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Dr. Ajith Kumar J MD
Dept. of Emergency Medicne
Travancore Medicity, Kollam
India
editor
Portal Hypertension
Hepatic Encephalopathy Hepato Renal Syndrome (HRS) Hepatopulmonary Syndrome Malnutrition | Coagulopathy
Bone disease
Hematologic abnormalities
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HRS
Hepatorenal syndrome is a form of functional renal failure without renal pathology that occurs in about 10% of patients with advanced cirrhosis or acute liver failure.
Condition is marked with increased renal vascular resistance (renal vasoconstriction) and accompanied by a reduction in systemic vascular resistance. The reason for renal vascular resistance is unknown.
It is diagnosed when person present with ascites with progressive rise in creatinine.
Type 1 HRS is characterized by a progressive impairment in renal function and significant reduction in creatinine clearance within 1-2 weeks.
Type 2 HRS is characterized by a reduction in glomerular filtration rate with an elevation of serum creatinine level, but it is fairly stable and is associated with a better outcome than type1.
Currently patients are treated with albumin & terlipressin.
Spontaneous Bacterial Peritonitis
SBP is a common and severe complication of ascites characterised by spontaneous infection of the ascitic fluid without an intrabdominal source .
Bacterial translocation is presumed mechanism for development of SBP with gut flora trasversing the intestine into mesentric lymph node, leading to bacteremia and seeding of the ascitic fluid.
Common organism are E.Coli, gram positive bacteria including streptococcus viridans, staphylococcus aureus and enterococccus species .
Patient present with fever, altered sensorium, elevated white blood count and abdominal pain or discomfort.
Absolute neutrophil count >250/mcl is considered diagnostic.
Cefotaxime is the recommended agent.
Splenomegaly & Hypersplenism
Congestive splenomegaly is common in patients with portal hypertension.
Clinical feature includes enlarged spleen , thrombocytopenia and leukopenia.
Ascites
Ascites is the accumulation of fluid within the peritoneal cavity.
In patients with ascites,there is an increase in intrahepatic resistance, causing increase in portal pressure, but there is also vasodilation of splanchic arterial system due substances like NO, which results in increased portal venous flow.
Both leads to increased production of splanchic lymph .
Hemodynamic changes leads to sodium retention by causing activation of RAAS with the development of hyperaldosteronism.
Hypoalbuminemia and reduced plasma oncotic pressure also contributes to the loss of fluid from the vascular compartment into the peritoneal cavity.
SAAG (Serum ascites to albumin gradient)
In patients with cirrhosis, the protein concentration of ascitic fluid is low.
SAAG is >1.1 g/dl, the cause of ascites is most likely due to portal hypertension.
SAAG < 1.1 g/dl, infectious or malignant causes should be considered.
Treatment
Salt restriction <2 gm/day
Sprinolactone 100 -200 mg/day is started and may be raised upto 400 – 600mg/day , furosemide 40 -80 mg/d may be also added.
Hepatopulmonary Syndrome
This characterised by refractory hypoxemia, intrapulmonary vascular dilatation and chronic liver disease with portal hypertension.
HPS causes digital clubbing, cyanosis, spider navei and a characteristic reduction in arterial oxygen saturation on standing.
The hypoxia is due to intrapulmonary shunting through direct arteriovenous communications.
It is believed to be a result of overproduction of nitric oxide.
Updated on 1/2/2015.
Reference
Harrison
Davidson
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emmedonline
Dr. Ajith Kumar J MD
Dept. of Emergency Medicne
Travancore Medicity, Kollam
India
editor