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Critical Care Patient Pathophysiology 
By Penny Rickenbach

Introduction

     P.C. is a 47-year old divorced Puerto Rican female, who has lived in the United States five years. Initially, P.C. moved to be close to her three children who reside here, but now lives by herself with her daughter next door. P.C. is retired. She has an allergy to aspirin and uses alcohol, cigarettes and caffeine routinely.
     P.C. thinks, reads and communicates in Spanish. She is slow to respond to English and understands very little English; however, she says, “Nurse, I need,” when she wants to express her needs. A nurse aid on the unit served as my interpreter.
     The Catholic religion was stated on her chart, but no artifacts, crosses, or active praying was observed. Her family and friends did visit and serve as her support system.
P.C. was admitted on January 17, 2002, with esophageal varices that were bleeding. Her past medical history indicates two previous hospitalizations in 2001 for the same problem. Her past medical history is alcohol-induced liver disease, thromobcytopenia, pancreatitis, esophageal varices and chronic hepatitis. Cirrhosis of the liver is the primary concern with resultant portal hypertension causing esophageal varices, splenomegaly, and pancreatitis.
     P.C. was admitted to the emergency department on January 17, 2002, with complaints of mid-epigastric pain, nausea, and vomiting of coffee ground blood.
     Immediately an intravenous line was established for fluid replacement. Oxygen at 2 liters via nasal canula was started. A foley catheter was inserted for fluid management. Data was ordered for blood products, a type and crossmatch was done, revealing type A positive blood, and two units of packed red blood cells were ordered. Other laboratory data was ordered: CBC with platelets and 5 part differential, chem 8 STAT, urine culture and urinalysis, and ammonia, magnesium, protime, amylase, lipase serum values and a complete liver profile. An electrocardiogram revealed a normal sinus rhythm.
     P.C. admitted consuming six aspirin, and one cup each of coke and coffee, which all could enhance bleeding, on the day of admission. She exhibited signs and symptoms indicating hypovolemia, an increased heart rate of 120, orthostatic hypotension and confusion.
An esophagogastroduodenoscopy was ordered and revealed four bleeding esophageal varices, which were ligated and banded to stop the bleeding.
     P.C. was stabilized by January 18, 2002, and transferred to a Medical-Surgical Unit for further observation.
      After talking to a Registered Nurse, who has followed P.C. on two past hospitalizations, I gathered information. P.C. is an alcohol abuser who is non-compliant with treatment and follow-up social service program. She fully understands the consequences of drinking and realizes that she is putting herself in jeopardy by its continued use. She understands that she may die if future episodes of variceal bleeding occur, but does not want or does not care to change her lifestyle. I feel her coping skills may be lacking or she feels isolated and unable to control her problem.

Alcoholic Liver Disease and Cirrhosis

Alcoholic cirrhosis is also referred to as portal Cirrhosis and microndular cirrhosis. Several steps occur before the liver becomes cirrhotic. Initially, subcellular changes develop and may progress to a fatty liver. Fat deposition (i.e. triglycerides) within the liver is caused primarily by increased lipogenesis and decreased fatty acid oxidation by hepatocytes (McCance, 1998, 1359). Non-specific symptoms include fatigue, weight loss, and anorexia. It is the continuing use of alcohol that causes the development of cirrhosis. At the fatty liver stage, damage is reversible with discontinued use of alcohol (Porth, 1998, p. 760).
     The intermediate stage, alcoholic hepatitis, is characterized by inflammation and necrosis of liver cells. As the disease progresses fibrosis occurs. Ballooning of hepatocytes and the toxic effects of alcohol metabolism, such as acetaldehyde, damage liver cells. This stage is characterized by hepatic tenderness, pain, anorexia, nausea, fever, jaundice, ascites and liver failure (Porth, 1998, p. 761).
     With repeated bouts of drinking and hepatitis, liver injury may progress to cirrhosis. The microscopic changes seen consist of degeneration and death of hepatocytes, proliferation of connective tissue, and regeneration of hepatoctes. The connective tissue spreads from the portal tracts and central veins throughout the liver and forms nodules on the liver surface. Development of fibrous cords throughout the liver alters structural function of the hepatic veins and portal veins. Scar tissue and nodular regeneration of hepatocytes compresses small branches of the portal vein, leading to veins that are engorged and dilated. The result is portal hypertension, which will be discussed in depth later in the paper.

Complications Associated with Hepatic Cirrhosis

Problems and complications depend upon the amount of damage the liver has sustained. The loss of hepatic function contributes to metabolic abnormalities, synthesis of proteins and excretory functions of the liver. Liver function tests measure enzymes to assess injury to the liver. Alanine aminotransferase (ALT) and asparate aminotransferase are enzymes that are present in acute hepatocellular injury (Porth, 1998, p. 752).
     The liver' s synthetic capacity is reflected in measures of serum protein levels and
prothrombin time. Hypoalbuminemia is present, along with deficiencies of coagulation factors and vitamin K factors, all increasing bleeding tendencies. Serum bilirubin and alkaline phosphatase (ALP) measure hepatic excretory function. Alkaline phosphatase is present in disorders affecting the bile duct. Protein synthesis dysfunction can lead to decreased albumin, which contributes to plasma colloid pressure and aids in binding and transporting of various substances, including hormones, anions, bilirubin and fatty acids. In advanced liver disease, urea synthesis is depressed, leading to an accumulation of ammonia, and subsequent reduction in blood urea nitrogen (Porth, 1998, p. 752).
     Liver cell degeneration may lead to portal hypertension, ascites, bleeding, esophageal varices, jaundice, portal-systemic encephalopathy (PSE), hepatorenal syndrome, coagulopathy and toxemia (Trevillyan, 1997, p. 1851).
     Portal hypertension is abnormally high blood pressure in the portal venous system. The portal veins carry blood from the GI tract, pancreas and spleen to the liver. Hepatic veins empty into the inferior vena cava. Any component that impedes blood flow may cause obstruction in the liver. Some components are thrombosis, inflammation and fibrosis.
High pressure in the portal veins causes collateral vessels to open between the portal veins and the systemic veins, in which the blood pressure is much lower. Collateral veins develop on the esophagus, anterior abdominal wall and rectum. High pressure and increased volume are transmitted to the systemic venous circulation causing several problems (McCance, 1998, p. 1349).
     Collateral circulation is influenced by hemodynamics. Because of high pressure, values become incompetent and reversal of blood flow from blood that normally goes form the coronary veins into the spenic vein occurs. This forces open the collaterals between the esophagus and the gastric veins, leading to esophageal varices, hemorrhoids and dilated veins around the umbilicus (Hegab & Luketic, 2001, p. 75). Esophageal varices consist of three or four large trunks, the larger they are, the more likely they are to bleed. The esophageal submucosa is quickly affected; it is friable and easily ruptured by tortuous veins under high pressure.
Varices develop in most patients with cirrhosis and 30% to 60% die from first episode bleeding. Rebleeding risk approaches 70% in the first year, and each hemorrhage episode carries a 30% to 40% mortality rate; consequently, the overall survival rate is about 5 years (Chedid et al., 2001, p. 49). 
     An EGD was ordered to manage bleeding varices. P.C. had a history of two previous bleeding episodes in 2001, so an EGD was done a few hours after admission to the hospital. The results were four varices were banded in the esophagus. The stomach and duodenum were negative for varices (Patient' s Chart, 2002).
     The procedure for banding is done by a flexible endoscope. Ligation accomplished by banding is done using a device attached to the end of the endoscope. (Giacchino & Houdek, 1998, p. 34). 
     Ischemic necrosis, thrombosis and fibrosis ensue eradicating the varices. Possible complications can occur as: tissue ulceration, esophageal perforation, bleeding at ligation site and obstruction of the esophagus. Bacteremia, sepsis and pleural effusion can occur as well. For these reasons, P.C. was kept under surveilance after being transferred to C/Unit in the hospital when she was stable.
     As a result of hemorrhaging, P.C. had coffee ground emesis, positive heme in occult blood stool sample, black tarry stools, and the hemodynamic profile revealed decreased hemoglobin, decreased hematocrit, decreased platelets, anemia, decreased red blood cells, midepigastric pain, decreased circulating blood volume, leading to oliguria (less than 500 cc over 12 hours). Her admitting vital signs indicated hypovoemia, by a heart rate of 120 and orthostatic hypotension as well as fatigue, lethargy, and confusion. Her heart sounds were within normal limits (WNL), bilaterally clear and bowel sounds positive in all four quadrants (Client Chart, 2001). Direct portal hypertension caused an enlarged unbilical vein in P.C. also.
     The hemorrhaging varices bleed into the stomach causing nausea and anorexia.
Consequently, P.C. had been anorexic three days prior to admission. She vomited coffee ground blood on the day of admission and was fatigued, a little confused and enhibited clubbed finger nails, all symptoms of hypoxemia caused by decreased oxygenation related to decreased hemoglobin. Decreased hemoglobin reduces its capacity to carry oxygen through the vasculature and symtpoms related to hypoxemia occur.
      Some of the fatigue and confusion could also be correlated to electrolyte imbalances such as P.C.’s hypokalemia and hypocalcemia, resulting from impaired liver metabolism. Scant hair on pubic and axillary areas is related to hormonal alterations, also seen in altered liver hormone metabolism. Men can exhibit gynecomastia in this altered hormonal state (McCance, 1998, p. 1347).
     Propranolol therapy is used as a standard treatment for variceal hemorrhage. But, in 20 to 30 percent of patients with portal hypertension, propranolol fails to decrease hypertension, and thereby decrease esophageal pressure by reducing azgos blood flow. (Trevillyan, 1997, p. 1852). P.C. was not taking propranolol upon admission. Her home maintenance medications were diuretics aimed at reducing and mobilizing excess fluid and edema (Furosemide) and spironolactone used in conjunction with diuretics to counteract potassium loss (Davis, 2000, p. 320). She also took folic acid. required for protein synthesis of red blood cells to help restore and maintain normal hematopoeisis (Davis, 2000, p. 320).
     Prior to the EGD procedure, P.C. received two units of packed red blood cells, type A positive to replace lost blood and increase hemoglobin and hematocrit levels. She also received two liters oxygen via nasal canula to reverse hypoxemia secondary to decreased hemoglobin.
Upon admission to the Emergency department, P. C. was started on IV therapy to replace fluid losses and correct electrolyte imbalances. She received Sodium chloride (NaCl) at 0.9% with 20 MEQ Potassium Chloride (KCl) infused at 83.3 ml/m. Initiallv 250cc NaCl at 0.9% with 20 MEQ KCl were infused over three hours then repeated two times. Her other IV therapy was NaCl at 0.9% infusing at 80 ml per hr over 13 hours. Her heart rate and blood pressure and potassium returned WNL after four hours of therapy (Client Chart, 2002).
     Her admitting electrolytes were low potassium at 3.5, and hioi chloride at 113.  Decreased liver metabolic function can alter electrolytes, and a chloride shift can occur from potassium loss. Also, an increase in chloride is seen in hypoaldosteronism secondary to decreased hormone function in the liver, which synthesizes aldosterone. Aldosterone indirectly regulates chloride in the renal tubules. When aldosterone causes sodium to be reabsorbed, chloride follows passivelv, attraction of cations and anions. P.C. had hypocalcemia, reflecting pancreatitis and hypomagnesia related to calcium depletion. The cellular pump that maintains homeostasis causes movement of magnesium and calcium from the intracellular space to the extracellular space or vice versa. Both magnesium and calcium are absorbed in the intestines, and phosphorous inhibits both their absorptions. Possibly the increase in alkaline phosphatase seen in hepatic biliary obstruction resulted in decreased absorption of these electrolytes. (Porth, 1998, pp. 585-624).
     Additional medications given were famotidine, whiich is compatible to "Y' site, (Pepcid) used to decrease secretion of gastric acid and decrease symptoms of esophageal reflux. In this case, the patient had nausea and vomiting secondary to blood flow to the stomach from esophageal bleeding, and pepcid is used to treat stress induced from upper GI bleeding in critically ill patients. It is also used in pancreatic insufficiency to prevent acid inactivation of pancreatic enzymes. The high amylase enzyme on the laboratory data indicates pancreatitis (Davis, 2000, p. 472). Dextrose with Prontonix was given for short-term treatment of erosive esophagitis. It binds to enzymes in the presence of acid gastric Ph and is used therapeutically to heal the esophagus (Davis, 2000, p. 751). Vitamin K (aqua mephyton phytonadione) was given to treat hypoprothrombihemia. In hepatic liver disease prothrombin is not synthesized in the liver, leading to deficient amounts necessary to coagulate and prevent bleeding (Davis, 2000. P.795). 
An additional note on blood administration is that hemodynaic stability is best achieved by maintaining a hematocrit at about 30% with paced red blood cells. This optimizes the oxygen-carrying capacity of the blood but avoids a hypervolemic state that would elevate portal pressure and potentiate further bleeding (Trevillyan, 1997, p. 1853). 
P.C.’s hematocrit post transfusion fell into those parameters.
     After P.C. was scheduled for transfer to C1, her new medication orders included Lopresor (Metroprolol), a beta adrenergic blocker, used to control hypertension in her case, portal hypertension (David, 2000, p. 638). 

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