Question about ETOH and clotting

[aerorunner80, ADN, BSN, MSN, APRN]

I'm working on a case study for my Patho class and am stumped on a question that I should know the answer to.

The question is asking me to explain the cause of the pts clotting defects.

Here is the hx we are given for the study:

50 yo man admitted for trtmt of acute GI bleed.

Hospitalized x4 in the past 24mos most recently for trtmt of upper GI bleed.

Has 40 hx of smoking and drinks an unknown quantity of liquor daily.

Previously treated for pancreatits, alcohol withdrawal seizures, cirrhosis and assoc ascites, coagulopathy, esophageal varicies, anemia, GI bleed, and gastritis.

Current probs: hepatic encephalopathy, GI bleed, coagulopathy, jaundice, hx of TB (age 15 w/trtmt), and hypoxia

Medications: spironolactone (25mg 2x/day), ranitidine (150mg 2x/day), antacid (Maalox), and multivitamins.

Please tell me if I'm thinking in the right direction here..........I'm thinking that the coagulopathy is due to the alcohol consumption which can cause thinning of the blood.

Is this right?

Thanks.

[GingerSue]

Please tell me if I'm thinking in the right direction here..........I'm thinking that the coagulopathy is due to the alcohol consumption which can cause thinning of the blood.

Is this right?

Thanks.

is the coagulation problem the result of the liver's inability to produce prothrombin and other factors essential for blood clotting

the alcohol leads to changes in the liver)?

Liver disease results in impaired synthesis of clotting factors

[leslie :-D]

etoh consumption does increase bleeding time by decreasing platelets, interfering with certain clotting factors and also by interfering w/production of fibrinogen.

excellent chance his alcoholism is the main contributor of his coagulopathy.

leslie

[BBFRN, BSN, PhD]

etoh consumption does increase bleeding time by decreasing platelets, interfering with certain clotting factors and also by interfering w/production of fibrinogen.

excellent chance his alcoholism is the main contributor of his coagulopathy.

leslie

Yep. And the esophageal varicies is a dead giveaway.

[purple1953reading]

Makes me wonder about his eye sight. Usually alcoholics, will beign to lose sight, once hgb, gets too low, from alcoholic coaglul.

[CRNI-ICU20]

This patient is in liver failure. Quite possibly close to the end of his life.

When the liver becomes toxic from the alcoholism, it can no longer make the clotting factors necessary for normal coagulation. He would be similar to treating a patient with induced coagulopathy, like say, someone who comes in with an INR of 7.0...but in his case, it is a liver that has failed....we drain the blood bank on these patients....and they still die! Usually they bleed to death, or end up on life support only to succomb to ARDS and pancreatitis. Many end up bleeding in their brains, lungs, etc.....and because of low volume depletion, their hearts and kidneys fail as well....it's not a pretty way to die....sigh.

[kmoonshine, RN]

As others stated above, the liver makes coagulation factors and if the liver is shot due to alcohol abuse and cannot make these factors as easily, this increases your bleeding time. Also, as cirrhosis sets in, the blood backs up (portal hypertension) and forms esophageal varicies, caput medusae (dialated, tortuous veins that can be seen on the abdomen), hemorrhoids, hepatic encephalopathy, splenomegaly (which may then sequester platelets, RBC's, WBC's), etc. As these veins dialate, they are prone to rupture; esophageal varicies are the worst in my opinion - it is never pretty and patients crash very, very fast...

Anytime I get a patient who is thin (usually very thin arms and legs with little muscle), a "sunken" looking face, and great peripheral veins (the kind where you can throw a 16 gauge needle in easily), I can guess they abuse ETOH. It's a very distinct look, but that's just my opinion. Sorry, this is a bit off topic but thought I'd add it!

[Diary/Dairy, RN]

Thank everyone for all the great information on ETOH and coagulopathies!