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 theres 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
channel
Stents- undergo stenosis or occlude over period of mos, prompting need for another tTIPS of another
approach
*Vasopressin- stop variceal bleeding; achieves lowering of portal pressure; maybe given in
conjunction w/ nitroglycerin, administered IV, sublingually
S/E: Hypothermia, myocardial and gastrointestinal tract ischemia and ARF
*Beta adrenergic blocking agents- for mgt of acute variceal bleeding (propranolol, metoprolol,
nadolol)
*Balloon tamponade-Applying pressure to ruptured vavrices may stop hemorrhage. Clinican inserts
sengstaken-blakemore or minnesota tube into the stomach and inflate esophageal and gastric
balloons; 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. Avoid straining maneuvers that increase intraabdominal or intrathoracic pressure
2. Avoid rough foods, w/c may traumatize the espohagus, 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, including melena or hematemesis because bleeding can precipitate hepatic
coma
*Protect from injury- 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- technique to create portal systemic shunt via
percutaneous approach
*Portosystemic shunt- 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, blood and fluid loss and anesthesia of surgery
Complications: MAJOR COMPLICATIONSo of shunt procedure: Bacteremia land DIC, heart
failure, shunt clotting and hepatic enceph
POST OP CARE:
Assess client after portosystemic shunt surgery by monitoring ff:
*Presence of hemorrhage, hypovolemia and oliguria
*F&E imbalances
*RR and rhythm (rales, atelectasis, labored breathing, 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- if clotting time is not w/in normal limits, administer
vit K; assess client for hepatic enceph; if portal HPN is due to liver dx, monitor for postop hemorrhage
because bleeding tendencies often arise from liver cell malfunction; monitor hgb, hct, PT, ammonia
lvl, BUN, bilirubin lvl; 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, 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; Ammonia is a CNS depressant
Reduced mental alertness, confusion Chnges during initail stages of hepatic enceph includes:
and restlessness
Loss of consciousness, seizures and Occur in terminal stage
irreversible coma
PATHO:
-Hepatic enceph is characterized by elevations of ammonia lvls in the blood and CSF.
-Ammonia is produced in the GIT when protein is broken down by bacteria, by liver and in lesser
amnts, by gastric juices and peripheral tissue metabolism
-More recently implicated as cause of enceph are false neurotansmitters, elevated lvl of
mercaptans(organic chemicals that contain sulfhydryl radical, formed when the O2 of alcohol
molecule is replaced by sulfur), phenol and short-chain fatty acids
The liver converts ammonia into the glutamine, 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, affecting glial and nerve cells; it leads to altered CNS metabolism and
function
CMS:
*Mild mental confusion to deep coma
*Hepatic enceph imparis memory, attention, 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, electrolyte levels, blood gases, and hepatic function test results
(bilirubin, albumin, 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. Severe livere disease include: GI bleeding, inccreased dietary portein,
constipation, infxn, CNS depressant drugs (opiates, 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, its must be avoided in clients w/ renal insuf
-Lactulos, w/c helps decrease blood ammonia lvls by reducing absorption of ammonia, is given to
clients to produce 2-4 stools a day
NSG MGT:
-Observe cleitn for persnlaity changes w/ labile feeling states, 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- client need to learn to manage diarrhea, 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- be alert ot possible harmful accumulation of ammonia
as result of duiuretic therapy. Hypokalemia from use of diuretics contributes to hepatic enceph by
increasing ammonia production in the kidney
*Avoid sedation- agents w/ CNS depressants may precipitate coma, adn their use should be avoided
*Prevent complications of immobility
FATTY LIVER (HEPATIC Lipid infiltraion may lead to hepatic stenosis, or fatty liver, one
STENOSIS) of the most common metabolic dx of liver
 This pathologic process causes liver enlargement and increased
firmness and may result to decreased function
Chronic alcoholism, protein MAJOR CAUSES OF LIPID INFILTRATION
malnutrition, DM, obesity, cushings
sx, jejunoileal bypass, 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