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Creutzfeldt-Jakob Disease (CJD)

Management Team

Creutzfeldt-Jakob Disease (CJD)

Overview

CJD is a life-threatening and rare neurodegenerative brain disorder. It can be sporadic, familial (inherited), iatrogenic (acquired) or variant (infection). The symptoms progress rapidly causing deterioration in sensorium and encephalopathy, usually terminating fatally within 6–12 months.

It is caused due to misfolding of prion protein

  • Rapidly progressive dementia
  • Behaviour changes
  • Hallucinations
  • Jerky movements/ myoclonus
  • Balance and coordination dysfunction
  • Speech impairment

  • Age. Sporadic CJD occurs around 60 years of age. Familial CJD is presented slightly earlier, whereas Variant Creutzfeldt-Jakob disease (vCJD) affects individuals usually in their late 20s.
  • Genetic changes that cause the disease
  • Exposure to contaminated tissue
  • Eating contaminated beef

Neurologist

  • EEG to determine bilateral periodic epileptiform discharges typically repeating at 1–1.5 seconds
  • CSF examination for biomarkers like 14-3-3, RT-QuIC for sporadic CJD
  • MRI to determine cortical ribboning and inverse hockey stick sign
  • Brain biopsy

  • No specific treatment
  • Symptomatic control of seizures and myoclonus
  • Supportive care for pain relief
  • Palliative care
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Corticobasal Degeneration (CBD)

Management Team

Corticobasal Degeneration (CBD)

Overview

CBD, also referred to as corticobasal syndrome, is a progressive and rare neurodegenerative disease, which generally starts between the age of 60–70 years.

It is caused due to abnormal deposition of Tau proteins in aging brain.

  • Asymmetrical loss of motor function, affecting one side more than the other
  • Axial rigidity with slowing of movements
  • Abnormal posturing of limbs (dystonia of hand/ leg)
  • Muscle twitches or jerks
  • Alien limb phenomenon- feeling that your hand has a mind of its own
  • Difficulty in doing learned motor activities (apraxia)
  • Difficulty in speech and language

  • Unknown

Neurologist

  • Clinical examination - to rule out Parkinson’s disease or other Parkinson plus syndromes
  • MRI brain to look for specific areas of atrophy
  • PET scan to detect areas of abnormalities

  • No curative treatment
  • Medication like levodopa to improve the slow movement
  • Medications to manage myoclonus
  • Physiotherapy, speech and occupational therapy
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Coma

Management Team

Coma

Overview

Coma refers to a deep state of unconsciousness characterized by lack of:

  • Response to stimuli
  • Voluntary movements
  • Meaningful verbal/visual response to sound
  • Sleep-wake cycle

  • Traumatic brain injury
  • Stroke and other vascular disorders
  • Meningitis and encephalitis
  • Metabolic disorders like hypoglycaemia or hyperglycaemia
  • Toxins
  • Mass lesions in brain
  • Hypoxic brain damage

  • An ischemic or haemorrhagic stroke
  • Serious brain infection of brain damage
  • Seizures
  • Brain cancer
  • Hypoxia
  • Metabolic disorders, such as hypoglycaemia and diabetic hyperosmolar coma
  • Toxins include poisons, alcohol, and other drugs (cocaine, barbiturates, sedatives)
  • Failure of the liver or kidneys

Neurologist

  • Clinical examination
  • EEG- shows slowing of background
  • Abnormal evoked potentials

Its severity is determined using Glasgow coma scale score:

  • 3–8 : Severe coma
  • 9–12: Moderate coma
  • 13–15: Mild coma

  • Supportive measures
  • Management of secondary complications
  • Treatment of underlying pathology
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Cluster Headache

Management Team

Cluster Headache

Overview

Cluster headache refers to a trigeminal autonomic cephalalgia affecting middle-aged males. It is a unilateral (on one side) excruciating headache and tends to recur during a particular time of the year and continues for a few days to a few months.

  • The exact cause is unknown
  • Sudden release of histamines or serotonin

  • Family history
  • Smoking
  • Alcohol consumption
  • Male sex
  • Head trauma

  • Rapid onset headache, reaching maximum intensity within 5–10 minutes
  • Always occurs on the same side
  • Lasts for 30–90 minutes
  • Attacks often recur approximately during the similar times in the day and around same time of the year
  • Attacks continue for 2 weeks to 3 months and the patient remains pain free between these periods
  • Severe pain around the eye associated with redness, tearing, nasal discharge, forehead and facial sweating with change in skin colour on the side of the headache
  • Occasionally associated with drooping of eyelid

Neurologist

Clinical examination

  • Abortive medication for instant pain relief
  • High flow oxygen therapy
  • Prophylactic medication to decrease frequency and intensity of pain
  • Lifestyle modification to avoid triggers
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C

Viral Hepatitis

Management Team

Viral Hepatitis

Overview

Viral hepatitis refers to inflammation of the liver caused by a viral infection. The most common types are Hepatitis A, B, C, D, and E, each caused by different viruses. While all types cause liver inflammation, they differ in transmission, severity, and treatment options.

Each type of viral hepatitis has a unique cause and mode of transmission:

  • Hepatitis A:
    • Caused by the hepatitis A virus (HAV).
    • Spread primarily through contaminated food or water, often in places with poor sanitation or through close contact with infected individuals.
  • Hepatitis B:
    • Caused by the hepatitis B virus (HBV).
    • Spread through blood, semen, or other body fluids, and can be transmitted via sexual contact, sharing needles, or from mother to child during childbirth.
  • Hepatitis C:
    • Caused by the hepatitis C virus (HCV).
    • Primarily spread through blood-to-blood contact, most commonly through sharing needles or receiving contaminated blood products. Sexual transmission is also possible but less common.
  • Hepatitis D:
    • Caused by the hepatitis D virus (HDV), which only infects people already infected with hepatitis B.
    • Spread in the same way as HBV, through blood and body fluids.
  • Hepatitis E:
    • Caused by the hepatitis E virus (HEV).
    • Spread primarily through contaminated water in areas with poor sanitation, similar to hepatitis A.

  • Hepatitis A:
    • Travel to regions with poor sanitation.
    • Close contact with infected individuals.
    • Poor hygiene practices, such as inadequate handwashing.
  • Hepatitis B:
    • Unprotected sex with an infected person.
    • Sharing needles or personal items (razors, toothbrushes).
    • Healthcare workers or others exposed to blood.
    • Birth to an infected mother.
    • Chronic kidney disease or dialysis patients.
  • Hepatitis C:
    • Sharing needles or drug paraphernalia.
    • Receiving blood products or organ transplants before the 1990s (before blood screening for HCV).
    • Unprotected sex, especially with multiple partners.
    • Tattooing or body piercings with unsterile equipment.
    • Healthcare workers exposed to blood.
  • Hepatitis D:
    • People already infected with hepatitis B are at risk.
    • Sharing needles, unprotected sex, or healthcare-related exposures.
  • Hepatitis E:
    • Travel to areas with poor sanitation (e.g., parts of Asia, the Middle East, and Africa).
    • Consumption of contaminated water or undercooked meat (especially pork or deer).
    • Poor hygiene practices.

Symptoms of viral hepatitis can vary, ranging from mild to severe. In many cases, especially in the early stages, hepatitis can be asymptomatic. When symptoms do occur, they may include:

  • Fatigue
  • Jaundice
  • Abdominal pain, particularly in the upper right side (over the liver)
  • Loss of appetite
  • Nausea and vomiting
  • Dark urine
  • Light-colored stools
  • Fever
  • Joint pain

The severity and presentation of symptoms differ depending on the type of hepatitis:

  • Hepatitis A: Often causes acute symptoms with jaundice, fatigue, and gastrointestinal distress, but generally resolves within a few months.
  • Hepatitis B: Acute infection can cause severe illness, but chronic infection may have no symptoms for years before leading to cirrhosis or liver cancer.
  • Hepatitis C: Often causes a long-term, chronic infection without symptoms until significant liver damage occurs.
  • Hepatitis D: Occurs only in people with hepatitis B and can worsen the course of hepatitis B infection, leading to more severe liver disease.
  • Hepatitis E: Typically causes acute illness with symptoms similar to hepatitis A, but can be severe in pregnant women, especially in the third trimester.

Diagnosing viral hepatitis typically involves a combination of blood tests, imaging studies, and sometimes liver biopsy. The diagnostic process includes:

  • Blood tests:
    • Liver function tests: Elevated liver enzymes (ALT, AST) suggest liver inflammation.
    • Hepatitis-specific antibodies and antigens: These blood tests help identify the specific virus causing the infection (e.g., anti-HAV IgM for hepatitis A, HBsAg for hepatitis B).
    • Polymerase chain reaction (PCR): Used to detect viral RNA (in hepatitis C, for example) or to quantify the level of the virus.
    • HCV genotype: Determines which strain of hepatitis C is present, which can influence treatment.
  • Imaging:
    • Ultrasound: Can help evaluate the liver for signs of scarring (fibrosis) or cirrhosis.
    • CT scan or MRI: Used for more detailed assessment if necessary.
  • Liver biopsy:
    • In cases of chronic infection, a biopsy may be needed to assess liver damage, especially for hepatitis B or C.

Treatment varies by type of viral hepatitis:

  • Hepatitis A:
    • There is no specific antiviral treatment for hepatitis A.
    • Supportive care: Rest, hydration, and a healthy diet help manage symptoms.
    • Vaccination: The hepatitis A vaccine is highly effective in preventing infection.
  • Hepatitis B:
    • Acute cases generally resolve without treatment, but chronic hepatitis B may require antiviral medications to prevent liver damage. These include:
    • Nucleos(t)ide analogs (e.g., entecavir, tenofovir).
    • Interferon therapy (less common).
    • Vaccination: A highly effective vaccine is available to prevent hepatitis B infection.
  • Hepatitis C:
    • Direct-acting antivirals (DAAs): Highly effective oral medications, such as sofosbuvir, ledipasvir, and velpatasvir, can cure most people with chronic hepatitis C. The treatment duration is typically 8-12 weeks.
    • No vaccine: Currently, there is no vaccine for hepatitis C, though new treatments have made the disease curable.
  • Hepatitis D:
    • Treatment for hepatitis D usually involves antiviral medications for hepatitis B, as it is dependent on the hepatitis B virus for replication.
    • Pegylated interferon may be used in some cases, but treatment can be complex.
    • Vaccination: Vaccination for hepatitis B can prevent hepatitis D, as it only occurs in those already infected with HBV.
  • Hepatitis E:
    • In most cases, hepatitis E resolves on its own without specific treatment.
    • Supportive care: Includes rest and hydration.
    • In severe cases, especially for pregnant women, antiviral therapy (e.g., ribavirin) may be considered.
    • No vaccine is available in many countries, but vaccines exist in some regions.

  • Vaccination:
    • Hepatitis A and Hepatitis B vaccines are widely available and highly effective in preventing infection.
  • Safe practices:
    • Avoid sharing needles or personal items (razors, toothbrushes) that may be contaminated with infected blood.
    • Practice safe sex, especially with new or multiple partners.
  • Improving Sanitation:
    • Ensuring clean drinking water and proper food hygiene can prevent hepatitis A and E.
  • Screening:
    • Routine screening for hepatitis B and C is recommended for high-risk groups, including people with a history of injection drug use or unprotected sex.
    • By focusing on prevention, early detection, and effective treatment, many cases of viral hepatitis can be managed successfully.
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V

Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)

Management Team

Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)

Overview

CIDP is a rare acquired autoimmune neuropathy affecting the peripheral nerves. Sometimes it occurs secondary to infections or vaccination, when the body recognizes self-proteins as foreign and forms antibodies against them. As a result, the myelin sheath around the nerves gets damaged, ultimately leading to neuronal loss.

CIDP is caused by an abnormal immune response

  • Age between 40 and 60 years
  • Male sex 
  • Uncontrolled type 2 diabetes
  • Infections such as HIV, hepatitis B, and Epstein-Barr infections 
  • Acute illnesses, vaccinations, and surgery can trigger CIDP

  • Muscle weakness, which is subacute in onset and sometimes waxes and wanes
  • Numbness of hands and feet
  • Sensory loss
  • Imbalance
  • Bilaterally symmetrical

  • Sensory CIDP
  • Multifocal CIDP (Lewis Sumner syndrome)
  • Motor CIDP
  • CISP- Chronic immune sensory polyradiculopathy
  • Distal CIDP (DADS)

Neurologist

  • Clinical examination and nerve conduction studies, which shows slowing of nerve conduction
  • Blood tests for antibodies and inflammatory markers

  • Corticosteroids to reduce inflammation
  • Immunomodulation by drugs like azathioprine, cyclophosphamide, IvIg, Rituximab, plasmapheresis
  • Physical therapy and rehabilitation
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C

Nonalcoholic Fatty Liver Disease (NAFLD)

Management Team

Nonalcoholic Fatty Liver Disease (NAFLD)

Overview

Nonalcoholic Fatty Liver Disease (NAFLD) refers to the accumulation of excess fat in the liver in people who consume little or no alcohol. It is a spectrum of liver conditions, which can progress from simple fatty liver (steatosis) to more severe forms like nonalcoholic steatohepatitis (NASH), cirrhosis, and even liver cancer.

The exact cause of NAFLD is not fully understood, but several factors contribute to its development:

  • Insulin resistance: The liver becomes more likely to store fat when the body becomes resistant to insulin. This is often associated with obesity, type 2 diabetes, and metabolic syndrome.
  • Obesity: Excess body fat, especially abdominal fat, significantly increases the risk of NAFLD.
  • Poor diet: Diets high in sugars, refined carbohydrates, and unhealthy fats can contribute to fat buildup in the liver.
  • Genetics: Genetic factors can predispose individuals to develop NAFLD, though the exact genes involved are still being studied.
  • Metabolic syndrome: Conditions like high blood pressure, high cholesterol, and high triglycerides can increase the likelihood of developing NAFLD.
  • Medications: Certain medications, such as corticosteroids, some cancer drugs, and anti-retroviral drugs, can contribute to the development of fatty liver.

Several factors increase the likelihood of developing NAFLD:

  • Obesity: Overweight individuals are at higher risk, especially those with a higher amount of abdominal fat.
  • Type 2 diabetes: Insulin resistance associated with diabetes often contributes to the development of fatty liver disease.
  • High cholesterol or triglycerides: People with dyslipidaemia (abnormal levels of fats in the blood) have an increased risk.
  • Sedentary lifestyle: Lack of physical activity can contribute to obesity and insulin resistance, both of which are risk factors for NAFLD.
  • Age: The risk increases with age, especially in individuals over 40.
  • Gender: Men are more likely to develop NAFLD, but postmenopausal women also have an elevated risk.
  • Genetics: Family history of NAFLD or other liver diseases increases the risk.
  • Other medical conditions: Conditions such as polycystic ovary syndrome (PCOS), hypothyroidism, and sleep apnea can increase the risk.

In the early stages, NAFLD often does not cause noticeable symptoms. However, as the condition progresses, some individuals may experience:

  • Fatigue
  • Abdominal discomfort or pain (especially in the upper right side of the abdomen)
  • Weight loss (in advanced stages)
  • Enlarged liver (hepatomegaly), which can be detected during a physical examination.
  • Jaundice in advanced cases with cirrhosis.
  • However, many individuals with NAFLD may remain asymptomatic until the disease reaches more severe stages, such as cirrhosis.

  • Blood tests: These can check for liver enzyme levels (ALT, AST) and other markers of liver function. While abnormal results may indicate liver damage, they are not conclusive for diagnosing NAFLD.
  • Imaging tests:
    • Ultrasound: The most common method for detecting fat in the liver. It’s non-invasive and can show liver enlargement or fatty changes.
    • CT Scan or MRI: These can also detect fat accumulation and assess liver structure.
  • Liver biopsy: If NASH or cirrhosis is suspected, a liver biopsy may be performed to assess the extent of liver damage. A biopsy is the gold standard for diagnosing NASH and determining the severity of liver damage.
  • FibroScan (Transient Elastography): This test measures liver stiffness, which is an indicator of fibrosis (scarring of the liver). It can help assess the extent of liver damage.

There is no FDA-approved medication specifically for treating NAFLD, but management focuses on lifestyle changes, monitoring, and treating related conditions.

  • Weight loss:
    • Diet: A balanced, healthy diet is essential. Low-calorie, low-fat diets, and diets high in fruits, vegetables, and whole grains are recommended. Reducing sugar intake, especially refined carbs, is important.
    • Exercise: Regular physical activity can help reduce liver fat, improve insulin sensitivity, and reduce obesity.
  • Control of risk factors:
    • Diabetes management: Keeping blood sugar levels under control is crucial.
    • Lowering cholesterol/triglycerides: Statins or other lipid-lowering medications may be prescribed if high cholesterol or triglycerides are present.
    • Blood pressure control: Managing hypertension can reduce the risk of complications.
  • Medications:
    • While no specific drugs for NAFLD exist, certain treatments may be used to manage related conditions:
    • Vitamin E may be prescribed for individuals with NASH (though it’s not suitable for everyone).
    • Pioglitazone (a diabetes medication) can sometimes be used in NASH with insulin resistance.
    • Avoiding alcohol and hepatotoxic drugs: People with NAFLD should avoid alcohol, which can worsen liver damage. Additionally, certain drugs that can stress the liver should be avoided.
  • Liver transplant: In cases of cirrhosis or end-stage liver failure, a liver transplant may be necessary.

Healthy lifestyle choices are the most effective way to prevent NAFLD. This includes maintaining a healthy weight, eating a balanced diet, exercising regularly, and managing underlying conditions such as diabetes and high blood pressure.

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N

Acute-on-chronic Liver Failure (ACLF)

Management Team

Acute-on-chronic Liver Failure (ACLF)

Overview

Acute-on-chronic liver failure (ACLF) is a severe and life-threatening condition characterised by the rapid deterioration of liver function in patients with pre-existing chronic liver disease. ACLF is distinct from general liver failure as ACLS exhibits a higher speed of onset, i.e., a rapid decline in liver function—whereas general liver failure can be either acute (rapid loss of liver function) or chronic (gradual loss of liver function)—causes multiple organ failure (kidney, liver, heart, brain, lungs) by inducing intense systemic inflammation (across the body).

ACLF typically occurs in individuals who have preexisting chronic liver disease, such as cirrhosis. The acute deterioration of liver function can be triggered by various factors, including:

  • Infections:
    • Bacterial infections: Spontaneous bacterial peritonitis (SBP), pneumonia, or urinary tract infections can trigger ACLF.
    • Viral infections: Hepatitis viruses (e.g., Hepatitis B, Hepatitis C) can trigger ACLF.
    • Fungal infections: In immunocompromised individuals with cirrhosis, fungal infections can trigger ACLF.
  • Alcohol abuse: Excessive alcohol consumption or sudden binge drinking can lead to liver injury, precipitating ACLF in patients with pre-existing liver disease.
  • Hepatotoxic drugs: Certain medications (e.g., acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs)) can worsen liver function.
  • Gastrointestinal bleeding: Excessive bleeding from varices (due to portal hypertension) or gastric ulcers can lead to ACLF.
  • Renal (kidney) failure: Pre-existing kidney issues or acute kidney injury (AKI) can worsen liver function, resulting in ACLF.
  • Metabolic disturbances: Electrolyte imbalances, dehydration, or hyperammonemia (a metabolic condition associated with high levels of ammonia in the blood) can exacerbate liver dysfunction.
  • Systemic inflammatory response: Conditions like sepsis, shock, or pancreatitis can trigger a systemic inflammatory response, thereby contributing to liver failure.
  • Hepatic encephalopathy: This condition can complicate the underlying liver disease, leading to ACLF.
  • Presence of comorbidities: Comorbidities, like kidney dysfunction (renal failure), cardiovascular disease, and metabolic disorders can contribute to the worsening of ACLF.
  • Poor nutrition: Malnutrition, which is common in liver disease, can weaken the body’s ability to recover from stressors like infection or injury, thereby enhancing susceptibility to ACLF.
  • Older age: Older patients with chronic liver disease are at higher risk of developing ACLF.

The symptoms of ACLF are related to acute deterioration of liver function as well as the multi-organ failure that can accompany it; these include:

  • Jaundice: This condition occurs due to bilirubin accumulation.
  • Ascites: Fluid accumulation in the abdomen due to liver dysfunction and portal hypertension.
  • Hepatic encephalopathy: Confusion, altered mental status, and in severe cases—coma—due to the inability of the liver to detoxify toxic substances in the blood.
  • Hepatorenal syndrome: Acute kidney failure, marked by low urine output and high levels of creatinine.
  • Gastrointestinal bleeding: Characterised by vomiting blood (hematemesis) or black, tarry stools (melena) due to variceal rupture or ulcers.
  • Fever and infection signs: In ACLF cases triggered by infection, fever, chills, and increased white blood cell counts may be observed.
  • Fatigue and weakness: Generalised malaise and lethargy due to liver and multi-organ failure.
  • Hypotension: Low blood pressure, often due to septic shock or liver dysfunction.

The diagnosis of ACLF is clinical, supported by laboratory tests and imaging. Key diagnostic steps include:

  • Clinical criteria:
    • History of chronic liver disease: The patient typically has a history of chronic liver disease, e.g., cirrhosis.
    • Acute deterioration of liver function: Sudden worsening of liver function, often identified by increasing bilirubin levels and INR (coagulation disorders), and worsening encephalopathy.
  • Blood Tests:
    • Liver function tests: Elevated AST, ALT, and bilirubin levels.
    • Coagulation tests: INR >1.5.
    • Kidney function tests: Creatinine and blood urea nitrogen (BUN) levels to assess renal (kidney) function.
    • Complete blood count (CBC): To check for infection or bleeding.
    • Arterial blood gas (ABG): To assess metabolic acidosis or respiratory dysfunction.
    • Serum ammonia: To assess hepatic encephalopathy.
  • Imaging:
    • Ultrasound: To assess the liver, portal vein, and presence of ascites or masses.
    • CT or MRI: To evaluate liver structure, complications (e.g., tumours, abscesses), and other organ involvement.
    • Endoscopy: To assess oesophageal varices.
  • Assessment of organ function: Multisystem organ failure (kidneys, lungs, cardiovascular system) is often evaluated, as ACLF can involve multiple organs.

The treatment of ACLF focuses on managing the underlying liver disease, treating the acute precipitating factors, and addressing multi-organ failure. The approach includes:

  • Treating the underlying cause(s):
    • Infections: Antibiotics, antivirals, or antifungals depending on the causative pathogen.
    • Alcohol: Systems and medications to enable complete cessation of alcohol consumption.
    • Discontinuation of hepatotoxic drugs: Stopping any drugs or substances that may have contributed to ACLF.
  • Supportive care:
    • Nutritional support: Adequate caloric intake, often through enteral feeding or parenteral nutrition if necessary.
    • Management of ascites: Diuretics (spironolactone, furosemide) to manage fluid accumulation.
    • Hemodynamic support: Intravenous fluids, vasopressors, and monitoring to stabilize blood pressure and manage septic shock if present.
    • Liver Support:
      1. Liver transplantation: The definitive treatment for patients with ACLF who have end-stage liver disease.
      2. Artificial liver support systems: In some cases, devices like the molecular adsorbent recirculating system (MARS) may provide temporary liver support.
  • Management of complications:
    • Lactulose and rifaximin: These drugs reduce ammonia levels in the blood, thereby managing hepatic encephalopathy.
    • Renal replacement therapy: Dialysis may be required for patients with acute kidney failure (hepatorenal syndrome).
    • Endoscopic treatments: For variceal bleeding.
  • Critical care: Intensive care management, including mechanical ventilation, continuous monitoring, and multi-organ support are needed for ACLF patients as the condition can rapidly progress to liver failure.
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A

Portal Hypertension

Management Team

Portal Hypertension

Overview

Portal hypertension refers to increased blood pressure within the hepatic portal system, which includes the portal vein—which carries blood from the digestive organs to the liver—and its branches. Portal hypertension generally arises as a result of liver disease, particularly cirrhosis, but it can also be caused by various other conditions that affect the liver and blood vessels.

The most common cause of portal hypertension is liver cirrhosis as scarring of the liver tissue blocks blood flow, resulting in increased blood pressure. Other causes and risk factors include:

  • Liver fibrosis: Progressive liver damage can lead to increased resistance to blood flow, and by extension, portal hypertension.
  • Schistosomiasis: This parasitic infection that can cause liver fibrosis, and by extension, portal hypertension.
  • Liver tumours: Tumours in the liver (both malignant (cancerous) and benign (non-cancerous) can obstruct blood flow, resulting in portal hypertension.
  • Budd‒Chiari syndrome: This condition—characterised by blockage of the veins that drain blood from the liver—can result in portal hypertension.
  • Non-cirrhotic portal fibrosis: Scarring of the portal vein without cirrhosis can also lead to portal hypertension.
  • Congenital abnormalities: Malformations of the blood vessels, particularly in children can also lead to portal hypertension.

The symptoms of portal hypertension include:

  • Ascites: Accumulation of fluid in the abdomen.
  • Variceal bleeding: Large veins in the oesophagus or stomach can rupture, leading to excessive bleeding.
  • Splenomegaly: Enlarged spleen due to blood pooling.
  • Hepatic encephalopathy: Confusion or altered level of consciousness due to toxins in the brain (often a result of liver failure); sometimes, the patient might also slip into a coma.
  • Caput medusae: Visible distended veins on the abdomen.
  • Portal system collaterals: Development of new blood vessels to bypass blocked areas, which can lead to abnormal blood flow.
  • Fatigue and weakness: Liver dysfunction and decreased blood flow to vital organs can result in fatigue and weakness.

Portal hypertension can be diagnosed using the following modalities:

  • Physical examination: Enlarged spleen (splenomegaly), ascites, or abdominal veins visible.
  • Blood tests:
    • Liver function tests to assess liver damage.
    • Complete blood count (CBC) to look for anaemia or signs of bleeding.
  • Imaging:
    • Ultrasound to detect ascites, enlarged spleen (splenomegaly), and assess liver structure.
    • CT or MRI to visualise liver damage and hepatic blood flow.
    • Endoscopy to detect oesophageal or gastric varices (dilated blood vessels at risk of bleeding).
    • Endoscopic ultrasound to assess the portal vein and surrounding structures.
  • Portal pressure measurement: Hepatic venous pressure gradient (HVPG) is the most accurate test for confirming portal hypertension (measuring the pressure in the portal vein).
  • Liver biopsy: This can confirm liver cirrhosis or other liver conditions.

  • Medical management:
    • Beta blockers: Medications like propranolol or nadolol are used to lower portal pressure and prevent variceal bleeding.
    • Diuretics: They are used to manage ascites by removing excess fluid from the body.
    • Antibiotics: They are used to prevent infections in patients with cirrhosis, especially if ascites is present.
    • Lactulose or rifaximin: They are used to manage hepatic encephalopathy as they reduce toxins in the blood that affect brain function.
  • Endoscopic treatment:
    • Endoscopic band ligation (EBL): This modality is used to prevent or treat oesophageal variceal bleeding; it involves placing rubber bands around the varices to stop bleeding.
    • Sclerotherapy: This involves injecting a sclerosing agent (irritant that has the ability to damage the endothelial layer of blood vessels) into varices to reduce bleeding risk.
  • Surgical treatment:
    • Transjugular intrahepatic portosystemic shunt (TIPS): In this procedure, a stent is placed in the liver to divert blood flow, thereby reducing portal pressure.
    • Liver transplantation: This intervention is used in cases of severe cirrhosis or liver failure where other treatments are not effective.
  • Lifestyle and diet:
    • Low-salt diet: To reduce fluid retention and manage ascites.
    • Avoidance of alcohol: Crucial to prevent worsening liver damage.
  • Managing the underlying liver disease: Addressing (managing) conditions like hepatitis or N/AFLD.
  • Managing complications of portal hypertension: Complications of portal hypertension, such as variceal bleeding (a potentially life-threatening complication where the dilated veins in the oesophagus or stomach rupture), ascites (fluid build-up in the abdomen, which can lead to infection (spontaneous bacterial peritonitis) or kidney failure), hepatic encephalopathy (altered brain function due to accumulation of liver toxins in the bloodstream), and portal vein thrombosis (a blood clot in the portal vein), should be managed to ensure a good quality-of-life for the patient.
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P

Hepatocellular Carcinoma (HCC)

Management Team

Hepatocellular Carcinoma (HCC)

Overview

Hepatocellular carcinoma (HCC) is the most common type of liver cancer. It generally occurs as result of abnormal growth of hepatocytes—the liver's main cells—and often develops in the background of chronic liver disease or cirrhosis. The prognosis for HCC (disease outcome, e.g., cure, relapse, etc.) depends on factors such as tumour size, liver function, presence of metastasis, and the underlying liver disease. Early stage HCC has a better prognosis, particularly if treated with surgery (or a liver transplant). Advanced HCC has a poorer prognosis, but new systemic therapies have improved the treatment outcomes in some patients.

Several factors increase the risk of developing HCC; these include:

  • Chronic viral hepatitis: Hepatitis B virus (HBV) and Hepatitis C virus (HCV) infections are the leading causes of HCC worldwide, particularly in regions with high prevalence of these viruses.
  • Cirrhosis: ALD and N/AFLD—both leading to cirrhosis—are significant risk factors.
  • Aflatoxin exposure: Exposure to aflatoxins (produced by certain moulds found in poorly stored grains and nuts) can increase the risk of HCC, especially in regions like sub-Saharan Africa and Southeast Asia.
  • Metabolic disorders: Conditions like hemochromatosis (iron overload), alpha-1 antitrypsin deficiency, and Wilson's disease can increase HCC risk.
  • Obesity and type 2 diabetes: Obesity and diabetes often contribute to the development of N/AFLD, which in turn increases HCC risk.
  • Family history: A family history of liver cancer or inherited liver diseases may increase HCC risk.
  • Age and gender: HCC is more common in older adults and is more frequent in men than in women.
  • Smoking: Smoking can increase the likelihood of developing HCC, particularly in individuals with preexisting liver disease.

In early stages, the symptoms of HCC may be apparent, but as the disease progresses, symptoms can become apparent; these include:

  • Abdominal pain or discomfort (especially in the upper right side of the abdomen).
  • Unexplained weight loss
  • Loss of appetite
  • Jaundice
  • Fatigue
  • Swelling of the abdomen (due to fluid buildup)
  • Nausea and vomiting
  • Fever
  • Easy bruising or bleeding (due to liver dysfunction)

HCC is typically diagnosed through a combination of clinical, imaging, and laboratory tests; these include:

  • Imaging studies:
    • Ultrasound: This is generally the first imaging modality to be used to detect liver masses (tumours).
    • CT or MRI: These provide detailed information about tumour size and location and extent of cancer spread.
    • Contrast-enhanced imaging (CT/MRI): This imaging modality can help differentiate HCC from benign (non-cancerous) lesions.
  • Blood tests:
    • Alpha-fetoprotein (AFP): Elevated levels of AFP can indicate HCC; however, it should be noted that other cancers can also elevate AFP levels.
    • Liver function tests: Individuals with damaged livers (including those with cancer) have elevated levels of ALT, AST, ALP, and bilirubin and low albumin levels.
    • Hepatitis markers: If a patient has a history of hepatitis, testing for HBV and HCV is important.
  • Liver biopsy: A biopsy, though less commonly performed, may be done if imaging findings are inconclusive or if there is uncertainty in diagnosis.
  • Endoscopy: In cases where cirrhosis is present, an endoscopy may be done to check for varices or signs of liver damage.

The treatment of HCC depends on the stage of the cancer, liver function, and the patient’s overall health. Treatment options include:

  • Surgical treatment:
    • Liver resection: Tumour-removal surgery may be an option if the tumour is confined to a particular part of the liver and the liver function is normal.
    • Liver transplantation: For patients with cirrhosis or large tumours, liver transplantation may be considered as severe liver and liver failure are a reality in these patients.
  • Ablation therapy: This is an umbrella term to describe minimally invasive surgical procedures (involving the use of very tiny cuts to perform surgery) that destroy small tumours.
    • Percutaneous ethanol injection (PEI)
    • Radiofrequency ablation (RFA)
  • Transarterial chemoembolization (TACE): TACE is used for patients who are not candidates for surgery. It involves delivering chemotherapy directly to the tumour while blocking the blood supply.
  • Systemic therapies: These therapies generally affect the entire body.
    • Targeted therapy: Drugs like sorafenib or lenvatinib that target cancer cell growth may be used for advanced HCC.
    • Immunotherapy: Drugs such as nivolumab or pembrolizumab (immune checkpoint inhibitors) have shown effectiveness in some patients with advanced or metastatic HCC.
    • Radiation therapy: In some cases, an external beam of radiation may be used to kill cancer cells, particularly when other treatments are not suitable.
    • Chemotherapy: Chemotherapy is generally not effective for HCC, so it is rarely used.
  • Palliative care: For advanced cases of HCC, the treatment focuses on relieving symptoms, improving quality of life, and managing complications like ascites or bleeding.

Strategies to prevent HCC occurrence include:

  • Vaccination against Hepatitis B virus.
  • Screening for liver disease in at-risk populations (e.g., patients with hepatitis B, hepatitis C, or cirrhosis).
  • Managing chronic liver disease (avoiding alcohol, controlling obesity, and treating hepatitis).
  • Healthy lifestyle choices (maintaining a healthy weight, avoiding tobacco, and managing diabetes).
  • Regular screening (e.g., ultrasound and AFP levels) for individuals at high risk of HCC.
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