EJERCICIO DE TRANSVERSALIDAD CURRICULAR: EL CONSUMO Y LA GENERACIÓN DE DESECHOS SÓLIDOS EN EL CENTRO EDUCATIVO Campo

A bile duct injury at the time of surgery should be suspected when postoperative extrahepatic obstructive jaundice occurs. Other more common causes of elevated unconjugated hyperbilirubinemia include hematoma reabsorption and hemolysis of transfused blood (Table 5.3). Hepatocellular injury is another possibility in the differential diagnosis of postoperative jaundice. Common etiologies are sepsis, low total hepatic blood flow, and infectious hepatitis. When all other factors are Table 5.2. Comparison of operative parameters between hepatic vascular isolation (HVI) and LCVP-aided hepatectomy (LCVP)

Author Technique Total Major Blood Transfusions

Cases Resections* loss (cc) (units

*Major resections include all lobectomies and extended lobectomies.

**Value are reported in mean ± S.D.

†Denotes inclusion of cirrhotic patients in series.

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Table 5.3. Differential diagnosis of postoperative jaundice*

Increased Bilirubin Load Biliary Obstruction Hepatocellular Injury Blood transfusion Intrahepatic cholestasis Hepatic hypoxemia

Hematoma Drug induced Exacerbated chronic

Hemolytic anemia Infection induced hepatitis

Extracorporeal circulation Extrahepatic cholestasis Acute hepatitis: viral,

Hemolysis Bile duct injury alcoholic

Pancreatitis Gilbert’s disease Retained gallstones Sepsis

Trauma Toxins, drugs

*(modified from Brown (1988) and Gelman (1992), with permission of F. A. Davis, J. B. Lippincott & Co., and W. B. Saunders, Philadelphia)

Fig. 5.1. Vena caval injury profile under various CVP conditions: a) high CVP, b) low CVP. Increased CVP leads to distention of vena cava with ensuing enlarge-ment in diameter of injury and increase in the bleeding driving pressure.

eliminated, the diagnosis of anesthetic related hepatotoxicity might be entertained if halothane was used. With newer, less controversial volatile anesthetics, it is rarely seen today.

78 Hepatobiliary Surgery

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Ascites

Ascites manifests as a result of:

1) impaired albumin and protein synthesis,

2) increased hydrostatic pressure in hepatic sinusoids and splanchnic capillaries,

3) over-production, transudation and low reabsorption of lymph into the peritoneal space,

4) renal sodium retention and,

5) impaired renal water excretion, partially due to increased concentrations of antidiuretic hormone (ADH). Albumin infusion has no beneficial effect even in the presence of severe hypoalbuminemia. The treatment of ascites underscores bed rest and sodium restriction, to be followed by spirono-lactone if a spontaneous diuresis is not restored. If life threatening com-plications such as cardiac or respiratory compromise occur, these patients require hemodynamic monitoring. Paracentesis should be attempted in case ascites persists.

Renal Failure

Following hepatobiliary surgery, rapidly progressive renal failure may occur. The differential diagnosis includes acute tubular necrosis, prerenal azotemia and hepatorenal syndrome. Hepatorenal syndrome is the development of otherwise unexplained renal failure with urine sodium < 10 meq/l, hyperosmolar urine, olig-uria (< 400 ml/24hrs), fractional excretion of sodium (FeNa⁺) < 1, and urine creati-nine to plasma creaticreati-nine ratio > 30:1 in patients with advanced liver disease. The pathophysiology of hepatorenal syndrome is based on the pooling of blood in the splanchnic bed and the resultant decrease in plasma volume. The kidney perceives a decreased glomerular filtration rate and causes a vasoconstriction that shunts blood away from the renal cortex. There is no specific treatment for hepatorenal syndrome.

Dopamine (1-2.5 mcg/kg/min) may help maintain urine output. Although sponta-neous recovery has been reported, mortality is very high. These patients, generally cirrhotic, may benefit from liver transplant.

Pulmonary Care

Hepatopulmonary syndrome is defined by liver disease, increased alveolar arte-rial gradients, and evidence of reduced intrapulmonary vascular resistance. In cir-rhotic patients, an increased synthesis of nitric oxide has been demonstrated that may lead to arteriovenous shunts in the lungs. The resulting hypoxemia requires oxygen supplementation and may progress to respiratory failure.

Glucose Metabolism

We might expect the postoperative patient to be prone to hypoglycemia second-ary to diminished glycogen reserves, increased insulin levels, and impaired gluco-neogenesis. Yet, dangerous hypoglycemia is rare. Routine (5%) dextrose solutions should be infused while monitoring glucose serum levels.

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Coagulation

Hypocoagulability derives from thrombocytopenia or reduced synthesis of vita-min K dependent factors; cholestasis also decreases vitavita-min K absorption and hepatic stores. Improvements in coagulation may be achieved with vitamin K 10 mg/day.

Another cause of bleeding is fibrinogen deficiency; this situation may benefit from fresh frozen plasma transfusion. Decreased serum concentration of protein S, protein C and antithrombin III result in hypercoagulable states that can lead to disseminated intravascular coagulation (DIC).

Sepsis

Abdominal sepsis is the most common cause of mortality after hepatic resection.

Preoperative biliary manipulation, infected bile, biliary stones, ascites, and blood loss may all predispose to abdominal sepsis. Other sources of sepsis include the respiratory and urinary systems. Wound infection and a central line catheter should also be considered as possible sources of infection.

Gastrointestinal Bleeding

The incidence of GI bleeding is 5%, with a mortality reaching 50%. The bleed-ing site can usually be identified by endoscopy. Treatment includes transfusions, antacids and H2 blockers. All postoperative hepatobiliary patients should be treated prophylactically. About 30% of cirrhotic patients have esophageal varices. The emer-gent treatment should combine blood product transfusion to correct the coagulopathy, gastric endoscopy with variceal banding or sclerotherapy, and possibly, octreotide 25-100 mcg/min to control bleeding. Life saving procedures may include compres-sion of the varices via a Sengstaken-Blakemore tube. As rebleeding occurs in 50% of patients, a definitive surgical treatment should be pursued.

Encephalopathy

Hepatic encephalopathy may be precipitated by GI bleeding, infection, drugs, diet or dehydration. It manifests as a sudden change in a patient’s mental status or the onset of asterixis. The precise pathogenesis remains unknown. The historical postulate has been the accumulation of endogenous ammonia. Other etiologies have been suggested, including changes in the blood-brain barrier permeability, abnor-mal neurotransmitter balance, altered cerebral metabolism, impairment of neuronal Na⁺-K⁺ ATPase activity, and increased endogenous benzodiazepines. Standard therapy is devised to reduce levels of ammonia and other potentially toxic metabolites.

Flumazenil has been administered with some improvement; however, protein restriction and lactulose administration are still practiced.