The Written Summary of the EM:RAP Monthly Audio

Transcription

The Written Summary of the EM:RAP Monthly Audio Program
January 2014: Volume 14, Issue 1
Editor-in-Chief: Mel Herbert
Executive Editor: Paul Jhun
Associate Editor: Marlowe Majoewsky, MD
www.emrap.org
Accidental Hypothermia Part 1
The duration of CPR does not predict outcome, and a long
transport time should not dissuade you from transferring.
Mel Herbert MD and Doug Brown MD
u
Brown DJ et al. Accidental hypothermia. N Engl J Med. 2012
Nov 15;367(20):1930-8 PMID: 23150960.
Case #1
Case presentation. A 29 year old orthopedic surgery
resident was skiing with friends in Norway. She fell into a
creek and became trapped upside down. Water flowed all
around her but she had an air pocket in front of her face.
Her friends were unable to extricate her so they watched
her while they waited for help. After 40 minutes, she lost
consciousness. After 80 minutes, rescuers arrived and extricated her. She was lifeless and in asystole. They started
CPR and transported her via helicopter to a tertiary care
center. At the time of her arrival, she had been down for
130 minutes and received 90 minutes of CPR. Her potassium was 4.3 mEq/L and her pH was 6.6. She was placed on
AV bypass. She had the lowest recorded core temperature of
13.7 degrees Celsius (56.7 degrees Fahrenheit).
10 minutes after bypass was initiated, she went into ventricular fibrillation. At 15 minutes, she had a pulsatile
rhythm. After 180 minutes, she was rewarmed. 24 hours
later, she went into florid pulmonary edema and remained
on extracorporeal membrane oxygenation (ECMO) for 5
days. She spent a month in the ICU with the usual complications: renal failure and ischemic colitis.
u
What is hypothermia? A core temp of less than 35 degrees
Celsius (95 degrees Fahrenheit).
u
The approach to patients with accidental hypothermia
can be broken down into two pathways: patients with
and without vital signs.
Hypothermic patients with no vital signs. This is a 3 step process.
#1. Is CPR needed? Do they have obvious signs of irreversible death: decapitated or death before cooling? If there is a
possibility that they were cooled (less than 28 to 32 degrees
Celsius [82.4 to 89.6 degrees Fahrenheit]) before their
heart stopped, they have a chance at recovery and should
be transferred to a center capable of performing ECMO or
cardiopulmonary bypass (CPB). These patients can survive
spectacular durations of CPR and still have a good outcome.
#2. Do you need to transfer to an ECMO center?
#3. Supportive care while transporting.
u
Who is cold and salvageable and who is cold and dead?
There are 5 criteria you can use to determine if they are dead.
1) A clear history of cardiac arrest prior to cooling.
2) If you have a core temperature greater than 32 degrees Celsius
(89.6 degrees Fahrenheit) and they are in asystole, hypothermia
is not the cause.
3) If they are frozen solid and the chest is not compressible.
4) They have potassium greater than 12 mEq/L.
5) Special circumstances: trauma, drowning and avalanche
burial.
q
Blunt traumatic arrest has a less than 1% survival
and hypothermia will decrease survival even further.
q
The history of drowning is important. Drowning can be
divided into submersion versus immersion.
• Submersion is when the patient goes under the
water immediately, has a hypoxic cardiac arrest
and then cools down. These patients have a dismal
prognosis. One caveat is the pediatric patient outlier:
there is a report of a 2.5 year old child who fell into
a 5 degrees Celsius (41 degrees Fahrenheit) creek and
was submerged for 66 minutes. He cooled extremely
rapidly and had simultaneous cardiac arrest. He had a
core temperature of 19 degrees Celsius (66.2 degrees
Fahrenheit) and asystole. He received 2 hours of CPR,
was transferred to ECMO and made a full recovery.
• Immersion is rare: patients are in the water but
the head is above the water and they continue to
breathe while they cool down before they eventually
arrest. The prognosis here can be good and these patients
may survive even after prolonged CPR time.
q
Selection of patients for ECMO should be judicious; using
ECMO in patients that are unlikely to benefit will dilute the
resource with cases that don’t do well.
EM:RAP Written Summary January 2014: Volume 14, Issue 1
1
The Written Summary of the
q
u
The unconscious, hypothermic patient with vital signs.
When should you not worry and when should you transfer to a
CPB center?
q Things
that are not worrisome in the unconscious hypothermic patient with vital signs: bradycardia, mild hypotension and atrial fibrillation. These are normal and to be
expected with accidental hypothermia. However, if you see
cardiac instability, ventricular arrhythmias, hypotension out
of proportion to the degree of cooling (this is difficult
to determine sometimes) or very low core temperature;
less than 28 degrees Celsius (82.4 degrees Fahrenheit)
and especially below 24 degrees Celsius (75.2 degrees
Fahrenheit): these patients are high risk for experiencing
cardiac arrest.
You come across a pulseless, hypothermic patient.
q
Should you start CPR immediately? Yes. This was controversial in the past due to a concern that the patient might
have a pulse that is not easily palpated and CPR might result
in asystole. However, the perfusion from CPR is better than
whatever limited perfusion they might still have.
q
Should you warm them, cool them or do nothing
during transport? The literature doesn’t give good
answers. The position taken in the paper is that you
should attempt minimally invasive rewarming. Insulate
them. Use warm water bottles or a Bair Hugger if you
have it. This won’t rewarm them, but it will prevent
further heat loss.
q
q
2
Most avalanche victims who die, do so as a result
of one of three things: severe trauma, the airway is
filled with snow and they have a hypoxic arrest, or they
have an air pocket and are able to breathe before cooling
down and arresting. If the patient has not been buried
long enough to get cold, you know hypothermia is not the
cause of the cardiac arrest. The magic number is 35
minutes. Patients buried in an avalanche cool at a rate
of 10 degrees Celsius per hour. If they are buried greater
than 35 minutes, their airway is not packed with snow,
and you don’t think that they died from massive trauma
immediately: this is the patient to consider for prolonged
CPR and transfer to a quaternary care center.
Monthly Audio Program
If you need to manage the airway, do it. If you need to give
fluids, give warm saline at 38 degrees Celsius (100.4 degrees
Fahrenheit).
In the emergency department, focus on high quality
CPR. Advocate for transfer to an ECMO/CPB center. If you
are within 6 hours of transfer to an ECMO center and have a
patient with a good history, the patient should be transferred,
even if you are able to achieve ROSC in your department.
There is a good chance the patient will progress to florid
pulmonary edema and require those services anyway.
q
A trial of epinephrine and electricity is reasonable.
But if it isn’t working, don’t persist. Give 1-2 doses, wait
until the patient is warmed 5-10 degrees Celsius and then
try again.
q
What about chest tube or peritoneal lavage? There is
no role for it unless you are not able to transfer the patient
to an ECMO/CPB center within 6 hours.
q
Is there any evidence to support thoracotomy with
rewarming of the heart? There is no literature on this.
There is literature supporting chest tube lavage with a
method of either one or two chest tubes. However, this is
a distant second best; the literature is not as robust as that
supporting transfer to an ECMO/CPB center.
q
Hypothermic patients who experience cardiac arrest
have a survival rate of 50% when treated in an ECMO
center but only 10% in a non-ECMO center. If you
have a patient with cardiac instability due to hypothermia,
you should package them up and transfer to an ECMO center; they will do much better.
Paper Chase 1:
A New Chest Pain Decision Rule
Sanjay Arora MD and Michael Menchine MD
u
Hess EP et al. The chest pain choice decision aid: a randomized trial. Circ Cardiovasc Qual Outcomes. 2012
May;5(3):251-9 PMID: 22496116.
u
Chest pain is a huge problem. We admit patients to obs
units and keep them there for 12-24 hours for serial troponins,
stress testing or CT angiogram. The yield is low, often in the
single percentage rates. It is expensive in terms of time lost,
actual cost and likelihood of indeterminate results leading to
additional testing.
u
Hess et al looked at whether providing patients with
information about their level of risk changes the
disposition. This assumes that we don’t really want to
admit these patients for work-up but do so out of a fear
of a rare bad outcome. It also assumes that if the patients
knew how low their risk was, they would not want admission
either.
q They
randomized 208 low-risk chest pain patients
and showed them an interactive card that provides
an assessment of risk. They asked the patients what
disposition they preferred: admission for urgent stress
test, follow-up in 2-3 days for stress testing, follow-up
with PCP or the decision be made by the ED physician.
q
The control group was asked the same series of
questions but did not receive a risk assessment.
77% opted for admission to the hospital. In the
group receiving the intervention, only 58% opted
for admission. This is a decrease of approximately 20%.
EM:RAP Written Summary | www.emrap.org
q
u
There were no negative outcomes.
What this study tells us.
q
Over half of patients still want to be admitted even knowing
they are low risk.
q
There is a substantial subset of patients who are willing
to forgo inpatient risk stratification and follow-up as an
outpatient. Patients were more satisfied with the intervention.
q
Shared decision making can reduce resource utilization.
u
u
The card given to the patients presented their risk in
several different ways. “Of every 100 people with factors
like yours who came to the emergency department with chest
pain, 2 had a heart attack or a pre-heart attack diagnosis within
45 days of the emergency department visit, 98 did not”. It also
showed a diagram representation of 100 figures, 98 are colored
blue and the 2 patients with a heart attack are identified by red.
If the patient is above 32 degrees Celsius (89.6 degrees
Fahrenheit), still in asystole and your clinical measures
are not working, hypothermia is no longer the cause.
u
Can you place a central line in these patients? What if
you tickle the heart with it? Do the things you need to do to
provide the necessary care for the patient. However, if you are
going to do a central line, try to place it shallowly.
u
The hypothermic, unconscious patient who has vital
signs can be divided into those with cardiac stability
and those with cardiac instability.
q
Any patient with cardiac instability should be
transported to an ECMO/CPB center. This is defined
as a systolic blood pressure less than 90, ventricular
arrhythmias or a core temperature less than 28 degrees
Celsius (82.4 degrees Fahrenheit). There is some literature
(mainly case series) indicating that hypothermic patients
with cardiac arrest may have improved survival when treated
at an ECMO center but it is much less clear for patients who
have a pulse but cardiac instability. However, these patients
are at high risk for arrest, and once they do, they are better
off at an ECMO center. For this reason, transport of patients
with cardiac instability to an ECMO/CPB center is recommended.
q
For all of your unconscious hypothermic patients,
you want to handle them carefully. Do minimally invasive rewarming. Expect that they may arrest.
q
Will rewarming patients cause cardiac arrest? There
is a concern that rewarming the patients may cause cold
blood to re-enter the circulation and lead to cardiac arrest
and death. This is controversial. Review of case reports in
the literature divides this into rescue collapse versus after-drop.
Rescue collapse is a real phenomenon. Once patients are
cold - under 32 degrees Celsius (89.6 degrees Fahrenheit) and
especially under 28 degrees (82.4 degrees Fahrenheit) - they
are at high risk for a malignant arrhythmia. They could go into
a cardiac arrest at any point during your resuscitation. It is not
caused by anything that you have done. It is the natural history
of accidental hypothermia. There are excellent physiology
studies that demonstrate after-drop; it is a real thing
but it is not clinically significant. If you take healthy
patients, cool them in ice water and then rewarm them,
the core temperature will drop between ¼ and ¾ of a
degree Celsius. This is not a clinically significant entity.
You should not worry about rewarming your patients.
We are still early in understanding how best to communicate
this to patients. This article is a great first step. It won’t change
practice (only 17% of chest pain patients were eligible for it),
but it does show that if you can communicate this to patients,
they can understand some of it and make decisions.
Accidental Hypothermia Part 2
Mel Herbert MD interviews Doug Brown MD
u
You have a hypothermic patient in a bad, death-defining
rhythm. Is there a temperature you need to warm them
to before you can consider giving medications? Can you
give ACLS drugs?
qThe
European Resuscitation Council recommends a
modified approach to support consisting of up to 3
defibrillations and withholding of epinephrine until
the core temperature is higher than 30 degrees Celsius
(86 degrees Fahrenheit). If you use epinephrine, the time
between doses should be doubled until the temperature
reaches 35 degrees Celsius (95 degrees Fahrenheit).
q
This is in opposition to the American Heart Association
recommendations, which say it might be reasonable to
consider the administration of vasopressors in cardiac
arrest.
q
Why are these recommendations different? They are based
on two different studies, one which shows epinephrine
works early on and one which shows it doesn’t work.
q
A practical approach. When beginning your ACLS
algorithm, give them one dose of epinephrine and one
trial of electricity (if you see a shockable rhythm). If
it doesn’t work, don’t persist with repeated doses but
wait until they warm up 5 to 10 degrees Celsius and
then try one more dose. Then wait until they are above
32 degrees Celsius (89.6 degrees Fahrenheit).
u
If you have a patient in hypothermic cardiac arrest with no
chance of transfer or ECMO, what should you do? Perform
high quality CPR. Prevent further heat loss by insulating the patient.
Place a Bair Hugger and warm up the room. Do a trial of
epinephrine and electricity (if indicated). Then insert bladder
lavage. If you have the capability to insert peritoneal lavage and
thoracic lavage, do those as well. Note: this is only for the
January 2014: Volume 14, Issue 1 | www.emrap.org
3
patient that you can’t get to ECMO. Rewarm the patient with
continued focus on high quality CPR. Watch their core
temperature; with every 5 degrees Celsius of increase, recheck
for a shockable rhythm and consider another dose of epinephrine.
q
u
You have a hypothermic patient who is still alive.
What are the triggers for aggressive rewarming? For
unconscious patients with hypothermia, there is no indication
for invasive rewarming. Place the patient in a Bair Hugger.
Handle them carefully to try to avoid triggering a malignant
arrhythmia. Bladder lavage has essentially no morbidity and
is reasonable. If you need to give them fluids, give them
warm saline at 38 degrees Celsius (100.4 degrees Fahrenheit).
Use normal supportive care.
q
u
If the patient has cardiac instability (ventricular arrhythmia, significant hypotension), there is evidence
that the patient may benefit from invasive rewarming.
Ideally this would occur in an ECMO/CPB center. There is
no evidence saying whether or not to perform chest tube or
peritoneal lavage.
The patient has a pulse but is very hypotensive. Should
you use vasopressors? Hypothermia causes some of the most
profound vasoconstriction and myocardial irritability of any
medical condition. Early in your resuscitation, there is no role for
vasopressors, as patients are as tight as they can get. You will just
increase their myocardial irritability. However, after you rewarm
the patient and the patient continues to experience hypotension
with an element of vasodilation, the risk/benefit may change and
you may consider using vasopressors. Remember that hypothermic
patients are very irritable and vasopressors have the potential
to increase irritability, causing a perfusing rhythm to progress
to cardiac arrest. You need to be especially careful if the patient
has frostbite. Vasopressors may worsen frostbite.
u
Shivering is the best way for patients to rewarm
themselves. Current research is examining strategies for
pain medication in trauma patients that does not inhibit the
shivering mechanism.
u
Hypothermic patients will become very volume depleted
due to vasoconstriction and cold diuresis. They will require
significant volume during rewarming to replace volume loss and
keep up with vasodilation. Expect 2-5 liters. Use of pressors during
rewarming should have the caveat that you have filled the tank or
need a temporizing measure while you catch up with the fluids.
u
4
Eventually you will reach 32 degrees Celsius (89.6 degrees
Fahrenheit). Once you are above 32 degrees Celsius
(89.6 degrees Fahrenheit) give it one more try. If
they are dead, then stop.
If the patient is rewarmed, rehydrated and in sinus
rhythm, but still requiring pressors, this is a red flag
that something else is going on such as sepsis or tox.
u
For more information on this, go to: drdougbrown.ca.
The review paper is available online and has an algorithm
detailing management of hypothermia.
u
The International Hypothermia Registry: https://www.
hypothermia-registry.org
The NNT: Aspirin for STEMI and IV PPIs
for Upper GI Bleed
David Newman MD
u
What is the number of patients needed to treat with
aspirin to save a life in patients with STEMI? There is
one major randomized controlled trial.
u
Randomised trial of intravenous streptokinase, oral
aspirin, both or neither among 17,187 cases of suspected
acute myocardial infarction: ISIS-2. Lancet, 1988 Aug
13;2(8607):349-60 PMID: 2899772.
q
This study was published in 1998. 17,187 patients with MI
were randomized to receive either streptokinase, aspirin,
streptokinase and aspirin, or two placebos.
q
This was a high quality study. It found that the aspirin groups,
compared to the placebo groups, had mortality of 9.4%
compared to 11.8%. This is a 2.4% difference. What is the
number need to treat? 42. We need to treat 42 patients
with MI with aspirin for one person to survive because of the
aspirin. 97.6% of patients were either going to die or live
and aspirin wasn’t the swing vote; however, for 2.4%,
the aspirin made the difference. This is a clinically
significant benefit. If you take a million MIs over several
years in the United States, 24,000 or 2.4% of them survive
because of the aspirin. This is major.
q
This is worth doing especially if you compare it to
the number needed to harm (167 patients). For every
167 patients you treat with aspirin, you will cause one minor
bleeding event. Aspirin did not increase intracranial hemorrhages or transfusion-requiring hemorrhages.
u
What is the evidence supporting proton pump
inhibitors (PPIs) for GI bleeds? Consultants seem to
love PPIs for GI bleeds; “Can you just give them a bolus before
they go upstairs?” Why do they love it? It is supposed to increase
the pH and make it more likely you can control the bleeding
and less likely they will experience rebleeds and death.
u
There are two Cochrane reviews. One is relevant to emergency
medicine and the other isn’t.
u
Dorward S et al. Proton pump inhibitor treatment
initiated prior to endoscopic diagnosis in upper gastrointestinal bleeding. Cochrane Database Syst Rev. 2006
Oct 18;(4):CD005415 PMID: 17054257. This is relevant to
emergency medicine as it looks at PPIs initiated before the
patient is taken to endoscopy. There are 4 randomized trials
including 1500 patients. The three effects evaluated were
mortality, rebleeding and going to the operating room (OR).
For those three effects, there was no benefit with PPI treatment prior to endoscopy. No patients benefited from PPI
therapy.
q
q
Patients with GI bleeds can be sick patients; they
often have multiple lines and are receiving transfusions, fluids, platelets, antibiotics, sedatives for
intubation. If you use a line for a drug that isn’t proven to
help a patient, you are likely doing more harm than good.
only is there no benefit to giving PPIs if you are in
Western industrialized country but there may be
some harm. However, this will take some time to become
well known by our consultants.
u
Check out the NNT website at www.thennt.com for links to
the reviews and additional info.
u
There are guidelines that support this: National Institute of Health
and Clinical Excellence in the United Kingdom 2012 guidelines
for upper GI bleed say do not give PPIs before endoscopy in the
acute non-variceal upper GI bleed. They do recommend PPIs if
an ulcer is seen.
u
If you are considering stopping the use of PPIs for upper GI
bleeds in the emergency department, read the Cochrane review
first. The findings were not all negative; the authors did find some
benefit with the use of PPIs such as a significant reduction in the
need for intervention with endoscopic hemostatic therapy at the
time of initial endoscopy. This may reduce costs.
There was no obvious harm to the PPIs.
second study wasn’t directly relevant to the emergency
department but still interesting. Leontiadis GI et al. Proton
pump inhibitor treatment for acute peptic ulcer bleeding.
Cochrane Database Syst Rev. 2006 Jan 25;(1):CD002094
PMID: 15266462.
uThe
q
q
q
If you wait to give PPIs until the patient goes to
the endoscopy suite and has confirmed peptic ulcer
disease, is there a benefit? The review included 24
randomized controlled trials with over 4000 patients.
They didn’t find a decrease in mortality or decrease need
for transfusion. They did find that it seemed to decrease
rebleeding by about 6.6% and need for the OR by about
3%. About 1 in every 15 patients avoided a rebleed
and 1 in every 30 people avoided going to the OR
because they had gotten PPIs compared to a placebo
or no treatment. This was in patients who had gone to the
endoscopy suite and had confirmed peptic ulcer disease.
The data suggests a benefit for patients with peptic
ulcer disease. If there is no harm for patients without
peptic ulcer disease, should we give PPIs (because
approximately 40-50% of patients with GI bleed will
have peptic ulcer disease)? If you look at the Cochrane
review, they did a number of different analyses of the data and
one was geographical.
Why did they do a geographical analysis? A number of
studies were done in Japan/China and others were done in
Western countries. These had very different results. When
averaged together, it seemed to show benefit for reducing
rebleeding and going to the OR. If you were in China and
suffering from a peptic ulcer bleed, there was a benefit in
mortality as well as a substantial benefit in rebleeding and
avoiding the OR. What happened in the other group?
Was there harm from PPIs? If you were in a study from
a Western country and received a PPI for acute peptic ulcer bleeding, you were more likely to die. There was not a
single benefit for any outcome.
q
Why is there a geographical difference? Nobody
knows.
q
This tells us in the Emergency Department that not
Paper Chase 2:
Head Trauma in the Anticoagulated Patient
u
The patient with blunt head injury and on warfarin who
now feels great is a very troubling clinical scenario.
Should you scan them? Should you get two CT scans? Admit
them for observation? Keep them in the ED for observation? We
know that there is the possibility of delayed bleed.
u
Menditto VG et al. Management of minor head injury in patients
receiving oral anticoagulant therapy: a prospective study
of a 24-hour observation protocol. Ann Emerg Med. 2012
Jun;59(6):451-5 PMID: 22244878.
q
This study only included patients on warfarin and did not
study other anticoagulation agents.
q
In 2002, a neurosurgical guideline recommended that patients
on warfarin with a head bonk should be observed for 24 hours.
This study looked at this protocol.
q
This is not a randomized controlled trial. It is a prospective
case series.
q
They included 97 patients with minor head injury
who had been on warfarin for at least a week. They
excluded patients with a positive initial head CT. 16% of
patients had a positive head CT. They included patients with
a GCS of 14 or 15.
q The
patients received a CT scan initially and then were
placed in an observation unit where their neurologic status
was monitored. The head CT was repeated in 24 hours. 10
patients refused repeat CT head.
q
They found 5 (or 6%) of these 87 patients, who had
5
an initially negative head CT and a GCS of 14 or 15,
had findings on repeat head CT. Only 1 of these had
any neurologic changes. What happened to these five
patients? 2 were discharged after additional observation.
3 were admitted and 1 had a craniotomy. Of the patients
who went home after two negative head CTs and a
period of observation, two patients later returned
with symptomatic subdural hematomas. One returned
2 days later and one returned 8 days later.
q
u
Nishijima DK et al. Immediate and delayed traumatic
intracranial hemorrhage in patients with head trauma
and preinjury warfarin or clopidogrel use. Ann Emerg
Med. 2012 Jun;59(6):460-8 PMID: 22626015.
q
This was a prospective observational study conducted in 6
different hospitals. They looked at clopidogrel as well as
warfarin.
q
The study included adult patients on warfarin or clopidogrel.
The patients had to be taking these medications within the
last 7 days. They looked at the incidence of acute and
delayed bleeds. The patients were followed out to two
weeks via either medical records, phone interviews or if they
were unable to contact the patient, they looked at the Social
Security Death Index.
q
1,064 patients were included in this study. About
70% were on warfarin and 30% were on clopidogrel.
About 10% of the patients did not get an initial CT
scan. This suggests that they included patients who were so
low risk that they didn’t even scan some of them.
q
What was the prevalence of a bleed on the initial
study? About 12% in the clopidogrel group and only 5%
in the warfarin group. These numbers are much lower than
traditional estimates.
q
They found the incidence of delayed bleed was 0%
in the clopidogrel group and 0.6% in the warfarin
group. Of the patients with delayed bleeds on warfarin, all
had a GCS of 15 and 50% died.
u
6
What can we conclude from this study? Delayed bleed
is a real entity. What is the frequency and what do we do with
these patients? They found a delayed bleed frequency of 6%
and another 2% returned with bleeds even after the 24 hour
observation period and two negative head CTs. Observing
people who are feeling fine for 24 hours and then repeating
a head CT is impractical for most of us. Patients with an
INR greater than 3 and those who were elderly were
at higher risk of delayed bleed.
Take home points. Immediate intracranial hemorrhage in
anticoagulated patients is real and happens 10-15% of the time.
Any patient who is coming in with head trauma and is taking
warfarin or clopidogrel should get an initial CT scan. Treat a
patient on clopidogrel just as you would a patient on warfarin.
The highest risk patients are those with high INRs and the elderly.
q
Do we observe the patient or repeat the CT scan? It is
still up in the air. Observation, a repeat CT head or sending
them home with good return precautions are all reasonable
options. What you do will depend on what the patient in front
of you looks like and what their support system is. At the very
minimum, the patient should be going home with someone
reliable who can watch them and bring them back for a
delayed scan. However, an observation period of 24 hours
for every patient with a GCS of 15 in our overcrowded
system is an impractical solution. You are going to have to
read the literature and come up with your own conclusion
of what to do. If the patient has risk factors such as a high
INR or elderly, it may be worth admitting them for observation
and a repeat CT.
q
Regardless of what strategy you use, remember that
there is still the possibility of a delayed bleed several
days later. You have to tell the family to watch for subtle
changes.
The Lin Sessions: PO vs IV Clindamycin,
the Dirty Epi Drip and Propofol for Migraines
Michelle Lin MD and Zlatan Coralic PharmD
Thoughts on vancomycin in the ED.
u
There has been a trend where healthy patients with
cellulitis are given 1 gram of vancomycin in the ED
and then are sent home on oral antibiotics. Is this
actually efficacious? There is no literature showing benefit
to giving one dose of vancomycin and then switching to oral
antibiotics. The IDSA guidelines do not recommend this
approach.
q
u
What are some downsides to this approach? You are
committing the patient to staying in the ED for another 1-1.5
hours or longer if there is an adverse reaction. It increases
the cost of the patient’s stay. It does not make sense from a
pharmacokinetic standpoint. Recent evidence shows that
ability of vancomycin to kill MRSA depends on the
concentration of the drug in the blood compared to
the minimum inhibitory concentration (MIC) of the
bacteria; the magic ratio is 400. It is almost impossible
to achieve this level with just one dose of vancomycin.
The average patient would need to receive one gram of
vancomycin every 8 to 12 hours to achieve these levels.
You will be increasing the potential for antibiotic resistance
by using just one dose.
There is the tendency to give a loading dose of
something via IV in the emergency department and
then send the patient home on oral antibiotics. If
you look at the antibiotics used to treat skin and soft tissue
infections, they are almost 100% absorbed from the GI tract.
Clindamycin is about 90%. Sulfamethoxazole-trimethoprim
(Bactrim) is 100% absorbed. Doxycycline is 100% absorbed.
Linezolid (which is not used as a first line agent) is also 100%
absorbed. There is no need to load someone on IV antibiotics;
this has never been proven to be efficacious. Giving them
an oral dose and discharging them home is likely the best practice.
u
There are a variety of presentations of soft tissue
infections in patients. There is no benefit to IV antibiotics
in the patient who is healthy and you know as soon as you see
them that they will be going home with oral antibiotics. If you
know you are going to admit the patient (they are septic, toxic
appearing, meet SIRS criteria, etc.), these patients need IV
antibiotics.
q
Deciding whether or not to give IV antibiotics to
patients in the gray zone is more challenging. For
example, the patient who is kind of sick looking
but you may be able to turn them around and send
them home with supportive care. What should you
do for these patients? Start the IV. Give them fluids and
supportive care. Give them the first dose of oral antibiotics.
If they improve within an hour, you can send them home on
PO antibiotics. If they aren’t improving, you can start them
on IV antibiotics and admit them.
q
What about patients who are admitted to the observation
units? Should these patients receive IV antibiotics or PO
antibiotics? Your intent is to admit these patients initially so
it is not unreasonable to start IV antibiotics in these patients
and then discharge them home if they are improving in 24
hours.
u
The “dirty epi drip” is a quick and dirty way to make an
epinephrine drip bedside for anaphylactic shock.
u
How do you do this? Take your epinephrine that you have
available. It does not matter if it is 1:1,000 or 1:10,000 as
long as it is 1mg and inject it into a liter bag of saline. This
can be the code cart epinephrine which is 1mg in 10cc or
the IM epinephrine which is 1mg in 1cc. This gives you a
concentration of epinephrine in the bag of 1mcg/mL. Hook this
up to the patient and run it wide open until the hemodynamics
stabilize. Others advocate starting at the 1mcg/min dose and
titrating up. This is not perfect, but it will buy you some
time until your team is able to set up the pump and follow
hospital protocols. This drug has been tested at such a dilute
concentration and found to be stable up to 24 hours.
u
The maximal rate of infusion will vary with a few things:
how high the IV bag is, the length of the tubing, and the size
of the catheter. With an open wide 18 gauge, the patient will
receive between 20 and 50 mcg/min (or between 20 and 50
mL/min). This is not something you walk away from; you need
to stay bedside with the patient with your hand on the roller
clamp. If your patient starts responding, you can decrease the
dirty epi drip by clamping down the line. If they aren’t doing
well you can squeeze the bag and give them more.
Case #2
Case #2. You are working at 3am in a low resource area.
You receive a patient who is an obese female of 47 years.
She presents to your triage area with shortness of breath
and difficulty speaking. She has an allergy to peanuts and
ate a candy bar prior to arrival. She has a history of hypertension and intubation for a prior episode. She becomes
more obtunded with a heart rate of 130, blood pressure
of 65/nothing and an oxygen saturation of 89% on O2.
Anaphylactic shock is on the top of your differential. The
nurse confirms administration of two separate shots of intramuscular epinephrine. The patient responds slightly but
remains hypotensive and wheezy.
u
u
Should you continue to give IM epinephrine or switch to
an IV drip? If you are giving the second IM dose of epinephrine,
you should also be ordering an IV epinephrine drip. The guidelines
say that IM epinephrine should be given to stable patients
exhibiting signs of anaphylaxis. The guidelines recommend
IV epinephrine in patients where the anaphylaxis appears to
be severe with immediate life-threatening manifestations.
What is the starting dose? Between 1 and 4 mcg/min. You
can start at 1mcg/min and titrate up.
Should you give the patient push dose epinephrine? The
guidelines suggest an IV push dose of 0.1mg of 1:10,000 over
5 minutes. This is a high risk drug and errors occur frequently.
There are multiple case reports of errors in IV administration
leading to death. There are no standardized guidelines for how
to mix this drug or which units to use. Once you dilute the
epinephrine, the drug is not stable for very long. It is unlikely
that most EDs will have premixed epinephrine drips ready to
use.
Propofol for migraines.
u
This is very controversial. This practice started in 2000 with an
open label trial where propofol was given to patient with migraines
at a migraine clinic. They found that propofol, when given to
patients at procedural sedation doses, terminates migraines for
most of the patients.
u
Krusz JC et al. Intravenous propofol: unique effectiveness
in treating intractable migraine. Headache. 2000
Mar;40(3):224-30 PMID: 10759925.
q This
trial included 77 patients with a pain score greater
than 7 out of 10 using a visual analog score. This was an
open label trial. They gave them 20-30mg IV push doses
every 5 minutes for up to an hour. The average reduction
in severity was 95.4% at 30 minutes which is the most
efficacious treatment so far for intractable migraines. 3
of the 77 patients returned with subsequent headache
but most had a sustained response. The average dose
of propofol was 110mg similar to procedure sedation.
They did not report any adverse events.
7
u
In 1995, the NINDS trial came out and was important in getting
tPA approved for stroke. It was only approved in patients with
symptoms with onset of less than 3 hours prior. Most of the
benefit seemed to occur in patients who had their stroke within
90 minutes prior to receiving drug. However, most patients do
not present within this window.
u
In 2003, the ECASS 3 trial showed that tPA was effective up to
4.5 hours after presentation. This is now a fairly widely adopted
recommendation.
u
This was a huge study. It included 3,035 patients in 156
hospitals in 12 countries. This study included people who
were able to get tPA versus nothing up to 6 hours after
symptom onset. How did this work? If the patient showed up
within 3 hours and was a slam dunk for tPA, they gave tPA
and didn’t enroll the patient in the trial. If the patient wasn’t
a great candidate but not a terrible candidate and the doctor
thought the patient might benefit from tPA (for example, the
85 year old presenting within 2 hours after symptom onset
or the healthy 47 year old presenting within 5 hours after
symptom onset), they were enrolled. This is exactly the
type of patient that presents a clinical conundrum in
the ED.
u
What did this mean for patient selection in the trial?
They were old. 50% were older than 80 years old. They tended
to have bigger strokes or were outside of the 3 hours window.
u
This was open label; patients were given tPA or nothing.
There was no placebo. Patients and their families were aware
that they were given tPA.
u
The primary outcome was alive and well at 6 months. This
was assessed using the Oxford Handicap Score which basically
asked if they had significant disability (bad outcome) or if they
were ok and able to attend to their basic activities of daily living
(good outcome).
u
The Paper Chase 3:
TPA up to 6 hours? Not!
What did they find? At 6 months, 37% of the patients in the
tPA branch had a good outcome versus 35% of patients in
the control group. This was insignificant both statistically and
clinically. There were bad outcomes overall; approximately
2/3 did poorly.
u
What did they conclude? “Despite the early hazards,
thrombolysis within 6 h improved functional outcome.”
u
IST-3 collaborative group et al. The benefits and harms of intravenous thrombolysis with recombinant tissue plasminogen activator within 6 h of acute ischaemic stroke (the
third international stroke trial [IST-3]): a randomised
controlled trial. Lancet. 2012 Jun 23;379(9834):2352-63
PMID: 22632908.
u
They stated their primary outcome and the primary
outcome was clearly negative. Then they did some fancy
math… They did ordinal rank logistical regression to say
that some more people moved from severely handicapped to
less handicapped due to tPA use. This is difficult to understand
and determine a number needed to treat.
u
This is an important article to understand. The conclusions
were misleading and if you rely on the abstract, you may be led
astray.
u
There was early harm with tPA. 11% in the tPA group died
compared with only 7% in the control group. Intracranial
hemorrhage within 7 days occurred in 7% of the tPA group
and 1% of the control group. More patients died initially in
u
Soleimanpour H et al. Effectiveness of intravenous dexamethasone versus propofol for pain relief in the migraine
headache: a prospective double blind randomized clinical
trial. BMC Neurol. 2012 Sep 29;12:114 PMID: 23020264.
q They
included 90 patients who presented to the ED with
migraines. The patients were divided into two groups: the
first group received propofol every 5 to 10 minutes with
a maximum of 80mg and the control group received
dexamethasone at 0.15 mg/kg. They found similar results
to the previous study.
q
u
Most patients had resolution of their migraine symptoms.
2 patients desaturated down to 89% but this resolved after
administration of oxygen.
Sheridan DC et al. Low-dose propofol for the abortive
treatment of pediatric migraine in the emergency department. Pediatr Emerg Care. 2012 Dec;28(12):1293-6 PMID:
23187986.
q This
was a case control trial with 7 pediatric patients
with migraines who received low doses of propofol and
compared these to patients who received the usual abortive
therapy which was prochlorperazine (Compazine), nonsteroidal anti-inflammatory (Toradol), and diphenhydramine
(Benadryl). Propofol was significantly better at decreasing
the pain: from 61% to 80%. They had no adverse events.
u
This is a pretty amazing thing to have in the ED. The
standard treatments such as triptans, prochlorperazine or
opiates have side effects. Now we have an intervention that can
completely obliterate a migraine in 20-30 minutes. However,
how many resources does using propofol require? Do
you have to do this as procedural sedation with end-tidal CO2
monitoring? This is difficult to do in a single coverage ED.
Will this make patients present repeatedly for treatment with
propofol? We need more research before this is ready
for primetime but it is something to consider in the
patient with refractory migraine.
8
founded fear as we have always been told that hypothermia
equals bleeding. Subarachnoid hemorrhage is not an uncommon
cause of cardiac arrest. The literature suggests that not only have
you not made things worse, you have probably made things better.
the tPA group but by six months it seemed to have evened out
and was equivalent to the control group.
u
There is no evidence that tPA is better than placebo out
to 6 hours. Although they claim improved functional benefit,
the data does not support it.
u
If you have a neurologist available, does this mean you
now have to call them for patients presenting within a 6
hour window? No. The neurologists seem to like to push this
drug. However, the data continue to show that that the benefit
is at best modest and when used outside of the window, you kill
people and you kill them early. The best data available for tPA
outside of 4.5 hours says that there is no difference in functional
outcome at 6 months.
u
However, we do things a little differently if we discover
a subarachnoid hemorrhage. You probably have a goal of
32-34 degrees Celsius (89.6 to 93.2 degrees Fahrenheit) in the
average post arrest patient. If the neurosurgeon wants to keep
the patient at that temperature, that’s fine. Most would let the
patient’s temperature drift up to 35 degrees Celsius (95 degrees
Fahrenheit). You do not want to rewarm these patients quickly;
aim for an increase of ¼ degree per hour: an increase from 33 to
35 degrees Celsius (91.4 to 95 degees Fahrenheit) over 8 hours.
At 35 degrees Celsius (95 degrees Fahrenheit), they probably
won’t experience an effect on their clotting factors but they will
get the benefits from mild hypothermia, such as decreased cerebral
metabolism and increased intracranial pressure.
u
Is the evidence strong for this? There is evidence that
induced hypothermia; between 32-35 degrees Celsius (89.6
- 95 degrees Fahrenheit) is good treatment for intractable
increased ICP. There is no data showing patient outcome
effects from the hypothermia but there is evidence showing
that it isn’t harmful. It is similar to giving mannitol or hypertonic;
the numbers improve but there is no evidence saying that it will
benefit mortality or neurologic outcome.
Critical Care Mailbag
Scott Weingart MD and Rob Orman MD
Who to get warm, who to get cold and who is still a mystery?
Hypothermia in Trauma
u
We cool down most of our post arrest patients to save the
brain. The hypothermic trauma patient often is intubated with
head injuries and some sort of thoracoabdominal trauma.
Is there any evidence to say that mild hypothermia in
these patients is a good or a bad thing?
u
#1. Bleeding. Once you start getting below 35 degrees Celsius
(95 degrees Fahrenheit), you begin to experience some mild
platelet effects. Between 32 and 35 degrees Celsius (89.6 and 95
degrees Fahrenheit), there is an anticoagulant effect and clotting
factors stop working as well. Things become horrible for trauma
patients at 32 degrees Celsius (89.6 degrees Fahrenheit). Your
goal should be a temperature above 35 degrees Celsius
(95 degrees Fahrenheit) the entire time. You should be
very afraid if the patient is at 32 degrees Celsius (89.6
degrees Fahrenheit).
u
#2. Is it good for the brain? Maybe. We don’t know if it
is good for the body yet. This is still up for debate in the post
arrest hypothermia patients. You should not be cooling down
your multi-trauma patients because they will bleed. If they are
cold, warm them up.
How to induce hypothermia in a remote setting
u
Strategies for cooling patients in EDs with limited
resources. Take 8 bags of normal saline and stick them in
one of your medication fridges (about 40F or 4C). Talk to
the nurse manager about checking the expiration dates every
so often. Now you have the means to cool a patient ready to
go. When a post arrest patient comes in, give them 2 liters
of the cold saline. Place ice packs (you can fill lab bags with
ice from the ice machine) in their groin and axilla. Is this
perfect? No, but it will do the job until you are able to transfer
them.
u
Continue the resuscitation as far as you can go. If you
can put an arterial line in, great. If not, don’t worry. Try to keep
their MAP above 65 and aim for 80. It is ok if you use a pressor
to get there. Keep their oxygen status in the middle ground;
hypoxia is bad and so is hyperoxia. Check their labs. Try to
figure out the cause of cardiac arrest. If it is something you can
intervene on, do it. If not, you will be transferring the patient
regardless.
u
Small hospitals should be cooling these patients but
not keeping them. If these things seem daunting in your ED,
your ICU probably will be unable to provide the same level of
care. Cooling is a small component of post cardiac arrest care.
It is important and necessary but the patients should be transferred to a cardiac arrest center.
Hypothermia in isolated head injury
u
The patient has isolated traumatic brain injury. Are these
patients better off at 35 degrees Celsius (95 degrees
Fahrenheit)? We don’t know for sure, but their intracranial
pressures (ICPs) might be less.
Hypothermia in subarachnoid hemorrhage
u
You cool down a post cardiac arrest patient and then
discover that they have a nontraumatic subarachnoid
hemorrhage. Have you done the patient a disservice?
No. Cooling the patient is the right thing to do. This is a well-
9
u
u
You are unable to transfer the patient for 4 to 5 hours.
You should have some means for core temperature monitoring.
The best way to do this is an esophageal/rectal probe. If you can
place an NG tube, you can place an esophageal probe. Try to
position it several inches above the xiphoid process. This hooks
into regular monitors using a cartridge (both the cartridge and
the probes are cheap so it is worthwhile to have them on hand).
If you don’t have this in the ED, your anesthesiologist should have
it. If you have nothing, do a rectal probe intermittently to check
the temperature.
Can you overshoot? If you are going too low, take off the ice
packs. Chances are it will be more difficult to achieve the desired
temperature than it will be to overshoot. You don’t want them too
far below 32 degrees Celsius (89.6 degrees Fahrenheit).
u
Shivering is your enemy. Make sure they are adequately
sedated. If they are still shivering, just paralyze them.
u
Why is there an emphasis on placing arterial lines? It
is not because it provides much additional benefit in terms of
the resuscitation but because it is a marker of the ability to do
post-arrest care at an ideal level.
Bag valve mask versus using the ventilator in cardiac arrest
u
For an intubated patient who arrests, should you
disconnect the ventilator and bag manually when doing
chest compressions? The safest way is to let respiratory therapy
or a colleague bag the patient if they are calm and know what
they are doing but there is the risk that the person may bag
the patient rapidly (for example, 60 beats per minute). This is
really bad for the patient’s outcome. However, the ventilator is
not a panacea either. Most ventilators have a set upper pressure
limit (usually between 40 and 60) so normal patients won’t get
an injurious level of ventilation. The chest compressions will be
read by the ventilator as increased pressure in the chest and the
ventilator will not deliver a breath. The ventilator doesn’t know if
the increased pressure is in the alveoli or external to them. If the
patient is receiving chest compressions at 100 beats per minute,
there is no time for the ventilator to deliver a breath between
those chest compressions. The ideal breath happens at the
downstroke of the chest compression.
you want to use the ventilator, if you understand
the settings, and if you are able to increase the
peak pressure limit to about 100, the ventilator
will now deliver breaths regardless of whether
or not the patient is getting a chest compression.
Nothing bad will happen to the alveoli as they are not actually experiencing that pressure. However, if you don’t
know how to adjust the settings, the ventilator can be
incredibly dangerous for these patients because they
won’t get any ventilation.
to the tube. Rate of 12 breaths a minute with a FiO2 of 100%.
PEEP of zero. If you know what it means, put them on a flow
rate of 30L/minute. This will deliver the 500cc over 1 second.
Increase the peak pressure to 100.
Ideal tidal volume for patients intubated in the Emergency
Department
u
q
The days of using 12-15 cc/kg are over. This is a bad idea.
You should be starting at 8ml/kg of predicted body
weight. If they have any signs that this is too much,
go down to 6ml/kg. What is predicted body weight? If you
have a patient that weighs 600lbs and is 5 foot 1 inch, they
get the tidal volume you predict based on the lung size for
someone who is 5 foot 1 inch. There are charts online for
this: ardsnet.org/node/77460
q
This is one of the few trials that showed mortality benefit.
More recent data shows that even healthy patients will be
less likely to develop acute lung injury if low tidal volumes
are used. The data is not definitive but there is no
good reason to use volumes of greater than 8ml/kg,
even in your healthy patients.
Paper Chase 4:
DKA and Cerebral Edema
u
Cerebral edema in kids with DKA is real, but rare. The
youngest children are at highest risk. Clinically apparent cases
occur in 0.5-1%. However, there may be more cases that go
unrecognized.
u
For those with clinically apparent cerebral edema, the
outcomes are devastating; up to 50% of these patients
will die. Of those that survive, 1/3 will be in a vegetative
state. There has been an association between severity of DKA
and intensity of treatment with development of cerebral edema.
u
Are fluids the culprit? Nobody knows. Early trials showed a
relationship with IV fluids but there were no controls and multiple
confounders. These were very sick kids who were more likely to
get the most fluid. There have been more than 20 retrospective
studies on this but no prospective trials until now. Both animal and
human studies have shown cerebral edema on MRI prior to
treatment.
u
The largest retrospective trial was published in
2001. Glaser N et al. Risk factors for cerebral edema in
children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the
qIf
Ideal ventilator settings in cardiac arrest
u
10
Put the ventilator on assist control at 550cc tidal volume. This will deliver 500cc to the patient and 50cc is lost
Ventilation with lower tidal volumes as compared with
traditional tidal volumes for acute lung injury and the acute
respiratory distress syndrome. The Acute Respiratory Distress
Syndrome Network. N Engl J Med. 2000 May 4;342(18):1301-8
PMID: 10793162.
American Academy of Pediatrics. N Engl J Med. 2001 Jan
25;344(4):264-9 PMID: 11172153.
q
u
This is a huge study. They included 61 children with cerebral
edema with 6 controls per patient. They found no
relationship between the amount or rate of IV
fluids and the development of cerebral edema.
Despite this data, some important people (like the AAP)
say that if you are going to give children with DKA more
than 10-20 cc/kg of IV fluid, you need to involve a pediatric
endocrinologist.
u
What is the pathophysiology? No one knows. Some believe
that osmotic changes result in rapid influx of fluid into brain cells.
However, others believe that it is caused by cerebral hypoperfusion
so you should get the fluids in fast.
u
Glaser NS et al. Subclinical cerebral edema in children with
diabetic ketoacidosis randomized to 2 different rehydration
protocols. Pediatrics. 2013 Jan;131(1):e73-80 PMID: 23230065.
q
This was a prospective trial including children between
the ages of 8 and 18 with DKA. They did not include the
children with the highest risk of DKA (less than 5 years).
q
The patients were randomized to receive Protocol
A, a fluid bolus of 20cc/kg initially and then rapid
replacement of their estimated fluid deficit (2/3 over
the first 24 hours and 1/3 over the next 24 hours)
or Protocol B, a fluid bolus of 10cc/kg followed by
slow, even replacement of their fluid deficit over the
next two days.
q
Both groups were given insulin at a rate of 0.1units/kg/h
with no bolus. They all got frequent neuro checks and labs.
Each patient got 3 MRIs: one MRI at 3-6 hours after
initiating treatment, one MRI at 9-12 hours and one MRI
after treatment was completed at approximately 72 hours.
q
The trial included 18 patients and two patients experienced
DKA twice so there were 20 total episodes. 2 of the cases
had to be withdrawn after randomization; one was too
claustrophobic for repeat MRI and the other was too sick
to have been enrolled in the first place. All of the kids did
fine at the end with no neuro deficits and no clinical
cerebral edema.
q
Remember that the likelihood of clinically apparent cerebral
edema is only 0.5 to 1% of cases and this was a small number
of patients. However, they were looking for subclinical cerebral
edema.
q
Note: One kid in the rapid rehydration group (Protocol
A) had a fast deterioration in his mental status. He was
treated for cerebral edema with mannitol with no improvement but then spontaneously improved after a few hours.
They eventually determined that this wasn’t cerebral edema,
but it is something to keep in mind.
q They
looked at the ADC (apparent diffusion coefficient)
and found no difference between the two groups. The ADC
reflects the diffusion speed of water molecules and changes
are a harbinger of cerebral edema.
q
However, based on the graphs, there was no real
difference in time to resolution of DKA. The kids with
rapid fluid administration did not do better. This was not
discussed much in the article.
u
What does this article tell us? In a small sample of kids,
there was no difference in terms of cerebral edema. So if you
have patient who is sick, shocky, septic and obviously
dehydrated or hypotensive, give them fluids. You are not
a bad doctor if you do so. However, be careful in what you
consider sick, shocky and septic in kids who are under
5 years old because these are more likely to get cerebral
edema.
u
Document the patient’s neurologic exam and mental
status prior to initiating treatment. If they are already
obtunded or lethargic before getting treatment, this can save
you if the kid develops cerebral edema. There is literature to
say that cerebral edema is present prior to treatment.
u
This same group (PECARN) is currently conducting a huge
prospective randomized controlled trial: the FLUID trial (Fluid
therapies Under Investigation in DKA). This is a 13 center,
nationwide study that includes 4 groups with fast and slow
rehydration with normal saline and half normal saline. The
protocol was published in Pediatric Diabetes earlier this year.
The primary outcome will be GCS of less than 14. They will
include children less than 8 years old.
Mythbusting Part 1:
Corneal Abrasions and Topical Anesthetics
Anand Swaminathan MD and Mel Herbert MD
u
Most of what we thought about the management of corneal abrasions is wrong. Patch the eye? No. Antibiotics? We
still do them but the evidence isn’t great. Don’t send your
patients home with topical Proparacaine?
u
Corneal abrasions are common. We see them multiple
times a day. You put the drops in. They feel better and ask if they
can take the drops home. We say no. We know that systemic
analgesics are inadequate for this. Our textbooks all say that it
is dangerous to give topical anesthetics because they will go on
to develop corneal ulceration and impaired healing.
u
What are the supposed dangers? #1. Physiologic. Topical
anesthetics supposedly inhibit mitosis and cellular migration and
impair the ability of the corneal epithelium to oxidize glucose
and pyruvate leading to decreased healing. #2. It decreases
corneal sensation to touch and the abrasion may worsen without
the patient knowing it. #3. There is direct toxicity. The agents
increase corneal thickness and cause opacification, stromal
infiltration or epithelial defects.
11
u
u
What do our textbooks say? Both say that topical anesthetics
are contraindicated in the management of corneal abrasions and
the healing will be different due to sensation issues. This is a
single line of text with no supporting references.
send patients home with. Of interest, they included 4 physicians.
u
Where does this come from?
q Most
of the literature comes from animal studies and
two main sources: enucleated rat and rabbit eyes or cell
preparations. There are number of different studies. Some
showed no difference in healing or corneal permeability,
others showed worse outcomes. Is an enucleated rat or
rabbit eye really equivalent to a living human eye?
q
The data that exists for humans is a series of case reports.
q
Epstein DL and Paton D. Keratitis from misuse of corneal
anesthetics. N Engl J Med. 1968 Aug 22;279(8):396-9
PMID: 4232838. Included 5 case reports of patients who
applied topical anesthetics for prolonged periods of time
and developed ulcerations, thickening of the corneal
epithelium and hypopyons or other infections. What
were these five cases? The first case used 5% tetracaine.
Most preparations in the emergency department are only
0.5%. The patient used it every hour for three weeks and
developed an ulcer. The second case used it every 20 minutes
for two months. The third case was a veterinarian who used
veterinary tetracaine in an unknown concentration, every
1-2 hours for two weeks. The fourth case was a pediatrician
who used it every 16 minutes for 5 days. The last case was
a patient who used it 10 times a day for three months. In
these cases the anesthetics were used much more
frequently than we are considering (at most 2-3
days).
q
q
q
12
Willis WE and Laibson PR. Corneal complications
of topical anesthetic abuse. Can J Ophthalmol. 1970
Jul;5(3):239-43 PMID: 5472832 . Described 9 cases
including a doctor who used 0.5% every 15 minutes for
seven days, a woman who used 8 bottles of Proparacaine
over 6 weeks and a 50 year old who used it every 30 minutes
for 9 days. All of the cases are very similar to this. There
was one patient who used Proparacaine 0.5% every
2 hours for three days and returned with ulceration.
Even though he used it sort of appropriately, he didn’t have a
good evaluation of his abrasion prior to initiating anesthesia
(he was a factory worker who was seen by the factory doctor
in 1969 and started on the regimen prior to evaluation by an
ophthalmologist).
Duffin RM and Olson RJ. Tetracaine toxicity. Ann Ophthalmol. 1984 Sep; 16(9):836, 838 PMID: 6508100. Included
one patient who used 0.5% tetracaine every 30 minutes for
more than 2 months.
Are there any safety studies? Initial studies were in the
ophthalmology literature with patients who received photorefractive
keratectomy and were given topical anesthetics agents for
between 24 and 72 hours. The healing was evaluated initially
and at 72 hours. All three studies agreed there was no difference
in corneal healing at 72 hours. They induced a laceration to
the cornea rather than abrasion and there was no
difference in wound healing.
q
Verma S et al. A comparative study of the duration and
efficacy of tetracaine 1% and bupivacaine 0.75% in
controlling pain following photorefractive keratectomy
(PRK). Eur J Ophthalmol. 1997 Oct-Dec; 7(4):327-33
PMID: 9457454.
q
Brilakis HS and Deutsch TA. Topical tetracaine with bandage soft contact lens pain control after photorefractive
keratectomy. J Refract Surg. 2000 Jul-Aug;16(4):444-7
PMID: 10939724.
q
Shahinian L Jr et al. Dilute topical proparacaine for pain
relief after photorefractive keratectomy. Ophthalmology. 1997 Aug;104(8):1327-32 PMID: 9261322.
u
There is one study in the emergency medicine literature.
Ball IM et al. Dilute proparacaine for the management of
acute corneal injuries in the emergency department. CJEM.
2010 Sep;12(5):389-96 PMID: 20880433.
q This
was a small study with only 33 patients but it was
randomized. 15 patients were given 0.05% proparacaine
as a topical anesthetic to take home. This is a 10-fold dilution
of what is normally used in the emergency department.
The patients were followed up at 72 hours with no adverse
events or change in wound healing. The group with topical
anesthetics needed less oral medication.
u
What are the take-home points? Most of the evidence
against topical anesthetics for corneal abrasion is from animal
studies with enucleated rabbit or rat eyes and case reports of
inappropriate use published years ago. There is some ophthalmology
literature saying that topical medications are safe after PRK.
The best literature in the ED says that there is no increased
risk of side effects but this is small. We need a larger study
looking at safety but the urban legend saying that
corneal anesthetics are unsafe appears to be based
on an unsound research base. We give patients medication that causes bleeding and death when they trip and fall; this
doesn’t seem so bad.
u
Both Herbert and Swaminathan have had corneal
abrasions. What did they do? Used proparacaine for several days…
Of the 15 case reports, 14 patients used it inappropriately.
All cases used a solution that was higher than we would
Paper Chase 5:
Patient Satisfaction and the Telephone
u
1 gram of calcium chloride has three times the amount of calcium
as calcium gluconate. This has to do with the size of the molecule.
There is very little literature on which one we should be using.
It has been said for years that calcium gluconate needs to go
through the liver for metabolism but there is little data
supporting this and no randomized controlled trials.
u
Brian Hayes Pharm.D discussed the data on Academic Life in
EM.
u
Martin TJ et al. Ionization and hemodynamic effects of
calcium chloride and calcium gluconate in the absence of
hepatic function. Anesthesiology. 1990 Jul;73(1):62-5 PMID:
2360741.
u
u
u
Patient satisfaction is important. It is how you get paid. It
is how you stay satisfied with your job. It may help the patient
avoid clinical deterioration and avoid a follow-up visit. It may
be the only way to measure quality in a healthy patient. It might
help patients follow your recommendations. It might help keep
you out of legal trouble and it is the right thing to do.
It is hard to influence patient satisfaction as there are multiple
variables beyond your control such as the cleanliness of the ED,
the waiting time, the rudeness of the clerk up front, etc. If you
can do something easy to improve patient satisfaction,
do it.
Patel PB et al. Physician e-mail and telephone contact after
emergency department visit improves patient satisfaction:
a crossover trial. Ann Emerg Med. 2013 Jun;61(6):631-7
PMID: 23465304.
q
This was a crossover trial done by Kaiser in Northern
California. The physicians contacted all of the patients
they saw. The physicians spent 2 minutes on average to
make the contact. Even if the contact was a phone call,
it was still usually only about 3 minutes.
patients were then surveyed about their satisfaction.
The patients who were contacted were satisfied with
their interaction with the physician 88% of the time
compared to 79% for the controls. Satisfaction was
assessed for the physician’s skills and abilities, care and
communication.
q
This study was performed in patients who were going to the
operating room for liver transplant. There was no way they
would be able to turn calcium gluconate into ionized calcium
if the liver was necessary. The patients received citrate as part
of the pre-transplant algorithm. This can cause hypocalcemia.
q
The patients became hypocalcemic and had serum calcium
levels measured. They were given either calcium chloride
at 10mg/kg or calcium gluconate at 30mg/kg.
q They
measured ionized calcium after administration and
found that the ionized calcium in both groups increased a
similar amount after 10 minutes. There was no difference
between the two. They concluded that you don’t need
the liver in order to turn calcium gluconate into
ionized calcium and it is safe to give either calcium
gluconate of chloride.
q The
q
There were some problems with this study; it was at
Kaiser, all of the patients had to have contact information,
the satisfaction scores were focused on the physician and
not the overall experience.
Mythbusting Part 2:
Calcium Chloride or Gluconate
q
u
u
u
A recent discussion recommended the use of calcium
chloride over calcium gluconate in the treatment of
hyperkalemia. Theoretically, it has quicker onset, has more
calcium in the same volume and doesn’t require first past
metabolism unlike calcium gluconate. However, most use
calcium gluconate as they are worried about extravasation
and sclerosis of the veins with calcium chloride.
A response by Chris Cresswell MD. This is BS and you need
to stop saying it. There is no difference in calcium levels regardless of what is given.
Cote’ CJ et al. Calcium chloride versus calcium gluconate:
comparison of ionization and cardiovascular effects in
children and dogs. Anesthesiology. 1987 Apr;66(4):465-70
PMID: 3565811.
q
Anand Swaminathan MD and Mel Herbert MD
This isn’t really applicable to emergency medicine, but it
does highlight that you don’t need a liver to activate calcium
gluconate.
Included 10 pediatric patients with significant burns going
to the operating room. These patients had hypocalcemia and
were given either calcium chloride or calcium gluconate with
the same outcome. The ionized calcium increased in the
serum in about the same amount of time regardless of
which formulation they were given. This paper was a little
weird as they also included 10 dogs.
Heining MP et al. Choice of calcium salt. A comparison of the effects of calcium chloride and gluconate on plasma ionized calcium. Anaesthesia. 1984 Nov;39(11):1079-82 PMID: 6507824.
u
These aren’t the greatest studies but they are probably
the best we will get. They both say there is no difference
between administering calcium chloride or calcium
gluconate.
13
u
Which is more effective to give for hyperkalemia?
There isn’t much literature on this. Calcium chloride has not
been compared directly to calcium gluconate for hyperkalemia.
Even the amount of calcium necessary is unknown. Calcium
gluconate is definitely superior to calcium chloride in terms of
safety through a peripheral line; it is less likely to cause tissue
necrosis if it extravasates. If you have central line access in a
patient with hyperkalemia, calcium chloride is a reasonable
choice at a dose of 1 gram. However, it is reasonable to
use calcium gluconate in everyone since we know it
works just as quickly with a better safety profile. You
can use a dose of 2 grams.
BONUS SECTION SUMMARIES
q
u
Child abuse cases can be dichotomized into two separate
areas.
q
1. Thinking about child abuse in the first place. If
you see a child with vomiting and without diarrhea, it is
difficult to think that it may be due to a brain injury. This is
the hardest thing to do: seeing a kid where no one is telling
you they are concerned for abuse, the child doesn’t have
an obvious injury and you have to be the one to say, “Well,
maybe this is from abuse.”
q
2. When the flag has been raised, deciding whether
or not abuse has occurred. Involve others. Don’t feel
like you have to do everything by yourself. If you are in
an academic center that has a pediatrician specializing in
child abuse, call them. They will know the literature and
can assist you in what tests to order. They will also be able
to go to court and talk with other experts.
u
How extensive should your work-up be? If you are
suspecting abuse, the work-up should include more studies
than you think. The more injuries you identify, the easier it
will be to protect the child in the face of opposition in court.
u
What injuries should heighten your suspicion of abuse?
q
Every injury in a child should be considered in the
context of the age of the child and the reported
mechanism of injury. For example: retinal hemorrhages,
rib fractures, subdural hematomas and skull fractures may
be consistent with a history of ejection in a motor vehicle
accident and are not always due to abuse. It can be difficult
to verify a fall. The most concerning time is age less than
3 years and especially less than 6 months old. Neurologic
exams are difficult in this age group and they are unable to
provide history. Once the child is able to talk to you and tell
you what happened, it is easier.
q
Spiral fractures have historically been considered
pathognomonic for abuse, but there is not a lot of
literature to support this. One of the most common
accidental fractures in children, the Toddler’s fracture, is
usually a spiral fracture.
q
It was previously thought that bruising of different ages
is concerning for abuse and the age of the bruise could
be determined based upon the color. However, a review
of the literature shows that we are often unable to agree
on the color of the bruise and there is no good evidence
associating the color of the bruise with its age. This theory
was based on studies performed decades ago that were
poorly done and not performed in children.
An Approach to Child Abuse
Ilene Claudius MD and Sol Behar MD with Dan Lindberg MD
u
How do you approach child abuse? It requires a different
way of thinking than usual. Why?
q
q
14
Unlike every other illness you may face in the pediatric
patient, the parents aren’t your partner when abuse
is involved, even when they are not responsible. Often
they are unaware the child has been abused. For example, even
though a father may have abused a child, the mother may just
think the child is limping. If they are responsible for the abuse,
they may give you a story that is very misleading or incomplete.
Our normal clinical gestalt is to look for clinically
important injury. If you miss a rib fracture in a patient
who fell down skiing and it heals by itself, it doesn’t really
make much difference. However, if you miss a rib fracture
in a child that is due to abuse and allow the child to return
home, it dramatically increases the risk of future abuse.
Evidence shows that if they are abused once, they are very
likely to be abused again if it remains unrecognized. The
abuse may be escalating.
One of the reasons the cases of child abuse we see
are so depressing is because we are often too late
for intervention. We are left trying to put someone in jail,
which is not a satisfying outcome. The satisfying outcome
is when we are able to recognize a mild abusive injury and
protect the child.
arm. You reported that the patient had fallen off of the bed. This
injury is more severe than we usually expect from a fall of this
type, so it is important for us to be sure that we are not missing
something else. It is important that we don’t miss something
medical that makes your child’s bones fragile or some other
kind of trauma that you are unaware of. Unfortunately, sometimes
we find that someone may have been hurting your child. We are
going take pictures of your child’s other bones to make sure that
there are no other injuries and do a CT or MRI to make sure that
their brain is ok. We will send some blood tests to make sure that
there are no signs of injury to their belly.”
q
Location of bruises is important. Active children are
expected to have bruises on their shins, forearms and
forehead. Bruising on the abdomen, neck, ears and under
the chin is more concerning. Pattern bruising is important.
Bruises in children under the age of 6 months or in
children who are not cruising are extremely rare in
normal children. In children under 6 months with bruising
and no other apparent injuries, the rate of fracture, brain injury
or abdominal injury is approximately 50%.
q
Rib fractures are concerning for abuse. This is true in
all age groups.
u
q
Fractures in different stages of healing.
q
q
The classic metaphyseal or bucket-handle fracture.
These are fractures around the growth plate. Most of these
are in infants.
q
Consider abuse in any case of subdural or subarachnoid
hemorrhage outside of major trauma such as a car
accident.
We need to weigh the risks and benefits of these
studies. The ALARA principle of radiation exposure (As
Low As is Reasonably Achievable) and new literature
describing which children do not need CT scans are
important. However, this is different for cases of suspected
abuse. Why? We are missing cases of abuse. This is not because
we are lazy or not trying; it can be difficult to detect.
q
The risk from missed abuse is very high. Children
with abusive head trauma have a mortality of about 20%
and of those who survive, about 60-80% will experience
long term neurologic problems. The lifetime disability and
risk of death is as high as any other disease we see. We are
much more likely to have seen a child die from abuse than
meningitis. Even in a newborn, the risk of cancer due to the
radiation from a head CT is only 1/500-1/1000 according
to the most conservative studies. The risk from abuse is
much higher.
q
The AAP guidelines say if you are concerned about
physical abuse in a child less than 2 years old, a
skeletal survey is mandatory. This recommendation
has the most supporting evidence. There are studies
showing the rates of positive findings on skeletal survey
in this population are about 20%. If you work at a center
that does not do skeletal surveys, you should consider
transferring the child to a center that does.
q
Your clinical exam is unlikely to be sufficient to
detect abusive abdominal injuries. You may screen
with AST and ALT in every child with concern for physical
abuse up to the age of 5. If these are elevated (>80 IU/L),
the likelihood of a positive abdominal CT is about 1 in 5. This
will not detect everything. If you have a child who reports
that they were punched in the abdomen or with bruising or
tenderness, it may be reasonable to go straight to CT.
q
Neuroimaging with CT head or MRI. There was a study
published with children under the age of 2 who were hospitalized for suspected abuse with no signs of brain injury.
Patients who were deemed high risk (<6 months, facial
bruising, rib fractures, multiple fractures) received neuroimaging. The rate of positive CTs was 37%.
q
Oropharyngeal injuries in a non-mobile infant. A
tear in the frenulum under the tongue is concerning for
abuse.
q
Any long-bone fracture in an infant outside of a
major car accident is concerning for abuse. The rate
of abuse associated with these fractures in infants is 20%
or more. If you are not going to screen for abuse in these
patients, you need a good reason (e.g. multiple people
unrelated to the family saw the accident happen the way
the family described, it was on videotape, it was a very
significant mechanism, etc.). The risk of screening is
much lower than the risk of missing abuse.
u
We do a bad job of identifying cases of abuse. Approximately
30% of cases of abusive head trauma are missed initially by
physicians. About 1/5 of kids with abusive fractures are seen by
physicians and sent home without a diagnosis of abuse.
u
Burns are complex. We are able to determine approximately
how long it would take a child to get burned based on the
temperature of the water heater at the house. The location of
the burn can indicate the position of the child at the time they
were burned. Consider consultation with a burn specialist or
a child abuse specialist in any burn case that is not obviously
due to the reported mechanism. If you do not have access to
an expert, take pictures of the burn.
u
How do we discuss performing a work-up for abuse with
the family in a way that is not punitive or stigmatizing?
Your decision to do a work-up should be uniform for a particular
injury and not based on whether or not you like the family or their
demographics. For example, a patient presents with a fracture of
both bones of the forearm after a reported fall off a bed. What can
you say to the family? “We found a fracture of both bones in the
What tests should you order?
15
Rubin DM et al. Occult head injury in high-risk abused
children. Pediatrics. 2003 Jun;111(6 Pt 1):1382-6
PMID: 12777556.
q
Neuroimaging should be obtained in any child
with signs of head trauma, altered mental status,
bulging fontanelle or if they are young and high
risk (rib fractures, multiple fractures, etc.). If it is
a stable infant, you can start with MRI. If they are unstable
or older, a head CT is more accessible. If you do not have
access to MRI, a CT is reasonable.
q
Every child needs a thorough physical exam. Get them
naked. Look in their ears. Feel their fontanelle. Look at their
genitalia. Look inside their mouth for chipped teeth, torn
frenulum and mucosal injuries.
u
What can you do to increase your odds of detecting
abuse? Make a list of injuries where you will decide to screen
every time. Make a list of screening studies, that when you think
about it, you do every single time. Batch order it once you are
thinking about abuse. Once this is triggered, your rate of positive
findings will be fairly high. Think less and screen more.
u
Kids that should trigger an abuse work-up. The story
is inconsistent with the injury. Children under 6 months with
bruising. Children of any age with bruising to unusual parts
of the body like the abdomen, ear, neck or pattern bruising.
Rib fractures at any age. Multiple fractures in different stages
of healing. Classic metaphyseal fractures. Subdural or
subarachnoid hemorrhage. Oropharyngeal injuries in
non-mobile injuries. Long bone fractures in non-mobile
infants.
u
Some instructive cases.
q
Children with frenulum tears or oral injuries in
non-mobile infants. These injuries are so minor and often heal without intervention. It hasn’t been well publicized
that these injuries are concerning for abuse. A child may be
crying or not eating food and someone may shove a pacifier,
finger, bottle or spoon in the mouth or strike the child in the
mouth.
q
Children presenting with vomiting without diarrhea
at a young age are challenging. Most of these children
will have gastroenteritis and not abuse but upon review of
missed cases of abuse, many of the children had a
presenting complaint of vomiting. Consider how long
it has been going on. If it has been more than 24 or 72
hours, it is less likely to be gastroenteritis. Do the full
physical exam and carefully examine the fontanelle.
u
16
for retinal hemorrhages. When we see retinal hemorrhage
we are probably correct but we are not good at ruling them
out. If the head CT is negative it is unlikely that there are
retinal hemorrhages. This is supported by the literature.
u
Consider trauma in reported medical cardiac arrests in
small children. During resuscitation of a toddler brought in
as a medical arrest, a bedside FAST showed positive free fluid
consistent with abdominal trauma. Another case was found to
have a rectal laceration due to sexual and physical abuse. If you
don’t think of it and do a thorough physical exam, you
won’t find it.
Retinal hemorrhages. Retinal hemorrhages obtained after birth trauma usually go away after a month. They are in
a different pattern then that seen in abuse. Whenever you
are concerned about abusive head trauma with a positive
CT or MRI, get a pediatric ophthalmologist involved to look

The Written Summary of the EM:RAP Monthly Audio

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