Name : Mr.XXX
Age : 64 year / male
Religion : Hindu
Address : Thiruvalla
Occupation : Retd. Govt. Employee
Presented on 12th Dec. 2003

Presenting Complaints
1. Sleeplessness (4 mths)
2. Increased frequency of urination (4 mths)at night
3. Drowsiness (4mths)
4. Repeated attacks of absent attacks and memory loss (4mths)
Associated with confusion of mind

History of presenting Symptoms
Complaints started about 6 months back as oedema of both lower limbs and he was diagnosed as having hypertension and took allopathic treatment. Then about 4 monthss back, he developed the Symptoms of Sleeplessness, anxiety, increased frequency of urination, weakness and occasional memory loss. Then he was undergone a detailed check-up in Amritha Institute of Medical Sciences and was diagnosed as having chronic liver disease with portal hypertension. There they done endoscopic bandaging of oesophageal varices, and went home. But after that his condition become worse. He developed absent attack and memory loss most frequently. During that absent attack, his mouth will be open and there will be dripping of saliva. He was not able to recognise anyone, and has disorientation & confusion. This will last for a few seconds. Then again he went to the hospital and diagnosed as having hepatic encephalopathy in its 1st stage. He was given medicines like lactulose solution and propananol for that, with no relief of his complaints.

Past history
No relevant history in the past.
Known hypertensive and diabetic for 6 years. He was taking allopathic medicines for that.
Family history :- No relevant family history
Personal history
I Habits :- Habit of drinking alcohol
II Life Situation
Born and brouht up at Thiruvalla
Educational Status : Pre-degree
Occupation : Rtd. Govt. Servant
Socioeconomic Status : Hailing from a middleclass family. Married and is having 3 children

III Patient as a person
a. Developmental landnmark :- Normal
b. Physical Characteristics
Prefes to lie on abdomen.
Stomach and abdomen
Appt N Desires fish+++, sweets & meat
Thirst increased Desires warm food and drinks.
Eliminations
Bowels (R)
Urine increased frequency at night
Sweat Reduced
Clothing :- want to be covered. chilly
Sleep :- decreased, disturbed sleep
No particular dreams
Sensorium :- disturbed, foregetfullness
c. Mental features
Very anxious and apprehensive
Has a childish behaviour. He is very sensitive and will cry on silly things. He is very slow in doing things and slow to comprehend things. Patient is very Sympathetic to others. He desires company and doesnot want to be alone. Has memory loss. Fear of disease.
d. Ailments from :- Alcoholism
Regionals
1. Dimness of vision
2. Oedema of both lower limbs

Physical examination
A. General
Moderate built. Moderately nourished
Slightly icteric
There is pedal oedema
No pallor, No cyanosis, No Cymphadenopathy
Pulse 62/mt.
Resp. rate : 16/mt.
BP : 120/80 mm. of Hg
Temp. : 98.60f.

Systemic Examination
1. CNS
a) Mental fuctions
Appearance, behaviour and communication
Idiotic appearance
Confusion
Talk irrelevent things occasionally
Emotional make-up
No signs of depression or elation
Anxious
Sleeplessness
Delusions & halluacination
Absent
Orientation of time and space
Disorientation of place & time.
Unable to recognise others occasionaly.
He was not able to remember the date and estimate time
Altered counciousness and lethargy.
Present occasionally
Confusion :- Present
Memory :- Recent memory loss.
Unable to remember the dates events correctly.
Intellegence :- Intellectual ability is low.
b) Speech and language :- No dysarthria or aphasia
c) Cranial nerves :- Normal functions
d) Motor functions :-
Movement & strength - Normal
Bulk of muscles - Normal
Tone of muscle - Normal
e) Sensory functions :- Normal
2. GIT
Abdomen is slightly distended
No visible pulsations, swelling and peristaltic movts are seen.
No tenderness on palpation. No fluid thrill
Abdominal organs are not palpable
3. Respiratory System - NAD
4. CVS - NAD

Diagnosis of the disease
Provisional diagnosis
Portal hypertension, with hepatic encephalopathy (1st stage)
Investigations
2nd Dec. ‘03
USG :- Impression:- Chronic Liver disease with portal hypertension. Liver is normal in size coarse eachotexture. Spleen is enlarged (12.5 cm.) Spleenorenal Collaterals.
Lab:- FBS 95 mg.%
PPBs 154 mg.%
S. bilirubin total 3.3 mg./dc. (N 0.2-1)
S. bilirubin direct 0.7 mg./dc. (N 0-0.3)
cholestrol total 137 mg./dc. (150-250)
LDL 73 mg./dc. (90-149)
Hb 15.6% platelet count 123 ok/ul (150-450)
ESR 8 mm./hr.

Final diagnosis
Portal hypertension with hepatic encephalopathy (1st stage)

Diagnosis of the patient
A. Analysis of Symptoms
Patient Symptoms                            Disease Symptoms
1. Anxiety                                        Mental confusion
2. Sensitive                                  Slow in comprehension
3. Sympathetic                                    Stagerring gait
4. Fear of disease                                    Insomnia
5. Desires company                             Pedal oedema
6. Desires:- fish              Increased frequency of urination sweets
warm food & drinks
7. Desires covering
8. Habit of alchoholism

Miasmalic expression
Psora         Syphilis                             Sycosris
Anxiety   Habit of alcoholism         Portal hypertension
Sensitive   Insomnia                        Pedal oedema
Sympathetic                              Impaired intellect
Desires covering
Desires:- fish
sweets
warm food & drinks

Evaluation
Mental general :- Anxiety
Fear of disease
Sensitive
Sympathetic
Weeps easily
Slow in comprehension
Loss of memory

Physical general
Desires :- Sweets
Warm food & drinks
Wants covering
Prefer to lie on abdomen
Sleeplessness

Particulars:- Pedal oedoma
Increased frequency to urinate Night

Repertorial totally
Mind - Sensitive
Mind - Confusion
Mind - Fear of disease
Mind - Dulness Repertorial result
Mind - Chrildish
Mind - Dipsomania
Stomach Desires - Sweets
Stomach Desires - Warm food
Stomach Desires - warm drinks
Sleep - Sleeplessness

Management
General:- Rest
Nutritious food. Restrict protien in take
Avoid alcoholism

Medicinal Management
12th Dec. ‘03
Avena sativa /(8-0-8) x 1 week (alcoholism, insomnia. As a specific medicine for brain complaints)19thDec`03
Cardus Mar /(8-0-8) x 10 days (As a specific medicine for liver complaints)
Sleep good
ed. frequency of urination was reduced.
Weakness - better
No staggering gait
No memory loss & absent attack.
30th Dec.‘03
Rpt for 10 days
FBS 70
Bilirubion - total 0.9
Sleep good
11th Jan. ‘04
Baryta carb 6 x /(1-1-1)
x 1 month
(As a constitutional medicine. Idiotic appearance. Difficult comprehension. Childish behaviour)
10th feb 04’
Much improvement of symptoms weakness was much better
BP - 100/50 mm. of Hg Rpt 1 month

(Stopped antihypertensive medicines. Take lacture solution occasionally only during weakness)
15th March 04’
Weakness Occasionally Baryta carb 30/2d daily
x 1 month
16th April 04’
Stopped all allopathic medicines Rpt for 1 more month
(No weakness,Sleep good,good memory).

PORTAL HYPERTENSION

   Portal hypertension is a condition characterised by prolonged elevation of the portal venous pressure (normally 2-5 mm Hg). Patients developing clinical features or complications of portal hypertension usually have portal venous pressure above 12 mm Hg. As portal hypertension produces no symptoms it is usually diagnosed following presentation with decompensated chronic liver disease and encephalopathy, ascites or varical bleeding.

ANATOMICAL AND PHYSIOLOGICAL CONSIDERATIONS
The liver has a dual supply from both hepatic artery and the portal vein. 80% of blood supply is from the portal vein and 20% from the hepatic artery.
Hepatic artery arises from coeliac trunk of the aorta, along with Spleenic artery. After branching to firm the gastroduodinal artery it branches to produce right and left hepatic arteries.
Portal vein is formed by the union of superior mesentric and spleenic veins, which in tern drain the splachnic and spleenic beds. Coronary or left gastric vein which drains the lesser curve of the stomach and the lower oesphagus, enter into the origin of portal vein. The inferior mesentric vein, which drains the left hemicolon, and most of the rectum, and joins the spleenic vein just before its confluence with the superior mesentric vein. After division into left and right branches, hepatic artery parallels the portal system, and subsequently divides into branches corresponding to the segmental anatomy of the liver.
The portal venous system is entirely devoid of valves. Numerous small tributaries connect the portal and systemic venous systems, and there can evolve into major collateral channels when portal hypertension superveins formation of such collaterals is triggered when portal pressure rises above the normal level of 5 to 10 mm Hg.
The most important of these portal - systemic channel is the
Left gastric or coronary vein, which connect the oesophageo-cardiac venous plexus with the spleenic or portal vein.
The short gastric and left gastroepiploic vein, connecting oesophageal and gastric plexus with the spleenic vein.
Numerous retroperitoneal portal radicles, which connect to the left renal via the left adrenal vein.
The umbilical and periumbilical veins connecting to the left portal vein.
The inferior mesentric vein connecting via the superior haemarrhoidal veins of the systemic circulation.
When flow to the sinusoids is significantly reduced, a compensatory increase in hepatic arterial inflow takes place to provoide the liver O2 requirements.

AETIOLOGY AND PATHOGENESIS
Portal venous pressure is determined by the portal blood flow and by the portal vascular resistance. Increased vascular resistance is usually the main factor producing portal hypertension irrespective of its cause.

Causes of portal hypertension according to site of portal venous obstruction.
I Presinusoidal obstruction
a) Portal vein thrombosis
Neonal umbilical sepsis
Dehydration
Portal pyaemia
Hypercoagulable states (polycythacmia, oral contraceptives)
Periportal inflammation (pancreatitis)
Trauma (accidental, iatrogenic)

b) Intrahepatic
Congenital heptic fibrosis
Idiopathic portal hypertension, non-cirrhiotic portal fibrosis
Schistosomiasis
Myeloproliferative disorder
Systemic mastocytosis
Primary biliary cirrhosis (early)
Toxic causes (Arsenic, vit - A intoxicion, Vinylchloride, Cytotoxins)
Sarcoidosis
Gaucher’s disease

c) Extrinsic compression
Periportal lymphadenopathy tumours
Pancreatitis

II Sinusoidal obstruction
Cirrhosis
Nodular regenerative hyperplasia
Fatty liver
Wilson’s disease

III Post - Sinusoidal obstruction
a) Intrahepatic
Cirrhosis (alcoholic, post necrotic, secondary biliary cirrhosis)
Alcoholic hepatitis
Viral hepatitis
Haemochromatosis
Budd - chiari syndrom (hyper coagulable state veno - ocelusive disease)
b) Extrahepatic
Budd-chiari syndrome (hepatic vein and inferior venacavathrombosis, congenital superheptic inferior venacava webs)
Extrisic inferior vena cava compression (hepatic, renal & adrenal tumour)
Chronic congestive cardiac failure
Constrictive pericarditis

IV. Increased flow portal hypertension
Hepatic arterial-portal venous fistula (congenital, traumatic or malignant)
Spleenic or mesenteric arteriovenous fistula
Portal-hepatic venous shunts
Massive spleenomegaly (tropical spleenomegaly syndrome)
Extrahepatic portal vein obstruction is frequently the cause of portal hypertension in childhood & adolescence, while cirrhosis causes 90% or more of portal hypertension in adults. Schistosomiasis is the most common cause in the world, but it is infrequent outside endemic areas.
Collateral vessel formation is widespread but occurs particularly in the gastrointestinal tract, espacially the oesophagus, stomach and rectum, in the anerior abdominal wall, and in the renal, lumbar, ovarian and testicular vasculature

ROLE OF VASOACTIVE SUBSTANCES IN PORTAL HYPERTENSION
Several substances have been implicated as hormonal factors which act on both splachnic and systemic circulation to produce hyperaemia. The most important of these are bile acids, serotonin, glucagon, and prostaglandins in particular prostacyclin. Elevated levels of bile acids have been demonstrated in patients with liver disease as promoters of splanchnic hyperaemia. Serotonin has a powerful vasoconstrictor effect on all vascular smooth muscles, and is normally released into the portal circulation by the enterochromaffin cells of GIP. Glucogon a patent splachnic vasodilator is elevated in patients with portal hypertension, and accounts for 30% of the increased splanchnic blood flow. Prostacyclin is another naturally occuring powerful vasodilator. Cirrhotic patients have extremely high levels of urinary 6-aceto prostaglandin, a stable metabolite of prostacyclin production reduces portal pressure in these patients.
There substances will remain vasoactive since they have avoided deactivation by the hepatocytes. They provide a likely explanation for the systamic hyperaemia of portal hypertension.

CLINICAL FEATURES
The clinical featuers of portal hypertension result principally from portal venous congestion and from collateral vessel formation. Spleenomegaly is a cardinal finding. Hyperspleenism
is common and frequently results in thromboiytopenia. Platelet counts are usually around
100x109/l. Leucopenia occurs occasionally. Collateral vessels may be visible on the anterior abdominal wall and several radiate from the umbilicus to form a capot medusae. Oesophageal varices causes severe bleeding. Rectal & Varices also cause bleeding. Fetor hepaticus can also be seen.

INVESTIGATIONS
1. Radiological and endoscopic examination of the upper Gap can show varies.
2. Ultrasonography can show spleenomegaly and collateral vessels.
3. Portal venography demonstrates the site of obstruction.
4. Portal venous pressure measurements are rarely needed.

Complications
1. Variceal bleeding
Oesophageal, gastric, other
2. Congestive gastropathy
3. Hyperpleenism
4. Ascites
5. Renal failure
6. Hepatic encephalopathy

HEPATIC ENCEPHALOPATHY
 

Heapatic encephalopathy is a neuropsychiatric syndrome caused by liver disease.

Aetiology
It is due to a biochemical disturbance of brain function. The nitrogenous substances produce in the gut are thought to be the main cause.

Precipitating factors
1. Uraemia
2. Drugs
3. Gastrointestinal bleeding
4. Excess dietary protein
5. Constipation
6. Paracentesis
7. Hypokalaemia
8. Infection
9. Trauma
10. Portasystemic shunts.

Clinical Featuers
1. Changes of intellect, personality, emotions and consciousness.
2. Inability to concentrate, confusion, disorientation, drowsiness, slurring of speech and eventually coma
3. Flapping tremor
4. Constructive apraxia
5. Hyper-reflexia and bilateral extensor plantar responses
6. Fetor-hepaticus (a sign of liver failure)
7. Cerebellar dysfunction
8. Parkinsonian syndromes
9. Spastic paraplegia & denentia

INVESTIGATIONS
EEG
Diffuse slowing of normal alpha waves with eventual development of delta waves

Management
1. Remove the precipitating factors
2. To reduce protein intake
3. Suppress the production of neutoxins in the bowel