“Ayurvedic Management of Hepatobiliary Disorders”
Part-1
Prof. Muralidhara Sharma
based on the lecture available at
Ayurvedic Management of Hepatobiliary Disorders
The one important sentence in all the clinical field is that the assessment of Dosha, Dushya, and Lakshana in a patient is the most important criteria to suggest any medicines or prescribe the medicines. As usual, we start with the theory of ‘Rakta’ and its theoretical uses. It’s very well-known. I will not go into the theory much, but what’s important is the relationship between Rakta and Yakrita Pliha, which is mentioned in all of the texts. However, a very interesting issue is that diseases related to Yakrita are mentioned very few times as a subject throughout the text.
Diseases of Yakrita-
सर्वाङ्गप्रग्रहस्तीव्रो हृदि शूलश्च दारुणः |
श्वासो यकृति तृष्णा च पिपासाक्लोमजेऽधिका ||
(Sushruta Nidan Sthan 9/22)
सव्येतरस्मिन् यकृति प्रदुष्टे ज्ञेयं यकृद्दाल्युदरं तदेव ||
(Sushruta Nidan Sthan 7/16)
If you see all the text together, it’s only about the Yakritodara. Even the description of Yakritodara is very limited, mainly explained as Plihodara. Charaka or Sushurta even state that when a similar condition is presented on the right side, it is called Yakritodara. You won’t find any further description. However, there’s another very interesting and paradoxical issue that is popular globally or among people. It’s widely believed that Ayurveda holds the solution for all liver disorders. Every Ayurvedic pharmacy would have some preparation for liver disorders. Practically, it’s true that many liver disorder conditions find better solutions in Ayurvedic textbooks. But it’s very interesting, and I don’t know how to bridge this gap. The textbook has very minimal descriptions of the Yakrita, which is virtually the least described organ in the body. If you read more about the Yakrita in the textbook, it would be about Aahara (food), Yakrita in Aahara dravya kalakhanda, and Yakrita being an important resource of food in Mamsa dravya. At times, the colour of the Yakrita is compared to disease presentations like haemorrhoids. Other than that, the Yakrita vyadhi related to the Yakrita is very minimal. Now, that’s one of the interesting issues. However, we can definitely and effectively treat patients related to the hepatic system. That’s a very interesting issue. Now, how is this possible, and how have I assessed this condition? Those are the points I’m going to discuss next.
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Definitions of Acute liver diseases
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http://www.emdocs.net/acute-liver-failure-evidence-based-evaluation-and-management/
Now, of course, as we know, the liver is a very important organ with wide functions. It’s considered to be the biggest chemical factory in the body. All diseases, irrespective of their type, can ultimately lead to liver failure. When the liver fails to function, it can present in two manners: acute hepatic failure or chronic hepatic failure. Most of the time, the real cause of the disease lies in the background, and effective management will solely be based upon the status of the failure. Managing that failure is the major and number one criteria in the management of hepatic pathologies. The underlying pathologies and diseases come next. So, from that point of view, I will try to discuss the same issues in the same order: the failures, different stages of the failures, and then of course, a bit about the specificity of the disease conditions that can cause the failure. Now, acute hepatic failure is generally believed to manifest in a certain manner. Jaundice is considered a hepatic pathology, but the definition of hepatic failure involves coagulation pathologies. In all hepatic disorders, there is a possibility that the coagulation time would be increased, and the patient tends to have a bleeding tendency. This bleeding tendency is the number one criterion for hepatic pathologies in every acute hepatic failure. It is very important. Acute hepatic failure is always defined as a condition where the bleeding time, particularly the prothrombin time, is increased by about 1.5 or more. The universal standard is one, and when it is more than 1.5, that’s one of the important issues. There would also be neurological dysfunction in acute hepatic failure. Due to ammonia toxicity, all hepatic failure conditions tend to involve the brain tissues. One of the important functions of the liver is to convert ammonia into urea, an inert substance. When the liver fails to function, ammonia becomes highly sensitive to the nerve fibers, causing irritation and different degrees of hepatic incapability. This can range from simple confusion to deep coma, which are other important pieces of evidence.
And of course, when you define acute hepatic failure according to international standards, it should occur within a period of less than four weeks. There should not be any underlying disease; otherwise, any patient presenting with the signs is considered to have hepatic failure.
There is some confusion regarding the universally believed duration of acute hepatic failure. While it is commonly believed to be less than four weeks, the WHO has extended it up to about 26 weeks. The total duration should not exceed 26 weeks; if the condition persists beyond this timeframe, it is considered chronic failure. However, this explanation alone is not sufficient for providing management strategies.
Subclassification of acute liver failure
- O’Grady JG, Schalm SW, Williams R. Acute liver failure: redefining the syndromes [published correction appears in Lancet 1993 Oct 16;342(8877):1000]. Lancet. 1993;342(8866):273-275. doi:10.1016/0140-6736(93)91818-7
- Bernal W, Auzinger G, Dhawan A, Wendon J. Acute liver failure. Lancet. 2010;376(9736):190-201. doi:10.1016/S0140-6736(10)60274-7
- European Association for the Study of the Liver. Electronic address: easloffice@easloffice.eu; Clinical practice guidelines panel, Wendon, J, et al. EASL Clinical Practical Guidelines on the management of acute (fulminant) liver failure. J Hepatol. 2017;66(5):1047-1081. doi:10.1016/j.jhep.2016.12.003
From a management point of view, acute hepatic failure needs to be further classified into hyperacute, acute, and subacute. This classification is important when selecting patients and planning for their management. In hyperacute conditions, the most significant factor affected is the bleeding time and coagulability. On the other hand, in subacute conditions, the presentation of jaundice becomes the most important aspect. I think that column explains the whole issue in hyperacute conditions. The first line is about the coagulability in hyperacute cases, where the bleeding tendency is the most important. All of a sudden, before the patient develops jaundice, they present with bleeding. So it’s also related to how you see the patients. Some patients may present with only bleeding tendencies, and jaundice may not be seen or may be minimal. Another set of patients may have jaundice as the most common or initial presentation, with lesser impairment of coagulability. This also has an impact on the immediate management. A patient with acute bleeding tendencies requires immediate and energetic management. If the bleeding is not addressed promptly, it can be immediately fatal. In most cases, hyperacute conditions are beyond our reach for ayurvedic management, as they are highly acute emergencies. However, subacute conditions, which are commonly seen in viral hepatitis cases, are more manageable. I don’t mean to say all patients, but a majority of patients in the viral hepatitis category present as subacute or acute cases, with jaundice being the major clinical presentation. Impairment of neurological functions and encephalopathy features are comparatively milder in subacute conditions, whereas they are more common in other conditions.
Regarding the causes, paracetamol is given as the number one important cause for hyperacute conditions based on global data. It’s a very interesting issue. In India, paracetamol is used more frequently than salt in the kitchen, and it is sold as an over-the-counter (OTC) product. Every ‘Paan dukan’ would have paracetamol available, and every ayurvedic student and doctor would have paracetamol in their pocket. It is one of the most important causes of acute hyperacute hepatic failure. This fact needs to be stressed upon. In India, the incidence of hyperacute failures statistically is lower because we have more viral-induced pathologies. However, globally, where viral hepatitis is less frequent, paracetamol-induced hepatitis becomes more significant, and the incidence is quite high. I am not stating this based on personal opinion; I have references for all the information.
Clinical manifestations of acute hepatic failure
Moncrief T, Koyfman A, Long B. Acute liver failure: A review for emergency physicians. Am J Emerg Med. 2019;37(2):329-337. doi: 10.1016/j.ajem.2018.10.032
As I mentioned earlier, acute hepatic failure is a critical condition that can affect every organ in the body, not just the liver itself. Once the liver is affected, it has a ripple effect on all other organs, making management challenging. Each patient needs to be assessed individually, and the management plan should consider the involvement of all organs, leading to a wide range of outcomes. Some patients may experience spontaneous recovery, while others may have poorer outcomes despite effective management.
One of the crucial organs that require assessment is the renal system. Every patient with hepatic failure is prone to develop hepatorenal syndrome, which involves the kidneys. This can lead to impaired urinary output, resulting in potassium loss and reduced urine production. Fluid accumulation becomes an initial and significant complication, and regular diuretics cannot be prescribed in cases of hepatic failure. Instead, potassium-preserving diuretics are needed. When water accumulation occurs, it can progress to cardiac pathologies, causing fluid overload and impacting heart function. Cardiac failure or related issues, along with fluid congestion, follow as the next stage. Additionally, fluid backlog can affect the lungs, leading to lung congestion and ventilation issues. These become the next affected organs in the cascade. Simultaneously, hepatic failure also results in ammonia toxicity, with a high tendency for brain involvement. Encephalopathy initially manifests as confusion, but it can progress to deep coma. Assessing encephalopathy is an important criterion in patients with hepatic failure, considering its impact on the brain. Furthermore, other systems in the body can also be involved.
Collagen tissue is another crucial aspect affected by hepatic failure. Fragility of collagen tissues can result in typical textbook signs of subcutaneous hemorrhages, manifesting as web-like markings on the body. These are additional clinical signs that can occur. In the end stage, hepatic failure can even affect the bone marrow, impacting hemopoiesis and the production of red blood cells and other cells, which becomes critical.
Principal etiologies of the hepatic acute hepatic failure
European Association for the Study of the Liver. Electronic address: easloffice@easloffice.eu; Clinical practice guidelines panel, Wendon, J, et al. EASL Clinical Practical Guidelines on the management of acute (fulminant) liver failure. J Hepatol. 2017;66(5):1047-1081. doi:10.1016/j.jhep.2016.12.003
The principal common etiologies of the hepatic acute hepatic failure in our conditions. Among our situation where we practice, viral hepatitis are the most common causes of hepatic failure in our condition. Whereas the next common condition which we see would be the vascular pathologies like blood flow to the liver is affected often as a result of the secondaries in the abdomen, like malignancies are so on. Budd- Chiari syndrome where there is a sudden stagnation of the blood flow and often it can also be a complication of the alcoholism also. The other important causes pregnancy is the next common cause drugs. Another hepatotoxic drug also is very common. Majority of the drugs used in the clinical practice and which belong to the category of antibiotics also have a hepatotoxicity. And among that hepatotoxic drug, one of the important issues which you should remember is that most of these hepato toxic drugs have a tendency to have entero-hepatic circulation. Entero-hepatic circulation is a drug given in the first dose. It tends to get metabolized easily. But as you administer consequently the drug which has been excreted by the liver, would be re absorbed by the system and there is a tendency for the accumulation toxicity consequent doses they tend to produce accumulation toxicity. The majority of the hepatotoxic drugs misleading would be initially. When you start with the doses initially first one week, we may not see any of the signs of hepatic failure, but when you continue the same regime for a longer duration it can result in a hepatic failure, either acute or chronic. Now of course in that condition it can even result in a chronic hepatic failure. And the protocols for such drugs are always there. The protocols are to be strictly followed protocols. You have to review the dosage of the drug at regular intervals and if necessary, the dose has to be reduced. Most of the times, even specialized practitioners do not do this. They give you a prescription and ask maybe it could be like negligence of the patient. Also, patient may be continuing to take the same dosage of the drugs for months together or years together and this itself can be a cause for hepatic failure and many of the patients who come to you with lots of such prescriptions. If we screen those prescriptions and if you identify some of those drugs and withdraw the drugs or maybe modify the drugs as per the necessity definitely as some of the patients can be saved from hepatic failure. That’s the important issue, particularly one of the drugs which is quite frequently prescribed in the tuberculosis management is Pyrazinamide. It is one of the drugs. Rifampicin also is known to be having the hepatic failure conditions. Rifampicin, hepatic failure conditions they can be assess easily somewhat the clinical signs are obvious. Pyrazinamide is a silent killer. Silent killer in a sense you will not see the impact of the hepatic failure initially for one or two months even. Later the hepatic failure changes to occur. The regular prescription will be how to reduce the doses after two or three months, maximum three months, not more than that, but many times the patients will be continuing with that. And when a patient comes with that prescription, if you can modify that naturally you can contribute a lot so we can prevent that. So that’s all the important issue. So, whenever the patient comes with a huge number of prescriptions where just together prescriptions, we have to review about all the possible drugs which have a hepato toxic property and they need to be reviewed they have to be assisted. Many of those so-called tonics, there are many plenty of tonics given and when a patient takes plenty of tonics two or three or many times it would be like some square bottle, round bottle and the bottle with the red color, green color and so on. Most of these tonics they would have some preservative and these preservatives, they are supposed to be inert. But when you take two or three bottles of that tonic one in the morning, one in the afternoon and so on. This is the usual trend. It results in accumulative toxicity and that’s again one of the causes of hepatic failure. And I have seen many patients and I have that credit of saving many patients were reducing the number of chronic but many of the patients may not like that. So it’s a general trend like the patients would like to have a tonic and more than the medicines and with trying those tonics also would be one of the important contributions which are generally not recognized very usual practitioners.
The principal common etiologies of acute hepatic failure in our conditions are as follows: viral hepatitis is the most common cause, followed by vascular pathologies that affect blood flow to the liver, such as abdominal malignancies or Budd-Chiari syndrome. Alcoholism can also lead to hepatic failure. Another important cause is pregnancy, as well as hepatotoxic drugs, which are commonly used in clinical practice. Many antibiotics, which fall under the category of hepatotoxic drugs, have a tendency for enterohepatic circulation. Initially, when these drugs are administered, they are easily metabolized, but with subsequent doses, the excreted drug can be reabsorbed, leading to accumulation toxicity. Most hepatotoxic drugs may not show signs of hepatic failure during the first week of administration, but prolonged use can result in acute or chronic hepatic failure. Protocols for such drugs are available and should be strictly followed. Regular dosage review is necessary, and if needed, the dose should be reduced. Unfortunately, even specialized practitioners sometimes neglect these protocols. Patients may inadvertently continue taking the same dosage for months or even years, which can contribute to hepatic failure. By screening prescriptions and identifying potentially hepatotoxic drugs, patients can be saved from such complications. One frequently prescribed drug for tuberculosis management, Pyrazinamide, is known to be hepatotoxic. Rifampicin is another drug with potential hepatic failure risks, but the clinical signs are more apparent. Pyrazinamide, on the other hand, can silently cause hepatic failure, with symptoms only becoming evident after one or two months or even longer. Modifying the prescription by reducing the dose after two or three months, and not exceeding three months of use, can help prevent complications. Reviewing all possible hepatotoxic drugs in a patient’s extensive prescription list, including various tonics, is crucial. Tonics often contain preservatives, which are considered inert. However, when multiple bottles of tonic are consumed, cumulative toxicity can occur, leading to hepatic failure. Although modifying tonics can contribute significantly to prevention, some patients may be resistant to such changes due to their preference for tonics over medication. This trend is common, and the importance of reducing tonics is generally unrecognized by practitioners
Etiology of the Hepatic Failure
In India, viral hepatitis is the most common cause of acute hepatic failure, accounting for 44% of cases. The incidence of viral hepatitis is also significantly high. In contrast, in Western countries like England and America, the most common cause is paracetamol-induced hepatic failure, accounting for 57% of cases in the USA. The ratio of hepatic failure incidence between India and the USA is approximately 1:25, with 25 cases occurring in India for every one case in the USA. It’s important to note that in India, the larger number of cases and drug-induced conditions, including paracetamol-induced pathology, are generally categorized as unknown in Indian statistics. This is not a criticism of Ayurveda or any system, but rather an awareness of existing loopholes in our recording system. The World Health Organization (WHO) has expressed concerns about the health delivery system in India, specifically regarding hepatic virus issues, and has directed India to review its system. This concludes the discussion on the causes of acute hepatic failure.
