NRSG353 Nursing Care Plan in Liver Cirrhosis: Assessment Task 1
Nursing care plan in Liver Cirrhosis
Outline the disease
Liver cirrhosis is a late stage of liver fibrosis caused by liver disease and conditions like hepatitis and consumption of excessive alcohol. It explains the damaging of the liver. In cirrhosis, the scar tissue formed in the liver which increases with the disease progression and altering the functional capabilities of the liver and results in life threatening situations.
Causes of Cirrhosis
The most common cause of the disease is viral infections of the liver along with fatty liver, obesity and diabetes and alcohol abuse. The other causes of disease development are (Schuppan & Afdhal, 2008):
- Cystic fibrosis
- Deficiency of Alpha-1 antitrypsin enzyme
- Autoimmune diseases like autoimmune hepatitis, primary sclerosing cholangitis, and primary biliary cholangitis.
- Blockage in the bile duct.
- Exposure to environmental toxins, infections, and consumption of unethical drugs.
In our case study, it has been identified that Mr. James has a previous case history of hepatitis C and drug abuse which increases the chances of cirrhosis. At present regular consumption of alcohol along with smoking is enhancing the risk factors for him.
The risk factors for the disease development identifies that excessive consumption of alcohol along with obesity is elevating the onset of disease. In obese, it has been recognised that non alcoholic fatty liver and non alcoholic steatohepatitis are a risk for the development of cirrhosis. Furthermore, the development of chronic hepatitis is responsible for liver cirrhosis (Mayo Clinic, 2019).
Incidence of Cirrhosis
In 2010-12, liver disease was the 11th leading cause of premature death in Australia (AIHW, 2019). The rate of death due to liver disease was increased 48% over the past three decades (AIHW, 2019). The premature death rate duet o liver disease is high among the men. It was 69%. In addition, the Aboriginal people are vulnerable to liver disease particularly in hepatitis B (AIHW, 2019). The death rate in indigenous people due to liver disease is higher compared to non indigenous Australians. It was recognised that in 2008-12 the rate is 3 times higher in the case of male and 5 times higher in the case of the female indigenous population (AIHW, 2019). The main reasons behind the aggressive onset of the disease development are fatty liver, overweight, diabetes, hypertension, and hypercholesterolemia in society. In addition, excessive consumption of alcohol is also interfering with disease development. Therefore, restricted life style with dietary modification and proper medication can eliminate the chances of disease development.
Impact on family
Liver cirrhosis is a progressive disease which develops slowly over many years. The process of the disease allows the development of scar tissue in the liver to stop the function of the liver(Murrell, 2017). It is a process of long term liver damage in which healthy liver tissues are replaced by the scar tissues and the functioning capabilities of the liver are altered. It can block the flow of blood through the liver and damage the tissue.
The person suffering from the illness can develop various symptoms which can increase their irritability and restlessness along with fatigue and loss of appetite. The disease not only affects the individual as it has a great impact on their family. The family member needs to support the patient in their intervention process.
Signs and symptoms of Cirrhosis
|Jaundice||High bilirubin level in blood is known as jaundice which is a common symptom of liver cirrhosis. Haemoglobin is breakdown into un-conjugated bilirubin and other substances in the blood. Therefore, albumin binds the un conjugated bilirubin and transport to the liver. In the liver, it is conjugated with glucuronic acid and excreted into the duodenum. Thus, in intestine bacteria metabolized the bilirubin and converted into urobilinogen which is eliminated with feces and reabsorbed by the hepatocytes. In liver cirrhosis, the functioning capabilities of the hepatocytes are decreased as a result the bilirubin reabsorbed process is inhibited (Herrine, 2018). In addition, lack of albumin in cirrhosis patients is also disturbing the transportation process of bilirubin. As a result, the blood bilirubin level is increased in cirrhosis patients which indicating the occurrence of jaundice.|
|Ascities or oedema|
The deposition of fluid in the abdomen is known as ascities and deposition of fluid in legs is called oedema. Both are common symptoms in liver cirrhosis. In cirrhosis, development of portal hypertension released the vasodilators which affect the splanchnic arteries and decrease the arterial blood flow and pressure. in addition, progressive vasodilation can cause activation of vasoconstrictor and antinatriurectic mechanisms to normalised the perfusion pressure. As a result of the sodium and water retention of the body precipitate. It has been recognised that in the late stage of liver cirrhosis water deposition is more pronounced compared to sodium retention. Furthermore, the patient with ascities has urinary sodium retention, and dilutional hyponatremia along with elevated total body sodium. It is indicating the inability of the liver cells to produce enough blood protein albumins (Such, 2018).
In cirrhosis, portal hypertension can cause the blood to be redirected towards the small veins. Therefore, scan in liver tissue can block the blood flow through the liver as a result of blood flow through the veins and extra blood flow can increase the pressure. The extra pressure can break the vein and cause serious bleeding. In addition, portal hypertension can cause enlarged veins in the esophagus or in the stomach which leads to life threatening bleeding in cirrhosis patients. The poor functioning capabilities of the liver are inhibiting the production of blood clotting factors which accelerate the continuous bleeding (Hilzenrat & Sherker, 2012).
Pharmacodynamics & Pharmacokinetics of Drug
It is a diuretic which can be used in anti-hypertensive therapy and for treating oedema. After oral consumption, 65% of the dose can be absorbed. It is a weak carboxylic acid exists in the separated form in the gastrointestinal tract. It is incompletely absorbed on oral administration but absorbs rapidly. The effects of the drugs can over within 4 hours of the administration. The prime absorption site of the drug is upper duodenum and the optimum pH is 5. The drug can bind to plasma protein up to 99% (Furosemide, 2019). It can bind albumin and exert its function. The drug can secrete efficiently by the transport of organic acid in the proximal tubule and bind the sites on sodium, potassium, chloride symporters in the ascending limbs. It has been recognise that 65% of furosemide is excreted in urine as unchanged compound and the rest can be conjugated with glucuronic acid in the kidney. The exceptional adverse effects can result due to fluid and electrolyte imbalance.
Mechanism of action:
It is a diuretics and the main renal action of the drug is to restrict the active chloride transport in the ascending limb of the body along with reducing the sodium re-absorption from the nephron and creating isotonic or hypotonic urine (Medicines, 2019).
The experimental studies indicating that furosemide acts on the entire nephron along with exception of distal exchange site of the kidney. The main affecting site is ascending limb of the Henley loop and the complex effects on the renal circulation. The drug can help in diverting the blood flow to the outer cortex from the juxta-medullary region.
The studies indicating that prostaglandin biosynthesis and rennin angiotesin system can get affected by the administration of furosemide and it can alter the renal permeability of the glomerulus to the serum protein. In addition, administration of furosemide can cause accumulation of sodium and chloride along with the fluid in the body. Thus, careful administration is essential to avoid consequences.
Nursing Care Plan
|The patient is suffering from fatigue, mood alteration, weakness, agitation.||After 4 hours of nursing, intervention patient will able to achieve sufficient sleep.|
Evaluate the stress level.
Reduce fluid intake.
Provide suitable and supportive atmosphere.
The complication of the condition can make the patient restless and interfere with his sleeping patterns (NRSNG, 2018).
Reduce sensory stimulation of the environment can help the patient.
|The patient is suffering from mild jaundice with poor muscle tone and abdominal distension||After 5 hours of nursing intervention, the patient appetite will be improved.|
During this period monitor the vital signs.
Consider the food preferences of the patient.
Administrate small and frequent meal without salt.
Motivate to take nutritious food.
It can stimulate the appetite of the patient.
Ascities has a strong impact on the patient appetite in cirrhosis (Wiegand & Berg, 2013).
The physiological disturbance can impair the food intake and digestion process of the patient.
Thus, conserving energy can reduce the metabolic demands and promote cellular regeneration in the liver cell(Wiegand & Berg, 2013).
|The patient has ascities, and respiratory distress along with fatigue||After 2 hours of nursing intervention, the patient will feel better and his complications will be partially released.|
Relaxing the patient by providing comfort and support.
Teach the relaxation techniques along with the breathing techniques.
Provide respiratory support in case of a severe respiratory problem.
Relaxation techniques and supportive environment can calm the patient and he can feel better.
The noisy environment along with physical discomfort stimulates the irritation (Nusrat, 2014).
|The patient has oedema, abdominal distension, jaundice and respiratory difficulties which needs attention||After 6 hours of intervention, the patient will achieve stabilise fluid volume and decrease the incident of oedema|
Monitoring the vital signs and measure fluid input and output.
Continually monitoring BP.
Measure the respiratory status.
Restrict the consumption of fluid and sodium intake.
Administration of diuretics.
Increase in BP indicating the elevation f fluid in the body.
Increase respiratory discomfort indicating further deposition of water in the body (Nusrat, 2014).
Sodium restriction can avoid fluid retention in extra vascular space.
Fluid restriction can avoid the onset of dilutional hyponatremia.
Administration of diuretics can remove the ascitis fluid.
|Physical discomfort of the patients along with anxiety and feeling of helplessness||After 8 hours of nursing intervention, the patient condition will be stable and he would feel better.|
Start the verbal communication with the patient.
Encourage the patient by showing positive and supportive attitudes.
Encourage the family to interact with the patient.
Verbal communication can help the patient to avoid the feelings of quit. In the case of James, control of alcohol consumption during the treatment is essential for his recovery (NRSNG, 2018)..
Therefore, supportive behaviour of the staffs and his family member can motivate him to stop the habits and concentrate on the intervention process (NRSNG, 2018).
The non judgemental and emotional behaviour of the nursing staff can ensure free access to patient participation in the intervention process.