Cirrhosis differential diagnosis: Difference between revisions
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* Transudate - SAAG > 1.1 g/dL (indicates the ascites is due to [[portal hypertension]]). | * Transudate - SAAG > 1.1 g/dL (indicates the ascites is due to [[portal hypertension]]). | ||
* Exudate - SAAG < 1.1 g/dL (indicates the ascites is due to non-portal hypertension etiology). | * Exudate - SAAG < 1.1 g/dL (indicates the ascites is due to non-portal hypertension etiology). | ||
{{reflist|2}} | {{reflist|2}} |
Revision as of 15:46, 7 September 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Govindavarjhulla, M.B.B.S. [2]
Overview
Differentiating Cirrhosis from other Diseases
Differentiating Cirrhosis from other Diseases Based on Ascitic Fluid
Ascites may be caused by portal hypertension due to cirrhosis of liver or due to other causes like malignancies etc.,
Ascitic fluid analysis should be done to broadly categorize the cause of ascites.
Ascites is broadly classified as two types based on the serum-ascites albumin gradient (SAAG):
- Transudate - SAAG > 1.1 g/dL (indicates the ascites is due to portal hypertension).
- Exudate - SAAG < 1.1 g/dL (indicates the ascites is due to non-portal hypertension etiology).
Condition | Differentiating Signs and Symptoms | Differentiating Tests |
Constrictive pericarditis | Increased jugular venous pressure, atrial fibrillation, and tachycardia. Quiet heart sounds with a third heart sound (ventricular knock) present. | *EKG will show tachycardia, atrial fibrillation, low-voltage QRS complexes and T wave abnormalities. Doppler ultrasound will show ventricular filling abnormalities. |
Budd-Chiari Syndrome | Delayed onset reaction caused by IgG or IgM antibodies, directed at drug-hapten coated cells. | Thrombocytopenia, anemia, cytopenia. |
Splenic vein thrombosis | Delayed in onset and caused by IgG immune complex formation and deposition, and complement activation. | Vasculitis, serum sickness, arthralgia, fever, rash. |
Portal vein thrombosis | The presentation of drug molecules by major histocompatability complexes to T cells, causing the release of cytokines and other inflammatory mediators. Also associated with the activation of eosinophils, monocytes, and neutrophils. | rashes, organ tissue damage, contact sensitivity. |
Schistosomiasis | The presentation of drug molecules by major histocompatability complexes to T cells, causing the release of cytokines and other inflammatory mediators. Also associated with the activation of eosinophils, monocytes, and neutrophils. | rashes, organ tissue damage, contact sensitivity. |
Sarcoidosis | The presentation of drug molecules by major histocompatability complexes to T cells, causing the release of cytokines and other inflammatory mediators. Also associated with the activation of eosinophils, monocytes, and neutrophils. | rashes, organ tissue damage, contact sensitivity. |
Inferior vena cava obstruction | The presentation of drug molecules by major histocompatability complexes to T cells, causing the release of cytokines and other inflammatory mediators. Also associated with the activation of eosinophils, monocytes, and neutrophils. | rashes, organ tissue damage, contact sensitivity. |