Thursday, July 7, 2016

Blood Medicine, Part Two



If the American Medical Association says blood transfusions do more harm than good, as we noted in Part One, why are so many doctors still doing them?

It’s your body. You need to understand what’s going on inside it, so that in an emergency you can make educated decisions, even if those decisions are contrary to what the experts are telling you. And if you can speak on an intelligent level with the experts, they are more likely to listen to you.

The primary justification given for blood transfusion is blood’s oxygen-carrying ability. The ASSUMPTION made by most medical people is that, 
1. Blood carries oxygen, 
2. If you've lost blood your ability to transport oxygen is impaired, and 
3. Replacing the lost blood will restore that lost oxygen-carrying ability.

Two of those assumptions are wrong.

Blood consists of four major parts:
  • Red blood cells or RBCs,
  • White blood cells (WBCs),
  • Platelets,
  • Plasma - the fluid the other three float in.
Blood in a container will, with very little help, separate itself into these four components. The “hematocrit,” that is, the combination of RBCs, WBCs, and platelets, will settle to the bottom third of the container, leaving the top two thirds of the test tube full of a straw-colored liquid, the plasma.

97% of the oxygen-carrying is done by the RBCs. (The other 3% is oxygen dissolved in the plasma; you can raise that number substantially, without a transfusion, with a hyperbaric chamber. Read more about that here.
 
Unlike nearly every other cell in your body, RBCs don’t self-replicate. They are produced in your bone marrow at the astonishing rate of 2 million per second. They survive in your body about 120 days (though they have a much shorter life span in storage.) Aging cells are filtered out of the bloodstream and recycled by your spleen and liver, again at the (normal) rate of a couple million per second. Having none of the breathing, repair, or reproducing machinery of other cells, RBCs are basically oxygen tankers, each packed full of a protein called hemoglobin.

Each hemoglobin molecule (of which each RBC has about 270 million!) is built around 4 iron ions, and has the ability to carry 4 atoms of O2. (Iron attracts oxygen… that’s why stuff at the junkyard rusts so quickly.) However, hemoglobin is different from a junkyard… its task is not simply to draw oxygen; it also has to be able to off-load oxygen.

Take another look at the diagram at the top of the page. To understand hemoglobin, picture one of those nylon pot-scrubbers with a magnet buried in the center of it. Then picture a ball-bearing, representing oxygen, balanced on top. If the pot scrubber is too floppy, the ball-bearing will get too close, maybe even touching the magnet, and then it's hard to get it loose. If the scrubber is too thick, though, there won’t be enough attraction to hold onto the ball-bearing.

A key to this balancing act is another chemical, manufactured inside the RBC, called BPG. Remember that name, we’ll come back to it.
RBCs are actually larger than your smallest capillaries, but that’s not a problem: dissolved in your blood is a gas called nitric oxide that signals the capillaries to dilate. The RBC deforms and squeezes tightly into the capillary; that skin-to-skin contact between the capillary wall and the RBC wall permits the offloading of its oxygen; then the RBC springs back into its donut-like shape when it gets back to roomier territory.

Now: here’s why it was important for you to wade through all that: Storing blood for any length of time changes it.
  • The first change that occurs in stored blood is off-gassing. The nitric oxide begins to dissipate immediately. Within 4 hours, half of it is gone. Remember, nitric oxide is the signal to your capillaries to let the blood cells in.
  • RBCs die in storage much more quickly than the normal 2 million a second. Blood is stored at 4 degrees centigrade to slow its degradation, but even at that temperature, chemical changes happen.
  • The low temperature of stored blood lowers the pH. Your body fights to keep your blood's pH at 7.35. As storage lowers that number blood becomes more acidic.
  • Those RBCs that survive in storage become frail and less flexible. The weakening RBCs begin to leak BPG – the chemical we spoke of earlier that performs the balancing act. RBCs with less BPG do a great job of attracting oxygen but are lousy at delivering it.
  • Potassium leaks into the plasma.
  • Ammonia levels (normal is 10-40) rise to 400 by day 20 of storage.
  • Most importantly, as the cell walls break, the hemoglobin gets loose.

When stored blood is transfused:

  • A burden is placed on the patient’s spleen and liver to quickly clean up the mess of old, inflexible cells and dead cell membranes.
  • While your doctor may view himself as a life-saver, stored blood has no conscience. Lacking nitric oxide, it actually robs it from the patient. Lacking BPG, the stored cells grab nutrients away from the patient to try to create it.
  • The low pH of the stored blood makes the patient’s blood more acidic. Since a blood pH outside the range of 7.35 to 7.45 will kill you, the patient’s body drops everything - including healing from whatever mayhem you're dealing with - and goes to work raising the blood pH.
  • The high ammonia level could put you into a coma, so your liver must work harder to get it under control.
  • The potassium that leaked out of the RBCs into the plasma can be high enough to stop the heart of an unhealthy patient... and some transfused patients have died from exactly this, although their death certificates usually list 'heart failure' as the cause of death, never 'blood transfusion'...
  • Being less flexible, the stored RBCs can’t deform as well to squeeze into the capillaries. Instead, they get stuck and pile up at the entrances of the capillaries, causing traffic jams - clots -  that prevent healthy RBCs from getting in with their load of valuable oxygen.
  • Free hemoglobin from broken RBCs is released into the patient. Hemoglobin is toxic to the kidneys (which is no doubt why it was designed to be inside a cell wall), putting another extra burden on the already sick recipient.
Free hemoglobin grabs oxygen out of the patient’s blood but, lacking BPG, it won’t release it – like the ball-bearing getting stuck on the magnet. After a transfusion the medical staff may pat themselves on the back for raising the patient’s oxygen – based on the reading from that light they clip on the patient's finger – but that oximeter only measures how red hemoglobin is. It does NOT tell them whether that hemoglobin is releasing oxygen, or hoarding it. The tissues could actually be starving for oxygen even with plenty of hemoglobin nearby!

“The clearance of damaged RBC reduces the therapeutic efficacy of the [transfused blood], stresses the …system of the recipient and adds an excess iron burden to chronically transfused patients. Moreover, transfusion of damaged RBC is suspected as a possible cause of clinically observed complications of transfusion therapy.” - Blood Transfusion, NIH, October 8, 2010.

In one study, it took 24 hours after transfusion to get BPG levels – not just of the donated blood but of the patient's entire blood volume - back up to 60% of normal! Their recommendation? 
 
“In [an] acute situation, when the organism needs restoration of the oxygen releasing capacity within minutes, the resynthesis is obviously insufficient.”
 
In other words, if the situation is critical, don’t take blood. And if the situation isn't critical... why would you need blood?

“The goal of packed red blood cell transfusion in the critically ill is to increase oxygen delivery to and hence consumption by tissues. An increase in hemoglobin should improve patient’s oxygen carrying capacity and help deliver oxygen to hypoxic tissues. Lactate, a clinically used surrogate of tissue hypoxia,should decrease with improved oxygen consumption. An abundance of literature over the past thirty years demonstrates that this clinical benefit is frequently not realized with transfusion in the critically ill.” - (medical magazine Journal of Blood Transfusion)

Translation: Blood lactate level is a better indicator of how well oxygen is getting to your tissues than that clip on your finger. Why?

When your tissues aren’t getting enough oxygen they send out a chemical signal – lactate. If you go for a jog it is lactate that tells your lungs to breathe harder; it is lactate that ultimately tells you when to stop running. Normal blood lactate level can be anywhere from 4.5 to 19.8, but the important thing to remember is that it is easily, accurately measurable. If you’re in the hospital for anything serious, they likely have already measured it. If they haven't, ask them to. When they measure it again, if it hasn’t gone up significantly, your tissues are NOT starving for oxygen.

Dr. Spiess, quoted in the previous article, refers to a blood transfusion as, “a liquid organ transplant. Through that transplant, the recipient's own immune system is altered for some period of time… there is debate in regard to how long and how important that immune suppression/alteration lasts; likely it lasts for weeks and perhaps up to years.”

Clearly, the AMA was right: A blood transfusion is more likely to harm you than help you.
 
However, there are therapies that can genuinely help a critically ill or injured patient. We’ll look at some of those advances in blood medicine in Part Three. 

Please leave a comment.To read Part One, click here.
 
Bill K. Underwood is a columnist and author of several books, available in either paper or ebook on Amazon.com. You can help support this site by purchasing a book. 

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