalasia, scleroderma, and other esophageal motility disorders are sometimes associated with GERD.

4. Is hiatal hernia an essential defect in patients with GERD?

Show answer
No. Not all patients with GERD have a hiatal hernia, and not all patients with a hiatal hernia have GERD. A total of 50% of patients with GERD have an associated hiatal hernia.

5. What studies are useful to diagnose GERD?

Show answer
Endoscopy with biopsy is essential in diagnosing GERD. Barium swallow with or without fluoroscopy can diagnose reflux but cannot identify esophagitis. Twenty-four-hour esophageal pH testing associates reflux with symptoms and is useful in some patients. Gastric secretory or gastric emptying tests are occasionally helpful. Manometry of the esophagus and LES is required whenever an esophageal motility disorder is suspected and before any surgical intervention.

6. What is the initial management of a patient suspected of having GERD?

Show answer

* Change diet to avoid foods known to induce reflux (e.g., chocolate, alcohol, and coffee).
* Avoid large meals before bedtime.
* Stop smoking.
* Do not wear tight, binding clothes.
* Elevate the head of the bed 4-5 inches.
* Take antacids when symptomatic.
* Weight loss can be very effective in reducing GERD symptoms.

7. If initial treatment fails, what should be recommended?

Show answer
About 50% of patients show significant healing with H2 blockers, but only 10% of these patients remain healed 1 year later. Metoclopramide promotes gastric emptying but rarely relieves symptoms consistently in the absence of acid reduction.

KEY POINTS: DIAGNOSTIC WORK-UP OF GERD

1. Underlying anatomic abnormality may cause functional incompetence of the lower esophageal sphincter (LES).
2. Endoscopy and biopsy are paramount in diagnosis.
3. Swallow studies delineate possible anatomic causes.
4. 24-hour pH monitoring can link reflux to patient’s symptoms.
5. Manometry of the LES is required if esophageal motility disorder is suspected.

8. What is the role of proton pump inhibitor (PPI) in GERD?

Show answer
PPIs (omeprazole and others) irreversibly inhibit the parietal cell hydrogen ion pump and are > 80% successful in healing severe erosive esophagitis. Two thirds of patients who continue the medication remain healed. A concern in prolonged PPI therapy is hypergastrinemia secondary to alkalinization of the antrum. Gastrin is trophic to gastrointestinal mucosa, but the initial fear of induced neoplasia has not been borne out by follow-up studies.

9. When should operation for GERD be recommended?

Show answer
Failure of nonoperative (medical) therapy is the primary indication for surgery. Noncompliance with prescribed treatment is a frequent cause of failure and even stricture unresponsive to dilation. With PPIs, most patients’ symptoms can be controlled for long periods of time. Current recommendations for surgical intervention include: (1) failed medical therapy (e.g., intractable disease, intolerance or allergy to medications, noncompliance, and recurrence of symptoms while on medical therapy), (2) complications (e.g., stricture, respiratory symptoms, medicosocial changes, and premalignant mucosal changes), (3) patient preference (e.g., cost-long-term medical prescriptions can be expensive-or lifestyle issues).

10. What is the goal of surgical treatment?

Show answer
Operations for GERD attempt to prevent reflux by mechanically increasing LES pressure and, in most procedures, to restore a sufficient length of distal esophagus to the high-pressure zone of the abdomen. Hiatal hernia, when present, is reduced simultaneously.

11. What procedures can accomplish this goal and how do they do it?

Show answer

1. In the Nissen fundoplication, which is used in > 95% of patients, the fundus of the stomach is mobilized, wrapped around the distal esophagus posteriorly, and secured to itself anteriorly (i.e., 360-degree wrap). The procedure alters the angle of the gastroesophageal junction and maintains the distal esophagus within the abdomen to prevent reflux. The operation is performed transabdominally by either laparotomy or laparoscopy. (See Figure 43-1.)
2. The Belsey Mark IV operation accomplishes the same anatomic changes but is done via a thoracotomy. (See Figure 43-2.)
3. The Hill gastropexy restores the esophagus to the abdominal cavity by securing the gastric cardia to the preaortic fascia. (See Figure 43-3.)
4. The Toupet (partial) fundoplication is used in patients who have associated motility disorders. Because the wrap is not circumferential, the incidence of postoperative dysphagia is significantly reduced with this partial wrap compared with a full 360-degree wrap (Nissen fundoplication). However, long-term durability may not be as good as with a Nissen fundoplication. This operation can be done transabdominally by either laparotomy or laparoscopy. (See Figure 43-4.)

Figure 43-1 In the Nissen fundoplication, which is used in > 95% of patients, the fundus of the stomach is mobilized, wrapped around the distal esophagus posteriorly, and secured to itself anteriorly (i.e., 360° wrap). The procedure alters the angle of the GE junction and maintains the distal esophagus within the abdomen to prevent reflux. The operation is performed transabdominally by either laparotomy or laparoscopy.

Figure 43-2 The Belsey Mark IV operation accomplishes the same anatomic changes as the Nissen fundoplication but is done via a thoracotomy.

Figure 43-3 The Hill gastropexy restores the esophagus to the abdominal cavity by securing the gastric cardia to the preaortic fascia.

Figure 43-4 The Toupet (partial) fundoplication is used in patients who have associated motility disorders. Because the wrap is not circumferential, the incidence of postoperative dysphagia is significantly reduced with this partial wrap compared with a full 360° wrap (Nissen fundoplication). However, long-term durability may not be as good as with a Nissen fundoplication. This operation can be done transabdominally by either laparotomy or laparoscopy.

12. What are the success rates for such procedures?

Show answer
All of the procedures described in question 11 eliminate GERD in almost 90% of patients who are followed for

10 years. But the Nissen fundoplication wins in comparison studies. Recurrent symptoms should be thoroughly worked up because they are frequently associated with other disorders and not recurrent GERD.
13. What are the long-term complications of such procedures?

Show answer
The repair may fail, with recurrence of reflux, after any of these operations. Incorrect placement or slippage of the stomach wrap can complicate Nissen fundoplication and the Belsey Mark IV procedure. Dysphagia and the inability to belch (i.e., gas-bloat syndrome) result from too tight a wrap.

14. How can stricture from GERD be managed?

Show answer
Pliable (unfixed) strictures can be dilated. Fixed strictures require surgical repair. A Thal patch expands the stricture by interposing a piece of stomach.

15. Is GERD better treated in the long term by PPI therapy or Nissen fundoplication?

Show answer
PPIs really work in resolving esophagitis and eliminating symptoms of GERD, but the long-term side effects are not fully known. Fundoplication potentially frees the patient from daily medicine (this has been challenged recently) and may cause morbidity in ≤ 10% of patients.

16. Should a Nissen fundoplication be performed by laparoscopy or laparotomy?

Show answer
The same procedure can be accomplished by either approach. Postoperative morbidity and mortality is comparable. The distinct advantages of laparoscopy are less postoperative pain, shorter hospitalization, and earlier return to work.

17. Can this disease be treated by other minimally invasive means?

Show answer
Yes. Other endoscopic methods include:

* Endoluminal suturing
* Radiofrequency treatment of the LES
* Injection of bulk-forming agents around the LES

References
WEB SITE
http://www.emedicine.com/med/topic857.htm
BIBLIOGRAPHY
1. Bremner RM, DeMeester TR, Crookes F, et al: The effect of symptoms and nonspecific motility abnormalities on outcomes of surgical therapy for gastroesophageal reflux. J Thorac Cardiovasc Surg 107:1244-1250, 1994. Medline Similar articles
2. DeMeester TR, Peters JH, Bremner CG, Chandrasoma P: Biology of gastroesophageal reflux disease: Pathophysiology relating to medical and surgical treatment. Annu Rev Med 50:469-506, 1999. Medline Similar articles
3. Hinder RA, Filipi CJ, Wetscher G, et al: Laparoscopic Nissen fundoplication is an effective treatment for gastroesophageal reflux disease. Ann Surg 220:472-481, 1994. Medline Similar articles
4. Lagergren J, Bergstrom R, Lindgren A, Nyren O: Symptomatic gastroesophageal reflux as a risk factor for esophageal adenocarcinoma. N Engl J Med 340:825-831, 1999.
5. Lord RV, Kaminski A, Oberg S, et al: Absence of gastroesophageal reflux disease in a majority of patients taking acid suppression medications after Nissen fundoplication. J Gastrointest Surg 6:3-9, 2002. Medline Similar articles Full article
6. Peters JH, DeMeester TR (eds): Minimally Invasive Surgery of the Foregut. St. Louis, Quality Medical Publishing, 1994.
7. Roy-Shapira A, Stein HJ, Scwartz D, et al: Endoluminal methods of treating gastroesophageal reflux disease. Dis Esophagus 15:132-136, 2002. Medline
8. Spechler SJ: Comparison of medical and surgical therapy for complicated gastroesophageal reflux disease in veterans. N Engl J Med 326:786-792, 1992. Medline Similar articles
9. Spechler SJ, Lee E, Ahnen D, et al: Long-term outcome of medical and surgical therapies for gastro-esophageal reflux disease: follow-up of a randomized controlled trial. JAMA 285:2331-2338, 2001.
10. Spivak H, Lulcuk S, Hunter JG: Laparoscopic surgery of the gastroesophageal junction. World J Surg 23:356-367, 1999. Medline Similar articles
11. Triadafilopoulos G, DiBaise JK, Nostrant TT, et al: The Stretta procedure for the treatment of GERD: 6 and 12 month follow-up of the U.S. open label trial. Gastrointest Endosc 55:149-156, 2002.
12. Trus TL, Laycock WS, Waring JP, et al: Improvement in quality of life measures after laparoscopic antireflux surgery. Ann Surg 229:331-336, 1999. Medline Similar articles Full article
13. Watson DI, Jamieson JG, Pike GK, Davies N, et al: Prospective randomized double-blind trial between laparoscopic Nissen fundoplication and anterior partial fundoplication. Br J Surg 86:120-130, 1999.

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1. What is upper gastrointestinal (GI) bleeding?

Show answer
Bleeding from proximal to the ligament of Treitz (the transition point between duodenum and jejunum).

2. What are the most common causes of upper GI bleeding?

Show answer
In descending order of frequency, they are gastritis, duodenal ulcer, esophageal varices, benign gastric ulcer, esophagitis, and Mallory-Weiss tear. All other causes account for < 5% of cases.

3. What is the overall mortality rate of upper GI bleeding?

Show answer
Approximately 10%. Mortality is usually associated with comorbid factors such as cardiac, pulmonary, hepatic, and renal disease as well as age (> 60 years) and large transfusion requirements (> 5 units of blood). Patients who rebleed during the same hospitalization have a mortality rate of 30%.

4. What is the most common presentation of upper GI bleeding?

Show answer
Eighty percent of patients present with melena (blood is a cathartic, and patients pass black, tarry, or maroon-colored stools) or hematochezia (bright red blood in the rectum). Hematemesis (bright red or coffee-ground emesis) is diagnostic of an upper source of GI bleeding. Occult bleeding may present only with guaiac-positive stool.

5. How much GI blood loss is necessary to cause melena?

Show answer
As little as 50 mL. Occult bleeding (guaiac- or Hematest-positive) can be detected with as little as 10 mL of blood loss.

6. A 45-year-old man presents to the emergency department with massive hematemesis, tachycardia, and hypotension. What should the initial approach be?

Show answer
Acute GI hemorrhage requires a prompt and systematic approach. As in all critically ill patients, initially assess the ABCs (airway, breathing, circulation). Start two large-bore intravenous (IV) lines, and give 1 L of Ringer’s lactate while monitoring the patient. Place a nasogastric tube (NGT) and Foley catheter and irrigate the NGT with saline. Send blood for type and crossmatch and coagulation and liver function tests.

7. This patient stabilizes after your interventions. Is a medical history of any value in determining a cause of the bleeding?

Show answer
Yes. The following are pertinent:

* Previous symptoms of peptic ulcer disease or nonsteroidal anti-inflammatory drug use: bleeding duodenal or gastric ulcer
* History of gastroesophageal reflux disease: esophagitis
* Heavy alcohol use: gastritis or bleeding varices
* Recent retching or vomiting: Mallory-Weiss tear
* Weight loss: upper GI malignancy

8. What physical finding may be helpful in establishing the source of bleeding?

Show answer
Physical examination is generally not helpful. The stigmata of liver disease (jaundice, caput medusa, ascites, muscle wasting) raise the suspicion of variceal bleeding or multiple superficial gastric erosions.

9. What percentage of patients with known esophageal varices are bleeding from the varices on presentation?

Show answer
Only 50%.

10. Does bilious or clear NGT aspirate rule out an upper GI source of hemorrhage?

Show answer
No. Although NGT aspiration can be useful in directing the search for a bleeding site, one should keep in mind that the false-negative rate may be as high as 20%.

11. What studies can be used to determine the source of bleeding?

Show answer
Esophagogastroduodenoscopy (EGD) is the first and best test. Barium studies may miss a significant source of upper GI bleeding, such as erosive gastritis, and interfere with other more definitive tests, especially arteriography. Nuclear scans are of limited value in acute upper GI hemorrhage.

12. What is the sensitivity of EGD?

Show answer
EGD identifies the source of bleeding in up to 95% of cases. EGD has the advantage of directly visualizing the source of blood loss and provides the opportunity to biopsy a lesion and perform therapeutic maneuvers such as cauterizing a bleeder in a duodenal ulcer.
KEY POINTS: UPPER GI BLEEDING

1. Upper GI bleeding is defined as bleeding proximal to the ligament of Treitz.
2. The most common causes are gastritis, duodenal ulcer, esophageal varices, benign gastric ulcer, esophagitis, and Mallory-Weiss tear.
3. Eight percent of patients present with melena or hematochezia.
4. EGD identifies the source of bleeding in 95% of cases.

13. How can EGD be used to control nonvariceal bleeding?

Show answer
Electrocautery and injection of vasoconstrictors are well-established techniques. Other modalities such as argon beam coagulation, hemoclips, and cyanoacrylates (super glue) are promising.

14. What amount of bleeding is required to see a “blush” on arteriography?

Show answer
Less than 5 mL per minute. Although angiography is the most invasive of these tests, the catheter can be left in place and used for delivery of therapeutic vasopressin or embolization.

15. What treatment options are available to control variceal bleeding?

Show answer
Upper endoscopy with sclerotherapy or band ligation. In experienced hands, placement of a Sengstaken-Blakemore tube (a double balloon tube that permits direct tamponade of both gastric and esophageal varices) temporarily controls bleeding in 90% of cases. IV infusion of vasopressin or octreotide should decrease blood flow to the varices but is less successful in patients with more severe liver disease.

16. What are the indications for surgery in patients with upper GI hemorrhage?

Show answer
About 10% of patients eventually require surgery. Indications include:

* Persistent hypotension or shock (failure of resuscitative therapy)
* Recurrent bleeding while on maximal medical therapy
* High-risk patients with significant comorbid disease
* Large transfusion requirements (transfusion of more than two thirds of the patient’s blood volume in 24 hours)

17. What is the surgical approach to an unstable patient with a nonlocalized upper GI bleed who does not respond to initial resuscitation?

Show answer
At laporotomy start with a generous gastroduodenotomy centered over the pylorus. If this does not reveal a source of bleeding, proceed with a proximal gastrotomy.

18. A patient presents with hematemesis and has a remote history of an abdominal aortic aneurysm repair. What uncommon cause of upper GI bleeding needs to be considered?

Show answer
Aortoduodenal fistula. Any patient with a history of aortic surgery and evidence of GI bleeding should be aggressively worked up for aortoenteric fistula. The study of choice is endoscopy.

19. What is a Dieulafoy’s ulcer?

Show answer
A gastric vascular malformation with an exposed submucosal artery, usually within 2-5 cm of the gastroesophageal junction. It presents with painless hematemesis, often massive (fortunately, this is uncommon).

20. A patient recently admitted with a traumatic liver laceration is treated nonoperatively and later develops painless hematemesis. What do you suspect? How should you treat this patient?

Show answer
Hemobilia, another rare cause of upper GI bleeding, usually occurs after liver trauma or hepatic resection. Treatment consists of angiographic embolization.

21. What are other rare causes of upper GI bleeding?

Show answer
Watermelon stomach, portal hypertensive gastropathy, arteriovenous malformations, upper GI neoplasm, duodenal diverticulum, and pancreatitis (resulting in erosion into the splenic artery or splenic vein thrombosis with portal hypertension).

References
BIBLIOGRAPHY
1. Cameron JL: Current Surgical Therapy, 7th ed. St. Louis, Mosby, 2001.
2. Conrad SA: Acute upper gastrointestinal bleeding in critically ill patients: Causes and treatment modalities. Crit Care Med 30:365-368, 2002.
3. Fallah MA, Prakash C, Edmundowitz S: Acute gastrointestinal bleeding. Med Clin North Am 84:1183-1208, 2000. Medline Similar articles
4. Jamieson GG: Current status of indications for surgery in peptic ulcer disease. World J Surg 24:256, 2000. Medline Similar articles
5. Savides TJ, Jensen DM: Therapeutic endoscopy for nonvariceal gastrointestinal bleeding. Gastroenterol Clin North Am 29:465-487, 2000. Medline Similar articles

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3. The most common location of an undescended testicle is the
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4. The most common solid renal mass in infancy is a congenital
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5. Ogilvie’s syndrome is acute massive dilatation of the cecum
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6. The best screening method for prostate cancer is digital
   rectal exam combined with serum prostate-specific antigen.
7. The most common histologic type of bladder cancer is
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8. Carcinoma in situ of the bladder is treated with
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9. Localized renal cell carcinoma is treated with surgery
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10. The most common cause of male infertility is varicocele.
11. The most common nonbacterial cause of pneumonia in
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12. Chimerism is leukocyte sharing between the graft and the
    recipient so that the graft becomes a genetic composite of both the
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13. OKT3 is a mouse monoclonal antibody that binds to and
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14. The most common disease requiring liver transplant is
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15. Cystic hygroma is a congenital malformation with a
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    as a soft mass in the lateral neck.
16. In neuroblastomas, age at presentation is the major
    prognostic factor. Children younger than 1 year have an overall
    survival rate > 70%, whereas the survival rate for children older
    than 1 year is < 35%.
17. The most feared complication of diaphragmatic hernia is
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18. The three most common variants of tracheoesophageal fistula
    are (1) proximal esophageal atresia with distal tracheoesophageal
    fistula, (2) isolated esophageal atresia, and (3) tracheo-esophageal
    fistula with esophageal atresia.
19. Atresia can occur anywhere in the GI tract: duodenal (50%),
    jejunoileal (45%), or colonic (5%). Duodenal atresia arises from
    failure of recanalization during the 8th-10th week of gestation;
    jejunoileal and colonic atresia are caused by an in utero mesenteric
    vascular accident.
20. The types of aortic dissection are ascending (type A)
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    descending aorta, and descending dissection (type B), which involves
    only the descending aorta.
21. A solitary pulmonary nodule is < 3 cm and is discrete on
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22. Mediastinal staging is indicated in patients with apparent
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23. The most common causes of aortic stenosis are now
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25. The indications for CABG are (1) left main coronary artery
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    depressed left ventricular (LV) function or two-vessel coronary artery
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    associated with a decrease in coronary flow in the setting of preserved
    myocardial viability. Some patients with global systolic dysfunction
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27. The surgical treatment of ulcerative colitis is total
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28. Dieulafoy’s ulcer is a gastric vascular malformation with
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29. The role of blind subtotal colectomy in the management of
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    patients in whom a specific bleeding source cannot be identified. The
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30. Colorectal polyps < 2 cm have a 2% risk of containing
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31. Patients with colorectal cancer with lymph node involvement
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32. Goodsall’s rule states the location of the internal opening
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33. Incarcerated inguinal hernia: structures in the hernia sac
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47. The absolute reduction in risk of stroke is 6% over a
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48. Abdominal aortic aneurysm’s average expansion rate is 0.4
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50. The patient with suspected intermittent claudication should
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52. Nitric oxide is synthesized in vascular endothelial cells
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56. Dextrose has 3.4 kcal/g, protein 4 kcal/g, fat 9 kcal/g
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67. Rebound tenderness implies peritoneal inflammation and
    irritation not simply abdominal tenderness.
68. The 5 Ws of post-operative fever are wound
    (infection), water (UTI), wind (atelectasis,
    pneumonia), walking (thrombophlebitis), and wonder
    drugs (drug fevers).
69. Cricothyroidotomy should not be performed in
    patients < 12 years old or any patient with suspected direct
    laryngeal trauma or tracheal disruption.
70. The radial (wrist) pulse estimates SBP > 80 mmHg;
    femoral (groin) pulse estimates SBP > 70 mmHg; and carotid (neck)
    pulse estimates SBP > 60 mmHg.
71. A general rule for crystalloid infusion to replace blood
    loss is a 3:1 ratio of isotonic crystalloid to blood.
72. Raccoon eyes (periorbital ecchymosis) and Battle’s sign
    (mastoid ecchymosis) are clinical indicators of basilar skull fracture.
73. CPP = MAP – ICP. Some debate exists on the minimum
    allowable CPP, but consensus indicates that a cerebral perfusion
    pressure of 50-70 mmHg is necessary.
74. Violation of the platysma defines a penetrating neck wound.
75. Tension pneumothorax is air accumulation in the pleural
    space eliciting increased intrathoracic pressure and resulting in a
    kinking of the SVC and IVC that compromises venous return to heart.
76. The most common site of thoracic aortic injury in blunt
    trauma is just distal to the take-off of the left subclavian artery.
77. The most common manifestation of blunt myocardial injury is
    arrhythmia.
78. Indications for thoracotomy in a stable patient with
    hemothorax include an immediate tube thoracostomy output of > 1500
    mL and ongoing bleeding of 250 mL/h for 4 consective hours.
79. Beck’s triad is hypotension, distended neck veins, and
    muffled heart sounds.
80. The hepatic artery supplies approximately 30% of blood flow
    to the liver while the portal vein supplies the remaining 70%. The
    oxygen delivery, however, is similar for both at 50%.
81. The Pringle maneuver is a manual occlusion of the
    hepatoduodenal ligament to interrupt blood flow to the liver.
82. Splenectomy significantly decreases IgM levels.
83. 90% of trauma fatalities due to pelvic fractures are due to
    venous bleeding and bone oozing; only 10% of fatal pelvic bleeding from
    blunt trauma is arterial (most common site is superior gluteal artery).
84. Intraperitoneal bladder rupture from blunt trauma:
    operative management; extraperitoneal rupture: observant management.
85. Pseudoaneurysm is a disruption of the arterial wall leading
    to a pulsatile hematoma contained by fibrous connective tissue (but not
    all three arterial wall layers, which defines a true aneurysm).
86. The earliest sign of lower extremity compartment syndrome
    is neurologic in the distribution of the peroneal nerve with numbness
    in the first dorsal webspace and weak dorsiflexion.
87. Posterior knee dislocations are associated with popliteal
    artery injuries and are an indication for angiography.
88. Management of suspected navicular fracture despite negative
    radiography is short-arm cast and repeat x-ray in 2 weeks; at high risk
    for avascular necrosis.
89. Parkland formula: lactated Ringer’s at 4 mL/kg x %TBSA
    (second- and third-degree only) of burn. Infuse 50% of volume in first
    8 hours and the remaining 50% over the subsequent 16 hours.
90. The metabolic rate peaks at 2.5 times the basal metabolic
    rate in severe burns > 50% TBSA.
91. Gallstones and alcohol abuse are the two main causes of
    acute pancreatitis.
92. Alcohol abuse accounts for 75% of cases of chronic
    pancreatitis.
93. Isolated gastric varices and hypersplenism indicate splenic
    vein thrombosis and are an indication for splenectomy.
94. The treatment for gallstone pancreatitis is cholecystectomy
    and intraoperative cholangiogram during the same hospital stay once the
    pancreatitis has subsided.
95. Proton pump inhibitors irreversibly inhibit the parietal
    cell hydrogen ion pump.
96. Definitive treatment of alkaline reflux gastritis after a
    Billroth II includes a Roux-en-Y gastro-jejunostomy from a 40-cm
    efferent jejunal limb.
97. Cushing’s ulcer is a stress ulcer found in critically ill
    patients with central nervous system injury. It is typically single and
    deep, with a tendency to perforate.
98. Curling’s ulcer is a stress ulcer found in critically ill
    patients with burn injuries.
99. Marginal ulcer is an ulcer found near the margin of
    gastroenteric anastomosis, usually on the small bowel side.
100. The most common cause of small bowel obstructions is
     adhesive disease; the second most common cause is hernias.