DUODENAL ULCER DISEASE

1. What is the risk of duodenal ulcer disease?

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The lifetime risk for duodenal ulcer is about 1 in 14. It usually occurs between ages 20 and 60 years, with peak incidence in the fourth decade of life. It is more common in males. Hemorrhage is the most common cause of hospital admission. The annual number of deaths in the United States is about 10,000 deaths caused by duodenal ulcers.

2. What is the role of Helicobacter pylori in duodenal ulcer?

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Helicobacter pylori, a gram-negative bacillus, is strongly associated with peptic ulcer disease. It is isolated from antral mucosa in 80% of patients with peptic ulcer disease. Ulcers may occur in the absence of H. pylori. These ulcers occur in the setting of hyperacid secretion, normal acid secretion, or after acid reduction operations such as vagotomy. Recurrent or multiple ulcerations may indicate an underlying endocrine disease. The breakdown of the duodenal mucosal barrier probably also contributes to ulcerogenesis.

3. Is acid hypersecretion necessary for peptic ulcer disease?

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No. Gastric hypersecretion of acid and pepsin plays an important role in ulcer formation; however, only 40% of ulcer sufferers manifest acid hypersecretion.

4. What are the clinically important complications of H. pylori infection?

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Peptic ulcer disease: As noted, H. pylori is present in 80% of peptic ulcers. Conversely, 50% of the general population harbors this organism, but only a small percentage of people develop ulcers. H. pylori may be part of the indigenous human gastric flora; antigens were detected in pre-Columbian Central American mummies whose last meal was 1700 years ago.
Gastric carcinoma: H. pylori is strongly linked to gastric cancer and is now classified as a group I carcinogen. It may also cause mucosa-associated lymphoid tissue lymphoma.
Barrett’s esophagus is a possible H. pylori-associated disease, although it is more commonly associated with chronic gastroesophageal reflux.
H. pylori probably synergizes with nonsteroidal anti-inflammatory drug (NSAID) use.

5. What is the most commonly used test for H. pylori?

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The CLO test detects the presence of H. pylori. H. pylori releases urease, which breaks down urea to ammonia and bicarbonate, thus increasing the pH. The CLO test can be performed at the time of endoscopy by obtaining scrapings from the antral mucosa.
If endoscopy is not available, the enzyme-linked immunosorbent assay (ELISA) may be used to detect anti-H. pylori IgA and IgG antibody titers.
Direct culture of the organism should be reserved for cases in which antibiotic resistance becomes the issue.

6. What other risk factors are associated with duodenal ulcer disease?

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* Cigarette smoking is a major risk factor; its cessation is a key component of ulcer therapy.
* Blood group O is associated with higher incidence of duodenal ulcer, as are leukocyte antigens HLA-B5, B12, and BW35.
* NSAIDs promote ulcer formation by suppressing systemic prostaglandin production.
* Chronic pancreatitis, cirrhosis, emphysema, and alpha-1 antitrypsin deficiency are also associated with the condition.

7. Which endocrine disorder is associated with severe ulcer disease?

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Patients with multiple endocrine neoplasia (MEN) type I have a 75% incidence of gastrinoma with severe ulcer diathesis.

8. What other endocrine disorders should be screened?

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Pituitary tumor and hyperparathyroidism should be suspected when MEN type I is considered.

9. What are the clinical presentations of peptic ulcer disease?

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* Pain is usually epigastric in origin, although radiation to the back may indicate pancreatic involvement. It is often relieved by food or antacid ingestion. Nausea and vomiting may occur.
* Upper gastrointestinal (GI) bleeding.
* Gastric outlet obstruction (GOO) may result from pyloric spasm, inflammatory mass constriction, duodenal scarring, or fibrosis.
* Perforation is a surgical emergency with a mortality rate as high as 10%. Perforation may occur without a history of peptic ulcer disease, especially if the ulcer is situated on the anterior surface of the duodenum.

10. How does the location of the ulcer affect its clinical presentation?

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Anterior wall ulcers (usually first portion of duodenum) may perforate and cause peritonitis with free air in the abdomen. Posterior ulcers may erode into the gastroduodenal artery or pancreas.

11. What are the differential diagnoses of epigastric pain?

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In addition to peptic ulcer disease, gastroesophageal reflux disease, gastritis, gastric carcinoma, biliary tract disease, pancreatitis or pancreatic carcinoma, aortic aneurysm, intestinal angina (ischemia), and myocardial ischemia should be considered.

12. What initial test should be performed when evaluating epigastric pain of presumed GI origin?

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Flexible esophagogastroduodenoscopy (EGD) is preferred, although the upper GI contrast study with barium may be acceptable. The CLO test can be performed at the time of the EGD if indicated. Ultrasound should be performed if gallbladder or vascular diseases are suspected. A lateral-view angiogram for intestinal angina, computed tomography (CT) scan for aneurysm, and a baseline electrocardiogram should be obtained because ischemic heart disease is always possible.

13. How are patients with duodenal ulcer treated?

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* Diet: Aspirin and NSAIDs must be discontinued. Alcohol and nicotine should be avoided.
* Antacids: Neutralizing gastric pH may alleviate symptoms, but its impact on ulcer healing is not well defined.
* H2 receptor antagonists: The use of cimetidine or ranitidine prevents gastric acid secretions by blocking the H2 histamine receptor.
* Sucralfate: A protective-barrier medicine adheres to the ulcer base, providing a protective coating. Medications that decrease acid secretion should not be used at the same time because sucralfate requires an acidic environment to be activated.
* Proton pump inhibitors: Omeprazole blocks the hydrogen-potassium adenosine triphosphatase pump in the gastric parietal cells and inhibits hydrogen ion release. It usually is reserved for failures of first-line therapy (i.e., H2 receptor antagonists).
* H. pylori eradication: If H. pylori infection is diagnosed, the combination of triple therapy (bismuth, tetracycline, and metronidazole) with an H2 receptor antagonist regimen appears to provide a 90% cure rate. Erythromycin, amoxicillin-omeprazole, or erythromycin-omeprazole may be added for initial failures.

14. What are the recurrence rates after medical therapy?

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Approximately 80% of duodenal ulcers heal in 6 weeks. The recurrence rate within 1 year of treatment is 70%; thus, repeated treatment may be necessary.

15. What complications are associated with medical therapy?

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H2 receptor antagonists may induce mental status changes and gynecomastia. Cimetidine, in particular, may affect hepatic metabolism of warfarin, phenytoin, theophylline, propranolol, and digoxin, leading to abnormal serum levels. Omeprazole may cause hypergastrinemia by blocking gastric acid secretion. H. pylori resistance to antibiotics may develop, especially to metronidazole; therefore, a triple combination of at least two antimicrobials with an acid inhibitory drug is recommended as initial therapy.

16. How should recurrent or multiple ulcers be evaluated?

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In addition to the previously mentioned workup, serum gastrin levels should be obtained to evaluate for possible endocrine disorder. Patients should not be taking omeprazole when gastrin levels are measured. In Zollinger-Ellison syndrome, gastrin hypersecretion from the pancreatic islet tumor results in multiple or intractable ulcers (normal serum gastrin, < 200 pg/mL; Zollinger-Ellison syndrome, usually > 500 pg/mL).

17. How do you evaluate a borderline serum gastrin value (200-500 pg/mL)?

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The secretin stimulation test may be used to diagnose Zollinger-Ellison syndrome. An intravenous bolus of secretin (2 U/kg) should result in an increase of gastrin of 150 pg/mL within 15 minutes if the patient has this syndrome.

KEY POINTS: HELICOBACTER PYLORI

1. H. pylori is a gram-negative urease-producing bacillus.
2. It has a strong association with peptic ulcer disease (80% of ulcer patients).
3. It is linked to development of mucosa-associated lymphoid tissue lymphoma (MALT).
4. Is is associated with development of gastric carcinoma.
5. H. pylori infection is diagnosed by EGD biopsy and CLO test.
6. Treatment includes triple antibiotic therapy supplemented with acid-reduction medication (90% cure rate).

18. What are the indications for operative treatment of duodenal ulcers?

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Failure of medical management to control pain, bleeding (< 6 units of packed red blood cell transfusions in 24 hours or, better yet, two thirds of the patients calculated blood volume loss in 24 hours), and obstruction are the usual indications. Perforation of the ulcer is usually treated surgically unless the patient presents 24 hours after the event without peritonitis and the Gastrografin upper GI series confirms that the perforation has been well sealed (usually with omentum).

19. What operations are used to treat duodenal ulcers?

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* Truncal vagotomy and pyloroplasty (V and P) or gastrojejunostomy
* Truncal vagotomy and antrectomy with Billroth I or II anastomosis
* Subtotal gastrectomy with Billroth I or II anastomosis
* Selective vagotomy (just the vagal branches to the parietal cells in the stomach)
* Total gastrectomy

20. What are Billroth I and Billroth II anastomoses?

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The Billroth I operation is an anastomosis between the duodenum and the gastric remnant (gastroduodenostomy). The Billroth II operation is constructed by sewing a loop of jejunum to the gastric remnant (gastrojejunostomy). Either method is acceptable.
21. Which procedure is preferred, Billroth I or Billroth II? Show answer
Billroth I has the advantages of eliminating the duodenal stump and requiring only one suture line instead of two (as in Billroth II). Duodenal stump blowout is a critical surgical emergency that requires immediate laparotomy. Afferent loop syndrome (i.e., sludging of stuff in the loop that is not in the enteric stream) is also a complication of Billroth II. Bile reflux gastritis may occur in both procedures. Billroth I is more physiologic; thus, it results in better protein and fat digestion. Billroth I is more susceptible to gastric outlet obstruction with ulcer or tumor recurrence; therefore, a Billroth I hook-up is not recommended for patients with gastric carcinoma.

22. What is afferent loop syndrome?

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Postprandial abdominal pain often is relieved by bilious vomiting. A narrowing at the junction of the stomach and duodenal side of a Billroth II anastomosis leads to biliary and pancreatic fluid build-up within the afferent limb of the intestine. Pain is relieved when the fluid content is emptied into the stomach, which may result in bilious vomiting and severe reflux gastritis.

23. How is afferent loop syndrome prevented?

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Prevention requires avoidance of a long or twisted afferent limb with too narrow an anastomosis during Billroth II construction. A Billroth I procedure eliminates this possible problem.

24. Who was Billroth?

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Christian Albert Theodor Billroth (1829-1894) was an Austrian surgeon credited with performing the first successful gastric resection in 1881 and introducing innovations to intestinal bypass surgery. The father of modern American surgery, William Halsted, was once an apprentice to Billroth in Vienna.

25. How does alkaline or bile reflux gastritis occur?

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Reflux of bile and pancreatic secretions into the stomach after a Billroth II (sometimes Billroth I) anastomosis may cause marked gastric irritation, leading to chronic postprandial pain. Persistent pain should be evaluated with endoscopy, and surgical reconstruction should be considered, usually with a Rouxen-Y gastrojejunostomy from a 40-cm efferent jejunal limb.

26. What is selective vagotomy?

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In this limited proximal vagotomy, the gastric parietal cells are selectively denervated. Fibers to antrum, pylorus, liver, biliary tract, and the rest of the intestinal tract are left intact, thereby precluding the need for a gastric emptying procedure. Recurrence of ulcer disease may be 10% or greater, but its side effects, namely dumping (caused by resection of the pylorus) or diarrhea (caused by the vagotomy), are minimized to 2%.

27. What is dumping syndrome?

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Resection of the pylorus can lead to uncontrolled, rapid emptying of hyperosmolar gastric contents into the proximal small bowel. The osmotic and glucose load in the intestine sucks intravascular volume into the gut, making the patient transiently hypovolemic. The physiologically appropriate adrenergic response to this volume shift produces tachycardia, sweating, flushing, weakness, nausea, abdominal cramps, and even syncope. Ingesting a small, dry, low-carbohydrate meal (to limit the available osmols) may prevent this syndrome. Anticholinergic drugs also may help. As many as 20% of patients experience the dumping syndrome in the early postoperative period, but only 2% develop chronic problems.

28. What must accompany truncal vagotomy?

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Truncal vagotomy denervates the stomach, resulting in gastric hypomotility. Some gastric emptying procedure such as a pyloroplasty or a side-to-side gastroduodenostomy should be performed.

29. What is a Heinecke-Mikulicz pyloroplasty?

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A pyloduodenal incision along the longitudinal axis followed by a transverse closure flops the pylorus open and promotes gastric emptying.

30. What is a Finney pyloroplasty?

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A side-to-side gastroduodenal anastomosis that transects and defunctionalizes the pylorus and promotes gastric emptying

31. What is a Jaboulay pyloroplasty?

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This gastric emptying procedure comprises a side-to-side gastroduodenal anastomosis that does not transect the pylorus. It is ideal if severe pyloric scarring is present.

32. What are the rates of ulcer recurrence after surgical treatment?

Vagotomy and pyloroplasty: 10%
Vagotomy and antrectomy: 2%
Highly selective vagotomy: 10%
Subtotal gastrectomy: 1%
Total gastrectomy: < 1%

33. What is the mortality rate of these operations?

Vagotomy and pyloroplasty: 1%
Vagotomy and antrectomy: 2%
Highly selective vagotomy: 0.1%
Subtotal gastrectomy: 2%
Total gastrectomy: 5%

34. How are patients with perforated duodenal ulcers treated?

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The patient must be resuscitated first, following the ABCs of airway, breathing, and circulation. The stomach contents are emptied via nasogastric tube. Surgical closure by omental patch (Graham closure) is widely practiced. For hemodynamically stable patients, oversewing of the ulcer followed by a selective vagotomy is appropriate. Antrectomy with vagotomy to remove the ulcer is appropriate if the patient has an intractable peptic ulcer.

35. What (ulcer-specific question) should you always ask before you proceed to the operating room?

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Past history of ulcer disease. Choice of operation will depend on acute versus chronic ulcer disease.
36. What is the long-term result after Graham closure of a perforated ulcer? Show answer
One third of patients remain asymptomatic, one third have symptoms controlled by medical treatment, and one third require an additional ulcer operation.

37. What are the complications of surgery for duodenal ulcers?

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Duodenal stump leakage may occur within the first week after antral resection and Billroth anastomosis. Treatment consists of prompt reoperation to drain and control the leak. Total parenteral nutrition may be required as a “bowel rest” adjunct.
Gastric retention may occur because of edema at the anastomosis or atony of the stomach after vagotomy. It usually resolves spontaneously in 3-4 weeks.
Bleeding may occur from a suture line, a missed ulcer, or other gastric mucosal lesions. Most postgastrectomy bleeding ceases spontaneously, but endoscopy may be necessary in some cases.

38. Where do ulcers recur after operation?

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Ulcers usually recur adjacent to the gastric anastomosis on the intestinal side (i.e., jejunum, duodenum).

39. Why do they recur?

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The responsible factors are inadequate gastric resection, incomplete vagotomy, inadequate drainage of the gastric remnant (stasis of gastric contents proximal to the anastomosis), or retained gastric antrum (gastrin-producing cells) after a Billroth II procedure.

40. How do you treat pyloric stenosis?

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Fluid resuscitation and nasogastric tube decompression should be initiated. Metabolic alkalosis may result from prolonged vomiting (loss of hydrogen ions) and should be corrected with normal saline infusion. Either vagotomy with gastrojejunostomy or resection of the stenosis with a Billroth II bypass is acceptable. Partial gastrectomy is required less often.

1. What are the four principles of medical ethics?

1. Beneficence describes the active role of doing good by intervention.
2. Nonmaleficence is equivalent to saying, “First do no harm.”
3. Autonomy accounts for informed consent, competence, and the patient’s right to refuse treatment and to know what’s going on.
4. Justice means that all patients should receive fair and equal care but that one patient’s care should not squander limited resources for others.

2. What is a do-not-resuscitate (DNR) order?

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A DNR order instructs the surgeon not to resuscitate the patient if cardiopulmonary arrest occurs; however, a DNR order is much more involved and complicated than the acronym would have you believe. DNR is not absolute.
The Joint Commission for the Accreditation of Healthcare Organizations mandates that hospitals have written guidelines that promote accountability for DNR orders. All DNR orders must be documented in writing, similar to all other orders, in the appropriate section of the patient’s chart. They should specify the treatments to be withheld and treatments that the patient wishes to have implemented. Patients and families must participate in the DNR decision. Moreover, the DNR status should be discussed and reviewed with the other members of the health care team. Finally, a DNR order does not mean that the patient should be medically abandoned.

3. What is the difference between withdrawing and withholding support?

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A decision to withdraw should not be more problematic than a decision to withhold, because one cannot be sure that an intervention will work until you try it. There is no moral or ethical distinction between withdrawal and withholding of support. Either of the two allows natural progression of disease without the interface of medical technology. The decision to withdraw or withhold support does not equate with patient death, although the probability of death may be greater. After the decision has been made, appropriate management should focus on the patient’s comfort and psychosocial support.

4. What is an advance directive?

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An advance directive is a method of delineating a competent patient’s wishes for application at a time when he or she is no longer competent. Medical management or the lack thereof can be based on the patient’s wishes rather than a perceived sense of what is best for the patient. Advance directives may be an informal document, such as a living will, or a formal legal document, such as medical durable power of attorney.

5. What is durable power of attorney?

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A durable power of attorney is a patient-appointed proxy decision maker. The proxy decision maker becomes active as soon as the patient is no longer able to make competent medical decisions. Hence, the durable power of attorney must have been established in advance of the cognitive decline of the patient.

6. What is a living will?

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A living will, much like a durable power of attorney, is a formal advanced directive in which a competent patient produces a pre-illness guideline for future care in accordance with his or her wishes.

7. What is included in informed consent?

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Information about the patient’s condition as well as risks and benefits of the recommended treatment are included. Moreover, the operative and nonoperative alternatives (including no treatment) should be discussed with the patient. The patient’s understanding of the information and alternatives should be assessed as part of the informed consent. Finally, informed consent is a voluntary decision made by the patient or on behalf of the patient by a proxy decision maker.

8. What are futile care and medical futility?

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Ultimately, old age and disease will conquer us all. The definition of medically futile or inappropriate treatment is still debated. Nonetheless, there are four main concepts of medical futility:

1. Health care professionals are not required to provide physiologically futile treatment.
2. Imminent demise argues against treatment if the patient has no likelihood of survival to discharge.
3. Under the concept of lethal condition, medical care is considered futile if the patient will survive temporarily but ultimately expire as a result of the ongoing disease process.
4. Quality of life or qualitative futility argues against treatment if the patient’s quality of life is so poor that it would be unreasonable to prolong life.

Care must be taken, however, in making medical decisions based on futility because these decisions may lead to self-fulfilling prophecies.

9. What are the clinical determinants of brain death?

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Many of the current concepts of brain death are based on the 1968 report from the ad hoc committee at Harvard Medical School, which called for a new neurologic definition of brain death. But it was not until 1981 that BEMAT justified the neurologic criteria of brain death by stressing the need for intact brainstem integrative function in order for a person to function as a whole. By definition, brain death requires loss of brainstem reflexes in an irreversibly comatose patient. Brain death includes loss of the pupillary, corneal, oculovestibular, oculocephalic, oropharyngeal, and respiratory reflexes for ≥ 6 hours. The patient also should undergo an apnea test, in which the pCO2 is allowed to rise to at least 60 mmHg without coexistent hypoxia. The patient should be observed for the absence of spontaneous breathing. Other ancillary tests are not essential; for example, it is not necessary to perform an intravenous radioisotope cerebral angiogram or a four-vessel contrast cerebral angiogram or to document an isoelectric (”flat”) electroencephalogram.
Of note, all of the above criteria for brain death require the absence of central nervous system depression caused by barbiturates, narcotics, or hypothermia.

10. What is a persistent vegetative state?

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In a persistent vegetative state, typically seen after improvement of a comatose state, the patient lies motionless and without activity. The patient appears to be awake but does not have awareness of his or her surroundings or higher mental activity. Other names for this entity are coma vigil and akinetic mutism.

11. What is euthanasia?

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Euthanasia requires that the physician play an active role in assisting in the death of the patient. The concepts of physician-assisted suicide and active and passive euthanasia are highly controversial. In 1992, the Society of Critical Care Medicine published the results of a survey of critical care specialists; 87% had withdrawn life-prolonging support from patients. In addition, the most recent U.S. law pertaining to assisted suicide was passed in Oregon in 1994. This law makes it legal for a physician to prescribe medication to terminally ill patients for the purpose of committing suicide.

12. Who should approach patients’ families about organ donation?

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Some claim that the physician who has established good rapport with the patient’s family should raise the issue of organ donation. Others believe that the local organ procurement personnel should approach the family because they have greater interest and training in the process. The best approach is probably a combined one.

13. What should patients’ families be told when organ donation is feasible?

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The surgeon should stress that the patient has died despite an actively beating heart. The family should be questioned about the patient’s wishes regarding organ donation. All topics should be based on the concepts of informed consent. The family should be informed of the likelihood that several patients will benefit from the donated organs. The family needs to understand that there is no guarantee that the organs will be suitable for donation. They should be assured that they are not responsible for the cost of care provided after brain death is determined and that they may refuse organ donation without fear of prejudice.

14. What is the role of the hospital ethics committee?

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The hospital ethics committee educates hospital staff members, creates policy, and provides a source of consultation.
The function of education is accomplished through grand rounds, seminars, special lectures, and journal clubs. The hospital ethics committee should be viewed as an intrinsic part of the hospital community. Developed policies should be reviewed by other committees and divisions of the hospital to foster a better sense of cohesiveness when ethical and moral dilemmas arise. The consultative function of the ethics committee produces the greatest amount of controversy. In fact, many hospitals negate this function by stating that it interferes with the physician-patient relationship. The hospital ethics committee can and should provide an arena for collaboration and general ethical education within the hospital.

References
BIBLIOGRAPHY
1. Ad Hoc Committee of the Harvard Medical School to Examine the Definition of Brain Death: A definition of irreversible coma. JAMA 205:337-340, 1968.
2. Aminoff MJ: The central nervous system. In Medical Diagnosis and Treatment. Norwalk, CT, Appleton & Lange, 1996.
3. Arnold RM, Siminoff LA, Frader JE: Ethical issues in organ procurement: A review for intensivists. Crit Care Med 12:29-48, 1996. Full article
4. Bernat JL, Culver CM, Gert B: On the definition and criterion of death. Ann Intern Med 94:389-394, 1981. Medline Similar articles Full article
5. Harken AH: Enough is enough. Arch Surg 10:1061-1063, 1999. Full article
6. Kelley DF, Hoyt JW: Ethics consultation. Crit Care Med 12:49-70, 1996.
7. McCollough L, Jones J, Brody B: Surgical Ethics. Oxford, Oxford University Press, 1998.
8. Nyman DJ, Eidelman AL, Sprung CL: Euthanasia. Crit Care Clin 12:85-96, 1996. Medline Similar articles
9. Society of Critical Care Ethics Committee: Attitudes of critical care medicine professionals concerning foregoing life-sustaining treatments. Crit Care Med 20:320-326, 1992.
10. State of Oregon: ORS.251.215, The Oregon Death with Dignity Act. Official 1994 Oregon General Election Handbook, 1994, pp 121-124.
11. Younger SJ: Medical futility. Crit Care Clin 12:165-178, 1996.

1. What infectious diseases are transmissible via blood transfusion?

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In developed nations with mature blood banking systems, by far the most common transfusion-acquired infections are hepatitis from the hepatitis B (HBV) and C (HCV) viruses. Other less commonly transmitted agents include the human immunodeficiency virus (HIV) and cytomegalovirus (CMV). Even rarer but still occasionally reported bloodborne infections are parasitic diseases such as malaria (genus, Plasmodium), babesiosis (genus, Babesium), Chagas disease (Trypanasoma cruzi), toxoplasmosis (Toxoplasma gondii), the lymphomas and leukemias caused by the human T-cell lymphotropic virus (HTLV-I), and infectious mononucleosis (Epstein-Barr virus). Bacterial contaminations are also rare but possible, especially in platelet preparations that are stored at room temperature. This may result in a toxic shock-like syndrome, the risk of which has been estimated as equivalent to the risk of HIV transmission.

2. What are the estimated risks of HBV, HCV, and HIV transmission by blood transfusion in the United States?

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3. Which bloodborne pathogens pose a risk to surgeons?

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Although the epidemic of HIV has increased general concern about bloodborne pathogens, the prevalence of hepatitis C virus (HCV) throughout North America has led to a shift of emphasis from HIV to hepatitis. Hepatitis B is an occupational risk in surgery, but vaccinations and a relatively efficient post-exposure protocol have reduced the consequences of contamination with HBV. Surgeons in the United States care for more patients with chronic hepatitis C than with chronic hepatitis B, and no vaccine is available for HCV infection. Although the rate of seroconversion for hepatitis C is 10% versus 30% for hepatitis B, when acute infection occurs, there is a much higher chance of developing chronic hepatitis (50% versus 10%) after HCV infection. Thus, HCV infection is the greatest threat to surgeons.

4. What is the risk to health care workers of exposure to HBV?

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The number of new infections in 2001 has dropped to approximately 78,000 from the estimated yearly incidence of 260,000 in the 1980s. At present, 1.25 million U.S. residents have chronic hepatitis B, with the highest prevalence occurring among 20-49-year-old individuals. Thirty percent of percutaneous hollow needle exposures are followed by acute infection. Thirty percent of hepatitis B cases are clinically occult, and ≤ 10% of infected people remain viral carriers for life. Many carriers are asymptomatic and suffer no active liver disease, although they are potentially infectious to others. Twenty-five percent of HBV-infected individuals eventually die from hepatic diseases.

5. What is the risk to health care workers of exposure to HCV?

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The number of new infections in 2001 was 25,000, down from 240,000 per year in the 1980s. Currently, 3.9 million (1.8%) U.S. residents have HCV infection, of whom 2.7 million are infected chronically. The risk of seroconversion from a percutaneous hollow needle injury is 10%, but 90% of acute infections result in the chronic carrier state, which is typically asymptomatic. Although these data are still controversial, 50% of HCV infected patients will develop cirrhosis, and 50% of these patients will develop a hepatoma.

6. What is the risk to health care workers of exposure to HIV?

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The risk of HIV seroconversion after percutaneous inoculation with HIV-contaminated blood is approximately 0.3%. Risk of infection also appears to be greater when the source of the blood is a terminally or severely ill patient. The U.S. Centers for Disease Control and Prevention (CDC) reports that 57 health care workers in the U.S. have been documented as seroconverting to HIV as a result of an occupational exposure to the virus. The majority of these individuals were either nurses (n = 24) or laboratory workers (n = 19); physicians accounted for only six of these cases. The routes of infection were percutaneous (puncture or cutting wounds) in 84% of the cases. Thus, the risk appears small relative to the large number of exposures that have probably occurred since the onset of the epidemic in the early 1980s. The CDC also reports that as of January 1, 1998, there has been no documented transmission of HIV infection from a patient to a surgeon secondary to occupational exposure.

7. How well does hepatitis B vaccination protect against the disease?

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Effective protection against hepatitis B correlates positively with post-immunization anti-hepatitis B surface antibody (anti-HBs) serum titers of ≥ 10 mIU/mL. These titers are achieved in 95% of young, healthy recipients of the standard three-dose immunization regimen, and the actual protective efficacy (i.e., ability of the vaccine to prevent the disease) is estimated to approach 100% in these individuals. Although about 50% of successfully vaccinated adults demonstrate a decrease in their anti-HBs levels to nondetectable levels by 10 years, continued immunologic protection is thought to persist via the amnestic humoral response. Because of the persistence of this “immune memory” to the viral antigen, healthy individuals appear to enjoy lifelong protection after vaccination and do not require booster doses. A bivalent vaccine immunizing against both hepatitis A and B was approved in 2001 by the U.S. Food and Drug Administration for individuals 18 years of age and older, and it is as successful as the monovalent vaccine in conferring protection from the HBV infection with the added benefit of protecting against hepatitis A viral infection.

8. Are patients at risk of infection from surgeons who are infected with HBV?

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Transmission of hepatitis B infection from surgeons to patients has been documented. Surgeons who are at risk for transmitting infection to patients are generally positive for the e-antigen of hepatitis B. The e-antigen is a degradation product of the nucleocapsid of the virus and represents active viral replication within the liver. People who test positive for the e-antigen have high viral titers and are quite infectious. The large number of documented transmissions of HBV to patients by surgical providers is particularly troublesome and may require restriction of clinical privileges. Furthermore, a recent report from England documented transmission of HBV infection from surgeons to patients even when the surgeon was negative for the e-antigen.

9. What is the proper response after percutaneous exposure to a patient with known hepatitis B?

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This depends on the provider’s vaccination status. Older individuals show a tendency to mount a weaker or delayed immunologic response as measured by peak serum titers of anti-HBs. If the provider has been vaccinated and has a positive antibody titer, no additional response is necessary. If the provider has not been vaccinated and is negative for antibodies to HBV or if the provider completed the series of vaccinations but exhibited a weak or absent antibody titer, then he or she should receive a dose of hepatitis B immunoglobulin and begin the hepatitis B vaccination series. For surgeons who were successfully immunized against HBV in the past, neither routine booster doses nor routine immunity status surveillance is recommended.

10. What are the recommendations for hepatitis C immunization?

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There is currently no effective vaccine available against HCV. Immunoglobulin for HCV does not confer protection. Using universal barrier precautions remains the best strategy.

11. Does laparoscopic surgery minimize the risk of HIV contamination?

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The laparoscopic technique reduces exposure to blood products and sharp instruments; however, the risks are different. The evacuation of the pneumoperitoneum during laparoscopic procedures releases aerosolized HIV-infected blood and peritoneal fluid into the operative suite. Evacuation of the pneumoperitoneum into a closed system diminishes this exposure.

12. Is double gloving an effective method of protection?

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Although double gloving may not prevent percutaneous injury, it clearly reduces blood exposure. The contact rates between blood and the surgeon’s skin are decreased by 70% when the surgeon wears two pairs of gloves. Whereas outer glove perforation occurs in 25% of cases, inner glove perforation occurs in only 10% of cases (surgeons, 8.7%; assistants, 3.7%). The longer the procedure, the more frequent are inner glove perforations. The nondominant index finger is the most common target.

13. Are eye splash injuries a major threat to surgeons?

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A CDC study demonstrated that approximately 13% of documented HIV transmissions occurred by mucocutaneous contact. Eye splash injuries during surgery are often underestimated, although they are the easiest type of contact to prevent. A recent study examined 160 eye shields used by surgeons and assistants. All operations lasted ≥ 30 minutes. The shields were inspected for macroscopic splashes and then tested for microscopic splashes. Forty-four percent of the shields tested positive for blood. The surgeon was aware of a spray in only 8% of cases. The splashes were macroscopically visible in only 16% of cases. The risk of eye splashes was higher for surgeons than for assistants and increased with the length of the operation. The type of operation also proved to be a determining factor; vascular surgery and orthopedic surgery had the higher risks for eye splash injuries. Eye protection should be mandatory.

14. What is the surgeons’ rate of exposure to blood and body fluids?

Show answer
Percutaneous blood exposure occurs in 1.2-5.6% of surgical cases and mucocutaneous blood contact in 6.4-50.4%. The discrepancy among reported rates reflects differences in data collection, procedures performed, surgical technique, and degree of precautions. No health care worker has ever been infected through exposure of intact skin to blood and body fluids. However, transmission of HIV after mucocutaneous contact with HIV-infected blood has been reported. The risk of contamination is real for all personnel in the operating room, but it is much higher for surgeons and first assistants, who account for 80% of all body contamination and 65% of injuries.

15. Again, what are the seroconversion rates for HIV and HBV exposure?

Show answer
Seroconversion rates from a hollow needle stick are 0.3% for HIV and 30% for HBV.

16. What is the lifetime occupational risk of HIV infection for surgeons?

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The risk of HIV infection for a surgeon can be calculated by obtaining the product of HIV seroprevalence in surgical patients (0.32-50.00%), percutaneous injury rate (1.2-6.0%), and seroconversion rate (0.29-0.50%). The calculated risk per case of acquiring HIV ranges from 0.11 per million to 66 per million. Assuming that a surgeon performs 350 operations per year over a 30-year career, the estimated lifetime cumulative risk ranges from 0.12% to 50.0%, depending on the variables. Several assumptions are inherent in this calculation:

* The formula assumes a constant HIV prevalence, but it is estimated that the prevalence increases by 4.0-8.6% annually in the United States.
* The formula assumes that exposure to HIV-infected blood occurs only through percutaneous injuries, disregarding the risk caused by mucocutaneous exposure.
* The formula assumes that whereas every operation carries the same risk, the risk varies with the length of procedure and amount of blood loss.
* The formula assumes that the risk per case is the same for a trauma surgeon in center city Detroit and a plastic surgeon in Beverly Hills.

Clearly, these assumptions are imprecise.

17. Are there effective methods to reduce the risk of transmission of bloodborne diseases to surgeons?

Show answer
For HBV infection, in addition to universal precautions, a highly effective vaccine is available, but it is not used as much as it should be. Most surgeons who are 45 years or older have not been vaccinated. A precisely defined postexposure protocol is also available. For HCV and HIV infections, the most pragmatic approach is to lower the rate of percutaneous and mucocutaneous injuries by observing barrier precautions and using safe surgical technique.
Finally, prompt response to blood exposure is required. Contamination of the hands or arms is best dealt with by immediate rescrubbing. If this is not practical, the area should be irrigated with povidone iodine, and rescrubbing should be accomplished soon thereafter.

References
BIBLIOGRAPHY
1. Barrie PS, Patchen Dellinger E, Dougherty SH, Fink MP: Assessment of hepatitis B virus immunization status among North American surgeons. Arch Surg 129:27-32, 1994.
2. Bell DM: Occupational risk of human immunodeficiency virus infection in healthcare workers: An overview. Am J Med 102(suppl 5B):81S-85S, 1997.
3. Cardo DM, Culver DH, Ciescielski CA, et al: A case-control study of HIV seroconversion in healthcare workers after percutaneous exposure. N Engl J Med 337:1485-1490, 1997. Medline Similar articles Full article
4. Dodd RY, Notari EP, Stramer SL: Current prevalence and incidence of infectious disease markers and estimated window-period risk in the American Red Cross blood donor population. Transfusion 42:975-979, 2002. Medline Similar articles Full article
5. Eubanks S, Newman L, Lucas G: Reduction of HIV transmission during laparoscopic procedures. Surg Laparosc Endosc 3:2-5, 1993. Medline Similar articles
6. Fry DE: Blood-borne diseases in 1998. Bull Am Coll Surg 83:13-18, 1998.
7. Gerberding JL: Reducing occupational risk of HIV infection. Hosp Pract 113-110, 115-118, 1991.
8. Klein HG: Allogenic transfusion risks in the surgical patient. Am J Surg 317:242-245, 1995.
9. Koff RS: Hepatitis A, hepatitis B, and combination hepatitis vaccines for immunoprophylaxis: An update. Digest Dis Sci 47:1183-1194, 2002. Medline Similar articles Full article
10. Lin EY, Brunicardi C: HIV infection and surgeons. World J Surg 18:753-757, 1994. Medline Similar articles Full article
11. Marasco S, Woods S: The risk of eye splash injuries in surgery. Aust N Z J Surg 68:785-787, 1998. Medline Similar articles
12. Megan J, Patterson M, Novak CB, et al: Surgeons’ concern and practices of protection against bloodborne pathogens. Ann Surg 228:266-272, 1998.
13. Pietrabissa A, Merigliano S, Montorsi M, et al: Reducing the occupational risk of infections for the surgeons: Multicentric national survey on more than 15,000 surgical procedures. World J Surg 21:573-578, 1997. Full article
14. Schreiber GB, Busch MP, Kleinman SH, et al: The risk of transfusion-transmitted viral infections: The retrovirus epidemiology donor study. N Engl J Med 334:1685-1690, 1996. Medline Similar articles Full article
15. Szmuness W, Stevens CE, Harley EJ, et al: Hepatitis B vaccine: Demonstration of efficacy in a controlled clinical trial in a high-risk population in the United States. N Engl J Med 303:833-841, 1980. Medline Similar articles

11. Is there any type of stone that cannot be seen on helical CT scan?

Show answer
Patients taking indinavir sulfate (Crixivan) for HIV infection can form stones from the crystals of the medication; these stones are not seen on CT scan.

12. What toxic substance can be produced by using the holmium:YAG laser on uric acid stones?

Show answer
Cyanide is produced from the uric acid. Although this sounds frightening, it is never a problem.

References
WEB SITE
http://www.transplantation-soc.org
BIBLIOGRAPHY
1. Menon M, Resnick M: Urinary lithiasis: Etiology, diagnosis and medical management. In Walsh PC, Retik AB, Vaughan ED, Wein AJ et al (eds): Campbell’s Urology, 8th ed. Philadelphia, W.B. Saunders, 2002, pp 3229-3305.
2. Teichman JM, Vassar GJ, Glickman RD: Holmium: YAG lithotripsy photothermal mechanism converts uric acid calculi to cyanide. J Urol 160:320-324, 1998. Medline Similar articles Full article

1. What are the most common types of urinary stones found in North America?

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* Calcium stones (calcium oxalate, calcium phosphate, or mixed calcium stones): 70%.
* Struvite or magnesium ammonium phosphate stones, often associated with infection: 20%.
* Uric acid stones (radiolucent): 5%
* Cystine stones, often with a genetic association: 5%

2. What are the typical presenting symptoms of a patient with an obstructing stone?

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* Pain, usually colicky in the flank or radiating to the groin; patients are usually agitated and cannot get in a comfortable position
* Hematuria, gross or microscopic
* Nausea and vomiting caused by obstruction and pressure on the renal capsule

3. What studies are best to diagnose stones?

Show answer

1. Excretory urogram, or intravenous pyelogram (IVP). Ninety percent of stones are radiopaque and can be seen on a plain radiograph of the kidney, ureter, and bladder (KUB). The IVP serves as a functional study to determine the degree of obstruction, level of obstruction, and presence of a contralateral kidney.
2. Currently, rapid-sequence helical computed tomography (CT) scan has gained popularity. Helical CT can accurately identify both renal and ureteral stones. Its advantages include no need for contrast; speed; and ability to identify calcium, uric acid, and cystine stones. Disadvantages include increased cost compared with IVP and inability to distinguish between radiolucent (uric acid) stones and radiopaque (calcium-containing) stones. A KUB should be obtained if the CT has positive results, to distinguish between radiolucent and radiopaque stones.
3. Ultrasound is particularly advantageous in pregnant women.

4. When should a patient with an obstructing stone be admitted to the hospital?

Show answer

* Any sign of infection (e.g., fever, leukocytosis, bacteriuria); infection behind an obstructing stone may result in urosepsis and death
* Intractable vomiting requiring intravenous (IV) fluids
* Pain requiring parenteral analgesics
* Bilateral obstructing stones or obstruction in a solitary kidney

5. What are the treatment options for ureteral calculi?

Show answer

* Wait and watch to see if the stone passes; it usually does. Approximately 90% of stones, 3 mm in size in the distal ureter, will pass. Fifty percent of 5-mm stones will pass, and 20% of stones larger than 6 mm will pass.
* Ureteroscopy and stone basketing or intraureteral lithotripsy (stone blasting) with a laser (holmium, pulsed dye) or electrohydraulic lithotripsy (EHL)
* Extracorporeal lithotripsy (ESWL), or shock waves directed at the stone to break it into small pieces that can then pass spontaneously
* Open ureterolithotomy, now rarely used because of the success of the less invasive techniques listed above

KEY POINTS: URINARY CALCULUS DISEASE

1. The most common stones in patients in the United States are calcium stones.
2. Excretory urogram or intravenous pyelogram, rapid-sequence helical CT, and ultrasound are the imaging studies used to diagnose stones.
3. Steinstrasse is a collection of small calculi that pile up together in the ureter and cause obstruction or symptoms.

6. What are the treatment options for renal calculi?

Show answer

* Expectant management in asymptomatic noninfectious stones
* ESWL
* Ureteropyeloscopy with lithotripsy using a laser. This has become more popular with smaller, flexible, deflectable ureteroscopes, but it is still a challenging procedure for large stones.
* Percutaneous nephrostolithotomy (particularly for stone burden > 2 cm)
* Combination of ESWL and percutaneous nephrostolithotomy
* Open lithotomy (less common because of the success of less invasive treatment options)

7. What is a steinstrasse?

Show answer
Steinstrasse (German for “stone street”) is a collection of small calculi that pile up together in the ureter and cause obstruction or symptoms. This problem may occur after lithotripsy treatment.

8. What is a stent?

Show answer
A stent is a small plastic catheter that coils in the renal pelvis, traverses the ureter, and coils in the bladder. Stents are useful to relieve ureteral obstruction temporarily and possibly facilitate stone passage after the stent is removed. Stents often cause some degree of ureteral dilatation after they have been removed.

9. What is a metabolic evaluation? Who needs one?

Show answer
A metabolic evaluation involves examining both serum and 24-hour urine specimens for factors that contribute to stone formation. The goals are to identify an abnormality and to treat it medically to prevent further stone formation. Indications for metabolic evaluation include recurrent stones, multiple stones, bilateral stones, stones in children, and non-calcium-containing stones.

10. Can stones be dissolved?

Show answer

* Uric acid stones often can be dissolved by alkalinizing the urine and with hydration therapy.
* Cystine, struvite, and apatite stones sometimes can be dissolved.
* Calcium stones cannot be dissolved.

1. What are branchial cleft anomalies?

Show answer
Cysts, sinuses, and fistulas that result from incomplete obliteration of the first, second, or third branchial clefts, and are present in early fetal development.

2. Which anomaly is the most common?

Show answer
Second branchial cleft anomalies are by far the most common, presenting near the mid- to upper border of the sternocleidomastoid (SCM) muscle. First branchial remnants are less common and third clefts are quite rare. (See Table 88-1.)
Table 88-1. BRANCHIAL CLEFT ANOMALIES

3. How do patients with branchial cleft anomalies present?

Show answer
Those with complete fistulas or sinuses present with intermittent drainage of a mucoid fluid on the neck. Patients with cysts usually present later with a mass (sterile or infected). Complete surgical excision is the treatment of choice.

4. What are the major operative hazards of branchial cleft remnant excision?

Show answer
The second branchial cleft tracts through the bifurcation of the carotid artery. The facial nerve is in close proximity to the first branchial cleft fistula. The superior laryngeal nerve and the recurrent laryngeal nerve are both at risk in dissection of a third branchial cleft.

5. What is a thyroglossal duct cyst?

Show answer
A thyroglossal duct cyst is the most common congenital cyst found in the neck. It is caused by failure of normal obliteration of the migration tract of the thyroid gland. Embryologically, the thyroid descends from the base of the tongue (foramen caecum) to its normal location in the low anterior neck.

6. How do patients with thyroglossal duct cysts present?

Show answer
They present with a paramidline mass in the upper neck; if infected, they may present with fever, tenderness, and erythema.

KEY POINTS: CONGENITAL CYSTS AND SINUSES OF THE NECK

1. The most common brachial cleft anomaly is the second brachial cleft anomaly presenting near the mid- to upper border or the sternocleidomastoid muscle.
2. A thyroglossal duct cyst is the most common congenital cyst found in the neck.
3. A cystic hygroma is a congenital lymphatic malformation that is benign an usually presents as a soft mass in the lateral neck.

7. How are thyroglossal duct cysts treated?

Show answer
The best treatment is complete excision of the cyst, along with the tract. Because embryologically the thyroid descends before formation of the hyoid cartilage, the tract may pass right through the hyoid. Therefore, complete tract removal requires excision of the central portion of the hyoid and dissection up to the base of the tongue (i.e., the Sistrunk procedure).

8. What is a cystic hygroma?

Show answer
A cystic hygroma is a congenital lymphatic malformation with a predilection for the neck. It is a benign lesion that usually presents as a soft mass in the lateral neck. Excision is often challenging because the lymph cysts do not respect the fascial planes and often intertwine with the neurovascular structures in the neck. Near-total excision is the treatment of choice.

References
BIBLIOGRAPHY
1. Alqahtani A, Nguyen LT, Flageole H, et al: 25 years experience with lymphangioma in children. J Pediatr Surg 34:1164-1168, 1999. Medline Similar articles Full article
2. Brown RL, Azizkhan RG: Pediatric head and neck lesions. Pediatr Clin North Am 45:889-905, 1998. Medline Similar articles
3. Kang L, Chang CH, Yu CH, et al: Prenatal detection of cystic hygroma using three-dimensional ultrasound. Ultrasound Med Biol 28:719, 2002. Medline Similar articles
4. Organ GM, Organ CH Jr: Thyroid gland and surgery of the thyroglossal duct: Exercise in applied embryology. World J Surg 24:886-890, 2000.
5. Smith CD: Cysts and sinuses of the neck. In O’Neill JA, Rowe MI, Grosfeld JL, et al (eds): Pediatric Surgery, 5th ed. St. Louis, Mosby, 1998, pp 757-771.
6. Telander RL, Filston HC: Review of head and neck lesions in infancy and childhood. Surg Clin North Am 72:1429-1447, 1992. Medline Similar articles

1. What is pyloric stenosis?

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Hypertrophic pyloric stenosis (HPS) is idiopathic thickening and elongation of the pylorus that produces gastric outlet obstruction. HPS is the most common surgical cause of nonbilious vomiting in infants. Offspring of an affected parent have an increased incidence of HPS (10%); the highest rate (20%) occurs in boys born to affected mothers.

2. Describe the typical presentation of HPS.

Show answer
The typical presentation is a healthy infant who initially fed normally but who presents at age 2-6 weeks with a history of “projectile” vomiting. The emesis is nonbilious. After vomiting, the infant appears hungry and will refeed immediately. With time, the infant becomes dehydrated and, if allowed to progress, malnutrition follows.

3. What are the physical findings?

Show answer
Affected infants suffer some degree of dehydration. The abdomen is nondistended and soft. A palpable pyloric tumor, known as the “olive,” confirms the diagnosis. An olive is palpable in 50% of patients. Associated findings are rare, but mild jaundice occurs in 5% of infants because of reduced glucuronyl transferase activity.

4. How is the diagnosis confirmed?

Show answer
Ultrasonographic criteria include pyloric diameter > 1.4 cm, wall width > 4 mm, and pyloric channel length > 1.6 cm. Alternatively, a barium upper gastrointestinal (UGI) examination may be used to confirm the diagnosis (gastric outlet obstruction, pyloric channel narrowing). Current analyses suggest that UGI is the most cost-effective initial radiologic diagnostic test because, unlike ultrasound, alternative causes of nonbilious vomiting (e.g., gastroesophageal reflux, malrotation, duodenal stenosis) can be identified.

5. Describe the likely electrolyte abnormalities.

Show answer
Electrolyte levels are often normal, but long-standing vomiting will eventually result in hypokalemic, hypochloremic metabolic alkalosis because of the loss of gastric acid (HCl). Earlier consideration of the diagnosis has led to a significant reduction in this classic electrolyte abnormality at presentation. Dehydration is corrected with either 0.9% NaCl or, in less severe cases, 0.5% NaCl with 30 mEq/L KCl. After dehydration and electrolytes are corrected, pyloromyotomy is performed.

6. What procedure is recommended for the correction of HPS?

Show answer

The Fredet-Ramstedt pyloromyotomy is recommended. A superficial incision is made longitudinally over the pyloric muscle in an avascular area, and the muscle fibers are fractured to expose the underlying mucosa. At the conclusion of the pyloromyotomy, the gastric mucosa should bulge upward into the cleft, and the pyloric muscle walls should move independently of one another. Air is injected into the stomach via the nasogastric tube to identify inadvertent mucosal perforation. Pyloromyotomy may be performed either via a transverse incision in the right upper quadrant (i.e., an open procedure) or via three small (3-mm) incisions in the epigastrium (i.e., a laparoscopic procedure). The results of open and laparoscopic pyloromyotomy appear equivalent.

7. What should be done if a perforation is identified?

Show answer
The mucosa should be closed with several fine sutures and covered with an omental patch. If the mucosal injury is too extensive, the myotomy should be closed with sutures and a second, parallel myotomy should be made at 45-180° from the original myotomy.

8. When can postoperative feeding begin?

Show answer
Small-volume feedings are started after the infant has recovered from anesthesia (2-3 hours) and advanced to goal. Small amounts of vomiting are common (20%), but most infants achieve full feeds within 24 hours postoperatively. Incomplete pyloromyotomy is uncommon (< 1%) and is not considered unless symptoms of gastric outlet obstruction persist for 7-10 days after surgery.

9. Describe several hypotheses about the pathogenesis of HPS.

Show answer
Recent studies of the abnormal pyloric complex demonstrate improper innervation of pyloric smooth muscle, excessive contraction of circular pyloric smooth muscle (decreased nitric oxide synthase), increased extracellular matrix proteins (collagen), and increased expression or local synthesis of growth hormones (i.e., insulin-like growth factor-1, transforming growth factor beta-1, platelet derived growth factor).

References
BIBLIOGRAPHY
1. Campbell BT, McLean K, Barnhart DC, et al: A comparison of laparoscopic and open pyloromyotomy at a teaching hospital. J Pediatr Surg 37:1068-1071, 2002. Medline Similar articles Full article
2. Chen EA, Luks FI, Gilchrist BF, et al: Pyloric stenosis in the age of ultrasonography: Fading skills, better patients? J Pediatr Surg 31:829-830, 1996. Full article
3. Garza JJ, Morash D, Dzakovic A, et al: Ad libitum feeding decreases hospital stay for neonates after pyloromyotomy. J Pediatr Surg 37:493-495, 2002. Medline Similar articles Full article
4. Hulka F, Campbell JR, Harrison MW, et al: Cost-effectiveness in diagnosing infantile hypertrophic pyloric stenosis. J Pediatr Surg 32:1604-1608, 1997. Medline Similar articles Full article
5. Miozzari HH, Tonz M, von Vigier RO, et al: Fluid resuscitation in infantile hypertrophic pyloric stenosis. Acta Paediatr 90:511-514, 2001. Medline
6. Ohshiro K, Puri P: Pathogenesis of infantile hypertrophic pyloric stenosis: Recent progress. Pediatr Surg Int 13:243-252,1998. Medline Similar articles Full article