Lecture Note: “Ayurvedic Management of Hepatobiliary Disorders” (Part-2)

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 “Ayurvedic Management of Hepatobiliary Disorders”
Part-2

 Prof. Muralidhara Sharma 

based on the lecture available at
 Ayurvedic Management of Hepatobiliary Disorders 

The chronic hepatic failure is not very clearly defined as such. Most of the time, chronic hepatic failure is when the duration is more than four weeks, and the patient has evidence of fibrosis or necrosis in the liver. This falls between categories such as cirrhosis. Cirrhosis is defined as necrosis, fibrosis, and regeneration of the liver, wherein partial regeneration and other related issues are present. In the case of chronic hepatic failure, jaundice may not be the typical clinical presentation. Instead, hypoalbuminemia, indicated by low albumin concentration, is observed. Albumin is an important substance synthesized by the liver. In earlier days, when we were students, we used to rely only on the albumin globulin ratio. However, now albumin can be directly accessed, and if the albumin level is less than 6 grams, it is one of the most common causes of chronic hepatic failure. Unfortunately, in many routine investigations of hepatic pathology conditions, the assessment of albumin is often missed, either due to negligence or oversight. Missing this assessment can lead to overlooking many cases of chronic hepatic failure. Therefore, whenever we conduct hepatic function tests or liver function tests, assessing the albumin level is crucial and should not be overlooked. This is another important point that is often missed.

  Acute on chronic liver failure  

Siba Y, Obiokoye K, Ferstenberg R, Robilotti J, Culpepper-Morgan J. Case report of acute-on-chronic liver failure secondary to diffuse large B-cell lymphoma. World J Gastroenterol. 2014;20(44):16774-16778. doi:10.3748/wjg.v20.i44.16774

Now there is one more variation: acute and chronic hepatic failure, which we frequently encounter in patients with chronic failure. Suddenly, the patient develops acute failure, and in most cases, this condition is almost a death sentence. The mortality rate is very high, almost 100%, despite the availability of treatment. The only other solution now available is liver transplantation, which I casually referred to earlier. This is one of the issues. Acute and chronic hepatic failure can often be misleading in clinical presentation because they may present with acute sepsis or acute septic pathology. Occasionally, the hepatic failure in these cases may be missed, and the patient may have an uncontrolled infective presentation elsewhere. It could be pulmonary infections, gastrointestinal tract infections resulting in mesenteric vein thrombosis and persistent rectal bleeding, or cutaneous infections leading to significant pyoderma-like presentations. In such conditions, even if it is a septic pathology, the total leukocyte count may not be very high. Normally, in septic pathology, we expect the total leukocyte count to be elevated, and it serves as one of the criteria to assess the severity of infections. However, in acute and chronic hepatic failure, the total leukocyte count will be moderately raised or, in many cases, even lower than normal, despite the presence of acute sepsis. This is another clinically misleading presentation.

  Hepatitis Viruses  

let’s discuss the general issues about acute and chronic hepatitis. Among the diseases we treat, the majority of them are viral hepatitis. Viral hepatitis is the most common, and many people mistakenly believe that all viral hepatitis is the same. But it’s not true. There are many varieties of hepatitis viruses that have been identified, ranging from A, B, C, D, and E, with the possibility of more categories being identified in the future. However, these new categories have not yet entered regular clinical practice. From our clinical perspective, the incidence of diseases we observe in our area shows that the majority of patients have hepatitis A, followed by hepatitis B. So, let’s discuss more about hepatitis A and B.

Hepatitis C is a budding disorder, a new issue emerging on the horizon. Information about hepatitis C in Indian circumstances is limited, and WHO has already provided guidelines for better screening methods for hepatitis C. Initially, when we were studying it, hepatitis C was considered exclusive to kidney transplantation or dialysis therapy, specifically affecting dialysis patients. However, this is not the case anymore.

Now, the primary difference between hepatitis A and B is important. Hepatitis A is transmitted through the fecal-oral route, typically through contamination of consumed food substances. On the other hand, hepatitis B is transmitted through body fluids such as blood serum or sexual transmission, as well as the possibility of fluid exchange. The hepatitis B virus can cause infections. Another important difference lies in the incubation period. Hepatitis A usually has an incubation period of about two weeks, 14 to 20 days, or 2 to 3 weeks. However, with hepatitis B, the incubation period can be much longer, even up to about 100 days, making it easier to miss the linkage between the infection and its presentation. In the case of hepatitis C, the incubation period can be as long as six months. These differences in incubation periods can create clinically misleading conditions. As for the other viruses, they are not significant from our current clinical standpoint. Let’s casually leave out D and B, as the differences are not substant

  Number of reported hepatitis outbreaks by state-India,2011 -2013  

A and B are very critical in our management and patient selection. C is also becoming important, and the outcomes in the case of A and B are different. So, I’ll try to discuss the differences between A and B to a certain extent. Before delving into that, it’s worth noting that Viral hepatitis A is particularly presented as an epidemic, and India is considered a treasure house for hepatitis A. India always has the highest incidence, with states marked in black having the maximum incidence, and those in dark blue come next, like Karnataka. Some states have comparatively lower incidences. This also holds significance when dealing with patients presenting with jaundice most of the time. Now, here, every person, or rather, the common man, would say that every jaundice case is hepatitis. They believe that every patient presenting with yellow color will have a uniform identification, but that’s not the true issue.

Kumar T, Shrivastava A, Kumar A, et al. Viral Hepatitis Surveillance–India, 2011-2013. MMWR Morb Mortal Wkly Rep. 2015;64(28):758-762. doi:10.15585/mmwr.mm6428a3

Another interesting issue is that initially, when we were studying hepatitis A earlier, it was considered a disease that predominantly presented in the summer or rainy season, usually in July. The incidence was higher during that time, while it was lower in winter and other seasons. However, the trend is gradually changing, as per our national statistics from 2007-2011. In the past four years, there has been a change in the incidence trend. Now, it has become prevalent almost throughout the year, although the incidence is still highest in the summer, particularly in North India during the rainy season in July or so. That’s the usual duration. Previously, the maximum incidence was only during that period, while it was lower in other seasons. Now, it is present almost throughout the year because the virus can grow much more effectively than human beings and can survive in various weather conditions.

  Changing trends in hepatitis A epidemics  

Another interesting issue is that initially, when we were studying hepatitis A earlier, it was considered a disease that predominantly presented in the summer or rainy season, usually in July. The incidence was higher during that time, while it was lower in winter and other seasons. However, the trend is gradually changing, as per our national statistics from 2007-2011. In the past four years, there has been a change in the incidence trend. Now, it has become prevalent almost throughout the year, although the incidence is still highest in the summer, particularly in North India during the rainy season in July or so. That’s the usual duration. Previously, the maximum incidence was only during that period, while it was lower in other seasons. Now, it is present almost throughout the year because the virus can grow much more effectively than human beings and can survive in various weather conditions.

  Basic difference between hepatitis A and B  

This virus produces an immunological reaction, and the immunoglobulin levels will be raised, remaining elevated for up to a maximum of about two months. After that, there will be no infectivity, indicating that the patient is cured .Once the patient experiences symptomatic relief after about two months, traces of the immunoglobulin will not be found in the body. However, with the HBsAg (hepatitis B virus), the situation is different.  The immunoglobulin levels reach their maximum in the initial stage, lasting for one or two months, and can persist for many years, or even for the patient’s entire life. The immunoglobulin may remain active while the virus stays dormant in the body, which is a dangerous aspect of hepatitis B. Many individuals may be clinically asymptomatic but still be carriers of hepatitis B. Their serum will test positive, and these individuals can silently transmit the disease to others without showing clinical symptoms.

Therefore, when dealing with a patient with hepatitis B, it is important to screen individuals who have come into contact with that patient and assess the potential contamination of serum products. Nowadays, there are universal criteria in place. For example, if there is a need to collect blood, it is mandatory to screen for HBsAg. This screening is not only necessary for blood transmission but also applies to the use of injections, syringes, needles, and potential contamination in surgical procedures.

If a patient undergoing surgery tests positive for HBsAg, there is a risk for the entire surgical team, including surgeons and others. Risk assessment is crucial in such cases, not only for the transmission to others but also because HBsAg is known to produce delayed complications. These complications can manifest years later, such as the development of hepatocellular carcinoma. Hence, it is essential to assess these patients and effectively manage their condition. This summarizes the key points about hepatitis.

 Clinical outcomes of Hepatitis B infection  

Hepatitis B World Health Organization, Department of Communicable Diseases Surveillance and Response WHO/CDC/LYO/2002.2: Hepatitis B

Now I consider this all these viral hepatitis, both A and B as Pittaja Jwara, It’s not kamala. I don’t consider this as kamala though in general. Again, something different from the usual trend. Kamala as such mentioned in the text easier complication of Pandu and in the delayed stages ultimate stages only the kamala is produced and it’s not only about the yellowish discolorations in kamala.

 Pittaja Jwara    

वेगस्तीक्ष्णोऽतिसारश्च निद्राल्पत्वं तथा वमिः |
कण्ठौष्ठमुखनासानां पाकः स्वेदश्च जायते ||
प्रलापः कटुता वक्त्रे मूर्च्छा दाहो मदस्तृषा |
पीतविण्मूत्रनेत्रत्वं पैत्तिके भ्रम एव च ||
( Su.U.T.39/31,32)

Samhitas would describe hundreds of diseases where there could be a yellowish discoloration; it’s not only the other. So I’ll come to the other certain of the other diseases later. But I consider it as Pittaja Jwara, and I treat all the patients of hepatitis as Pittaja Jwara. The differences, in terms of this A and B, would be in terms of the total outlook about the treatment. But my prescription would be the same. And the description in the text is exactly the same, like where you have a Tikshana vega and Vami, i.e., the vomiting or gastrointestinal tract abnormality, and at the same time, the possibility of encephalopathy.

Pralapa where the patient would have the possibility of encephalopathy sense and even the possibility of bleeding from the oral or other areas.EIn advanced stages, it can result in hepatic coma like Mada, Murcha, etc., which also can be the other clinical sense.

Hence, it is very practical to consider all the hepatitis variety patients as a Pittaja Jwara.

  Encephalopathy-  

स गात्रस्तम्भशीताभ्यां शयनेप्सुरचेतनः ||
अपि जाग्रत् स्वपन् जन्तुस्तन्द्रालुश्च प्रलापवान् |
संहृष्टरोमा स्रस्ताङ्गो मन्दसन्तापवेदनः ||
ओजोनिरोधजं तस्य जानीयात् कुशलो भिषक् ||
((Sushruta Uttartantra 39/43,44,45)

Only the differences will be in advanced conditions where there would be encephalopathy. Encephalopathy is described as Ojovisransa, which is also a complication of Pittaja jwara or Sannipataja jwara and can produce the same ” Ojovisransa, yasya pittanilsamuchhayata.”When there is a possibility of Pittaja jwara and Vata, that results in the Ojovisransa, and that’s considered as Asadhya. “Ojonirodhjam tasya janiyat kushlo bhisaka” and these are considered as Asadhya as such. That’s about the other important signs which we can make out.

  Workout and management A and E  

दीपनी पाचनी लघ्वी ज्वरार्तानां ज्वरापहा |
अन्नकाले हिता पेया यथास्वं पाचनैः कृता ||
(Sushruta Uttartantra 39/109,110)

When a patient comes to me with a history of jaundice and fever, which is usually limited to that category of hepatitis conditions, the important investigations that are necessary are a liver function test. In this, the albumin level is one of the crucial issues. And then, the Prothrombin time is a very important criterion. Screening HBsAg is also important and it is important to note that HBsAg may not be positive in patients with the B virus in the first week. So, many times you may have to repeat that HBsAg after about two weeks, and then the USG is also necessary to see whether there is a chronic change or not. Hepatic changes like fibrosis and so on are not important issues.

The management would be the most important part, particularly in hepatitis virus A. It’s usually a self-limiting disorder, even if you do not give any medicines. Patients may recover, provided there are no other complications, and the best means to prevent complications is rest. So, absolute rest is required. When I say rest, it’s not only sleeping; you also support the rest of the gastrointestinal tract. The maximum energy-consuming activity of the body is the digestion of food. You do not really spend more energy when you climb the stairs, but you spend more energy when you have taken the food and that food is being digested. And hence, the principle of Langhana is the most important crucial part in the management, particularly of hepatitis fever. In every Jwara condition, it is crucial, but there has to be a more important priority. Langhana doesn’t mean fasting. Langhana means the administration of Laghu Dravyas. It’s the most important part, more than any of the medicines and diet also. The only hepatoprotective diet is a carbohydrate-containing diet with lesser protein and no fat. That’s the usual diet that has to be given, and that’s exactly what is mentioned as deepanam, paachanam, etc. The quality of the drug should be of the same diet should be any of that.

My prescription remains the same: Mritunjaya, Arogyavardhini, and Kumariasava. The only important point is that I would avoid treating hyperacute liver failure conditions, as our medication cannot manage them. As I mentioned before, severe coagulopathy cases with prolonged bleeding time or prothrombin time exceeding 1.5 times or more cannot be effectively managed with our medicines. These conditions can undergo sudden and potentially fatal complications, so I prefer to avoid such patients. However, subacute conditions can definitely be effectively managed by following this regimen. Another important issue to consider is electrolyte imbalance. Many patients may experience hypokalemia, where potassium levels tend to decrease during the course of treatment. If necessary, potassium supplementation may be prescribed occasionally. I do occasionally prescribe a potassium-preserving diuretic like Aldactone, depending on the individual case, but it is not necessary for all patients. However, monitoring for hypokalemia is necessary and supplementation should be provided if there is a tendency for low potassium levels during the treatment duration.

 Key points: 

 Management 

  • Rest
  • Diet: -only cooked fat-free, carbohydrate-rich

Prescription:
Mritunjaya
Arogyavardhini
Kumari Asava

3 weeks in HAV, 3 months in HEV, and 6 months in HBV

  Investigations to be performed:   LFT, Prothrombin time, HbsAg, USG

The other difference between A and B is in A virus, our total treatment can be three weeks, and after three weeks, we can definitely stop the treatment. But in the case of Hepatitis B pathology, it cannot be limited to that; it has to be either six months or even longer until the patient becomes HBsAg-negative. One group of patients who come to us falls into that category. They are diagnosed as HBsAg carriers, and I don’t know who coined the term “white jaundice,” but it’s quite popular in society. Some people consider white jaundice to be anemia, while others associate it with the diagnosis of HBsAg. These patients often discover their positive status when applying for a visa or attempting to donate blood, and then they seek Ayurvedic treatment. Based on my clinical observation, I have noticed that patients who have had an episode of jaundice can definitely test negative with our treatment if they persist with it for either three months or six months, sometimes even longer. The treatment includes the use of Mritunjaya, Arogyavardhini, and Kumariasava. However, patients who have never experienced clinical jaundice but test positive for HBsAg often fail to achieve negativity. Although their globulin levels may slightly diminish, they tend to remain positive. This information is crucial when counseling patients about the possible outcomes. It’s challenging to manage these cases, and I don’t know the exact reason. I don’t have any scientific explanation to substantiate this observation, but it is purely based on clinical experience. Patients who have never had jaundice but test positive for HBsAg are difficult to treat in terms of achieving negativity. Although they appear clinically normal, the risk of being a carrier persists.

  Hepatitis B Carrier State  

Poortahmasebi, Vahdat & Salarian, Ali & Amiri, Mehdi & Poorebrahim, Mansour & Jazayeri, Seyed Mohamad & Ataei, Atousa & Asghari, Matin & Alavian, Seyed. (2017). Integrated Analysis of Gene Expression Profiles Reveals Deregulation of the Immune Response Genes during Different Phases of Chronic Hepatitis B Infection. Hepatitis Monthly. In press. 10.5812/hepatmon.42237

Now, the carrier state, as I mentioned before, the patients with the carrier state, they are the silent killers and can potentially harm others more than they damage themselves. So it’s important to screen the family members. Screening the family members is an important issue because many times the whole family may be HBsAg positive without being aware of the situation. Thus, it becomes an issue. Moving on, the final outcome for all these patients could be recurrent hepatitis. It may also lead to fibrosis, cirrhosis-like changes, or even hepatocellular carcinoma. However, the exact duration for these complications cannot be determined in many cases. It could take many years, such as 20-30 years, or even until the end stage before a specific carcinoma is diagnosed. Such difficult complications remain a concern for the patient.

Nevertheless, what I have observed is that if the patient follows the diet restrictions and takes these medicines, we can delay the onset of complications for a longer period. However, predicting whether the treatment has truly benefited the patient is difficult because we don’t know the exact timeframe for the development of complications. So, as long as the patient is under our treatment and has not developed complications, we can conclude that our treatment has prevented them. Therefore, the idea of results remains somewhat uncertain. However, I still manage the patients with the same line of treatment: Mritunjaya, Arogyavardhini, Kumariasava, and diet restrictions.

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