Just One Time
Are you being the focused, exacting medic that your service needs in order to be a “high reliability
Is your goal getting to work just in time and hoping the shift passes quickly, or is each patient care
experience your best effort. Sometimes we forget that “ho hum” for us can make a huge difference for
We must keep our preparedness and each patient encounter in focus to deliver our best to our
We will examine a few areas that related to trauma, where a less than enthusiastic effort can be
devastating to the patient. We will examine why we need to be “on our game” all the time.
First, consider that a small overlooked detail or one that you at first think is inconsequential could
easily develop into a problem. Sometimes a small deviation can end up becoming a big deal.
The first focus on trauma is immediate Damage Control Resuscitation. We must stop the bleeding
immediately. We must get air in and air out. If available, we may need to administer blood to the
patient. We must be ever vigilant for shifts in the “Lethal Triad”. The three sides of the triad are
Hypothermia, Acidosis, and Coagulopathy. We also need to consider the effect of hypocalcemia on all
sides of the triad. The effect of the calcium has is great enough that our understanding of this needs
to see that calcium as a fourth side to the triange.
We must assume the patient is hypothermic upon our arrival, evaluate and take immediate corrective
action. Hypothermia starts at 35°C or 95°F. (Normal temps are 35.6 to 37.8 C and 96 to 100 F.)
100% mortality begins as temps drop to 32°C or 89.6°F. Consider the effect of temperatures in your
ambulance on the patient and fluids that you store there. Room temperature fluids worsen
Remove wet clothing and cover the patient with warm layers, then occlusive layers. The best options
come in the form of a cocoon type wrap the prevents heat loss circumferentially . IV fluids can be
warmed with a Ready Heat II® and a roll of soft, roller bandage, in the absence of a warmer. Roll up a
small coil of IV admin tubing and tape it to the disposable heater. Adding a squirt of water soluble jelly
will help transfer the heat to the tubing and into the patient. This will not overheat the solution. Larger
Ready Heat® blankets can be used under or on the patient, but use care not to burn the patient,
especially on the bottom side.
Acidosis is the second side of the triangle. Use care in relying on inexpensive lactic acid meters…the
elevated values you get may be from falling values from previous activities, instead of current trauma.
Remember that Normal Saline has a pH of 5.5, whereas Lactated Ringers is safer at 6.5. Increasing
acidosis leads to worsening coagulopathy, and lower temperatures. This leads to a vicious downward
spiral. Consider normal blood pH of 7.35 to 7.45. When the pH drops to 7.2, we see reduced cardiac
contractility, and therefore reduced cardiac output; vasodilation, hypotension, bradycardias, increased
dysrhythmias, and reduce hepatic and renal blood flow. This leads to nausea, vomiting, headache,
SOB, confusion, LOC, coma, seizures, weakness and diarrhea. We also see reduced clotting, so
bleeding increases. In a world where normal exist in a range of .10, a fluid pH difference of 1.0 could
be devastating. Realizing that the body normally begins to neutralize these changes immediately
cannot be relied on in the traumatized patient.
Acidosis contributes more to coagulopathy than the hypothermia does, and it is harder to correct in
Resuscitation with crystalloids or packed red blood cells do not provide the clotting factors that the
body needs to prevent the lysing of clots that are attempting to form. Critical dilution begins at 1.2
blood volumes. In the future we may see more pre-hospital use of fresh frozen plasma, as it provides
clotting factors and is great for use in burns, where we do not see as much loss of red cells.
Reconstitutable lyphilized plasma is also in the testing phases. For reasons not yet understood,
plasma replacement also appears to be protective of the vessel lining itself, making it less likely to
develop permeability as soon, preventing leaking into the tissues.
Thermal Coagulopathy occurs when hypothermia causes the enzymatic pathway to degrade, affecting
the coagulopathy cascade. This can lead to Disseminated Intravascular Coagulation. In DIC, the
clotting cascade becomes uncontrollable. This over-activity consumes all the body's clotting factors.
The worst issue is the hypocalcemia. Most people in our modern cultures are walking around in a
chronically hypocalcemic state. Loss of blood leads to hypothermia and further loss of calcium. For
every 100 ml of blood we lose, we also lose 10 mg of calcium. Hypothermia leads to decreased citrate
metabolism, which leads to more calcium binding by the citrate. This takes more calcium out of play.
Citrate is used as a blood component preservative. In healthy patients, this citrate is normally quickly
hepatically metabolized. However, in patients with hemorrhagic shock, this clearance is greatly
decreased, and the often-concomitant rapid transfusion of large amounts of blood products also
contributes to citrate accumulation. A Royal British Military study proved a substantial loss of calcium
due to citrate binding, with each unit of blood given. Replacement must occur in a timely manner to
protect organ systems. This is important because calcium plays an important role in platelet adhesion
and coagulation, as well as contractility of myocardial and smooth muscle cells. Calcium is required by
clotting factors II, VII, IX, and X, as well as proteins C and S for activation at the damaged endothelium.
Finally, calcium has a role in stabilizing platelets and fibrinogen in the developing thrombus. It also
binds with the citrate preservative in component blood products such as pRBC.
Acute hypocalcemia usually first presents as perioral paresthesia. You can easily evaluate the patient
for Trousseau’s sign by placing a BP cuff on the upper arm for three minutes. If this elicits a spasm of
the arm, hypocalcemia is present. You can also evaluate Chvostek’s sign by tapping on the facial
muscle just in front of the ear. A muscle spasm will occur if positive for hypocalcemia. You may also
see developing fatigue, prolonged QT, and eventually seizures.
Provide better perfusion support: Permissive hypotension, minimal use of fluid (especially NS), GET
THE PATIENT TO BLOOD, (or blood to the patient) and target respirations to EtCO2. Remember, for
every increase of 10 mmHg in EtCO2, the pH drops by 0.08 and the K+ increases by 0.5. If we don't
get a handle on this with a BVM or vent, it will be time to reach for the drug box.
Realistically, every substantial trauma patient needs calcium replacement whether the patient receives
blood or not. IV access X2. Blood (or components) through one line via warmer. Calcium admixed
into 100 ml NS for bolus, flush the line, followed by 1 Gm of TXA over 1-2 minute push. (CaCl is 13.65
meq/10 ml; CaGlu is 4.65 meq/10 ml, so if you use gluconate give three times as much.)
If you are not concerned with TBI, consider a permissive MAP of 65 mmHg…don’t pop the clots!
Consider TXA. TXA does not cause blood to clot. It prevents blood clots that have formed from
Learn and use the SHOCK INDEX. The shock index is the heart rate divided by the systolic blood
pressure. SI=HR/SBP. Normal is 0.5. If the SI goes above 0.9 the mortality rate at 24 hours rises
from under 4% to almost 60%.
REMEMBER. Missing any part of the Lethal Triad, JUST ONE TIME, can be lethal to your
Simple crush injuries involve muscle swelling and neurological injury. Crush Syndrome is a systemic
manifestation. These injuries do not have to be circumferential. Extended contact with a hard
surface, such as a floor will cause the same metabolic injury. This is particularly true of older patients
with low muscle mass.
Unless there is a threat to life, do not move this patient until you have taken a complete history, and
begin treatment. If IV access is not readily possible, consider a tourniquet prior to moving the patient.
Try to get IV access before moving this patient.
Moving the patient prior to treatment prevents providing the patient with a buffer against injury. You
essentially poison the patient by the release of muscle break-down products. These include
myoglobin, potassium, and, phosphorus, which are all nephrotoxic. Traumatic rhabdomyolysis occurs
as dying cells absorb water, sodium and calcium. This releases potassium, myoglobin, phosphate,
thromboplastin, creatine, and creatine kinase. This can quickly result in a fatal outcome, either
acutely or within a few days.
In addition to a good history, you should monitor this patient’s cardiac rhythm. Do serial 12 leads, look
for serum potassium changes. Remember peaked T-waves generally mean potassium has reached
5.5 to 6.0 mEq. As the potassium increases to 6.1 to 7.0 mEq you will see a prolonged PR interval,
flattened or absent P waves and a widening QRS. Patients with potassium above 7.0 mEq will develop
AVB, BBB, and or PVC’s. Guess what happens with a potassium of 10.0 mEq. Often, it is the
unmistakable sound of charging the defibrillator.
This patient should receive oxygen. An IV with .45% Normal Saline (1/2 normal saline) should be run
at 150/hr, unless a bolus is needed to maintain SBP. Albuterol can be given by small volume
nebulizer. As soon as possible a second IV of ½ NS with 100 mEq of sodium bicarbonate added
should be started. Any open wounds should have antibiotic coverage, if it is available. Cefazolin
If a hyperkalemic ECG is still evident, consider administering regular Insulin, 10 iu SQ with 25 gm of
D50. (Better yet: Use 125 ml of D10.) This will effectively pump potassium from the cells. Most of
these patients are hypocalcemic, consider calcium chloride 10%, 5 ml over two minutes. It is important
that this patient be transported to a dialysis capable hospital.
Remember, missing this JUST ONE TIME can be fatal to your patient.
Five concerns with head injuries include: Pressure, Seizurea, Herniation, Temperature, and
Hypercarbia. Positioning at a 30° incline is more physiologically neutral. As ICP goes up MAP must
follow or the resulting CPP will not be high enough to perfuse the brain.
In some cases our previous treatment modalities have created iatrogenic damage. For instance, rigid
C-collars have been proven to slow the flow of blood out of the brain via the external jugular veins.
This congestion increases ICP. We sometimes hamper carotid flow to the brain with our airway
choices. In a cadaveric study, endotracheal tubes were proven to have no more systolic carotid flow
or pressure restriction that a patient without an airway installed. Mean arterial pressure and flow
deviated by less than 2% which would be clinically irrelevant. The ET is considered the standard in
this study and assigned a factor of 3.0. Supraglottic airways tested to ascertain how they fared
against that standard. The iGel airway scored 2.75, a typical LMA scored 2.0, with the KIng Airway
scoring 1.75. For clarification, the lower the index number, the more restriction in carotid pressure
Maintain the MAP between 60 and 150 with a target of 90 to 95. This is important to maintain cerebral
perfusion pressure and blood flow.
Prevent seizure activity with prophylactic Fosphenytoin, 15 – 20 mg/kg, as warranted.
Monitor the patient for signs of herniation, which is usually preceded by Cushing’s Triad.
(Hypertension, Bradycardia, and Irregular respirations). If pupillary changes are noted, hyperbag the
patient until the pupils return to normal. Watch the EtCO2.
Spot check the temperature as soon as possible, but rely on core temperature. Maintain a
euvothermic core state. Becoming hypothermic just once is very detrimental to the patient.
If the patient becomes hypoxic, hypothermic, or hypotensive just one time the mortality increases to
Remember, missing this JUST ONE TIME can be fatal to your patient!
Create the mindset that you will tolerate no less than a “DASH 1A”. This means you will create a
Definitive Airway, Sans Hypoxia/Hypotension, in One Attempt!
Many organizations are using Delayed Sequence Intubation (DSI). This is undertaken using
ketamine. The ketamine calms the patient, and but does not take the airway from their natural control,
provided you use an appropriate dose and don't push it too fast.
Place the patient in an upright position, if possible. Apply a high flow nasal cannula, administer 1
mg/kg of Ketamine, which can be re-dosed in 0.5 mg/kg increments if needed. Consider the 15/15/15
protocol. Bag the patient with a BVM with PEEP set at 15 cm of H20 pressure, with a liter flow of 15.
Under the mask place a high flow nasal cannula at 15 Lpm. Dropping in bilateral NPs works well also.
This massive pre-oxygenation is designed to de-nitrogen the patient, giving you much more working
time to intubate before the patient desaturates. When monitoring your intubation, remember that
pulse ox lag is only about 30 seconds in a healthy patient, BUT can be 3-4 minutes in a compromised
patient. Using a nasal or ear clip SpO2 clip responds to changes like de-sat much faster.
One recent study suggests that patients often fare better if paramedics do not attempt intubation.
There are procedural concepts we can do that reduce that danger, such as the DSI concept. Another
is constant vigilance for Peri-Intubation hypotension. If a patient’s Shock Index is greater than 0.8,
they will experience hypotension caused by the intubation itself. We can get around this with a low
dose “push dose pressor”. The safest and simplest of these is epinephrine, which is readily available
on the truck. Draw up 9 ml of Normal Saline in a syringe, add one ml of 1:10,000 epi. This yields a
dose of 10 mcg/ml. This micro-dose of epi can be given to a patient experiencing a hypotensive
response to the intubation, without frying the brain with vasoconstricting doses of the drug.
Close blood pressure or MAP monitoring, with judicious use of the Epi PDP, can bring a patient
through the intubation process without the detrimental effects of the intubation in a patient in extremis.
Times when we don’t need to intubate.
A recent British Army study of 492 patients that were injured enough to allow intubation without
pharmaceuticals: Only one patient survived. If the patient has reached that level of extremis, a
surgical cryc is far safer. Perform the cryc before it is absolutely needed. Whether you use a
seldinger type airway, with aspiration needle and a wire for placement or a standard open surgical
cryc with an appliance or 6 mm ET, accomplish this airway sooner rather than later. If the patient is
semi-conscious, consider low dose ketamine, and local lidocaine prior to the procedure.
Remember. Missing this JUST ONE TIME can be fatal for the patient!
Recent studies have shown that pain control reduces the recovery period by 2/3. Not providing pain
relief can lead to chronic pain syndrome. The use of poly-pharmacy addresses multiple pain
receptors and allows relief with less opiod use. DO NOT use Cox-1 inhibitors like aspirin on trauma
patients. IV acetaminophen allows for temperature and pain control, as it works faster and more
efficiently than its oral counterpart. Ketamine addresses different receptors than drugs like fentanyl
and morphine and creates far less histamine response.
A one-centimeter square space has 2 heat receptors, 12 cold receptors, 50 pressure receptors, but
over 200 pain receptors.
Remember. Missing this JUST ONE TIME costs your patient extra days of hospital confinement,
and may cause chronic pain issues.
Stop the Bleed
This needs to become foremost in your mind for trauma victims. Teach the “immediate responders”
(Active Bystanders) in your community and your household.
Identify patients in trouble in the first five minutes, then get them to definitive care (blood).
Clotting factors are proteins in the blood that control bleeding. When a blood vessel is injured, the
walls of the blood vessel contract to limit the flow of blood to the damaged area. Then, small blood
cells called platelets stick to the site of injury and spread along the surface of the blood vessel to stop
At the same time, chemical signals are released from small sacs inside the platelets that attract other
cells to the area and make them clump together to form what is called a platelet plug.
On the surface of these activated platelets, many different clotting factors work together in a series of
complex chemical reactions (known as the coagulation cascade) to form a fibrin clot. The clot acts like
a mesh to stop the bleeding.
Coagulation factors circulate in the blood in an inactive form. When a blood vessel is injured, the
coagulation cascade is initiated, and each coagulation factor is activated in a specific order to lead to
the formation of the blood clot. Coagulation factors are identified with Roman numerals (e.g. factor I or
Penetrating wounds must be packed using roller gauze, z-fold gauze or hemostatic gauze. Packing
the wound stops the blood flow at the point of origination, helping the clotting cascade do its job.
Immediate blood flow in an extremity may require a tourniquet. A TQ should be applied in 20 seconds
or less. Two may be required on a large thigh, etc. Monitor for collateral circulation and tighten as
The body's clotting factors may not meet demand. Transexamic acid is used to prevent the natural
lysing of clots, supporting clot development. TXA should be started within the first three hours, but
best if started as soon as possible. The initial dose is one gram mixed in 100 ml of NS, administered
over 10 minutes. Secondary dosing consists of an additional gram diluted in 500 ml of NS for
administration over 8 hours. The use of TXA does not change the requirement for blood products.
Remember. Missing this JUST ONE TIME can be lethal for your patient.
As EMS providers we are considered the liaison between circumstance and fate. How many hours of
training do you invest yourself in each year? Are you well educated and mentally prepared?
Thanks for your interest. Be safe out there.
You can find information about classes we teach at www.publicservantsolutions.com .
©2019-2020, Public Servant Solutions, All Rights Reserved.