Mirandaliang.files.wordpress.com



Nursing Care For Hepatic Encephalopathy Miranda LiangApril 24, 2016University of New HampshireIn the United States, alcoholism is a major problem facing the population today. An estimated 70% of adults in the United States drink alcohol, with 10% of them being heavy drinkers and 5-10% alcohol-dependent (Robinson, 2015). It is the most widely abused drug in the US. This substance is so addictive because it produces a general, nonselective reversible depression of the central nervous system. Alcohol abuse is a dangerous field because it is a drug that affects almost every part of the body. With chronic alcohol use, some of the major consequences are gastritis, esophagitis, recurrent pancreatitis, and most commonly, hepatitis and cirrhosis. Some other effects are cardiomyopathy, sexual dysfunction, peripheral neuropathy, Korsakoff’s and Wernicke’s syndrome, and leukopenia and thrombocytopenia. In the intoxication phase, some symptoms are disinhibition, mood lability, impaired judgment, impaired social or occupational functioning, slurred speech, incoordination, nystagmus, and unsteady gait. Chronic alcoholism is characterized by a progressive and physical dependence on alcohol, with withdrawal symptoms present in the absence of it (RN Mental health nursing, 2013). What makes alcoholism potentially life threatening is a complication of liver disease that often occurs with liver failure called hepatic encephalopathy. Another name for this is portosystemic encephalopathy. A patient with hepatic encephalopathy may show no signs and symptoms but will have abnormalities in neurological assessments. The pathophysiology behind this is that with chronic alcoholism, the liver, progressively damaged by alcohol, is unable to detoxify the byproducts of metabolism, causing a build up of ammonia in the blood. When ammonia enters the brain, it causes stimulation of gamma-aminobutyric acid (GABA), a neurotransmitter that causes depression of the central nervous system causing sleep and behavioral changes, and in some severe cases, coma (Hinkle & Cheever). Hepatic encephalopathy also causes portosystemic shunting, which is the development of collateral vessels as a result of portal hypertension. The collateral vessels allow the portal flood that is filled with toxins and unfiltered by the liver to enter the systemic circulation, going to the brain and exaggerating the neurological deficits (Carey, 2014). Patients suffering with hepatic encephalopathy are a common and complicated population often seen on medical surgical floors and in intensive care units. Winningham’s book Critical Thinking Cases in Nursing covers a case study on hepatic encephalopathy and the course of treatment for this acute illness. The case study will be examined here, and the scenario is: “John Doe, approximately 50 years old, is admitted to your unit for observation from the emergency department (ED) with the diagnosis of rule out hepatic encephalopathy with acute alcohol intoxication. This man was sent to the ED by local police, who found him lying unresponsive along a rural road. Examination and x-ray studies are negative for any injury, and you are awaiting the results of the blood alcohol level and toxicology tests. He has no identification and is not awake or coherent enough to give any history or to answer questions. He is lethargic, has a cachectic appearance, does not follow commands consistently, and is mildly combative when aroused. He smells strongly of alcohol and has a notably distended abdomen and edematous lower extremities. He has a Foley catheter and an IV of D5?NS with 20mEq KCl and 1 ampule of multivitamins infusing at 75 mL/hr.John Doe’s admission orders are:IV D5?NS with 20mEq KCl at 75 mL/hr; add 1 ampule multivitamins to 1L of IV fluid per dayInsert Salem Sump NG tube and attach to low continuous suctionInsert Foley catheter to gravity drainageElevate HOB at 30-45 degrees at all timesCheck all stools for occult bloodLactulose (Cephulac) 45mL PO qid until diarrheaAbdominal ultrasound in AMVitamin K (AquaMEPHYTON) 10 mg/day IV or PO (when alert and able to swallow) x3 dosesVitamin B1/thiamine 100 mg/day IV; change to PO when alert and able to swallowVitamin B9/folic acid 0.4 mg/day IMVitamin B6/pyridoxine 100 mg/day POLabs: CBC with differential, BMP, LFTs, PT/INR and PTT, serum ammonia now and in AMOnce patient is alert and able to swallow, may have low-protein diet. Observe for any difficult swallowing, and offer assistance with meals if neededCall house officer for any sign of GI bleed; delirium tremens; systolic BP over 140 or less than 100 mmHg; diastolic BP less than 50 mmHg; or pulse over 120 beats/min,” (Harding, Snyder, Preusser, & Winningham, 2013).With this long list of orders, sometimes it is necessary for a registered nurse (RN) to ease the workload and delegate certain tasks to nursing assistive personnel (NAP), as long as these tasks are within their scope of practice. One of the above orders that can be delegated to the NAP is positioning John Doe, by elevating the head of bed to 30 to 45 degrees. They can also alert the RN when stools are passed so they can be tested for occult blood. NAP can also ensure a low-protein diet when receiving meals for John Doe, as well as assisting with feeding if any difficulty swallowing is present. Lastly, they can take vital signs on John Doe and notify the RN when any of the findings are out of the expected parameters specified in the orders.Some of the lab work drawn in the emergency department have come back. The blood alcohol level is 320 mg/dL, and the blood ammonia level is 155 mcg/dL. His total protein is 5.2 g/dL and albumin is 2.1 g/dL. This blood alcohol level is excessively high, indicating John Doe has a significant amount of alcohol in his system. His blood ammonia level is also excessively high, indicating his liver is not working correctly to convert ammonia into its healthy byproducts and ammonia ends up in the blood. It excites and stimulates GABA, the neurotransmitter that depresses the central nervous system, therefore causing John Doe to be drowsy. His protein level is low, showing that alcohol has prevented the ability of his body to absorb proteins. Lastly, his low albumin level indicates his body has the inability to main blood volume. Albumin plays an important role in keeping the fluid from the blood from leaking out into the tissues. The medication that would be most helpful with the elevated ammonia levels is Lactulose (Cephulac), an ammonium detoxicant and osmotic laxative. The breakdown of lactulose to organic acids by colonic bacteria acidifies colonic contents, thereby subsequently inhibiting diffusion of ammonia back to the blood. It also enhances the diffusion of ammonia from blood into the gut, where it is converted to ammonium (Weber, 1996). Lactulose traps and expels the high levels of ammonia in the feces. Two to three soft stools per day are expected, but excessive watery diarrhea is a sign of overdose. Because it is a laxative, it is a perfect treatment for John Doe since constipation can further exaggerate the effects of encephalopathy. While receiving Lactulose, the patient will be closely monitored for hypokalemia and dehydration, which explains why John Doe is receiving an intravenous infusion of dextrose 5% half normal saline with potassium chloride as a supplement. John Doe has a multitude of vitamins ordered. Due to his significant reduction in food intake during his stay in the hospital, it is reasonable to conclude that these were ordered to replenish necessary vitamins needed for regular functioning. Also, it is highly likely that his diet prior to hospitalization was not providing adequate nutrition. In cirrhosis, there is a decreased production of clotting factors due to deficient absorption of vitamin K from the gastrointestinal tract because the liver cells are impaired and cannot use vitamin K to make prothrombin. The absorption of other vitamins is also impaired from the decreased secretion of bile salts into the intestine (Hinkle & Cheever). John Doe needs vitamin supplements to meet one hundred percent of his dietary allowance because the stress of a lack of vitamins can further exaggerate his liver damage. The case study progresses further:“While you get John Doe settled, you continue your assessment.Neurological findings: PERRL (Pupils Equal, Round, Reactive to Light), moves all extremities, but patient is sluggish, pulling away during assessment, and follows commands sporadically.Cerebrovascular findings: Pulse is regular but tachycardic without adventitious sounds. All peripheral pulses are palpable, with 3+ bilateral and 3+ pitting edema in lower extremities.Respiratory assessment: Breath sounds decreased to all lobes, no adventitious sounds audible, patient not cooperating with cough and deep breathing, and SaO2 at 90% on room air.GI assessment: Tongue and gums are beefy red and swollen, abdomen is enlarged and protuberant, girth is 141 cm, and abdominal skin is taught and slightly tender to palpation. His Salem Sump NGT is patent, connected to LCS with small to moderate greenish drainage; bowel sounds positive with NGT clamped.Genitourinary (GU) assessment: Foley to gravity drainage, with 75 mL dark amber urine since admission (2 hours).Skin: Pale on torso and lower extremities; heavily sunburned on upper extremities and head. Skin appears thin and dry. Numerous spider angiomas are found on the upper abdomen with several dilated veins across abdomen.Vital signs: 120/60, 104, 32, 99.1 degrees F (37.3 C),” (Harding, Snyder, Preusser, & Winningham, 2013).The spider angiomas found are characteristic of alcoholic liver disease. Spider angiomas are small lesions with tiny blood vessels radiating away from the center. They are a result of neovascularization and the development of collateral vessels. The blood pressure is so high in the portal vein that these tiny vessels are created and they transport the toxic, unfiltered blood to systemic circulation. The dilated abdominal veins come from resistance from the increased blood pressure from portal hypertension. Peripheral edema is a result of John Doe’s low albumin levels, activating the renin-angiotensin-aldosterone-system (RAAS), causing the kidneys to retain salt and water. His distended abdomen is another result of the portal hypertension and indicates ascites (Hinkle & Cheever). The common cause of all these problems is portal hypertension, the abnormally high blood pressure in the portal vein. This is the vein that brings blood from the intestine to the liver.John Doe’s distended abdomen is called ascites. It is caused by fluid that leaks across the endothelium causing abdominal swelling. This is a result of both increased pressure in the vein system and the development of collateral vessels, as well as his low level of albumin, the protein responsible for maintaining blood volume and preventing leakage. With portal hypertension, the blood being delivered to the liver meets resistance and the pressure rises. Collateral blood vessels dilate, and blood is redirected away from major organs and increased blood flow goes to the liver. The kidneys interpret this as a low blood pressure and activate the RAAS further, and the retained water leaks out of the vessels, causing ascites. The way to assess this is to inspect first, looking for signs of injury, bruises, wounds, skin texture, and prominent veins. Next, the abdomen should be auscultated before palpation and percussion because the external pressure can cause a change in bowel sounds. Palpation detects pain and tenderness, while percussion detects the accumulation of fluid. Percussion starts with the patient lying supine, and the free fluid in the abdomen will collect around the flanks due to gravity. Next, the patient is positioned on his/her side, and the fluid should move to the front of the abdomen and air will be percussed at the top. This is called shifting dullness and presence of it indicates a positive test for ascites. Nursing interventions include administering prescribed diuretics and restricting sodium intake. Diuretics most commonly used are spironolactone and furosemide. Expected weight loss is about one to two pounds a day with careful monitoring of electrolytes and renal functioning before administration. It is also essential for nurses get daily weights of the patient at the same time of day wearing the same amount of clothing for consistency, (Lee & Grap, 2008). Limiting sodium is a controversial subject, because hyponatremia, a low sodium level in the blood, is a common potential complication for this specific population of patients. As stated by Fullwood and Purushothaman, “salt should be restricted to 70-90 mmol/day. This equates to a non-added salt diet rather than the more traditional recommendation of a low salt diet of 22-40 mmol/day. The traditional regimen has been found to compromise protein and calorie intake in a patient group that is already experiencing malnutrition as a result of chronic liver disease, and therefore is no longer recommended,” (Fullwood & Purushothaman, 2014). John Doe’s nutritional status is especially concerning because alcohol interferes with the ability to absorb vitamins, and alcoholics typically have bad diets to begin with. Objective findings indicating his poor nutrition are that he is sluggish and only follows commands sporadically, and he has edema in lower extremities, a beefy red and swollen tongue and gums, taut abdominal skin tender to palpation, dark amber urine, and pale, thin, dry skin. It is evident he is malnourished and dehydrated by his poor skin quality and concentrated urine. The most significant assessment factor is his abnormal neurological status that is characteristic with a thiamine deficiency. Inadequate thiamine can lead to beriberi, polyneuritis, and Wernicke-Korsakoff psychosis, a permanent form of brain damage (Xiong, 2015).Although John Doe’s protein levels are low, he still has an order for a low protein diet. This is because John Doe’s alcoholism has impaired the ability to absorb and digest proteins. The breakdown of protein actually increases the production of ammonia, and would therefore exaggerate his hepatic encephalopathy. The high ammonia levels are responsible for his neurological changes of being sleepy and unresponsive. Although the science behind it supports a low protein diet, research has been done regarding the effectiveness of it. Protein restriction could perhaps worsen the nutritional status of a patient with cirrhosis and may have no resulting improvements in hepatic encephalopathy. A study was done to see if a low-protein diet for fourteen days resulted in improvements in neurological status compared to a normal-protein diet in cirrhotic patients with episodic hepatic encephalopathy. It was found that there was no significant difference between the two groups, showing that diets with normal protein content could be safely administered to cirrhotic patients to improve their metabolic status and will not have any negative effects on hepatic encephalopathy, (Córdoba et.al, 2004). This randomized study had a population size of only 30, so more research should be done on this topic to investigate the best protein diet for patients with cirrhosis to ensure proper nutrition without decreasing neurological function. When an alcoholic is admitted to the hospital, it is common for nurses to stereotype and judge them, with remarks like “Why are we wasting time with this ‘wino’? He isn’t worth the time or money. Why don’t they let him die?” In a situation like this, it is important to remember that as nurses, our responsibility is to treat our patients rather than passing judgments. In addition, he has not provided a specific history so we do not know if there is a reason why he is a heavy drinker. Our nursing ethics of beneficence, nonmaleficence, and justice require us to do good, avoid harm, and give fair treatment of all patients, regardless of their condition and social habits. A nursing problem relative to John Doe’s care is the possibility of injury. Ensuring safety is a priority when caring for a person who might be withdrawing from alcohol. Because of his excessive alcohol abuse, his body has built up a tolerance over time to GABA. When the body is so used to it and the alcohol is stopped abruptly, the opposite effect of GABA happens, called delirium tremens (DT). DT is alcohol withdrawal symptoms with an altered mental status and sympathetic overdrive, characterized by anxiety, tremors, diaphoresis, arrhythmias, irritability, agitation, tremors, and seizures (RN Mental health nursing, 2013). A calm environment should be maintained to reduce stimulation. Seizure precautions must be implemented for John Doe ensuring he has IV access, seizure pads and his bed in the lowest position, and potentially having a tele-sitter to continuously monitor him. Some medications that can prevent seizures are benzodiazepines and barbiturates, but they can only be given if there is an order. Often times, giving benzodiazepines is concerning because of the highly addictive nature of these drugs, which is especially dangerous in a population already addicted to alcohol. When used in combination, there is a high risk for toxicity and respiratory depression (Doyle, Keogh, & Lynch, 2010). Another reason he is at a fall risk is because he is not alert and oriented and might try to ambulate, even though he is unaware of his situation. Lastly, his poor nutrition and fluid balance puts him at an even higher risk for falls. It is important to reorient him as appropriate and prevent dehydration and malnutrition. In monitoring John Doe for signs and symptoms of alcohol withdrawal and DT, he is restless, has tremors, and a low-grade fever. Some more severe symptoms of DT are hallucinations, extreme diaphoresis, tachycardia, and vomiting, (Doyle, Keogh, & Lynch, 2010). It is important to educate John Doe of early signs of withdrawal and to report them to prevent him from developing the more serious symptoms. Falls are especially important in John Doe because his cirrhosis indicates he has low clotting factors. If he were to fall, it could cause bleeding that could not stop and puts him at risk for hemorrhage. In addition, a fall could cause trauma to his face, dislocating the NG tube hooked up to suction. Lastly, his poor nutrition would cause poor wound healing, so if he were to sustain a fall, he would have a complicated and lengthy recovery process with a high risk for infection.During John Doe’s hospitalization, a staff psychiatrist evaluates him for mental decline associated with alcohol abuse and dependence, including alcoholic dementia, or Korsakoff’s psychosis. This is a chronic memory disorder caused by severe deficiency of thiamine (vitamin B1). Thiamine is essential for glucose use and axonal conduction. The damaged liver impairs the body’s ability to store thiamine, and low levels restrict the brain from carrying signals and generating enough energy to function properly. Wernicke’s encephalopathy often precedes Korsakoff’s psychosis, with symptoms like confusion, staggering, stumbling, lack of coordination, and abnormal involuntary eye movements. This is an acute episode. If it develops into Korsakoff’s psychosis, the patient will have problems learning new information, the inability to remember recent events, and long-term memory gaps (Xiong, 2015). John Doe survives a rocky course of hepatic encephalopathy and near-renal failure. After 27 days, including a week in the ICU, he is discharged to a drug and alcohol rehabilitation facility. He is employed as a longshoreman; fortunately, his insurance covers his month of in-house rehabilitation. When caring for patients going through alcohol withdrawal, the priority nursing intervention is safety. These patients are at a high fall risk because of their changes in neurological status, high risk for seizures, sympathetic overdrive and withdrawal symptoms, and poor nutritional status. They should be closely monitored and re-oriented appropriately. Medications can be given to prevent seizures, but must be carefully administered to prevent addiction and overdose. More research should be done to investigate the most beneficial diets for this population in terms of protein and sodium restrictions. Electrolyte and vitamin supplements are a crucial part in their recovery process too because an adequate balance is necessary for proper functioning. After ensuring the patient is safe and stable, it is important to provide education on the multitude of effects that alcohol has on the body and what they can do to change their lifestyles to prevent further hospitalizations related to alcohol.The patient should be given education and resources on how to quit drinking to prevent further lasting effects on the body. Although hepatic encephalopathy is an acute complication, alcoholism is a chronic disease and should be treated as such. There are some medications that can help with addiction like Disulfiram (Antabuse) that gives unpleasant side effects when consumed in combination with alcohol. It will condition to patient to refrain from drinking because negative side effects like flushing, nausea, tachycardia, and chest pain will occur if it is taken with alcohol. This medication will require follow-ups and counseling to ensure medication compliance. As nurses, we can also give referrals to support groups like Alcoholics Anonymous and Smart Recovery. This will allow alcoholics to openly share and listen to others’ journeys related to alcoholism, providing them with a support system and assuring them that they are not alone in their struggle. Lastly, it is important to remember that alcoholism is a disease and should be treated like one. Even though it is easy to pass harsh judgments and assume John Doe did this to himself, we must be unbiased and provide care to him like we would to any other sick patient.ReferencesCórdoba, J., López-Hell??n, J., Planas, M., Sab??n, P., Sanpedro, F., Castro, F., . . . Guardia, J. (2004). Normal protein diet for episodic hepatic encephalopathy: Results of a randomized study. Journal of Hepatology, 41(1), 38-43. doi:10.1016/j.jhep.2004.03.023Carey, W. D. (2014, June). Hepatic Encephalopathy. Retrieved April 16, 2016, from , L., Keogh, B., & Lynch, A. (2010). Pharmacological management of alcohol dependence syndrome. Mental Health Practice, 14(1), 14-19 6p.Fullwood, D., & Purushothaman, A. (2014). Managing ascites in patients with chronic liver disease. Nursing Standard, 28(23), 51-58 8p. doi:10.7748/ns2014.02.28.23.51.e8004Harding, M., Snyder, J. S., Preusser, B. A., & Winningham, M. L. (2013). Winningham's critical thinking cases in nursing: Medical-surgical, pediatric, maternity, and psychiatric. St. Louis, MO: Elsevier/Mosby.Hinkle, J. L., & Cheever, K. H. (n.d.). Brunner & Suddarth's textbook of medical-surgical nursing.Lee, L., & Grap, M. (2008). Care and management of the patient with ascites. MEDSURG Nursing, 17(6), 376-381 6p.RN Mental health nursing. (2013). ATI Nursing education.Robinson, J. (2015, March 01). Understanding Alcohol Abuse -- the Basics. Retrieved April 16, 2016, from , J. F. (1996). Lactulose and Combination Therapy of Hepatic Encephalopathy: The Role of the Intestinal Microflora. Digestive Diseases, 14(1), 53-63. doi:10.1159/000171583Xiong, G. L. (2015, August 19). Wernicke-Korsakoff Syndrome. Retrieved February 29, 2016, from ................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download