Portal hypertension

Nursing

1. PORTAL HYPERTENSION

4. Causes of portal hypertension
Pre hepatic
•Congenital portal atresia
•Portal vein thrombosis
•Phlebitis of portal vein
Hepatic
•Cirrhosis
•Chronic hepatitis
•Parasitic infections (schistosomiasis)
Post hepatic
•Budd-chiari syndrom ( Hepatic venus thrombosis)
•Constructive pericarditis
•Tricuspid valve incompetence

5. Pathophysiology

6. Symptoms
Symptoms of portal hypertension include the following:
• Weakness, tiredness, and malaise
• Anorexia
• Sudden and massive bleeding, with or without shock on
presentation
• Nausea and vomiting
• Weight loss
• Abdominal discomfort and pain - Usually felt in the right
hypochondrium or under the right lower ribs (front, side, or back)
and in the epigastrium or the left hypochondrium
• Jaundice
• Edema and abdominal swelling

7. • Pruritus
• Spontaneous bleeding and easy bruising
• Symptoms of encephalopathy
• Impotence and sexual dysfunction
• Hematemesis or melena - May indicate
gastroesophageal variceal bleeding
• Increasing abdominal girth - May indicate ascites
formation
• Abdominal pain and fever - May indicate spontaneous
bacterial peritonitis
• Hematochezia

8. Complications of portal hypertension
ASCITES

•The mechanisms responsible for the development of ascites are
not completely understood. Portal hypertension and the resulting
increase in capillary pressure and obstruction of venous blood flow
through the damaged liver are contributing factors.
•The failure of the liver to metabolize aldosterone increases sodium
and water retention by the kidney. Sodium and water retention,
increased intravascular fluid volume, and decreased synthesis of
albumin by the damaged liver all contribute to fluid moving from
the vascular system into the peritoneal space.

9. Pathophysiology
Cirrhosis with portal hypertension

Splanchnic vasodilation

Decrease in circulating arterial blood volume

Activation of renin-angiotensin and sympathetic nervous systems and antidiuretic
hormone

Kidney retains sodium and water

Hypervolemia

Persistent activation of systems for retention of sodium and water; ascites and edema
formation

Continued arterial underfilling; cycle repeats

10. Clinical Manifestations

•Increased abdominal girth
•Rapid weight gain
•Short of breath and
uncomfortable from the
enlarged abdomen
•Striae and distended veins may
be visible over the abdominal
wall (caput medusa).
•Umbilical hernia
•Fluid and electrolyte
imbalances are common.

11. ESOPHAGEAL VARICES

Esophageal varices are dilated veins usually
found in the submucosa of the lower
esophagus, but they may develop higher in
the esophagus or extend into the stomach.
This condition nearly always is caused by
portal hypertension, which in turn is due to
obstruction of the portal venous circulation
within the damaged liver.

12. Risk factors
Risk factors that contribute to hemorrhage
are;
•Muscular exertion from lifting heavy
objects
•Straining at stool
•Sneezing, coughing, or vomiting
•Esophagitis; irritation of vessels by poorly
chewed foods or irritating fluids; or reflux
of stomach contents.

13. Pathophysiology
Portal hypertension
Development of pressure gradient of 12 mm Hg or greater
Venous collaterals develop

from high portal system pressure to systemic veins
Formation of abnormal varicoid vessels

Vessels may rupture causing life-threatening hemorrhage.

14. Clinical Manifestations

•Hematemesis
•Melena or hematochezia
•Signs and symptoms of shock (cool clammy
skin, hypotension, tachycardia) may be
present.

16. Medical Management

DIETARY MODIFICATION

The goal of treatment for the patient with
ascites is a negative sodium balance to
reduce fluid retention.
DIURETICS

Use of diuretics along with sodium
restriction is successful in 90% of patients
with ascites.
PARACENTESIS

Paracentesis is the removal of fluid (ascites)
from the peritoneal cavity through a small
surgical incision or puncture made through
the abdominal wall under sterile conditions.

17. Beta-blockers
Beta-blockers (nadolol or propranolol) may be
prescribed to reduce the pressure in varices and further
reduce the risk of bleeding.
BALLOON TAMPONADE
To control hemorrhage in certain patients, balloon
tamponade may be used. In this procedure, pressure is
exerted on the cardia (upper orifice of the stomach) and
against the bleeding varices by a balloon tamponade.
The tube has four openings, each with a specific
purpose: gastric aspiration, esophageal aspiration,
inflation of the gastric balloon, and inflation of the
esophageal balloon.

19. ENDOSCOPIC SCLEROTHERAPY

In endoscopic sclerotherapy (also referred to as injection
sclerotherapy), a sclerosing agent is injected through a fiberoptic
endoscope into the bleeding esophageal varices to promote thrombosis
and eventual sclerosis.

20. ESOPHAGEAL BANDING THERAPY (VARICEAL BAND LIGATION)

In variceal banding, a modified endoscope loaded with an elastic rubber
band is passed through an over-tube directly onto the varix (or varices) to be
banded. After suctioning the bleeding varix into the tip of the endoscope, the
rubber band is slipped over the tissue, causing necrosis, ulceration, and
eventual sloughing of the varix.

21. TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC
SHUNTING

Transjugular intrahepatic portosystemic shunting (TIPS) is a method of
treating esophageal varices in which a cannula is threaded into the
portal vein by the transjugular route. An expandable stent is inserted
and serves as an intrahepatic shunt between the portal circulation and
the hepatic vein, reducing portal hypertension.

22. SURGICAL MANAGEMENT

Several surgical procedures have
been developed to treat
esophageal varices and to
minimize rebleeding, but they are
often accompanied by significant
risk. Procedures that may be used
for esophageal varices are;
splenorenal and portacaval
venous shunts to relieve portal
pressure.