Doing it all over again

Practice does not make perfect, and familiarity does not ease the pain.  

Xanax wears off to quickly, fentanyl cannot be taken forever, and the journey out of anesthesia happens all too quickly as far as I'm concerned.

Tuesday was probably my 8-12th esophageal varice ligation.  I'm going to try to explain the whats and whys as best as I can, but impaired liver function prolongs drug processing, therefore making me still pretty much all over the place from all the pain meds and anesthetics.   Then there's the post-anesthesia headache and abdominal pressure of a tornado trying to knock me over.  But I'm trying, so here goes...

Breakdown what I have: Primary sclerosing cholangitis.  Primary meaning basic, sclerosing meaning enabling abnormal hardening or thickening, choloangitis meaning inflammation of the bile ducts.  So basically, it's an abnormal inflammation (including hardening and thicknening) of the liver's bile ducts and vasculature.  Over time, the tissue just dies (whch is where PSC turns into cirrhosis).  If you think about the liver's size of a football and the amount of bodily functions it executes, fluids it excretes, and nutrients it processes, it's easy to see how even slight tissue death is detrimental.  Even as the tissue continues to die, the blood, bile, nutrients, and waste products still need somewhere to go.  Something called the portal vein is capable of handling 75% of hepatic blood flow, but it's no match to a badly damaged liver.  Ducts and vasculature inherently form collaterals and develop shunts in efforts to find somewhere to go, and what better place to go to than the large portal vein?  Unfortunately, the portal vein is not equipped for such volume and a complication called portal hypertension develops.

The cirrhosis-driven portal hypertension causes many implications, one being the developoment of varices, blood vessels that are stretched and weakened from all of the pressure.  They develop anywhere the pressure is intense, and advanced cases like mine eventually produce them all over all of the organs in the body.  The danger is rupture from the pressure, as internal bleeding will happen.  There's not much to do with internal varices, but due to many factors, a common site of varices is the esophagus.  The esophagus is accessible enough that it is the least minimal site to safely treat at least some of the varices, so doctors have begun "banding" esophageal varices in patients at risk for variceal rupture.  Rupture is an enormous concern since liver patients typically have low blood volumes and minimal clotting factors, so being prophylactic in this situation is not only ideal but critical.  To band a varice, a liver surgeon will go down an anesthesized patient's esophagus (throat) with special tools, locate dilated varices (essentially blood vessels), and release  tiny rubber bands around each bumpy varice.  Eventually (usually within a few days), the tight band is enough to shut down complete blood supply to the varice and cause it to simply fall off and be eliminated.  The downfall is repeated occasions can cause nerve damage, spasms, and severe choking episodes (which is all where I am now), but when held to the alternative option of death from rupture, it's easy to know which to choose.

Surprisingly, and thankfully, things didn't look too bad on Tuesday.  (Relatively speaking!)  Here's the images my doctor took:

Compared with an image I found from 2 years ago:

(As you can see, in this photo, my doctor is actually banding a group of varices)

So we just wait awhile until it's time to do it all over again......

 

For more clarification, here is one of the best videos of this procedure I've ever seen.  It is by Dr. Galati of Texas Liver Specialists.  

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