Portal HPN Persistent increase in BP in the portal venous system occuring

as a result of increased resistance or to obstruction of blood
flow through portal venous system into liver
Increased resistance to flow Factors in the pathogenesis of cirrhotic Portal HPN
Portal or splenic vein occlusion
Schistomiasis
Congenital hepatic fibrosis
Sarcoidosis
Cirrhosis
PATHO
-The normal blood flow to and from the liver depends on the proper functioning of portal vein (70%
inflow), the hepatic artery (30%) and hepatic vein (outflow)
-It results either from increased blood flow in the portal vein or from an increased resistance to flow
w/in the portal venous system
-Most common cause of portal HPN is cirrhosis
-The pathoplysiologic mechanism in cirrhosis is increased, resistance, w/c is intrahepatic and
primarily sinusoidal
-It may also arise from presinusoidal obstruction, either outside the liver (portal vein thrombosis) or
w/in it (as in schisto).
-Lesions leading to portal HPN may be postsinusoidal, either w/in the liver (as in venoocclusive
disease) or distal to it (as in Budd-chiari syndrome or R sided heart failure).
-Normal portal venous BP is 5-10mmHg
-Portal HPN exists when the pressure rises 5mmHg higher than the inferior vena cava pressure
S/SX:
Slightly tortuous epigastric vessels that branch off the area of the umbilicus and lead toward the
sternum and ribs(caput medusae); an enlarged, palpable spleen; internal hemorrhoids; bruit, which
may be hear over the upper abdoen and ascites which appears when there’s concurrent liver disease
-ONE OF THE MOST SERIOUS DISABLING COMPLICATIONS OF PORTAL HPN IS
DILATION OF THE SUPERIOR RECTAL VEINS, ABDOMINAL WALL VEINS AND
ESOPHAGOGASTRIC VEINS
Varices Swollen dilated veins
Increased portal venous pressure, Factors that can contribute to rupture of varices
increased thoracic pressure, irritation
by food or alcohol, and eroiion by
gastric juices
Veins of stomach and esophagus Most subject to rupture
To stop hemorrhage, health practitioners perform emergency measures: Injection sclerotherapy,
transjugular intrahepatic portosystemic shunt, admin of vasopressin, balloon tamponade, beta
adrenergic blocking agents, endoscopic electrocautery etc.
MEDICAL MGT
1.Control hemorrhage
*Sclerotherapy- passes an endoscope into esophagus and injects sclerosing agent taht flows into
varices. The agent causes inflam of vein and then fibrosis
*Tranjugular intrahepatic portosystemic shunt- an expandable metal stent is advanced w/ aid of
fluoroscopy to the hepatic veins during angiogram and then through liver to create direct portacaval

you should have scissors at bedside to be able to remove tube in an emergency NURSING MGT: DX: Ineffective tissue perfusion interventions: *Prevent hemorrhage: 1.for mgt of acute variceal bleeding (propranolol. nadolol) *Balloon tamponade-Applying pressure to ruptured vavrices may stop hemorrhage. Avoid rough foods.technique to create portal systemic shunt via percutaneous approach *Portosystemic shunt.undergo stenosis or occlude over period of mos. prompting need for another tTIPS of another approach *Vasopressin.keep side rails up and bed in lowest position SURGICAL MGT *Endoscopic band ligation -Esophageal varices are ligated and strangulated w/ small elastic O-rings placed in the appropriate place during endoscopy *Tranjugular intrahepatic portosystemic shunt. maybe given in conjunction w/ nitroglycerin. metoprolol. sublingually S/E: Hypothermia. heart failure. shunt clotting and hepatic enceph POST OP CARE: .stop variceal bleeding. Avoid straining maneuvers that increase intraabdominal or intrathoracic pressure 2.channel Stents. w/c may traumatize the espohagus. Clinican inserts sengstaken-blakemore or minnesota tube into the stomach and inflate esophageal and gastric balloons. and spicy foods w/c irritate esophageal mucosa 3. Develop and emergency plan in case severe esophageal varices should rupture DX: Impaired gas exchange Interventions: *Prevent esophageal necrosis *Prevent aspiration pneumonia *Prevent nares erosion *Prevent airway obstruction DX: Acute confusion Interventions: *Monitor lvl of consciousness -Assess for dvpt of asterixis (liver flap or flapping tremor) -Monitor GI bleeding. blood and fluid loss and anesthesia of surgery Complications: MAJOR COMPLICATIONSo of shunt procedure: Bacteremia land DIC. myocardial and gastrointestinal tract ischemia and ARF *Beta adrenergic blocking agents. administered IV.reduces portal HPN by sending portal venous blood directly into the inferior vena cava bypassing the liver MAIN CONTRA TO PORTOSYSTEMIC SHUNT: Poor general health so that client is not able t w/stand the trauma. including melena or hematemesis because bleeding can precipitate hepatic coma *Protect from injury. achieves lowering of portal pressure.

if portal HPN is due to liver dx. by gastric juices and peripheral tissue metabolism -More recently implicated as cause of enceph are false neurotansmitters. pneumonia) *Hypoalbuminemia *Hypogly *Manifestation of infection *Pain lvls *Mental status DIAGNOSIS: EXCESS FLUID VOL Interventions: *Assess for excess fluid vol *Monitor and treat postprocedure complications. monitor for postop hemorrhage because bleeding tendencies often arise from liver cell malfunction. seizures and Occur in terminal stage irreversible coma PATHO: -Hepatic enceph is characterized by elevations of ammonia lvls in the blood and CSF. assess client for hepatic enceph. elevated lvl of mercaptans(organic chemicals that contain sulfhydryl radical. PT. affecting glial and nerve cells. w/c is stroed in the liver and is later converted to urea and excreted through kidneys -Failure of liver to perform this function may be due to liver cell damage and necrosis -Ammonia also is a CNS toxin. labored breathing. by liver and in lesser amnts. hypovolemia and oliguria *F&E imbalances *RR and rhythm (rales. it leads to altered CNS metabolism and function . monitor hgb. hct. Ammonia is a CNS depressant Reduced mental alertness. BUN. formed when the O2 of alcohol molecule is replaced by sulfur).Assess client after portosystemic shunt surgery by monitoring ff: *Presence of hemorrhage. atelectasis.if clotting time is not w/in normal limits. ammonia lvl. bilirubin lvl. depress CNS or are known hepatototxins *Maintain nutrition *Maintain sterile technique *Maintain patency if GI tube is in place etc PLEASE READ ESOPHAGEAL BLEEDING SECONDARY TO PORTAL HPN CRITICAL MONITORING PAGE 1155 :) HEPATIC ENCEPH Etiology and risk factors: Cause is the livers inabilty to metabolize ammonia to form urea so that it can be excreted. administer vit K. confusion Chnges during initail stages of hepatic enceph includes: and restlessness Loss of consciousness. -Ammonia is produced in the GIT when protein is broken down by bacteria. administer blood transfusion if needed Other areas w/c you may need to intervene for clients who have undergone portosystemic shunt surgery: *Administer IV fluids pus blood or vol expanders *Monitor blood and urine values and note any manifestation of inection *Eliminate meds that sedate. phenol and short-chain fatty acids The liver converts ammonia into the glutamine.

client need to learn to manage diarrhea. concentration and rate of response *Hand writing and speech show significant changes as intellectual deterioration occurs *Hyperventilation w/ respi alkalosis develops because high ammonia levels stimulate respi center *The presence of methylmercaptan causes a characteristic odor on the on breath called fetor hepaticus *Monitor serum ammonia lvls. constipation. Severe livere disease include: GI bleeding. CNS depressant drugs (opiates. attention. adn their use should be avoided *Prevent complications of immobility FATTY LIVER (HEPATIC Lipid infiltraion may lead to hepatic stenosis.be alert ot possible harmful accumulation of ammonia as result of duiuretic therapy. is given to clients to produce 2-4 stools a day NSG MGT: -Observe cleitn for persnlaity changes w/ labile feeling states. or fatty liver. and hepatic function test results (bilirubin. a possible S/E of action of lactulos or neomycin SO4 DX: DEFICIENT FLUID VOL DX: RISK FOR INJURY Interventions: *Prevent hypoxemia *Prevent infection *Prevent ammonia toxicity and hypokalemia. its must be avoided in clients w/ renal insuf -Lactulos. w/c helps decrease blood ammonia lvls by reducing absorption of ammonia. blood gases. one STENOSIS) of the most common metabolic dx of liver . albumin. benzodiazepines) and dehydration -Protein may be totoally eliminated w/ fruit juices and IV fluids -Chronic hepatic enceph need low protein diet (50-60 g/day) *Reduce nitrogenous waste in blood and bacteria in the colon -Neomycin and lactulose are given to reduce bacteremin in the intestinal tract -Neomycin is nephrotoxic.agents w/ CNS depressants may precipitate coma. electrolyte levels.CMS: *Mild mental confusion to deep coma *Hepatic enceph imparis memory. Hypokalemia from use of diuretics contributes to hepatic enceph by increasing ammonia production in the kidney *Avoid sedation. inccreased dietary portein. prothrombin and enzymes) -Client may die of circulatory or PROGNOSIS respi complciations. infxn or delirium and convulsions MEDICAL MGT: *Identify and treat precipitating causes Factors that precipitate w. infxn. and elicit liver flap or flapping tremor (asterixis) by asking client to dorsiflex the hand w/ rest of arm resting on bed DX: INEFFECTIVE THERAPEUTIC REGIMEN MGT AND INEFFECTIVE FAMILY THERAPEUTIC REGIMEN MGT Interventions: *Promote low protein diet *Monitor for GI bleeding *Encourage bowel cleansing.

prolonged IV hyperalimentation etc NURSING INTERVENTIONS: *Directing attention to correction of cause *Preparing client for dx procedures *Giving emotional support by allowing verbalization of concerns and fears *Giving support physical care *Designing teaching guidelines that promote proper diet and prevent recurrence . jejunoileal bypass. cushings sx. obesity. DM. protein MAJOR CAUSES OF LIPID INFILTRATION malnutrition. This pathologic process causes liver enlargement and increased firmness and may result to decreased function Chronic alcoholism.