In my short presence here tonight, let me fix some really bad medicine on this thread, before the trainees start drinking the Kool-Aid, too (especially the latest generations which have been discouraged to transfuse blood).
Before I start, let me remind everybody that some people live with Hgb of 4 g/dL, without complications. But that anemia is CHRONIC, and those people's blood pressures are at baseline.
The problem in this case wasn't that the Hgb was 6 and the patient was not transfused. Heck, she could have paralyzed even with a Hgb of 8. The crux of this case is that we have a patient who loses a lot of blood, an anesthesiologist that thinks like a CRNA and keeps giving crystalloids, despite the hypotension not resolving, a PACU team that discharges the patient with a borderline/low BP, and a surgeon who's also stupid and uses protocols instead of medical knowledge and brain. I wouldn't be surprised if this was a patient with a baseline MAP of 110 (BP 150/90), and the postop MAP was 60-70 (BP 80/50-90/60).
Now back to the physiology. Why does chronicity matter in this case? Because chronicity allows the body to compensate, especially by adjusting its Hgb-O2 dissociation curve. Those 2,3-DPG changes don't just happen in hours. This was untreated severe ACUTE anemia. What makes it severe? It's not the Hgb of 6. Had the patient started with a chronic Hgb of 8, she probably wouldn't have even noticed the anemia. It's the DELTA, the difference between the starting hemoglobin and the one the patient ended up with. She must have lost like 1/3 of the blood volume.
Let's mention again the stupid protocols that say that one should transfuse at 7 g/dL (and 8 for patients with cardiac comorbidities). Not at 7.1, and definitely at 6.9, say the protocol bureaucrats. Those numbers are based on weak studies. There is no proof that 8 is safe, especially not in ACUTE anemia. There is no proof that 7 is the magic number, just that a transfusion target of 9-10 is no better than 7-8. It's just that the studies most protocols are based on were done with a transfusion threshold of 7 g/dL in the restrictive group. We don't have good studies with 6-7, AFAIK. So do NOT transfuse based on numbers, but based on the patient's clinical status.
What does oxygen delivery to tissues depend upon? I am not going to use some stupid formula, just common sense:
1. Flow to tissue. More flow, more O2. Vasoconstriction, e.g. due to hypotension, is bad.
2. Amount of Hgb in the blood.
3. Saturation of said Hgb with O2.
4. The extraction ratio in the periphery (e.g. the heart can extract way more oxygen than other tissues), aka the difference in the oxygen content of the blood between the arteriolar and venous end of the peripheral capillary. (Most healthy tissues get about 4-5x more O2 than they need, but that's also because most suck at oxygen extraction when ischemia hits the fan. What's the lowest SvO2 you have ever seen in sepsis? Even the heart can't extract more than 75%.)
What happened in this case? The patient bled, A LOT. The blood loss was replaced by the CRNA++ only with crystalloid. Bad move. The persistent hypotension should have been a serious red flag that the patient needed blood, even if the finger O2 sat was OK. Let me explain why.
BP is directly proportional to CO and SVR. If one replaces acute blood loss with crystalloid, the CO remains unchanged. However, if you take a careful look at the formula of resistance to laminar blood flow through a vessel (image borrowed from Wikipedia):
where
- R = resistance to blood flow
- L = length of the vessel
- η = viscosity of blood
- r = radius of the blood vessel
Everybody who looks at this equation tends to forget about η. Every anesthesia trainee will recite that the resistance is directly proportional to the length of the IV line, and inversely proportional to the fourth power of the radius, but usually not one remembers VISCOSITY as a component of resistance to flow. If viscosity drops, as when there is significant blood loss diluted by crystalloid-only replacement, SVR drops. If SVR drops, BP drops, and then peripheral flow drops as a result of reflex vasoconstriction. And, voila, ischemia!
OP, your anesthesiologist friend was extra-lucky for not being found responsible for 50% of the damages. Had I been an expert witness, that's what I would have suggested. An anesthesiologist's work doesn't end until the patient is discharged from the PACU. If the patient was hypotensive at the time, the anesthesiologist of record (or the on-call anesthesiologist s/he had signed out the patient to) was responsible.
tl;dr:
"Kids", do not transfuse patients based on numbers, but on clinical status. Humans are not machines; each individual is different. Do not treat numbers, treat patients. A Hgb of 8, coming from 13, is way more dangerous than a Hgb of 6, coming from 7. A blood loss of 1.5L in 3 hours is way more dangerous than the same over a month. Acute anemia should be treated with blood (at least partially), whenever the blood loss is significant (e.g over 1L). Postoperative hypotension that does not easily resolve with crystalloid requires administration of blood. It doesn't take much; many times, just 1-2 units of PRBC for all problems to go away. Like magic.
If you EVER get into a similar situation, do 4 things:
1. Tell the nurse to call the in-house surgical team and the surgeon.
2. Call the surgeon yourself, if you feel it's warranted.
3. Call your in-house colleague and have them go evaluate the patient, and even order blood transfusion if needed.
4. Document everything, either remotely, or have your colleague write a note that you will addend the next day.
Always do what's right for the patient. NEVER LET BUREAUCRACY OR LAZINESS,
OR THE SURGEON, STAY IN THE WAY OF GOOD PATIENT CARE! "Not my patient" doctors don't deserve a medical license. Don't abandon your patients the second they roll out of the PACU. Use the Silver Rule: don't do onto other people's loved ones what you wouldn't want to be done to yours, especially in an urgent/emergent situation.
Good night and good luck! The break is over.