Download Oct 2011

EMERGENCY
MEDICINE UPDATE
MARCH 2012
1) Can't take anything from this study on cadavers but it does go against
myths that ATLS has given us and this in itself is worthy to mention.
The recommendations of ATLS were always to log roll patients 90
degrees and then to slide the board out from under them while
checking the back. This according to the authors can cause
unacceptable neck motion. It is believed that maintaining in line
stabilization is thought to cause less movement and therefore lifting
the patient and sliding the board out is safer. OK well, this was
cadavers, and who knows if the movement is significant but it makes
some sense that it will be harder to maintain neck stabilization when
revolving the patient.(J Trauma 70(5)1282). PLEASE REMEMBER- the
spine board is for transport only and provides no stabilization of the
spine. It causes back pain in normal volunteers for up to three weeks
afterwards when left on the board for the usual time most EDs leave
patients on these boards. Also can cause pressures sores. Take them
off the board immediately. TAKE HOME MESSAGE: The log roll is not
holy and may not be the best way to take the patient off a long board.
But do get him off fast.
2) This study was surprisingly well done- what was it doing in such a
obscure journal? They claim that NTPROBNP levels are high when A
fib starts and then go down after 48 hours- how well do they predict
left atrium thrombus? If they are good, then you can use this to
convert them. Are you a family doc? Do the test, then give some
Propafenone and you saved your patient time and money. In this
study they took patients with no heart failure and a fib of unknown
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duration and did the test. It worked actually very well. (Heart
97(11)914) The problems- there were few patients in each group and
even in the low values there were still 5% that had a thrombus so it
isn't perfect. False positives aren't so important here because the
absence of the NTPROBNP is what we are looking for. But like D
Dimer it could be that this is rarely negative. Needs a bigger study.
TAKE HOME MESSAGE: NTPROBNP is a new possible way of
determining if there is a right atrial thrombus but it needs more study.
3) Good Grief- just when you thought it was safe to go out. Like my pals
Rick and Jerry, I can't resist not including one pulmonary embolism
article per issue and here we are (did we lose everyone yet? You in the
corner- Why aren't you leaving? Oh sorry, didn't mean to wake you
up) But this is an important one. There is an entity of non thrombotic
pulmonary embolism which can be due to air, amniotic fluids, a variety
of other gases and materials, infectious emboli, and fat. D dimer is
often negative and CT can be unreliable. (J Thromb Thromb 31(4)436)
Of course clinical picture will be very helpful here but little else –
perhaps MRI? TAKE HOME MESSAGE: PE can be from other causes
than thrombosis- and nothing much will help you with clinching the
diagnosis. While we are at it we should mention the Lancet
(378(9785)41) article about sending some PE patients home. I do not
think there is any argument here the study was well done and the
question is just- who qualifies? It is worthwhile mentioning that in this
study no one died at home and even in the hospital only one died.
Those who were sent home had category one or two PE which has a
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mortality of up to 10% but it is clear that probably more could have
been sent home since so few died in the hospital.
4) OK, this month's clinical challenge is actually quite easy. This patient
underwent a thyroidectomy. (CMAJ 183(8)e498)
5) I have an interest in flight medicine and this is a reminder that the air
in the ET tube can expand when ascending. The numbers- if they are
important to you are that tracheal mucosal perfusion is impaired at 30
cm H2O and by 50 total blood perfusion is impaired. The study used
an in vitro model with ascent to 2400 meter which is less than most
airplanes fly but it is what the cabin is pressurized to. Interestingly
enough but not surprising from a physics viewpoint is that water filled
balloons were unaffected. (PEC 27(5)367).TAKE HOME MESSAGE: In
ascent whether they are to mountains or in planes- you must remove
air from balloons that may cause impaired perfusion. Now the article
that I wanted to do but never got around to. A dermatologist- of all
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folks, huh?- did a study to see if air lines in Europe were in compliance
with international standards for required equipment for in flight
emergencies. None were. A lot of them had weird stuff in their kits
including IV aspirin and po placebo. (Trav Med Inf Dis 8(6)388) Now in
deference to my Asian readers, EL AL, Qantas (leave off guys, I know
Australia is not part of Asia) and Air India were not included in the
study. These issues were also discussed in JAMA, 305(19)2003 and
they found that flight attendants were ill prepared for in flight
emergencies even thought the FAA mandates drills in use of the AED
and CPR skills. Standardized recording systems for emergencies do
not exist and while on ground medical support exists it is rarely used.
TAKE HOME MESSAGE: Be prepared to not be prepared on in-flight
emergencies.
6) An article that was just a survey of their center in dealing with nail bed
lacerations but the important point here is that plastics repair showed
no better results than EPs. I assume the same for FPs as well. This is
a laceration- while ugly- that most of us should be able to handle- just
be careful if it crosses the germinal matrix. (ibid p375). TAKE HOME
MESSAGE: Everyone can sew nailbed lacerations pretty well with good
results
7) A great idea and I am sure that the ultrasound geeks that read EMU
are already salivating. For pleural effusions, pulmonary edema,
pneumothorax and lung consolidation- ultrasound at bedside
performed just as well as chest x ray (when CT was used as the gold
standard). (Chest 139(5)1140) The kappa was 95% which is very
impressive, although not clear to me why they used p values for some
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comparisons and Kappas for others. The study did not look at
pneumonia and lung masses so you probably have to still do films for
these conditions. TAKE HOME MESSAGE: Beside ultrasound can
replace chest films for many conditions.
8) We discussed upper extremity PE in last month's issue. Here is some
more data. 1% of these patients get PEs which is low for DVTs but 5
of their patients who were on Coumadin fell and bled in their brains
and died. (Ann Vasc Suyrg 25(4)442) So do you treat these folks with
Coumadin or not? Good question. No answer. There was referral bias
in this study as it came from a DVT clinic but this doesn't ehlp us
answer this question. TAKE HOME MESSAGE: Upper Extremity DVT
needs Coumadin- or maybe not. Or maybe yes.
9) Fads come and go and I have to admit I was a doubter as to how
important Vitamin D is. Recently the daily recommended allowances
for Vitamin D have increased and we do know that is related to
immune function. In this study, patients with sepsis who were vitamin
D deficient did worse. They designed the study using APACHE scores,
and SOPFA scores. (AEM 18(5)551). This study was not randomized
and only had 81 patients, in addition APACHE score is just that – a
score. Some patients may have been worse in some aspect of
APACHE that may be worse in sepsis or in vitamin D deficiency or
both- it is hard to tell. But yes, I probably will go out and get those
vitamin D pills. Or at least take my intubated septic patients outside to
get some good sun. TAKE HOME MESSAGE: Vitamin D deficient
patients may do worse in septic shock. And yes, I did buy those pills
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10)
Adam Singer is our guest speaker for this year's scientific
assembly. Adam is known to be a paper factory but the great thing
about Adam is the originality of his research. Adam brought us a lot of
the first articles on gluing wounds, and the article on the use of
Docusate for ear wax and many others that I enjoyed. The originality
continues- Adam found in a meta analysis that in four countries they
sew up abscesses after opening them- which we do not generally do.
They healed faster and had no more septic complications. Adam
admits that most of this research was done on surgical patients by
surgeons on anogenital abscesses but the studies were randomized
and showed this works. (AJEM 29(4)361) The big question is that
these studies came out of basically four countries- Nigeria, Australia,
India and the UK- can it be repeated elsewhere? Adam is an EMU
reader for years now, and I am privileged to have spoken to him on
many occasions. However, if you are one of those salivating geeks I
spoke about before- doing ultrasound guided needle aspiration of skin
abscesses did not do as well as traditional incision and drainage. My
first inclination was to say, that incision is always better than needle
aspiration because needle aspiration is a dynamic process- it is to be
done multiple times until the problem resolves. But that was not the
point of the article- despite seeing the abscess cavity on ultrasound
they frequently came up with taps that had no pus in them. (Ann Emrg
Med 57(5)483) Really sounds like this is operator dependant. TAKE
HOME MESSAGE: You can sew up abscesses that have been drained
but if you use ultrasound to aspirate them, you may not be as
successful as incision.
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11)
How about some more name dropping. EMU reader and peer
reviewer in the past Prof Pinny Halpern has also appeared at our
roundtables. They recently published a paper on the use of lidocaine
jelly for the insertion of NG tubes (Zonde) versus KY jelly. While this is
hard to be double blinded because the jellies do look different but
indeed the lidociane jelly caused less gagging and less pain. However
it was harder to insert the tube (AJEM 29(4)386). I discussed this with
Pinny and this could be because the swallowing mechanism becomes
anesthetized and therefore they can't swallow the tube or it could be
that KY is more viscous and therefore spreads better and goes further
down the GI tract. In either case in Israel we exclusively use lidocaine
jelly, but in the USA the use is less common. Nebulized lidocaine is
another option that Chris Nickson uses. Give it a try, Huh? TAKE HOME
MESSAGE: Lidocaine jelly causes less gagging than KY Jelly
12)
OK, I know you are smart. You not only get EMU, but you
subscribe to EMA, read Life in the Fast lane and go up on EM Central.
So you knew that the case above in # 4 was the Trousseau sign seen
in hypocalcemia. But this case is tougher. A fifty year old man has an
abscess of the appendix- He is previously healthy. He got cefotaxime
and metronidazole in the hospital and was discharged with
metronidazole and ciprofloxacin for continuing therapy. 5 days later he
is found with hearing loss, vomiting, ataxia and dysarthria. MRI shows:
bilateral and symmetric swellings of the cerebellar dentate nuclei, dorsal medulla, dorsal pons,
midbrain, corpus callosum and increased signal intensity in the supratentorial periventricular white
matter.
PS- he was admitted to the ICU. Viral and bacterial cultures
were all normal, as was the LP. What happened? TFTs and
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Autoimmune markers were also negative. If you are not an ultrasound
geek but an IM geek, you should know the answer immediately.
(Lancet 378(9787) 288), If you are both an ultrasound and IM geek,
you should be writing EMU, not me.
13)
OK let's say you are a pediatrician. And you think that despite
last month's roundtable on pediatrics I do not spend enough time
speaking about kids. So since you immediately knew that the case
above was metronidazole induced encephalopathy, so I will give you
one. Really not too difficult but I am surprised how many do not know
about this condition. Age of onset- 7-12. Girls more than boys.
Colicky abdominal pain, often incapacitating, with vomiting and
occasional headaches. Nothing really has been proven as helping for
treatment. Diagnosis please J Ped Health Care 24(6)372)
14)
I won't drag things out- this one was pretty easy. And I didn’t
know the original description of the entity goes back to 1986
(Cephalagia 6(4)223). This is abdominal migraine which is very similar
to its head equivalent. You do need to rule out other causes of course.
15)
ICU corner. These two articles in the same journal (CCM 39(6)
1562) and (ibid 1576) deal with refractory hypoxemia usually due to
ARDS. The first article points out that with H1N1 we suddenly had a lot
of patients with ARDS who did not have past medical problems and
therefore rescue therapies could be tried, in contradistinction to the
usual ARDS patients with multiple medical problems who generally die
from multi organ failure fairly quickly. The first steps are usually PEEP
and prone positioning, but now there are some new players to tryECMO, which worked in 51% of the patients – a very high percentage
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of survival for this malady, but it resulted in blood loss. Other
therapies include high frequency ventilation which is favored by the
Canadians, and airway pressure relief ventilation . If you are not
familiar with these therapies, I have hyperlinked you to Wikipedia and
CCM tutorials. TAKE HOME POINT: PEEP is the standard for treatment
for ARDS. ECMO is an exciting new option. Other therapies are very
interesting but unproven.
16)
This is an opinion article on acute chest syndrome in Sickle cell
Anemia, and while we live very close to Africa and have many patients
from Eritrea, Ethiopia and Sudan- I rarely see this disease anymore.
The approach they use in Brooklyn at King's County in patients with
SCA and a new infiltrate is antibiotics, fluids, oxygen, simple
transfusion and occasionally steroids. They like macrolides although I
do not and sometimes use exchange transfusions if the patient is
doing poorly despite other therapies. (Blood 117(20)5297) The
problem is that this is fine when the etiology is pneumonia, may be OK
if the etiology is fat embolism but the large majority are of unknown
etiology and therefore you can not really know what helps. TAKE
HOME MESSAGE: SCA acute chest syndrome is a dangerous disease,
but the therapies used are fairly standard- oxygen, transfusion and
antibiotics. Harder cases need an exchange transfusion
17)
I do a lot of CVP lines-EMU readers know that for fluid status
measurements CVP lines are not very accurate. And they also know
that we are putting a lot fewer of these. However, we are doing a lot
more critical care medicine in the ED, and while you don't have to put
in a CVP to give vasopressors, it is what the ICU guys want and it is
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probably safer. Furthermore, in my elderly population often we can not
find a good vein and this makes life easier in patients who need fluids
or meds fast. This article from Hadassah reminds us that CVP
placement can cause cardiac tamponade- which is rare but can
happen- and if it does it is lethal 50% of the time and can take time to
develop so you may not see it immediately. This can be prevented by
noticing that the pericardium reflects up 3 cm onto the SVC so if you
want to avoid placement in the heart and anywhere near the
pericardium so use 15 cm as the maximum insertion of the CVP and
the guide wire. The other bad things that can happen with CVP are
well known, so I mention this article just as a caution – but I still will
be doing them when there is an indication.(Anest Analg 112(6(1280).
What I have seen in the literature indicates that femoral lines are the
fastest, IJ lines are the safest, SC lines are the ones most often done.
TAKE HOME MESSAGE: do not abandon CVP lines but use caution and
remember that tamponade is a preventable complication
18)
Urinary catheters are often inserted for no good reason,- we
know that already- but while in this hospital they were indicated less
than half the time- also they showed no benefit most of the time - but
the criteria for benefit were not clear to me. What is important from
this study is that many who got the catheter could not be weaned
from it. (Am J Med Sc 341(6)474) Good work, Dr. Niven who is an
EMU reader- did you think I would miss this? TAKE HOME MESSAGE:
Think twice before automatically putting in a catheter. You may never
be able to get it out.
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19)
This is a review article that gives the basics on Trigeminal
Neuralgia- but since we do not see so many cases, I will just mention
it. Pain is in the trigeminal distribution and it is usually idiopathic but
can be due to a tumor or of course, and Multiple Sclerosis which is not
a surprise because any neuro complaint can be caused by MS. CT
should help if there is a doubt (I am not sure how CT helps in MS)
Tegretol is the accepted treatment, but sometimes surgery is the way
to go if meds do not help (Post grad Med J 87(1028)410). Now the
article doesn't mention Lyrica which may help and I often do infra
orbital nerve blocks with a lot of success. TAKE HOME MESSAGE:
Tegretol is first line treatment for trigeminal neuralgia, but consider
nerve blocks.
20)
We mentioned last month about people abusing propofol, but
ketamine is now becoming a drug of abuse as well. But if you do
abuse drugs- be careful. Other than being stupid you take a risk of
significant problems in your GU tract including painful bladder,
papillary necrosis, uretic dysfunction and hepatic necrosis. (BJU
107(12)1881) This is only in very high dosages with continual use- our
use of ketamine is safe. However, if your colleague is jumping up and
down and having hallucinations you may think about….. TAKE HOME
MESSAGE: Ketamine abuse is growing and can cause hepato- GU side
effects.
21)
I have written often about hyperemesis gravidarum but there
have been many new subscribers so as long as the literature speaks
about this nauseating subject, so will I. I won't describe the condition
–we are all familiar with it, but it does recur in people who had it
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before. Interestingly the risk is reduced if there is a change in
"paternity" although I will not be the one to recommend it to patients.
(Not sure my wife would be as hesitant). Tall thin women have a
higher rate. H Pylori is often found and should be treated. Here is an
interesting statistical error- Twin pregnancy has been associated with
having more HG but there is the same incidence of twin pregnancies
whether the patients vomit or not which does not say the same thing.
In any case ketones can damage the developing fetus and often
thiamine deficiency occurs. Amylase can be 5 times the normal value
but is of no significance. In the USA they are trying home care, in
Israel it is the accepted way of treating this. What works?
metoclopramide, antihistamines, ondansetron, pyridoxine (vitamin b 6)
all work AND ARE SAFE; Phenothiazines may not be so avoid them.
Steroids -not so clear if they work or not, use only if necessary and
after the tenth week as cleft palate can occur. Ginger may not be as
safe as we thought as it affects testosterone binding and
thromboxane synthesis but it is not clear to me if these are really
clinically important (Arch Gyn Obstet 283:1183) TAKE HOME
MESSAGE: Aside from phenothiazines all medications usually used for
vomiting work well in hyperemesis
22)
Diuretics- urinating your way to health and happiness? Well,
there is very good evidence that diuretics improve symptoms. However
they may damage too. They could worsen renal function in high doses
and cause neurohumoral activations which make CHF worse. However
other research shows some improvement in function due central
venous pressure reduction. Hemoconcentration also occurs which
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increases the creatinine but improves outcome. There is also
additional evidence that KIM 1 receptors and NAG concentrations- no
idea what this is- show that diuretics do improve the renal function.
(JACC 57(22)2242). I do not think we really know the answer and but
we should know that diuretics do not work that fast and are not the
first choice in acute pulmonary edema- use CPAP and nitrates which
work faster. TAKE HOME MESSAGE: Diuretics definitely improve quality
of life. Whether they damage renal function seems to be less clear but
new evidence says no. Now Chris Nickson is on the money with what
KIM1 and NAG are- here is what he has to say- They're markers of kidney injury
http://www.ncbi.nlm.nih.gov/pubmed/11873947 and
http://www.ncbi.nlm.nih.gov/pubmed/18414680
23)
I really do not want to discuss this article. I think it is
reprehensible. That may be a big word for some of you so I will say it
differently- this is sick. And sad. Baruch Krauss- an EMU reader writes
on the strife between anesthesiologists and EPs with regard to use of
sedation. The anesthesiologists want us to take a training program
which includes a written knowledge based test and supervised clinical
experience on no less than 35 patients. Deep sedation would be
granted on a one time limited basis and as decided on by the hospital's
anesthesiologists. And only for adults. They claim this is for patient
safety but of course the articles show that EPs give sedation just fine
with out any more adverse events than the Masters themselves. They
do not want us using propofol and I guess after the Murray case I
understand, but I agree with Baruch that deep sedation is not equal to
anesthesia. Baruch gives some ideas how to handle this at your
hospital but one must take into consideration that once it is an official
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document it is very hard to get legal footing if G-d forbid something
does happen (Ann Emerg Med 57(5)470). In Israel the government
has agreed to make this a hospital decision as to who gives the
courses on sedation but the anesthesiologists are still fighting this.
Silence kills gentlemen, silence kills.
24)
This is an article for radiologists but there are some tips for us.
We often- maybe too often- do portable chest x rays. I will summarize
a few points that may be helpful in understanding these films. Most of
the portables are ICU patients so are less relevant to us, but here are
some things to remember. We know that AP supine x rays show
magnification of the mediastinum, and that low respiration breathing
can also cause this. So how do you know if there is real mediastinal
widening? Actually kind of surprised about the answer that was givendo a second film and compare it. Another point: White lung. It could
be be empyema – which can look a lot like a hemothorax- but
empyema takes more time to develop but do not forget lobar collapse
Lobar collapse shows crowding and re orientation of pulmonary vessels
and elevation of the diaphragm. Next point: Pneumothorax. If it is
small it may only be hinted by a deep sulcus sign on the side of the
pneumothorax- check for sulci that are unequal. Next point:
Pneumomediastinum is often missed – it is multiple lucent streaks that
do not change when there is different position of the patient.
Pulmonary embolism: often you see nothing, but pleural effusions,
lower lung atelactasis, point to this and a Hampton Hump (looks like a
pulmonary infarct with a convex medial border and a Westermark sign
pulmonary oligema) are rarely there but if they are, they are pretty
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sensitive. (AJR 196(supp6) s45) This probably didn't help you so much
but let's give you some examples. Here is
pneumomediastinum
(Courtesyemphysemasymptoms.gass) now for Hampton's hump:
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( Courtesy of Emory) and Westermark's
sign:
(Courtesy of
Medscape).I have to admit that one didn't help me much and I didn't
find too many good examples.
25)
This review of Toxic Epidermal Necrolysis and Stevens Johnson
Syndrome is from CCM 39(6)1521 and it says what you already knewthese patients are really sick and need critical care. But remember
how people get into this bad shape- most cases are because of
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medication misadventures. You knew that TMP- SMX (Resprim,
Bactrim, Septra) causes this. But Cepahlosporins, Penicillins and
Quinolones are also on the list although at a Risk Ratio much lower but
still very significant. The point is that antibiotics are not innocuous
and if you used antibiotics for bronchitis or otitis media and the patient
ended up with Steven Johnson, you will find your hind quarters dealing
with the men in the black robes. TAKE HOME POINT: antibiotics are
not benign!
26)
And now some letters from our readers. I heard from Barry
Brenner (who was mentioned in our essay two months ago) who
reminded me that propofol is a bronchodilator. If so, this may replace
ketamine in intubations of respiratory distressed patients with normal
blood pressures such as cardiogenic asthma and COPDers who need
intubation. Ken Iserson reminds us that that once the the patient has
seizures this is eclampsia and not pre eclampsia. There is increase of
reflexes in Preeclampsia. Ken we knew that. Really. We were only
testing you. I also want to give a plug for Ken's new book which is on
a very interesting topic which I have heard Ken lecture on- Improvised
Medicine. Some of his ideas are really cool in trying situations. I got a
couple of e mails from Life in the Fast Lane. Steve Wake noted that
people really do not know about foreign bodies and unnecessary
testing gets done for no reason. He brings a case of a patient that
had daily x rays until the foreign body passed and he is correct that
this was totally unnecessary unless they planned to evaporate the
foreign body via radiation. Lastly, Jay Baker reports that his wife
doesn't buy the virus –can't do anything schpiel so he uses the
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menthol rubs for their placebo effect (and presumably to make his wife
happy- you are a nice man). They also use honey for coughs. Actually
there is some evidence it may work.
EMU LOOKS AT: Movement Disorders and
Disorderly Conduct.
The first article deals with a subject we tackled a while back. It is on
emergency neurology. The source article is Arch Neuro 68(5)567. The
second article is the most important article I have read in the last few
years- don't miss it. See JEM 41(6)598. It is written by Greg Moore one
massively intelligent guy who is an MD/JD and who I have heard speak
twice- once at ACEP and once on Risk Management Monthly
MOVEMENT DISORDERS
1) NMS-Neuropleptic Malignant Syndrome- this is due to
dopaminergic blocking drugs which basically means neuroleptics
event the newer ones. Common drugs that must be thought about
besides the obvious ones are prochlorperazine (Comapzine),
metoclopramide (Pramin, Reglan), Droperidol, and Promethazine
(Phenregan). This is a high risk disorder and missing it could be
fatal. Often it occurs after changes in dosing.
2) The signs are fever, rigidity- often described as lead pipe, mental
status changes, autonomic dysfunction, myoclonus, dystonia and
tremor. Since you see these signs and symptoms in Parkinson'sif your patient has Parkinson's and fever, consider NMS.
3) The key lab test here is CPK .Albumin and iron levels are
decreased, although many ED s can not check those.
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4) Since these patients have muscle breakdown and are immobile
they can suffer from rhabdo, kidney failure, and aspiration
pneumonia.
5) Treatment is definitely not evidence based but giving
dopaminergic agents seems to help. Bromocriptine is the usual
drug. Dantrolene can relax the muscles enough that there will
less CPK leak. Do use this therapy for at least a week no matter
what the half life of the offending agent is. Do stop the offending
med and do not restart it for at least two weeks until after
symptoms resolve. In the interim, electric convulsive therapy can
resolve the psychosis in the mean time
6) Parkinson Hyperexia Syndrome can look exactly like NMS but this
is in a patient with- you guessed it- Parkinson's. We do not do
Leovdopa Holidays any more, but if you reduce their dopamine
medications you could cause this. Treatment is the same as NMS
but methylprednisilone may help here. Here they may not get
better and their Parkinson's may become worse permanently.
7) The usual mimic for both these disorders is Serotonin Syndromefever, myoclonus and altered mental status. Here there is much
less incidence of rigidity and there may be additionally
hyperreflexia, seizures and restlessness which are less seen in
NMS. NMS is usually acute while serotonin syndrome improves
much faster. CPK is usually not elevated. Causes include SSRIs
of course and MAOs, but remember opiates (except morphine),
lithium, triptans, LSD and cocaine. Cyproheptadine is the
treatment in severe cases, but go find this drug- I haven't seen or
used it since the late eighties. This is what the article said- but
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MEDICINE UPDATE
Chris has some updated info: We tend to use benzos as the mainstay – if severe
intubate and paralyse. We'd use cyproheptadine in mild-moderate cases that benzos weren't
sufficient on. Chlorpromazine and olanzepine also have anti-serotonergic effects. By “we”, I mean
the Western Australia Poisons Information Centre (WA PIC) I used to work for.
8) Parkinson causes many ED visits and I know the disease
unfortunately up close- I diagnosed my father with this early on
and while his brain is clear as ever, the physical effects have
reduced him to an invalid. He is 87, and we hope for good health
and happiness for him. The most common reason for
presentation to the ED for these patients is falls. Postural
instability is a major part of this disease, but it does not respond
to levodopa. Other effects include rigidity bradykinesia, which
occur during off periods. Dysautonomia including tachycardia
may occur and psychiatric effects may become more
pronounced. Consider also concurrent infection, medication
changes and metabolic derangements. Dyskinesia may only
respond to amantadine or deep brain stimulation. For psychosis,
they like clozapine and quietipine.
9) Acute Parkinson's is not Parkinson's! Consider stroke, subdural
hematoma, chemo, antiepilptics, anti depressants, CO poisoning,
CN, methanol, Whipple disease, HIV encephalitis, central pontine
mylenosis, and of course, psychogenic. Remember all this?
There will be a test at the end.
LEGAL MEDICINE
1) I have refrained from talking about this topic because the legal
systems are so different between all the countries that EMU goes
to. For example, the USA uses juries and convincing juries is
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often more of a case of theatrics and less justice. I have been
told that Australia uses a non partial government sponsored
panel of medical experts instead of using experts for both sides
which is rarely impartial. In Israel, the loser pays court costs.
However the principles in this article are very relevant to all
systems. Let's get started.
2) You need four elements to prove medical malpractice. You must
prove that the physician had a duty to treat that there was a
breach of that duty, there was harm to the patient and the harm
was caused by the physician's negligence. The main point of this
article is that even with all four elements being there you can still
get out of a malpractice action. Here is how:
3) Firstly- assumption of risk. If the patient took the risk they can not
reasonably sue and win. In Schnieder vs Revici- the patient had a
breast lump which was treated in a non traditional manner. She
had singed a statement assuming risk. When the cancer spread
she sued- and lost. However this defense requires excellent
documentation and the signing of consent forms are often in
language that is not understandable and therefore not defensible.
4) Good Samaritan: you probably already know about this one
however it needs five elements – it has to be an emergency, the
provision of care was voluntary, the patient accepts the care, the
care is given in good faith to help, and there can be no gross
negligence. Now here is the kicker- it can not be for any
reimbursement. There are some caveats- in some locales even if
you have no duty and relationship to the patient—if you work in
that hospital you are responsible for the care rendered. Disasters
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may require physicians to come in and render services may be
exempted under Good Samaritan. Responding to in hospital
emergencies as part of a code team is not exempted from the
Good Samaritan law. In an airplane it actually depends on where
the plane took off from, where it is when the care is given and
where it is going to land. All three jurisdictions could apply.
However most countries do have a Good Samaritan law. Be
careful- even accepting a drink from the airline that would not
have been otherwise provided may drop you from this protection.
5) The next concept is contributory negligence and comparative
fault. The former refers to the fact that a patient who contributes
to the negligence that led to the malpractice event – then she
shares or bears the responsibility. In Ray versus Wagner, the
patient had a positive pap test and was unable to be contacted
with the results. It was proven that she provided incorrect
contact information and therefore bore responsibility. The case
was thrown out. In comparative fault percentages of negligence
are computed and the patient gets a reduced reward based on the
percent of negligence they contributed. In Ostrowski versus
Azzara case the plaintiff was a hypertensive diabetic with
peripheral vascular disease who was overweight and had
uncontrolled diabetes. The defendant removed her toenail that
looked infected and gangrene resulted. The defendant showed
that the failure to heal was related to the plaintiff's smoking and
poor health habits and the court found the defendant only 49%
responsible. Of course, to use this defense you must document
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MEDICINE UPDATE
very well. If the patient fails to follow through at least you told
them what to do.
6) “Sudden emergency” is a concept that a person would not use
the same judgment under the pressure of a sudden emergency as
they would in a controlled situation. In Ross versus Vanderbilt, a
first year resident was injecting lidocaine into a laceration when
the patient syncopized. The resident went for help and neglected
to protect the patient's head. The patient claimed he had memory
loss and tinnitus as a result. The resident claimed that the
emergency caused him to do what he normally would not have
done and won the case.
7) Respectable minority: is the premise that if there is a respectable
minority of physicians that do practice in this manner then
malpractice cannot be claimed. In Hamilton versus Hardy, the
defendant continued to prescribe oral contraceptives even after
that patient claimed she had headaches. In the end she suffered
a stroke. The court ruled that the few doctors that would continue
prescribing the medication were not enough to drop the case.
Had a respectable amount of physicians existed that would
continue contraceptives under these conditions- the case would
have been dropped. Another example the article brings is that PE
in some cases can be sent home based on recent articles (see
EMU in Jan) and so if the patient did not do well- it still could be a
clean case under respectable minority rule.
8) Two schools of thought is similar. Jones versus Chidester was a
case where a tourniquet was used for a bloodless field in
orthopedic surgery. Despite opening the tourniquet several times
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during the surgery, there was nerve damage. The doctor won
because there are many who do use this. Keep in mind that two
schools of thought may not necessarily mean professors and
academics- it only means what is done in the community.
9) Clinical innovation can be defense when no good evidence exists
for the proper treatment. In Brook versus St John’s contrast was
injected into the calf instead of the buttocks. There was
shortening of the Achilles tendon. The patient then needed
surgery. The package insert said specifically injection in the
buttocks. But the physician was able to bring articles that said
that buttock injection would cause damage to the sciatic nerve
and the physician had used the calf successfully in the past.
Obviously this requires documentation and explanation to the
patient why standard practice is not being followed. This is a
difficult defense; try not to go there.
10)
Liked this? If you did, let me recommend Risk Management
Monthly – Rick Bukata's excellent monthly series on legal issues.
In the May issue of EMU we will have a roundtable on legal
issues- stay tuned.
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