CASE DISSCUSSION 7 : A 45 year old with seizures secondary to hepatic encephalopathy with alcoholic hepatitis

The entire analysis of this case is found in the link below

http://jayanth1802.blogspot.com/2021/02/45-year-old-with-seizures-secondary-to.html

Here is a case i have seen: 

A 45 yr old male patient ,resident of chityala,came to the opd with 

CHIEF COMPLAINTS :

– Involuntary movements of upperlimbs (2episodes) - 15 days ago

– Fever, Loss of appetite and Vomitings 2 episodes in morning 10 days back

HISTORY OF PRESENT ILLNESS : The patient was apparently assymptomatic 15 days back,then he developed involuntary movements of upperlimb(seen by neighbours) lasted for 5 mins. After 30mins he had another episode of involuntary movements of upperlimb , associated with tongue bite lasted for 1-2 mins & not associated with aura. The patient lost consciousness for 10 min and has woke up.He had postictal confusion,drowsiness,apathy and couldnt recognise anybody present there.

– No involuntary defecation,micturition or uprolling of eyes.

 – 10 days ago he developed fever which was insidious in onset,low grade,continuous relieved on tepid sponging. He had vomitings 2 episodes/day Which is non projectile, non bilious, contains food particles,non foul smelling.

– 6 days ago he developed abdominal distension

 and 

– Swelling of both legs with pain in the left leg.swelling is of pitting type.No diurnal variations

PAST HISTORY : patient had similar complaints in the past,10yrs back he had multiple episodes.Recently 6months back had 2episodes of seizures.

– He had a surgery in the past for abdominal trauma

– Not a k/c/o DM2,HTN,Asthma,TB,CAD

PERSONAL HISTORY : 

– Mixed diet

– Appetite normal

– Disturbed sleep

– Regular bowel and bladder movements

– Patient is chronic alcoholic having 180ml/day whisky since 20yrs

FAMILY,DRUG & ALLERGIC HISTORY : not significant

GENERAL EXAMINATION :
Patient c/c/c , moderately built and nourished

ICTERUS : present 

EDEMA : present (grade 4 pitting type)

No signs of pallor, clubbing, koilonychia lymphadenopathy, cyanosis. 

BP-110/70 mmHg
RR-17cpm
PR-98bpm
SPO2-98% @room air
GRBS- 165 mg/dl
CVS - s1 s2+, No murmurs heard
RS - NVBS, BAE+, No added sounds heard
PER ABDOMEN 

Inspection : Umbilicus central and slit like, abdominal distension with fullness of flanks,scar present over umbilicus (9*11cm)

 Palpation : Abdomen is soft, non tender.skin is tense and shiny, organomegaly cant be assesed

Percussion : 

DULL NOTE,SHIFTING DULLNESS PRESENT.

– Bowel sounds heard

CNS - NFD HMF intact. 

INVESTIGATIONS DONE - 

HbSAg, HIV1/2, HCV- Non reactive 

Dengue NS1, IgM, IgG- Negative 

PT 20, INR 1.45, APTT 39.

 DIAGNOSIS : SEIZURES SECONDARY TO HEPATIC ENCEPHALOPATHY WITH ALCOHOLIC HEPATITIS? 

THE FOLLOWING ARE THE DIFFERENT CAUSES OF HE :-

• Chronic parenchymal liver disease

• Chronic hepatitis.

• Cirrhosis. 

• Fulminating hepatic failure

 • Acute viral hepatitis. 

• Drugs. 

• Toxins e.g. Wilson’s Disease, CCL4. 

• Surgical Portal-systemic anastomoses,

 - portacaval shunts, or Transjugular intrahepatic portal-systemic shunting

– RULING OUT CIRRHOSIS : No circulatory changes - palmer erythema, spider telangiectasia, cyanosis.

• No endocrine changes - gynecomastia, testicular atrophy.

• No bleeding tendency- bruises, purpura, epistaxis.

– NO H/O DRUG INTAKE : such as opiates, benzodiazepines, antidepressants, and antipsychotic agents

– RULING OUT WILSON DISEASE : NO H/O Fatigue,Abdominal pain

Golden-brown eye discoloration (Kayser-Fleischer rings,Problems with speech, swallowing or physical coordination

Uncontrolled movements or muscle stiffness

• There is h/o fever,yellowish discoloration of eyes,vomitings,loss of appetite...might probably be alcoholic hepatitis

Hence,the probable mechanism of pathology may be due to alcoholic hepatitis or porto-systemic shunts.

1. ANATOMICAL LOCATION :

Presence of yellowish discoloration of eyes (jaundice), swelling of legs (pedal edema), abdominal distension (ascitis). Suggests that the pathology is in the liver

ETIOLOGIC DIAGNOSIS :  Hepatic encephalopathy due to  ALCOHOLIC  hepatitis

2. INVOLUNTARY MOVEMENTS (seizures) :

 

➞ DIFFERENTIAL DIAGNOSIS:

 

• Intracranial lesions- subdural hematoma, intracranial bleeding, stroke, tumor, and abscess

 • Drug or alcohol intoxication

 • Toxic encephalopathy from alcohol intake, such as acute intoxication, alcohol withdrawal, and Wernicke encephalopathy • Toxic encephalopathy from drugs, such as sedative hypnotics, antidepressants, antipsychotic agents, and salicylates

 • Metabolic encephalopathy, such as hypoglycemia, electrolyte imbalance, anoxia, hypercarbia, and uremia

 • Infections- meningitis, encephalitis, and intracranial abscess 

• Hyperammonemia from other causes- secondary to ureterosigmoidostomy and inherited urea cycle disorders

– As the patient is chronic alcoholic, the cause of seizures in this patient may be due to alcohol intoxication/withdrawl 

SIGNS & SYMPTOMS suggesting hepatic encephalopatgy are in this patient:-

– Involuntary movements

– Confusion, drowsiness, apthy and

– loss of consciousness , unable to recognise family members

➞ Types of HE :The following three types of HE:

Type A

Type A HE results from acute liver failure (ALF), which occurs when someone with no preexisting liver disease experiences a rapid decline in liver function. This decline usually takes place over days/weeks.

The most common cause of ALF is acetaminophen overdose. Some other 

Causes include:

•Excessive alcohol consumption

•Hepatitis infection

•Wilson’s disease, a hereditary condition that involves an accumulation of copper in the body

Type B

Type B HE results from a portal-systemic bypass. This involves blood flowing around the liver when it would ordinarily flow to the liver. The redirection prevents the liver from effectively filtering toxins from the blood.

Two potential causes are congenital abnormality and trauma.

Type C

Type C HE results from severe scarring — cirrhosis— of theliver. Cirrhosis develops during late stage liver disease.

Over time, as scar tissue increasingly replaces healthy tissue, the liver is less able to remove toxins from the blood and perform its other functions.

WEST HAVEN CRITERIA OF HE :

– Grade 0 :  Minimal hepatic encephalopathy. Lack of detectable changes in personality or behavior. Minimal changes in memory, concentration, intellectual function, and coordination. Asterixis is absent.

– Grade 1 : Trivial lack of awareness. Shortened attention span. Impaired addition or subtraction. Hypersomnia, insomnia, or inversion of sleep pattern. Euphoria, depression, or irritability. Mild confusion. Slowing of ability to perform mental tasks. Asterixis can be detected.

– Grade 2 : Lethargy or apathy. Disorientation. Inappropriate behavior. Slurred speech. Obvious asterixis. Drowsiness, lethargy, gross deficits in ability to perform mental tasks, obvious personality changes, inappropriate behavior, and intermittent disorientation, usually regarding time.

– Grade 3 : Somnolent but arousable, unable to perform mental tasks, disorientation about time and place, marked confusion, amnesia, occasional fits of rage, incomprehensible speech 

– Grade 4 : Coma with or without response to painful stimuli

Pathogenesis :

a). Shunting of portal blood directly into systemic circulation bypassing liver.

 b). Severe hepocellular damage and dysfunction. In both circumstancestoxic substances absorbed from intestine not metabolised by liver toxins accumulate in the brain.

PATHOPHYSIOLOGY : 

3. MECHANISM OF ASCITIS :

• Ascites in cirrhosis results from a combination of the following:

– Liver failure

– Portal hypertension.

☆ Mechanisms Involved in Pathogenesis :

• Renal mechanism

– Liver failure leads to redistribution of blood flow, resulting in a decrease in renal blood flow. This in tum causes

a reduction in the glomerular filtration rate and excessive reabsorption of salt and water by the renal tubules. This

results in salt and water retention and hence, ascites.

• Secondary hyperaldosteronism

– Decreased renal blood flow leads to increased release of renin, which stimulates the angiotensin system, that in

turn leads to secondary hyperaldosteronism. The secondary hyperaldosteronism results in salt and water retention.Failure of liver to metabolise aldosterone intensifies secondary hyperaldosteronism.

• Vasopressin

– Failure of liver to metabolise vasopressin reduces renal water clearance that results in fluid retention.

• Increased capillary hydrostatic pressure

– Portal hypertension raises the hydrostatic pressure within the splanchnic capillary bed. This results in extravasation

of fluid from plasma into the peritoneal cavity.

• Reduced plasma oncotic pressure

– Hypoalbuminaemia results in a reduction of plasma oncotic pressure. This again results in an extravasation of fluid

(ascites and oedema).

• Hepatic lymph

– Hepatic lymph oozes freely from the surface of cirrhotic liver into the peritoneal cavity. This adds to the develop-

ment of ascites.

• So, portal hypertension and lymphatic ooze predispose to localisation of fluid within the peritoneal cavity.

4. EDEMA (BILATERL PITTING ): 

Edema in this case is bilateral .The cause for bilateral edema can be of cadiac,renal and hepatic pathology 

Causes of bilateral edema :

• Congestive heart failure, right or overall – due to increased capillary hydrostatic pressure

• Cirrhosis – due to deceased capillary oncotic pressure

• Nephrotic syndrome (loss of proteins in the kidneys), or acute glomerulonephritis – decreased capillary oncotic pressure

– As there is no periorbital puffiness we can rule renal cause.

– Heart failure is ruled out as there is no JVP elevation

– In this case Long term alcohol consumption, yellowish discoloration of eyes and urine and abdominal distension due to ascitis indicate hepatic cause

MECHANISM OF HEPATIC EDEMA :

5. JAUNDICE :

Jaundice results from high levels of bilirubin in the blood. Bilirubin is the normal breakdown product from the catabolism of haem, and thus is formed from the destruction of red blood cells.

Under normal circumstances, bilirubin undergoes conjugation within the liver, making it water-soluble. It is then excreted via the bile into the GI tract, the majority of which is egested in the faeces as urobilinogen and stercobilin (the metabolic breakdown product of urobilingoen). Around 10% of urobilinogen is reabsorbed into the bloodstream and excreted through the kidneys. Jaundice occurs when this pathway is disrupted.

TYPES OF JAUNDICE

There are three main types of jaundice: pre-hepatic, hepatocellular, and post-hepatic.

Pre-Hepatic

In pre-hepatic jaundice, there is excessive red cell breakdown which overwhelms the liver’s ability to conjugate bilirubin. This causes an unconjugated hyperbilirubinaemia.

Any bilirubin that manages to become conjugated will be excreted normally, yet it is the unconjugated bilirubin that remains in the blood stream to cause the jaundice.

Hepatocellular

In hepatocellular (or intrahepatic) jaundice, there is dysfunction of the hepatic cells. The liver loses the ability to conjugate bilirubin, but in cases where it also may become cirrhotic, it compresses the intra-hepatic portions of the biliary tree to cause a degree of obstruction.

This leads to both unconjugated and conjugated bilirubin in the blood, termed a ‘mixed picture’.

Post-Hepatic

Post-hepatic jaundice refers to obstruction of biliary drainage. The bilirubin that is not excreted will have been conjugated by the liver, hence the result is a conjugated hyperbilirubinaemia