Skip to main content

Portal Hypertension; Definition, Etiology and Management!

 PORTAL HYPERTENSION

Definition:

"Portal Hyperension is present when the hepatic venous pressure gradient exceeds 10mmHg and risk of variceal bleeding increases beyond a gradient of 12mmHg."



Classification: According to The Site of Action:

1. Pre-Hepatic, Pre-Sinusoidal:

    Caused by;

  •          Portal vein thrombosis due to sepsis
  •          Abdominal trauma including surgery.


2. Intra-hepatic pre-sinusoidal:

   Caused by; 

  •         Schistosomiasis
  •         Congenital hepatic fibrosis
  •         Drugs
  •         Sarcoidosis


3. Sinusoidal:

    Caused by; 

  •         Cirrhosis
  •         Polycystic liver disease
  •        Nodular regenerative hyperplasia
  •        Metastatic malignant disease


4. Intrahepatic Post-sinusoidal:

    Caused by; 

  •       Veno-occlusive disease


5. Post-hepatic post-sinusoidal:

  Caused by;

  •       Budd-Chiari syndrome


Etiology:

  1. Cirrhosis
  2. Schistosomiasis
  3. Portal vein thrombosis
  4. Drugs
  5. Fibrosis


Clinical Features:

  1. Variceal bleeding
  2. Congestive gastropathy
  3. Renal failure
  4. Iron deficiency anemia
  5. Hepatic encephalopathy
  6. Splenomegaly


Pathophysiology:

  • Increased portal vascular resistance leads to gradual reduction in flow of portal blood to liver and simultaneously to the development of collateral vessels, allowing portal blood to bypass liver and enter systemic circulation directly.
  • Poly systemic shunting occurs, particularly in the GIT and especially in the distal esophagus, stomach and rectum, in the anterior abdominal wall and in the renal, lumbar, ovarian and testicular vasculature.



Investigations:

  1. Portal venous Pressure is measured: by using a balloon catheter inserted using a trans jugular route.
  2. Endoscopy
  3. Ultrasonography
  4. CT scan
  5. MRI


Management of Bleeding:

1. IV Fluids: To replace the extracellular volume.

2. Vasopressor: To reduce the portal pressure, acute bleeding and risk of early bleeding.

3. Prophylactic Antibiotics (Cephalosporins IV): To reduce incidence of spontaneous bacterial peritonitis.

4. Emergency Endoscopy: To confirm variceal rather than ulcer bleeding.

5. PPI: To prevent peptic ulcer.

6. Variceal Band Ligation: To stop bleeding.

7. Phosphate Enema/ Lactulose: To prevent hepatic encephalopathy.


Management of Acute Bleeding From Esophageal Varices:

  1. If suspected variceal hemorrhage.
  2. Start IV Terlipressin (Vasopressor) and Antibiotics prophylaxis.
  3. Urgent Upper GI Endoscopy:
  4. If Varices present, go for, Endoscopic Therapy. (If no varices present; stop Terlipressin.)
  5. Is there hemostasis. If yes; continue Terlipressin to 72hr. Introduce Beta-blocker as secondary prophylaxis. Enter the patient to endoscopic banding program to obliterate varices. (If no Hemostats; Further endoscopic therapy or Ballon Tamporate and Emergency Trans jugular Intrahepatic Portosystemic Stent Shunt (TIPSS)).



Labels:

Comments

Post a Comment

Popular posts from this blog

Diabetes Mellitus: Types!

TYPES OF DIABETES MELLITUS 1. TYPE1 DM Type 1 DM is usually diagnosed before age 30 years, but it can develop at any age. T1DM is an autoimmune disease in which insulin producing B-cells are destroyed. The presence of Human Leucocyte Antigens (HLAs ) is associated with the development of T1DM. In addition, these individuals often develop Islet cell antibodies , Insulin Autoantibodies or Glutamic Acid decarboxylase autoantibodies . At the time of development of diagnosis of T1DM, it is usually believed that most of the patients have 80-90%loss of beta cells. The remaining beta cells function at the diagnosis creates a " HONEYMOON PERIOD" during which the blood glucose levels are easier to control, and smaller amounts of insulin are required. after this, the remaining beta cells function is completely lost, and the patients become completely deficient of insulin and hence require exogenous insulin.  2. TYPE1.5 DM:  Also referred as Latent autoimmune diabetes in Adults (LAD)
Post a Comment
Read more

Diabetes Mellitus: Pharmacotherapy- Gliptins and a-Glycoside Inhibitors!

  PHARMACOTHERAPY:  Medications classifications include:  Sulfonyl Urea's Nonsylfonylurea Secretagogues (a-Glinides) Biguanides Thiazolidinediones a-Glucosidase Inhibitors Dipeptidyl Peptidase-4 Inhibitors (Gliptins) Sodium-glucose co-transporter (SGLT) Inhibitors  Central-Acting Dopamine Agonists Bile Acid Sequestrants Insulin therapy 5. a-GLUCOSIDASE INHIBITORS Acarbose and Miglitol are a-glucosidase inhibitors currently approved in the United States. Mechanism of Action: An enzyme that is along the brush border of the intestine cells called a-glucosidase; breaks down the complex carbohydrates into simple sugars, resulting in absorption. The a-glucosidase inhibitors work by delaying the absorption of carbohydrates from the intestinal tract, which reduces the rise in postprandial glucose levels. Therapy: As a monotherapy , a-glucosidase inhibitors primarily reduce post-prandial glucose excursions.  Clinical Use: FPG concentrations have been decreased by 40-50mg/dL and A1c level
Post a Comment
Read more

GASTRO-ESOPHAGEAL REFLUX DISEASE (GERD)!

MANAGEMENT OF GASTRO-ESOPHAGEAL REFLUX DISEASE  "GERD refers to the endoscopically determined esophagitis or endoscopy-negative reflux disease" . "GERD is the term used to describe any symptomatic clinical condition or histopathological alteration resulting from episodes of reflux of acid, pepsin and occasionally, bile into the esophagus from the stomach". Patients with uninvestigated "reflux-like" symptoms should be managed as patients with uninvestigated dyspepsia. There is currently no evidence that H.pylori should be investigated in patients with GERD. Symptoms: Heartburn is the characteristic symptom of GERD. Acid regurgitation Dysphagia Belching Upper abdominal discomfort Bloating and postprandial fullness Chest pain Hoarseness Cough Complications include: Esophageal ulceration Formation of specialized columnar-lined esophagus at the gastro-esophageal junction known as Barretts Esophagus . Mechanism of Acid Reflux: The mechanism of acid reflux is mu
Post a Comment
Read more