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Jaundice In Viral Hepatitis: Symptoms and Management Overview

M3 India Newsdesk Sep 07, 2022

The frequency of jaundice has increased steadily and alarmingly despite the appalling record-keeping practices in the majority of the states of the union. In this article, the author talks about the occurrence of jaundice due to Hepatitis A and E, its transmission and management.

Jaundice and hepatitis

Over the last 20 years, the number of deaths caused by jaundice has increased. According to the data from the National Institute of Communicable Diseases (NICD) research, jaundice is a significant public health issue in India. Physicians reported and verified an annual incidence of 2.76 per 1000 people.

Virus infections of the liver are quite frequent in the rainy season. Water is a vector for the hepatitis virus to propagate. This infection is really dangerous. Jaundice, which is caused by hepatitis, causes yellow urine and eyes. During the monsoon, people are more prone to getting Hepatitis A or E.

Contaminated water or food might lead to hepatitis A or E. Due to most regions' water being polluted during the monsoon, it is frequent. Being that we don't have a decent sewage infrastructure, it is particularly widespread in South Asia. It spreads because of poor hygiene, raw food, or fruits and vegetables that have been washed in polluted water.

Adult jaundice evaluation

Adult jaundice might be indicative of a serious underlying condition. It is caused by increased amounts of unconjugated or conjugated bilirubin in the serum. Evaluation of jaundice is based on the patient's medical history and physical examination.

Fractionated bilirubin, a complete blood count, alanine transaminase, aspartate transaminase, alkaline phosphatase, -glutamyltransferase, prothrombin time and/or international normalized ratio, albumin, and protein should be part of the initial laboratory evaluation.

Ultrasound or computed tomography imaging may distinguish between extrahepatic obstructive and intrahepatic parenchymal diseases. Ultrasonography is the least intrusive and most affordable imaging modality. Additional cancer screening, biliary imaging, autoimmune antibody assays, and liver biopsy may be part of a more extensive evaluation.

Unconjugated hyperbilirubinemia is caused by an increase in bilirubin production due to the loss of red blood cells, as in hemolytic diseases, and disorders of defective bilirubin conjugation, such as Gilbert syndrome.

Illnesses causing hepatic injury, such as viral and alcoholic hepatitis, and cholestatic disorders, such as choledocholithiasis and neoplastic blockage of the biliary system, may cause conjugated hyperbilirubinemia.

When the blood bilirubin level surpasses 3 mg/dL, jaundice develops. It might be difficult to identify along with a physical examination. Acute jaundice is often an indication of a serious underlying condition and may have intrahepatic or extrahepatic causes.

55% of adults with acute jaundice have intrahepatic disorders, such as viral hepatitis, alcoholic liver disease, or drug-induced liver injury. The remaining 45% of instances of acute jaundice are extrahepatic, including gallstone disease, hemolysis, and cancer. This article presents a systematic method for diagnosing jaundice during the monsoon season only i.e. viral infective causes of hepatitis.

Adult jaundice assessment using an algorithm

Hepatitis A

The hepatitis A virus, which causes hepatitis A, causes liver inflammation (HAV). When an uninfected (and unvaccinated) individual consumes food or water that has been tainted by an infected person's faeces, the virus is most often disseminated. Oral-anal sex, contaminated food or water, poor sanitation, and poor personal hygiene, and these factors are all strongly linked to the illness.

Hepatitis A may induce crippling symptoms and, less often, fulminant hepatitis (rapid liver failure), which is frequently deadly. Hepatitis A does not cause chronic liver disease, unlike hepatitis B and C. According to WHO estimates, 7134 people worldwide passed away from hepatitis A in 2016 (which accounts for 0.5% of the mortality from viral hepatitis).

How it spreads

Primarily, the hepatitis A virus is spread by the faecal-oral route, which occurs when an uninfected person consumes food or drink contaminated with the faeces of an infected person. This may occur in households when an infected individual prepares meals for family members with unclean hands. Infrequent waterborne epidemics are often linked to sewage-contaminated or improperly cleaned water. Close physical contact (such as oral-anal sex) with an infected individual may also transfer the virus, although casual touch between persons does not spread the infection.

Clinical manifestations

Generally, the incubation time for hepatitis A is between 14 and 28 days.

Hepatitis A may cause moderate to severe symptoms, including fever, malaise, lack of appetite, diarrhoea, nausea, stomach pain, jaundice, and dark-coloured urine (yellowing of the eyes and skin). Not all infected individuals will exhibit all symptoms.

Children exhibit fewer signs and symptoms of sickness than adults. In senior age groups, illness severity and mortality consequences are greater. Infected children under the age of six often display no symptoms, and just 10% develop jaundice. It is possible for someone who has just recovered from an acute bout of hepatitis A to have a recurrence. This is often followed by recuperation.

Who is at risk?

The hepatitis A virus may infect anybody who has not been immunized or who has not previously been infected. In regions where the virus is prevalent (high endemicity), the majority of hepatitis A infections occur in young children.

Risk factors include:

  • Inadequate sanitation
  • Lack of clean water
  • Living in a home with an infected individual
  • Being a sexual partner of someone with acute hepatitis A infection
  • Recreational drug use
  • Intercourse between males
  • Travel to high-endemic regions without vaccination

How to diagnose?

Hepatitis A is clinically indistinguishable from other acute viral hepatitis strains. The identification of HAV-specific immunoglobulin G (IgM) antibodies in the blood provides a definitive diagnosis. Additional tests, such as reverse transcriptase polymerase chain reaction (RT-PCR) to identify hepatitis A viral RNA, may need specific laboratory equipment.


Hepatitis A has no particular therapy. After infection, symptoms may be sluggish to go away and may take weeks or months. Prescriptions that are not essential should be avoided.

Avoid using acetaminophen, paracetamol, and anti-vomiting medications. In the absence of abrupt liver failure, hospitalisation is not required. The goal of treatment is to preserve comfort and a healthy nutritional balance, which includes replacing lost fluids from vomiting and diarrhoea.


  1. The best approaches to fight hepatitis A are improved sanitation, food safety, and vaccine.
  2. Adequate supplies of clean drinking water, efficient sewage disposal within communities, and personal hygiene habits like routine handwashing before meals and after using the restroom may all help to stop the spread of hepatitis A.
  3. Internationally, several injectable inactivated hepatitis A vaccinations are accessible. They all have equivalent negative effects and provide comparable viral prevention. There are no authorised vaccines for infants under 1 year of age.

Hepatitis E

Infection with the hepatitis E virus (HEV) is a more frequent cause of acute hepatitis in India. After the Yamuna river flooded in 1955 and tainted the city's drinking water, HEV was discovered (retrospectively, as non-A, -B, -C, or -D) in India. An estimated 30,000 instances of HEV infection were documented.

The hepatitis E virus causes hepatitis E, an infection of the liver (HEV). There are at least four distinct strains of the virus: genotypes 1, 2, 3, and 4. Only humans have been discovered to have genotypes 1 and 2. In addition to circulating in a variety of species without producing illness, including pigs, wild boars, and deer, genotypes 3 and 4 sometimes infect people.

The virus enters the human body via the intestine and is passed on in the faeces of infected people. It mostly spreads via tainted drinking water. Usually self-limiting, the illness clears itself in 2 to 6 weeks. A rare but potentially deadly condition called fulminant hepatitis (acute liver failure) may appear.

How it spreads

Infection with hepatitis E is widespread around the globe, but it is more prevalent in low- and middle-income nations where access to basic services for hygiene, water, sanitation, and health is poor. Both sporadic instances and outbreaks of the illness may be seen in these regions. The epidemics, which may impact several hundred to several thousand people, often occur after intervals of faecal contamination of drinking water sources. Some of these outbreaks have happened in conflict zones and humanitarian crises, such as refugee camps and places where people have been internally displaced when access to sanitary facilities and clean drinking water is particularly difficult.

Smaller-scale water pollution is thought to be the cause of sporadic occurrences as well. Most of the cases in these regions are brought on by genotype 1 viral infection, with genotype 2 virus infections occurring significantly less often.

Hepatitis E infection is uncommon in places with superior water cleanliness, with just rare instances occurring on occasion. The majority of these cases are brought on by the genotype 3 virus and are brought on by infection with an animal-borne virus, often by consumption of undercooked animal flesh (including animal liver, particularly pork). These incidents have nothing to do with tainted water or other foods.

Clinical symptoms

Following HEV exposure, the incubation period lasts between two and ten weeks, on average between five and six. The virus is excreted by the infected individuals from a few days before to 3–4 weeks after the commencement of the illness.

Young individuals between the ages of 15 and 40 are most often infected with symptoms in regions with high disease endemicity. Although infections do affect children in these places, they often go misdiagnosed because they frequently show no symptoms or simply a minor sickness without jaundice.

Hepatitis often manifests as the first stage of mild fever, decreased appetite (anorexia), nausea, and vomiting that lasts for a few days, stomach discomfort, itching, skin rash, or joint pain, jaundice (yellow skin colour), dark urine, and pale faeces, as well as a slightly enlarged, sensitive liver (hepatomegaly). These symptoms generally last 1-6 weeks and are frequently difficult to differentiate from those brought on by other liver disorders.

Rarely, acute hepatitis E may become fulminant and be quite severe (acute liver failure). These patients run the danger of passing away. Hepatitis E in pregnancy increases the risk of severe liver failure, fetal loss, and death, especially in the second and third trimesters. If they have hepatitis E during the third trimester, up to 20–25% of pregnant women risk dying.

Immunosuppressed individuals, especially organ transplant patients using immunosuppressive medications, have been found to have cases of persistent genotype 3 or genotype 4 HEV infection. These are still rare.


Hepatitis E cases cannot be distinguished from other acute viral hepatitis cases clinically. However, inappropriate epidemiologic settings, such as when several cases occur in areas where the disease is known to be endemic, in locations where there is a risk of water contamination when the disease is more severe in pregnant women, or if hepatitis A has been ruled out, a diagnosis can frequently be strongly suspected.

The discovery of specific anti-HEV immunoglobulin M (IgM) antibodies to the virus in a person's blood is often sufficient in regions where the illness is prevalent for the diagnosis of hepatitis E infection. For field usage, rapid testing is available.

Reverse transcriptase polymerase chain reaction (RT-PCR) assays are additional procedures used to find hepatitis E virus RNA in faeces and blood. Specific lab equipment is needed for this experiment. In places where hepatitis E is uncommon and in rare instances of persistent HEV infection, this test is very necessary.


There is no particular therapy for acute hepatitis E that can modify its course. Hospitalization is often not necessary since the condition is typically self-limiting. The avoidance of unneeded drugs is crucial. Acetaminophen, paracetamol, and antiemetic drugs should be taken with caution or avoided. People with fulminant hepatitis must be hospitalized, and symptomatic pregnant women should also be given this option.

People with chronic hepatitis E who are immunosuppressed benefit from specialized therapy utilizing the antiviral medication ribavirin. Interferon has also been effectively employed in a few particular circumstances.


The best way to combat the illness is via prevention. At the community level, the transmission of HEV and hepatitis E infection may be decreased by maintaining public water supply quality standards and putting in place appropriate faeces disposal systems.

Individually, infection risk may be decreased by following hygiene procedures and refraining from consuming unpurified water and ice. Although not FDA-approved, hepatitis E virus (HEV239) vaccines are accessible in China. Research on the effectiveness of pre- or post-exposure immunoglobulin prophylaxis for preventing HEV in people is limited.

This is the next article of our monsoon series. To read the earlier articles of the series, click here: Malaria in monsoon: Recent updatesManaging dengue fever: What you should knowLeptospirosis: A commonly misdiagnosed diseaseKnow cholera: Diagnosis and treatment approachChikungunya: An overview of diagnosis and treatmentTyphoid Treatment in OPD: Recent UpdatesTreating Skin Infections in MonsoonInfluenza in Monsoon: How to Differentiate Between Flu and Common Cold?

Click here to see references


Disclaimer- The views and opinions expressed in this article are those of the author's and do not necessarily reflect the official policy or position of M3 India.

About the author of this article: Dr Monish Raut is a practising super specialist from New Delhi.

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