Management of chronic liver disease

Sivagami*

ANS, Nursing Department, Kauvery Hospital, Salem, Tamil Nadu

*Correspondence

Abstract

Chronic Liver Disease (CLD) is a progressive liver disorder caused by long-term injury leading to fibrosis and Cirrhosis. Common causes include alcohol use, viral hepatitis, and metabolic conditions. Patients may present with jaundice, ascites, and complications like portal hypertension. Early diagnosis and appropriate management are essential to prevent disease progression and improve outcomes.

Key words: Chronic Liver Disease (CLD); Cirrhosis; Jaundice

Introduction

Chronic liver disease is a progressive liver condition lasting more than six months, leading to fibrosis and cirrhosis. It is commonly caused by viral hepatitis, and metabolic disorders. Early detection is important to prevent complications and improve outcomes.

Case Presentation

Patients came with history of decreased food intake x 10 days
Decreased orientation x 3 days
Decreased mobility (+)
Easy fatigability and drowsiness
Known to have DM / SHTN / hypothyroidism /DCLD
Known to have pituitary micro adenoma – 5 months’ back
S/p Thyroidectomy – 30yrs back

Relevant clinical findings

On examination the patient appeared ill, drowsy, and moderately dehydrated. General examination revealed pallor, icterus, bilateral pedal edema, spider angiomas and palmar erythema, indicating chronic liver dysfunction. His blood pressure was 100/70 mmHg, pulse rate 96 beats per minute, respiratory rate 24 breaths per minute, temperature 37.8 ℃, and oxygen saturation 95% on room sir. Abdominal examination revealed mild distension, suggestive of moderate ascites. The liver was shrunken and difficult to palpate, while splenomegaly was present. Neurological examination showed grade II hepatic encephalopathy with altered mental status.

Relevant investigation

USG abdomen scan report (bed side) – 20.04.26.

Impression :

Chronic liver parenchymal disease with mild splenomegaly
No portal vein thrombosis
Mild to moderate ascites
no peri cholecystic collection
No IHBR / CBD dilatation

Trans thoracic ECHO report – 20.04.2026

Impression :

No RWMA /Normal LV & RV systolic function
Grade I LV diastolic dysfunction
Mild mitral regurgitation /Aortic valve sclerosis: Mild AR / No AS
Mild tricuspid regurgitation / Mild pulmonary artery hypertension
No clot / vegetation / pericardial effusion

Investigation

CBC
Haemoglobin	9.5	11.3	11.4
Haematocrit	29.2	32.8	33.3
WBC count	6390	6890	8350
RFT
Urea	34
Creatinine	0.67
Sodium	126	128	130	134	136
Potassium	3.3	3.7	3.9	4
LFT
Bilirubin Total	3.2	3.6	4.4
Bilirubin Direct	1.4	1.7	2.2
Bilirubin indirect	1.8	1.9	2.2
SGOT	100	107	194
SGPT	72	85	154
Alkaline phophatase	168	169	241
Albumin	2	2.1	2.7
Ammonia	97	110
Coagulation profile
Test (P time)	17	21
Control (P time)	13	13
INR	1.32	1.64

Diagnosis

Based on the patient’s history, clinical examination, laboratory findings, and imaging studies, a diagnosis of decompensated chronic liver disease. The patient also had grade II hepatic encephalopathy and coagulopathy. Non-alcoholic fatty liver disease.

ICU Management

The patient was admitted to the ICU for close monitoring aggressive supporting management Oxygen therapy was initiated and intravenous fluids were administered to cautiously maintain adequate circulation while avoiding fluid overload. Lactulose was started to reduce blood ammonia levels and improve hepatic encephalopathy, while rifaximin was added to decrease intestinal ammonia production. Intravenous volume and support renal perfusion. Spironolactone was prescribed to manage ascites and peripheral edema. Broad-spectrum intravenous antibiotics were initiated empirically to prevent bacterial infections until culture reported become available. Vitamin K administered for correct coagulopathy, Nutritional therapy included a high -calorie, high protein diet. Daily laboratory investigation performed to monitor liver function, coagulation profile, renal function and electrolytes.

Outcome

Following ten days of intensive care, the patient’s neurological status improved significantly with resolution of hepatic encephalopathy. Serum bilirubin levels gradually decreased, renal function stabilized, and urine output improved. Ascites reduced following diuretic therapy, and abdominal discomfort was relieved. The patient remained hemodynamically stable without evidence of gastrointestinal bleeding. She was successfullytransferred from the ICU to ward for continued treatment.

Discharge

The patient was discharged after two days of hospitalization in stable condition. At discharge she was conscious, oriented, tolerating oral diet, and able to perform basic activities. She was prescribed antibiotics and other supportive drugs.

Conclusion

Chronic liver disease is a progressive condition that requires early identification, proper medical treatment, and effective nursing care. Good management helps prevent complications, improve quality of life, and reduce mortality. Patient education, lifestyle modification, and regular follow-up play a vital role in long-term outcomes.

Reference

Harrison’s principles of internal medicine 21^st
Oxford Handbook of clinical medicine, 11^th

Management of chronic liver disease

Management of chronic liver disease

Sivagami*

Nightingale Journals