He had already survived one transplant.
But this time, the odds were stacked higher.
Sadam — a man with polycystic kidney disease, diabetes, and hypertension — had a kidney transplant years ago.
Later, Hepatitis C led to liver failure. He arrived in the ICU with ACLF: unconscious, with multi-organ failure.
His son Arif stood by him. A combined transplant wasn’t possible due to family history.
We managed sepsis, stabilised him, and timed his liver transplant perfectly.
This episode explains how time, teamwork, and tenacity save lives.
We frequently see ACLF — Acute-on-Chronic Liver Failure — in our emergency rooms. Patients with known or sometimes undiagnosed chronic liver disease arrive critically decompensated. They’re not just jaundiced or confused — they often present with multi-organ failure.
Altered mental status, kidney shutdown, fluid overload, haemodynamic instability, or respiratory distress are common at first contact. At this point, it’s no longer just about the liver.
The involvement of the brain, kidneys, heart, and lungs makes the clinical picture far more complex.
Our initial focus is always resuscitation and stabilisation, followed by ICU transfer. But simultaneously, we start assessing whether liver transplantation is a viable and urgent option, or whether it’s already contraindicated based on the extent of organ involvement.
ACLF is different from acute liver failure. In ACLF, transplant eligibility is dictated by which and how many organs are involved. Clinically, we categorise organ systems into what we call “organs of utility” — primarily the kidney and brain, which are more likely to recover after transplant — and “organs of futility”, such as the circulatory and respiratory systems, where failure significantly worsens outcomes.
If more than three organs are failing, or if there’s respiratory or circulatory collapse, a liver transplant is generally considered futile. On the other hand, if the failure is limited to the liver and utility organs — and the patient remains hemodynamically stable — we may consider an urgent transplant. Even in patients with no obvious organ failure, a MELD score above 30 prompts early transplant evaluation due to the high risk of rapid deterioration.
In recent years, there has been growing evidence and clinical acceptance of therapeutic plasmapheresis (or plasma exchange) as a bridge therapy in ACLF. We now know that low-volume plasmapheresis, in particular, can be more beneficial than earlier large-volume approaches. It works by reducing the systemic inflammatory response (SIRS) that drives much of the multi-organ damage in ACLF.
By modulating this inflammatory cascade, plasmapheresis can help prevent further organ failure, buying time for the liver to recover or for a transplant to be arranged. In alcohol-related ACLF, the combination of low-volume plasma exchange with low-dose corticosteroids has shown especially promising results. While not a cure in itself, plasmapheresis can stabilise patients during that critical window when decisions must be made fast, and outcomes are still reversible.
This blog is my attempt to walk you — the patient or the caregiver — through the real-life complexity of ACLF: what it looks like, how we approach it, what treatment options exist, and how we decide who can make it to transplant. I hope it offers clarity, comfort, and a better sense of control during what is often a chaotic and overwhelming time.
2023 guidance from the American Association for the Study of Liver Diseases (AASLD) addresses the diagnosis, evaluation, and management of Acute-on-Chronic Liver Failure and critically ill cirrhotic patients in intensive care settings. It offers expert consensus instead of formal guidelines, due to limited randomised controlled trial data.
Podcast: ACLF
💡 1. Understanding ACLF: Definition and Framework
- Acute-on-Chronic Liver Failure occurs in patients with chronic liver disease (CLD) with or without cirrhosis.
- It is characterised by:
- Acute onset with rapid deterioration.
- Hepatic failure: Elevated bilirubin and INR.
- ≥1 extrahepatic organ failure: Neurologic, circulatory, respiratory, or renal.
- Causes include: Alcohol-associated hepatitis, drug-induced liver injury, viral infections, bacterial infections, and surgery.
🧠 2. Prognostic Scoring: Assessing Severity and Mortality
- Recommended over MELD: NACSELD, CLIF-C ACLF, AARC ACLF.
- All consider organ failures, some include lactate levels and systemic inflammation markers.
- CLIF-C ACLF ≥ 70 = ~90% 90-day mortality.
- NACSELD ACLF (≥2 OFs) = ~3% 28-day survival.
- MELD-LA outperforms MELD/Na.
- Dynamic evaluation (serial scores over days 3–7) predicts prognosis more accurately than static scores.
📊 Scoring Tools Comparison:
| Score | Includes the Brain, Kidney, Liver, and Respiratory | Lactate | Use |
|---|---|---|---|
| NACSELD | ✅ | ❌ | Easy bedside tool |
| CLIF-C ACLF | ✅ | ✅ | Dynamic, good predictive value |
| AARC | ✅ | ✅ | Widely used in Asia |
🩺 3. Organ-Specific Management of Acute-on-Chronic Liver Failure
Each organ has distinct recommendations. Here’s a focused breakdown:
🧠 Understanding Brain Involvement in Acute-on-Chronic Liver Failure (Hepatic Encephalopathy)
One of the earliest and most alarming signs of Acute-on-Chronic Liver Failure is when the brain starts to slow down. Family members often notice confusion, odd behaviour, or sudden sleepiness. In the hospital, we call this hepatic encephalopathy (HE) — a direct result of toxins building up in the bloodstream when the liver is unable to clear them.
We assess the severity using two clinical tools: the West Haven criteria and the Glasgow Coma Scale (GCS). If a patient reaches Grade 3 or 4 HE on West Haven (meaning they’re very confused, disoriented, or even unresponsive), or if their GCS drops below 8, it means the brain is significantly affected, and they often require ICU care and airway protection.
But not all confusion is caused by liver toxins. If it’s the first episode of altered mental status, or if a patient doesn’t respond to typical HE treatment, we always investigate other possibilities — things like alcohol withdrawal, stroke, or head injury. We don’t assume it’s just “liver-related.”
For treatment, we usually start with lactulose — either orally or rectally — to help remove toxins from the gut. If the patient is bloated or can’t tolerate lactulose, we may use polyethene glycol instead. Rifaximin, a commonly used antibiotic to prevent recurrent HE, is still being studied in critically ill Acute-on-Chronic Liver Failure patients and isn’t a standard add-on at this stage.
If the patient becomes unresponsive or needs to be put on a ventilator, we use short-acting sedatives like propofol or dexmedetomidine, which don’t linger in the body and allow us to reassess brain function sooner.
One thing we avoid: doing routine brain scans or checking ammonia levels unless there’s a strong reason. If the clinical picture fits the usual pattern of HE, and there’s no suspicion of other causes, these tests usually don’t change management.
💧 Kidney Involvement in Acute on Chronic Liver Failure (Hepatorenal Syndrome–AKI)
In patients with acute or chronic liver failure, kidney failure is one of the most frequent and serious complications. Many arrive at the hospital with reduced urine output or rising creatinine levels, even though their kidneys were functioning reasonably well just days before. This is a condition called Hepatorenal Syndrome–Acute Kidney Injury (HRS-AKI). It’s not because the kidneys are damaged directly, but because the failing liver creates circulatory changes that severely affect kidney function.
Our first step in managing HRS-AKI is to stop any diuretics the patient may be on, address any precipitating infections, and perform a volume challenge using intravenous albumin. This is usually given at a dose of 1 gram per kg body weight, up to a maximum of 100 grams per day, over 48 hours. If there is no improvement after this initial resuscitation, we move to vasoconstrictor therapy — but only in patients who meet criteria for Stage 2 or higher HRS-AKI, and who do not have contraindications.
These patients receive a combination of vasoconstrictors (to improve kidney blood flow) and albumin (20–40 grams per day). The most commonly used medication is terlipressin, either in intermittent doses or as a continuous infusion. However, terlipressin is avoided in patients with severe acute or chronic liver failure (ACLF Grade 3) or those with significant heart or lung disease. In patients with circulatory shock, norepinephrine is often the preferred agent.
If pharmacological treatment fails, renal replacement therapy (RRT) — such as dialysis — may be considered. But in the setting of acute or chronic liver failure, we use RRT only when the patient is already listed for liver transplant or is being actively evaluated. Starting dialysis in a patient who is not a transplant candidate often does not improve outcomes and may add to the burden of critical care.
Ultimately, a liver transplant is the definitive treatment for HRS-AKI in the context of acute on chronic liver failure. However, this decision is never made in isolation — we always assess how many other organs are failing, and whether the overall clinical picture supports transplant candidacy.
🫁 Respiratory Involvement in Acute on Chronic Liver Failure
Breathing difficulties are not uncommon in patients with acute or chronic liver failure, and they can arise from multiple causes, some related to the liver itself. Conditions like hepatic hydrothorax, massive ascites, or hepatopulmonary syndrome can lead to low oxygen levels and significant respiratory distress. In such cases, our first step is to identify and treat the specific complication, for example, draining fluid from the abdomen (paracentesis) when it’s compromising lung expansion.
If a patient is struggling to maintain oxygen levels, we often start with high-flow nasal cannula (HFNC) therapy. It’s less invasive than a ventilator but still delivers a good amount of oxygen and helps reduce the effort of breathing. However, this requires close monitoring — if the patient remains tachypneic or their oxygen levels don’t improve, we may have to escalate to mechanical ventilation.
Now, when a patient with Acute-on-Chronic Liver Failure does need a ventilator, how we set it up matters a lot. We use what’s called a lung protective strategy — low tidal volumes (around 6 mL per kg of predicted body weight) and keeping the plateau pressure under 30 cm H₂O. This minimises further lung injury, especially important in critically ill patients who are already vulnerable.
In cases where acute lung injury (ALI) is present, the approach becomes even more tailored. For mild ALI (oxygen ratio between 200–300), we go with a low PEEP (positive end-expiratory pressure) setting to avoid reducing venous return and cardiac preload, which is especially sensitive in cirrhotic patients. But if the ALI is moderate to severe (oxygen ratio less than 200), we may have to increase the PEEP to improve oxygenation, even though it comes with some hemodynamic trade-offs.
Our goal is always the same: support the lungs without harming the heart, kidneys, or liver any further — a careful balance that requires minute-to-minute adjustments in the ICU.
🩸 Bleeding, Clotting, and the Confusion Around INR in Acute on Chronic Liver Failure
In patients with acute or chronic liver failure, bleeding and clotting issues can be extremely confusing, not just for families, but often even for clinicians who are unfamiliar with how the liver affects the body’s coagulation system. One of the most misunderstood lab values in this setting is the INR (International Normalised Ratio). Many assume that a high INR automatically means the patient is at a high risk of bleeding, but in cirrhosis and Acute-on-Chronic Liver Failure, this is simply not true.
The bleeding risk in these patients is not determined by INR alone. INR does not accurately reflect the real balance between clotting and bleeding in patients with advanced liver disease. That’s because the liver produces both pro-clotting and anti-clotting factors, and in cirrhosis, both sets are reduced, often balancing each other out in unpredictable ways.
We now know that more advanced tools — like viscoelastic tests (e.g., TEG or ROTEM) or thrombin generation assays — give a more accurate picture of the patient’s overall hemostatic state. However, these are still not widely available or validated enough for routine use. So we often rely on clinical judgment and the overall picture, especially when procedures or bleeding concerns arise.
When it comes to anticoagulation, especially for conditions like portal vein thrombosis or venous thromboembolism, research shows that patients with cirrhosis — even those with abnormal INRs — don’t necessarily bleed more than the general population. However, in patients with very low platelet counts (less than 50,000), decisions around starting blood thinners must be taken case-by-case, carefully weighing the risk of bleeding versus the benefit of preventing or treating dangerous clots.
So while bleeding is a concern in acute or chronic liver failure, it’s often not as straightforward as it seems. More importantly, not all abnormal labs mean the patient will bleed, and not all clotting risks should be ignored. It’s about balance, and in Acute-on-Chronic Liver Failure, that balance is fragile and dynamic.
❤️ Circulatory Collapse in Acute on Chronic Liver Failure
One of the most critical issues we manage in acute-on-chronic liver failure is circulatory collapse — a situation where the patient’s blood pressure drops dangerously low, and vital organs are starved of adequate blood flow. This isn’t just “low BP.” It’s a shock, and it requires immediate, careful intervention.
As soon as a patient reaches the ICU, we begin a baseline assessment of their volume status, perfusion, and heart function. This includes bedside clinical exams and point-of-care echocardiography, especially if the patient is hypotensive or in shock. These tools help us determine whether the patient needs fluids, vasopressors, or both.
When fluids are required, we use a judicious strategy. That means not giving fluids blindly but instead tailoring them based on real-time hemodynamic monitoring. We typically use balanced crystalloids like lactated Ringer’s solution and, in select cases, intravenous albumin, especially if the patient has ongoing ascites, hypoalbuminemia, or HRS.
Our target is to restore the mean arterial pressure (MAP) to around 65 mm Hg, which is considered adequate for organ perfusion, but we don’t stop there. We continue to assess end-organ response, like kidney function, mental status, and urine output. If needed, we insert invasive monitors (arterial lines and central venous catheters) to guide vasopressor support more precisely.
When medications are required to support blood pressure, norepinephrine is our first choice. It effectively tightens the blood vessels to raise pressure without overburdening the heart. If the blood pressure doesn’t stabilise with norepinephrine alone, we may add vasopressin as a second-line agent to enhance vasoconstriction and reduce norepinephrine requirements.
In cases of refractory shock, where even high-dose vasopressors are not enough, we sometimes consider adrenal insufficiency as a hidden cause. In such situations, we may initiate an empiric trial of intravenous hydrocortisone — typically 50 mg every 6 hours or as a 200 mg daily infusion — for up to 7 days or until ICU discharge.
This phase of hemodynamic support in Acute-on-Chronic Liver Failure is often delicate and time-sensitive. Every intervention — fluid, medication, monitoring — must be balanced carefully to avoid tipping the patient into further organ failure while keeping transplant options viable.
🦠 Infections in Acute on Chronic Liver Failure: A Hidden Trigger That Can Turn Deadly
One of the most important — and often underestimated — factors in acute-on-chronic liver failure is infection. Even something as seemingly minor as a urinary tract infection or chest infection can act like a matchstick on dry grass, pushing an already fragile patient into multi-organ failure. That’s why in Acute-on-Chronic Liver Failure, we treat infection as a medical emergency, both in terms of finding it and fighting it early.
When a patient with cirrhosis or Acute-on-Chronic Liver Failure is hospitalised — especially if they have symptoms like fever, confusion, new or worsening ascites, kidney issues, or general clinical decline — we immediately start a full infection workup. This usually includes diagnostic paracentesis (to check for spontaneous bacterial peritonitis), blood cultures, urinalysis, urine cultures, and a chest X-ray. If the clinical condition changes at any point — for example if mental status worsens or new organ dysfunction develops — we repeat the infection workup without waiting for obvious signs.
Once we suspect or identify an infection, we start antibiotics right away — but not just any antibiotics. We choose them based on where the infection started, how severe it is, and whether the patient acquired it in the hospital or outside, while also keeping in mind local antibiotic resistance trends. This helps us stay one step ahead of the pathogens.
For patients already diagnosed with Acute-on-Chronic Liver Failure, or those who aren’t improving despite being on antibiotics for 48 hours, we often have to widen the coverage to include multidrug-resistant (MDR) bacteria or even fungal infections, which are increasingly common in ICU settings. These are tricky, and delays in appropriate treatment can be fatal.
We also work hard to prevent infections in the first place. That means limiting the use of proton pump inhibitors (PPIs), which increase the risk of bacterial overgrowth, and avoiding unnecessary urinary catheters (Foleys), which are one of the most common sources of hospital-acquired infections.
In short, infections don’t just complicate Acute-on-Chronic Liver Failure — they often cause it. And the faster we find and treat them, the better the chances we have to stabilise the patient and keep transplant options on the table.
🏥 Liver Transplant in Acute on Chronic Liver Failure: Timing, Triage & Tough Decisions
⏳ When is Liver Transplant Considered?
In some patients with acute-on-chronic liver failure, an expedited liver transplant (LT) can be life-saving, but it has to be the right patient, at the right time.
🚨 Transplant isn’t always possible, even when the liver is failing. That decision depends on:
- The number and type of organs involved
- Whether the patient is stable enough to undergo surgery
- Reversibility of the current organ failures
- The availability of a liver
- ICU resources and team readiness for fast-tracking transplant
🧪 There’s no perfect score that tells us exactly who will survive and who won’t — we make this decision daily based on clinical judgment, experience, and continuous reassessment.
The success rate of liver transplantation for Acute-on-Chronic Liver Failure (ACLF) has improved significantly over the years due to advances in surgical techniques and critical care. While ACLF patients are often critically ill with multiple organ failures, timely transplantation offers a strong chance of survival, with one-year survival rates commonly reported between 75% to 80%. Early evaluation and proper patient selection remain crucial to maximise outcomes, making liver transplants a life-saving option for many suffering from ACLF.
🛑 What is “Futility of Care”?
If a patient is not a transplant candidate — due to irreversible multi-organ failure or involvement of “futility organs” (lungs and circulation) — we may reach a point where continuing aggressive ICU care is not beneficial.
This doesn’t mean we give up.
It means we shift focus to comfort, dignity, and supportive care, and guide families with honesty and compassion.
🔍 Key Points:
- High MELD, lactate >9 mmol/L, FiO₂/PaO₂ <150 = poor outcomes.
- Assess for futility using NACSELD (≥2 OFs = ~3% 28-day survival) or CLIF-C >70 = ~90% mortality.
Contraindications for Liver Transplant in Acute-on-Chronic Liver Failure:
- Severe respiratory failure.
- Lactate >9 mmol/L.
- Ventilatory support >72h with encephalopathy.
- Progressive vasopressor needed.
- Active sepsis.
🍽️ Nutrition in Acute on Chronic Liver Failure
👥 Team Involvement:
Early referral to a nutrition support team
⚖️ Weight for Calculation:
Use ideal body weight, not actual weight (due to ascites/fluid retention)
🍛 Caloric Target:
Start with 12–25 kcal/kg/day
• Use a higher range in non-obese
• Increase gradually as the condition improves
🥩 Protein Needs:
1.2–2.0 g/kg/day (ideal body weight)
🚫 No protein restriction
🧃 Route of Feeding:
Enteral nutrition is preferred over parenteral
(unless there’s a clear contraindication)
⚠️ Feeding Precaution:
Hold enteral feeds if on high-dose vasopressors
(e.g., norepinephrine > 0.15 µg/kg/min)
🧪 Refeeding Syndrome Risk:
Watch for low potassium, phosphate, and arrhythmias
Use routine electrolyte and ECG monitoring in malnourished patients
🩸 Blood Sugar Target:
Maintain glucose between 140–180 mg/dL (7.8–10 mmol/L)
Prevention of Acute-on-Chronic Liver Failure
- Avoid unnecessary PPIs.
- Minimise catheter use.
- Vaccinate against HAV, HBV, pneumococcus, and influenza.
- SBP prophylaxis when indicated.
- Avoid sedatives and opiates; prevent aspiration.
🧭 Final Words: When Every Hour Matters
If you’re reading this because your loved one has been diagnosed with acute-on-chronic liver failure, I know the ground beneath your feet may feel like it’s crumbling. One minute, they were doing okay, and the next, they were in the ICU, surrounded by machines, numbers, alarms, and endless medical terms.
As someone who’s stood at the bedside of hundreds of such patients — resuscitating, stabilising — let me tell you this:
You are not powerless.
Understanding what’s happening is the first step toward making strong, informed decisions. Whether it’s asking the right questions about transplant candidacy, understanding organ support, or simply knowing what “futility” truly means, knowledge gives you footing.
Acute-on-Chronic Liver Failure is fast, fierce, and unpredictable.
But with the right care, timely decisions, and a coordinated team, recovery is still possible.
Some patients make it to transplant. Some recover without it. And in some cases, we must pivot toward peace, comfort, and presence.
Whatever your journey looks like, I hope this blog helps you feel more anchored in a moment when everything else feels out of control.
You’re not alone in this.
Dr. Tanuja Mallik
Liver Transplant Anaesthetist | Critical Care Specialist
Founder – Dr. Tanuja Mallik Wellness Venture
Frequently Asked Questions
What is Acute-on-Chronic Liver Failure (ACLF)?
Acute-on-Chronic Liver Failure (ACLF) is a complex condition that occurs in patients with chronic liver disease (usually cirrhosis) when they experience an acute deterioration, leading to the failure of one or more organs. It is associated with high short-term mortality. The sources highlight that ACLF is a significant healthcare burden, with varying definitions and scoring systems used globally to assess its severity and predict outcomes.
Different consortiums, such as the European Association for the Study of the Liver (EASL) – Chronic Liver Failure (CLIF), the North American Consortium for the Study of End-Stage Liver Disease (NACSELD), and the Asian Pacific Association for the Study of the Liver (APASL), have developed their diagnostic criteria and scoring systems (like CLIF-C ACLF, NACSELD ACLF, and AARC ACLF) based on factors such as organ failures (liver, kidney, cerebral, respiratory, coagulation, cardiovascular), age, white blood cell count, albumin, and lactate.
How is altered mental status managed in critically ill patients with cirrhosis?
Altered mental status in critically ill patients with cirrhosis is often due to hepatic encephalopathy (HE), but it is crucial to consider other causes such as alcohol intoxication and withdrawal, drug-related issues, infections, metabolic disorders (like diabetic ketoacidosis), intracranial bleeding, non-epileptic seizures, and psychiatric disorders. Initial management involves investigating and treating potential precipitating factors. Empiric therapy with lactulose is recommended if no obvious alternative cause is immediately apparent.
For patients with severe HE (Grade 3 or 4), lactulose enema may be considered. Polyethene glycol is another alternative to lactulose, especially in the ICU setting, potentially reducing the risk of ileus. Short-acting sedatives like propofol or dexmedetomidine are preferred for intubated patients requiring sedation. Routine brain imaging and ammonia level testing are generally not recommended for diagnosis in typical HE presentations.
What are the key considerations for managing cardiovascular failure in critically ill patients with cirrhosis?
Critically ill patients with decompensated cirrhosis often have hyperdynamic circulation with low blood pressure and increased cardiac output, which can worsen with inflammation in ACLF. Assessment of volume status, cardiac function, and fluid responsiveness is essential. Bedside echocardiography can help evaluate fluid and cardiac status. Fluid resuscitation with balanced crystalloids and/or albumin is recommended, with careful monitoring to avoid fluid overload. For patients with septic shock, a mean arterial pressure (MAP) target of 65 mm Hg is suggested, with individualised targets based on assessment of end-organ perfusion. Norepinephrine is the recommended first-line vasopressor, with vasopressin as a second-line agent. Considering adrenal insufficiency, an empiric trial of hydrocortisone may be necessary for refractory shock.
What ventilatory strategies are recommended for critically ill patients with cirrhosis and respiratory failure?
Management of respiratory failure in critically ill patients with cirrhosis involves investigating and treating coexisting pulmonary issues like hydrothorax, ascites, or hepatopulmonary syndrome, with therapeutic thoracentesis/paracentesis if needed. High-flow nasal cannula (HFNC) therapy can be considered for acute hypoxemic respiratory failure, with close monitoring for escalation to invasive mechanical ventilation.
For patients requiring mechanical ventilation for reasons other than acute lung injury (ALI), a lung protective strategy with low tidal volumes (6-10 mL/kg predicted body weight) and low plateau pressures is advocated. In the setting of ACLF with ALI requiring mechanical ventilation, a stricter lung protective strategy with low tidal volume (6 mL/kg PBW) and low plateau pressure (<30 cm H2O) is recommended. The use of positive end-expiratory pressure (PEEP) should be considered carefully, with a low PEEP strategy for mild ALI and potentially a higher PEEP strategy for moderate-severe ALI, while monitoring for hemodynamic side effects.
How is acute kidney injury (AKI) managed in patients with cirrhosis, particularly Hepatorenal Syndrome (HRS-AKI)?
AKI in patients with cirrhosis can stem from structural causes (like acute tubular necrosis) or, more commonly, functional causes related to hemodynamic abnormalities, such as Hepatorenal Syndrome (HRS-AKI). Differentiating these causes can be challenging. Diagnostic criteria for HRS-AKI include cirrhosis with ascites, at least Stage 2 AKI, lack of response to diuretic withdrawal and albumin volume expansion, absence of shock or nephrotoxic drugs, and no evidence of parenchymal kidney disease. Initial management involves withdrawing diuretics, treating precipitating factors (like infections), and administering a volume challenge with intravenous albumin (1 g/kg body weight, maximum 100 g/day for 48 hours).
If this doesn’t reverse Stage 2 or higher HRS-AKI, vasoconstrictor therapy with albumin (20-40 g/day) is recommended, provided there are no contraindications. Terlipressin is a primary vasoconstrictor used, but caution is advised in patients with ACLF-3 or significant cardiopulmonary disease. Norepinephrine is an alternative, particularly in the setting of shock.
What are the considerations for coagulation management and venous thromboembolism (VTE) treatment in patients with cirrhosis?
Patients with cirrhosis have a complex hemostatic balance and are at increased risk of both bleeding and VTE. While the INR (international normalised ratio) is often elevated, it is not a reliable indicator of bleeding risk in cirrhosis. Global tests of hemostasis, like thromboelastography, may better capture the hemostatic status but are not yet clinically validated. Despite the theoretical risk of bleeding, therapeutic anticoagulation for VTE in patients with cirrhosis appears to have similar non-portal hypertensive bleeding complication rates compared to the general population.
Low molecular weight heparin (LMWH) is favoured for VTE treatment. Direct-acting oral anticoagulants (DOACs) are generally contraindicated in patients with Child-Turcotte-Pugh Class C cirrhosis due to liver metabolism. Decisions regarding anticoagulation in patients with severe thrombocytopenia (<50,000) should be made on a case-by-case basis.
What is the role of liver transplantation (LT) in critically ill patients with cirrhosis and ACLF?
Liver transplantation is the definitive treatment for HRS-AKI and can be considered for critically ill patients with cirrhosis and ACLF, especially those with high MELD scores and multiorgan failure who are considered LT candidates. However, waitlist mortality for these patients is high, and only a minority ultimately undergo transplants. While some predictive models exist, identifying which critically ill patients with ACLF will benefit from LT remains a challenge. Patients with HRS-AKI who fail pharmacotherapy and are LT candidates should be referred for evaluation without delay. In some cases, a simultaneous liver-kidney transplant may be considered for patients with prolonged pre-transplant renal replacement therapy.
Why is palliative care important in critically ill patients with cirrhosis and ACLF?
Palliative care plays a crucial role in the management of critically ill patients with cirrhosis and/or ACLF, irrespective of transplant listing status. Given the high mortality rates and the burden of symptoms, early integration of palliative care principles is essential. This includes discussing goals of care, defining and explaining prognosis, identifying surrogate decision-makers, and documenting medical power of attorney and code status. Palliative care or hospice should be offered to patients with a limited prognosis and those who are not candidates for potentially life-sustaining interventions like liver transplantation or renal replacement therapy. This approach aims to improve quality of life, manage symptoms, and support patients and their families through the trajectory of their illness.