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Acute Disseminated Encephalomyelitis (ADEM)

Management Team

Acute Disseminated Encephalomyelitis (ADEM)

Overview

ADEM is an acquired condition wherein demyelination takes place in the brain and spinal cord secondary to antecedent infection or immunization. It generally affects younger population, is usually monophasic, and does not tend to recur.

  • Fever
  • Headache
  • Meningism
  • Seizures
  • Altered mental state
  • Multiple neurological deficits

  • More common among children than adults
  • One is more likely to get ADEM soon after having an infection

Neurologist

  • CSF examination to determine the number of white blood cells, protein levels, and oligoclonal bands
  • MRI to check lesions involving grey matter, mass effect and enhancement after instilling contrast
  • Other diseases such as multiple sclerosis, myelin oligodendrocyte glycoprotein antibody disease (MOGAD), neuromyelitis optica, neurosarcoidosis, malignancy, and granulomas need to be ruled out

Five-day-course of intravenous immunoglobulin.

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Acute Ischemic Stroke

Management Team

Acute Ischemic Stroke

Overview

Acute ischemic stroke is a neurological pathology caused due toa blocked blood vessel in the brain, resulting in decreased blood flow and hence, reduced oxygen supply in the area supplied by that blood vessel. It is a medical emergency and requires immediate medical attention to reverse the symptoms and dissolve the clot. In severe cases, the condition can prove to be life threatening or result in permanent neurological deficit in the patient.

  • High blood pressure/ cholesterol
  • Obesity
  • Diabetes
  • Smoking habits
  • Family history/ genetics
  • Sleep disorders

  • High blood pressure
  • High cholesterol
  • Diabetes
  • Smoking
  • Obesity
  • Family history/ genetics
  • Sleep disorders

  • Sudden numbness or weakness in arm, face, or leg
  • Difficulty in talking with slurring of speech
  • confusion or imbalance
  • Visual disturbance
  • Severe headache

Neurologist/ Neurosurgeon/ Neuro-interventionist

  • Computed tomography (CT)
  • Magnetic resonance imaging (MRI)-brain with angiography of brain
  • CT/ MRI perfusion
  • 2D Echo, Holter monitoring and blood tests to determine the underlying cause of stroke

  • Thrombolysis of clot using injection alteplase or tenecteplase within 4.5 hours of symptom onset
  • Surgical treatment involves clot lysis or aspiration using thrombectomy devices within 24 hours of onset of symptoms
  • Medical management is attempted the using blood thinner medications to minimize the risk of future episodes
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Acoustic Neuroma

Management Team

Acoustic Neuroma

Overview

Acoustic neuromas, also known as vestibular schwannomas, are benign (non-cancerous) tumours that develop from the Schwann cells, responsible for insulating the eighth cranial nerve (vestibulocochlear nerve). Acoustic neuromas rarely turn malignant.

Acoustic neuromas may occur suddenly. Bilateral occurrence may be associated with Neurofibromatosis type 2, which is a genetic disorder.

Genetic risk factor: A family history of the rare genetic condition neurofibromatosis type 2 significantly increases the risk.

Environmental risk factor: Exposure to radiation, particularly the head, has been conclusively associated with a higher risk of acoustic neuroma. However, there is currently no evidence suggesting a link between the use of cell phones and the development of these tumours.

  • Hearing loss on the side of the lesion
  • Ringing in the ear (Tinnitus)
  • Giddiness
  • Imbalance on walking
  • Facial weakness
  • Headache, nausea, or vomiting, if the tumour is large or is compressing the ventricular outflow system.

Neurologist/ Neurosurgeon

  • Audiogram- For high frequency hearing loss
  • CT scan- For contrast enhancing lesion with expansion of internal auditory canal
  • MRI brain- For detecting ice cream cone appearance in posterior fossa

  • Usually, conservative treatment is required with monitoring through serial MRI
  • Expanding or large lesions may be excised (through suboccipital or translabyrinthine or middle fossa approach)
  • Excision carries the risk of morbidities  such as hearing loss, facial nerve injury or vertigo
  • Stereotactic radiotherapy has low morbidity risk compared with surgery
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Alcoholic Liver Disease (ALD)

Management Team

Alcoholic Liver Disease (ALD)

Overview

Alcoholic liver disease (ALD) or alcohol-related liver disease is an umbrella term for a group of liver diseases caused due to excessive alcohol consumption over time. ALD is a progressive condition and individuals with early ALD may be asymptomatic (not outwardly show any symptoms), with simple steatosis (fat accumulation in liver also known as alcoholic fatty liver disease) or alcoholic steatohepatitis (an advanced stage of alcoholic steatosis associated with inflammation and cell damage) and early-stage fibrosis (reversible accumulation of collagen in the liver), while patients with advanced ALD may have advanced fibrosis (irreversible, widespread fibrosis), which can cause cirrhosis and associated complications (hepatocellular carcinoma), alcohol-associated hepatitis with jaundice, portal hypertension, and/or acute-on-chronic liver failure. Thus, ALD includes a range of conditions, including alcoholic fatty liver disease (alcoholic steatosis), alcoholic steatohepatitis, fibrosis, portal vein hypertension, alcohol-associated hepatitis, cirrhosis, liver failure, and hepatocellular carcinoma.

Excess and prolonged consumption of alcohol is the primary cause of ALD. The liver breaks down alcohol into smaller molecules, leading to detoxification but drinking too much alcohol over a prolonged duration can overwhelm this ability, leading to the development of ALD.

  • Heavy drinking
  • Genetic factors  
  • Nutritional deficiencies: Alcohol interferes with the absorption of essential nutrients, a phenomenon that can contribute to liver disease.
  • Coexisting conditions: Pre-existing conditions, like metabolic syndrome, viral hepatitis, or obesity, can increase the risk of developing ALD.

Symptoms may vary depending on disease severity. Common symptoms have been enumerated below:

  • Fatty liver (alcoholic steatosis)  
  • Slight discomfort in the upper abdomen.
  • Jaundice
  • Swelling of the lower limbs (oedema)
  • Fluid buildup in the abdomen (ascites)
  • Itchy skin
  • Fever and shivering
  • Excessively curved fingernails
  • Muscle weakness
  • Blood in vomit or stools
  • Easy bleeding and bruising  
  • More sensitive reactions to alcohol or drugs
  • High blood pressure in the liver (portal hypertension)
  • Bleeding from veins in the oesophagus (oesophageal varices)
  • Confusion and behavioural changes (hepatic encephalopathy)
  • Enlarged spleen

One of the first steps in the diagnosis of ALD involves going through an individual’s medical history (alcohol consumption patterns, including the quantity and frequency of drinking). The other steps include:

  • Physical examination
  • Laboratory tests: Several blood tests help assess liver function and detect ALD-associated damage.
    • Liver function tests (LFTs):
      1. ALT and AST: High ALT and AST values indicate liver damage. Further, in case of liver damage, AST values are generally higher than ALT values.
      2. ALP and GGT: Increased ALP and GGT values can indicate liver damage or biliary obstruction.
      3. Bilirubin: High levels of bilirubin may indicate liver dysfunction that can lead to jaundice.
      4. CBC: A low platelet count or anaemia in a complete blood count test can suggest liver damage.
      5. Coagulation studies (PT, INR): The liver produces clotting factors, so a longer blood clotting time (i.e., prolonged PT (prothrombin time) or elevated INR (international normalized ratio)) indicates liver dysfunction.
      6. Serum albumin: Low albumin levels can be a sign of chronic liver disease.
      7. Ammonia level: Elevated levels of ammonia may indicate hepatic encephalopathy, a severe complication of advanced liver disease.
  • Imaging studies:
    • Ultrasound
    • CT and MRI
    • Elastography (FibroScan)
    • Magnetic resonance elastography (MRE)
  • Liver biopsy: In some cases, a liver biopsy—removing a small piece of liver tissue for examination under a microscope—may be used to assess the degree of liver damage. It helps determine the extent of liver inflammation, presence of fat in the liver (steatosis), the degree of fibrosis or scarring (cirrhosis), and whether alcohol is responsible for the damage observed.
  • Exclusion of other liver diseases: As the symptoms of ALD can overlap with those of liver disease arising from other causes (e.g., viral hepatitis, fatty liver disease unrelated to alcohol, or autoimmune liver diseases), doctors may conduct additional tests to rule out other conditions:
    • Hepatitis B and C tests: To rule out viral hepatitis as the cause of liver disease.
    • Autoimmune markers: To rule out autoimmune hepatitis.
    • Iron tests: To exclude hemochromatosis (excess iron accumulation in the liver).
    • Alpha-1 antitrypsin deficiency test: To rule out genetic liver diseases.

Once ALD is diagnosed, the severity of liver damage is assessed. This is typically done through:

  • MELD score: Used to determine the severity of cirrhosis and predict survival by considering bilirubin levels, creatinine levels, and INR.
  • Child‒Pugh score: Used to determine the prognosis of liver disease (prediction of the likely disease course, including the probability of recovery/recurrence), particularly cirrhosis, by looking at factors, like serum albumin and bilirubin levels, encephalopathy, and ascites.

The most important step in managing ALD is to completely stop drinking alcohol (abstinence), which may stop the progression of liver damage and, in some cases, allow the liver to heal; however, a drastic decrease in alcohol consumption can result in severe withdrawal symptoms, for which medicine may be prescribed. Other strategies include:

  • Nutritional support: Individuals with ALD often suffer from malnutrition and deficiencies. A balanced diet with vitamin supplementation (especially B vitamins) is therefore crucial for recovery.
  • Liver transplantation: A liver transplant may be necessary in cases of advanced ALD. However, it is generally only considered for people who have stopped drinking for at least six months.
  • Management of complications: This may include:
    • Diuretics: To counter fluid buildup.
    • Lactulose: To prevent encephalopathy.
    • Endoscopic treatments: For variceal bleeding.
    • Medications: For managing complications, like infections, bleeding, or ascites (fluid accumulation).

Preventing ALD involves reducing or eliminating alcohol consumption and taking steps to protect liver health. 

  • Limiting the alcohol intake: Adhering to recommended guidelines for alcohol consumption can significantly reduce the risk of developing ALD.
  • Maintaining a healthy diet: A balanced diet and regular exercise are necessary for maintaining liver health and prevent malnutrition, which is common in ALD.
  • Early intervention: Regular check-ups and liver function tests for high-risk individuals (e.g., individuals with heavy drinking habits) can help detect liver damage early, thereby improving the chances of recovery.
  • Vaccinations: For individuals with ALD, vaccination against hepatitis A and B is recommended as infections can further harm the liver.
  • Avoiding other liver toxins: Limiting the use of over-the-counter medications like acetaminophen (which can be toxic to the liver) and avoiding exposure to harmful chemicals can help protect the liver.
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A

Peritoneal Dialysis

Management Team

Peritoneal Dialysis

Overview

Peritoneal dialysis is a home-based dialysis method that uses the peritoneal cavity to filter waste, excess fluids, and toxins from the blood stream. A catheter (a flexible tube), surgically placed near the umbilicus (belly button), facilitates the exchange of dialysis fluid (dialysate).

The process involves filling the peritoneal cavity with dialysate through the catheter (called a dwell), usually for several hours. The lining of the abdominal cavity (the peritoneal membrane) acts as a natural filter, enabling the removal of fluids and waste products. Once the exchange is complete, the used dialysate is drained and replaced with fresh dialysate solution.

Peritoneal dialysis treatments may be done by hand four to five times a day (Known as CAPD) or by using a machine (called a cycler- CCPD/APD) while you sleep. Some people use a cycler at night and also do one or two exchanges during the day.

  • Compared to haemodialysis the Peritoneal dialysis allows more uninterrupted time for work, family, and social activities.
  • Home-based treatment eliminates the need for frequent hospital visits.

  • Requires the patient or a caregiver to be trained in setting up equipment and managing connections
  • May not be suitable for individuals with limited dexterity or support at home.
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P

Dialysis

Management Team

Dialysis

Overview

Haemodialysis is an artificial method for removing waste, toxins, and excess fluids from the blood when the kidneys are unable to perform this function. During the procedure, blood is drawn from the body through small tubes, cleaned using special filter in the haemodialysis machine, and then returned to the body. Importantly there is no blood loss during this process. Each session typically lasts four hours and is conducted three times a week.

Our dialysis department offers a comprehensive range of services, including: Haemodialysis and haemodiafiltration procedures to address various clinical needs.

Access creation for dialysis through temporary HD catheters, Permanent tunnelled catheters, and AV fistulas.

Our dedicated team of nurses, physicians, urologists, radiologists and interventional radiology team is ensures seamless care and efficient management of any dialysis-related issues. The multidisciplinary approach guarantees optimal outcomes and patient comfort.

Diseases treated:

  • Chronic Kidney Disease
  • Acute Kidney Injury
  • ESRD
  • Electrolyte Imbalances
  • Fluid overload
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D

Renal Transplant

Management Team

Renal Transplant

Overview

Our centre offers both ABO-compatible and ABO-incompatible kidney transplants, catering to a wide range of donor-recipient pairs.. Transplant options include live-related donors and deceased donors. A dedicated multidisciplinary team ensures comprehensive care, managing transplant rejections, as well as post-transplant surgical or infectious complications.

Plasmapheresis: Available for pre-transplant immunological optimization and for managing post-transplant rejection episodes.

Laparoscopic donor nephrectomy: Laparoscopic donor nephrectomy is a minimally invasive removal of donor kidney.

Robotic laparoscopic donor nephrectomy: Enhances precision and accuracy, offering improved outcomes with minimal disfigurement or scarring.

  • Kidney transplant is used to treat the following conditions:
  • Chronic Kidney Disease (CKD)
  • ESRD
  • Diabetic Nephropathy
  • Polycystic Kidney Disease (PKD)
  • Glomerulonephritis
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R

End-stage Renal Disease (ESRD)

Management Team

End-stage Renal Disease (ESRD)

Overview

End-stage renal disease (ESRD) represents the final stage of CKD, where the kidneys lose their functional reserve and require renal replacement therapies to support daily activities. These therapies include initiation of dialysis or undergoing pre-emptive renal transplantation.

ESRD may present with:

  • Fluid overload, causing swelling, breathing difficulties, and abdominal distension.
  • Uremic gastritis symptoms such as indigestion, acidity, reduced appetite and itching.
  • Neurological issues like altered sensorium or irrelevant talk due to uremic encephalopathy.
  • Metabolic complications, including hyperkalaemia and metabolic acidosis.

Patients with ESRD should consult a kidney specialist (nephrologist) for optimal management and treatment.

  • Urine tests, blood tests to assess renal function,
  • Ultrasound (USG) for kidney imaging and evaluation

Management of ESRD involves renal replacement therapies, including:

  • Haemodialysis or peritoneal dialysis to support kidney function.
  • Kidney transplantation, which may be performed pre-emptively (before starting dialysis) or after initiating dialysis.
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E

Acute Kidney Injury (AKI)

Management Team

Acute Kidney Injury (AKI)

Overview

AKI or acute kidney injury is a sudden and often reversible decline in renal function over a short period of time. If identified and treated promptly, kidney function can frequently be restored. AKI can result from acute dehydration such as in cases of severe diarrhoea or burns, secondary sepsis, certain medications, or following surgical procedure.

The underlying causes of AKI can be classified as follows:

  • Pre-Renal AKI: Pre-renal AKI is caused by reduced blood flow to the kidneys due to dehydration, low blood pressure, or heart failure.
  • Intrinsic Renal AKI: Results from direct damage to the kidney tissue, such as infections, toxins, or autoimmune diseases.
  • Post renal AKI: Occurs due to the obstruction in the urinary tract, such as from kidney stones, tumours, or an enlarged prostate.

The presentation of AKI can vary:

Mild cases may be asymptomatic and identified only during laboratory investigations.

Severe cases of AKIs may present with:

  • reduced urine output
  • swelling in the face and feet
  • reddish discoloration of urine
  • Aabdominal pain

A kidney specialist (nephrologist) should be consulted for the diagnosis and management of AKI.

Accurate diagnosis of AKI involves:

  • Urine tests
  • Blood tests to assess renal function
  • Imaging studies, such as an ultrasound, to confirm normal kidney size and identify potential structural abnormalities.

The management of AKI is tailored to address the underlying cause, including:

  • Rehydration therapy for patients suffering from diarrhoea or burns,
  • Antibiotic therapy for treating sepsis
  • Discontinuation of nephrotoxic medications, i.e. drugs that cause AKI.
  • In some severe cases, advanced interventions such as immunosuppressive therapy or temporary dialysis may be necessary to support kidney function until recovery.
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A

Interstitial Nephritis

Management Team

Interstitial Nephritis

Overview

Acute interstitial nephritis (AIN) is a condition in which there is inflammation and damage to the kidney tubules and interstitium (inner part of the kidney). This may be a reaction to a drug or infection or kidney transplant rejection.

Common causes of AIN include certain medications such as antibiotics, non-steroidal anti-inflammatory drugs, infections and in some cases, autoimmune conditions or reactions to kidney transplants. If the condition is related to a drug, discontinuation of the medication is essential.

In some cases, acute interstitial nephritis may be asymptomatic. Patients may have a normal urine output, but renal function tests will show a concerning increasing trend., indicating kidney dysfunction. Haematuria (blood in the urine) and proteinuria (protein in the urine) may also be present, depending on the severity.

To properly manage this condition, a kidney specialist (nephrologist) should be consulted.

Diagnosis often involves urine tests, blood tests to evaluate renal function, and imaging tests such as ultrasound KUB (Kidney, Ureter, and Bladder). In some cases, the diagnosis is confirmed through a USG-guided Kidney Biopsy to examine tissue samples from the kidney.

If the condition is drug-induced, discontinuing the offending medication is crucial. Treatment may include a short course of steroids to reduce inflammation and improve kidney function. If infection is the cause, appropriate antibiotic therapy will be necessary.

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