Central Serous Chorioretinopathy (CSCR)

Management Team

Central Serous Chorioretinopathy (CSCR)

Overview

Central serous chorioretinopathy (CSCR), a common ophthalmic disorder, affects the macula, which is crucial for sharp, clear central vision. In CSCR, fluid accumulation below the macula causes the temporary distortion and blurring of vision. CSCR is common in people aged 20–50 years. Its incidence in men is higher than that in women.

No exact cause of CSCR has been identified. However, several risk factors for this condition have been identified:

  • Psychological stress, including traumatic life events or work-related stress.
  • Excessive or prolonged corticosteroid use (oral, inhalational, or topical administration).
  • The risk of developing CSCR may be particularly high in individuals with a Type A personality (who are highly competitive, ambitious, and driven and exposed to high levels of psychological stress).

The severity and duration of the symptoms of CSCR vary. These symptoms include:

  • Blurring or distortion of central vision in one eye (the most common symptom).
  • Appearance of dark spots in the central field of vision.
  • Heightened contrast sensitivity.
  • Decreased colour perception.
  • Objects appearing smaller than they are (micropsia).

To diagnose CSCR, an ophthalmologist will perform a comprehensive eye examination, which includes:

  • Retinal examination. The doctor dilates the pupils with special eye drops to examine the retina using a slit-lamp or ophthalmoscope for identifying cataracts and assessing any damage to the retina.
  • Visual acuity tests.
  • Collection of comprehensive medical history.
  • Accessory diagnostic tests, such as the estimation of choroidal thickness using enhanced depth imaging optical coherence tomography (OCT), OCT angiography (a non-invasive technique used to visualise the vasculature of the retina and choroidal layers), fluorescein angiography (injection of fluorescein into a vein to detect blood vessels in the eyes), and indocyanine green angiography (an invasive technique used to visualise the vasculature of the retina and choroidal layers). These tests help assess the degree of retinal involvement and confirm fluid leakage in the retina.

CSCR often resolves spontaneously even without specific treatments over a period of few months. However, various treatment options are available for patients showing persistent symptoms or those facing a high risk of complications:

  • Routine eye checkups and observations: As mild or early-stage CSCR is self-limiting, only regular monitoring may be required.
  • Lifestyle modifications: Adopting healthy lifestyles, reducing stress levels, and ensuring mental well-being can help prevent and treat CSCR.
  • Photodynamic therapy (PDT): This may be recommended to seal leaks in the choroidal blood vessels for patients with advanced CSCR and can help mitigate fluid accumulation in the retina.
  • Micro-pulse and low-power laser therapies. These are also useful in sealing leaks in the retina, promoting fluid absorption.
  • Anti-vascular endothelial growth factor (VEGF) agents: Intravitreal injections of specific therapeutics, such as anti-VEGF drugs, can help treat CSCR. These agents suppress abnormal angiogenesis (formation of new blood vessels) below the retinal layers.

Although CSCR causes discomfort and temporarily impairs vision, early diagnosis and the timely administration of appropriate treatments can ensure a complete recovery.

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Cataract

Management Team

Cataract

Overview

A cataract refers to the clouding of the lens inside the eye, which ultimately becomes opaque and results in the gradual blurring of vision. The lens of a normal eye is clear, which helps focus light rays onto the retina (back of the eye) and the transmission of visual signals to the brain, enabling us to see. During cataract development, the clouding of the lens prevents the light rays from being focussed onto the retina. Thus, the picture received by the retina is dull and blurry.

Most forms of cataracts develop in adult life. Ageing causes the lens to become cloudy and harden. This represents the most common type of cataract and is referred to as an age-related cataract. Cataracts usually occur in patients aged > 40 years. However, other age-independent types include congenital (present at birth), traumatic (injury to the eye), and drug (steroids)-induced cataracts. Furthermore, the risk of cataract development among individuals with certain pre-existing conditions, such as diabetes, is higher than that among healthy individuals.

Cataracts, which usually form slowly over a few years, cause gradual vision blurring. Thus, corrective glasses are not sufficient for visual correction. In some cases, the deterioration of vision is rapid. Cataracts may also cause glares and the formation of multiple images in the retina of the affected eye, markedly affecting visual acuity and complicating daily activities, such as reading, driving, and recognising faces.

Cataracts are diagnosed by ophthalmologists during routine eye examinations. To confirm the diagnosis, the following examinations can be performed:

  • Visual acuity test to indicate the sharpness of vision.
  • Slit-lamp examination to closely examine the structures at the front of the eye (cornea, iris, lens) and spot abnormalities in the lens that may indicate cataracts.
  • Retinal exam, where the doctor dilates the pupils with special eye drops to examine the retina using a slit-lamp or ophthalmoscope for identifying cataracts and assessing any damage to the retina.
  • Refraction and contrast sensitivity tests to measure how the cataract is affecting vision and to check for other refractive errors, such as myopia, hyperopia, or astigmatism.

Currently, automated eye surgery, one of the most prolific hallmarks of advanced eye care, represents the primary method for treating cataracts (to remove the cataract). During the cataract surgery, the natural lens, which has turned cloudy and opaque, is replaced with an intraocular lens (a clear, artificial lens). This is a safe, painless, and routine outpatient surgery. Cataract surgeries are performed on a day-care basis, where the admission, surgery, and discharge happen on the same day. Cataract surgeries are of the following two types:

  • Refractive surgery: This is the most common cataract treatment. It involves a refractive lens exchange operation to replace the cloudy lens with an intraocular lens. The procedure is quick, takes 20–30 minutes, and can greatly improve vision.
  • Laser cataract surgery: For this procedure, a femtosecond laser is used to partially break down the cataract. The subsequent procedure is similar to that of conventional (non-laser) cataract surgery. Currently available evidence shows that both conventional and laser cataract surgery are equivalent in terms of vision and safety.

In recent years, precision surgery, such as that using the Alcon Lens Laser (a cutting-edge technology used in ophthalmology for precise and automated cataract surgery), and advanced robotic surgery have also emerged as efficient surgical modalities for cataract removal. These advanced techniques are associated with high accuracy and rapid treatment and recovery, resulting in reduced levels of stress for patients, increased levels of comfort, and enhanced cataract surgery outcomes.

Cataract surgery recovery durations differ for every person. Usually, outpatient recovery is possible. Most patients recover quickly within approximately 3–4 days. During recovery, it is normal for vision to take a few days to improve. The eyes may also be sore, scratchy, and light-sensitive. Antibiotic and anti-inflammatory drops are initiated the day after surgery. Patients can return to work a few days after surgery. However, if a job is physically demanding, recovery may require a longer duration. The treating physician determines the recovery duration.

Once the cloudy (cataractous) lens has been removed in surgery, it does not recur. However, after a few months or years after cataract surgery, the thin membrane behind the new lens implant (posterior capsule) may become opaque. This creates a “filter effect” and can cause the deterioration of vision. A simple laser treatment (YAG laser capsulotomy), which is usually an outpatient procedure, can be performed to clear this membrane and restore vision.

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Colorectal Cancer

Management Team

Colorectal Cancer

Overview

Colorectal cancer arises from abnormal cell growth in the colon or rectum, leading to tumour formation. This cancer may occur in different segments of the large intestine, and its management has evolved significantly due to advancements in minimally invasive surgical techniques.

The main types of colorectal cancer include:

  • Adenocarcinoma: The most common type, accounting for over 90% of cases, originating in the glandular cells lining the colon and rectum.
  • Carcinoid Tumours: Develop in the hormone-producing cells of the intestine.
  • Gastrointestinal Stromal Tumours (GIST): Rare tumours originating in the connective tissues.
  • Lymphomas and Sarcomas: Rare types of colorectal cancers that arise in the lymphatic or connective tissues.

Colorectal cancer develops due to genetic mutations in the cells of the colon or rectum, leading to uncontrolled growth and tumour formation.

  • Lifestyle Factors:
    • Diet high in red and processed meats.
    • Sedentary lifestyle and obesity.
    • Smoking and excessive alcohol consumption.
  • Medical Conditions:
    • Family history of colorectal cancer or inherited syndromes (e.g., Lynch syndrome).
    • History of polyps or inflammatory bowel disease (Crohn’s disease, ulcerative colitis).
    • Type 2 diabetes.
  • Age and Genetics:
    • Risk increases after age 50.
    • Mutations in genes like APC, KRAS, and TP53.

In the early stages, symptoms may be mild or absent. As the disease progresses, the following symptoms can appear:

  • Changes in bowel habits (diarrhoea, constipation, or stool narrowing).
  • Blood in the stool or rectal bleeding.
  • Abdominal pain or cramping.
  • Unexplained weight loss.
  • Fatigue and weakness.
  • Persistent feeling of incomplete bowel evacuation.

The diagnosis of colorectal cancer involves a combination of the following:

  • Screening Tests:
    • Colonoscopy: The gold standard for detecting polyps and tumours.
    • Faecal Occult Blood Test (FOBT) or Faecal Immunochemical Test (FIT): Detects hidden blood in stool.
  • Imaging Studies:
    • CT Colonography (virtual colonoscopy).
    • MRI and CT scans for staging and detecting metastases.
  • Biopsy: Tissue samples taken during colonoscopy to confirm cancer diagnosis.
  • Blood Tests: EA (carcinoembryonic antigen) levels to monitor treatment response.

Treatment options depend on the stage, location, and patient factors:

  • Early-Stage Cancer:
    • Polypectomy: Removal of polyps during a colonoscopy.
    • Endoscopic Mucosal Resection (EMR): For larger, localised tumours.
  • Locally Advanced Cancer:
    • Surgery:
      - Open, Laparoscopic, or Robotic Approaches for tumour removal.
      - Total Mesorectal Excision (TME) for rectal cancer.
    • Neoadjuvant Therapy: Chemotherapy or radiotherapy before surgery to shrink tumours.
  • Advanced Cancer:
    • Chemotherapy: Used to shrink tumours or as adjuvant therapy post-surgery.
    • Targeted Therapy: Monoclonal antibodies (e.g., bevacizumab) targeting cancer pathways.
    • Immunotherapy: For certain patients with high microsatellite instability (MSI-H).
    • Palliative Care: To manage symptoms and improve quality of life in metastatic cases.

  • Neo-Adjuvant Chemo and Radiotherapy: Modern radiotherapy techniques have enabled sphincter-preserving surgeries for low rectal tumours, reducing the need for more invasive procedures like abdomino-perineal resection (APR), which often result in incontinence or stoma formation.
  • Total Mesorectal Excision (TME): Introduced by Heald et al., this technique emphasizes precise dissection along the mesorectal plane, ensuring complete removal of vasculo-lymphatic pathways and reducing local recurrence. TME is pivotal for achieving optimal oncological outcomes.
  • Complete Mesocolic Excision (CME) with Central Vascular Ligation (CVL): Hohenberger et al. extended the principles of TME to colonic cancers, emphasizing the removal of intact mesocolic tissue and extensive lymph node dissection. This approach has been associated with better oncological outcomes and reduced systemic disease spread.
  • Laparoscopic Colorectal Surgery (LCS): Minimally invasive laparoscopic techniques have evolved significantly, offering comparable long-term outcomes to open surgery for colorectal cancer. Short-term benefits, including faster recovery, reduced pain, and shorter hospital stays, have been well-documented in multiple studies.
  • Robotic Colorectal Surgery (RCS): Robotic surgery addresses many limitations of laparoscopy, such as restricted instrument mobility, tremor amplification, and the absence of three-dimensional vision. With robotic systems like the da Vinci Surgical System, surgeons gain enhanced precision, better ergonomics, and improved control over surgical instruments.

    Advantages of Robotic Surgery

    • Enhanced Precision: Greater maneuverability with EndoWrist instruments.
    • Improved Ergonomics: Surgeons experience reduced fatigue and better control.
    • Reduced Conversion Rates: Studies report conversion rates as low as 0–4.9%.
    • Positive Oncological Outcomes: Comparable or superior lymph node yields, low circumferential resection margin (CRM) positivity, and reduced local recurrence rates.

    Supporting Evidence for Robotic Surgery

    • Several prospective and retrospective studies validate the safety and efficacy of robotic colorectal surgery. For instance:
    • Long-term outcomes demonstrate three-year disease-free survival rates of 73.7% to 79.2% and overall survival rates of 92% to 97%.
    • Studies, including hybrid and fully robotic approaches, consistently show promising results for rectal cancer management.
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Cholangitis

Management Team

Cholangitis

Overview

Cholangitis is an inflammation of the bile ducts, which can disrupt the flow of bile from the liver to the intestines. It is often a serious condition requiring prompt medical attention.

  • Acute cholangitis (ascending cholangitis): Caused by bacterial infection, often due to bile duct obstruction.
  • Primary sclerosing cholangitis (PSC): Chronic, progressive disease leading to scarring and narrowing of bile ducts. Often associated with inflammatory bowel disease (IBD).
  • Secondary sclerosing cholangitis: Resulting from a secondary cause like infection, trauma, or ischemia. 
  • IgG4-related cholangitis: Autoimmune condition, often linked with IgG4-related disease.
  • Recurrent pyogenic cholangitis: Common in East Asia, characterized by recurrent infections with stone formation.

There are many causes and risk factors for this condition, these include:

  • Infections:
    • Bacterial infections (e.g., E. coli, Klebsiella, Enterococcus)
    • Parasites (e.g., liver flukes)
  • Obstructions:
    • Gallstones
    • Bile duct strictures
    • Tumours (e.g., cholangiocarcinoma)
  • Autoimmune:
    • IgG4-related cholangitis, PSC
    • Iatrogenic:
    • Post-surgical or post-endoscopic procedures (e.g., ERCP)
    • History of IBD (e.g., ulcerative colitis in PSC)

Multiple symptoms exist depending on the type of disease. These have been enumerated below.

Acute cholangitis (Charcot's Triad):

  • Fever and chills
  • Right upper quadrant abdominal pain
  • Jaundice

Obstructive ascending cholangitis (Reynolds' Pentad):

  • Fever and chills
  • Right upper quadrant abdominal pain
  • Jaundice
  • Hypotension (low blood pressure)
  • Altered mental status.

Chronic cholangitis (e.g., PSC):

  • Fatigue
  • Pruritus (itching)
  • Progressive jaundice
  • Weight loss

Multiple types of diagnostic modalities are available cholangitis; these include:

  • Blood tests:
    • Liver function tests: Elevated ALP, GGT, AST, ALT, and bilirubin levels
    • Complete blood count (CBC) test: Leukocytosis (high white blood cell (WBC) counts
    • Autoimmune marker analysis: Elevated IgG4 and ANCA (in PSC)
  • Imaging:
    • Ultrasound: Detects bile duct dilation
    • MRCP (Magnetic resonance cholangiopancreatography): Non-invasive visualisation of bile ducts
  • ERCP (Endoscopic retrograde cholangiopancreatography): For diagnosing and treating cholangitis
  • Microbiological studies: Blood cultures in suspected infection

Treatments vary depending on the type of cholangitis; the same have been enumerated below.

  • Acute cholangitis:
    • Antibiotics: Broad-spectrum targeting gram-negative and anaerobic bacteria.
    • Biliary decompression: Via ERCP or percutaneous drainage if obstructed
    • Supportive care (intravenous (IV) fluids, pain medication)
  • Primary sclerosing cholangitis (PSC):
    • No curative treatment; focus on symptom control.
    • Ursodeoxycholic acid (UDCA) may help bile flow.
    • Liver transplant in advanced cases.
  • IgG4-related cholangitis: Steroids or other immunosuppressants
  • Recurrent pyogenic cholangitis: Antibiotics and removal of stone
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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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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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Cirrhosis

Management Team

Cirrhosis

Overview

Liver cirrhosis is a chronic condition in which healthy liver tissue is replaced by scar tissue (i.e., progression of fibrosis), leading to impaired liver function, which can have serious health implications. 

As with all other manifestations of ALD, chronic alcohol abuse is one of the most common causes of liver cirrhosis. Other causes include:

  • Fatty liver disease (N/AFLD): This condition—linked to obesity, diabetes, and metabolic syndrome—can promote cirrhosis.
  • Chronic viral hepatitis: Hepatitis B and C can promote cirrhosis.
  • Autoimmune hepatitis: In this condition, the immune system attacks the liver cells.
  • Biliary diseases: Diseases that affect the gall bladder and bile ducts, such as primary biliary cholangitis or primary sclerosing cholangitis, can lead to cirrhosis.
  • Genetic conditions: Hemochromatosis (iron overload) and Wilson’s disease (copper buildup) can also cause cirrhosis.
  • Medications and toxins: Long-term use of certain drugs or toxins can also cause cirrhosis; they can also serve as risk factors.
  • Infections: Schistosomiasis or other parasitic infections can also cause cirrhosis.
  • Obesity: Increases risk of N/AFLD, and by extension cirrhosis.
  • Diabetes and insulin resistance: These factors can serve as risk factors for liver cirrhosis.
  • Family history: A family history of liver diseases (genetic predisposition) can also serve as a risk factor.

Cirrhosis shares many symptoms with N/AFLD, N/ASH, and liver fibrosis. The same has been enumerated below.

  • Fatigue
  • Loss of appetite
  • Nausea (urge to vomit)
  • Weight loss
  • Jaundice
  • Ascites (fluid accumulation in the abdomen)
  • Oedema (swelling in the legs)
  • Oesophageal varices (enlarged veins prone to bleeding)
  • Hepatic encephalopathy (confusion, memory problems, drowsiness)
  • Spider angiomas (spider-like blood vessels on the skin)

As cirrhosis shares many symptoms with N/AFLD, N/ASH, and liver fibrosis, it also shares the diagnostic modalities; the same have been enumerated below.

  • Blood tests:
    • Liver function tests (ALT, AST, bilirubin, albumin)
    • Coagulation profile (INR, PT)
    • Platelet count
  • Imaging studies:
    • Ultrasound (detects liver size, texture, ascites)
    • CT or MRI (detailed liver structure)
    • Elastography (evaluates the extent of fibrosis by measuring liver stiffness)
  • Liver biopsy: To confirm the diagnosis in uncertain cases.
  • Endoscopy: To check for oesophageal varices.
  • Serology and genetic tests: To identify underlying causes.

Cirrhosis treatment generally focuses on managing the underlying cause, slowing down disease progression, and preventing complications. The strategies used have been enumerated below.

  • Lifestyle changes:
    • Alcohol cessation
    • Weight loss and dietary management (low sodium, balanced diet)
  • Medications:
    • Antivirals for hepatitis B or C
    • Diuretics for ascites (spironolactone, furosemide)
    • Lactulose or rifaximin for hepatic encephalopathy
    • Beta-blockers for oesophageal varices (e.g., propranolol)
  • Management of complications:
    • Paracentesis for ascites
    • Endoscopic treatment for variceal bleeding
  • Advanced therapies:
    • Liver transplantation: For end-stage liver disease. (advanced cirrhosis and liver cancer).
    • TIPS (transjugular intrahepatic portosystemic shunt): For refractory ascites or variceal bleeding.
  • Nutritional support: Adequate protein intake and vitamin supplementation to manage cirrhosis-associated liver damage.

Strategies for cirrhosis prevention have been enumerated below.

  • Vaccination against hepatitis A and B.
  • Avoidance of excessive alcohol consumption.
  • Regular screening and early management of viral hepatitis.
  • Healthy lifestyle with balanced diet and exercise.
  • Avoiding hepatotoxic drugs and chemicals.
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