welcome to chapter 24 where we will be discussing the nursing management of patients with hepatic and bilary disorders today's objectives are to relate jaundice portal hypertension aites vyses nutritional deficiencies and hepatic coma to pathophysiologic alterations of the liver also to describe the medical Surgical and nursing managements of patients with hepatic dysfunction compare the types of hepatitis and their causes prevent clinical manifestations and management and lastly to discuss the management of chysis over the next few slides we're going to look at the manifestations of hepatic dysfunction up first is jaundice jaundice is caused by the impairment of the liver's ability to metabolize and secrete belly ribbon there are four different types of jaundice aat cellular often caused by viral hepatitis autoimmune hepatitis hepatotoxins such as drugs or alcohol metabolic disorders esema or pregnancy obstructive jaundice caused from an obstruction of the bile duct gallstones inflammation of the bod duct often caused from sclerosing colangitis biliary strictures malignancy such as pancreatic cancer liver cancer or even pancreatitis another cause can be hemolytic where we have an increased production of Billy Rubin due to homolysis also hematologic disorders or the re reabsorption of a hematoma and multiple transfusions last cause is hereditary hyperbar rubinia an inherited disorder of the Billy ruon metabolism often requiring a liver transplant jaundice is often found during the physical exam showing signs of yellowing of the skin and Scara lethargy weakness AES or partis fluid retention nause and vomiting blood can be found in the stool or the vomit spontaneous bruising and increased bleeding and shortness of breath our next manifestation of hepatic dysfunction is Portal hypertension most commonly caused from therosis the scarring of the liver portal hypertension is an elevated pressure in the portal Venus system caused by that increased resistance and blood flow through the liver and that increased blood flow due to vasod dilation two major complic are aites and gastrosoph varices both which we will be discussing further on the next coming slides let's look more closely at aites aites is a fluid accumulation within the peronal cavity caused by portal hypertension and increased capillary pressure and obstruction of Venus blood flow through the damaged liver Key signs and symptoms of aites include an increase in abdominal growth it is key to measure and assess that abdominal growth daily the patients may also experience weight gain or dependent edema treatment options are nutritional education and sodium restrictions of 2 gram or less daily medications may be prescribed such as diuretics like spaalone and Lasix it is key with diuretics to monitor weights daily and assess for side effects like dehydration volume depletion electrolyte imbalances kidney impairment and hepatic and sephy opathy another treatment option is a paracentesis during a paracentesis the parital cavity fluid is removed through a puncture or surgical incision with a trocar catheter this is a sterile procedure complications can include the infection of the acidic fluid treatment for an infection does involve IV antibiotics and long-term prophylactic po antibiotics as a cites often redevelops and multiple pair centesis are not uncommon the last treatment is a trans jugular intrahepatic portosystemic shunt also called a tips in a tips a canula is threaded into the portal vein by the trans jugular route a stent is then inserted to help with the circulation please review both Associated YouTube videos for further information regarding a parentesis and the tips procedure next let's look at our second complication to portal hypertension and another manifestation of hepatic dysfunction called esophagal varices esophagal varices are dilated tortuous veins that are usually found in the sub mucosa of the lower esophagus caused from that collateral circulation development esophagal varices are at high risk for bleeding the veins become very fragile procedures such as NG tube insertions should be avoided for the this reason it is not uncommon to see esophageal varices with those that experience alcohol abuse it is key for nursing staff to assess for signs of rupture which include monitoring vital signs for signs of hypovolemic shock such as low blood pressure high heart rate and cool and clammy skin another key finding is hematosis where there's blood in the vomit treatment options do include medications like Vaso constrictors such as arrio tide or soost Statin vasopressors and even IV antibiotics to prevent infection another treatment options are endoscopic therapies that we will discuss further on the next few slides our first endoscopic therapy is veral banding in this procedure a rubber band like ligature is slipped over the esophageal veric blood flow is cut off the verx becomes necrotic and eventually slops off our next endoscopic therapy is endoscopic injection sclerotherapy in this procedure there's an injection of a sclerosing agent straight into the esophago veres this medication promotes thrombus and eventual sclerosis thereby obliterating the varices our last endoscopic therapy is a balloon tampen in this procedure a four Lumin esophagal tampon tube is placed into the esophagus where balloons are then inflated to compress the bleeding esophagus varices now these do have four lumens which do include a gastric and esophageal outlet for aspiration of secretions if all these treatment options fail both phological and endoscopic a TIPS procedure can again Lower that portal hypertension and lessen the likelihood of bleeding and should be considered as small addendum to the previous recording stages of hepatic hopy can be found on table 24-2 on page 827 of the honin book edition three let's discuss our next manifestation of hepatic dysfunction hepatic Andy opathy hepatic Andy opathy is a life-threatening complication to liver disease and results from the accumulation of ammonia and other toxic metabolites within the blood ammonia is a byproduct of protein and amino acid breakdown the liver is responsible to convert that ammonia into Uria and excrete it into the urine to prevent tox toxic buildup when the liver fails this detoxification and conversion does not occur it is important to understand the stages of hepatic and sephy opathy found on your in your book on table 25-2 it can be seen that there are four different stages to hepatic and sephy opathy in these stages the level of Consciousness declines in our first stage you'll see a normal level of Consciousness with periods of lethargy and Euphoria reversal of day and night sleep patterns in our second stage you'll have increased drowsiness disorientation inappropriate behavior mood swings and agitation in the third stage you'll see a stupis difficult to arouse sleep most of the time marked confusion and incoherent speech in our fourth stage they may become comos and may not actually respond to painful stimuli at all during all of these stages an additional clinical sign is Axia a flapping or Tremor of the hands you can see this better in the attached YouTube link another possible sign is Vector hepaticus a sweet slightly feal odor to the breath that originates from the intestinal track treatment for hepatic and cyop is lactose lactose can reduce that Ser serum ammonal Levels by promoting the excretion of ammonia through the stool your goal with El lactose treatment is to have two to three soft bowel movements daily let's review a patient with a history of heavy alcohol use is receiving lactose for the treatment of hepatic and cyop what is the desired outcome of this treatment a two to three soft bowel movements daily B watery diarrhea several times daily C prevention of constipation or D the maintenance of feal continents the correct answer is a 2 to three soft bowel movements daily again the purpose of lacos is to excrete ammonia through the stool in the form of two to three soft bowel movements let's take a look at our last manifestation of hepatic dysfunction where we focus on vitamin deficiencies such as a decrease in absorption of vitamin K from the GI TR which leads liver cells unable to use vitamin K to make prothrombin we also have the impaired absorption of vitamin A D and E from a decreased secretion of Bio salts into the intestines let's take a closer look at what inadequate intake of the following vitamins can cause a vitamin A deficiency can lead to night blindness and ion skin changes thyine deficiency can lead to warx cor off's psychosis roof Flavin deficiency can lead to lesions of the skin and mucus membranes vitamin B6 deficiency can lead to lesions of the skin mucus membranes and neurologic changes vitamin C deficiency can lead to hemorrhagic lesions of scurvy vitamin K can lead to hypoprothrombinemia or spontaneous bleeding and ecosis anop folic acid deficiency can lead to microtic anemia let's discuss our next topic viral he hepatitis viral hepatitis is a systemic viral infection involving the necrosis and inflammation of liver cells this can either result in acute or chronic liver dysfunction and disease patients typically present asymptomatically or have non-specific symptoms including Bays GI distress jaundice or elevation of aminot transferase there are many types of hepatitis that we will dive into further as we go these types include hepatitis A Hepatitis B hepatitis C hepatitis D Hepatitis E and even hepatitis G let's take a closer look at hepatitis A virus hepatitis A is often transmitted through a FAL oral Ro rout personto person or ingestion of fecal contaminated food or water diagnosis is usually through a positive anti-hepatitis a virus test where we look at some imunoglobulin antibodies that react to the hepatitis A virus to confirm the acute infection patients present either asymptomatically or with an acute symptoms such as fever malaise anorexia nausea vomiting diarrhea abdominal pain and JIS medical management focuses more on supportive care such as IV fluid for hydration and activity as tolerated if there are signs of liver failure they will be referred to a liver transplant center it is our job to ensure and educate on proper hand hygiene proper food presentation education on the transmission of the disease and prevention tips vaccination is also highly encouraged let's review a nurse is conducting a health promotion class what would the nurse describe as the best method to prevent the transmission of hepatitis A virus a follow proper handwashing techniques B avoid chem that are toxic to the liver C using a conduct during sexual contact or D wearing a mask when in a large crowd the correct answer is a follow proper handwashing techniques as the transmission of hepatitis A does occur through the feal and oral Roots next let's take a look at Hepatitis B virus Hepatitis B virus is a public health problem with 350 million people worldwide diagnosed transmission occurs primarily through blood but can also be found in both saliva and semen transmission routs primarily include prenatally percutaneously through sexual exposure or close person-to-person contact risk factors can include frequent exposure to blood bodily fluids hemodialysis male homo or bisexual activity IV drug use multiple sexual partners history of STDs recipients of blood products or those with travel or res in an area of Uncertain sanitary conditions Diagnostics often include lab work such as CBC hepatic function testing PTINR values hepatitis A and hepatitis C virus testing and HIV testing signs and symptoms vary as Hepatitis B virus has a long incubation period some may experience anorexia sleep disturbances fever dyspepsia pain in the right upper quadrant generalized aching malays weakness or jaundice and skin rashes chronic Hepatitis B virus is often asymptomatic until curosis can occur there's a large push for the prevention of infection through vaccination currently there's a three series vaccine available after the initial dose a second dose is given 1 month later and then a third dose is given at 6 months post that initial vaccine hbig can provide passive immunity to those that were exposed but don't fully develop the Hepatitis B virus a second dose of hbig can even be given 28 Days Later if the vaccine is refused other preventative methods are the use of protective devices during sexual intercourse the avoidance of sharing razors and toothbrushes the covering of wounds and the cleaning of blood spills with bleach the goal of medical management of hepatitis B is to prevent the replication of the active Hepatitis B virus with viral suppression and to reduce the effects of chronic liver inflammation often antivirals can be prescribed and frequent labs and ultrasounds are utilized to assess the liver function nursing management often focuses on symptom support such as maintaining nutrition fluid intake and adequate rest some may be referred to a transplant center depending on their symptoms such as altered mental status severe vomiting or increased jaundice there's also a large focus on education of transmission of hepatitis B virus this includes to healthcare workers healthcare workers are at equal risk for Hepatitis B virus as many can be exposed to blood or bodily fluids the use of protective devices is highly encouraged let's discuss hepatitis C virus hepatitis C virus is the leading cause of liver disease and liver transplants transmission often occurs Through Blood risk factors include injection of drugs blood transfusions parental contact with blood sexual transmission less common are causes like hemodialysis needle sticks and tattooing 20 to 50% will clear the acute affection but most will develop chronic infection risk factors that contribute to the severity of liver disease include increased alcohol use males older age at the time of infection HIV or Hepatitis B virus and obesity Diagnostics include the anti-hepatitis C virus antibodies being present genotyping and liver biopsies and ultrasounds many remain asymptomatic for decades but it can progress to sosis if left untreated where you may present with jaundice nausea vomiting and malaise medical management does focus on the use of antivirals protase Inhibitors can lead to a sustained viral response if the viral load is undetectable 12 weeks post treatment nursing management focuses on education of transmission and the education on risk factors often time there are health promotion regarding needle safety such as safe capping and safe disposal communities may also support the use of clean needle exchange programs for those that use and inject IV drugs next we have nonviral hepatitis or alcoholic hepatitis caused by excessive ingestion or abuse of alcohol ethanol is broken down by our liver the byproduct aceta alahh is toxic to the liver and can cause impairment to liver function alcoholic hepatitis is the cause of about 40% of deaths related to sosis co-actors contributing to the development of sosis are hepatitis C virus smoking and obesity takes about 20 grams of alcohol daily over 10 years in females and about 60 to 80 gram of alcohol daily over 10 years in males to to develop Diagnostics include the known history of alcohol use or abuse in conjunction with liver failure patients present differently key findings are jaundice or malaise anorexia nause of vomiting abdominal pain fever muscle wasting Stigmata or spider angomas when there is hepatic decompensation a key finding is the development of aites P edema and hepatic Andy opathy medical management does involve the abstinence of alcohol oral ental nutritional therapy they're often malnourished depleted of protein stores and have significant vitamin deficiencies nursing management involves a nutritional support signs and symptoms of infection or bleeding and breast and fluid overload treatments let's take a look at our last hepatitis drug rated hepatitis cause from the unintentional or intentional ingestion or exposure to medications toxins or Herbal Remedies you may have heard of Tylenol or nids being common causes but there's also antibiotics anti-convulsants or anti-tuberculosis agents that can have the same effect clinical manifestations can include the abrupt presence of chills fever rash parius and anorexia or nausea delayed presence of jaundice dark urine or even enlarged and tender liver the medical and nursing management shows a priority in stopping the offending medication administering any available antidotes such as n ayto sytin for Tylenol overdoses Andor prescribing steroids if there's hyp sensitivity an additional focus is on education and health promotion this includes education on proper dosing recommendations for over-the-counter medications such as Tylenol and Nets let's discuss sosis sorosis is when normal liver tissue is replaced by a fibrotic tissue and response to damage there are two types compensated or decompensated compensated curosis may present asymptomatically or there can be reports of intermittent fever vascular spiders Palmer Eda unexplained epistaxis ankle edema vague mourning and digestion flatulent dispepsia abdominal pain firm enlarge liver or speno megly decompensated therosis is attributed to worsening signs like aites jaundice weakness and muscle wasting weight loss continuous mild fever clubbing of the fingers perpa or that thrombocytopenia spontaneous bruising epistaxis hypotension Barse body hair white nails gonad atrophy gastrosoph varices and hepatic andopa promoting rest providing skin care and reducing the risk of injury from thrombocytopenia there's also a focus on monitoring for complications second secondary to thrombocytopenia like the risk for bleeding and Hemorrhage hepatic andypath and fluid volume excess let's review is the following statement true or false a patient with decompensated therosis is likely to exhibit increased abdominal girth and pedal edema the following statement is true increased abdominal girth and pedal edema are two signs of aites aites is associated with decompensated sorosis let's move on to the galbladder first we'll look at kisis or G Stones G stones are formed in the gallbladder from solid constituents of bile these Stones can be comprised of either pigments or cholesterol patients can present asymptomatically or report mild GI distress symptoms like epigastric fullness abdominal distension big right upper quadrant pain often associated with the ingestion of high fat or fried foods complications to G stones are an obstructing chth Isis or a peritonitis symptoms often present then with abdominal tenderness distension rebound tenderness rigidity loss of bowel sounds fever hypotension pness nausea vomiting and M Murphy sign positive Murphy sign means that there's right upper quadrant pan on deep inspiration that prevents the full inspiratory Excursion when the examiner's fingers are underneath the liver border treatment for G Stones is AIC sectomy and anti- lipidemia medications lastly let's look at kystis kystis is defined as an acute inflammation of the gallbladder the gallbladder May even develop an Emma which means to fill with pus common causes are repeated obstructions from the cystic ducts by G stones or a calculus chitis which means without stones caused from major surgery trauma or even Burns kestis can be diagnosed through the elevation of white blood cells and a positive Murphy sign additional signs are often right upper quadrant pane that radiates to the back or right shoulder shoulder and scalpa and nausea and vomiting medical management focuses on bowel rest fluid and electrolyte imbalance Corrections pain management antibiotics endoscopic procedures or even surgery medications can also be used to dissolve the small cholesterol G Stones surgical complications are bile duct injury a bile duct leak which may even lead to a bile duct stent and biop peritonitis nursing management focuses on postsurgical care to resume normal activity wound care dietary restrictions such as avoiding high fat foods or fried foods and Pain Management in addition to necessary follow-up care please review the attached YouTube video for additional surgical Care on colitis let's review the Nur is caring for a patient diagnosed with aites the nurse would expect which of the following to be restricted from the patient's diet a potassium B calcium C sodium or D magnesium the correct answer is C sodium dietary restrictions of salt intake is a mainstate of treatment for aites to achieve a negative sodium balance to reduce fluid retention the recommended daily sodium intake of patients with aites should be no more than 2 gr a patient diagnosed with hepatic enop is receiving lactose when preparing to administer this medication the RN understands that it is used to decrease which of the following serum levels a calcium B ammonia C potassium or D sodium the correct answer is B ammonia lacos is administered to reduce the serum ammonia levels through the excretion of ammonia in this stool your goal is two to three soft bowel movements daily question patients with severe chronic liver dysfunction often have problems related to inadequate intake of sufficient vitamins which of the following vitamin deficiencies would result in hemorrhagic lesions of scurvy a riboflavin B vitamin C C vitamin A or D vitamin K the correct answer is B vitamin C a vitamin C deficiency may result in hemorrhagic lesions of scurvy a riboflavin deficiency may result in the characteristic skin and mucous membrane lesions a vitamin A deficiency may result in night blindness or eyon skin changes and a vitamin K deficiency may result in hypoprothrombinemia which is characterized by spontaneous bleeding and ecosis last question a patient with hepatitis A is admitted to a general Med surge floor the AA knows that this type of hepatitis is spread through which of the following modes of transmission a injection of drugs B blood C semen or D feal oral the correct answer is D fecal oral the mode of transmission for Hepatitis A virus occurs through fecal oral route primarily through personto person contact and or ingestion of thally contaminated food or water uncooked or poor food handling is also a common method of transmission