Friday, March 12, 2021

Cirrhosis Case File

Posted By: Medical Group - 3/12/2021 Post Author : Medical Group Post Date : Friday, March 12, 2021 Post Time : 3/12/2021
Cirrhosis Case File
Eugene C. Toy, MD, Lawrence M. Ross, MD, PhD, Han Zhang, MD, Cristo Papasakelariou, MD, FACOG

A 38-year-old man comes into the emergency department presenting with fatigue and abdominal swelling. For several months, he has noticed that his abdomen has been growing larger and that his skin has turned yellow. He denies any medical problems but admits to drinking alcohol almost every day. On examination, his skin clearly has a yellow hue indicative of icterus. His palms have some redness. His abdomen is markedly distended and tense, and a fluid wave is present. Prominent vascular markings appear on the surface of the abdomen.

What is the most likely diagnosis?
What organs are likely to be affected?


Summary: A 38-year-old icteric man who abuses alcohol enters the emergency department for fatigue and abdominal “swelling.” He has palmar erythema and abdominal distention with a positive fluid wave and prominent vascular markings.
• Most likely diagnosis: Alcoholic cirrhosis with portal hypertension
• Organs likely affected: Liver and those drained by the portal venous system

This patient abuses alcohol and has manifestations of end-stage liver disease (cirrhosis). Cirrhosis results in severe fibrotic scarring of the liver, which decreases blood flow through the organ. Hypertension in the portal venous system is the result, with collateral venous flow, especially in organs having venous drainage by the portal and vena caval systems, such as the abdominal surface, and the esophagus. The spleen is frequently enlarged, and the ascites, fluid within the peritoneal cavity, is due to liver insufficiency. Death may ensue as a result of bleeding from esophageal varices or bacterial peritonitis of the ascitic fluid. Marked hepatic insufficiency is another complication.

The Liver

1. Be able to describe the anatomy of the liver and its unique blood supply
2. Be able to sketch the anatomy of the portal venous system and the clinically important sites of anastomosis with the vena caval system

CIRRHOSIS: Disease of progressive degeneration of the liver in which damage to the liver cells results in nodular regeneration, fibrosis, and impedance
PORTACAVAL ANASTOMOSIS: Communication between tributaries of the portal venous system and the systemic venous system
PORTAL HYPERTENSION: Increased pressure in the portal venous system with resultant reverse flow, typically due to obstructed venous flow through the liver, as in cirrhosis
FLUID WAVE: A maneuver during physical examination in which tapping on one side of the abdomen leads to the sensation of a force traveling to the other side of the abdomen, suggesting the presence of intraabdominal fluid

The liver, the largest internal organ, has a convex diaphragmatic surface that conforms to the curvature of the diaphragm and an irregular concave visceral surface. The liver is covered with visceral peritoneum over most of its surface and is suspended by several mesenteric structures called ligaments. The falciform ligament (with the round ligament of the liver, the adult remnant of the umbilical vein, in its free margin) is reflected onto the anterior abdominal wall and divides the liver into apparent right and left anatomical lobes. As the falciform ligament passes onto the superior surface of the liver, the two layers of peritoneum diverge to the right and to the left, creating the anterior layers of the coronary ligaments. These pass to the right and to the left to the extremes of the superior liver surface, turn back on themselves (creating the triangular ligaments), and turn posteriorly to form the posterior layers of the coronary ligaments. In this manner, an area devoid of visceral peritoneum is created, the bare area of the liver. The posterior layers of the coronary ligaments converge to form the lesser omentum, which passes from the visceral surface of the liver to the lesser curvature of the stomach (hepatogastric ligament) and the first part of the duodenum (hepatoduodenal ligament).

The liver is divided anatomically into four lobes by external landmarks and is delineated on the visceral surface by fissures and fossae, which form the letter H (see Figure 23-1). The right side of the H is formed by fossae for the gallbladder and the IVC, and the right lobe lies to the right of these structures. The left side of the H is formed by the fissure for the round ligament and the ligamentum venosum (adult remnant of the ductus venosus); the left lobe is to the left of this fissure. The crossbar of the H is the porta hepatis, through which the hepatic artery, portal vein, and nerves enter the liver and the bile ducts and lymphatics exit.


Figure 23-1. The visceral surface of the liver. (Reproduced, with permission, from Lindner HH. Clinical Anatomy. East Norwalk, CT: Appleton & Lange, 1989:399.)

The crossbar subdivides the central portion into quadrate and caudate lobes. Functionally, the right portal lobe lies to the right of the fossae of the gallbladder, IVC, and a portion of the caudate lobe. The left portal lobe is the left anatomical lobe, quadrate lobe, and the remainder of the caudate lobe. The portal lobes are supplied by lobar branches of the hepatic artery, portal vein, and bile ducts. Although lacking external landmarks, the portal lobes are further divided functionally into hepatic segments.

The liver receives a dual blood supply; approximately 30 percent of the blood entering the organ is from the hepatic artery, and 70 percent is from the portal vein. The proper hepatic artery is a branch of the common hepatic artery, one of the three major branches of the celiac artery. As it approaches the liver, it divides into right and left hepatic branches that enter the liver and divide into lobar, segmental, and smaller branches. Eventually, blood reaches the arterioles in the portal areas at the periphery of the hepatic lobules and, after providing oxygen and nutrients to the parenchyma, drains into the hepatic sinusoids. The majority of blood entering the liver is venous blood rich in nutrients and molecules absorbed by the gastrointestinal organs. Intrahepatic branches of the portal vein follow the arteries to the portal areas, where portal venules empty into the sinusoids from which molecules are extracted and added. Sinusoidal blood flows to the central vein of each lobule from which increasingly large veins are formed until typically three hepatic veins exit the liver to join the IVC (Figure 23-2).

The portal venous system arises from the capillary beds within the abdominal organs supplied by the celiac artery, superior mesenteric artery (SMA), and inferior mesenteric artery (IMA), and blood will flow to and through the liver for metabolism of its contained molecules. Veins from these organs for the most part accompany arteries of the same name. The portal vein itself is formed by the union of the splenic vein and SMV posterior to the neck of the pancreas. This short, wide vein ascends within the hepatoduodenal ligament, posterior to the bile duct and hepatic artery, and enters the liver through the porta hepatis. Typically, the IMV drains its blood into the splenic vein.

Portacaval (systemic) venous anastomoses occur at sites where blood may ultimately drain into the portal system and/or the vena caval system. If venous flow through the portal system is prevented by liver disease, for example, the absence of valves within the portal system veins allows reverse flow. This dilates the smaller veins, and blood is drained by veins emptying into the vena cavae. This occurs at several sites and may produce clinical signs or symptoms (Table 23-1).

Cirrhosis anatomy
Figure 23-2. The portal system: 1 = portal vein, 2 = superior mesenteric vein, 3 = splenic vein, 4 = inferior mesenteric vein, 5 = superior rectal vein, 6 = right gastroepiploic vein, 7 = left gastric vein, 8 = esophageal vein, 9 = hepatic veins. (Reproduced, with permission, from the University of Texas Health Science Center Houston Medical School.)



Portal Venous Drainage

Vena Cava Venous




Left gastric vein

Hemiazygous vein

Esophageal varices,



Superior rectal vein

Inferior rectal vein


Anterior abdominal wall

Paraumbilical vein

Intercostal vein

Caput medusa


Duodenal, pancreatic, right

and left colic veins

Lumbar vein

Intestinal bleeding


23.1 You are examining the liver during a surgical procedure. The gallbladder will be found in its fossa between which two anatomical lobes?
A. Quadrate and left lobes
B. Quadrate and caudate lobes
C. Right and quadrate lobes
D. Caudate and right lobes
E. Caudate and left lobes

23.2 If you ligated the right hepatic artery, the arterial supply to which of the following portions of the liver would remain intact?
A. Right lobe only
B. Right and quadrate lobes
C. Left lobe only
D. Left and quadrate lobes only
E. Left, quadrate, and a portion of the caudate lobe

23.3 Your patient who had cirrhosis has symptoms of esophageal varices. This is due to dilatation of the anastomosis between which of the following pairs of veins?
A. Left gastric and azygous veins
B. Right gastric and azygous veins
C. Right gastric and hemiazygous veins
D. Left gastric and hemiazygous veins
E. Azygous and hemiazygous veins


23.1 C. The gallbladder is located between the right lobe and the quadrate lobe.
23.2 E. The left hepatic artery supplies the left and quadrate lobes and a portion of
the caudate lobe.
23.3 D. Esophageal veins drain to the left gastric and hemiazygous veins.

 The left anatomical lobe, quadrate lobe, and a portion of the caudate lobe constitute the left portal lobe.
 Hemorrhage from the liver can be controlled by clamping the hepatoduodenal ligament (Pringle maneuver), which contains the hepatic artery and portal vein.
 The portal vein drains blood from organs supplied by the celiac artery, superior mesenteric artery (SMA), and inferior mesenteric artery (IMA).
 Esophageal varices with bleeding is the most clinically significant symptom of portal hypertension.


Gilroy AM, MacPherson BR, Ross LM. Atlas of Anatomy, 2nd ed. New York, NY: Thieme Medical Publishers; 2012:164−167. 

Moore KL, Dalley AF, Agur AMR. Clinically Oriented Anatomy, 7th ed. Baltimore, MD: Lippincott Williams & Wilkins; 2014:268−277, 285−286. 

Netter FH. Atlas of Human Anatomy, 6th ed. Philadelphia, PA: Saunders; 2014: plates 277−279, 291−292.


Post a Comment

Note: Only a member of this blog may post a comment.