I welcome Matthew Reed's article emphasising the role of nitrates in
the emergency management of severe acute cardiogenic pulmonary oedema
(ACPO). I also welcome his appreciation of the dead space involved in the
use of any cannula, which so often seems to be ignored.
ACPO occurs as a result of decompensation of the left ventricle
initiating a circle of increasing preload, often with incr...
I welcome Matthew Reed's article emphasising the role of nitrates in
the emergency management of severe acute cardiogenic pulmonary oedema
(ACPO). I also welcome his appreciation of the dead space involved in the
use of any cannula, which so often seems to be ignored.
ACPO occurs as a result of decompensation of the left ventricle
initiating a circle of increasing preload, often with increasing
afterload, in the presence of worsening oxgenation. Any intervention that
acutely improves oxygenation and/or reduces preload (and afterload) will
often initiate a recovery. The quicker this occurs the more likely the
patient will make a prompt recovery.
The use of intravenous nitrates is a very effective means of reducing
preload and subsequently improving cardiac output but there is inevitably
a delay in initiating this therapy. This delay, as Matthew Reed points
out, will be exacerbated by using a slow infusion rate through a wide bore
cannula.
I would therefore advocate the use of sublingual or buccal nitrates
as soon as the condition is recognised (and this is often in the pre-
hospital phase) which 'buys time' to set up a nitrate infusion. I would
also advocate initiating any nitrate infusion at the higher end of the
recommended dose schedule (12mg/hour for glyceryl trinitrate, 10mg/hour
for isosorbide dinitrate). This not only overcomes the potential dead
space issue but more importantly ensures the patient will receive an
effective dose in an appropriate timescale. These patients are usually
critically unwell and will be managed in a high dependency area of any
hospital. They will therefore be closely observed. Any adverse effect of
high dose nitrates on perfusion pressure, which is uncommon in ACPO in my
experience, can be easily managed by titrating back on the infusion rate.
We must overcome many practitioners, in Emergency as well as other
specialities, use of less effective treatments in what is an extremely
distressing and potentially life threatening condition.
I enjoyed the article on shock and circulatory support in the
Emergency Department.[1] Early and aggressive resuscitation of patients
with shock is known to improve outcome, as shown in the Emmanuel Rivers et
al paper used as the first reference.[2] I was disappointed, however, to
find an important component of that study had not been mentioned.
Following the establishment of an adequate centr...
I enjoyed the article on shock and circulatory support in the
Emergency Department.[1] Early and aggressive resuscitation of patients
with shock is known to improve outcome, as shown in the Emmanuel Rivers et
al paper used as the first reference.[2] I was disappointed, however, to
find an important component of that study had not been mentioned.
Following the establishment of an adequate central venous pressure
and mean arterial blood pressure, the next step of the protocol was to
measure the patients’ mixed central venous saturations. This was used as
an indication of the oxygen delivery and consumption. If the ScvO2 fell
below 70%, the patient was given red blood cell transfusions to achieve a
haematocrit of at least 30% to optimise oxygen delivery. If ScvO2 remained
below 70% after these measures, dobutamine was administered to improve
cardiac output. This method of balancing systemic oxygen delivery and
consumption was shown to improve subsequent oxygen delivery to tissues,
pH, lactate, base deficit and severity-of-illness scores.
The optimisation of the three parameters in the first six hours of
presentation significantly reduced mortality(2) .Dr Rivers said himself of
goal directed therapy, “Mainly the key is to look at three things: volume,
pressure and oxygen delivery (via central venous oxygen)…”. While Graham
and Parke’s review covered the first two, it was a shame that the equally
important third was omitted.
References
1. Graham C, Parke T. Critical care in the emergency department: shock
and circulatory support. Emerg Med J 2005;22: 17-21.
2. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy
in the treatment of severe sepsis and septic shock. N Engl J Med
2001;345:1368-77.
We were interested in the recent NICE guideline review by Dunning
& Lecky [1], in particular the extrapolation of the Canadian head CT
rule for adults to a paediatric population. We retrospectively audited
children with head injury presenting to the emergency department of
Birmingham Heartlands & Solihull hospital for the months of June 2003
and December 2003. Case notes were reviewed to dete...
We were interested in the recent NICE guideline review by Dunning
& Lecky [1], in particular the extrapolation of the Canadian head CT
rule for adults to a paediatric population. We retrospectively audited
children with head injury presenting to the emergency department of
Birmingham Heartlands & Solihull hospital for the months of June 2003
and December 2003. Case notes were reviewed to determine whether skull
radiograph, CT scan of the head, or admission to hospital would be
indicated if NICE guidelines for head injury were followed.
During the 2 months 206 children attended with head injury (90 in
June 2003 and 116 in December 2003). Median age was 5 years, (range 0.03-
16 years) . Of the 206 children, 88 (42.7%) had skull radiographs (one
skull fracture detected), 10 (4.9%) had CT scan of the head performed (no
abnormality detected) and 34 (16.5%) were admitted under existing head
injury guidelines. No children required transfer to a neurosurgical unit.
Application of the NICE guidelines for head injury would result in 14
(7.0%) children still requiring skull radiographs, 26 (12.6%) children
having a CT head performed and 16 (7.8%) children being admitted for
persisting symptoms.
Of the additional 16 CT scans that would be performed under NICE head
injury guidelines [2], 12 were due to “dangerous mechanism of injury”, 3
due to more than two vomits, and 1 due to amnesia for greater than thirty
minutes of events prior to head injury. All 16 patients were discharged on
the day of hospital attendance with head injury advice. None re-attended
the hospital.
Our study suggests that if we implemented the new NICE guidelines the
number of CT head scans performed would increase from an average of 5 to
13 a month, with a reduction in hospital admissions for head injury.
Extrapolating adult CT guidelines to children may be inappropriate,
especially since children may have a higher risk of harm from ionising
radiation [3]. Paediatricians need to decide whether the risk of increasing childrens’ exposure to ionising radiation is justified or whether to await
studies involving children due to report next year.
P Debenham, S Adalat, F A Riordan
Department of Child Health, Birmingham Heartlands Hospital, Birmingham, UK
Correspondence to: Dr P Debenham, Department of Child Health,
Birmingham Heartlands Hospital, Bordesley Green East, Birmingham, B9 5SS,
UK; phillip.debenham@heartsol.wmids.nhs.uk
References
(1) Dunning J, Lecky F. The NICE guidelines in the real world: a
practical perspective. Emerg Med J 2004;21:404-7
(2) National Institute for Clinical Excellence. Head injury. Triage,
assessment, investigation and early management of head injury in infants,
children and adults. Clinical guideline 4. Developed by the National
Collaborating Centre for Acute Care. London: National Institute for
Clinical Excellence, 2003
(3) Hall P, Adami H, Trichopoulos D, Pedersen N, Lagiou P, Ekbom A,
Ingvar M, Lundell M, and Granath F. Effect of low doses of ionising
radiation in infancy on cognitive function in adulthood: Swedish
population based cohort study
BMJ, Jan 2004; 328: 19 - 23
In his letter entitled ‘Counting Angels’, Dr Mason dismisses our
attempt to challenge the doctrine of always using an un-cuffed tracheal
tube for emergency intubation of children as irrelevant and meaningless
(1). His arguments are that we should challenge the perceived ‘gold
standard’ role of emergency tracheal intubation in the pre-hospital
setting (for all patients) and consider using supra-glot...
In his letter entitled ‘Counting Angels’, Dr Mason dismisses our
attempt to challenge the doctrine of always using an un-cuffed tracheal
tube for emergency intubation of children as irrelevant and meaningless
(1). His arguments are that we should challenge the perceived ‘gold
standard’ role of emergency tracheal intubation in the pre-hospital
setting (for all patients) and consider using supra-glottic airway devices
more often. We don’t disagree. There are, as Dr Mason points out, a number
of reasons why non-specialist teams and individuals should carefully
consider these matters. This was not however the subject of our paper.
Our paper was stimulated by direct personal experience of managing
critically injured children within the context of established active pre-
hospital critical care and retrieval teams in the UK (the Magpas Emergency
Medical Team (EMT) and the London Helicopter Emergency Medical Service).
We emphasized that our discussion “rests with not whether these children
should be intubated but what they should be intubated with” (2). The key
point, as Dr Mason reminds us, is that “patients die from a failure to
oxygenate and a failure to ventilate, not from a failure to intubate”.
While there is clearly an evolving role for other forms of ventilation
and/or airway devices, pre-hospital emergency anaesthesia and tracheal
intubation is an established, safe and efficient way of optimizing
oxygenation and ventilation when undertaken by competent practitioners
within a properly supported system. It also mirrors current in-hospital
practice. We stand by our conclusion that practitioners should consider
using cuffed tracheal tubes in this highly selected group of critically
injured and ill children.
Of course ATLS needs to be reformed,[1] and perhaps we could start
by abandoning the tortured ABCDE mnemonic.
Many major trauma patients are conscious and in this situation the
first thing to do is take a brief History. Breathing and Airway are part
of the same process, and surely the patient should be immediately Exposed
to allow examination. And if Disability means a core neurological
exami...
Of course ATLS needs to be reformed,[1] and perhaps we could start
by abandoning the tortured ABCDE mnemonic.
Many major trauma patients are conscious and in this situation the
first thing to do is take a brief History. Breathing and Airway are part
of the same process, and surely the patient should be immediately Exposed
to allow examination. And if Disability means a core neurological
examination, then please can we say so.
As to the ATLS course itself, this takes too long and this causes
problems filling faculty places. This in turn limits the number of courses
held, and how many providers can be trained. With modern distance learning
techniques it should be possible to do most of the coursework beforehand,
requiring only a 36hr event to teach practical skills and to examine.
Dr Gori, Cinotti and Papagallo's concerns [1] reflect the
inexperience of many medical staff in the use of adrenaline to treat
anaphylaxis, a misunderstanding of the ethical issues relating to our
trial, and perhaps over-reliance on invasive measures of severity that are
a sign of sustained and untreated cardiorespiratory collapse. To deal with
each comment in turn:
Dr Gori, Cinotti and Papagallo's concerns [1] reflect the
inexperience of many medical staff in the use of adrenaline to treat
anaphylaxis, a misunderstanding of the ethical issues relating to our
trial, and perhaps over-reliance on invasive measures of severity that are
a sign of sustained and untreated cardiorespiratory collapse. To deal with
each comment in turn:
- Even Mueller Grade I reactions can be extremely uncomfortable; in
many patients these are florid, cause significant discomfort, and are
associated with unbearable itching, severe malaise and marked anxiety. In
our experience these symptoms respond immediately to adrenaline, but
respond slowly (and unreliably) when treatment is limited to
antihistamines and steroids.
- Ethically we were required to offer patients the opportunity to
withdraw from the study at any time. This included the use of adrenaline
to treat extremely uncomfortable and distressing symptoms. Nevertheless,
no patient requested the use of adrenaline prior to our objective criteria
for intervention being met.
- Intravenous adrenaline infusion, regulated by an electronic infusion pump
and supervised by experienced doctors as in our study, is a safe method of
giving adrenaline. Because there is no absorption phase and a very short
half-life, the effect of any infusion rate change is almost immediate and
adverse effects can be stopped immediately by ceasing or reducing the rate of
infusion. Conversely, intravenous, large intramuscular, and even subcutaneous
boluses of adrenaline can result in significant adverse reactions [2].
- Gori et al claim that "late side effects due to adrenaline
intravenous (may occur in) cardiopathic patients". We are unaware of any
evidence or anecdotal experiences for this occuring in the absence of
earlier signs such as ECG changes, ischaemic chest pain and cardiovascular
instability.
- So-called "biphasic" reactions are a poorly understood phenomenon.
In our experience many such reactions are actually due to an ongoing
(rather than biphasic) reaction, unmasked as an intramuscular bolus of
adrenline slowly wears off. An advantage of using an intravenous infusion
of adrenaline is that when turned off, ongoing reactions are immediately
unmasked. In our study this occured in 7/11 (64%) of people with Grade
III/IV reactions [3]. After discharge according to our criteria, no
patient suffered a biphasic reaction. True biphasic reactions are
exceedingly rare (and generally mild) in the setting of ant sting
anaphylaxis [4]. Prolonged &/or biphasic reactions may be more
frequent in severe reactions due to ingested allergen [5]. Therefore, the
discharge criteria used in our very select study group was appropriate,
but of course should not be extrapolated to the general management of
anaphylaxis.
- The measurement of arterial pH and pO2 were not performed because
firstly, the invasiveness (and risk) of arterial puncture/line insertion
was not justifiable for a condition almost always manageable without this
intervention. Secondly, significant changes in PaO2 (<_60 mmhg="mmhg" are="are" reliably="reliably" detected="detected" by="by" an="an" spo2="spo2" below="below" _92="_92" this="this" was="was" continually="continually" monitored.="monitored." thirdly="thirdly" a="a" fall="fall" in="in" ph="ph" would="would" be="be" late="late" feature="feature" due="due" to="to" tissue="tissue" hypoxia-="hypoxia-" we="we" did="did" not="not" feel="feel" it="it" ethical="ethical" wait="wait" so="so" long="long" before="before" treating="treating" with="with" adrenaline="adrenaline" p="p"/> Finally, we must emphasise that our study was performed in an
idealised setting on a select group of patients treated by experienced
consultant emergency physicians. Further studies are required in the
general emergency department setting. In the meantime we encourage doctors
not to use treatments with which they are unfamiliar, and to instead
consider established consensus guidelines. That is, intramuscular
adrenaline (0.3-0.5 mg in adults) as first line treatment, repeated if
necessary after 5 minutes.
References
(1) Gori L, Cinotti S, Pappagallo S. Risks of Overzelous Adrenalin
Administration [electronic response to Brown et al. Insect sting
anaphylaxis; prospective evaluation of treatment with intravenous
adrenaline and volume resuscitation] emjonline.com 2004
http://emj.bmjjournals.com/cgi/eletters/21/2/149#277
(2) Horowitz BZ, Jadallah S, Derlet RW. Fatal intracranial bleeding
associated with prehospital use of epinephrine. Ann Emerg Med 1996;28:725-
7.
(3) SGA Brown, KE Blackman, V Stenlake, and R J Heddlel.: Insect sting
anaphylaxis; prospective evaluation of treatment with intravenous
adrenaline and volume resuscitation. Emerg Med J 2004; 21: 149-154.
(4) Brown SGA, Franks RW, Baldo BA, Heddle RJ. Prevalence, severity,
and natural history of jack jumper ant venom allergy in Tasmania. J
Allergy Clin Immunol 2003;111:187-92.
(5) Stark BJ, Sullivan TJ. Biphasic and protracted anaphylaxis. J
Allergy Clin Immunol 1986;78:76-83.
After reviewing Drs. Boudreaux and Bewley report entitled “Death from
paracetamol overdose despite appropriate treatment with N-acetylcysteine
“(1) we must disagree with their conclusions. The authors described a
patient who was treated appropriately with N-acetylcysteine after a large
acetaminophen overdose. The patient was initially stable, but
decompensated after 8 hours, developed multi-system...
After reviewing Drs. Boudreaux and Bewley report entitled “Death from
paracetamol overdose despite appropriate treatment with N-acetylcysteine
“(1) we must disagree with their conclusions. The authors described a
patient who was treated appropriately with N-acetylcysteine after a large
acetaminophen overdose. The patient was initially stable, but
decompensated after 8 hours, developed multi-system organ failure after 72
hours and then died 84 hours after admission. During this time the only
evidence of liver injury was a mild elevation of serum transaminase and a
transient elevation of the INR. The authors attribute this patient’s
death to the failure of acetylcysteine to prevent acetaminophen toxicity.
The course of acetaminophen poisoning has been described numerous
times since the mid 1970s. Typical acetaminophen toxicity results in
hepatic necrosis and death from hepatic failure over several days. N-
acetylcysteine effectively prevents hepatic injury when administered early
in the course of poisoning.
In the past 20 years, another pattern of toxicity has been described
following massive overdose. These cases developed a marked lactic
acidosis, coma and hyperglycemia (2;3). However, hepatic damage is
minimal and most patients recover with supportive therapy and
acetylcysteine. One case report even described a patient who goes on to
developed multi-system failure similar to the current case3. The
manifestations are due to mitochondrial dysfunction, an effect not
reversed by acetylcysteine. The case described by Boudreaux and Bewley is
consistent with this presentation. Parenthetically, this case report does
not provide sufficient information to determine if other causes (such as
ethylene glycol) were excluded, and these alternative causes would also
not be expected to respond to acetylcysteine.
The authors imply that this patient’s death was a failure of N-
acetylcysteine therapy. An alternative interpretation is that this
patient developed renal and pulmonary failure and died as a complication
of metabolic disturbances from his massive acetaminophen poisoning or
another, unrecognized cause, and acetylcysteine prevented the hepatic
injury that would have otherwise occurred.
Case reports are a valuable source of information for medical
toxicology. Many poisonings are rare and case reports offer the only
available information. However, authors, reviewers and editors must
assure that the report provides sufficient information to assess the
validity of the author’s conclusions, and that the authors consider
alternative interpretations of that information.
Kennon Heard MD
Richard C. Dart MD, PhD
Rocky Mountain Poison and Drug Center, Denver Health
University of Colorado School of Medicine
Department of Surgery (Emergency Medicine)
Denver CO, USA
Reference List
1. Bourdeaux C,.Bewley J. Death from paracetamol overdose despite
appropriate treatment with N-acetylcysteine. Emerg Med J 2007;24:e31.
2. Roth B, Woo O, Blanc P. Early metabolic acidosis and coma after
acetaminophen ingestion. Ann Emerg Med 1999;33:452-6.
3. Flanagan RJ,.Mant TG. Coma and metabolic acidosis early in severe
acute paracetamol poisoning. Hum Toxicol 1986;5:179-82.
I am interested in the nurological effects of N2O. At a seminar that
I attended 6 years ago it was brought out that N2O was very similar in
nurological side effects as wine. It was stated by a medical professor
that N2O did indead kill about the same amount of brain cells due to the
lack of oxegen to the brain cells. Recentlly a inter-office discussion
resulted in that question being raised again. Does...
I am interested in the nurological effects of N2O. At a seminar that
I attended 6 years ago it was brought out that N2O was very similar in
nurological side effects as wine. It was stated by a medical professor
that N2O did indead kill about the same amount of brain cells due to the
lack of oxegen to the brain cells. Recentlly a inter-office discussion
resulted in that question being raised again. Does N2O kill brain
cells(although it only be a few)? Doing resurch I have come acrossed two
different views on that. Can you clear up this matter with factual proof
and references?
The UK criteria for the diagnosis of brain death[1] would prevent the
diagnostic confusion encountered by Agarwal et al.[2] Included in the
preconditions, before brainstem testing can proceed, is that the patient’s
condition should be due to irremediable brain damage of known aetiology.
Whilst this may be immediately apparent such as in massive head injury or
intracerebral haemorrhage, for patients wit...
The UK criteria for the diagnosis of brain death[1] would prevent the
diagnostic confusion encountered by Agarwal et al.[2] Included in the
preconditions, before brainstem testing can proceed, is that the patient’s
condition should be due to irremediable brain damage of known aetiology.
Whilst this may be immediately apparent such as in massive head injury or
intracerebral haemorrhage, for patients with possible global hypoxic
damage it may take days to establish that the injury is irremediable.
The authors do not mention which agents were used to facilitate
endotracheal intubation in their case. The UK criteria stipulate that
there should be no evidence that the patient’s clinical state is due to
depressant drugs or the effects of neuromuscular blocking agents. Use of
a nerve stimulator to exclude neuromuscular blockade may have aided
diagnosis in this patient.
The ‘locked-in’ syndrome consists of quadriplegia and anarthria with
preservation of consciousness.[3] Vertical eye movements are retained. The
syndrome is usually caused by damage affecting the ventral pons or more
rarely by destruction of corticobulbar and corticospinal tracts. Whilst
extremely rare, the condition should be considered as ten-year survival
for these patients has been reported to be as high as 80%. Non-verbal
communication may be established using the preserved vertical eye
movements.
Guidance for the performance of brain death tests varies worldwide.[4] The
UK criteria recommend the use of ancillary tests such as cerebral
angiography, transcranial doppler or EEG in situations where testing is
clinically difficult such as local trauma that precludes full assessment
of cranial nerve function. In other countries, the use of such tests is
mandatory. Reassuringly, a follow-up survey of over 1300 patients
diagnosed as brain dead on the basis of the UK criteria, found that all
patients suffered cardiorespiratory death even if full supportive measures
were continued.[5]
Published reports have identified a number of other conditions that may
mimic brain death.6 To these should be added envenomation with
neuroparalytic agents such as that descibed by Agarwal et al.
References
1.Health Departments of Great Britain and Northern Ireland. A code of
practice for the diagnosis of brain stem death including guidelines for
the identification and management of potential organ and tissue donors.
London: HMSO,1998.
2.Agarwal R, Singh N, Gupta D. Is the patient brain-dead? Emerg Med J
2006;23:e5.
3.Smith E, Delargy M. Locked-in syndrome. BMJ 2005;330:406-409
4.Wijdicks EFM. Brain death worldwide; accepted fact but no global
consensus in diagnostic criteria. Neurology 2002;58:20-25.
5.Pallis C. Brain stem death – the evolution of a concept. Med Leg J.
1987;2:84-104.
6.Powner DJ, Hernandez M, Rives TE. Variability among hospital policies
for determining brain death in adults. Crit Care Med 2004;32:1284-1288.
I read with interest and agreement over the article by Kane et
al.,[1] as well as the eletter response of Reed published on 16 September.
For trauma patients requiring mechanical ventilation it is vitally
important to diagnose pneumothorax promptly. However these are the
conditions (supine anteroposterior films) in which chest radiography is
likely to perform not as well. Thoracic CT scan is super...
I read with interest and agreement over the article by Kane et
al.,[1] as well as the eletter response of Reed published on 16 September.
For trauma patients requiring mechanical ventilation it is vitally
important to diagnose pneumothorax promptly. However these are the
conditions (supine anteroposterior films) in which chest radiography is
likely to perform not as well. Thoracic CT scan is superior, but more time
is required. Another modality for the diagnosis of pneumothorax is
ultrasound.
It has recently been shown that thoracic ultrasound can reliably
diagnose pneumothorax, and that surgical residents are able to complete
the focused scanning within 2-3 minutes.[2] Hence this modality is faster
than radiography or CT scan. Its utility may benefit the trauma patient
about to undergo mechanical ventilation, and may be incorporated in the
focused abdominal sonography for trauma (FAST) exam. More research in the
ultrasound diagnosis of pneumothorax is needed before it can be widely
used.
References
(1) Kane TP, Nuttall MC, Bowyer RC, and Patel V. Failure of detection
of pneumothorax on initial chest radiograph. Emerg Med J 2002;19:468-469.
(2) Dulchavsky SA, Schwarz KL, Kirkpatrick AW, Billica RD, Williams
DR, Diebel LN, Campbell MR, et al. Prospective evaluation of thoracic
ultrasound in the detection of pneumothorax. J Trauma 2001;50:201-205.
Dear Editor,
I welcome Matthew Reed's article emphasising the role of nitrates in the emergency management of severe acute cardiogenic pulmonary oedema (ACPO). I also welcome his appreciation of the dead space involved in the use of any cannula, which so often seems to be ignored.
ACPO occurs as a result of decompensation of the left ventricle initiating a circle of increasing preload, often with incr...
Dear Editor
I enjoyed the article on shock and circulatory support in the Emergency Department.[1] Early and aggressive resuscitation of patients with shock is known to improve outcome, as shown in the Emmanuel Rivers et al paper used as the first reference.[2] I was disappointed, however, to find an important component of that study had not been mentioned.
Following the establishment of an adequate centr...
Dear Editor
We were interested in the recent NICE guideline review by Dunning & Lecky [1], in particular the extrapolation of the Canadian head CT rule for adults to a paediatric population. We retrospectively audited children with head injury presenting to the emergency department of Birmingham Heartlands & Solihull hospital for the months of June 2003 and December 2003. Case notes were reviewed to dete...
Dear Editor,
In his letter entitled ‘Counting Angels’, Dr Mason dismisses our attempt to challenge the doctrine of always using an un-cuffed tracheal tube for emergency intubation of children as irrelevant and meaningless (1). His arguments are that we should challenge the perceived ‘gold standard’ role of emergency tracheal intubation in the pre-hospital setting (for all patients) and consider using supra-glot...
Dear Editor
Of course ATLS needs to be reformed,[1] and perhaps we could start by abandoning the tortured ABCDE mnemonic.
Many major trauma patients are conscious and in this situation the first thing to do is take a brief History. Breathing and Airway are part of the same process, and surely the patient should be immediately Exposed to allow examination. And if Disability means a core neurological exami...
Dear Editor
Dr Gori, Cinotti and Papagallo's concerns [1] reflect the inexperience of many medical staff in the use of adrenaline to treat anaphylaxis, a misunderstanding of the ethical issues relating to our trial, and perhaps over-reliance on invasive measures of severity that are a sign of sustained and untreated cardiorespiratory collapse. To deal with each comment in turn:
- Even Mueller Grade I re...
Dear Editor,
After reviewing Drs. Boudreaux and Bewley report entitled “Death from paracetamol overdose despite appropriate treatment with N-acetylcysteine “(1) we must disagree with their conclusions. The authors described a patient who was treated appropriately with N-acetylcysteine after a large acetaminophen overdose. The patient was initially stable, but decompensated after 8 hours, developed multi-system...
Dear Editor
I am interested in the nurological effects of N2O. At a seminar that I attended 6 years ago it was brought out that N2O was very similar in nurological side effects as wine. It was stated by a medical professor that N2O did indead kill about the same amount of brain cells due to the lack of oxegen to the brain cells. Recentlly a inter-office discussion resulted in that question being raised again. Does...
Dear Editor,
The UK criteria for the diagnosis of brain death[1] would prevent the diagnostic confusion encountered by Agarwal et al.[2] Included in the preconditions, before brainstem testing can proceed, is that the patient’s condition should be due to irremediable brain damage of known aetiology. Whilst this may be immediately apparent such as in massive head injury or intracerebral haemorrhage, for patients wit...
Dear Editor
I read with interest and agreement over the article by Kane et al.,[1] as well as the eletter response of Reed published on 16 September. For trauma patients requiring mechanical ventilation it is vitally important to diagnose pneumothorax promptly. However these are the conditions (supine anteroposterior films) in which chest radiography is likely to perform not as well. Thoracic CT scan is super...
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