In this presentation we will go through a case

you're called to see a patient who is unconscious and making a loud snoring noise

He’s receiving O2 at 2l/min via nasal prongs and the saturation is 98%

does this patient require any airway intervention

yes the snoring suggests he has partial airway obstruction

the saturation does not exclude obstruction particularly in a patient receiving oxygen

it is important to realize that airway management can be extremely difficult even for an expert so
call for help early

start with the basic airway maneuver the head tilt chin lift

place your hand firmly on the patients head and tilt the head backward on the atlanto-occipital joint
then left the chin by placing the fingers of your other hand under the bony part of your lower jaw
and lift forward

As you do this the tongue and anterior pharyngeal wall will be lifted away from the posterior
pharynx

If this fails, then perform a triple maneuver. Tilt the head back in a similar fashion. Do the head
tilt chin lift then grasp the ramus of the mandible with the fingers of both hands and push it upward
and forward. Finally use both thumbs to open the mouth

note that the head should not be tilted in patients who may have a cervical spine injury

in these patients use a modified jaw thrust this is covered in the trauma lecture

if these maneuvers fail use an artificial airway the gudel airway is inserted upside down with
concavity facing the palate and then is rotated into position

however gudel airway is uncomfortable for the patient and the patient was not deeply unconscious
may not tolerate one. In that case a nasopharyngeal airway may be useful

note that the nasopharynx passes directly posteriorly from the nares and the airway should be
inserted on the same direction not superiorly

returning to our case. Airway patency has now been restored and confirmed by looking listening
and feeling but the respiratory rate is low

the patient needs some form of ventilatory assistance. usually with a manual self-inflating bag
valve resuscitator.

use of this equipment requires time and experience to master and will be covered at one of the skill
sessions the equipment which may need to be assembled consists of: mask ideally transparent so
the patient's mouth can be seen , which connects to an expiratory valve to prevent rebreathing of
the expired gas. this in turn connects to the self inflating bag which is squeezed to ventilate the
patient. at the distal end of the bag is a one way valve which allows oxygen to pass into the self
inflating bag but prevents backward flow of gas when the self inflating bag is squeezed. beyond the
valve is an oxygen inlet and a reservoir bag . the oxygen flow rate is typically set at 15 litres per
minute. check that the reservoir bag inflates. The additional positive end expiratory pressure PEEP
valve may improve arterial oxygenation and help to overcome airway obstruction due to laryngeal
spasm

the pitfalls of mask ventilation include gastric insufflation and overdistension of the lungs

gastric insufflation is common and increases the risk of vomiting and aspiration. in addition severe
intra abdominal distension may cause cardiovascular compromise

if gastric insuflation is occurring carefully apply cricoid pressure which may prevent further
insufflation

the volume of an adult sized self inflating bag is approximately 2 liters. a tidal volumes of 1 and a 1/2
to two litres can easily be delivered by excessive squeezing of the bag

rapid delivery of high tidal volumes can lead to gas being retained in the lungs and progressive
distension and progressive rises in intrathoracic pressure. And these may cause profound
hemodynamic instability

it's important therefore to concentrate on providing tidal volumes to only about 300 to 500 mls at
respiratory rates of 10 to 16 per minute

look at the chest as you squeeze the bag and check the chest is moving adequately. if it does not.
check the airway is open and if necessary adjust position of the head and neck .. alternatively the
seal of the mask against the face may not be adequate

if adjusting the mask position does not help then use two hands to hold the mask and ask someone
else to squeeze the bag

what next

Should we intubate the patient

indications for intubation are: the patient is unlikely to be able to maintain an unobstructed airway

protection against aspiration

high peep or requirement for pharmacological paralysis

or need for frequent airway suction

it's important to understand that airway obstruction due to an anatomical lesion as opposed to
decreased consciousness is difficult to manage and you must find expert help urgently

In particular patients with an obstructing lesion in the oropharynx or larynx should not receive
paralyzing agents . as there's a high risk of failure to intubate and failure to ventilate.

the urgency of the situation must be considered. the patient may need to be intubated urgently but
may not need to be intubated immediately . allowing time for help to arrive.

the urgency will depend on the situation for example a patient with very severe hypoxia will require
intubation more urgently than the patient who requires intubation to prevent aspiration

other considerations are your own personal level of skill and the anticipated difficulty of intubation

before attempting intubation always assess the patient to determine whether intubation is likely to
be difficult or not
clues to difficult intubation include:

neck swelling or short muscular neck

decreased distance between the chin and the thyroid cartilage less than 6 centimeters is worrying

a beard as this frequently hides a receding chin and makes bag mask ventilation more difficult

lower incisors are anterior to the upper incisors or protruding teeth a

small mouth or limited mouth opening

severe facial trauma

high curve palate

large or swollen tongue

and limited neck movement

if you think intubation will be difficult call for help immediately while continuing with basic airway
techniques and administration of high flow oxygen via bag valve mask resuscitator

prepare the equipment for advanced airway techniques and wait for help to arrive

however if the patient develops complete airway obstruction or cardiorespiratory arrest is

imminent before help arrives. attempt to advance airway technique yourself

the choice of technique is dependent on the situation and your skill in performing the technique

our case has no features suggestive of difficult intubation and we decide to go ahead with direct
laryngoscopy . had the patient been conscious it would of course have been important to obtain
verbal consent

we start by assembling the appropriate equipment and making sure it works

the equipment should include: intubation equipment

monitoring

suction

bag valve resuscitator

and artificial airway

intubation equipment includes 2 laryngoscopes with at least two sizes of blade

endotracheal tubes

forceps

stylet

bougie

and syringe

note that a laryngoscope blade has both horizontal and vertical parts
 the vertical part allows the operator to move the tongue to the left the horizontal part allows the
tongue or epiglottis to be elevated at the appropriate time

check the light works and it's bright

we will also need drugs including an agent for inducing anesthesia

muscle relaxants for producing paralysis

oxygen

a sedative to keep patients sedated when the induction agent wears off

resuscitation drugs and fluids

administration of these drugs requires reliable IV access. check cannula is in place and is
working

assistants are crucial. it is not possible to safely intubate a patient on your own

before starting make sure that each person is clear about the role he or she needs to play

typically there are three main roles

Drug Administration

passing you the equipment

and cricoid pressure

the person giving the drugs must be given clear instructions on what drug to give how much and
when

the person performing cricoid pressure should not be given any other role during laryngoscopy

these are the important landmarks you're aiming to see

the epiglottis

the vocal cords and the arytenoid cartilages

most ICU patients are at risk of aspiration of gastric contents during intubation and therefore rapid
sequence induction and intubation is required

this minimizes the risk of aspiration by minimizing the time between loss of consciousness and
intubation and by the use of cricoid pressure

start by positioning the patient with the neck flexed. this is best achieved by elevating the occiput
by about seven to 10 centimetres with a foam pillow or wedge and extend the head

positioning is crucial to the success of the procedure

then preoxygenate the patient with 100% oxygen for two to five minutes

give a predetermined dose of induction agent and paralyzing agent. giving the paralyzing agent
without waiting for loss of consciousness . and apply cricoid pressure as the patient starts to lose
consciousness
to find the cricoid cartilage first find the thyroid cartilage moving caudally you will then feel the
cricothyroid membrane and then the cricoid cartilage

to apply cricoid pressure. place one finger on the center of the cartilage and one finger on each
side pushing the cricoid cartilage backwards to occlude the esophagus

pick up the laryngoscope in your left hand and turn it on by extending the blade. with the head and
neck in a good position, advance the laryngoscope blade gently along the right hand side of the
tongue, pushing the tongue to the left until the tip of the epiglottis is seen. Continue to
advance the laryngoscope to the base of the epiglottis

note that the laryngoscope blade is in front of the epiglottis and not covering it.

Lift the larynegoscpe in the direction of the handle to reveal the cords behind the epiglottis

do not look away from the courts insert the endotracheal tube from the right with your right hand

measurement of expired CO2 by capnography is an accurate way to confirm the tubes and position
in the trachea.

carbon dioxide is only produced in the lungs and therefore only expired gas can contain carbon
dioxide

note that in a pre-oxygenated patient this saturation may remain high for some minutes even after
mistaken esophageal intubation. Capnography may produce false positive results ie detect end tidal
CO2 were the first few breaths after inadvertent esophageal intubation, as a result of gastric
insufflation from prior mask ventilation

a false negative. a decrease of very low carbon dioxide despite correct position may occur with
cardiac arrest without CPR and low cardiac output states

clinical signs such as auclulation of breath sounds over the chest and epigastrium are useful but less
reliable. Auscultation is however useful to detect a tube that is too deep and in the right main
bronchus in most men the tip of the Andrew killed tube will be appropriately deep when the tip is 23
centimetres from the front teeth in women 21 centimeters secure the end of Q2 carefully with taped
or this may be catastrophic if it is unrecognized or if the patient cannot be adequately opinionated
by backmask ventilation it is therefore essential to have a plan for a carnage debate can't ventilate
situation this is an example of a very simple algorithm for integer equal incubation failure it can be
found in your course manual however if your unit has a standard algorithm for this situation that
maybe you saw this is bad lubrication water soluble Jelly position the patient as for endotracheal
intubation with flexion of the neck and extension of the adds up to
today I wanted to talk about massive transfusion mainly because anesthesia providers give a lot of
blood in fact we're one of the leading providers of blood transfusions in the health care system

additionally there may be instances where you may get involved in multiple massive transfusion
scenarios some people have actually been in excess of 100 units of blood products and it's one of
those clinical scenarios where everything you read in the textbooks is very real in terms of effect and
complications so I think it's critical to know how to recognize and manage those complications
additionally complications related to blood product transfusion appear to be frequently tested on
exams and that is very clinically relevant and certainly there's no shortage of topics that can be
addressed regarding complications of blood product utilization

there's ongoing debate about restrictive or liberal transfusion strategies proper transfusion ratios
transfusion reactions ethical questions related to blood transfusion and then certainly much debate
about the use of adjutants like factor 7 …its far too much to be covered in the single podcast so my
goals for today are to

define massive transfusion

discuss some of the basic principles and strategies for administering a massive transfusion

and then discuss the complications of massive transfusion

and how to potentially recognize and treat those

lastly I may throw in tidbits about pediatric patients but overall we'll focus on adult patients so I
think we're ready to get started

And it's really important to know both for that reason and of course for taking care of patients when
it happens

so let's dive in you wanna start by knowing a little bit about the epidemiology of this

hemorrhage is the most common cause of death in the first hour of arrival to a trauma center 80% of
OR deaths and 50% of deaths in the first 24 hours after injury are due to exsanguination and
Coagulopathy 3% of civilian trauma patients receive massive transfusion but these patients actually
consume 70% of the blood in a trauma center and mostly today we'll be speaking more so about
civilian trauma though certainly a lot of this data has come from military studies and I often think
about massive transfusion in terms of trauma and it's generally the best studied but certainly many
other common scenarios for massive transfusion including cardiac surgery liver transplant surgery or
major vascular surgery specifically aortic surgery GI bleeding and obstetric hemorrhage

yeah I think we really hear a lot about obstetric cases that can end up using dozens of units of blood
so this is as you say definitely not limited only to trauma really important as you mentioned major
cause of death in major centers is exsanguination and 70% of the blood I just want to highlight what
you say 'cause it's such a striking statistics 70% of the blood in in major centers going to 3% of the
patients so when it happens it happens pretty big

indeed all right so why don't we back up a second and talk about what exactly is massive transfusion
is there a definition what can you tell us about how how we should think about this term

perfect because of course it is important to define the term we're focusing on and interestingly
there's quite a few definitions of massive transfusion in the literature historically massive transfusion
was defined as transfusion of 10 units of red blood cells in 24 hours and this historically came about
because approximately 10 units of blood is the amount of blood a 70 kilogram adult has in their
vasculature but 10 units in 24 hours undoubtedly sounds laughable to anyone who's been involved
in a major trauma or other keys were massive hemorrhage occurs where we might give 10 units of
product in a matter of minutes

so I've found some additional useful definitions as we mentioned loss of entire blood volume within
24 hours which is quite similar to the 10 units in 24 hours
another definition is 50% of the blood volume in three hours

ongoing bleeding at greater than 150 milliliters per minute

or rapid bleeding with circulatory failure despite volume replacement

interestingly there's also a scoring system to predict the need for massive transfusion one of the
best validated and simplistic is the assessment of blood consumption score or the ABC score and for
civilian trauma has a sensitivity of 75 to 90% with the specificity of 67 to 88% that looks at

whether the injury is penetrating or not

the first Ed systolic blood pressure of less than 90 millimeters of mercury

and eD heart rate of greater than 120 beats per minute

and a positive fast exam

each of those is awarded a point and a score greater than two predicts the need for massive
transfusion

but ultimately I think there is an element of gut feel or intuition or intuition to activating a massive
transfusion the polytrauma that's coming up to the OR who's unstable or you hear about the
ruptured AAA it's a liver transplant take back who's pouring blood out of his drains I'm likely to call
the blood bank in these scenarios and initiate massive transfusion protocol to mobilize the necessary
resources to have blood products available quickly and voluminously

and you'll notice important that I've mentioned specifically a massive transfusion protocol and that's
important because both the American College of surgeons and the ASA committee on blood
management advocate for institutional protocol for massive transfusion

the general goal is for the protocol to mobilize the necessary resources while also providing guiding
principles for damage control resuscitation as well as giving a standard way to assess the endpoints
of resuscitation and to assess and manage the complications of massive transfusion all in order to
attain the best outcomes for the patient

now they're likely variations from institution to institution but the overall principles tend to be
similar and we'll review some of them here

usually four components of the ABC score is whether the injury is penetrating or not the first blood
pressure in the emergency room to stock blood pressure less than 90 a heart rate greater than 120
and a positive fast exam

the score greater than two predicts the need for massive transfusion for that patient right so you got
3 4/4 of these is gonna be a positive outcome of that test

and then massive transfusion protocols as you said differ from place to place who can activate them
differs and what they entail differs as well

but find out if you're out there at an institution you don't know what your massive transfusion
protocol is you wanna find out how to activate it and what it gets you when you activate it

alright so I think I am gonna give you some information on our here at NICVD what we do in terms of
our massive transfusion protocol just so people have an example
a little bit about the principles of how this works sure and even before we get into the principles of
massive transfusion have to speak just a little bit about IV access

so arterial lines are fun and central lines are even better and it may it may very well be that the
patient may be requiring those things but I cannot overemphasize the importance of good
peripheral IV access

the atls guidelines first step for resuscitation in terms of access are two large bore peripheral IVS in
the upper extremities so if I'm working in a team and delegating task I certainly make sure that
someone is working on peripheral IV access with a 14 gauge IV you can run a rapid infusion device
such as the Belmont full blast can transfuse blood products over 500 ml per minute with acceptable
line pressures

so just had to say a quick word you may remember from your physics or your pre Med classes or
Med school that the determinant of how fast you can give fluid through a line depends on as we all
know on the diameter but also on the length and that's really key

so a central line is much longer than a peripheral line and so a peripheral IV that is a decent diameter
and certainly a 14 gauge has a healthy diameter will give you higher flow rates than a thinner or
even a similar diameter long central line

that's why if you can get good peripheral IVS you can really resuscitate through those in a very fast
and efficient manner

and then just in case anyone was wondering Steven mentioned atls and that's advanced trauma life
support so yet another one of these like acls BLS eight protocolized life support and they put out
some guidelines and that's what you mentioned in case anyone was wondering what atls was alright

guiding principles of massive transfusion is that in the treatment of acute hemorrhage hemorrhagic
shock first priority is to stop the hemorrhage

but the second although it will be concurrent priority is blood transfusion the aim of hemorrhagic
shock treatment is the rapid and effective restoration of adequate blood volume all in order to
maximize tissue oxygen delivery that's really the endpoint of everything

furthermore the goal of transfusion of blood and blood products is to maintain the patients blood
composition within safe limits with regards to hemostasis the oxygen carrying capacity oncotic
pressure and just generalized biochemistry really trying to keep it as similar to the patient starting
blood composition as we can therefore the initial administration of other blood components and
addition to pack red blood cells namely plasma platelets and sometimes cryoprecipitate is necessary
for the prevention of dilutional coagulopathy and dilutional thrombocytopenia so that's where the
overall goal of massive transfusion

some additional principles that have kind of complement that goal is number one is to give blood
early obviously it might be necessary to start with crystalloid or colloid resuscitation and certainly
the crystalloid versus colloid is a debate one in its own right that we certainly won't get into today
but if massive losses occur, if massive losses are expected to be continued there's some evidence to
suggest it's better to start giving blood product early and this is primarily to avoid that dilutional
effect

number two is to transfuse blood products using standardized ratios again the whole point here is to
replicate transfusion of whole blood there actually are institutions that have whole blood but there's
very few and the problem is the storage time for whole blood is so short so we do the best we can
with our broken blood products to help replicate whole blood

some debate exactly to where that ratio lies the perfect ratio but the general consensus is that the
pack red blood cells two fresh frozen plasma ratio should be between one to one and one to two of
note the proper trial and JAMA in 2015 by Holcomb ET al investigated patients with severe trauma
and major bleeding and looked at early administration of plasma platelets and red blood cells either
in a one to one to one ratio compared to one to one to two ratio 2 being the red blood cells so
they're getting slightly less platelets or plasma in that case

and they did not notice any significant difference in mortality at either 24 hours or 30 days

however more patients in the one to one to one group achieved quicker hemostasis and fewer
experienced death due to exsanguination by 24 hours

and even though there was an increased use of plasma and platelets transfused into one to one to
one group no other safety differences were identified between the two groups

so largely as a result of that study our trauma massive transfusion protocol if you activated the blood
bank will send you a cooler 6 red blood cells, an apheresed platelets and basically apheresis pack is
equal to a 6 pack therefore giving the one to one to one ratio

another guiding principle for massive transfusion is to transfuse to the restoration of perfusion but
to allow normotension or even hypo tension basically you're trying to ensure palpable pulses
adequate urine output observant down-trending lactate but potentially to allow for a low even a
normal to even low blood pressure often termed hypotensive resuscitation

this may allow for better hemostasis and even might suggest better end organ perfusion in that you
have better end organ flow additionally a lot of these patients were referring to specifically in
trauma are otherwise young healthy adults who can likely tolerate a lower blood pressure

another key component of massive transfusion frequent laboratory testing for this reason the
patient will require arterial line but as I mentioned probably more important to their survival is to
have good Iv access to get the products in among the frequent laboratory test to be performed
would be an arterial blood gas with base deficit electrolytes particularly sodium potassium glucose
ionized calcium lactate coagulation studies like PT INR PTT platelet count and fibrinogen and
certainly a growing and important role for visco elastic testing either tag or thromboelastography or
or ROTMG rotational thromboelastometry and then the other huge point for massive transfusion is
that there needs to be endpoints of the transfusion and these can vary based upon the literature
search that you do but as guiding principles from the massive transfusion and trauma guidelines
from the American College of surgeons and trauma quality improvement programs include the
following hemoglobin greater than 10 certainly some evidence suggests 7 to 8 is at adequate but
we're often aim higher for a patient who is actively bleeding complete pT of less than 18 seconds
which would correspond to an INR of 1.4 to a PTT of less than 35 seconds platelet count greater than
50,000 a fibrinogen greater than 150 to 180 is often the range you'll see in the literature and then
normalization of your viscoelastic testing additional components or endpoints of resuscitation would
be lactate less than four

and perhaps most importantly it would be some of the clinical signs declaration of surgical
hemostasis by the surgeons and observation of improving blood pressure heart rate urine output or
decreasing vasopressor requirement and then sadly but an important endpoint to consider is futility
if it is deemed that there's so many injuries that cannot be sort of surgically controlled in a
reasonable amount of time with a sort of controlled massive transfusion one has to consider the
economic effects and effects it can have on the greater patient population and sadly some of these
cases are in fact futile to continue with the massive transfusion

you how accurate do you think of hemoglobin being in the setting of ongoing bleeding

That's a great question because with ongoing bleeding you're essentially losing an equivalent
hematocrit so in the immediate sort of resuscitation. period a Normal or low normal hemoglobin is
not necessarily a good indicator that everything is OK often you'll need some time for it equilibration
or crystalloid resuscitation to give you an idea that your hemoglobin has actually fallen so that's a
great point

yeah I think that's really important and also another reason why though normally we would shoot
for a lower hemoglobin than 10 and patient for example in the ICU who's not you know massively
bleeding we shoot for greater than seven or greater than eight if they have cardiac disease but in a
patient who's massively bleeding in the OR even if we get a hemoglobin back and it says it's eight it
may well be significantly less than that once everything settles out so we would shoot for a little bit
higher as you said some recommendations even say higher than 10 great

couple other things so you mentioned tissue oxygenation is being really key and I think there's a lot
of different ways to think about measuring this in your experience what do you normally looking for
you mentioned some important things like just clinical signs as a patient look perfused anything else
in terms of numbers that particularly speak to you about tissue oxygenation

certainly we mentioned lactate and lactate less than four is often one of the things we look at
importantly and certainly the utilization of mixed venous oxygen saturation though often at times
with these patients the priority is administering the blood product and running laboratory results or
a little bit easier to obtain so being able to draw mixed venous from a central line or even a swan
isn't something that we've done as often but it certainly isn't important marker of end organ
perfusion

yeah I think that's great the lactate is gonna be a big indicator clinical signs as you said and then if
you do pull either from a central line a central venous sat or from a from swan if you have one a
mixed venous sat that'll give you some idea of tissue oxygenation and of course if your lactates going
down you're probably perfusing just fine

alright you mentioned the ratios I think that's key and if people wanna look closer look more closely
at the proper trial certainly I think a lot of centers as you said have now gone to one to one to one at
least for trauma because of that trial

urine output so definitely if you've got good urine output it's probably a good sign unless you have
head injury and maybe you have DI but low urine output's really tough and I don't know we sort of
what you think Steven but I tend to think low urine output if everything else looks good I don't worry
too much about the stress of surgery and certainly trauma can really frequently lead to the release
of ADH and so I think if you're an output is not a great sign of perfusion of the kidneys which it it
traditionally is taught to be but I I'm a little iffy about that I think if everything else looks good I don't
worry end up immediate perioperative setting about low urine output too much

I completely agree but often in these patients they're not doing well so looking at urine output in
the course of your resuscitation can be an important marker that if you're having adequate urine
output of a half CC per kilo per hour so one cc per kilo per hour in the concurrent time course of
your resuscitation I think is a good sign if other things suggest that you're adequately resuscitated
but your urine output might have dropped off some I don't necessarily think it's crucial that you keep
chasing that urine output and I agree with you I think having that robust or good urine output is
really nice to see if you can do it

great alright you mentioned the kind of hypotensive resuscitation may actually improve end organ
flow any any kind of thoughts on how that works

essentially what you're trying to do again accomplishes with Physiology in general we're often using
blood pressure systolic blood pressure as a surrogate marker for flow or perfusion and that's
certainly not a perfect marker so the thought process is again to use lower blood pressures to
maintain better hemostasis therefore there's less surge force on blood clots and things of that
nature to help from sort of almost a surgical standpoint but in terms of tissue oxygenation again
using systolic blood pressure alone is not a great marker for end organ perfusion and therefore by
using lower blood pressures but having markers of adequate tissue perfusion otherwise might
suggest that you're perfusing that organ better than a higher blood pressure might suggest in which
case you might actually have an element of vasoconstriction and not as much blood being directly
delivered to the to that organ

yeah so absolutely I think those are all really important key things and the other thing is that the
human body evolved so that blood loss leads to hypotension it turns out that anemia leads to
hypotension even in the absence of hypovolemia and the reason for that is you probably know is
that hemoglobin scavenges nitric oxide and so as you have less hemoglobin around you scavenge
less nitric oxide and you vasodilate so it makes sense from an evolutionary standpoint that it is
probably advantageous if you are losing blood to have some amount of hypotension and we don't
totally understand all of that you've pointed out some good reasons certainly to help stop ongoing
bleeding but also there's probably a tissue level increase in perfusion that happens based on the
microenvironment that's happening certainly we don't want to cause hypertension for a variety of
reasons and counter that evolutionary advantage that we've kind of evolved to have

alright let's move on so you've done your massive transfusion you followed your protocol there's a
lot of advantages to doing it this way certainly you can save a life by getting them resuscitated
appropriately but there's downsides to everything So what are some of the complications of massive
transfusion

exactly and that's one of the most important things to consider is in the whole process of a massive
transfusion protocol is managing the complications of the massive transfusion

so the first one will address are the acid base disturbances that can occur with massive transfusion
now classically massive transfusion associated with metabolic alkalosis and that's as a result of the
citrate that is part of the storage anticoagulation solution for the blood products stored blood is
actually acidic but the metabolism of citrate in the blood produces bicarbonate however in the
presence of lacteMia from the massive transfusion or being hypoperfused or as a result of the
hyperkalemia which we will address later acidaemia might in fact be present I've actually seen both
metabolic disorders separately during massive transfusion and often you'll have a mixed disorder in
where you're essentially managing both

alright so you can see out acidosis as you can see alkalosis certainly the citrate itself is going to cause
the alkalosis citrate also can cause you mentioned hypocalcemia correct we will talk more about that
great
alright So what are there great alright So what are there other complications you think about
absolutely another key complication that I think about or that one will see with massive transfusion
is hyperkalemia

now that's primarily because the potassium in the supernatant of red blood cells specifically
increases by about 1 mil equivalent per day however because the volume of the supernatant is small
the amount of free potassium infused tends to be less than 7 mil equivalents per unit and this
potassium typically moves intracellularly rapidly went warmed into the circulation but this can
rapidly become a problem in patients with renal failure renal hyporperfusion and pediatric patients
and namely in massive transfusion with large volumes are being transfused especially into the
central circulation

in fact for this reason pediatric patients at least here at Johns Hopkins received fresher blood so to
speak that have lower levels of potassium and the patients do better for that reason

importantly other than looking at your frequent lab draws and seeing the actual potassium value
some signs that look for hyperkalemia assuming on an anesthetized patient would be peaked T
waves on your EKG this can then progress to prolong PR interval a widened QRS the sort of classical
sine wave EKG of severe hyperkalemia which can progress to ventricular fib and asystole

so importantly one has to be familiar with the treatment of hyperkalemia and you might remember
from med school step one and certainly carrying into anesthesia and critical care training first step is
administering calcium and this is to stabilize myocardium other interventions to help combat
hyperkalemia would be insulin in combination with dextrose if needed if the patient is not in fact
hyperglycemic hyperventilation and using beta agonist like albuterol and these three interventions
the insulin the hyperventilation and the beta agonist like albuterol and these 3 intervention the
insulin the hyperventilation and beta agonist is all entirely to shift potassium intracellularly you're
not changing total body potassium at this point and these are probably the interventions most easy
to accomplish in a massive transfusion scenario

potassium excretion methods like diuresis with loop diuretics or even hemodialysis are pretty
difficult to implement in a trauma patient especially one who's combating hypovolemia and
hypotension in general

importantly the evidence is somewhat controversial regarding using bicarb for combating
hyperkalemia certainly jED is not in huge favor of bicarb especially if it's to treat lactic acidosis
specifically but certainly there's more literature to suggest a movement away from using
bicarbonate to treat hyperkalemia

yeah definitely not a big fan as as listeners know bicarb the lactic acidosis setting and I agree with
you Steve and I think that the the kind of

the evidence is moving a little bit away from using it to treat hyperkalemia certainly I would first go
to insulin and dextrose hyperventilation and maybe even albuterol before I thought about going to
bicarb I would probably try to avoid the bicarb regardless

absolutely next complication as we mentioned briefly before was hypocalcemia this is really
important complication this is because the citrate anticoagulant chelates calcium and causes the
hypocalcemia and high citrate content is in FFP and platelets actually it's five times the amount of
citrate then in the rbs so when transfusing in a one to one to one ratio for example requires a lot of
calcium to keep up with the hypocalcemia that would otherwise be caused
again assuming anesthetized patient some of the findings you’l have with hypocalcemia would be
hypo tension decreased pulse pressure and increase LV EDP among others

the hypocalcemia is especially problematic in liver patients or for example if the Pringle maneuver is
performed in the Pringle maneuver is essentially clamping of the hepatenodeudnal ligament
interrupting the flow of blood to the liver in order to help control bleeding from the liver and either
a patient with coexisting liver disease or if the Pringle maneuver is performed the liver can no longer
metabolize citrate adequately leading to worsening hypocalcemia

additionally infusions in excess of 50CC's per minute which would certainly addressed were often
well above and in neonates hypocalcemia can particularly a problem

the recommendations in general are 500 to 1000 milligrams of calcium gluconate or 250 to 500
milligrams of calcium chloride for every 500 milliliters of product transfused

so practically when I'm working with a team or what I'm thinking about in massive transfusion for
every two products that go in this patient should be receiving a dose of calcium yeah I think that's

absolutely right I think I used to think that when I was giving a couple of units of FFP so about
500CC's of FFP I would give a gram of calcium chloride to 1000 milligrams and similarly if I gave
maybe two to three units of packed cells that I'm thinking about the same thing maybe 4

when you're thinking about wanting to see where you're at you wanna make sure you're looking at
the I-Cal right the ionized calcium so that's what's getting bound by the citrate and you may not see
a big change in your overall calcium but most of the time if you're sending a blood gas you're getting
a stat lab that is going to come back with an ionized calcium and that's what you're going to want to
look at to figure out where you're at with your calcium balance

you mentioned the things you see with hypocalcemia I think all really important to keep in mind one
way to help remember this is if you've done any kind of cardiac anesthesia we often for hypotensive
post-op cardiac patients we give calcium all the time and we see an increase in the contractility and
in the blood pressure and so if you think the reverse when they're hypocalcemic Steven mentioned
they have decreased LV EDP's that's left ventricular end diastolic pressure or volume in other words
their LV is not working as well because it needs that calcium to squeeze that's why we give it

other complications there’s no shortage of them next want to talk about is hypothermia and
hypothermia can develop rapidly with the transformation of products and an hour of surgery plus
transfusion of 10 units of cold product can drop the core temperature by three degrees Celsius and
this hypothermia can lead to arrhythmia and worsen Coagulopathy in fact often referred to in the
literature as the lethal triad of hypothermia Coagulopathy acidosis because they all kind of work in
this vicious cycle and worsen each other so to speak and it's known that bleeding worsens below 35
degrees Celsius

additional important concept to keep in mind is that viscoelastic testing by tegs and even coag tests
are run at 37 degrees Celsius therefore they will come back normal if otherwise normal in a bleeding
patient if they're cold so that can be one way to be falsely to be misled essentially and the ways to
combat hypothermia would certainly be using the blood warmer using a forced air warmer and
increasing room temp and I will say that in bleeding trauma patient is often one of the few scenarios
where we can get the surgeons to agree to increase room temperature with very little debate yeah
those trauma ors are often pretty warm you're setting up in there and sweating right from the
beginning but then as you said they need to be
so I just want to stress what you said the rotem if you took a patient who had a Coagulopathy but
then because they were cold and then you warm up the blood to do your coags or to do your rotem
or to do your teg that may come back normal even though in the patient its going to be they have
the coagulopathy because they're cold exactly that's the key thing

the viscoelastic testing is a great and we'll talk more about it but viscoelectic is a great model for in
vitro Croaulation status but you will miss the contribution of hypothermia with those tests because
the blood is warmed

right so patient who's got platelets of 10 you're gonna see it on your rotem no matter what
temperature they are but a patient with everything normal in terms of their numbers but who's got
just a cold Coagulopathy you're not going to see exactly alright what's next

I think that takes us really nicely into coagulopathy and that's one of the other biggest complications
to manage a lot of this is from dilutional effect so if you're giving crystalloid or giving pack red blood
cells in excess of the ratio we've talked about you'll dilute out all your clotting factors

however there's more to than that and there's a lot of mechanisms proposed from tissue injury and
activation of anticoagulant and thrombolytic pathways and fibrolytic pathways and overall it's a
multifactorial process the Coagulopathy of trauma both being dilutional and a prolific cascade of
mediators that can affect the coagulation cascade

so importantly you have to be able to measure your coagulation activity and these would include
sending labs like your platelet count fibrinogen the PT inR every 30 to 60 minutes however these
tests have limitations namely both platelet count fibrinogen are only quantitative tests it can give
you a number but that doesn't necessarily tell you anything about how well those factors or those
platelets are functioning so that's an important thing to keep in mind additionally those tests
typically take about 30 to 60 minutes to run so by the time you get a result back it might be tough or
too late to act on so to speak and largely for that reason there's this growing use of viscoelastic
testing again the teg or rotems up here at Johns Hopkins because tag there faster to result and they
give a better idea of in vivo coagulation status so often with the massive transfusion patient will send
tegs about every hour

so in a brief way to sort of review teg in terms of the therapy for the coagulopathy for a patient who
has a prolonged R time that often indicates or and also it indicates if they have prolonged PT INR but
in this case the R time indicates that there's deficiency in clotting factors and for that suggests that
the patient needs plasma or ffps

Steven tell us what is the R time….so the R time is basically the time from the initiation of the teg
study until there's first detection of a clot in the piston cup module.. OK so it's the time for a clot to
form

exactly and if as you said if it takes longer than usual it means that you are missing coagulation
factors and So what are you gonna give.. FFPs… great…

alright what's our next part teg… the next part of the teg to look at would be the maximum
amplitude and a decreased maximum amplitude typically suggest platelet dysfunction or
thrombocytopenia so we'll typically transfuse platelets to help correct the MA or again if you have a
platete count less than 50,000 We are often using both test simultaneously

reduce MA can also be in a fibrinogen defect but I often typically think of it more in terms of
platelates…. yeah I think exactly right to me either one often you're gonna know its fibrenogen
because you have that number and so if you're low you're going to give cryo but if your fibrinofen is
a reasonable number and the ma is low you know it's the platelets either low number of platelets or
poor platelet function I think of the ma as the strength of a clot. so you gotta have platelets and
fibrinogen to make that clot strong. You ganna need the coagulation factors to start building it and
then it's going to get strong based on the interweaving of the platelates and the fibrinogen so that's
why the ma represents those two factors alright anything else you look at

the other thing to look at in terms of treating the coagulopathy would be as mentioned looking at
the fibrinogen level or the alpha angle often represents fibrinogen activity. We are shooting for an
angle less than 60 we are often transfusing cryoprecipitate to achieve a fibrinogen level greater than
ranging between 150 to 200 is often we shoot for ////great and then you look at fibrinolysis on a
teg…..absolutly so fibrinolysis is the last component of the teg and that would suggest that you need
an antifibrinolytic like TX or AMocar interestingly from the crash two study was a randomized
controlled trial from The Lancet in 2010 and it demonstrates the use of tranxamic acid in trauma
patients suffering from significant hemorrhage reduces all 'cause mortality without any significant
increase in the incidence of fatal or non fatal vasoocclusive events,,,,, we don't typically use anti
fibrinolytics for all trauma patients here at Johns Hopkins we use it for many other surgeries like
cardiac surgery or large spine surgery but certainly there are institutions that are more regularly
using anti fibrinolytics for all trauma patients right so when you are running that teg and you see
that clot form that kind of graph of the clot form on it and then if it starts to go down back to a point
as opposed to staying at the maximum amplitude that's where you worry about fibro lysis and where
you might wanna give the transaminicacid or the amicar exactly lastly there's a couple other
adjuvants for the treatment of coagulopathy that are more controversial we won't get too much
into them but certainly for recommbitant factor 7A is controversial and very expensive but it has
been used sometimes prothrombin concentrates or PCcs are given in massive transfusion or even
giving desmopressin to help with platelet function but those are certainly more controversial and
not as well studied and we'll do them occasionally here for really in sort of desperation mode but
they're used less frequently yeah sounds good

factor seven a lot of complications a lot of possibility for clot and thrombosis but I think usually
when you're kind of throwing the kitchen sink at people often that gets broken out you also want to
make sure if you're gonna use it that you have replenished your factors because it needs the
presence of the factors in order to be effective ,,

alright what's next now should be addressing the lung injury that can occur from massive transfusion
or often any blood transfusion but specifically in the setting of massive transfusion these two types
primarily being trali or transfusion associated lung injury which is defined as acute onset it must be
during within six hours of transfusion hypoxemia with the presence of bilateral infiltrates on frontal
chest radiograph no evidence of circulatory overload or left atrial hypertension and no pre-existing
acute lung injury or ARDS before the the transfusion.. but because certainly trali can look almost
identical to ARDS otherwise

and important board question here that I've seen more than once is that trali is the leading cause of
transfusion related mortality some will actually argue that it's Taco which we'll talk about tacos often
more common but the correct answer I've seen for number one cause of transfusion mortality is trail

I think that's right and people by the way are gonna be sitting out there think of what's why is he
talking about tacos is transfusion associated circulatory overload which we’ll talk about in a second I
think that we can also point out that in especially in countries that have stopped taking FFP from
women who have had children the incidence of trali has gone way down because it's thought to be
related to the HLA antibodies from the interaction with women that went pregnant they develop
these antibodies which then get into the plasma, which when they donate can lead to trail. so that is
hopefully as more and more as we go more and more away from those donations we’ll be seeing
less trail.. exactly and related to that and another board question that I've seen is that trali can
actually be associated with leucopenia and that's specific to trali as a result of pulmonary
sequestration of the neutrophils related to this HLA incompatibility often from donations from
plasma from pregnant women

absolutely and another important board question is that trali is most associated with plasma rich
components so namely the answer you'll probably be looking to select would be FFP it is plasma but
also to keep in mind platelets and whole blood also do have plasma components to them

so now moving away from trali the other primary lung injury we look at is Taco which I referred to
earlier which is arguably the best acronym of all time …so this is transfusion associated circulatory
overload it's very similar to trail but the big difference is there signs of volume overload and this is
specifically defined as a wedge pressure of greater than 18 and this is the second most cause of
transfusion related death yeah now so wedge pressure obviously you only get if you have a swan
ganz in which we often won't and So what it what are some sort of classic symptoms of circulatory
overload that you may see in someone without sawn….. so things like pulmonary edema, peripheral
edema, JvD (jugular venous distension) things of that nature

absolutely great OK alright Steven do you worry about infection when you're giving this much blood
to people

certainly infection is a risk that we worry about with this much volume of blood over all.. people
certainly think of viral transmission as being the main concern…the leading transmitted virus by
bloodis still hepatitis B virus and the incidence being about one and 250,000 …..HIV and HCV did a
better screening now was much much lower looking at less than one and two million but the
important thing to think about and is another board question I've seen is actually the most common
type of infection transmitted is actually bacterial infection and what the product most associated
with this is platelet transfusion and this is because platelets carry a higher risk of contamination
because platelets are stored at room temperature

alright so anything else we've covered a lot of great stuff anything else you think we should cover

I think those are the big ones a couple smaller ones to still keep in mind would be that massive
transfusion or any transfusion the blood has it decreased 2-3 DPG level and what this causes is left
shift in oxyhemoglobin dissociation curve and you essentially have decreased O2 unloading at the
tissue level of course there's something very difficult to measure but it's important to think about
because that's defeating or against the ultimate goal of what we're trying to accomplish with
massive transfusion

other smaller things are not necessarily a small thing but transfusion reactions you want always has
to keep in mind that can occur with any blood transfusion and the main types being hemolytic
transfusion reaction due to ABO incompatibility, febrile transfusion reactions due to antibodies to
the leucocytes in the donor blood, allergic reactions which are due to reaction to the donor plasma
proteins and then any of the delayed immunological reactions and specifically related to
immunomodulation is that allogeneic transfusion suppress cell mediated immunity and may place
patients at risk or post operative infection so there's just some of the smaller things to keep in mind
and I can't say I've they seem to be as frequently tested but they are very real complications
absolutely so a couple other things when you are massively transfusing someone we talked about
infection but what about antibiotics..we are giving prophylactic antibiotics how often do you feel like
you need to redose if you're transfusing a ton of blood

there's a great point I'm not as familiar with the evidence regarding that but typically our protocol
here at Johns Hopkins is to reduce our antibiotics at approximately every 1500 milliliters of blood
loss

yeah that's what I do as well and I think that's pretty evidence based and then the other thing
maybe we can just touch on briefly someone comes in massively bleeding we don't have a type in
screen what are you gonna do in terms of type of blood you're gonna give

so it's ideal to obtain type and screen for the patient so they can get properly cross match blood if
that's not available the first choice would be to give O positive blood it's the blood type is the
universal donor that you can give to any patient and if it's woman of childbearing age so the
preference is to give O negative blood in order to avoid developing antibodies to the RA antigen
which could potentially predispose that woman to hydropsfetalis if she were to become pregnant in
the future

right so that's exactly right so we our practice here at Hopkins and I think in most places is a man
who comes in or a postmenopausal woman can get a positive but there's really no downside ..as
emergency blood.. the obviously preference as you said is to type and screen them but a woman of
childbearing age should get O negative and again if we there is actually no harm in the moment right
to a woman who gets O positive blood it's that if she later gets pregnant and she's developed those
antibodies and the baby is O positive then that woman’s antibodies the anti RA antibodies that she's
now developed can attack that baby's blood cells and as you said cause hydrops fatality in that baby
which can't be fatal in utero

alright so that's what we wanna do O positive except for childbearing age women get old negative if
we don't have a type and screen

alright we talked about redosing antibiotics we talked about O negative blood Steven any last words
you've covered a lot of great stuff

thing that's all I have for us it’s just a little bit of brief rapid review

please

so mass transfusion is when you anticipate replacement of blood volume in less than 24 hours or
greater than 50% of blood volume in three hours or essentially when I think about it is if things look
really bad I activate massive transfusion

badness activated

again you want to activate your institutions protocol and then transfuse in a systematic manner you
need good I/v access use appropriate ratios for damage control resuscitation ,transfuse to specific
endpoints and monitor those parameters and the immediate complications that you're likely to see
OR and need to manage acidbase disturbance, hyperkalemia hypocalcemia Coagulopathy and
hypothermia

this is fantastic Steven thank you so much thanks for being the inaugural resident you did a fantastic
job thanks for coming on the show well thank you I wanna thank Jim for having me I was really
excited to be here wanna give a quick thanks to doctor Steve frank he's one of my mentors and he's
really the blood management guru here at Johns Hopkins and then of course the biggest thanks to
all my fantastic Co residents and attending to make coming to work every day rewarding and exciting
thanks so much David alright that's it for today remember you can check out the website at at
cracked.com that's ACC rac.com or you can sign up for mailing list in the

Many many reasons that we can talk about in a whole other episode why people bleed during
cardiac surgery that's actually very interesting but you know the consequence is that bleeding and
anemia that results from it can have very real consequences and bad outcomes you know but on the
other hand transfusions can have consequences two and so you know many of you are familiar a lot
of the debate has kind of centered around these restrictive versus liberal transfusion practices but
on the extreme end we also have this really fascinating population of people who cannot receive
blood transfusions for religious reasons and I thought this would make a really good topic so I'm
really excited actually to introduce doctor Steve frank

Formulas for Finding the Ideal Weight

IBW formulas were developed mainly to facilitate drug dosage calculations. All of the
formulas, have the same format of a base weight given a height of 5 feet, with a set
weight increment added per inch over the height of 5 feet. For example, if you are a
5'10" male estimating your ideal weight with the Devine formula, you would add (2.3
× 10) kg to 50 kg to get 73 kg, or ~161 lbs.
The formulas differ in the values used based on the research of the scientists
involved in their development, and their findings. The Devine formula is the most
widely used formula for the measurement of IBW.
G. J. Hamwi Formula (1964)
Male: 48.0 kg + 2.7 kg per inch over 5 feet
Female: 45.5 kg + 2.2 kg per inch over 5 feet
Invented for medicinal dosage purposes.
B. J. Devine Formula (1974)
Male: 50.0 kg + 2.3 kg per inch over 5 feet
Female: 45.5 kg + 2.3 kg per inch over 5 feet
Similar to the Hamwi Formula, it was originally intended as a basis for medicinal
dosages based on weight and height. Over time, the formula became a universal
determinant of IBW.
J. D. Robinson Formula (1983)
Male: 52 kg + 1.9 kg per inch over 5 feet
Female: 49 kg + 1.7 kg per inch over 5 feet
Modification of the Devine Formula.
D. R. Miller Formula (1983)
Male: 56.2 kg + 1.41 kg per inch over 5 feet
Female: 53.1 kg + 1.36 kg per inch over 5 feet
Modification of the Devine Formula.

Base excess or base deficit is characterized by the amount of base that is required to
normalize the pH of the blood. Normal values range from -2 to +2 mEq/L.

Regular And Healthy Urine Output Rate ; Adult, >0.5 mL/kg/hr ; Child, >1 mL/kg/hr ; Neonate,

>2 mL/kg/hr ...

Normal urine output is 1-2 ml/kg/hr. To determine the urine output of your patient, you need
to know their weight, the amount of urine produced, and the amount of time it took them to
produce that urine.