A case report on DCLD with hepatic encephalopathy and multidrug resistant sepsis

Muthulakshmi1*, Shalini H S2, Vijayakumari. D3

1Infection Control Nurse, Kauvery Hospital, Electronic City

2CNO, Kauvery Hospital, Electronic City

3Nurse Educator, Kauvery Hospital, Electronic City

*Correspondence

Abstract

Liver cirrhosis is a major cause of mortality in the world, which constitutes around 2.4% of the global death. Clinical complications such as ascites, jaundice, hepatic encephalopathy, infections, or portal-hypertensive haemorrhages are common with acute decompensation of liver cirrhosis, which marks a turning point in the prognosis. Men account for almost two-thirds of all liver-related fatalities. Alcohol, non-alcoholic fatty liver disease, and viral hepatitis (HBV and HCV) are the three main causes of cirrhosis in the world. Many acute hepatitis cases are caused by hepatotropic viruses, although a growing percentage of cases are caused by drug-induced liver injury. Massive upper gastrointestinal (UGI) bleeding is a life-threatening complication commonly associated with portal hypertension and oesophageal varices. When compounded by hepatic encephalopathy and sepsis, it significantly increases morbidity and mortality. We report a case of a 42-year-old male presenting with massive UGI bleeding, severe anaemia, hepatic encephalopathy, and subsequent multidrug-resistant (MDR) sepsis, who was managed successfully with a multidisciplinary approach including endoscopic intervention, ventilatory support, and targeted antimicrobial therapy.

Key words: Liver cirrhosis; Upper gastrointestinal (UGI) bleeding; Multidrug-resistant (MDR)

Introduction

Liver diseases remain a major health concern in developing countries like India, with a rising burden of chronic liver disease (CLD) impacting the economy. Hepatic encephalopathy (HE), also known as portosystemic encephalopathy, is a severe complication of chronic liver disease, characterized by altered mental status and cognitive dysfunction. It is reversible with early diagnosis and treatment but significantly impacts quality of life and survival. Nearly 70% of patients have subtle symptoms, while 30-45% of cirrhotic individuals develop overt HE.1 Ammonia, produced by gut bacteria, and is processed by the liver, but impaired clearance due to portosystemic shunting leads to hyperammonaemia. Hepatic encephalopathy results from neurotoxic accumulation in the blood and brain. The correlation between ammonia levels and her severity is inconsistent. Other contributing factors include false neurotransmitters and mercaptans. Minimal hepatic encephalopathy presents with subtle symptoms, detectable only through specialized tests. Hepatic encephalopathy is diagnosed clinically, requiring a skilled physician to recognize its varied symptoms. Patients may present with confusion, personality changes, aggression, or excessive drowsiness. In severe cases, it can progress to hepatic coma, which may be fatal. Identifying precipitating factors is crucial for timely management. Asterixis, or “liver flap,” is a common finding in hepatic encephalopathy, induced by asking patients to extend their arms and bend their wrists back. The West Haven criteria are widely used for grading HE. While ammonia levels are often elevated, they are not a reliable diagnostic marker. Most HE episodes in cirrhotic patients result from identifiable precipitating factors or spontaneous portosystemic shunting.

Common precipitating factors of hepatic encephalopathy include GI bleeding, infections, hypovolemia, azotaemia, constipation, electrolyte imbalance, and high protein intake, with infections and GI bleeding being the most frequent. Management involves ruling out other causes, identifying triggers, and assessing response to empirical treatment. Lactulose and rifaximin, approved by the FDA, help reduce ammonia production and absorption. Early detection and prompt management of precipitating factors are crucial for better patient outcomes.5, 6 Therefore this study aimed to analyse the clinical profile of HE in cirrhosis, identify precipitating factors, and assess their correlation with outcomes.

Case Presentation

History

Patient with nil comorbidities presented to emergency department with complaints of 1 episode of hematemesis along with 3 episodes of dark coloured loose stools since today morning. No history of fever / abdominal pain. Patient initially treated at elsewhere and referred here for further management.

Clinical Examination

On Arrival, 42 years / Male.

Body builtAverage
Heart Rate130/min
BP 130/70mmHg
Respiratory Rate17/min
Temp 98°F
SPO298% on RA
Respiratory SystemBilateral normal vesicular breath sounds present.
Cardiovascular SystemS1 S2 +.
AbdomenSoft, non-tender
Central Nervous SystemConscious and oriented

Course in the Hospital

A 42-year-old male, Mr. K, presented to the emergency department with massive hematemesis and altered sensorium. Initial evaluation revealed a haemoglobin drop from 9.0 g/dL to 3.2 g/dL, indicating severe acute blood loss anaemia. The patient was immediately shifted to the ICU for further management. On admission, he was hemodynamically unstable and required aggressive resuscitation. The patient was admitted to the ICU and managed with fluid resuscitation and multiple packed red blood cell (PRBC) transfusions. Pharmacological therapy with Inj. Terlipressin was initiated for suspected variceal bleeding. Emergency upper GI endoscopy revealed large oesophageal varices, and Endoscopic Variceal Ligation (EVL) was performed successfully. During the ICU stay, the patient developed seizures, which were managed with anticonvulsants including Lorazepam infusion, and a neurology consultation was obtained. He was diagnosed with Grade I hepatic encephalopathy, contributing to his altered mental status. Due to worsening sensorium, the patient was intubated and mechanically ventilated, with sedation maintained using Fentanyl infusion. The patient also developed acute kidney injury, with creatinine levels improving from 2.8 mg/dL to 1.5 mg/dL with supportive care. Despite stabilization, the patient had persistent encephalopathy, requiring continued ventilatory support. Broad-spectrum antibiotics including Meropenem, Teicoplanin, and Fluconazole were initiated empirically. Blood culture grew multidrug-resistant Acinetobacter baumannii complex, necessitating escalation of antibiotics based on sensitivity. However, BAL and urine cultures were negative.

The patient had four episodes of melena between 01.07.2025 and 02.07.2025, requiring ongoing transfusion support. A total of 4 units of PRBC were transfused, improving haemoglobin from 3.2 g/dL to 7.5 g/dL. Bronchoscopy on 03.07.2025 showed no significant abnormalities. The patient remained critically ill with severe anaemia and lactic acidosis. Pulmonology consultation was sought due to cough and breathlessness, and appropriate management was provided.

On 04.07.2025, the patient was on volume control ventilation with stable vitals: pulse 72/min, blood pressure 102/54 mmHg, and FiO₂ 40%. Relatives were counselled regarding the critical condition and prognosis. In view of decompensated liver disease with recurrent variceal bleeding, liver transplantation was discussed, and surgical gastroenterology consultation was obtained.

Investigations

Lab investigations were done showed

Hb 3.2 gm/dl
PCV12.6%
TLC 96000
Platelet count80000/ml
Sodium 137mEq/L
Potassium5.7 mEq /L
Creatinine 2.9 mg/dl
Total bilirubin5.5
Direct bilirubin 3.6
Protein6.1gm/dl
Albumin2.3gm/dl
SGPT 132U/L
SGOT 1400U/L
ALP116IU/L
GGT 328U/L

2D Echo done on 01.07.2025 showed Normal Chamber Dimensions, MR- Grade I, TR – Mild, Mild PAH (PASP – 39mmHg), No RWMA, Normal LV Systolic Function, LVEF – 60%. MRI Brain done on 02.07.2025 showed Symmetrical T1 hyperintensities involving bilateral lentiform nuclei, internal capsule and cerebral peduncle (along the CST Territory) – Metabolic / Toxic Etiology. Small foci of FLAIR hyperintensities in the subcortical white matter of left frontal lobe. No acute ischemic lesions by DWI.  USG abdomen and pelvis (03.07.2025) which showed Features are suggestive of Chronic Liver Disease. Mild splenomegaly. Mild-to-moderate ascites. Supraumbilical hernia.

Discussion

Variceal bleeding is a severe complication of portal hypertension and carries high mortality if not managed promptly. Early administration of vasoactive agents like terlipressin and timely endoscopic intervention such as EVL are the cornerstones of management. Hepatic encephalopathy further complicates the clinical course, often necessitating airway protection and ventilatory support. In this case, early intubation helped prevent aspiration and ensured adequate oxygenation. The development of multidrug-resistant Acinetobacter baumannii infection highlights the growing challenge of nosocomial infections in critically ill patients. Prompt identification and escalation of antibiotics based on culture sensitivity were crucial in management. Acute kidney injury and lactic acidosis added to the complexity, requiring careful fluid and metabolic management. Multidisciplinary care involving intensivists, gastroenterologists, neurologists, and pulmonologists played a key role in stabilizing the patient.

The development of multidrug-resistant Acinetobacter baumannii infection highlights the growing challenge of nosocomial infections in critically ill patients. Prompt identification and escalation of antibiotics based on culture sensitivity were crucial in management. Acute kidney injury and lactic acidosis added to the complexity, requiring careful fluid and metabolic management. Multidisciplinary care involving intensivists, gastroenterologists, neurologists, and pulmonologists played a key role in stabilizing the patient.

Conclusion

This case underscores the critical complexity and high mortality risk associated with massive upper GI bleeding in the setting of decompensated liver disease, especially when compounded by hepatic encephalopathy, severe anaemia, acute kidney injury, and multi drug resistance sepsis. The patient’s presentation with profound haemoglobin drops, altered sensorium, and haemodynamic instability required immediate, aggressive well-coordinated critical care interventions. Timely initiation of resuscitative measures including massive transfusion and vasoactive therapy with terlipressin, played a pivotal role in stabilizing the patient. Early endoscopic intervention with variceal band ligation (EVL) was lifesaving in controlling the source of bleeding. The development of hepatic encephalopathy and seizures further complicated in clinical course, necessitating ventilatory support and continuous neurological monitoring, highlighting the importance of airway protection in such patients.

The occurrence of multi drug resistant Acinetobacter baumannii sepsis emphasizes the growing challenge of nosocomial infections in ICU Settings. Prompt microbiological diagnosis and appropriate escalation of antibiotics were crucial in preventing further deterioration. Additionally, the improvement in renal function reflects the effectiveness of supportive care in reversing organ dysfunction when addressed early. Importantly this case also highlights the need for early identification of patients for liver transplantation in patients with DCLD, as definitive management to prevent recurrence and improve long term survival.

In conclusion, early recognition, rapid resuscitation, timely endoscopic management, vigilant infection control. And coordinated multidisciplinary care are the cornerstones in managing such critically ill patients. This case reinforces that even in severe and complicated presentations, Structured ICU protocols and timely interventions can significantly improve clinical outcomes and survival.

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