By: Farhan J. Mohamed
A 45 year old truck driver presented to the Casualty Department (brought by his wife). The patient had a history of disturbed sleep and irrelevant talking for the last day. His wife said that he had general weakness and abdominal distension (on and off, lasting for 3 months)-subsides with medication-for the last 5 years. He has a habit of consuming 2 bottles of arrack (liquor) everyday for the last 20 years. Examination revealed that the patient was drowsy, but arousable upon shouting/painful stimuli. He had flapping tremors in both hands, gynecomastia, ascites, splenomegaly (dipping method) and pitting edema (both feet). Vital signs were stable and other systems were normal.
Q1) What is the likely diagnosis?
Q2) Mention other relevant findings
Q3) Outline the investigation and management Q4) Mention other causes of ascites
2 important clues
45 year old truck driver
Habit of consuming liquor everyday for the last 20 years
45 yr old truck driver
During general examination, patient should be asked about his habits, social history and nutritional status. Patient susceptible to:
heart diseases, hypertension
STDs (HBV) Accidents/trauma Likely to be a cigarette smoker Poor nutrition
Habit of drinking 2 bottles of liquor/day for past 20 years
Chronic alcoholic Nutritional status is very important
Ask about # in household, whether meals are regular, etc.
chronic liver disease should be strongly suspected in patients with a history of prolonged or excessive alcohol intake
Q) What is the likely diagnosis?
Alcoholic Liver disease, with portal hypertension and hepatic cellular destruction/cirrhosis
Rule out Other cause of liver cirrhosis:
Hepatitis B infection
May be HBV because patient’s occupation puts him at risk of exposure to STDs. Serological tests for: HBsAg, anti-HBs, anti-HBc
Hepatitis C infection
diagnosed when serum aminotransferases are elevated and anti-HCV is present in serum.
In contrast to alcoholic cirrhosis (which has an elevated AST level), viral hepatitis has an elevated ALT relative to AST.
Alcoholic Liver Disease (ALD)
In western societies, alcohol is the most common cause of liver disease Quantity & duration of alcohol intake are the most important risk factors for developing ALD.
Consistent drinking, with an intake of >60g/D for approximately 10 years, is required to produce severe ALD. A steady daily intake is more hazardous than intermittent drinking. If patient is an intermittent drinker, then the liver has time to heal itself, therefore cirrhosis is unlikely.
Three stages of ALD
Chronic alcohol consumption has a variety of adverse effects, however there are three distinctive forms of lesions in the liver:
Fatty Change/hepatic steatosis Alcoholic hepatitis Cirrhosis
Stages often overlap, rarely present alone.
Fatty liver/hepatic steatosis
Initial & most common lesion that affects 90% of binge drinkers.
May become evident as hepatomegaly with mild elevation of serum bilirubin & ALP levels.
Alternatively, there may be no clinical or biochemical evidence of liver disease. REVERSIBLE
Alcohol withdrawal & proper diet are sufficient treatment.
Differentiation of alcoholic fatty liver from non-alcoholic fatty liver is difficult unless an accurate drinking history is verified.
Transition between fatty liver & alcoholic hepatitis is difficult to pinpoint.
Tends to appear relatively acutely, usually following a bout of heavy drinking.
Liver is normal or enlarged in size, with a mottled red appearance. Clinical features include fever, spider nevi & abdominal pain, but many patients remain asymptomatic. REVERSIBLE
Alcohol withdrawal & proper diet are sufficient treatment in most. However, if left untreated or with repeated bouts, cirrhosis appears in 1/3 of patients within a few years.
Cirrhosis is a consequence of chronic liver disease characterized by replacement of liver tissue by fibrous scar tissue as well as regenerative nodules, leading to a loss of liver function. Manifestations of alcoholic cirrhosis are similar to those of other forms.
Cirrhosis is the final & IRREVERSIBLE form of ALD, usually evolves slowly & insidiously.
Alcoholic cirrhosis—signs and symptoms
Symptoms are insidious, occurring usually after 10 years of steady alcohol intake. Initial signs:
Anorexia and malnutrition Easy bruising, weakness and fatigue
Eventually the clinical manifestations of hepatocellular dysfunction/portal HT will ensue:
Splenomegaly, ascites, encephalopathy, etc.
Positive examination findings/ case symptoms
Drowsy but arousable upon shouting/painful stimuli
Disturbed sleep and irrelevant talking Flapping tremor Gynecomastia Ascites
symptom of alcoholic cirrhosis
malnourishment Anemia psychiatric problems (i.e. depression) DM
Patient is drowsy but arousable upon shouting/painful stimulus
Grade 0= fully conscious & aware Grade 1= drowsy/sleepy state (alert upon stimulus) Grade 2= Stupor (semi-conscious, drowsy & only responds to pain) Grade 3= Unconsciousness (even painful stimuli will not elicit a response)
Grade 4= coma (no response, but vital signs are normal)
Grade 5 = deep coma (vital signs are affected/ brainstem lesion)
Disturbed Sleep and irrelevant talking
due to recent onset of problems with patient’s higher mental functions. increased ammonia level is the likely causative factor. Feature of hepatic encephalopathy.
bilateral, coarse movement which is characterized by sudden relaxation of muscle groups holding a sustained posture (most common in fingers & wrists). To elicit, the patient is asked to extend the arm, forearm & dorsiflex the hand. Hallmark of hepatic encephalopathy Other causes:
o o o
Severe respiratory insufficiency Uremic syndrome Thiamine deficiency
What is hepatic encephalopathy?
Disorder of neurotransmission in the CNS and neuromuscular system that is associated with elevated blood NH3 levels, which impair neuronal function & cause generalized brain edema. Marked by changes of intellect, personality & consciousness Diagnosis via clinical/neurological signs:
Flapping tremor/asterixis (hallmark) Rigidity hyperreflexia
Usually readily reversed (until terminal stages occur)
Hepatic encephalopathy—differential DX
Must be differentiated from other causes of confusion & coma Subdural hematoma
Measure plasma ethanol levels
Alcoholic patients with delirium tremens
These patients are usually alert rather than drowsy, and are nervous, confused and hallucinating.
Psychiatric diseases, such as Wilson’s disease
enlargement of male breasts, an important sign of liver cell dysfunction. The liver is an important metabolic organ, hormone metabolism is disturbed in case of liver disease.
Deficiency in testosterone production the metabolism of estrogen is lowered, resulting in elevated estrogen levels, which can feminize male tissues, resulting in gynecomastia, alopecia & hypogonadism.
Collection of excess fluid in the peritoneal cavity (clinically evident when >500ml). Pathogenesis: Liver failiure and portal HT in cirrhosis cause general Na and water retention in the body, with localization of fluid in the peritoneum owing to the high venous pressure in the mesenteric circulation. Clinical features: Abdominal distension Shifting dullness on percussion Fluid thrill on palpation Everted umbilicus
Other causes of ascites
Cardiac failure Hypoproteinemia
Malnutrition, nephrotic syndrome
TB, bacterial perotinitis
Lymphatic obstruction (chylous ascites)
Due to congestion of the red pulp as a result of portal HT. May result in anemia.
Spherocytosis Viral hepatitis Typhoid fever TB
Portal hypertension in cirrhosis
Condition characterized by prolonged elevation of the portal venous pressure, which leads to a gradual reduction in portal blood flow to the liver.
There is simultaneous development of collateral vessels, allowing portal blood to bypass the liver and enter the systemic circulation directly.
In adults, cirrhosis causes 90% of portal HT Clinical features: Splenomegaly Bleeding varices (esophageal, gastric) Ascites Hepatic encephalopathy Renal failiure
Likely due to the decreased levels of albumin> decreased COP. May be due to the Na and water retention in liver failiure. Elicited by putting pressure (for 30 seconds) over a bony prominence, such as the distal end of the tibia.
Mention other findings to look for in this patient…
Bleeding Esophageal varices
General definition= Yellow appearance of skin, sclerae and mucous membranes resulting from an increased plasma bilirubin level (>3mg/dl). In liver disease:
Bilirubin transport across the hepatocytes is impaired. Swelling of cells/edema may cause obstruction. Increase in BOTH conjugated & unconjugated bilirubin is seen.
Varices are dilated blood vessels usually in the esophagus or stomach. They cause no symptoms unless they rupture and bleed. Bleeding from varices is a lifethreatening complication of portal hypertension. Symptoms of bleeding varices:
hematemesis Black, tarry, or bloody stool hypotension tachycardia Shock (in severe cases)
Radial array of tiny arterioles that commonly occur in pregnant women and in patients with hepatic cirrhosis. In men, they are related to high estrogen levels secondary to liver disease.
reddening of the palms at the thenar and hypothenar eminences. Principal cause is portal hypertension. Also due to increased estrogen levels.
is a fixed flexion contracture of the hand where the fingers bend towards the palm and cannot be fully extended (straightened). idiopathic
is the appearance of distended and engorged umbilical veins which are seen radiating from the umbilicus across the abdomen to join systemic veins. It is a sign of severe portal hypertension. Differential DX:
Caput Medusae - flow is towards the legs IVC obstruction - flow is towards the head.
Aminotransferases – AST and ALT are moderately AST > ALT. Alkaline phosphatase - GGT -- chronic liver disease from alcohol. Bilirubin - Globulins -
due to shunting of bacterial antigens away from the liver to lymphoid tissue.
Prothrombin time & clotting time- the liver synthesizes clotting factors.
Albumin - levels as the synthetic function of the liver declines with worsening cirrhosis since albumin is exclusively synthesized in the liver Serum sodium -
hyponatremia due to inability to excrete free water resulting from high levels of ADH and aldosterone.
Thrombocytopenia - due to both congestive splenomegaly as well as decreased thrombopoietin from the liver. However this rarely results in platelet count < 50,000/mL.
Barium swallow or endoscopy to diagnose esophageal/gastric varices. Abdominal paracentesis for examination of ascitic fluid Fluid in cirrhosis is clear, with a low protein content and <250 PMNs/mm3.
Liver biopsy With a special needle, usually through an intercostal space
Measuring portal pressure by wedging a catheter into a hepatic vein
ALD is a serious illness requiring long term medical management. GOLDEN RULE: Alcohol should be absolutely forbidden An alcohol rehabilitation program or counseling may be necessary. provide a high-carbohydrates, high-calorie diet to reduce protein breakdown in the body. Vitamins, especially B1 and folic acid, are associated with improvement.
In advanced cases of cirrhosis, a liver transplant may be necessary.
All medicines should be administered with caution, since the liver’s function of drug metabolism is greatly compromised.
Specific treatments for the patient
For general weakness, Anti-anemic Treatment: B12 & Folic Ac blood transfusions protein supplements & a salt restricted diet For ascites, administer a diuretic (furosemide or spiranolactone), while carefully monitoring electrolyte levels and blood volume. Give beta blockers, such as propanolol, for portal HT. Vitamin K injections Lactulose syrup for portal systemic encephalopathy Somatostatin analogues Branched chain amino acids
The LT outlook for alcoholics with liver disease is variable. In the end-stage alcoholic, the proximate causes of death are:
Hepatic coma Massive GIT hemorrhage Intercurrent infection Hepatorenal syndrome Hepatocellular Ca (3% to 6%)
Harrison’s Internal Medicine Davidson’s Medicine Robbins Pathological Basis of Disease
Dr. Anjusha Dr. Rao Nitya