This document discusses Kamala or jaundice according to Ayurveda. It describes: 1. The pathogenesis of Kamala where excess pitta aggravated by rakta and mamsa dhatu causes the condition. 2. The clinical features of Kamala including yellowing of eyes, skin, urine and stool. 3. The progression of Kamala into more severe types like Kumbha Kamala over time if left untreated. 4. The treatment approach focuses on pacifying aggravated pitta and eliminating associated kapha dosha. So in summary, the document outlines the Ayurvedic view of the causes, presentation and management of jaundice or Kam

1. Dr. Vijay Singh Yadav
SENIOR RESIDENT & PHD SCHOLAR

2. KAMALA

3. Nidan & Samprapti
पाण्डुरोगी तु योऽत्यर्थं पपत्तलापि पिषेवते|
तस्य पपत्तमसृग्ाांसां दग्ध्वा रोगाय कल्पते||३४||
हाररद्रिेत्रः स भृशां हाररद्रत्वङ् िखाििः|
रक्तपीतशक
ृ न्मूत्रो भेकवर्णो हतेन्द्रियः||३५||
दाहापवपाकदौर्बल्यसदिारुपिकपषबतः|
कामला र्हुपपत्तैषा कोष्ठशाखाश्रया मता||३६||

4. If a patient of pandu roga excessively follows pitta vitiating diet and
regimen, the pitta so aggravated by involving the rakta and the mamsa
dhatu causes kamala.
Its clinical features are the-
 eyes, skin, nails and face of the patient become exceedingly yellow;
 stool and urine become reddish-yellow in color;
 complexion develops a coulor similar to that of a frog (found in rainy
season);
the senses get impaired;
 Burning sensation, indigestion, weakness, prostration and anorexia.
This kamala is caused by excess of pitta is known
as koshthashakhashrita.

5. कालान्तरात् खरीभूता क
ृ च्छ्
र ा स्यात् क
ु म्भकामला|
क
ृ ष्णपीतशक
ृ न्मूत्रो भृशां शूिश्च मािवः||३७||
सरक्तापिमुखच्छ्पदबपवण्मूत्रो यश्च ताम्यपत|
दाहारुपितृषािाहतिामोहसमन्द्रितः||३८||
िष्टापिसञ्ज्ञः पिप्रां पह कामलावाि् पवपद्यते|३९|

6. With the due course of time the disease (kamala) becomes deep seated
(kharibhuta) resulting in excessive dryness of the body or afflicted tissue and thus
becomes difficult to cure. This condition is called kumbha kamala.
Asaadhya Lakshan-
If the stool and urine of the patient (of kamala) become black and yellow;
develops excessive edema;
Eyes and face becomes red colored;
Vomit, stool and urine are mixed with blood;
The patient feels like going in darkness;
Burning sensation, anorexia, morbid thirst, constipation, drowsiness and
fainting;
The person looses his agni and consciousness;

7. पतलपपष्टपिभां यस्तु विबः सृजपत कामली||१२४||
श्लेष्मर्णा रुद्धमागं तत् पपत्तां कफहरैजबयेत्|
रूिशीतगुरुस्वादुव्यायामैवेगपिग्रहैः||१२५||
कफसम्मून्द्रच्छ्बतो वायुः स्र्थािात् पपत्तां पिपेद्बली|
हाररद्रिेत्रमूत्रत्वक
् श्वेतविाबस्तदा िरः||१२६||
भवेत् साटोपपवष्टम्भो गुरुर्णा हृदयेि ि|
दौर्बल्याल्पापिपाश्वाबपतबपहक्काश्वासारुपिज्वररैः||१२७||
क्रमेर्णाल्पेऽिुसज्येत पपत्ते शाखासमापश्रते|१२८|

8.  A patient of kamala if passes stools of the color of sesame paste (tila
pishta nibhama), then it denotes obstruction in the passage of pitta by
the kapha.
 Therefore, the pitta of such patient should be won by administration of
drugs which also eliminate kapha.
The excess usage of-
 Ununctuous, cold and sweet ingredients;
 Excessive exercise;
 Suppression of the natural urges leads to the aggravation
of vata infilterated with kapha and the displacement of pitta from its
site, resulting in the development of the following features:

9. The eyes, skin and urine of the patient become yellow while
his stools become white in color.
Other symptoms are-
 Atopa (tympanitis),
 Vishtambha (constipation associated with flatulence),
 Heaviness in the cardiac region,
 Due to the displacement of pitta in the peripheral tissues
(shakha), there is diminution in the flow of pitta resulting in
the gradual development of -weakness, agnimandya , parshva
shool , hikka , shvasa , aruchi and jwara.

10. jaundice
Jaundice is defined as a yellowing of skin, mucous membranes and
sclera due to the deposition of yelloworange bile pigment i.e. bilirubin.
The word Jaundice is actually a derivative of French word ‘Jaune’ which
means ‘yellow’.
Jaundice indicates the hyper bilirubinemia and that excessive level of
bilirubin may be in conjugated or unconjugated form.
The clinical presentations of jaundice appear when bilirubin level
exceeds 34.2 µmol/L or 2 mg/dL.

12. 80 % of bilirubin is derived from the heme group of haemoglobin.
This haemoglobin comes from the destruction of red blood cells in the
reticuloendothelium of liver, spleen and bone marrow.
The remaining 20% of bilirubin comes from multiple sources like
myoglobin, cytochromes etc.
The bilirubin produced is then transported to the liver in the bound
form with plasma albumin.
Conjugation of bilirubin takes place in the liver by UDP-glucronyl
transferase and this conjugation is essential for water solubility and
elimination.

13. The activity of UDP-glucronyltransferaseis influenced by
age, gender, thyroid hormones and microsomal enzyme
inducing agents, such as phenobarbital, rifampicin etc.
Conjugated bilirubin is excreted into the bile.
The bile is then passed to the duodenum via biliary system.
Inside the intestine some bilirubin is metabolized by the
intestinal flora into urobilinogens and then reabsorbed.
These urinobilinogens are then removed by the kidney and
excreted via urinary system.

14. Bilirubin metabolism

15. Bilirubin Metabolism
RBC Destruction(85%) Conjugated Bilirubin(<0.3mg/dl)
Spleen Biliary Duct
Release of Heme+Globin Intestine
Fe(Ferritin) Protoporphyrin Gut Bacteria
Unconjugated Bilirubin(Lipid Sol.)
Stercobilinogen(Stool color)
UCB+Albumin>>Circulation
*UDP:Uridine Diphosphate
*UGT:UDP Glucuronyl Transferase
Blood Kidney *UCB:Unconjugated Bilirubin
*CB:Conjugated Bilirubin
Urobilinogen (Normal Total Serum Bilirubin:0.1-1.2 mg/dl)
UCB UDP
Liver UGT
CB(Water Soluble)

16. Types
On the basis of causes Jaundice
can be classified into three types-
1. Pre-hepatic
2. Hepatic
3.Post-hepatic

17. Unconjugated
Hyper-
bilirubinemia
More Destruction
of RBC’s
Eg.Hemolytic
Anemia
Liver
Immaturity
New Borns
Physiological
Jaundice
Breast Milk
Jaundice
UGT
Defects(Reduced
enzyme activity)
Gilbert
Syndrome
Stress Induced like
Fasting,infection etc.
Criggler-
Najjar
Syndrome
Type 1(ZERO Activity of
Enzyme)
Type 2 (Reduced Enzyme
Activity)
Unconjugated Hyper-Bilirubinemia

18. Conjugated Hyper-
bilirubinemia
Bile Duct Obst.
Stone
Cancer
Infection
Biliary Tract
Disease
Primary Biliary Cirrohsis
Primary Sclerosing Cholangitis
Genetic Disease
Dubin-Johnson Syndrome
Rotor Syndrome
Clinical Features
Jaundice
Pruritis
Clay Color Stool
Stetorrhea
Mal absorption of Fat
Soluble Vitamins

19. Pre-Hepatic Jaundice
Pre hepatic jaundice is caused due to hemolysis therefore it is also
known as hemolytic jaundice.
The major cause of enhanced hemolysis is defective plasma
membrane of red blood cells.
This vulnerable cell membrane cannot bear the shear stress and
hence ruptures resulting in hemolysis thus causing the increased
serum bilirubin level.

20. Etiology
Congenital Causes
Spherocytosis
Elliptocytosis
Congenital LCAT deficiency
 Thalassemia
 Sickle cell anemia
Stomatocytosis
Acanthocytosis
Echinocytes
GSH synthase deficiency
Pyruvate kinase deficiency
G6PD deficiency
Erythroblastosis fetalis
Acquired causes
Resorption of extensive hematomas
Auto immune hemolysis
Transfusion reactions
Trauma
Microangiopathy
Infections e.g. malaria, etc.
Toxins e.g. snake venoms, etc.
Chemicals e.g. nitrites, aniline dyes,etc.
Paroxysmal nightly hemoglobinuria
Thrombotic thrombocytopenic purpura
Hypophosphatemia
Vitamin B12 deficiency
Folic acid deficiency

21. Clinical presentations
Patients with hemolytic jaundice are presented with-
Anemia
Yellowing of sclera
dark yellow-brown colored urine
yellowish skin
high bilirubin levels.

22. Hepatic jaundice
Hepatic jaundice is a type of jaundice in which the basic defect lies
within the liver mainly in the hepatocytes.
The liver captures bilirubin from plasma proteins mainly albumin, then
after conjugation excretes in the bile via biliary system.
Any pathology of the liver leading to defect in capture, conjugation and
excretion can cause hepatic jaundice.
Main enzyme of conjugation is UDP-Glucronyltransferase.
This is commonly immature at birth and its under-activity can cause so
called Neonatal Physiological Jaundice.

23. Further this enzyme can be defective due to the genetic mutation of
the UTG1A gene on chromosome 2.
This gene encodes for UDP-Glucronyltransferase and thus the defective
conjugating enzyme leads to the hepatic jaundice.
Any defect in the hepatic excretory mechanism of bilirubin can also
cause hepatic jaundice.
The excretory mechanisms involve hepatocytic bile acid-independent
secretion, hepatocytic bile acid-dependent secretion and bile ductular
secretion.
Any defect in the above mentioned excretory mechanisms can lead to
the accumulation of bilirubin in blood causing hepatic jaundice.

24. Etiology
Congenital causes
Wilson’s Disease •
Rotor’s Syndrome
Haemochromatosis
Crigler Najar syndrome
Gilbert’s syndrome
Dubin-Johnson’s syndrome
Acquired causes
Viral Hepatitis
Alcoholic Hepatitis
Auto immune Hepatitis
Drug related Hepatitis (e.g. NSAIDs)
Sepsis
Pregnancy
Systemic Diseases (e.g. celiac disease)
Malnutrition
Physical Trauma
Hepatic Adenoma

25. Clinical presentations
The clinical presentations of hepatic jaundice include-
Abdominal pain,
Fever,
Vomiting and nausea along with the complications involving satiety,
gastrointestinal bleeding, diarrhoea,
Anemia,
Edema
weight-loss and associated weakness,
if unchecked leading to mental disturbances like kernicterus, coma or even
death

26. Post hepatic jaundice
Post hepatic jaundice is such type of a jaundice in which the cause
lies in the biliary portion of hepatobiliary system.
The major cause of post hepatic jaundice is extra-hepatic biliary
obstruction.
Therefore it is also known as obstructive jaundice.

27. Etiology
Congenital causes
Biliary Atresia
Cystic Fibrosis
Idiopathic dilation of common
bile duct
Pancreatic biliary malfunction
Choledochal Cyst
Acquired Causes
Portal biliopathy
Cholecystitis
Trauma
Pancreatitis
Strictures
Choledo cholithiasis
 AIDS
 Intra-Abdominal Tuberculosis
 Tumors
 Common bile duct Obstruction

28. Clinical presentation
The clinical manifestations of obstructive jaundice are –
Dark urine, pale stools
Generalized pruritus
History of fever
Biliary colic
Weight loss
Abdominal pain and
Abdominal mass are also the representatives of obstructive jaundice
Obstructive Jaundice may lead to various complications including cholangitis,
pancreatitis, renal and hepatic failure.

29. Differential diagnosis
The pre-hepatic jaundice can be differentiated from hepatic and
post hepatic jaundice exclusively on the basis of elevated serum
levels of unconjugated bilirubin and urobilinogen, which are raised
in case of pre-hepatic jaundice.
The serum levels on conjugated bilirubin, alkaline phosphatase,
Alanine transferase and Aspartate transferase are seen normal in
the case of pre-hepatic jaundice. The urinary excretion of conjugated
bilirubin is also not present in pre-hepatic jaundice.

30. The hepatic jaundice can be differentiated from post hepatic
and pre hepatic jaundice on the basis of five times high
bilirubin levels.
In hepatic jaundice due to hepatitis the bilirubin levels may be
ten times higher than their maximum values.
Hepatic jaundice can be differentially diagnosed from post
hepatic jaundice on the basis of abdominal ultrasonography
and other radiological technique.

31. However the hepatic jaundice can be differentiated from pre-
hepatic jaundice on the basis of diagnostic markers, like alpha-
1 Antitrypsin, Ceruloplasmin,Immunoglobulins,etc.
Elevated serum bilirubin level along with the conjugation is a
key diagnosis of post hepatic jaundice.
Serum bilirubin is usually less than 20 mg/dL.
In pancreatic cancer the serum bilirubin may rise up to 40
mg/dL.

32.  Serum Gama-glutamyl transpeptidase (Serum GGT), alkaline
phosphatase and transaminases may be elevated.
 Tumour markers like CA-125, CA19-9 and CEA are usually
elevated in cancerous obstruction.
 The diagnosis of obstructive jaundice can further be
confirmed by-
 Ultrasonography, plain abdominal x-ray, computed
tomography, contrast-enhanced multi sliced computed
tomography, endoscopic retrograde cholangiopancreatography
(ERCP), Percutaneous trans-hepatic cholangiography (PTC),
Endoscopic Ultrasound, Magnetic Resonance
cholangiopancreatography (MRCP), Cholescintigraphy,
Radionuclide scanning angiography and Staging Laparoscopy.

33. Thank You