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Queries 5

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Liver Transplantation

admin — Mon, 13 Jul 2009 18:48:40 +0000

89 LIVER TRANSPLANTATION
Thomas E. Bak M.D., Michael E. Wachs M.D., Igal Kam M.D.

1. When and where was the first liver transplant performed?

Show answer
Dr. Thomas Starzl performed the first operation on March 1, 1963, at the University of Colorado in Denver.

2. Is liver transplantation considered a safe and effective operation?

Show answer
Yes. Although still a major operation with significant risks, patient and graft survival have continuously improved. One-year survival should be well over 90% in major centers.

3. What are the most common indications for liver transplantation in the United States?

Show answer
Noncholestatic cirrhosis characterizes > 50% of the recipients. This group includes those with viral hepatitis, alcoholic cirrhosis (Laennec’s), and Budd-Chiari syndrome. Cholestatic cirrhosis makes up an additional 15%, with primary sclerosing cholangitis (PSC) and primary biliary cirrhosis heading this group. Other indications include biliary atresia, acute hepatic necrosis, malignant neoplasms, and metabolic disease.

4. Has the most common disease requiring transplantation shifted over the years?

Show answer
Yes. The largest percentage of people now being transplanted have hepatitis C. There are also more retransplants performed because some diseases such as hepatits C and PSC can recur in transplanted livers.

5. How is the waiting list run?

Show answer
Changes have been made to the list so that the sickest patients get transplanted first. New scoring systems (Mayo End-stage Liver Disease [MELD] score) have been devised to give more weight to objective markers of illness rather than the more subjective medical criteria used in the past. This point system has also minimized the importance of time spent on the waiting list. The goal of these changes is to reduce waiting list mortality.

6. What are some of the recent advances in liver transplant surgery?

Show answer
Operative techniques have improved such that some liver transplant recipients do not require a stay in the intensive care unit, venovenous bypass, or external biliary drainage, and operative times are shorter (4-5 hours). Improved immunosuppression medications have reduced rejection rates and side effects.

7. How long can a liver be kept “on ice”?

Show answer
Optimal cold ischemia should be < 12 hours.

8. What are some common postoperative complications of liver transplantation?

Show answer
Postoperative bleeding, infection, and biliary complications are the most common. Primary nonfunction (< 5%) and early hepatic artery thrombosis (5%) are less common, but they usually require an urgent retransplant.

9. What is the “piggy-back” technique?

Show answer
This is a technique in which the recipient’s sick liver is carefully resected off of his or her vena cava, which is left in situ. The upper donor cava is then sewn to a common cuff of native hepatic veins. The donor’s lower cava is ligated. Using this method, it is possible to do the complete transplant with minimal if any vena caval occlusion, resulting in less intraoperative hemodynamic instability.

10. Is living-donor liver transplantation an option?

Show answer
Yes. Initially used in the pediatric population using an adult left lateral segment graft, this procedure has evolved into fairly common practice. The Far East has had a large number of adult-to-adult left lobe graft series. Elsewhere, this has been replaced with a right lobe donor operation. Both the donor and recipient liver lobes quickly regenerate to normal size. Results in experienced centers mimic those of cadaveric transplant with similar patient survival, albeit at higher complication and retransplant rates.
KEY POINTS: LIVER TRANSPLANTATION

1. The most common indication for liver transplantation in the United States is noncholestatic cirrhosis.
2. Optimal cold ischemia time for the liver is < 12 hours.
3. Transjugular intrahepatic portosystemic shunts can be used in potential transplant recipients as a bridge to transplantation.

11. How have transjugular intrahepatic portosystemic shunts (TIPS) improved this field of surgery?

Show answer
TIPS can be used in potential transplant recipients as a bridge to transplantation. This procedure is very effective in controlling portal hypertension without the need for a major abdominal operative shunt. A prior portocaval shunt does complicate a liver transplant, but it is not a contraindication to liver transplantation.

Portal Hypertension & Esophageal Varices

admin — Wed, 08 Jul 2009 14:58:46 +0000

42 PORTAL HYPERTENSION AND ESOPHAGEAL VARICES
Ramin Jamshidi B.S., B.S., Gregory V. Stiegmann M.D.

1. Describe the blood supply to the liver.

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

2. How is portal hypertension defined?

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

3. What is hepatopetal flow?

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

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

Show answer

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

5. What are schistosomiasis and Katayama fever?

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

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

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

Show answer
Presinusoidal:

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

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

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

Show answer

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

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

8. Define sinistral portal hypertension.

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

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

Show answer

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

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

Show answer

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

11. Liver function is classified according to what system?

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

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

12. What is MELD?

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

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

13. How is MELD calculated?

Show answer

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

Result is rounded to the nearest integer.

14. How common are esophageal varices?

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

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

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

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

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

17. What factors are predictive of variceal bleeding?

Show answer

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

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

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

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

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

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

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

Show answer

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

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

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

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

Show answer

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

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

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

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

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

25. What is a Sengstaken-Blakemore tube?

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

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

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

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

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

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

28. What is TIPS?

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

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

29. Describe the basic options for surgical shunting.

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

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

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

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

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

Hepatic & Biliary Trauma. Surgical Anatomy Of The Liver

admin — Tue, 07 Jul 2009 20:45:21 +0000

SURGICAL ANATOMY OF THE LIVER

7. How many anatomic lobes are present in the liver? What is their topographic boundary?

Show answer
The liver is divided into two anatomic lobes, the right and the left. Their boundary lies in an oblique plane extending from the gallbladder fossa anteriorly to the inferior vena cava posteriorly. The three hepatic veins define the division between the lobar segments and the planes of surgical resection. Lobar segments are numbered I-VIII, according to Couinaud’s nomenclature. (See Figure 25-1.)

Figure 25-1 The functional division of the liver and the segments according to Couinaud’s nomenclature. (From Bismuth H: Surgical anatomy and anatomical surgery of the liver. World J Surg 6:6, 1982, with permission.)

8. What is the blood supply to the liver and the relative contribution of each structure to hepatic oxygenation?

Show answer
The hepatic artery supplies approximately 30% of the blood flow to the liver and 50% of its oxygen supply. The portal vein provides 70% of the liver’s blood flow and 50% of its oxygen. The relative significance of arterial flow in cirrhotic patients is greater; therefore, hepatic artery ligation is not recommended in patients with cirrhosis.

9. What are the most common variations in hepatic arterial supply to the right and left lobes of the liver?

Show answer
In most people, the common hepatic artery originates from the celiac axis and divides into right and left hepatic arterial branches within the porta hepatis. Approximately 15% of people have a replaced right hepatic artery (sole arterial supply to the right lobe) that originates from the superior mesenteric artery (SMA). A replaced right hepatic artery always supplies a cystic artery; thus, ligation should be followed by cholecystectomy. A replaced left hepatic artery (approximately 15% of people) arises from the left gastric artery; it may be the sole blood supply to the left lobe or may contribute to blood supply in conjunction with a normal left hepatic artery. In 5% of people, the hepatic arterial supply does not arise from the celiac axis. In these people, either the right and left hepatic arteries are replaced or a single main hepatic trunk derives from the SMA.

10. What is the venous drainage of the liver?

Show answer
The right, middle, and left hepatic veins are the major venous tributaries and enter the inferior vena cava below the right hemidiaphragm.

KEY POINTS: BLOOD SUPPLY AND DRAINAGE OF THE LIVER

1. Hepatic artery delivers 30% of blood flow.
2. Portal vein delivers 70% of blood flow.
3. -In 15% of the population the right hepatic artery originates from the superior mesenteric artery.
4. In 15% of the population the left hepatic artery originates from the celiac artery.
5. In 5% of the population neither hepatic artery originates from the celiac artery.
6. Venous drainage: right, middle, and left hepatic veins drain into the inferior vena cava.

Portal Hypertension & Esophageal Varices. Controversy

admin — Wed, 08 Jul 2009 17:32:34 +0000

CONTROVERSY

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

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

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

Abdominal Tumors

admin — Mon, 13 Jul 2009 08:39:51 +0000

87 ABDOMINAL TUMORS
Frederick M. Karrer M.D., Denis D. Bensard M.D.

1. What are the most common malignant solid abdominal tumors in children?

Show answer
Neuroblastomas, Wilms’ tumors, and hepatoblastomas, in that order. Neuroblastomas are derived from neural crest tissue; in the abdomen, they originate from the adrenal glands and paraspinal sympathetic ganglia. Wilms’ tumor (nephroblastoma) derives from the kidney, and hepatoblastomas originate in the liver.

2. Is it tough to differentiate Wilms’ tumor from neuroblastomas clinically?

Show answer
Yes. Both tumors present as an asymptomatic abdominal mass. The differences are summarized in Table 87-1. In addition, because neuroblastomas produce hormones, affected children may exhibit flushing, hypertension (catecholamine release), watery diarrhea, periorbital ecchymosis, and abnormal ocular movements.
Table 87-1. DIFFERENTATION BETWEEN WILMS’ TUMOR AND NEUROLASTOMA

	Wilms’ Tumor	Neuroblastoma
Age at presentation	3-4 yr	1-2 yr
Extend across midline	Rare	Common
Surface on palpation	Smooth	Knobby
X-ray calcifications	No	Yes

3. How are Wilms’ tumors and neuroblastomas treated?
Table 87-2. TREATMENT OF WILMS’ TUMOR AND NEUROBLASTOMA

	Wilms’ Tumor	Neuroblastoma
Primary surgical excision	Important (likely)	Important (less likely)
Chemotherapy	Enormous impact	Less responsive

4. What are the major prognostic factors in neuroblastomas and Wilms’ tumor?

In neuroblastomas, age at presentation is the major prognostic factor. Children younger than 1 year have an overall survival rate > 70%, whereas the survival rate for children older than 1 year is < 35%. Shimada proposed a prognostic classification based on evaluation of histologic parameters (tumor differentiation, mitosis-karyorrhexis index [MKI]) as well as age. Aneuploid tumors, tumors with low MKI, and tumors with < 10 copies of the n-myc gene also have better outcomes.

Age is also important in children with Wilms’ tumors, but the prognosis is better because the tumors are more readily excised and much more sensitive to chemotherapy.
5. What are the differences between hepatoblastomas and hepatocellular carcinomas? How are the tumors treated?
Hepatoblastomas usually occur in infants and young children, whereas hepatocellular carcinoma usually occurs in children older than 10 years. Hepatocellular carcinoma usually is associated with cirrhosis and hepatitis B and is histologically identical to the adult form. Surgical resection is the primary therapy for both tumors. Hepatoblastomas often have a good response to adjunctive chemotherapy, whereas hepatocellular carcinoma rarely responds to chemotherapy.

Nutritional Assessment & Enteral Nutrition. Nutritional Assessment

admin — Mon, 06 Jul 2009 21:33:48 +0000

8 NUTRITIONAL ASSESSMENT AND ENTERAL NUTRITION
Margaret M. McQuiggan M.S., R.D., CNSD, Frederick A. Moore M.D.

NUTRITIONAL ASSESSMENT

1. What does a nutritional assessment include? Show answer

1. The medical and surgical history is used to establish preexisting (comorbid) conditions, metabolic stress, and alterations in organ function.
2. The physical examination focuses on the muscle mass, adipose stores, skin integrity, and hydrational state.
3. Laboratory data include the chemistry profile (Na, K, CO2, Cl, BUN, creatinine, glucose), ionized Ca, serum PO4, and Mg, complete blood count (CBC) with differential, arterial blood gases (ABGs; to assess acid-base status and CO2 retention), albumin, transferrin, prealbumin, and urinary nitrogen.
4. The drug profile can reveal agents that affect the metabolism of nutrients (insulin, levothyroxine, corticosteroids) or alter energy expenditure (beta-blockers, Diprivan).
5. Anthropometric data include height and weight; skinfold testing with calipers is only useful once edema has resolved but is rarely used in the acute care setting. Although information on adipose reserve, body cell mass, intra- and extracellular water, and third space fluid may be elucidated, standards for bioelectrical impedance analysis (BIA) have yet to be determined.
6. A nutrition history reveals preexisting nutritional practices.
7. The social history explores economic data or substance abuse behaviors and may predict the likelihood of adequate home care for the patient upon discharge.

2. What are primary and secondary malnutrition?

Show answer
Primary malnutrition is the consumption of inadequate kilocalories, protein, vitamins, or minerals. It may occur because of poor food choices, anorexia, poverty, alcoholism, suboptimal support regimens, or after bariatric surgery. Secondary malnutrition may occur even when adequate food is infused or consumed. It results from organ dysfunction (hypoalbuminemia with cirrhosis), malabsorption (Crohn’s disease), immobility (muscle wasting), drug therapy (insulin resistance with corticosteroids), or the inflammatory response (reprioritization of hepatic synthesis of acute phase instead of constitutive proteins).

3. What is the significance of serum proteins in nutritional assessment?

Show answer

Table 8-1. SERUM PROTEINS

TIBC = total iron-binding capacity.

KEY POINTS: HALF-LIVES OF SERUM PROTEINS USED AS NUTRITIONAL MARKERS

1. Pre-albumin: 2-4 days
2. Transferrin: 8-10 days
3. Albumin: 20-21 days

The most readily available proteins for nutritional assessment are albumin, transferrin, and prealbumin, which are all constitutively produced in the liver. Their half-lives are 20-21 days, 10-12 days, and 2-4 days, respectively. The level of all three plummets shortly after injury or surgery as the liver reprioritizes the production of acute phase proteins. Then, as inflammation, infection, and stress begin to resolve, the liver resumes production of constitutive proteins. Adequate kilocalories and protein facilitate this process. Because of their shorter half-lives, prealbumin and transferrin are most useful in the intensive care unit (ICU) setting and should be limited to patients with creatinine clearance > 50 mL/min. Levels of both proteins may be depleted in patients with hepatic failure or cirrhosis because of decreased synthetic function. Prealbumin travels in the circulation bound to retinol-binding protein (RBP) and vitamin A. Levels of prealbumin may be elevated in renal failure despite nutritional compromise, because of decreased catabolism and decreased excretion of RBP. Transferrin is elevated with iron depletion, independent of the effects of nutrition. (See Table 8-1.)

4. What is the significance of urinary nitrogen in nutritional assessment?

Show answer
Total urinary nitrogen (TUN) is the most reliable indicator of nitrogen utilization and excretion in surgical ICU patients. However, urinary urea nitrogen (UUN) is more readily available in most hospital laboratories. Although TUN and UUN are nearly equal in healthy ambulatory patients, critically ill patients exhibit a poor correlation between the two. Optimal nutrition support should place a patient in 13 to 15 nitrogen balance. One may estimate the protein needs of the patient by adding:

[24 h UUN (g) + 2 g N insensible losses + 3] x 6.25 = required amount of protein (g)

The total in brackets is multiplied by 6.25 to convert nitrogen grams to protein grams. Thus, if the laboratory reported a 13-g UUN/24 hours and a 2-g N insensible loss (skin, hair, feces) + 3 g for optimal anabolism, the patient would require 18 g N × 6.25 = 112.5 g of protein for anabolism. Urinary nitrogen is not useful as a guide for nutritional prescription in hepatic failure, renal dysfunction (< 50 mL/min creatinine clearance), or recent spinal cord injury.

5. How are protein requirements determined?

Show answer
Protein need is determined based on the weight of the patient, current stress factors, extraordinary skin losses, and organ function. Although the recommended daily allowance (RDA) for protein for healthy individuals is only 0.8 g protein/kg body weight, the following guidelines may be used in surgical patients. (See Table 8-2.)
Table 8-2. PROTEIN REQUIREMENTS IN RELATION TO INJURY LEVEL

Injury Level Protein Requirement
Mild stress or injury 1.2-1.4 g/kg
Moderate stress or injury 1.5-1.7 g/kg
Severe stress or injury 1.8-2.5 g/kg

6. Should protein be severely restricted in surgical patients with hepatic failure or renal failure?

Show answer
Protein should be restricted to 0.7 g/kg in patients with encephalopathy, only if the hepatic encephalopathy produces significant clinical consequences. Only 10% of chronic liver disease patients are protein sensitive; thus, other causes of encephalopathy such as infection, constipation, and electrolyte disturbance should be explored. Otherwise, a more typical postsurgical protein load may be adopted (1.4 g/kg). In injured patients with renal failure, one must balance the need for increased protein with the need for increased dialysis. One should provide the amount of protein required and dialyze more frequently.
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7. How are kilocalorie needs determined?

Show answer
There are several methods for setting kilocalorie targets in the surgical patient: standard prediction equations, kilocalorie per kilogram estimations, and indirect calorimetry. One common prediction equation, the Harris Benedict (HBE), was developed in 1919 for use on ambulatory, fasted, healthy people. Basal energy expenditure (BEE), the number of kilocalories required at rest daily, is calculated using the following equations:

Female BEE = 655 + 9.6 (kg) + 1.8 (cm) -4.7 (age)
Male BEE = 67 + 14 (kg) + 5 (cm) – 6.7 (age)

Subsequently, the above sums are multiplied by stress factors to determine total kilocalorie goals. (See Table 8-3).
Many clinicians use a total kcal/kg goal as shown in Table 8-4.
Table 8-3. KCAL NEEDS IN RELATION TO STRESS LEVELS

Stress Level Example Kcal Needs
Mild Closed fracture, pneumonia, or splenic laceration BEE × 1.2
Moderate Bowel resection, hepatorrhaphy, or thoracotomy BEE × 1.4
Severe Major bowel perforation with resection, major open wounds,
intraabdominal abscess BEE × 1.6

Table 8-4. KCAL / KG GOALS

Patient Feeding Level (kcal/kg) Level by Indirect Calorimetry
Normal weight patients 25-30 REE† × 1.0
Underweight patients 35-40 REE × 1.2
Obese patients 20-25* REE × 0.85
Morbidly obese 10-20* REE × 0.75

†Resting energy expenditure (REE) is the measure of energy expenditure in a fed state and is generally 10% higher than BEE.
*Use adjusted weight.

8. What is indirect calorimetry?

Show answer
It is a bedside test in which the patient’s production of carbon dioxide and consumption of oxygen are measured for approximately 30 minutes until steady state is achieved. Results are inserted into the modified Weir equation:

REE = [(3.796 x VO2) + (1.214 x VCO2)] x 1440 min/day

where REE = resting energy expenditure (kcal/day), VO2 = oxygen consumption (L/min), and VCO2 = CO2 exhaled (L/min).

The chart reports the number of kilocalories the patient is predicted to consume in 24 hours and the respiratory quotient (RQ). RQ = VCO2/VO2 and provides information on the type of substrate being used. The RQs for the metabolism of fat, protein, and carbohydrate are 0.7, 0.83, and 1.0, respectively. Overfeeding results in an RQ > 1.0.
KEY POINTS: RESPIRATORY QUOTIENT

1. Defined as ratio of CO2 produced to O2 consumed
2. Easy to perform on mechanically ventilated patients
3. Identifies principal metabolic substrate used by the patient
4. Ratio for fat (0.7), protein (0.83), and carbohydrates (1.0)
5. 5. Ratio < 1 indicates starvation or underfeeding; ratio > 1 indicates overfeeding, lipogenic status
6. Increased CO2 production linked to difficulty with ventilator weaning and impaired immune response

9. When is indirect calorimetry useful?

Show answer
The test may be performed on mechanically ventilated patients as soon as they are relatively stable, with a fractional concentration of oxygen in inspired gas (FiO2) < 60% and peak end-expiratory pressure (PEEP) < 10. Studies are helpful:

* When overfeeding (e.g., in diabetes mellitus, chronic obstructive pulmonary disease [COPD]) would be undesirable
* When underfeeding (e.g., renal failure, large wounds) would be especially detrimental
* In patients whose physical or clinical factors promote energy expenditure deviant from normal
* When drugs are used that might alter energy expenditure (e.g., paralytic agents, beta blockers)
* In patients who do not respond as expected to calculated regimens

UPPER GASTROINTESTINAL BLEEDING

admin — Wed, 08 Jul 2009 20:47:30 +0000

51 UPPER GASTROINTESTINAL BLEEDING
G. Edward Kimm Jr. M.D., Allen T. Belshaw M.D.

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