• Postoperative fever workup
• opss sepsis 14 days
• solitary pulmonary nodule breast cancer patient
• honeymoon period bochdalek
• relation between breathlessness and total thyroidectomy
• colon surgery diverticulitis
• Hematest-positive NGT
• nonoperative management of spleen injury
• when is the parental nutrion discontinued
• grading for splenic laceration
• having a solitary nodule with calcium flecks
• how many milliequivalents in gatorade

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

1. Why is there a different approach to stab and gunshot wounds?

Show answer
Whereas one third of stab wounds to the anterior abdomen do not penetrate the peritoneum, 80% of gunshot wounds violate the peritoneum. Furthermore, penetration of the peritoneum by a bullet is associated with visceral or vascular injuries in > 95% of cases, whereas only one third of stab wounds violating the peritoneal cavity produce significant injury. (See Figure 24-1.)

Figure 24-1 Management of patients witih penetrating abdominal trauma.

2. What is the secondary survey for a penetrating abdominal wound?

Show answer
The ABCs (i.e., airway, breathing, and circulation) are the first priority in every trauma patient. Look everywhere-watch out; it is easy to overlook synchronous injuries. This includes looking for additional entry or exit sites; evaluation for blood in the gastrointestinal (GI), genitourinary (GU), and gynecologic systems; and blunt mechanism injuries (e.g., some unfortunate patients are both stabbed and beat up). The “mechanism” of injury includes the time of injury, type of weapon, length or caliber of the weapon, depth of penetration, and estimated blood loss at the scene.

3. What are the appropriate initial studies in patients with penetrating abdominal trauma?

Show answer
In stable patients, a chest radiograph excludes hemo- or pneumothorax and determines the position of intravenous catheters (e.g., endotracheal, nasogastric, and pleural tubes). Biplanar abdominal radiographs are helpful in locating retained foreign bodies, such as bullets, and may reveal pneumoperitoneum. Entrance and exit wounds should be identified with a radiopaque marker. This may be helpful in determining the trajectory of missiles. Injuries in proximity to the rectum obligate sigmoidoscopy (see Chapter 28), whereas injuries in proximity to the urinary tract should be evaluated with computed tomography (CT) scanning (see Chapter 31).

Figure 24-2 An example of how the path of a bullet through contorted body can produce confusion when the patient is examined in the emergency department. An entrance wound will be found at the left upper arm and an exit wound at the medial aspect of the right knee. The bullet could have damaged any structure that was in between these two wounds when the patient’s body was contorted.

4. What are the indications for prompt laparotomy in patients with stab wounds?

Show answer
Abdominal distention and hypotension, overt peritonitis, and obvious signs of abdominal visceral injury (hematuria, hematemesis, proctorrhagia, evisceration; palpation of diaphragmatic defect on chest tube insertion; radiologic evidence of injury to GI or GU tracts) mandate immediate exploration.

5. What are the indications for immediate laparotomy in patients with gunshot wounds?

Show answer
Because of the high incidence of visceral injury, early exploration is indicated for all gunshot wounds that violate the peritoneum.

6. When is emergency department (ED) thoracotomy indicated for a penetrating abdominal wound?

Show answer
Almost never. But it should be considered when a patient, after penetrating trauma, presents in cardiac arrest or profound hypotension (< 60 mmHg) refractory to initial resuscitation. Thoracotomy allows open cardiac massage and access to cross clamp the descending aorta to improve coronary and cerebral perfusion as well as decrease subdiaphragmatic hemorrhage. Closed cardiac massage is ineffective when the patient is hypovolemic. (See Figure 24-3.)

7. What is the general plan for abdominal exploration in patients with penetrating trauma?

Show answer

A midline abdominal incision provides rapid entry and wide exposure; it may be extended as a median sternotomy to access the chest or continued inferiorly into the pelvis. The aorta should be palpated to assess blood pressure (BP). All findings, including a low BP, should be communicated to the anesthetist. Evacuation of blood and placement of tamponade packs into areas of suspected blood loss should be followed by exploration of the wound tract. Actively bleeding areas are digitally controlled until the culprit vessel can be occluded. Hollow visceral injuries are temporarily isolated with noncrushing clamps. The entire abdomen is systematically explored before undertaking extensive repairs so that injuries can be prioritized.

Figure 24-3 Treatment of gunshot wounds.

8. How is an anterior abdominal stab wound evaluated in asymptomatic patients?

Show answer
The first step is local exploration of the wound to determine peritoneal penetration. If the tract clearly terminates superficially, above the fascia, no further evaluation or treatment is required. If the fascia is penetrated or the peritoneum violated, diagnostic peritoneal lavage (DPL) is performed. Double-contrast (oral and intravenous) CT scanning is not routinely used because of its relative insensitivity for detecting hollow visceral injuries. Ultrasonography is useful for detecting intraperitoneal fluid but is helpful only if the results are positive. (See Figure 24-4.)

Figure 24-4 Treatment of stab wounds.

9. What constitutes a positive DPL result after penetrating trauma?

Show answer
A grossly positive tap (aspiration of >10 mL of blood or aspiration of GI or biliary contents) mandates immediate exploration. A negative initial aspirate result is followed by the instillation of 1000 mL of saline (15 mL/kg in children) into the abdomen through a dialysis catheter, followed by gravity drainage of the fluid back into the saline bag. The finding of > 100,000/mm3 red blood cells (RBCs), the combined elevation of amylase > 20 IU/L and alkaline phosphatase > 3 IU/L, or elevated bilirubin level are also indications for exploration.

10. How are stab wounds to the flank and back evaluated?

Show answer
The incidence of significant injuries is 10% for stab wounds to the back and 25% for stab wounds to the flank. However, evaluation of such wounds is problematic because the retroperitoneum is not sampled by DPL and physical examination is even less sensitive. The major concern is missed colonic perforation. At present, triple-contrast (oral, intravenous, and rectal) CT scan and serial physical examination are the two primary modes of assessment. Operative exploration is advisable if CT scanning demonstrates wound trajectory in the vicinity of the colon.
KEY POINTS: CLINICAL APPROACH TO PENETRATING ABDOMINAL TRAUMA

1. Gunshot wounds to the abdomen generally require operative exploration (> 80% violate the peritoneum).
2. Stab wounds with evisceration or hypotension are operatively explored.
3. Stab wounds in stable patients are managed with local wound exploration (66% violate the peritoneum) plus DPL, ultrasound, or CT scan. If tests are positive, the patient goes to the operating room.
4. During celiotomy, pack the upper quadrants and pelvis; then address vascular, solid organ, and alimentary tract injuries in succession.
5. Prophylactic antibiotics for the first 24 hours decrease postoperative wound infection.

11. How is a lower chest stab wound evaluated?

Show answer
The lower chest is defined as the area between the nipple line (fourth intercostal space) anteriorly, the tip of the scapula (seventh intercostal space) posteriorly, and the costal margins inferiorly. Because the diaphragm reaches the fourth intercostal space during expiration, the abdominal organs are at risk (even after what appears to be a clear “chest” wound). Stab wounds to the lower chest are associated with abdominal visceral injury in 15% of cases, whereas gunshot wounds to the lower chest are associated with abdominal visceral injury in nearly 50% of cases. Thus, wounds to the lower chest should also be managed as abdominal wounds to rule out intraabdominal injury. In the case of lower chest stab wounds, an RBC count of > 10,000/mm3 warrants laparotomy to rule out a diaphragmatic injury; thoracoscopic exploration (not thoracotomy) may also be performed for counts of 1000-10,000/mm3.

12. Which patients with abdominal gunshot wounds are managed nonoperatively?

Show answer

Stable patients with tangential missile tracts or equivocal peritoneal penetration are candidates for DPL. The cutoff for RBC counts is reduced to 10,000/mm3, above which laparotomy is indicated. Patients with a negative DPL result are observed for 24 hours. For RBC counts of 100-10,000/mm3, laparoscopy may be used to exclude intraperitoneal injury. Selective management of gunshot wounds to the back and flank are generally based on triple contrast CT.

13. What is the role for presumptive antibiotics?

Show answer
Short courses (< 24 hours) of high-dose antibiotics are initiated only when the decision has been made to perform a laparotomy. Coverage of both anaerobic and aerobic flora is desirable. Tetanus prophylaxis should be given to all patients with penetrating injuries.

23. How fat is fat?

Show answer
Lean body mass is three times more metabolically active than adipose tissue. Multiple definitions of clinical obesity exist: > 120% ideal body weight (IBW), > 130% IBW, body mass index (BMI) > 30, body fat > 24-28% of body weight in men and > 30-35% in women. Measured weight is a poor indicator of relative adiposity. Self-reported weights or weights reported by family members are often erroneous in the ICU setting. Fluid resuscitation and edema make visual assessment challenging and limit the usefulness of noninvasive technology such as bioelectrical impedance (BIA) for measuring body composition. Although measured energy expenditure in kcal/kg of actual weight may sometimes approach that of normal-weight patients, feeding at the measured body weight level may be associated with profound hyperglycemia, hypercapnea, and the inability to clear triglycerides.

24. Should actual, ideal, or adjusted body weight be used in nutrition calculations for obese patients?

Show answer
Studies using an obesity-adjusted weight in kilocalorie calculations (IBW + 0.25 [actual IBW]) report greater correlation with measured energy expenditure than when using actual weight.

25. Which is more important, nitrogen or caloric balance?

Show answer
Ultimately, maintaining a positive nitrogen balance may be more important than achieving a positive kilocaloric balance.

26. Are postpyloric feedings superior to gastric feedings?

Show answer
After major surgery or injury, the stomach exhibits decreased motility for several days. Early enteral feeding, with its known benefits, may not be accomplished through a gastric feeding in the early stages of injury. Jejunostomy feedings have been associated with higher kilocalorie intake, more timely return to anabolism, and a lower pneumonia (aspiration) rate than continuous gastric feeding.

27. When should immune-enhancing formulas be used?

Show answer
Rarely. PRCTs have demonstrated that immune-enhancing diets (IEDs) improve outcome and reduce septic morbidity in patients prone to intraabdominal sepsis after major torso trauma and after major operative resection of upper GI cancers. The use of IEDs should be restricted to these patients, and the duration of use should be limited because of the increased expense. The IEDs have not been adequately tested in other types of patients and, when tested in mixed ICU patients, some evidence suggests that they might even be harmful in addition to being expensive.

28. Are arginine-containing formulas contraindicated in patients with sepsis?

Show answer
Arginine is thought to be a semi-essential amino acid in critically ill patients. It is a metabolic fuel for lymphocytes and fibroblasts. It is also a secretagogue for a variety of hormones (most notably growth hormone). PRTs have shown that supplemental arginine improves wound healing and immune responsiveness in high-risk surgical patients. Arginine is also one of the key ingredients of the newer IEDs. The other key ingredients include glutamine, omega-3 fatty acids, and nucleotides. A large number of PRTs have compared IEDs with standard enteral formula and have shown that IEDs reduce infections and decrease hospital length of stay. The most convincing data come from PRTs that have enrolled patients undergoing major upper GI cancer resections. PRTs that have enrolled less homogenous ICU patients have had a difficult time demonstrating improved outcome, and subset analysis suggest that IEDs may be harmful in ICU patients with sepsis. Reviewing the potential immunomodulating effects of the key ingredients in IEDs has led some authorities to hypothesize that arginine supplementation is harmful in the patients with sepsis. These patients exhibit increased levels of inducible nitric oxide synthase (iNOS). Arginine is a substrate for iNOS and, in its presence, arginine combines the molecular oxygen to produce citrulline and nitric oxide (NO). The resulting NO may have numerous adverse effects in sepsis, including vasodilation, cardiac dysfunction, and direct cytotoxic injury by generating potent reactive oxygen (peroxynitrite) species. Unfortunately, little data support or refute this hypothesis.

29. Should formula with increased fish oil be used in patients at risk for acute respiratory distress syndrome (ARDS)?

Show answer
One industry-funded PRCT demonstrated superior outcome in patients with ARDS when provided a high omega-3 fatty acid enteral product versus a high-omega-6 “pulmonary” formula. Unfortunately, the control diet is not the standard of care and may worsen ARDS. High omega-6 fatty acids increase inflammation and production of lipid mediators, which worsen V/Q mismatch in the lung, which worsen oxygenation in ARDS. Duplication of the results and comparison with standard, moderate-fat polymeric formula is needed.

References
WEB SITE
http://www.gpnotebook.co.uk/simplepage.cfm?ID=516948028

BIBLIOGRAPHY
1. ASPEN Board of Directors and the Clinical Guidelines Task Force: Guidelines for the use of enteral and parenteral nutrition in adult and pediatric patients. J Parent Enter Nutr 26(suppl 1):1SA-138SA, 2002.
2. Cutts ME, Dowdy RP, Ellersieck MR, Edes TE: Predicting energy needs in ventilator dependent critically ill patients: Effect of adjusting weight for edema or adiposity. Am J Clin Nutr 66:1250-1256, 1997.
3. Gadek JE, DeMichele SJ, Karlstad MD, et al: Effect of enteral feeding with eicopentaenoic acid, gamma-linolenic acid, and antioxidants in patients with acute respiratory distress syndrome. Crit Care Med 27:1409-1420, 1999. Medline Full article
4. Konstantinides FN, Konstantinides NN, Li JC, et al: Urinary urea nitrogen: Too sensitive for calculating nitrogen balance studies in surgical clinical nutrition. J Parent Ent Nutr 15:189-193, 1991.
5. Kozar R, McQuiggan M, Moore F: Nutritional support of trauma patients. In Shikora S, Martindale RG, Schwaitzburg S (eds): Nutritional Considerations in the Intensive Care Unit. Silver Spring, MD, Aspen, 2002, pp 229-244.
6. Malone AM: Is a pulmonary formula warranted for patients with pulmonary dysfunction? Nutr Clin Practice 11:189-191, 1997.
7. McClave SA, Snider HL: Understanding the metabolic response to critical illness: Factors that cause patients to deviate from the expected pattern of hypermetabolism. New Horizons 2:139-146, 1994. Medline Similar articles
8. Montecalvo MA, Steger KA, Farber HW, et al: Nutritional outcome and pneumonia in critical care patients randomized to gastric versus jejunal tube feedings. Crit Care Med 20:1377-1387, 1992. Medline Similar articles
9. Moore FA, Feliciano DV, Andrassy R, et al: Enteral feeding reduces post operative septic complications: A meta analysis. Ann Surg 216:62-71, 1992.
10. Talpers SS, Romberger DJ, Pingleton SK: Nutritionally associated increased carbon dioxide production: Excess total kilocalories vs high proportion of carbohydrate kilocalories. Chest 102:551-555. 1992. Medline Similar articles
11. Van den Berghe G, Wouters P, Weekers F, et al: Intensive insulin therapy in critically ill patients. N Engl J Med 345:1359-1367, 2001. Medline Similar articles

1. What infectious diseases are transmissible via blood transfusion?

Show answer
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?

Show answer
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?

Show answer
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?

Show answer
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?

Show answer
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?

Show answer
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?

Show answer
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?

Show answer
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?

Show answer
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?

Show answer
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?

Show answer
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?

Show answer
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?

Show answer

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

1. How does a pulse oximeter work?

Show answer
Light-absorption characteristics differ for the four most common circulating species of hemoglobin in adults:

1. Reduced hemoglobin (RHb)
2. Oxygenated hemoglobin (O2Hb)
3. Methemoglobin (Met Hb)
4. Carboxyhemoglobin (CO Hb)

Current pulse oximeters transmit two wavelengths of light, red (680 nm) and infrared (940 nm), and these differentiate O2Hb from RHb. Using optical plethysmography, the pulse oximeter measures hemoglobin saturation only during arterial pulsation.

2. How accurate is pulse oximetry?

Show answer
The device is highly accurate at saturations > 80%. This results in an overall accuracy of ± 5%.

3. Are clinicians accurate in determining arterial desaturation by “visual oximetry” (how red is the blood)?

Show answer
No. Pulse oximetry should be regarded as the fifth vital sign.

4. How does the pulse oximeter respond to an abnormal species of hemoglobin?

Show answer
In carbon monoxide or cyanide poisoning, the oximeter interprets an abnormal hemoglobin as a combination of O2Hb and RHb, which results in an erroneously high saturation. Based on the light absorption of Met Hb, the pulse oximeter may display a saturation of 85%.

5. Can any other environmental or clinical conditions result in inaccurate pulse oximetry values?

Show answer
Reliability depends on a strong arterial pulse plus good light transmission. Inaccuracy results with hypotension (mean arterial pressure < 50 mmHg), hypothermia (< 35°C), vascular disease (poor peripheral perfusion), and vasopressor therapy (vasoconstriction). Bright lights, intravenous dyes, nail polish, and excessive motion each may produce bad information.

6. What is the relationship between oxyhemoglobin saturation (Sao2) and partial pressure of oxygen (Pao2)?

Show answer
Proper interpretation of pulse oximetry requires recall of the oxyhemoglobin dissociation curve. A rightward shift (decreased hemoglobin affinity for oxygen) facilitates oxygen unloading at the tissue level. Increasing temperature, increasing Paco2, increasing 2,3-diphosphoglycerate, and increasing hydrogen ion concentration-all “increases”-shift the curve to the right. When the Pao2 is > 100 mmHg, however, the curve is virtually flat. Consequently a large drop in Pao2 (e.g., from 200 to 100 mmHg) may occur with no discernible change in Sao2. (See Figure 11-1.)

7. What are the indications for continuous pulse oximetry?

Figure 11-1 Oxyhemoglobin dissociation curve.
Any patient who either is or might get sick. Pulse oximetry should be considered standard monitoring in critical care units. Pulse oximetry is uniquely valuable during patient transport, when weaning from the ventilator, and after major ventilator changes. Critically ill patients who are outside the intensive care unit (ICU) (emergency department or radiology suite) also should be monitored by pulse oximetry.

8. How does a continuous mixed venous oximeter work?

Show answer
Mixed venous oximetry uses reflective spectrophotometry. Narrow wavebands of light are transmitted via a fiberoptic bundle to the blood flowing past the tip of the catheter and are reflected by a separate fiberoptic bundle to a photodetector that determines relative absorption of the specific wavelength. A microprocessor calculates mixed venous hemoglobin saturation (Svo2).

9. What is the normal value for mixed venous oxygen saturation?

Show answer
The normal oxygen tension in mixed venous blood (Pvo2) is 40 mmHg. Under physiologic conditions, this is equivalent to an Svo2 of 75%, which is on the steep portion of the oxyhemoglobin dissociation curve. Three fourths of the oxygen (see Chapters 4, 5, and 6) delivered out of the aorta (Do2) returns to the right heart unused.

10. Using a pulmonary artery catheter, how can oxygen delivery and consumption be determined?

Show answer
The Fick equation shows the relationship between systemic oxygen delivery (Do2) and oxygen consumption (Vo2):

VO2 = CO x (CaO2 – CVO2)

where Cao2 is arterial oxygen content, Cvo2 is mixed venous oxygen content, and CO is cardiac output. Oxygen delivery is determined by the following equation:

DO2 = CaO2 x CO

where Cao2 is (1.36 × [hemoglobin concentration] × [arterial oxygen saturation] + Pao2 × 0.003) and Cvo2 is (1.36 × [hemoglobin concentration] × [venous oxygen saturation] + Pao2 × 0.003).

11. Describe the four primary causes of a sudden fall in Svo2.

Show answer
A stable, normal Svo2 ensures a balance of Do2 and Vo2, whereas a sudden fall in Svo2 provides an early warning of (1) low CO, (2) arterial oxygen desaturation, (3) drop in hemoglobin, or (4) increased Vo2.

12. Why does Svo2 rise during general anesthesia?

Show answer
General anesthesia suppresses metabolic demands; vo2 decreases (extracting less oxygen peripherally), and Svo2 rises.

13. Why does Svo2 rise with septic shock?

Show answer
During sepsis, large peripheral shunts, high cardiac output, and poor oxygen extraction contribute to an elevated Svo2.

14. State the advantages of continuous monitoring of Svo2.

Show answer
Svo2 provides prompt feedback about therapeutic interventions and disease progression. Svo2 trends are more important, however, than absolute values. With time, the catheter tip gets progressively gummed up with tissue proteins; the catheter should be recalibrated every 12-24 hours.

15. Are there any disadvantages to computer-generated hemodynamic profiling?

Show answer
Yes-even when it is wrong, we tend to believe it. Comprehensive hemodynamic profiling includes a constellation of parameters: cardiac output, Pao2, Svo2, urine output, serum lactate level, and great-toe temperature.

16. What is dual oximetry?

Show answer
Dual oximetry consists of simultaneous monitoring of arterial (Sao2) and mixed venous (Svo2) hemoglobin saturation to provide real-time, continuous information about pulmonary function, oxygen transport, and oxygen extraction ratio. Dual oximetry is particularly useful for real-time assessment during a best trial of positive end-expiratory pressure.

17. What is transcutaneous oxygen monitoring (TCM)?

Show answer
TCM is a method of continuously recording skin Po2 (Ptco2), which is not equal to arterial Po2. In 1975, Van Duzee observed that the lipid component of the stratum corneum melts as skin temperature increases, and gas diffusion can increase by 1000-fold. The Ptco2 electrode is designed to heat the skin to 44°C. The elevated temperature also increases dermal blood flow and “arterializes” the capillary blood. The interpretation of pulse oximetry and TCM are the same, however.

18. If the skin beneath the sensor is arterialized, why is the Ptco2 not equal to the Pao2?

Show answer
Four factors contribute to the difference between Ptco2 and Pao2:

1. The rightward shift of the oxygen-hemoglobin dissociation curve with heating
2. Variations in the skin oxygen permeability
3. Metabolic consumption of oxygen by the dermal tissue
4. Cutaneous blood flow

Because factors 1 and 3 tend to cancel each other, the relationship between Ptco2 and Pao2 is effectively linear and depends only on oxygen permeability and skin blood flow.

19. What is an oxygen debt?

Show answer
An oxygen debt is the net cumulative difference between oxygen consumption measured at baseline and during any pathologic state. It is the amount of oxygen needed by the cells to compensate for the mismatch between oxygen delivery and oxygen demand.

20. Name the five physiologic mechanisms responsible for causing hypoxemia. Do they all result in a widened alveolar-arterial gradient (A-a gradient)?

Show answer

1. Low inspired oxygen fraction (e.g., high altitude)
2. Alveolar hypoventilation (physiologic dead space)
3. Diffusion limitation
4. Ventilation/perfusion mismatch (most common cause for hypoxemia-this really includes both mechanism 2 and 5)
5. Shunt (adult respiratory distress syndrome, severe pneumonia)

Alveolar hypoventilation and a low FiO2 may result in hypoxemia with a normal A-a gradient.

KEY POINTS: PHYSIOLOGIC CAUSES OF HYPOXEMIA

1. Low FiO2: normal A-a gradient
2. Alveolar hypoventilation or dead space: normal A-a gradient
3. Diffusion defect: abnormal A-a gradient
4. Ventilation/perfusion mismatch: most important cause with abnormal gradient
5. Shunt: abnormal A-a gradient; does not correct with oxygen therapy alone

21. How should a hypoxic event be managed?

Show answer
Before you even start trying to make the diagnosis, give oxygen. The first maneuver for intubated patients is to hand-ventilate with an ambu-bag. A ruptured endotracheal tube cuff is self-evident, whereas difficult bagging implies airway obstruction, bronchospasm, or tension pneumothorax. Inability to pass a suction catheter confirms endotracheal tube obstruction. If the obstruction is not reversible by changing head position or by cuff deflation, the endotracheal tube must be replaced immediately. If there is difficulty with bagging and no evidence of airway obstruction, listen to the chest for breath sounds to exclude a tension pneumothorax. The mechanical ventilator and breathing circuit must be examined for malfunction. Send arterial blood gases to confirm hypoxia (low Po2) and rule out hypoventilation (high Pco2).
Next, get a chest x-ray (to rule out a pneumothorax and to confirm the correct position of the endotracheal tube) and review recent medications, interventions (e.g., suctioning, position changes, nursing care), and changes in clinical status. Most acute hypoxic events in the ICU are due to easily identified and reversible mechanical problems, such as disconnects from oxygen delivery systems or mucus plugging that requires suctioning. (See Figure 11-2).

1. What are the “hard signs” of arterial injury?

Show answer

* Distal circulatory deficit: ischemia or diminished or absent pulses
* Bruit
* Expanding or pulsatile hematoma
* Arterial (pulsatile) bleeding

2. What are the four ways in which an arterial injury may present?

Show answer

1. Hemorrhage
2. Thrombosis
3. Arteriovenous fistula
4. Pseudoaneurysm

3. What are the “soft” signs of arterial injury?

Show answer

* Small- or moderate-sized stable hematoma
* Adjacent nerve injury
* Shock not explained by other injuries
* Proximity of penetrating wound to a major vascular structure

4. What are the symptoms of acute arterial occlusion?

Show answer
The six P’s: pain, pallor, pulse deficit, paresthesia, paralysis, and poikilothermia (cold).

5. What initial screening test is used to evaluate an extremity for occult vascular injury?

Show answer
Calculation of arterial pressure indices (APIs).

6. What are the APIs for the upper extremity and lower extremity called?

Show answer
An API for the upper extremity is the wrist brachial index (WBI).
An API for the lower extremity is the ankle brachial index (ABI).

7. How are WBI and ABI measured, and what is considered a normal value?

Show answer
A hand-held Doppler and blood pressure cuff are used to measure systolic blood pressure in the brachial, radial, ulnar, dorsalis pedis (DP), and posterior tibial (PT) arteries bilaterally. The ABI for each leg is the highest DP or PT divided by the highest brachial pressure. The WBI for each arm is the highest radial or ulnar artery pressure divided by the highest brachial pressure. A value of 1.0 is normal.
8. What API value raises concern for arterial injury, and what is the sensitivity and specificity? Show answer

* An API value < 0.9 has a sensitivity of 95% and specificity of 97% for major arterial injury.
* An API > 0.9 has a negative predictive value of 99%.

9. When the API value is < 0.9 in an injured extremity, what should be the next diagnostic test?

Show answer
Arteriography to establish the diagnosis and plan for operative intervention.

10. What abnormalities on arteriography determine a positive test result?

Show answer

* Obstruction of flow
* Extravasation of contrast
* Early venous filling or arteriovenous fistula
* Wall irregularity or filling defect
* False aneurysm (pseudoaneurysm)

11. What study should be performed for patients with proximity injury or soft signs (API > 0.9)?

Show answer
Duplex ultrasonography to rule out occult vascular injury.

12. What occult vascular injuries can be detected by duplex ultrasonography?

Show answer

* Intimal flap
* Pseudoaneurysm
* Arteriovenous fistula
* Focal vessel narrowing
* Nonoperative observation of these injuries is safe and effective: 89% of them do not require surgery

13. What is a pseudoaneurysm?

Show answer
It is a disruption of the arterial wall leading to a pulsatile hematoma contained by fibrous connective tissue (but not all three arterial wall layers). (See Figures 32-1 and 32-2.)

Figure 32-1 Subtraction angiography demonstrating intimal flap with stenosis of superficial femoral artery.

Figure 32-2 Duplex ultrasound of common femoral artery demonstrating pseudoaneurysm sac and associated neck between pseudoaneurysm sac and femoral artery after percutaneous access for angiography.

14. What is a true aneurysm?

Show answer
Dilatation of all three layers of the vessel wall (i.e., intima, media, and adventitia).

15. What is the most effective way to control arterial bleeding in an injured extremity?

Show answer
Direct digital pressure.

16. What means of controlling vascular injury should be avoided? Why?

Show answer
A tourniquet should be avoided because collateral circulation is occluded and leads to increased tissue ischemia.
Blind clamping should also be avoided because it causes further vessel damage, making reconstruction more difficult.

17. How should a patient with an extremity vascular injury be prepared and draped in the operating room?

Show answer
The entire involved extremity should be in the sterile field. The major arterial trunk proximal to the site of injury (for proximal control) and a portion of lower extremity permitting access to saphenous vein should be included in the sterile field.

18. What else should be prepared and draped for proximal extremity injuries?

Show answer
The chest should be prepped for proximal injuries of the upper extremity. The abdomen should be prepped for proximal injuries of the lower extremity. (Access to the chest or abdomen may be necessary to obtain proximal vascular control.)

19. What are the operative principles relative to repair of vascular injuries?

Show answer

* Perform longitudinal incisions over vessels to be explored.
* Initial dissection should be away from the site of suspected injury and adjacent hematoma.
* Obtain proximal and distal control of the injured vessel.
* Debride the injured vessel.
* Perform primary repair if tension free (fully extend extremity to ensure tension-free repair).
* Repair with autogenous interposition vein graft if there is inadequate length (tension).

20. What is the best conduit to use if primary repair is not possible? Why?

Show answer
Saphenous or cephalic vein from the uninjured extremity to preserve venous flow.

21. Should injuries to major veins of the extremities be repaired?

Show answer
Yes. Repair of a major vein enhances the success of a concomitant arterial repair by improving outflow. Late thrombosis often occurs after venous repair, but initial patency helps by allowing collateral circulation to develop. This may also reduce the incidence of postoperative venous insufficiency.

22. When should injured major veins be ligated?

Show answer
Major veins should be ligated rather than repaired when the patient is hemodynamically unstable or the repair is too complex.

23. What complications can develop after ligation of major extremity veins?

Show answer
Possible complications include rapid increase in muscle compartment pressure, leading to compromised venous or arterial flow and compartment syndrome. Also, postoperative venous stasis may occur, which can be alleviated with intermittent pneumatic calf compression and leg elevation.

24. What is a compartment syndrome?

Show answer
Development of pathologically elevated tissue pressures (preventing perfusion) within nonexpansile envelopes (inside fascial compartments) of the arm or leg.
KEY POINTS: COMPARTMENT SYNDROME

1. Pathologically elevated tissue pressures in nonexpansile fascial compartments prevent tissue perfusion.
2. The most common cause is ischemia-reperfusion injury following traumatic extremity injuries.
3. The earliest clinical sign is numbness in the first dorsal webspace associated with compromise of the deep peroneal nerve. Other signs: pain with passive joint motion, pain out of proportion to injury, tense and tender muscle compartments.
4. Distal pulses are evident until late in the diagnosis and should not be used to rule out compartment syndrome.
5. Hand-held manometer is used to measure muscular compartments. Normal pressure = < 10 mmHg; pathologic pressure = > 30 mmHg.
6. Treatment is emergent fasciotomy.

25. What is the most common cause of a compartment syndrome?

Show answer
Ischemia-reperfusion injury when ischemia depletes intracellular energy stores and then reperfusion leads to toxic oxygen radicals, causing cellular swelling and interstitial fluid accumulation.

26. What is the earliest sign of compartment syndrome after vascular repair of an extremity?

Show answer
Neurologic deficit in the distribution of the peroneal nerve with weak dorsiflexion and numbness in the first dorsal webspace.

27. Are there any other signs of a developing compartment syndrome of an extremity?

Show answer

* Increased pain with passive motion of the ankle
* Pain out of proportion to clinical findings (ischemia hurts)
* Tense muscle compartments that are tender to palpation

Distal pulses can remain intact.
28. How is the objective diagnosis of a compartment syndrome made?

Show answer
By measuring compartment pressures with a percutaneous needle and pressure transducer. Criteria for compartment syndrome are as follows:

* When diastolic pressure-compartment pressure is ≤ 20 mmHg or
* When mean arterial pressure-compartment pressure is ≤ 30 mmHg

29. What is the treatment for compartment syndrome of an extremity?

Show answer
Emergent fasciotomy, with decompression of the four compartments of the lower leg (anterior, lateral, superficial posterior, and deep posterior) or decompression of the forearm compartments.

30. What is the result of untreated compartment syndrome?

Show answer
Loss of perfusion promotes eventual myoneuronecrosis.
31. Which are the most commonly injured arteries in the upper extremity?

32. Which are the most commonly injured arteries in the lower extremity?

33. Can a patient with an extremity arterial injury have palpable distal pulses?

Show answer
Yes. In ≤ 20% of proven arterial injuries, a distal pulse is palpable (often because of collateral circulation).

34. What orthopedic injuries commonly have associated vascular injuries?

Show answer

* Supracondylar humerus fractures are associated with brachial artery injuries.
* Knee dislocations are associated with popliteal artery injuries.
* Femur fractures can be associated with injury to the superficial femoral artery.

35. For an injured extremity with concomitant fracture and vascular injury, which repair should be performed first?

Show answer
The vascular repair should be performed first to restore flow and reverse tissue ischemia.

36. After reducing or fixing an extremity fracture, what must you always do?

Show answer
Evaluate the distal pulses to ensure adequate vascular inflow (especially if fixation or any manipulation follows a vascular repair).

37. What is the likely diagnosis in a patient with repetitive palmar trauma and finger ischemia or necrosis?

Show answer
Hypothenar hammer syndrome (HHS). The mechanism is thought to be repetitive palmar trauma in patients with preexisting palmar artery fibrodysplasia. (The arteriogram shows digital artery occlusions with segmental ulnar artery occlusion or “corkscrew” elongation.) (See Figure 32-3.)

Figure 32-3 Angiography demonstrating intimal flap in superficial femoral artery associated with femur fracture.

38. What complications can occur after angiography when a percutaneous closure device is used on the femoral artery?

Show answer

* Thrombosis, ischemia, or both when the closure suture involves the posterior wall (back wall) of the artery
* Infected pseudoaneurysm
* Distal embolization when a hemostatic plug closure device is used

References
WEB SITES

1. http://www.east.org/tpg/lepene.pdf
2. http://www.surgery.ucsf.edu/eastbaytrauma/Protocols/ER%20protocol%20pages/extremity.htm

BIBLIOGRAPHY
1. Ferris BL, Taylor LM Jr, Oyama K, et al: Hypothenar hammer syndrome: Proposed etiology. J Vasc Surg 31:104-113, 2000. Medline Similar articles
2. Rutherford RB (ed): Vascular Surgery, 5th ed. Philadelphia, W.B. Saunders, 2000, pp 862-870.
3. Schwartz SI (ed): Principles of Surgery, 7th ed. New York, McGraw-Hill, 1999, pp 158-177.

1. How common is prostate cancer?

Show answer
It is the most common malignancy diagnosed in men in the United States; almost 200,000 new cases were diagnosed in 2001.

2. Do most men die with prostate cancer, rather than from it?

Show answer
Yes, but approximately 31,500 men died of prostate cancer in 2001 in the United States. Thus, it should not be treated as benign.

3. What are the early symptoms of prostate cancer?

Show answer
There are none. By the time significant symptoms develop, the disease is likely to be advanced. This is an argument for screening to detect prostate cancer.

4. What is the best screening method for prostate cancer?

Show answer
Digital rectal examination (DRE) combined with serum prostate-specific antigen (PSA). Since PSA testing was introduced, there has been a stage migration with less metastatic disease and more local-regional disease being detected.

5. How is prostate cancer diagnosed?

Show answer
It is diagnosed with prostate biopsy, which is a biopsy using transrectal ultrasound for guidance. Many cancers are discovered incidentally at transurethral resection of the prostate (TURP) for benign prostatic hyperplasia (BPH).

6. When is prostate biopsy indicated?

Show answer
When either the PSA or DRE result is abnormal.
KEY POINTS: PROSTATE CANCER

1. Prostate cancer is the most common malignancy diagnosed in men in the United States.
2. The best screening method is a combination of digital rectal exam and serum prostate-specific antigen.
3. Clinically localized prostate cancer is treated with surgery, radiation, cryotherapy, or watchful waiting.

7. Does an elevated PSA level mean a man has prostate cancer?

Show answer
No. PSA can be elevated with BPH, prostatitis, or after prostate trauma. It is prostate specific, not prostate cancer specific.

8. What is a free PSA?

Show answer

Free PSA is the percentage of PSA that is not bound to a serum protein carrier. The ratio of free to total PSA is helpful in determining when to do a prostate biopsy. “Free” is good because a higher ratio of free to total PSA is less likely to represent a prostate cancer.

9. Are there any known risk factors for prostate cancer?

Show answer
Yes. African-American men and men with a family history of prostate cancer are at an increased risk. A high-fat diet may play a role in increasing risk of many cancers, including prostate cancer.

10. What is Gleason’s sum?

Show answer
It’s a score that the pathologist gives prostate cancer to estimate its aggressiveness. The two predominant patterns of cancer are scored 1 to 5, and the sum is, therefore, between 2 and 10. Tumors can be well differentiated (2, 3, 4), moderately differentiated (5, 6, 7), or poorly differentiated (8, 9, 10).

11. How is clinically localized prostate cancer treated?

Show answer
Surgery (radical prostatectomy), radiation therapy by external beam or interstitial seed implant, cryotherapy, or watchful waiting.

12. How is advanced metastatic prostate cancer treated?

Show answer
Hormonal ablation therapy (orchiectomy or luteinizing hormone-releasing hormone agonist drugs) or chemotherapy, but these treatments are palliative and not curative.

13. What is the best treatment for prostate cancer?

Show answer
This is highly controversial. Patients must weigh factors such as age, overall health, grade and stage of the disease, and risk of side effects versus complications from the various treatment options.

References
WEB SITE
http://www.transplantation-soc.org
BIBLIOGRAPHY
1. Catalona WJ: Clinical utility of free and total prostate specific antigen. Rev Prostate 7(suppl):64-69, 1996.
2. D’Amico AV, Whittington R, Malkowicz SB, et al: Biochemical outcome after radical prostatectomy, external beam radiation therapy, or interstitial radiation therapy for clinically localized prostate cancer. JAMA 280:969, 1998.
3. Greenlee RT, Hill-Harmon MB, Murray T, Thun M: Cancer statistics 2001. CA Cancer J Clin 51:15-36, 2001.
4. Keetch DW, Humphrey PA, et al: Clinical and pathological features of hereditary prostate cancer. J Urol 155:1841-1842, 1996. Medline Similar articles Full article
5. Polascik TJ, Pound CR, et al: Comparison of radical prostatectomy and iodine-125 interstitial radiotherapy for the treatment of clinically localized prostate cancer: A 7-year biochemical (PSA) progression analysis. Urology 51:884-890, 1998. Full article
6. Resnick MI, Novick AC: Urology Secrets, 2nd ed. Philadelphia, Hanley & Belfus, 1999.
7. Reiter RE, deKernion JB: Epidemiology, etiology, and prevention of prostate cancer. In Walsh PC, Retik AB, Vaughan ED, et al (eds): Campbell’s Urology, 8th ed. Philadelphia, W.B. Saunders, 2002, pp 3003-3024.

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 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.

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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?

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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?

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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.

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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?

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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?

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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?

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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.

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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