Fulminant hepatic failure-Mr Mulundano

This Presentation is about the Nursing management of Patients with Fulminant Hepatitis. Nurses will find it helpful in terms of management.

1. FULMINANT HEPATITIS January 2019 intake

2. General Objective At the end of this lecture/discussion, students should acquire knowledge on Fulminant Hepatic Failure and be able to provide nursing care to patients with this disease.

3. Specific Objectives At the end of the lecture/discussion students should be able to: Define Fulminant Hepatic Failure. Mention the causes of Fulminant Hepatic Failure. Describe the pathophysiology of Fulminant Hepatic Failure State the clinical manifestations of Fulminant Hepatic Failure  

4. Outline the medical management of a patient with Fulminant Hepatic Failure. Discuss the specific nursing care for a patient with Fulminant Hepatic Failure. Mention the complications of Fulminant Hepatic Failure.

5. DEFINITION Fulminant Hepatic Failure , also known as acute liver failure, is a disease in which the liver cells fail to regenerate, characterised by the development of hepatic encephalopathy within 8 weeks of onset of disease in a patient without prior evidence of hepatic dysfunction/disease. It can occur rapidly in as little as 48 hrs and can be difficult to detect initially. It is a rare but potentially fatal condition as it leads to massive hepatocellular injury and necrosis. This condition is a Medical Emergency.

6. CAUSES Viruses ; viral hepatitis being the major cause. Toxins or Autoimmune Responses . Poisons/Chemicals Amanita mushrooms or any poisonous wild mushroom. Some Herbal medicines High doses of drugs such as Paracetamol, Isoniazide and Alcohol. Most of these cause Hepatotoxicity

7. PATHOPHYSIOLOGY Following the introduction of a causative agent into the body, such as a virus or poisons, there is acute inflammatory reaction with hepatic vascular occlusion, leading to ischaemia and hypoxia of the hepatic parenchyma.

8. Ischaemia will lead to progression of hepatocellular injury and necrosis with development of hepatic encephalopathy leading to dramatic and rapid clinical deteroriation . Liver Failure is the end result. Mortality rate is extremely high (60% to 85%) despite intensive treatment.

9. CLINICAL FEATURES General body malaise due to impaired carbohydrate Metabolism. Anorexia, nausea and vomiting due to accumulation of metabolites. Pruritis caused by bile salts being deposited on the skin. Light Coloured stool with steatorrhoea and diarrhea due to poor absorption of food. Dark Coloured Urine . Due to passage of excess uncongugated bilirubin Hepatomegaly due to the inflammatory process and fat infiltration.

10. Portal obstruction and ascites; partly due to prolonged failure of liver function and partly due to obstruction of the portal circulation. Lack of albumin also facilitates Ascites. Fever due to accumulation of metabolites and viral toxins.

11. Peripheral Oedema due to depletion of plasma proteins such as albumin, resulting in reduced oncotic pressure making body fluids to move from the intravascular Space into the interstitial space. Oedema may also result from venous stasis. Vitamin deficiency and anaemia due to inadequate formation, storage and use of certain vitamins (e.g. vitamin A, C and K) Mental deterioration, irritability, confusion, altered level of consciousness and coma due to accumulation of unconjugated bilirubin and Ammonia.

12. Jaundice due to accumulation of unconjugated bilirubin and bile stasis as the bile ducts get obstructed. Bleeding tendencies such as epistaxis due to protein deficiency and vitamin K deficiency Menorrhagia in women (excessive bleeding)

13. Investigations HISTORY; Patient may reveal exposure to drugs, chemicals, hepatitis or any toxic substances.  LABORATORY TESTS  Liver function tests which indicate low serum albumin level and increased serum globulin level Enzyme tests indicate liver cell damage; serum alkaline phosphatase, cholinesterase level may decrease. Bilirubin tests are performed to measure bile excretion or retention Blood Test may reveal Increased Prothrombin time. Urine Test may reveal excess Ammonia and other metabolites. Ultrasound scanning is used to measure the difference in density in parenchymal cells and scar tissue. CT Scan and MRI give information on liver size,hepatic blood flow and obstruction.

14. Drugs therapy Management is usually based on the presenting symptoms; Potassium sparing diuretic like Spironolactone ; 100mg per day orally to decrease ascites and reduce oedema but conserve potassium for cell metabolism.  Antacid; Magnesium trisilicate ; Dose adult-250 to 500mg TDS and H 2 Receptor antagonists; Cimetidine; 200mg daily per oral to reduce the risk of bleeding from stress ulcers.

15. Manage cerebral oedema by giving mannitol; which is a cerebral diuretic. Vitamin A supplement, Vitamin B Complex 1 tablet daily, Vitamin C and K to improve integrity of the mucous membranes of the GIT, and increase prothrombin levels for proper blood coagulation.  

16. Antibiotics such as Cloxacillin 500mg qid or Amoxicillin 500mg tds per oral for 5 to 7 days to treat any underlying bacterial infection that may be suspected. Neomycin ; orally 500mg is administered if jaundice is present to suppress intestinal bacteria so that absorption of protein is blocked so as to prevent ammonia intoxication. Abdominal Paracentesis is done to decrease ascites.

17. The Goal of all these intervention is to preserve whatever part of the liver which is still viable. Some causes of acute liver failure can be reversed with treatment. However, if this is not possible, Liver transplantation can also be done.

18. SPECIFIC NURSING CARE Aims of nursing care To promote patient’s rest To improve nutritional status To provide skin care To reduce risk of injury To Prevent infection To Promote Pulmonary function

19. Promote patient’s rest Rest is important to permit the liver to reestablish its functional ability. Patient’s position in bed should be adjusted to promote maximal respiratory efficiency especially if ascites is marked. Rest reduces the demands on the liver and increases the liver’s blood supply. Do procedures in blocks. Nurse the patient in a quiet place. Restrict unnecessary visiting.  

20. Improving nutritional status If there is no ascites, oedema or signs of impending hepatic coma patient should receive a nutritious Low-protein diet, supplemented with vitamins; B complex as well as vitamins A, C and K. Encourage patient to eat while in a sitting position to prevent feeling of fullness especially if there is ascites. Provide small frequent meals to support the body’s metabolic activities. The meals should look appetizing and served in a clean environment.  

21. Oral care is done to promote comfort and stimulate appetite. In severe cases, restrict Sodium and protein intake to prevent further oedema and ascites and loading the liver with more work to breakdown proteins for body usage, as this will raise ammonia levels and increase encephalopathy.

22. Provide skin care Skin care is important because of subcutaneous oedema, patient’s immobility, jaundice and increased susceptibility to skin breakdown and infection. Irritating soaps and adhesive tapes are avoided to prevent trauma to the skin. Frequent changing of position is necessary to avoid pressure sores. Avoid trauma to the patients skin through friction while turning him, be gentle.

23. Bath patient with a mild soap and apply a soothing lotion to prevent cracks. Since the patient may experience pruritis and scratch himself, employ nail care and keep her nails short to prevent injury to his skin.

24. Reduce risk of injury Patient should be oriented frequently to the environment and the room should be well Lit and floor not slippery to prevent falls. Assist the patient with ambulation to prevent falls. A soft-bristled tooth brush should be used to minimize bleeding from the gums  

25. Patient should be protected from falls and other injuries by being nursed in a bed with side rails in case a patient become agitated or restless. Any injury should be evaluated carefully because of the possibility of internal bleeding.

26. Observations The nurse should closely monitor the patient’s condition by frequent observation of vital signs (4 hourly observation of temperature, respiration, pulse and blood pressure) to detect any deviation from normal. Observe for evidence of coughing or increasing dyspnoea which may indicate evidence of pulmonary compromise. Assess the mental status and change in the level of consciousness, sleep patterns and whether encephalopathy is worsening. Observe skin for pruritis. Observe for signs of infection such as Fever and abnormal breath sounds.

27. Look out for abdominal distension to ascertain the development of ascites. Assess for hepatomegaly by abdominal palpation. Check for oedema to ascertain worsening of the condition. Observe the characteristics of urine and stool for colour to determine severity of the disease.  

28. Psychological support Explain the disease process and all the procedures to the patient to allay anxiety and gain patients cooperation. Reassure him that everything possible is being done to manage his condition. Attend to his questions and concerns genuinely and refer to relevant authorities what you cannot handle. Involve patients’ relatives in the care so that the patient can feel loved and cared for.

29. Body fluid replacement Because of some degree of circulatory dysfunction, careful attention should be paid to fluid management. In the presence of ascites, assess the abdominal girth daily to ascertain its reduction. Although there is fluid restriction and control, electrolytes are administered as advised. Sodium is restricted due to oedema. Dextran is given to improve blood flow in areas of stasis by reducing cellular aggregation.

30. Albumin is also administered as advised to maintain plasma oncotic pressure thus reducing oedema . Maintain an intake and output balance chart to prevent fluid overload or under hydration.

31. Prevention of infection Restrict visitors to the patient since his immunity is low and can easily contract infection. Always wash hands with antiseptics before attending to the patient. Advice the patient not to scratch his body to prevent injury to the skin and exposing himself to infection.

32. Patient education Patient is advised to avoid scratching to prevent cracking the skin & To use a soft-bristled toothbrush to prevent bleeding from the Gums.

33. Advise patient on the important of ; Nutritious diet, but low in fat, protein & sodium to promote recovery Avoidance of alcohol and unprescribed drugs to promote recovery Drug compliance to promote healing Follow up care is emphasized to monitor prognosis of the condition

34. COMPLICATIONS Haemorrhage (Bleeding Tendencies) The patient is at increased risk of bleeding because of decreased production of prothrombin and decreased ability of the liver to synthesise necessary clotting factors. Hepatic encephalopathy Hepatic encephalopathy is as a result of the liver’s inability to detoxify toxic by products of metabolism and portal-systemic shunting, in which collateral vessels develop as a result of portal hypertension which allow potentially toxic substances usually extracted from the liver to enter the systemic.

35. Chronic Hepatitis as a result of repeated inflammation and regeneration. Hepatic Coma due to replacement of viable cells with a fibrotic tissue. Liver Cirrhosis resulting from chronicity of the disease. Cancer of the Liver due to prolonged fibrosis and calcification of the liver parenchyma Acute Hepatic necrosis due to massive destruction of hepatocytes. Increased Intracranial Pressure due to cerebral oedema.

36. Thank you You are destined for Greatness…