into the aircraft upholstery, the patient’s vital
signs seem to improve.
On a sullied monitor screen, you note that
her heart rate is 90; blood pressure appears to
have climbed to 135/85 mmHg; EtCO2 is 37
mmHg; and her oxygen saturations are holding and reaching as high as 98%, so you can
begin to titrate her FiO2 down. With attention to the finishing touches, the patient is
given further sedation as well as analgesia to
ease her through her ride on the vent.
Thankfully, the flight proceeds without
further incident as does your final handoff
to staff at the receiving hospital. Repeat labs
done on admission at the bedside find your
patient’s INR to have reversed course; now
a sterling 1. 5.
In one final moment, you watch from the
ED hallway as your patient is wheeled away
to the operating room. She’s found to have a
bleeding ulcer, which is cauterized.
The good news eventually comes that
she was extubated several days later and discharged within a week to a skilled nursing
facility … which is meaningful to hear, because
you feel like it took nearly that long to clean
There are few cases more challenging in
EMS than the critical geriatric patient. These
become all the more so when we’re handed
the long list of medications they may—or may
not—have been taking, and then left asking
how our treatment plan should now change.
Among those medications it’s not uncommon
to find blood thinners prescribed specifically
to help protect the patient to some extent from
the risk of stroke, emboli and coronary events.
Within this broader realm of pharmacology, the prescribed medications fall into one
of two larger groupings: antiplatelet agents
or anticoagulants. The former group includes
medications such as aspirin, clopidogrel
(Plavix), dipyridamole (Persantine), ticagrelor
(Brilinta) and ticlodipine (Ticlid). The latter
constitutes a list we might find just as familiar,
with names such as warfarin (Coumadin or
Jantoven), enoxaparin (Lovenox), dalteparin
(Fragmin), rivaroxaban (Xarelto), apixaban
(Eliquis) and dabigatran (Pradaxa).
Collectively, these act on the body to thin
the blood along a number of different path-
ways. In order to understand how to deal with
each of these medications in an emergency
setting, we need to first understand how each
of them contribute to clot formation.
An article on the coagulation cascade
could fill an entire journal with the minutiae involved, and attempting to memorize
every nuance could have you forgetting other
important details in life such as birthdays and
the location of your car keys. In this case, we
focus on aspects of the clotting cascade that
relate to the practicality of our jobs.
A blood clot consists of two components:
platelets and cross-linked fibrin strands. Platelets will gather initially at the site of any tissue injury or bleeding, but in order to bind
together and form a stable blood clot they
require something more. A meshwork of fibrin
is necessary for clot formation, and it’s what
we have to blame for the confusing array of
factors, proteins and other mediators that so
many of us find intimidating.
These two requirements for blood clotting—platelets and cross-linked fibrin
strands—are the reason there are two classes
of prescribed medications to work against
coagulation. Antiplatelet agents (e.g., aspirin, Plavix, etc.) target platelets specifically.
Meanwhile, anticoagulants act at a number
of different points on the formation process
of the fibrin meshwork.
To further appreciate the steps that lead to
fibrin activation and cross-linking, we should
take a step back. With any vessel damage and
bleeding, there’s also activation of an enzyme
called tissue factor (otherwise known as factor III), in addition to platelet activation. This
sets off the extrinsic pathway in the coagulation cascade.
A number of other factors are subsequently
involved and activated, leading us into the
common pathway of the clotting cascade.
The common pathway begins with factor X
which, by way of its activation (Xa), catalyzes
the formation of thrombin (factor IIa), fibrin
(IIa), and finally a stable fibrin meshwork at
the site of bleeding. Within this sequence,
the activation of prothrombin ( 2) to thrombin (2a) triggers a separate and accelerating
process known as the intrinsic pathway. This
chain of reactions, involving still other clotting factors, all the more gainfully activates
factor X in a positive feedback loop, leading
to substantially greater thrombin and fibrin
The positive feedback thrombin loop
involves numerous other factors (I–XIII) as
well as their activated forms), however, we’ll
limit ourselves to briefly mentioning only two
other players in the coagulation cascade to the
treatments placed at our fingertips. The first
is vitamin K and the second is calcium. Each
plays the role of a necessary cofactor in acti-
vation of specific clotting factors within both
the extrinsic and intrinsic legs of the coagu-
lation cascade, as well as along the common
pathway (targeting factor Xa and thrombin).
In the absence of either vitamin K or calcium,
a patient can suffer from serious coagulopathy.
Warfarin, perhaps the most commonly seen
anticoagulant in our modern-day pharmacopeia, specifically acts to reduce the amount of
vitamin K available for use in the clotting cascade, and subsequently interferes with coagulation, as it did in this case.
Also in the case of this patient, a dose of
calcium was given to the patient before providers administered a fourth unit of blood
products. This was done because of blood
product administration. Each unit of PRBCs
(also FFP or whole blood) contains a preservative called citrate which acts to keep the
Reversal of drug-induced coagulopathies can be an
important part of treating an upper GI bleed or any
other type of hemorrhage in the prehospital setting.
Photo courtesy Ryan Hodnick