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By Ian Halim

About 20 miles north of New York City, a massive stone dam, nearly 300 feet high and almost as wide, holds back as much as 19 billion gallons of water. The New Croton Reservoir, behind that dam, helps supply New York City’s 8.8 million residents with water. Across the crest of the dam runs a foot path. Part of that crossing is formed by a steel arch. Under that arch, water from the reservoir pours over a spillway.

That spillway acts as a kind of release valve for the dam, letting some of the water escape. On one half, water flows over a structure that looks like a series of curved steps. On the other, water sprays over boulders, like a natural waterfall. Standing on the top of the dam, you can survey the reservoir on one side and the wide-open gorge created by the dam on the other.

A dammed-up reservoir draining over a spillway offers a rough but useful analog for thinking about the way that blood flows through the liver. Some spillways have a gate that can be set to control the outflow of water. Narrow that gate too much and the outflow slows to a trickle, and the reservoir rises. Eventually, the dam overflows. If it does, water won’t just pour over the spillway like it’s supposed to. It will flow anywhere it can, including over the edges of the dam that aren’t designed to handle these forces and can buckle and break.

This is a little like what happens in liver disease. When the liver is functioning well, blood moves through it easily, so that the reddish-brown organ can disarm harmful things flowing in the blood – toxins, drugs, or infectious virus or bacteria. But when the liver is diseased, blood moves through it more slowly. Like a narrowed spillway, blood gets caught behind the liver. The liver becomes a bottleneck of blood. The vessels that drain into the damaged organ overfill with blood and stretch. Some of these vessels are in the throat and the stomach. They can break under the rising pressure – like water flowing perilously over the top of a dam. When this happens, blood pours into the throat and stomach. Someone who had appeared quite healthy can suddenly find themselves doubled-over, retching, vomiting up large amounts of blood. This is a medical emergency.

One pathway to this kind of liver disease is drinking a lot of alcohol for a long time. When we drink, the liquid sloshes down the narrow esophagus, into the stomach, and then down into the small and large intestine. Some alcohol gets absorbed into the stomach, but most crosses into our blood through the wall of the narrow small intestine. From there, it travels to the liver through a special set of blood vessels called the portal venous system.

“Portal” is a good name, since this system of vessels acts as a kind of gateway between what we eat and drink, and the rest of our circulating blood. The veins of the portal system drain blood from the gut, stomach, and the lower food pipe (also known as the lower esophagus). And their purpose is to bring blood enriched by orally-absorbed nutrients, toxins, and drugs to the liver. Like a sentry stationed upon the gate of a castle, the liver surveys these absorbed substances from our food and drink for signs of danger before allowing them to intermingle freely with the rest of our blood.

This sentry, our liver, does its best to “disarm” anything extracted from what we eat or drink before allowing it within the “castle” of our body. The liver uses enzymes, for instance, to break the alcohol molecule into smaller pieces. The first fragment we get when alcohol is broken down contributes to hangover (this fragment is called acetyl aldehyde). Next, the liver converts this hangover culprit into the harmless acetic acid that gives vinegar and kambucha their distinctive tang. But too much alcohol for too long overwhelms the liver and damages it. Alcohol is not the only pathway to this kind of liver damage, however. Viral infections of the liver, or accumulation of fat in the liver, can trigger the same cascade of damage. Regardless of the cause, end stage liver disease is known as cirrhosis.

Once cirrhosis develops, the scarred, nodular liver tissue can stop blood from flowing through the organ easily. The portal system gets jammed up and acts like the narrowed spillway I described at the beginning of this essay – a bottleneck, but of blood rather than water. The veins of the stomach and lower esophagus within this portal system can no longer drain into the liver easily. They grow plump. They can get so big that they would be visible to the naked eye, if you could look that far down someone’s throat.

When swollen, these vessels are known as “varices” (pronounced like, “vara-seas”). This is the same word root as “varicose veins” which are also swollen, but which are often found in the legs rather than the throat. Varicose veins are typically more of a concern because of how they look, but gastric and esophageal varices pose a different kind of problem. When their walls get too stretched and swollen, they can burst open and bleed, like a balloon that pops after someone has forced too much air into it. And, when gastric or esophageal varices bleed, they tend to bleed fast. So fast, that it’s a medical emergency, requiring a swift and effective response.

A classic medical school exam question asks the test-taker to identify the first step in responding. The most immediate problem caused by this kind of massive blood loss is the loss of blood pressure. Imagine allowing water escape slowly from the opening lips of a taut balloon filled with water, and watching it sag as it’s drained – drooping as the volume within diminishes. 

We often think of high blood pressure as a problem, which it is, but blood pressure serves an important function too, pushing oxygenated blood out to the tissues so that it can bathe them with its life-sustaining power. When blood pressure drops too far, this prevents blood from delivering oxygen effectively.

So, the right answer to the test question is to insert two large IV lines, to deliver salt water (known as saline) to restore blood pressure. The IV lines channel fluids or medicines into the venous blood (hence IV for “intravenous”).

This can be a life-saving step. So, its status as a classic exam question is well-earned. Because variceal bleeding is rapid, a lot of fluid must be given quickly in order to compensate for all that blood loss. So, the clinician should place two IV lines and they should be wide, or large bore, meaning that the needle should be thick, with a wide inner space or lumen, so that fluid may pass through the two IVs as quickly as possible to restore blood pressure.

Once adequate blood pressure has been achieved, clinicians must then check to see if there are enough red blood cells per volume of blood. When a large volume of blood loss is replaced by salt water, the resulting blood is diluted, with fewer oxygen-carrying red blood cells per unit of volume. If the blood becomes too dilute, however, the effect is similar to low blood pressure: poor oxygen delivery, threatening the body’s oxygen-dependent tissues. Patients with cirrhosis often already have a low red blood cell count to begin with (a condition called anemia). So, the loss of blood from a variceal bleed is especially dangerous, and often it’s necessary to transfuse donor red blood cells to make up for this.

Once a patient is stabilized with IV fluids and with blood transfusion, if needed, it’s important to verify the cause of the bleeding. A camera mounted on a flexible tube can be inserted into the throat (the procedure is called an endoscopy, meaning an “inside” endo- “look” -scopy). Looking through this camera, the gastroenterologist (a doctor who specializes in the esophagus, stomach, gut, and related organs) can check for plump or bleeding variceal veins, which confirms the diagnosis. This is a crucial step, since other things can cause someone to vomit blood, and the treatment will differ, depending on whether it’s a variceal bleed or another kind of bleed.

People who are sick often are in danger on multiple fronts, and this is true of variceal bleeding in liver disease too. The liver not only detoxifies portal blood; it also produces critical small molecules suspended in the blood that help the blood to clot. A damaged liver isn’t as good at making these clotting factors, and the blood’s ability to clot can be compromised. This impaired ability to clot and close up a burst, bleeding vessel can make variceal bleeding even more dangerous.

Vomiting blood – hematemesis, in medical terms – can be caused by other things too. The surface of the stomach or the small intestine can become irritated and bleed – a condition known as peptic ulcer disease. Or forceful vomiting can tear the esophagus and cause it to bleed. But for those with severe liver disease, one of the greatest perils is variceal bleeding. Take a deep breath and begin by placing two large bore IV lines.

Somerville Bagel Bards member and physician-humanist, Ian Halim, writes about how medicine relates to everything from ethics to botany – aiming to make science accessible to the widest possible audience. Ian earned his PhD in Greek & Latin literature and his MD at Columbia University in New York City and is now training at a hospital in Boston.