The Physiology of Bleeding to Death

This is what happened to that patient, in physiological simple speak. This patient
Young man, on his bike. Side-swiped by another vehicle going in the opposite
did suffer many many injuries; abrasions, lacerations, a few fractures of the limbs.
direction. Crash, dragged, rolled and left almost lifeless by the road. Passers-by
These injuries bled quite a bit, but they were not killers. Nope. He had, instead,
spot him, load him up into their car, drop him off at the nearest Emergency
suffered a high force impact onto his left torso which broke multiple ribs, resulted
Department and leave.
in a severely lacerated spleen and severe pulmonary contusions. Which was not
recognized, and which continued to bleed until he bled to death. That was the
killer.
The ED doctor on duty there identifies a patient with multiple injuries; very
restless, not obeying commands, hypotensive (80/40) and tachycardic (130) with
an SpO2 of 80%. Automatic mode kicks in - oxygen is given via non-rebreather
The reason why he came in very restless was because of hypoxia and hypotension,
high-flow mask at 15 L/min, Normal Saline is started at full flow, bloods are taken
NOT because of head injury. Being very short of oxygen and deprived of blood
for inx, and documentation of injuries ensues. Repeat BP comes back at 130/60,
supply to the vital organs would make every single one of us become highly
HR 135, SpO2 94% and doctor sighs relief. Would you do the same ? Same sigh
agitated and distressed. This is the reason why GCS is not a useful tool for
of relief as well ?
estimation of head injury until the ABCs have been stabilized.

Patient gets sent to X-ray; spends an hour there with X-rays of just about
In severe bleeding, the body compensates to try to maintain the blood pressure.
everything unimportant, when the accompanying staff notices that the patient was
The pressure is maintained to try to preserve blood flow to the most vital of
gasping and rushed him back to the ED; in time for them to note asystole and
organs; the brain, heart and lungs. But this pressure is maintained mainly by
commence CPR. The patient succumbs to his injuries (and the doctor's failure to
squeezing all the main blood vessels (vasoconstriction). Blood is now shunted
understand physiology of bleeding to death) about 45 minutes later.
away from the skin, limbs and intestines to the brain, heart and lungs. The limbs
become cold and bluish from the lack of fresh oxygenated blood, and the SpO2
reading drops.
What was the doctor thinking about ? I thought I would ask some of the new
doctors who were posted to our ED. Scenario presented; and this reply was their
This entire compensation mechanism maintains pressure, but the total amount of
COMMON thought process. Initially restless and then obtunded (must be head
blood flow and oxygen supplied decreases, to the rest of the body. Cells in the
injury - must do CT scan as priority). Initially hypotensive (must be bleeding -
body, deprived of enough oxygen, are now forced use their fuel without oxygen;
need to look for source of bleeding - but since BP improved with fluids, should be
in an inefficient manner that starts producing huge amounts of acids, mainly lactic
getting better). Very tachycardic (must be due to pain, anxiety). Low SpO2
acid. This leads to worsening acidosis.
(something wrong with the breathing - better look for pneumo- or haemothorax -
but since improved with oxygen, must be getting better - let's do x-rays to find out
more). Yup, that's right. This was their COMMON reply. So it is not merely that
So this patient has severe bleeding from his lacerated spleen, and had lost so much
particular doctor's failure to understand the physiology of bleeding to death, it is
blood that his compensation mechanisms were beginning to fail; that was why he
ALL our YOUNGER DOCTORS FAILURE to do so as well.
came in hypotensive. He was definitely restless from all that lack of oxygen and
blood to his brain. His peripheries were cold as no blood was reaching his fingers
and toes; his SpO2 was obviously going to be low.
Let's look at what happened next. He was given oxygen, a good thing. What it did,
was filled the little blood that was still available with oxygen. Which made the
saturation SpO2 of the little blood that was available, 95%. Although 95%, it was
still too little blood to really carry the oxygen needs of the patient. NO, the SpO2
of 95% did not mean he was any better.
And he was given fluids. So all those fluids would have rushed into the
"squeezed" blood vessels and immediately raised the pressure within those blood
vessels. This gave the impression of "improvement" to the doctor. In fact, it
probably made things worse. There are two main down-sides to this. Firstly, the
sudden increase in the pressure has the tendency to suddenly burst some of the
newly formed clots, causing bleeding to resume. Secondly, the fluid now dilutes
the clotting factors in the blood making it more inefficient at formed a clot to stem
the bleeding.
So, none of the initial therapy really helped much. What was worse, was the
assumption that he was now "better" and could be sent to the X-rays Dept for
further xrays. What happened there was this. The bleeding continued, and the
compensations were not able to maintain his blood pressure anymore. The
decreased blood supply to the brain made the patient obtunded (accompanying
staff may have just thought that the patient was now more quiet and easier to
handle). He would also have lost his airway control reflexes, and regurgitation of
food may have partially blocked his airway, further worsening his overall
hypoxia.
By now, the amount of blood circulating would have been minimal, and acid
levels would have skyrocketed. This acidosis would be the final nail. Reaching a
particular dangerous level, it would essentially have prevented the heart from
working properly. The heart essentially stops and the quick spiral to death ensues.
What was reversible, and when was it reversible ? Could things done right made a
difference ? What things, done differently in what ways ?
Firstly, any person in trauma, with tachycardia, is in SHOCK until proven
otherwise. SHOCK in a patient presents with various degrees of anxiety and
restlessness, tachycardia, cool peripheries, rapid breathing and signs of poor organ
perfusion (low urine output, acidosis and altered mental states). SHOCK is almost
always due to bleeding from trauma (significant alternatives include only tension
pneumothorax, cardiac tamponade and airway obstruction; but always think of
bleeding as well). So, the first right thing to do is to recognize the SHOCK state.
Next, look very carefully for the source of bleeding. Search carefully for spilled
blood, either on-the-floor (external bleeding) or in only 4 other areas of significant
internal bleeding. Massive haemothorax (diagnosed clinically and with the
bedside ultrasound), bleeding into the pelvis and retroperitoneal space (almost
always related to pelvic fractures, lower spinal injuries and associated vascular
injuries), bleeding into the peritoneal space (mainly due to liver and splenic
lacerations, as in this case; and diagnosed with a FAST ultrasound scan) and the
tissue spaces of the thighs (which are easily seen, and associated with fractures
and vascular injuries). That's it. No X-rays other than the bedside trauma X-ray of
the chest and pelvis. No other x-rays needed. Search carefully for bleeding, and
once you find it, get the surgeon.
And lastly, this patient needed blood. Lots of blood. Preferably fresh whole blood.
If not, packed cells and the freshest plasma you can get. What needs to be done is
to replace the lost blood with actual blood. And with it, hopefully some additional
coagulation factors to help stop the bleeding.
The physiological derangements needed to be reversed. To do that, young doctors
must must simply must understand the physiology first. That was the only way to
save this patients life.