Letter to the Editor
Henry G Watson* & James Ferguson
*Department of Haematology
Aberdeen Royal Infirmary,
Foresterhill,
Aberdeen,
Scotland
AB25 2ZN
Email: henrywatson@nhs.net
Tel 00-44-1224-553394
Department of Emergency Medicine
Aberdeen Royal Infirmary,
Foresterhill,
Aberdeen,
Scotland
Email: j.ferguson@nhs.net
Tel 00-44-1224-550506
Keywords: Intracranial haemorrhage, warfarin, prothrombin complex
concentr...
Letter to the Editor
Henry G Watson* & James Ferguson
*Department of Haematology
Aberdeen Royal Infirmary,
Foresterhill,
Aberdeen,
Scotland
AB25 2ZN
Email: henrywatson@nhs.net
Tel 00-44-1224-553394
Department of Emergency Medicine
Aberdeen Royal Infirmary,
Foresterhill,
Aberdeen,
Scotland
Email: j.ferguson@nhs.net
Tel 00-44-1224-550506
Keywords: Intracranial haemorrhage, warfarin, prothrombin complex
concentrate
Word Count 675
We welcome the review of this common clinical problem and broadly
agree with the conclusions arrived at by Leiblich and Mason1. One aspect
of management that requires further investigation is the appropriate
strategy for reversal of anticoagulation.
Clinical studies consistently demonstrate that there is a higher incidence
of intracranial haemorrhage (ICH) in patients who are anticoagulated with
warfarin compared with controls who are not. Whilst there may be an
increased risk of ICH, which is attributable to the indication for
anticoagulation, there is a strong rationale to indicate that
anticoagulation per se contributes to the increased bleeding risk in this
group. As such, in the context of ICH in an anticoagulated patient there
is a rationale, although little evidence, for reversal of anticoagulation.
Our contention is that if anticoagulation is to be reversed then there is
a strong rationale for achieving this as quickly and completely as
possible. Although in the Swedish study, cited by Leiblich and Mason, the
outcomes were apparently poorer for recipients of PCC compared with FFP it
is highly likely that this observation resulted from clinical bias towards
the use of PCC in patients with more severe head injury or in those
perceived by the investigators to be at a higher risk of ICH than those
given FFP or nothing2. In reality, prothrombin complex concentrates are
likely to provide significant benefits over fresh frozen plasma for the
rapid reversal of the anticoagulant effect of warfarin. PCCs are
manufactured from pooled non-UK donor plasma, and subjected to two virus
inactivation or removal steps while FFP is a single donor product which,
at present in the UK, is still made from UK donor plasma with the
attendant risks of vCJD transmission. FFP is blood group specific and the
delay associated with determining blood group and thawing plasma for
clinical use is not shared by PCC, which may be stored in a pharmacy,
clinical areas or blood banks and is available for immediate release upon
request. PCC requires about 10 minutes for re-constitution from its
lyophilised state. The reversal of warfarin anticoagulation using
coagulation factors is all about replacing the factors II, VII, IX and X,
which are depleted by the action of warfarin. PCC contains all of these
factors in a high concentration but no other procoagulant factors while
FFP contains all the circulating prothrombotic factors in a dose of
approximately 1u/ml. Although, this is subject to significant variation
between units. To reverse an INR of >5 in a 70 Kg patient, based on
manufacturers recommendations, would entail giving a dose of around 3000
units of PCC which would be delivered in a volume of 120-140 ml over
between 18 and 40 minutes. The equivalent dose of FFP to deliver this dose
of coagulation factors is around 3000 ml, which would predictably take
hours to infuse and which would be more likely to be associated with
circulatory overload. The only possible caveat of the use of PCC is that
there have been reports of subsequent thrombotic events in recipients3.
The role of PCC in these events is unclear as they are occurring in a
group with a pre-existing risk of thrombotic events sufficient to warrant
warfarin therapy. In addition, these patients may have had an additional
acute prothrombotic event which resulted in the need for reversal.
However, even bearing this small risk in mind, the prognosis for
anticoagulant related ICH is so poor that this small risk is unlikely to
detract from the overall potential benefit of reversal. Finally, a recent
economic appraisal comparing the use of FFP and PCC within the UK
healthcare system indicates that there is a cost benefit for the use of
PCC as opposed to FFP in anticoagulated patients presenting with ICH4.
In summary, although there are few good data to support rapid reversal of
anticoagulation in patients on warfarin who sustain ICH, there is a strong
rationale for this. We would suggest, in fitting with UK national
guidelines5, that where reversal is considered appropriate this should be
achieved using PCC as opposed to FFP for the reasons outlined above
Conflict of interest declaration
HGW received a lecture fee from CSL Behring in 2007
JF has no conflict of interest to declare
References
1. Leiblich A & Mason S Emergency management of minor head injury in
anticoagulated patients. Emerg Med J. 2011;28:115-118
2. Sjoblom L, Hardemark HG, Lindgren A et al Management and prognostic
features of intracerebral hemorrhage during anticoagulant therapy: a
Swedish multicenter study. Stroke 2001;32:2567-2574
3. K?hler M, Hellstern P, Lechler E et al. Thromboembolic complications
associated with the use of prothrombin complex and factor IX concentrates.
Thromb Haemost. 1998;80(3):399-402.
4. Guest JF, Watson HG, Limaye S. Modelling the cost-effectiveness of
prothrombin complex concentrate compared to fresh frozen plasma in
emergency warfarin reversal in the UK. Clinical Therapeutics 2011 (in
press)
5 .Baglin TP, Keeling DM, Watson HG; British Committee for Standards in
Haematology. Guidelines on oral anticoagulation (warfarin): third edition
-2005 update. Br J Haematol. 2006;132(3):277-85.
We read with interest the study published in this month's EMJ by
Aldous et al. High-Sensitivity troponin T for early rule-out of
myocardial infarction in recent onset chest pain. (1) This study adds to
the growing body of published evidence that points to the safe use of new
high-sensitivity troponin assays earlier in the patient journey.(2,3,4)
The authors quite rightly point out that further prospective testing is...
We read with interest the study published in this month's EMJ by
Aldous et al. High-Sensitivity troponin T for early rule-out of
myocardial infarction in recent onset chest pain. (1) This study adds to
the growing body of published evidence that points to the safe use of new
high-sensitivity troponin assays earlier in the patient journey.(2,3,4)
The authors quite rightly point out that further prospective testing is
required.
The current aim of emergency department research surrounding
suspected cardiac chest pain is to allow identification of a patient group
that can be safely discharged following rapid rule-out of MI with very
low (ideally <1%) Major Adverse Cardiac Event (MACE) rates. In the
recently published ASPECT Study (5) Than et al. identified such a group
using a combination of risk-scoring (using the TIMI score), ECG and
negative point-of-care biomarkers for myocardial necrosis (CK-MB,
myoglobin and "low-sensitivity" troponin) tested at 0 and 2 hours giving
MACE rates of 0.08%. However, the cost effectiveness of point-of-care
biomarker testing has recently been questioned,(6) and therefore the focus
has switched to new laboratory high-sensitivity troponin assays.
We note that the cohort of patients investigated by Aldous et al. had
a high prevalence of high-risk clinical features prior to troponin
testing (52% had ischaemic heart disease and 33% had prior
revascularisation). This may have contributed to the relatively higher
MACE rates of 1.2% observed in this study, and highlights the Bayesian
argument regarding pre-test probability. We suggest that improved early
risk stratification using a combination of history, risk factors and ECG
may improve the accuracy of early high-sensitivity troponin. However, a
risk score appropriate for this purpose has yet to be identified. One
problem with current risk score systems, such as the TIMI(7) and GRACE(8),
is that they were developed to identify high rather than low risk
individuals. Furthermore, they often require knowledge of troponin and
angiography results. Further validation of risk scores is required.
At a time when there is increased focus on the new Emergency
Department Quality Indictors, it is strongly recommended that Patient
Satisfaction should be taken into account. (9) We have found no published
evidence that patients have increased satisfaction when discharged earlier
following an episode of chest pain assessed by accelerated chest pain
protocols. Rather, may patients actually prefer to be admitted to
hospital for a longer period of observation following what is an
undoubtedly a high-anxiety presentation? Qualitative research in this
area is also required.
REFERENCES
1. Aldous S, Pemberton C, Richards AM, et al. High-sensitivity
troponin T for early rule-out of myocardial infarction in recent onset
chest pain. Emerg Med J 2011
2. Keller T, Zeller T, Peetz D, Tzikas S, Roth A, Czyz E, Bickel C,
Baldus S, Warnholtz A, Frohlich M, Sinning CR, Eleftheriadis MS, Wild PS,
Schnabel RB, Lubos E, Jachmann N, Genth-Zotz S, Post F, Nicaud V, Tiret L,
Lackner KJ, Munzel TF, Blankenberg S. Sensitive troponin I assay in early
diagnosis of acute myocardial infarction. N Engl J Med 2009; 361:868-77.
3. Reichlin T, Hochholzer W, Bassetti S, Steuer S, Stelzig C,
Hartwiger S, Biedert S, Schaub N, Buerge C, Potocki M, Noveanu M,
Breidthardt T, Twerenbold R, Winkler K, Bingisser R, Mueller C. Early
diagnosis of myocardial infarction with sensitive cardiac troponin assays.
N Engl J Med 2009; 361:858-67.
4. Body R, Carley S, McDowell G, Jaffe AS, France M, Cruickshank K,
Wibberley C, Nuttall M, Mackway-Jones K. Rapid exclusion of acute
myocardial infarction in patients with undetectable troponin using a high-
sensitivity assay. J Am Coll Cardiol 2011; 58:1332-9.
5. Than M, Cullen L, Reid CM, Lim SH, Aldous S, Ardagh MW, Peacock
WF, Parsonage WA, Ho HF, Ko HF, Kasliwal RR, Bansal M, Soerianata S, Hu D,
Ding R, Hua Q, Seok-Min K, Sritara P, Sae-Lee R, Chiu TF, Tsai KC, Chu FY,
Chen WK, Chang WH, Flaws DF, George PM, Richards AM. A 2-h diagnostic
protocol to assess patients with chest pain symptoms in the Asia-Pacific
region (ASPECT): a prospective observational validation study. Lancet.
2011 Mar 26;377(9771):1077-84.
6. Fitzgerald P, Goodacre SW, Cross E, Dixon S. Cost-effectiveness of
point-of-care biomarker assessment for suspected myocardial infarction:
the randomized assessment of treatment using panel Assay of cardiac
markers (RATPAC) trial. Acad Emerg Med. 2011 May;18(5):488-95.
7. Antman EM, Cohen M, Bernink PJ, McCabe CH, Horacek T, Papuchis G,
Mautner B, Corbalan R, Radley D, Braunwald E. The TIMI risk score for
unstable angina/non-ST elevation MI: A method for prognostication and
therapeutic decision making. JAMA. 2000 Aug 16;284(7):835-42.
8. Fox KA, Eagle KA, Gore JM, Steg PG, Anderson FA; GRACE and GRACE2
Investigators. The Global Registry of Acute Coronary Events, 1999 to 2009-
-GRACE. Heart. 2010 Jul;96(14):1095-101.
9. Department of Health (UK). A & E Clinical Quality Indicators.
Epub 2010 Dec.
I have recently read the case report "A complication of the use of an
intra-osseous needle" by Helm, Goller, Hackenbroch and Hossfeld published
online in your Emergency Medicine Journal June 2, 2011. This is a well
written and informative article that discusses the uses and potential
complications of intra-osseous infusion.
I am concerned about the actual FAST1 device that was used in this
case report. This wa...
I have recently read the case report "A complication of the use of an
intra-osseous needle" by Helm, Goller, Hackenbroch and Hossfeld published
online in your Emergency Medicine Journal June 2, 2011. This is a well
written and informative article that discusses the uses and potential
complications of intra-osseous infusion.
I am concerned about the actual FAST1 device that was used in this
case report. This was an older version that still provided a removal tool
to remove the metal portal ("end of the needle"). Pyng, the manufacturer
of the FAST1 redesigned the FAST1 over 4 years ago because of a limited
number of reports of the portal being left in the sternum during the
removal procedure. The redesigned FAST1 strengthened the portal-plastic
tubing connection and did away with the need for a removal tool. The last
of the FAST1's with the removal tool was shipped over 3 years ago.
Specifically, these devices were last shipped in AUG 2008. The newly
designed devices without the removal tool began to be shipped in NOV 2007.
Additionally, the product has a stated shelf life or expiration date 2
years after manufacturing.
Therefore the device that was reported in this case study was over 3
years old. Some of the reasons that the FAST1 has a 2 year shelf life are
sterility and a possible degradation of components exposed to the
potentially harsh climates (extremes of heat, cold and humidity) that the
military routinely trains and operates in.
As a retired military physician I am well aware of the military
logistics systems, cost constraints and the need sometimes to "use what
you have". This brings up the more significant issue of patient safety
and in this case, training safety. Almost all medical materiel, from the
FAST1 to medications, IV fluids and various electronic monitoring,
treatment and diagnostic devices have a designated shelf life or
expiration date. These dates are determined by detailed studies and
regulatory practices. Use of any medical materiel beyond its expiration
date for any reason poses a serious risk to the patient or in this case
training volunteers. Regardless of where one practices medicine from a
"brick and mortar" medical center or hospital to austere frontline care it
is imperative to check and examine the expiration dates of all medical
materiel on a routine basis, from receipt through storage and prior to use
with a patient to ensure quality care and patient safety.
DR. Alan Moloff, MPH
COL (RET) U.S. Army
CMO, Pyng Medical Corp.
We read with interest the short report by Wood et al[1], and support the idea of the Emergency Department as an observatory for emerging licit/illicit novel substances. We would caution however, against the assumption that legislation has a significant impact on the consumption patterns of young drug users.
For that assumption, one would require significantly more data, from a much wider range of EDs than the relatively...
We read with interest the short report by Wood et al[1], and support the idea of the Emergency Department as an observatory for emerging licit/illicit novel substances. We would caution however, against the assumption that legislation has a significant impact on the consumption patterns of young drug users.
For that assumption, one would require significantly more data, from a much wider range of EDs than the relatively small numbers provided in their report. In our data set of 138 cases over two hospital sites, there have been 2 subsequent spikes in presentation following the banning of mephedrone, and no real signs of long-term abatement. The only effect of the ban that we could identify was a surge in presentations related to the drug, immediately prior to its ban- this also appears to be the case in Woods et als data. One could argue that the high profile announcement of the ban of mephedrone, and the associated media coverage[2] actually caused the spike in consumption, in ingénues unfamiliar with the product and keen to sample it prior to it becoming illegal. As consumers became more familiar with the less desirable, but nevertheless predictable side effects of the drug, it is possible they became less inclined to seek medical care. Even worse, it may be that consumers became reluctant to seek medical care for the effects of a now-illegal product, for fear of recriminations. Our findings reflect those of others[3], providing very little evidence that the ban on mephedrone has had any meaningful impact on its consumption.
Even if the pattern of ED presentations seen by Woods et al is merely a local one, it doesn’t necessarily imply that that is a ‘good thing’ for their population. It has been suggested that the increased use of mephedrone had resulted in a reduction of cocaine related deaths in 2009[4]- has that reversed? The likeliest reason for the diminution in the use of mephedrone is the fickle nature of the market itself, rather than any legislation, with consumers of legal highs moving on to whatever next big thing is waiting in the wings. Experience has shown, as in the cases of p-methoxyamphetamine (PMA)[5] and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)[6], that the next ‘big thing’ might not be a ‘better’ thing, but may in fact have effects far worse that those of its banned predecessor.
In an effort to avoid such oversimplifications, the Welsh Emergency Department Investigation of Novel Substances (WEDINOS) has set up a programme of systematically identifying potential novel products as they present to the emergency departments of Wales. A three pronged approach of chemical characterization of substances arriving at the Emergency Department, epidemiological tracking using GIS software, and the planned introduction of on-site rapid patient interventions allow for patterns of harm associated with consumption to be definitively delineated.
There is very little evidence that the simple ‘banning’ of any recreational product has ever had a significant impact on its availability. To assume that anything is different with mephedrone seems a little naïve. The real hazard of the legal high market are not the individual drugs themselves, but the rapid cycling of products that leaves clinicians, toxicologists and legislators alike bewildered in its wake, and the potential for the emergence of something profoundly dangerous in the evolutionary crucible that is the current online market.
Interdiction is a very crude tool to manage the subtle nuances of the ‘legal highs’ market, and data provided in the form that it has by the authors, with unsophisticated attributions of causality, are usually the remit of government departments. This report will certainly be seized upon by political bodies as a justification for action; whereas it might reflect the efficacy of government interventions in London SE1, we remain to be convinced of its validity elsewhere.
1. David M Wood, Shaun L Greene and Paul I Dargan Emergency department presentations in determining the effectiveness of drug control in the United Kingdom: mephedrone (4-methylmethcathinone) control appears to be effective using this model Emerg Med J published online October 27, 2011 doi: 10.1136/emermed-2011-200747
2. Editorial (2010). "A collapse in integrity of scientific advice in the UK". The Lancet 375 (9723): 1319–1319.
3. McElrath K, O'Neill C. Experiences with mephedrone pre- and post-legislative
controls: perceptions of safety and sources of supply. Int J Drug Policy. 2011
Mar;22(2):120-7
4. Daly, M. (September/October 2010). "Booze, bans and bite-size bags". Druglink. Drugscope. pp. 6–9. http://www.drugscope.org.uk/Resources/Drugscope/Documents/PDF/Publications/DruglinkSept-Oct2010.pdf. Retrieved 2011-01-29.
5. Caldicott DG, Edwards NA, Kruys A, Kirkbride KP, Sims DN, Byard RW, Prior M,
Irvine RJ. Dancing with "death": p-methoxyamphetamine overdose and its acute
management. J Toxicol Clin Toxicol. 2003;41(2):143-54.
6. Fahn, Stanley. The Case of the Frozen Addicts: How the Solution of an Extraordinary Medical Mystery Spawned a Revolution in the Understanding and Treatment of Parkinson's Disease. The New England Journal of Medicine. Dec 26, 1996. Vol. 335, Iss. 26; pg. 2002
We were very glad to reply your letter posted online on the emj
website in october, 6 2011. We read very carefully your concerns regarding
the verifiability of cyanide as the poisoning agent. Certainly You can
agree with us that, in a brief report with a fixed length, it is very
difficult to give all the information and in some case you have to choose
what you consider more important .
In this c...
We were very glad to reply your letter posted online on the emj
website in october, 6 2011. We read very carefully your concerns regarding
the verifiability of cyanide as the poisoning agent. Certainly You can
agree with us that, in a brief report with a fixed length, it is very
difficult to give all the information and in some case you have to choose
what you consider more important .
In this case we thank you for giving us the opportunity to clarify some
points that obviously were not so clear in the original paper.
First of all, the patient was uncooperative but not unresponsive; so
we asked her if she had effectively chewed and swallowed the apricot seeds
and she confirmed it, enjoying the bittersweet taste. We also visualized
many fragments of seeds on gastric lavage, so we were sure that she had
masticated and swallowed the seeds.
For your second objection, unfortunately we are not able to measure
cyanide levels in our emergency department, so we consider the possibility
that the metabolic acidosis with increased anion gap was due to an
abnormal lactate production, as we can see in cyanide poisoning [1].
Moreover the anamnesis of the patient was negative for
inappropriate ingestion of drugs of any kind, and she confirmed to us that
she did not ingest any other substance. She did not take medications at
home and she has no access to medications of her parents.
Finally, we reported that the patient was dyspnoic, hypotensive and she
developed metabolic acidosis with increased anion gap [2].
These symptoms, according with the anamnesis of recent ingestion of
cyanide-releasing substance, suggested us the diagnosis of cyanide
poisoning [3]. In addition the quick response of the patient to the
antidotal therapy for cyanide poisoning indirectly confirm the cyanide
intoxication.
Thank you again and best regards
Cigolini Davide, MD
Ricci Giorgio, MD
References
[1] Beasley DM, Glass WI. Cyanide poisoning : phatophysiology and treatment reccomendations. Occup Med (Lond) 1998;48:427-31
[2] Cigolini D, Ricci G, Zannoni M et al. Hydroxocobalamin treatment of acute cyanide poisoning from apricot kernels. Emerg Med J. Sep 2011;28(9):804-05
[3] Vogel SN, Sultan TR, Ten Eyck RP. Cyanide poisoning. Clin Toxicol 1981;18:367-83
Left-without-being-seen patients and nurse counselling
It is with great interest that we acknowledge the recent publication
concerning improvements that could prevent departures of patients that
left-without-being seen (LWBS) (1). Children who LWBS are an important
concern in our emergency department (ED) and we have previously reported a
proportion of LWBS of 17% during the year 2008 (2). With the
implementatio...
Left-without-being-seen patients and nurse counselling
It is with great interest that we acknowledge the recent publication
concerning improvements that could prevent departures of patients that
left-without-being seen (LWBS) (1). Children who LWBS are an important
concern in our emergency department (ED) and we have previously reported a
proportion of LWBS of 17% during the year 2008 (2). With the
implementation of many strategies, we were able to reduce that number to
10% in two years. Such improvements include screening patients for minor
symptoms using pre-established criteria during the quick look evaluation.
Once identified, these patients can be fast tracked without being triaged,
to a minor care clinic within the ED where they are seen by a physician
that is working collaboratively with a nursing assistant. Other measures
have also been suggested (3).
Ibanez et al suggest that when the personnel is aware of a patient
who is about to LWBS, appropriate information should be provided (1). This
should be emphasized, as we have recently demonstrated that patients who
receive counselling by a nurse before leaving have a 24% relative risk
reduction in their return visits within the next 48 hours compared to
those who left without warning and thus could not be warranted the
appropriate counselling (2). Indeed, only 6.1% of patients counselled
prior to departure returned to the ED compared to 8.1 % who did not
benefit from any advice before leaving the ED (2). Without necessarily
decreasing the rate of LWBS, this measure, also greatly improves the
quality of care provided to these patients.
Interestingly enough, our waiting room is about to undergo a major
make-over using a Cirque du Soleil theme. We are hopeful that, with your
results suggesting that patients request more comfortable waiting rooms,
this measure will also contribute to decreasing the LWBS in our ED.
Benoit Bailey MD MSc FRCPC, Michael Arseneault MD FRCPC, Arielle Levy
MD MEd FRCPC, Jocelyn Gravel MD MSc FRCPC
Division of Emergency Medicine
Department of Pediatrics
CHU Sainte-Justine
Montreal, Qc
Competing Interest: None to declare.
Word count: 296 (excluding title and references)
Key word: paediatric emergency medicine; management.
References
1. Ibanez G, Guerin L, Simon N. Which improvements could prevent the
departure of the left-without-being-seen patients? Emerg Med J 2011; 28:
945-947.
2. Gaucher N, Bailey B, Gravel J. For children leaving the emergency
department before being seen by a physician, counselling from nurses
decreases return visits. Int Emerg Nurs 2011; 19: 173-177.
3. Wiler JL, Gentle C, Halfpenny JM, et al. Optimizing emergency
department front-end operations. Ann Emerg Med 2010; 55: 142-160.
We have previously expressed concerns about the validity of the
"clinical bottom line" published alongside the popular Best BETS. (1) Best
BETS should be based on specific clinical scenarios and should aim to
provide a clinical bottom line which indicates, in the light of the
evidence, what the clinician would do if faced with the same scenario
again. (2) The report by Olaussen and Williams serves to...
We have previously expressed concerns about the validity of the
"clinical bottom line" published alongside the popular Best BETS. (1) Best
BETS should be based on specific clinical scenarios and should aim to
provide a clinical bottom line which indicates, in the light of the
evidence, what the clinician would do if faced with the same scenario
again. (2) The report by Olaussen and Williams serves to remind us, again,
that unless Best BETS are rigorously conducted their conclusions may be
highly inappropriate.(3)
Olaussen and Williams wonder how different intraosseous (IO) access
techniques and devices compared in the pre-hospital setting. Their review
of the literature to May 2010 concluded that: "Traditional manual
intraosseous infusion devices have better success rates and faster
insertion times compared with semi-automatic intraosseous infusion devices
in the prehospital setting".
Evidence based medicine is the conscientious, explicit, and judicious
use of current best evidence in making decisions about the care of
individual patients.(4) Good evidence answers a highly specific question
and the results are similarly specific to the circumstances. Olaussen and
Williams ask a poorly focused question and do not define (a) the
circumstances surrounding pre-hospital IO access,? (b) the range of
devices and points of access or (c) the outcome measures. Available IO
devices include hand held needles (e.g. Cook and Jamshidi), spring-loaded
needle devices for the limbs (e.g. Bone Injection Gun) and sternum (e.g.
FAST device) and electric drill type devices (e.g. EZ-IO).
The structured question used by Olaussen and Williams does not
sufficiently distinguish the patient group, intervention, comparator or
outcome. To compound this, the 2100 reports identified in the literature
search were, without any explanation of the filter used, reduced down to
two. Indeed one of the two selected reports does not even involve the use
of manually inserted IO devices, lending no support to their conclusions.
Even a cursory search of the primary literature will identify several
relevant reports comparing first attempt success rates, ease of use and
speed of insertion for a variety of IO devices.(5-9) Olaussen and Williams
synthesis of the two reports they chose to review may well be correct but
the information is out-of-date, the search strategy is incomplete and the
conclusion entirely inappropriate and clinically misleading.
The EMJ has a responsibility to ensure that Best BETS are properly
conducted and reviewed. This is not the first time that clinical bottom
lines with major implications have been questionable - perhaps it is time
to review the process again?
Dr Alistair Steel, Consultant Anaesthetist, The Queen Elizabeth
Hospital, Kings Lynn
Dr David Bevan, General Practitioner, Upwell, Cambridgeshire
Mr Dan Cody, Paramedic, East of England Ambulance Service
Dr Simon Lewis, Consultant in Emergency Medicine, Addenbrookes
Hospital, Cambridge
Dr Rod Mackenzie, Consultant in Emergency Medicine, Addenbrookes
Hospital, Cambridge
Dr Ben Teasdale, Consultant in Emergency Medicine, Leicester Royal
Infirmary, Leicester
Mr Ryan Warwick, Paramedic, East of England Ambulance Service
All authors are members of the Magpas Prehospital Emergency Medical
Team and have been trained in and have used clinically a variety of
devices for intra-osseous access in the prehospital setting.
1. French J, Steel A, Clements R et al., Best Bets: A call for
scrutiny. Emerg Med J 2006;23:490.
2. Mackway-Jones K. Towards evidence based emergency medicine: Best
BETs from the Manchester Royal Infirmary. Emerg Med J2005;22:887.
3. Olaussen A, Williams B. Which intraosseous device is best in the
prehospital setting. Emerg Med J 2011;28:717.
4. Sackett DL, Rosenberg WMC, Gray JAM, et al. Evidence based
medicine: what it is and what it isn't. BMJ1996;312:71-72.
5. Sunde GA, Heradstveit BE, Vikenes BH, Heltne JK. Emergency
intraosseous access in a helicopter emergency medical service: a
retrospective study. Scandinavian Journal of Trauma, Resuscitation and
Emergency Medicine 2010
6. Frascone RJ, Jensen JP, Kaye K, Salzman JG. Consecutive field
trials using two different intraosseous devices. Prehospital Emergency
Care 2007;11:164-71.
7. Calkins MD, Fitzgerald G, Bentley TB, Burris D. Intraosseous
infusion devices: a comparison for potential use in special operations. J
Trauma. 2000;48:1068-1074
8. Shavit I, Hoffmann Y, Galbraith R, Waisman Y.
Comparison of two mechanical intraosseous infusion devices: a pilot,
randomized crossover trial. Resuscitation. 2009;80:1029-33.
9. Leidel BA, Kirchhoff C, Braunstein V, Bogner V, Biberthaler P,
Kanz KG.
Comparison of two intraosseous access devices in adult patients under
resuscitation in the emergency department: A prospective, randomized
study. Resuscitation. 2010;81:994-9.
Conflict of Interest:
All authors are members of the Magpas Prehospital Emergency Medical Team and have been trained in and have used clinically a variety of devices for intra-osseous access in the prehospital setting.
We congratulate Cigolini and colleagues on their case report of
apparent cyanide poisoning from apricot kernels[1]. However, we have
several concerns regarding the verifiability of cyanide as the poisoning
agent. These concerns were not addressed in the case description or in a
limitations section.
First, while the patient was surrounded by apricot kernels, ingestion
of the kernels was not verified visually (...
We congratulate Cigolini and colleagues on their case report of
apparent cyanide poisoning from apricot kernels[1]. However, we have
several concerns regarding the verifiability of cyanide as the poisoning
agent. These concerns were not addressed in the case description or in a
limitations section.
First, while the patient was surrounded by apricot kernels, ingestion
of the kernels was not verified visually (on lavage), on questioning of
the patient, or radiographically. In addition, to release hydrogen
cyanide, the kernels must be masticated, which was not described in the
case[2,3].
Second, cyanide exposure was not documented. A cyanide level was not
reported. A lactate acidosis is common, but a serum lactate level was not
reported after the patient became symptomatic, which would support a
diagnosis of cyanide toxicity[4]. In addition, a "mentally ill" and
"uncooperative" patient could have ingested almost any chemical, object,
or medication (including her own, which were not mentioned). Confirmatory
drug or chemical urine and blood testing with gas chromatography mass
spectrometry or thin layer chromatography was not reported.
Finally, cyanide toxic patients typically develop significant
sedation, apnea, and lactic acidosis before developing hypotension5. None
of these symptoms was reported. The patient's tachycardia and hypotension
could have been from antipsychotic medications, tricyclic antidepressants,
or dihydropyridine calcium channel blocker as from cyanide.
Hydroxocobalamin increased the patient's blood pressure; however, with its
nitric oxide scavenging effects, it increased blood pressure even in
healthy volunteers.
In summary, as written the case description does not confirm this
patient was exposed to and intoxicated by cyanide.
Vikhyat Bebarta, MD
Shawn M. Varney, MD
References
1. Cigolini D, Ricci G, Zannoni M, et al. Hydroxocobalamin treatment
of acute cyanide poisoning from apricot kernels. Emerg Med J. Sep
2011;28(9):804-805.
2. Kerns W, Isom G, Kirk MK. Cyanide and Hydrogen Sulfide. In:
Goldfrank LR, ed. Goldfrank's toxicologic emergencies. 7th ed ed. New York
:: McGraw-Hill, Medical Pub. Division; 2002:1498-1510.
3. Suchard JR, Wallace KL, Gerkin RD. Acute cyanide toxicity caused
by apricot kernel ingestion. Ann Emerg Med. Dec 1998;32(6):742-744.
4. Baud FJ, Borron SW, Megarbane B, et al. Value of lactic acidosis
in the assessment of the severity of acute cyanide poisoning. Crit Care
Med. 2002;30(9):2044-2050.
5. Bebarta VS, Tanen DA, Lairet J, Dixon PS, Valtier S, Bush A.
Hydroxocobalamin and sodium thiosulfate versus sodium nitrite and sodium
thiosulfate in the treatment of acute cyanide toxicity in a swine (Sus
scrofa) model. Ann Emerg Med. Apr 2010;55(4):345-351.
Luscombe et al [1] are to be congratulated for developing a more
accurate age-based paediatric weight estimation tool than that previously
commonly used in the UK. Perhaps modesty prevented them mentioning that
their formula has also been incorporated into the 5th edition of the
Advanced Paediatric Life Support manual, for 6-12 year olds [2]. It is
important for readers to realise that in their art...
Luscombe et al [1] are to be congratulated for developing a more
accurate age-based paediatric weight estimation tool than that previously
commonly used in the UK. Perhaps modesty prevented them mentioning that
their formula has also been incorporated into the 5th edition of the
Advanced Paediatric Life Support manual, for 6-12 year olds [2]. It is
important for readers to realise that in their article, the inaccurate
'APLS formula' refers to the previous edition of APLS.
However, it is unfortunate that their study makes no mention of the
precision of either formula. Although the new formula has minimal bias
(ie, the mean difference between estimated and actual weight), all age-
based weight formulae have very poor precision, which can be indicated by
the standard deviation of the differences. In our study published in this
journal in May [3], we demonstrated the results of Bland Altman analysis
of 11 different age-based formulae. For all these formulae, the 95% limits
of agreement (defined as +/- 2 standard deviations of the difference) were
approximately +/- 40%. In other words, using any age-based formulae, 95%
of estimated weights can be expected to lie within +/- 40% of actual
weight. Many readers might consider that such imprecision is potentially
very unsafe: weight-dependent drug and fluid doses do not all have such a
large safety margin.
Luscombe et al suggested that the Broselow tape is particularly
useful 'if the age is not known'. The Broselow tape has far better
precision that any age-based formula, and is extremely accurate (ie,
minimal bias) as well. It's true that it can sometimes be difficult to
measure a child's length, but we have also shown that mid-arm
circumference (MAC, cm) can be used to estimate weight with comparable
bias and precision to the Broselow tape, in 6-12 year olds. The formula is
simple: weight = 3x(MAC-10).[4]
This formula needs to be validated in a UK population, and until then
we would recommend the use of the Broselow tape to ensure precision of
weight estimation in children. Age-based formulae should only be used when
other more precise methods are unavailable.
Sincerely,
Dr Giles N Cattermole (South London Healthcare NHS Trust)
Prof Colin A Graham (Chinese University of Hong Kong)
Prof Timothy H Rainer (Chinese University of Hong Kong)
1. Luscombe MD, Owens BD, Burke D. Weight estimation in paediatrics:
a comparison of the APLS formula and the formula 'Weight=3(age)+7'. Emerg
Med J 2011;28:590-3.
2. Advanced Life Support Group. Advanced paediatric life support. 5th
edn, London: BMJ Publishing Group, 2011.
3. Cattermole GN, Leung MPY, So HK, Mak PSK, Graham CA, Rainer TH.
Age-based formulae to estimate children's weight in the emergency
department. Emerg Med J 2011;28:390-6.
4. Cattermole GN, Leung PYM, Mak PSK, Graham CA, Rainer TH. Mid-arm
circumference can be used to estimate children's weights. Resuscitation
2010;81:1105-10.
We read this intriguing case report with great interest. However, it
contained two specific weaknesses which undermined its strength, leaving
it inconclusive. The critical point is not whether caffeine excess might
cause seizures (this is known), or the theoretical pathophysiology
(comprehensively discussed in the article), but whether it was the
definitive cause of seizures in this case.
We read this intriguing case report with great interest. However, it
contained two specific weaknesses which undermined its strength, leaving
it inconclusive. The critical point is not whether caffeine excess might
cause seizures (this is known), or the theoretical pathophysiology
(comprehensively discussed in the article), but whether it was the
definitive cause of seizures in this case.
Firstly, without measuring the serum caffeine concentration (or at
least its metabolite, theophylline - a widely available assay in acute
hospitals for therapeutic purposes) it is impossible to know how much
credence to place on the role of caffeine in this case.
Secondly, there was no mention of serum sodium, potassium or
creatinine kinase measurements. Sodium and potassium gradients across the
cell membrane exert a major effect on the stability of excitable cells,
especially neurone and skeletal muscle respectively[1]. Potassium
gradients are affected directly by hydrogen ion concentrations.
Hypokalaemia predisposes to tachyarrhythmias, potentially leading to
seizures through secondary cerebral anoxia. There is a complex interplay
between electrolyte disturbances (especially hypokalaemia and acid-base
disturbance), cardiac arrhythmias and seizures - each predisposing to the
others, and in turn being predisposed to by the others. Arguably, the
biochemical data in this case were consistent with recent seizure
activity, irrespective of its precipitant.
In a patient with a previous cerebral infarct and 'vascular
encephalopathy', both significant risk factors for seizure, it is very
difficult to know what part each of the relevant contributory factors
played. The reference cited for seizure incidence post-stroke [2] looks
at the influence of major co-morbidities (which this patient did not
apparently have) on the outcome, in particular mortality, and without
mentioning seizure per se. That said, the incidence of idiopathic
epilepsy is well known to vary greatly by age and other factors, none of
which was discussed quantitatively for this case.
As the report says, any seizure occurs when the seizure threshold is
lowered sufficiently by the prevailing circumstances. With so many
interdependent co-variates in this case (underlying structural brain
lesion, past history of substance abuse and possible withdrawal, acute
kidney injury, electrolyte and acid-base disturbances, as well as possible
rhabdomyolysis) in addition to the possibility of caffeine, it is
impossible to judge the latter's likely contribution. Sadly this adds no
weight to the quoted case report [3] which also omitted relevant
toxicological data.
A case report needs the relevant data to allow a conclusive judgement
to be made!
[1] Goldstein LB et al. Charlson Index comorbidity adjustment for
ischaemic stroke outcome studies. Stroke 2004;35:1941-5
Letter to the Editor Henry G Watson* & James Ferguson *Department of Haematology Aberdeen Royal Infirmary, Foresterhill, Aberdeen, Scotland AB25 2ZN Email: henrywatson@nhs.net Tel 00-44-1224-553394
Department of Emergency Medicine Aberdeen Royal Infirmary, Foresterhill, Aberdeen, Scotland Email: j.ferguson@nhs.net Tel 00-44-1224-550506 Keywords: Intracranial haemorrhage, warfarin, prothrombin complex concentr...
We read with interest the study published in this month's EMJ by Aldous et al. High-Sensitivity troponin T for early rule-out of myocardial infarction in recent onset chest pain. (1) This study adds to the growing body of published evidence that points to the safe use of new high-sensitivity troponin assays earlier in the patient journey.(2,3,4) The authors quite rightly point out that further prospective testing is...
I have recently read the case report "A complication of the use of an intra-osseous needle" by Helm, Goller, Hackenbroch and Hossfeld published online in your Emergency Medicine Journal June 2, 2011. This is a well written and informative article that discusses the uses and potential complications of intra-osseous infusion.
I am concerned about the actual FAST1 device that was used in this case report. This wa...
Dear Collegues,
We were very glad to reply your letter posted online on the emj website in october, 6 2011. We read very carefully your concerns regarding the verifiability of cyanide as the poisoning agent. Certainly You can agree with us that, in a brief report with a fixed length, it is very difficult to give all the information and in some case you have to choose what you consider more important . In this c...
Left-without-being-seen patients and nurse counselling
It is with great interest that we acknowledge the recent publication concerning improvements that could prevent departures of patients that left-without-being seen (LWBS) (1). Children who LWBS are an important concern in our emergency department (ED) and we have previously reported a proportion of LWBS of 17% during the year 2008 (2). With the implementatio...
Dear Sirs,
We have previously expressed concerns about the validity of the "clinical bottom line" published alongside the popular Best BETS. (1) Best BETS should be based on specific clinical scenarios and should aim to provide a clinical bottom line which indicates, in the light of the evidence, what the clinician would do if faced with the same scenario again. (2) The report by Olaussen and Williams serves to...
We congratulate Cigolini and colleagues on their case report of apparent cyanide poisoning from apricot kernels[1]. However, we have several concerns regarding the verifiability of cyanide as the poisoning agent. These concerns were not addressed in the case description or in a limitations section.
First, while the patient was surrounded by apricot kernels, ingestion of the kernels was not verified visually (...
Dear Editor,
Luscombe et al [1] are to be congratulated for developing a more accurate age-based paediatric weight estimation tool than that previously commonly used in the UK. Perhaps modesty prevented them mentioning that their formula has also been incorporated into the 5th edition of the Advanced Paediatric Life Support manual, for 6-12 year olds [2]. It is important for readers to realise that in their art...
We read this intriguing case report with great interest. However, it contained two specific weaknesses which undermined its strength, leaving it inconclusive. The critical point is not whether caffeine excess might cause seizures (this is known), or the theoretical pathophysiology (comprehensively discussed in the article), but whether it was the definitive cause of seizures in this case.
Firstly, without meas...
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