Hepatic Encephalopathy

In: Other Topics

Submitted By bird1980
Words 5461
Pages 22
Hepatic Encephalopathy
Raven Dunn, SRN
Augusta Technical College
Adult Nursing II
RNSG 2210
Ms. Kandace Chariff, BSN, MSN
July 23, 2012

Table of Contents
Abstract Page 3
Case Study Etiology and Pathophysiology Page 4 Clinical Manifestations Page 5 Diagnostic Findings Page 7 Treatment and Nursing Interventions Page 7 Patient Presentation Page 8
Conclusion Page 9

References Page 10
Appendix I Page 11
Appendix II Page 11
Appendix III Page 12
Appendix IV Page 13
Appendix V Page 13
Appendix VI Page 16

This paper will focus on the clinical manifestations of hepatic encephalopathy and its effects on Mrs. X. She is a 64 year old female who has been an alcoholic for more than 40 years. The constant abuse of alcohol has left her with cirrhosis of the liver. One problem of cirrhosis is the inability of the liver to filter ammonia. When the levels of ammonia build up in the body, it affects various organs and systems. In Mrs. X’s case, it affected her brain. She manifested impaired cognitive abilities as well as physical limitations. This case study will expand on these processes as well as her prognosis and nursing implications.

Hepatic Encephalopathy
Mrs. X is a 64 year old white female and was a functional alcoholic and smoker for more than 40 years. She presented to the E.R. from home with complaints of lethargy, confusion, and decreased mobility. This paper will discuss the clinical manifestations of hepatic encephalopathy and the effects it has had and still do on Mrs. X’s mind, body, and soul. Mosby’s medical dictionary (2007) defines hepatic encephalopathy as:
A neuropsychiatric manifestation of extensive liver…...

Similar Documents


...with cirrhosis are portal hypertension, hepatic encephalopathy, ascites, and esophageal varices. 6. After reading this patient’s history and physical, identify her signs and symptoms that are consistent with the diagnosis. • Mrs. Wilcox’s signs and symptoms include a diagnosis of hepatitis C, constant fatigue, poor appetite, nausea and vomiting, rapid weight loss and weakness. 7. Hypoglycemia is a symptom that cirrhotic patients may experience. What is the physiological basis for this? Is this a potential problem? Explain. • Hypoglycemia is a common problem associated with cirrhosis. To avoid this it is advised to follow a diet of small frequent meals that include complex carbohydrates such as breads and rice. This problem occurs in those with cirrhosis because the liver is not able to store enough energy in the form of glycogen. Since the body is able to break down carbohydrates quick and use them for energy, this diet is recommended in order to avoid problems caused by hypoglycemia. Hypoglycemia in someone who has cirrhosis can present a problem is not addressed by altering the diet. 8. What are the current medical treatments for cirrhosis? • There are four main treatments for cirrhosis. These treatments include preventing damage to the liver, treating the complications of cirrhosis, preventing liver cancer or detecting it early, and lastly liver transplant. 9. What is hepatic encephalopathy? Identify the stages of encephalopathy and outline the major theories......

Words: 842 - Pages: 4

The Nature and Characteristics of Research

...in actively growing tubercle bacilli. | * TB, all forms in which organisms are susceptible. * Prophylaxis in specific patient who are tuberculin reactors or household members of recently diagnosed tuberculars or who are considered to be high risk. | * Contraindicated with allergy to Isoniazid, Isoniazid-associated hepatic injury or other severe adverse reactions to isoniazid, acute hepatic disease. * Use cautiously with renal impairment. | * CNS: peripheral neuropathy, seizures, toxic encephalopathy, optic neuritis and atrophy, memory impairment, toxic psychosis. * GI: nausea, vomiting, epigastric distress, bilirubinemia, bilirubinuria, elevated AST, ALT levels, jaundice, hepatitis. * Hematologic: Agranulocytosis, hemolytic or aplastic anemia, thrombocytopenia, eosinophilia, pyridoxine deficiency, pellagra, hyperglycemia, metabolic acidosis, hypocalcemia, hypophosphatinemia due to altered vitamin D metabolism. * Hypersensitivity: fever, skin eruptions, lymphadenopathy, vasculitis. * Others: gynecomastia, rheumatic syndrome, SLE syndrome | Assessment * History: allergy to Isoniazid, Isoniazid-associated adverse reactions; acute hepatic disease; renal impairment * Physical: skin color, lesions; orientation, reflexes, peripheral sensitivity, bilateralgrip strength, ophthalmologic examination; adventitious sounds; liver evaluation; CBC, LFTs, renal function tests, blood glucose.Interventions * Give on an empty stomach, 1 hr before or 2 hrs after meals;......

Words: 349 - Pages: 2

Hyperammonemia and Liver

...Hyperammonemia Ammonia is a normal constituent of all body fluids. At physiologic pH, it exists mainly as ammonium ion. Reference serum levels are less than 35 µmol/L. Excess ammonia is excreted as urea, which is synthesized in the liver through the urea cycle. Sources of ammonia include bacterial hydrolysis of urea and other nitrogenous compounds in the intestine, the purine-nucleotide cycle and amino acid transamination in skeletal muscle, and other metabolic processes in the kidneys and liver. Increased entry of ammonia to the brain is a primary cause of neurological disorders associated with hyperammonemia, such as congenital deficiencies of urea cycle enzymes, hepatic encephalopathies, Reye syndrome, several other metabolic disorders, and some toxic encephalopathies. Ammonia is a productof the metabolismof proteinsand other compounds,and itis required for the synthesis of essential cellular compounds. However,a 5- to 10-fold increase in ammonia in the blood induces toxic effects in mostanimal species, withalterations in the functionof the central nervous system. Bothacuteand chronic hyperammonemia result inalterationsof the neurotransmitter system. Based onanimal study findings, the mechanismofammonia neurotoxicityat the molecular level has been proposed.Acuteammonia intoxication inananimal model leads to increased extracellular concentrationof glutamate in the brainand results inactivationof the N-methyl D-aspartate (NMDA) receptor.Activationof this receptor......

Words: 4293 - Pages: 18

Patho Unit 1 Case Study

...leaves the lining beneath the mucosa very susceptible for rupture, leading to major bleeding. Since F.C. has already had several incidents with GI bleeding, he is at an even greater risk for re-bleeding (Copstead, pg. 761). F.C’s mental deterioration is most likely caused by a disorder called hepatic encephalopathy. When cirrhosis occurs, the parts of the liver cannot function the way that they are supposed to. Since once of the major jobs of the liver is to clean out, or “detox” the blood, this function can be inhibited or even stopped if cirrhosis becomes too severe. When the blood is not being filtered correctly, these toxins can continue through the blood stream and begin to effect the brain, leading to mental disorders (National Institute of Health, 2014). This is a major problem and must be treated as one. The first steps that must be taken are to stop drinking alcohol, and go to the hospital to have the bleeding stopped and blood in the intestines removed. Antibiotics and diuretics may be prescribed to flush out the body of the toxins and protein will need to be restricted. This is a very serious disorder and should be managed before treatment is no longer an option. The encephalopathy may be treatable, but if it is left alone there is a very good chance that F.C. may go in to a coma or pass away from complications. References Be Responsible About Drinking (2013, January 22). BAC Charts. Retrieved May 30, 2014, from......

Words: 545 - Pages: 3

Case Study

...Pathophysiology II Digestion/Hepatic Case Study Worth 15 pts; July 15, 2014. Name: ___________________________ Directions: Please read the following scenarios and answer the questions that accompany each. Use complete sentences when answering your questions. You will likely need to use your textbook, the class BB site, additional web sites, and your own analytical skills to answers these questions in full. No two people should turn in word for word answers even if you are in the same group. Likewise, information found in resources other than your brain, should also not be copied word for word, but should be rephrased in your own word. Word for word copying in either case will count as plagiarism and no points will then be given for the assignment. Please TYPE out your answers on a separate sheet of paper. Case 1 (7.5 pts) S.M., a young woman in her twenties arrives at your clinic complaining of feelings of pyrosis in her neck, shoulders and jaw. She has had difficulty swallowing her food lately. She self-reports as a smoker. She also reports that she has a low alcohol intake but does drink two or more cups of coffee a day. She is six months along in her first pregnancy. She has a BMI of 22, her BP is 145/90 and her temperature is 37.7oC. Her only reported medications are vitamin C and prenatal tablet supplements daily. Her reported occupation is as a waitress. 1. Give a possible diagnosis for S.M.’s clinical presentations, explaining which......

Words: 1037 - Pages: 5


...inside and out, causes millions of deaths world wide, and casues many personal problems between people. Alcohol has many effects on the human body that can cause long term physical and metal damage. One major organ that alcohol effects in the human body is the brain. When the liver is breaking down the alcohol and its toxins that it releases, the alcohols byproducts damage the liver cells. Once the liver cells have been damaged, they will not work like how they are suppose to ever again causing toxic substances, ammonia, and manganese in particular, to travel to the brain. All these toxins are caused from alcohol use. After reaching the brain, they start damaging brain cells causing a disorder known as hepatic encephalopathy. Hepatic encephalopathy leads to many problems. These problems are sleep disturbances, mood and personality changes, anxiety, depression, shortened attention span, coordination problems, including asterixis, which results in hand shaking or flapping, coma, and even death! Another major organ alcohol effects is the heart. Over the years of heavy alcohol drinking, alcohol weakens the heart muscle which causes a condition called alcoholic cardiomyopathy. When the heart is weakened, it can not pump blood efficiently throughout the body causing severe damage to organs and tissues. This will cause shortness of breath, fatigue, swollen legs and feet, and irregular heartbeat which leads to heart failure and death. Not only does alcohol affect you......

Words: 919 - Pages: 4

Patho Case Study 1

...secondary to hepatocellular failure because the bilirubin metabolism becomes impaired due to malfunction of liver tissue. * Spontaneous Bacterial Peritonitis: acute bacterial infection of ascetic fluid caused by contamination of dialysate. This condition is considered secondary to portal hypertension because the normally, the fluid passes the portal vein into the liver to be killed off, but with a fluid back up, bacterial infection grows due to the increased fluid retention within the portal vein. * Hepatic Encephalopathy: accumulation of toxic substances in blood that are not removed because with a damage liver, the liver cannot kill of toxins leading to infection or constipation. This condition is secondary to both hepatocellular failure and portal hypertension. The relation to hepatocellular failure is due to the hepatocytes being incapable of metabolizing causing the liver to not function properly. Then, with portal hypertension, hepatic encephalopathy can continuously circulate the waste in the portal vein if liver damage has caused surgeries to bypass the liver causing an endless systemic circulation. * Hepatorenal Syndrome: defined as a rapid deterioration in kidney function that manifests from an acute insult to the liver. Changes in blood flow due to decreased kidney function causes toxins to begin impairment of the kidneys since the liver cannot kill off the toxins before-hand. This condition is considered secondary to portal hypertension......

Words: 764 - Pages: 4

Hepatic System

...metabolism: which increases the vulnerability for drug-induced hepatitis and increase risk for drug interactions * Decrease ability to respond to injury Hepatitis Most common cause for liver inflammation is viral infection Acute Infection: * Inflammation causes damage liver cell and may develop into hepatic cell necrosis. * If there are no complications, the liver cells can regenerate and regain its normal appearance and function. Chronic Infection: * Last longer than 6 months * May persist for years * Continuous inflammation and damage done to the liver will slowly develop into liver cirrhosis, then liver failure, and then liver cancer. Clinical Manifestations: Acute Phase: 1-4 Months: Icteric Phase * Jaundice begins * Clay Color stools Convalescence Phase: Post-Icteric phase (healing phase) * Jaundice starts to disappear * Last about 2-4 months. * Major complaint is easy fatigue and malaise. Priority Nursing Diagnosis: * Activity Intolerance r/t decrease physical energy and strength. Recovery Phase: Most patients recover completely Chronic Infection/Condition: * Develops into: Chronic hepatitis, Cirrhosis, Hepatic Failure, Heptocellular cancer Assessment: Health History: * Medications: Some medications that can be toxic to the liver Physical Assessment: * Normal liver cannot be palpated * Percussion is used to determine if the liver is normal size. (8 to 10cm) Diagnosis: Liver Enzyme: *......

Words: 4061 - Pages: 17

Chronic Traumatic Encephalopathy

...! ! ! ! ! ! Chronic Traumatic Encephalopathy ! ! ! ! ! ! ! ! There is a dark cloud hanging over the world of contact sports and it is growing at an alarming rate. With the size and speed of today’s athletes, the sports of football and hockey have become more exciting, fast paced, wide open, and fun to watch. However, there is another consequence of these ever growing athletes on their sports. They have made the collisions in them increasingly more violent. The velocity that these athletes hurl themselves through the air has created an atmosphere that could not have been imagined when these sports were created. First described in the year 1928 (McKee 2010), Chronic Traumatic Encephalopathy, or CTE, is a progressive neurodegenerative disease. ! CTE is famously regarded to be the cause of retired NFL linebacker, Junior Seau’s suicide. The disease deteriorated his brain and hindered his ability to think logically. Seau is not the only retired NFL player found to have had CTE through autopsy following their death. Mike Webster was the first football player found to have CTE, when scientists found the characteristic buildup of the tau protein in his brain. Another significant find in CTE affected brains such as his, includes the shrinkage of the hippocampus, the part of the brain responsible for memory and thinking processes. The disease was originally noticed in boxers, first being called “punch drunk.” These boxers were described......

Words: 1068 - Pages: 5

Wgu - Biochemistry

...function deteriorate, resulting in hyperbilirubinemia, coagulopathy, hypoglycemia, acidosis, hepatic encephalopathy, and hepatorenal syndrome [22]. Multiorgan failure, disseminated intravascular coagulation, mesenteric thrombosis, convulsions, and death may result within 1–3 weeks after ingestion [23]. In contrast, in those patients with a favourable outcome, a rapid International Journal of Hepatology 3 Table 1: Criteria for urgent liver transplantation in patients with ALF. Only Ganzert’s criteria are developed specifically for Amanita phalloide poisoning. Clichy’s criteria King’s College criteria for nonparacetamol causes King’s College criteria for paracetamol causes Ganzert’s criteria Escudie’s criteria (a) Combination of a decrease in factor V below 30% of normal in patients over 30 years or below 20% of normal in patients below 30 years (b) Grade 3-4 en cephalopathy (a) Prothrombin time over 100 s (≈INR over 7) or (b) At least three of the following criteria: (i) prothrombin time over 50 sec (INR over 3.5), (ii) serum bilirubin over 300 μmol/L, (iii) age below 10 years or over 40 years, (iv) an interval between jaundice and encephalopathy over 7 days, (v) drug toxicity (a) Arterial pH below 7.3 or arterial lactate above 3 mmol/L after adequate fluid resuscitation or (b) Concurrently, serum creatinine above 300 μmol/L, INR above 6.5 and encephalopathy of grade 3 or more (a) A decrease in prothrombin index below or equal to 25%......

Words: 4886 - Pages: 20

Cirrhosis and Related Liver Disorders

...approximately 1.2-1.5 kilograms in a healthy adult. The liver is divided into four lobes. The falciform ligament divides the liver into left and right halves. The right lobe is substantially larger than the left. The ligamentum venosum and the ligamentum teres create the caudate lobe and the quadrate lobe. (Kasper, 2008) The liver is an extremely vascular organ. The hepatic artery and the portal vein deliver the liver’s blood supply. Twenty five percent of this blood comes from the hepatic artery and is rich in oxygen. The remainder is carried by the portal vein. This blood is saturated with nutrients absorbed through the digestive tract. Merging into capillaries, the blood makes its way to the hepatocytes, the functional cellular unit of the liver. Blood leaves the liver via hepatic veins which eventually flow into the inferior vena cava. Approximately 90 liters of blood flow through the liver per hour. (Kasper, 2008) The liver’s excretory products flow through the spaces between hepatocytes call bile canaliculi. These join to form intra hepatic ducts which coalesce into the left and right hepatic ducts. The hepatic ducts lead to the common bile duct of the gallbladder. The gall bladder secretions are then expelled into the duodenum of the small intestinal. Hepatocytes make up about eighty percent of the liver. These cells perform most of the functions in the liver including protein synthesis, detoxification, and synthesis of bile. These cells are also responsible......

Words: 3669 - Pages: 15

Cte Chronic Traumatic Encephalopathy

...Chronic Traumatic Encephalopathy CTE is a deterioration of the brain and can also be defined as a progressive neurodegenerative disease, which is caused by repetitive head trauma. CTE first came along in 1928 and was described by New Jersey medical examiner, Dr. Harrison Martland. Martland began to notice a group of related symptoms in boxers (confusion, speech problems, tremors, and slow movement). He published an article entitled “Punch Drunk,” in which he describes the boxers as, “cuckoo,” “goofy,” “cutting paper dolls,” or “slug nutty” (Journal of the American Association, 1928). Later, this was termed dementia pugilistica, which actually means dementia of a fighter. With the growth of our sports like American football, symptoms of CTE were being reported in a number of athletes other than boxers and in the 1960s, it was renamed Chronic Traumatic Encephalopathy. CTE has become a very popular topic because of its close association with American football, soccer hockey, boxing, and professional wrestling. Several of the affected athletes are retired, but have struggled in their late years with anger, depression, substance abuse, memory/motor disturbances, and suicide. Autopsy results from these particular athletes have proposed a link between these cognitive, emotional, and physical manifestations and CTE. In addition to athletes, soldiers have become another group of concern being that many are returning from the battlefield and have brain injuries along with......

Words: 1104 - Pages: 5

Is Vipi

...Unit 5: Hepatic/Pancreatic Dysfunction * Functions of the liver * Metabolism of carbohydrates * Glucose energy * Dysfunction = fatigue * Metabolism of proteins * Proteins muscle * Dysfunction: weak, tired, fatigue, lethargic * Metabolism of fats * Dysfunction: atherosclerosis/ N&V * Production of bile: helps metabolize fats * Synthesis of blood clotting factors * Dysfunction: increased risk for bleeding * Blood storage: holds 400 ml – loss of blood and will put into system * Filters blood: decrease infections – remove bacteria from system * Metabolism of medications * Dysfunction: can’t metabolize and get hepatotoxicity * Hepatitis A * Transmission: Fecal-oral route * Wash veggies b/c migrant workers use fields as bathrooms * Occurrence * Poor hygiene * Improper handling of food * Poor sanitation * Foods or water in third world country * Risk Factors * Close personal contact/ handling feces contaminated waste * Animal workers/handlers from endemic areas * Handling food * Day care center workers * Seafood – clams & muscles * Natural Course * Does not progress to chronic state * Symptoms......

Words: 2257 - Pages: 10

Symptoms Associated with Renal and Hepatic Disease

...  Week 13: Symptoms Associated with Renal and Hepatic Disease 1       Symptoms Associated with Renal and Hepatic Disease  Case Study  November 23, 2013                      Week 13: Symptoms Associated with Renal and Hepatic Disease 2     Renal Case Study Introduction  Glenda  is  a  41  year   old  woman  with   end  stage  renal  disease  related  to polycystic kidney  disease.  She  has been on dialysis for ten years while waiting for a donor.  She has recently made  the  choice  to  stop  her  dialysis  sessions  and  her  medications.  She  acknowledges  this  will  mean  the  end  of  her  life,  but  she   has  come  to  feel  that  she  has  no  quality.  She  has  come  to  discuss  what you can do for her current symptoms and what death might look like.     Glenda  tells  you  she  is  chronically  fatigued,  has  diminished  appetite  and  is  always  constipated.  She  reports  getting  a  little  foggy  before  her dialysis and sometimes has neuropathy   in  her  fingers  and  feet.  She  goes  crazy  from the uremia. She is currently on an ACE inhibitor to  control  her  blood  pressure,   calcium  carbonate  PO  TID  to  bind  phosphate,  docusate 100 mg TID  for constipation.   Medication and Dosing Considerations  Since  Glenda  has  chosen   to  stop  her  dialysis  treatments  as  well  as  her  medications,  I  would  first  review  the  medical  treatments  that  Glenda  is  currently  receiving ......

Words: 876 - Pages: 4

Hepatic Encephalopathy

...Hepatic Encephalopathy Name________ Directions: Gender: Male Age: 47 Setting: Hospital Ethnicity: African American Preexisting Conditions: Cirrhosis secondary to alcohol hepatitis, hypertension, esophageal varices Coexisting Conditions: Disability: Unemployed (on disability) for past four years Socioeconomic: Married, father of two boys (ages 19 and 17 years old), history of drinking one quart of hard liquor each day for three years prior to diagnosis of cirrhosis Pharmacologic: Lactulose (Cephulac), neomycin sulfate (mycifradin sulfate) Client Profile: Mr. Escobar is a 47-year old male with a history of cirrhosis. He lives with his wife and teenage sons. His wife brought him to the emergency department today because she noticed that her husband had increasing confusion and lethargy and was having difficulty walking. His wife states, “ He is probably acting a little fun because he is sleep deprived. He hasn’t slept very much in the past few days.” Case Study: Mr. Escobar is afebrile. His blood pressure is 136/68, pulse 88, and respiratory rate 18. His oxygen saturation is 98% on room air. He is awake, alert, and oriented to person only. His speech is slow and he appears tired. The nurse notices a foul odor to his breath. Upon physical examination, he is found to have a slightly distended abdomen. The health care provider (HCP) does not note any asterixis. The HCP requests an abdominal ultrasound, which reveals fatty infiltration of......

Words: 2207 - Pages: 9