Cirrhosis is
a consequence of chronic liver disease, resulting in loss of function of liver.
Despite all advances in the fields of medicine and surgery, the progress of the
disease cannot be prevented; symptomatic treatment remains the mainstay of therapy.
Clinical
picture of the disease includes frequent complaints of weakness, fatigue,
muscle cramps and digestive symptoms such as anorexia, vomiting, abdominal
discomfort and peripheral oedema; ascites is most frequently encountered in
such patients, which is due to excess accumulation of fluid in peritoneal
cavity consequent upon portal hypertension.
Hepatic
encephalopathy is a complex neuropsychiatric syndrome characterized by
disturbances of behavior and consciousness, and personality changes. As the
condition becomes more severe confusion, disorientation, drowsiness and
eventual coma develop. A flapping tremor, hyper-reflexia and extensor planter
responses are usually present.
It is established
that Lithium ion (Li+) inhibits the hydrolysis of inositol-1-phosphate
in brain cells and selectively modulate the function of hyperactive neurons
which are responsible for the symptoms in manic state. The occurrence of
toxicity is related to plasma concentration of Li+, and its rate of
rise in plasma. Early toxic effects include nausea, vomiting, abdominal pain,
diarrhea, sedation and fine tremor.
Lithium
Carbonate increases total body water volume by increasing Aldosteron secretion
and sodium retention, thus playing causative role in production of oedema.
The
toxicological picture of Lithium Carbonate bears a great similarity to the
clinical picture of cirrhosis; thus Lithium carbonate in potency form would be
a reasonable therapy to get symptomatic benefits in the disease. Lithium
Carbonate was prepared in micro dose (2X and 3X) according to methods
enumerated in Homoeopathic Pharmacopoeia, and was administered to patients
suffering from cirrhosis of liver with Ascitis and oedema. Also, in some cases
in which neurological symptoms of encephalopathy developed, micro doses of
Lithium Carbonate were given. Doses and
duration were recommended separately for cases of cirrhosis with Ascites and oedema
and cases with neurological features.
Clinical
observations show that general symptoms like anorexia, nauea, vomiting and
abdominal discomfort improved remarkably in 75% cases within two weeks.
Cases of
ascites and oedema responded well in relatively early stages (less than six
months duration), and moderately in more chronic ones (more than six months
duration). Along with diminution of ascites, size of spleen reduced by ½”to 1”
in 60% cases and by less than ½” in 40% cases after 4 weeks of therapy, and
after 8 weeks it reduced by ½” to2”. Since Ascites and splenomegaly are both
outcome of portal hypertension, reduction of spleen was concomitant with
diminution of Ascites.
Early
neurological features like emotional and personality changes and flapping
tremor showed good response in 4 weeks which continued during follow up
observation.
Cases with
advanced neurological features such as mental confusion, drowsiness, extension
rigidity etc. exhibited objective improvement; but subjective symptoms of
mental aberrations persisted even after eight weeks of therapy.
Comatose
patients could not be treated with Lithium doses.