This 55 yo man presented with a plasma paracetamol level of 534 mg/L
at 4 hours post ingestion and was treated with adequate doses of
intravenous acetylcysteine. Peak ALT was 145 U/L and peak INR was 2.5
both drawn 72 hours post ingestion. He met none of the King's College
criteria for paracetamol-induced liver failure and transplant. The patient
died of ARDS and a "deteriorating cardiovascular st...
This 55 yo man presented with a plasma paracetamol level of 534 mg/L
at 4 hours post ingestion and was treated with adequate doses of
intravenous acetylcysteine. Peak ALT was 145 U/L and peak INR was 2.5
both drawn 72 hours post ingestion. He met none of the King's College
criteria for paracetamol-induced liver failure and transplant. The patient
died of ARDS and a "deteriorating cardiovascular status" at 84 hours post
ingestion. The autopsy revealed a normal liver.
The authors conclude that acetylcysteine failed. I would argue that
the antidotal therapy was hepatoprotective since the patient did not die
of hepatic failure. Extensive toxicological analysis should have been
performed, as per history this is a mixed drug overdose. In my
experience, review of 300-400 toxicological deaths reported to my Poison
Center over the last 10 years, I have found that post mortem toxicological
analysis changes the cause of death in up to 25% of cases.
Suzanne Doyon, MD
Medical Director
Maryland Poison Center
Baltimore, MD 21201
Maxwell-Armstrong et al[1] have apparently done a significant amount
of work in sampling the current state of knowledge among haematology
technicians on the performance of Diagnostic Peritoneal Lavage (DPL)
analysis. They also report on surgeons’ experience of the procedure. Their
analysis and conclusions, however, seem not to be supported by this data.
Indeed, their paper climaxes with propos...
Maxwell-Armstrong et al[1] have apparently done a significant amount
of work in sampling the current state of knowledge among haematology
technicians on the performance of Diagnostic Peritoneal Lavage (DPL)
analysis. They also report on surgeons’ experience of the procedure. Their
analysis and conclusions, however, seem not to be supported by this data.
Indeed, their paper climaxes with propositions relating to the use of
ultrasound, for the relative superiority of which they have collected as
much evidence as for fortune-telling.
Despite my own high level of interest in the use of ultrasound, I
cannot but disagree with the methods used by the authors in analysing the
use of its “rival” – DPL.
The authors surveyed technician’s experience in the analysis of DPL
specimens and this was found apparently lacking. They then still accepted
these same technicians’ opinions about how this procedure is or should be
performed. They question the fine details of which fluid is used and in
which container it is send when a surgeon would struggle to find a fluid
or container which would be inadequate regardless of what the technician
knew of this. And I would not trust an estimate of an hour to analyse a
sample – it is likely that this was received from those less experienced
technicians who were merely guessing.
To suggest that an investigation be abandoned because it is not as
available as one would like is irresponsible. Only a few years ago, one
would have envied such a level of accessibility to, say, CT scanning for
head injuries or cardiac enzymes for chest pain, as has been identified
herein for DPL. Gratefully, we did not abandon the use of CT then for
these reasons. It would only take a minimal investment to reach an
acceptable level of knowledge and protocols in labs.
As for surgeons’ experience, the data presented was poorly
representative (48% response) and poorly analysed. To claim that there is
little increase in experience with duration in post is misleading. A
closer look at their own data would have reassured the authors. For
example, 51 of 54 consultants with fewer than 2 years’ experience
performed DPL (94%) – an average of 47% per year of work. The figure is
282 of 333 (85%) for those with over 10 years’ experience, which, assuming
10-25 years of practise in this group, is 3.4-8.5% per year worked.
Ignoring pre-consultant exposure for both groups, this shows recently
trained consultants are around 10 times more likely to perform DPL per
year of practise and will thus be more experienced by the time they have
10 years behind them.
No comparative figures were presented on surgeons’ experience in the
performance of ultrasound or on the availability of other trained users
and the costs involved in ultrasound equipment and training. To reach
competence (and hence sensitivity) in the use of ultrasound is certainly
more time-consuming and costly than to perfect the use of DPL.
In addition, the ATLS guidelines referred to in the article were compiled
primarily for physicians working in smaller set-ups, not for the “major
units” surveyed. In the latter, most patients will have CT scans unless
unstable enough to need immediate surgery.
Despite the problems presented by ultrasound in the circumstances of
suspected intra-peritoneal haemorrhage – operator
inexperience/unavailability, obese or previously operated patients,
subcutaneous air, etc. – it is still probably worthy of attention. But our
approach must be scientific.
References
(1) Maxwell-Armstrong C, Brooks A, Field M, Hammond J, Abercrombie J.
Diagnostic peritoneal lavage analysis: should trauma guidelines be
revised. Emergency Medicine Journal 2002;19(6): 524-525.
Dr Halpern's article about the development of EM training in Israel
is quite informative and can be relevant to many other countries in the
middle east.
However, I would like to enquire about how senior physicians who are
already trained in their respective specialties and run their own private
clinics were persuaded to leave all that and enter another 2.5 years of EM
specialist training - th...
Dr Halpern's article about the development of EM training in Israel
is quite informative and can be relevant to many other countries in the
middle east.
However, I would like to enquire about how senior physicians who are
already trained in their respective specialties and run their own private
clinics were persuaded to leave all that and enter another 2.5 years of EM
specialist training - the so called 'Grandfather clause'.
I'm sure this wasn't an easy task to do. Is EM in Israel still looked
upon as a young specialty run by young single (i.e. no family commitment)
doctors or has that view changed like in the US and UK? Was EM portrayed
to them as a 'glamorous' specialty or do EM physicians have a better
salary than other specialists? Did they choose to train or were they
formally asked to join an EM training program? Are these physicians still
allowed to run private clinics after being trained in EM and what are
their working hours like?
Article named Lower limb amputation with CPR in progress: recovery
following prolonged cardiac arrest(Ref1) is very interesting as well as
thought provoking. Such clinical scenario is not only rare but needs a
good team effort to come to a clinical judgement. Amputation in acute
scenario in the absence of obvious vascular injury is definitely a brave
decision.
Article named Lower limb amputation with CPR in progress: recovery
following prolonged cardiac arrest(Ref1) is very interesting as well as
thought provoking. Such clinical scenario is not only rare but needs a
good team effort to come to a clinical judgement. Amputation in acute
scenario in the absence of obvious vascular injury is definitely a brave
decision.
I would be grateful for the authors if my doubts can be clarified
1) There are many causes of hyperkalemia and how the team treating
could come to a conclusion that the hyperkalemia was caused by the
rhabdomyolysis of foot.
2) Drugs like cocaine, heroine can cause rhabdomyolysis (of any muscle), disseminated intra vascular coagulation, hyperkalemia and
arrythmias which can be made worse by naloxone (Ref2). In the presented
clinical situation these possibilities cannot be ruled out.
3) Arterial blood gas values of this patient would be very
interesting to see as well, with particular emphasis on acidosis and anion
gap.
4) If limb ischaemia and reprfusion of the ischaemic limb are
considered as the cause of hyperkalemia, application of tourniquet or
clamping of the vessels can act as diagnostic test rather than going for
an amputation.
5) What are the parameters that the teams used to determine the level
of initial amputation and what was the initial level of amputation.
Thanking you
Yours sincerely
Mr Sreenadh Gella
SPR Orthopaedics
Calderdale Royal Hospital
Reference
1. R Wise1, I Higginson2, J Benger2 and N Rawlinson1 Lower limb
amputation with CPR in progress: recovery following prolonged cardiac
arrest, Emergency Medicine Journal 2006;23:e20; doi:10.1136/emj.2005.
2. McCann B, Hunter R, McCann J. Cocaine/heroin induced
rhabdomyolysis and ventricular fibrillation.Emerg Med J. 2002
May;19(3):264-5.
We thank Dr Duby for his interest in our paper and comments.
We think he
misses its fundamental points - the majority of haematology technicians
cannot analyse DPL specimens, and the paucity of experience with the
procedure. Similarly this paper is not a review of the efficacy of
ultrasound.
Dr Duby comments on our asking technicians on how DPL samples are
analysed, even though they f...
We thank Dr Duby for his interest in our paper and comments.
We think he
misses its fundamental points - the majority of haematology technicians
cannot analyse DPL specimens, and the paucity of experience with the
procedure. Similarly this paper is not a review of the efficacy of
ultrasound.
Dr Duby comments on our asking technicians on how DPL samples are
analysed, even though they felt they could not perform it. The
heterogeneity in the responses obtained merely highlights the fact that
these technicians really dont have a clue. His comments regarding
investing in DPL are risible - why invest in DPL, when you have a probably
better alternative - US? What exactly was the alternative to head CT all
those years ago
We accept his criticisms about a response rate of 48%. This does however
reflect 854 responses...His comments about "recently trained
consultants..." assumes that these consultants use DPL for the next 10
years, and are actually involved in trauma care at the sharp end. The
comments in the final two paragraphs are valid.
While I normally find the Best BETs both informative and useful, I was
surprised at the publishing of one concerning gastric lavage in drug overdose
[1].
Gastric lavage is both dangerous and without benefit in all but a few
overdoses. The 1997 Joint Position Statement made by the American Academy
of Clinical Toxicology, and the European Association of Poisons Centres
stated that gastric lavage s...
While I normally find the Best BETs both informative and useful, I was
surprised at the publishing of one concerning gastric lavage in drug overdose
[1].
Gastric lavage is both dangerous and without benefit in all but a few
overdoses. The 1997 Joint Position Statement made by the American Academy
of Clinical Toxicology, and the European Association of Poisons Centres
stated that gastric lavage should never be routinely used [2].
A statement on the National Poisons Information Website (TOXBASE)
indicates that gastric lavage should only be considered in a case of a
potentially life-threatening overdose taken within the last hour of a
poison that is not adsorbed by charcoal.
To state that gastric lavage is no better than charcoal as a clinical
bottom line at reducing toxicity following aspirin or non-steroidal anti-
inflammatory drugs is at Best misleading.
References
(1) Teece S. Gastric lavage in aspirin and non-steroidal anti-
inflammatory drug overdose. Emerg Med J 2004;21:591-592.
(2) American Academy of Clinical Toxicology and European Association
of Poisons Centres. Gastric Lavage. J Clin Toxicol-Clin Toxicol
1997;35:711-719.
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The considerable pain caused by common partial thickness cutaneous
burns is widely acknowledged to be a difficult therapeutic problem.
Growing evidence has shown peripheral opioid receptors to be a potentially
exploitable target for topical analgesic intervention. The efficacy of
topical opioids at various time points following burns, and the relative
effectiveness of their use for various burn dept...
The considerable pain caused by common partial thickness cutaneous
burns is widely acknowledged to be a difficult therapeutic problem.
Growing evidence has shown peripheral opioid receptors to be a potentially
exploitable target for topical analgesic intervention. The efficacy of
topical opioids at various time points following burns, and the relative
effectiveness of their use for various burn depths remains to be
elucidated, so we welcome Welling’s contribution to this field.
We work within a large burns service, and have used 10 to 30mg of
topical morphine on a selection of burn wounds for over a year, mixing it
primarily with Flamazine® cream. Thus far, we have been impressed by its
efficacy and the longevity of its action. In our hands however, its use
has been confined to cases responding poorly to conventional systemic
analgesic regimes and has therefore rarely seen use as early in the post-
burn period as the scenario described by Welling’s study.
Interpretation of published burns research is unfortunately often
compromised by disparity in nomenclature pertaining to burn depth.
Unfortunately, as the study’s title alludes, this is also true in this
study. During Peter Shakespeare’s editorship of the International Journal
of Burn Care, he attempted to standardise this nomenclature to the
anatomical definitions of:
• deep dermal partial thickness (epidermis & deeper dermis)
• full thickness
“Partial thickness” essentially refers to all burns less than full
thickness, and therefore in itself is inadequate to describe burn depth.
It is unclear from the published study what depths of burns have been
included. Elucidation of burn depth warrants further attention, as it may
correlate with the efficacy of topical morphine, because where the
epidermis is retained (superficial burns) this may provide a barrier to
topical absorption. Also, the deeper the burn, the greater the oedema and
the worse the vascularity, which is likely to influence tissue penetration
and the bioavailability profile. Furthermore, the absorption of morphine
through glabrous skin (palms & soles) is likely to be considerably
impaired and we would anticipate hand burns to have made a substantial
contribution to the subjects studied, but no distinction has been made.
There are certain problems we commonly see with burns treated by non-
specialists. Firstly, there is inadequacy of burn debridement; all
blisters should be removed, as they represent an infection risk.
Admittedly, at first attendance in A&E, they are often initially absent or
incompletely formed, complicating this first assessment. This problem
should be approached by rubbing the burned area with gauze to mechanically
shear off the roof of blisters-to-be. This is required if TBSA is to be
correctly assessed (purely superficial burns are excluded from TBSA
assessment). Failure to debride blisters will present a considerable
barrier to absorption of topical analgesics (epidermis + thick fluid
layer). It may be the case that such burn assessment and debridement was
performed, but simply not reported.
Following thorough debridement and wound toilet, any burn deeper than
superficial depth which is not being directly referred for specialist
management should be dressed with antimicrobial dressings. The rate of
infection in burns treated without topical antimicrobials (or inadequately
debrided) is unacceptably high and this carries the consequence of
increasing burn depth, delaying healing, worsening scarring and increases
the proportion of burns requiring skin-grafting. This common misconception
is in part attributable to advice given by burns services, who generally
prefer the omission of topical antimicrobials in cases they have been
referred, so that on admission the wound surface is not obscured by such
substances (however antimicrobials are then applied after assessment). The
omission of topical antimicrobials to burns should be the exception, not
the rule, and is reserved almost exclusively for cases experiencing
hypersensitivity to such agents. Paraffin tulle dressings are now falling
from favour due to a high incidence of adherence to the burn wound and
granuloma formation. Favoured alternatives include the silicone based
Mepitel® and lotion impregnated Atrauman® dressings. Six-layer Jelonet®
dressings are not to be recommended, as at this thickness they are
relatively impermeable, compromising the function of the dressing. We
therefore take exception to the dressings chosen for the study.
The study unfortunately has no statistically significant findings, in
part due to inadequate subject inclusion, failing to meet the calculated
requirement of 21 subjects in each arm of the study. The results of the
visual analogue pain scores are compromised by systemic analgesia
administration not having been standardised. However, all subjects
received paracetamol and/or ibuprofen at admission, and assessment of the
VAS over the duration of action of these analgesics is therefore the least
biased. Over this period, the morphine group was the only group to see a
VAS reduction of >20mm on two consecutive time intervals and overall,
the VAS for the morphine group fell to 30% of its pre-treatment value,
compared to 43% and 40% for the other two groups. Whilst this does not
reach statistical significance, this is likely attributable to inadequate
numbers rather than an absence of therapeutic effect. The finding closest
to reaching statistical significance was of subjects in the morphine group
requiring less analgesia after discharge.
The results presented in Table 5 summarise the total analgesic units
for each group; the topical morphine has also been attributed analgesic
units for each subject and this included in the final analysis. We would
argue that to test the hypothesis of whether topical morphine works
topically on fresh burn wounds, this treatment arm should not be
attributed these additional analgesic units as their effect as analgesia
is unproven and this is what is on test. This amendment would lend support
to the hypothesis that topical morphine is effective in burn wounds as
other studies have shown.
Previous work includes the cited pilot study by Long , in which
subjects <72h following <25% TBSA burns were divided into two
treatment arms, each comprising two patients. One arm received morphine
infused silver sulfadiazine cream, whilst the control arm received plain
silver sulfadiazine cream. Twice daily dressing changes using these
compounds occurred twice daily for 4 days, but none of the patients
remained in the study until its conclusion. The study found pain levels
and anxiolytic usage to be reduced, but was limited by small study size.
More recently, Robertson showed peripheral opioid receptor
stimulation by fentanyl is opposed by naloxone in healthy subjects with
standardised experimental burns. Volunteers’ bilateral forearm burns had
saline subcutaneously injected on one side and naloxone on the other. Heat
pain threshold and mechanical pain ratings were found to be similar at the
two sites. Subsequently, fentanyl was injected at both sites, and
following this, heat pain threshold was increased and mechanical pain
decreased at the site without naloxone. This gives further evidence of the
presence of peripheral opioid receptors very shortly after burn injury.
The bioavailability of topical opioids applied to burn wounds remains
unclear. Ribeiro’s work on topical morphine in cutaneous ulcers showed
poor bioavailability, with plasma penetration only demonstrable in 17%,
and this at only 20% of the administered dose . In the canine model,
morphine applied to peri-articular intact skin does not achieve measurable
plasma penetration, although after 2 – 4 hours it is measurable in urine
and synovial fluid in half of subjects . In view of burn eschar and burn
related hyperaemia, these findings are not necessarily transferable to the
burn scenario. Furthermore, the optimum opioid for such topical
administration remains unknown, morphine sulphate has a relatively poor
absorption profile, which diamorphine improves upon, or indeed the
enhanced lipophilicity of fentanyl may be exploited to ensure better
penetration, but this may sacrifice duration of action.
The potential for targeting of peripheral opioid receptors as a locus
of pain control early in the course of cutaneous wounds has been
established. It remains to be conclusively proven that topical morphine is
effective on burns, and from what time point this is effective, as it is
uncertain how long opioid receptors take post-injury before they appear in
peripheral tissues, though “minutes to hours” has been quoted by Stein,
who has carried out much research into peripheral opioid receptors . From
the results of Robertson’s study, it is likely that topical opioids are an
appropriate intervention as early as the first dressing. It also remains
to be elucidated what is the most appropriate opioid, at what dose, and
what nuances exist within specific wounds such as burns (efficacy in
different burn depths, duration of action etc.). Welling’s study is a
welcome addition to the sparse research in this area, although we would
interpret her results differently and urge reconsideration in the choice
of burn dressings used.
1. Shakespeare PG. Standards and quality in burn treatment. Burns.
2001; 27(8): 791-792
2. Long TD, Cathers TA, Twillman R, O’Donnell T, Garrigues N, Jones
T. Morphine-infused silver sulfadiazine (MISS) cream for burn analgesia: a
pilot study. Journal of Burn Care and Rehabilitation. 2001; 22(2): 118-123
3. Robertson LJ, Drummond PD, Hammond GR. Naloxone antagonizes the
local antihyperalgesic effect of fentanyl in burnt skin of healthy humans.
The Journal of Pain. 2007; 8(6): 489-493
4. Ribeiro MDC, Joel SP, Zeppetella G. The bioavailability of
morphine applied topically to cutaneous ulcers. Journal of Pain and
Symptom Management. 2004; 27(5): 434-439
5. Moore DP, Parikh R, Vernick SH, Petroski GF, Pryor WH, Kazmierczak
SC. Topical morphine in a canine model: a pilot study. Archives of
Physical Medicine and Rehabilitation. 1998; 79(9): 1034-1037
6. Stein C. The control of pain in peripheral tissue by opioids. New
England Journal of Medicine. 1995; 332(25): 1685-1690
Thank you for the interesting case of metformin-associated lactic
acidosis. It is a very rare complication of the most widely used drug
treatment for Type 2 diabetes.
In this case, we do not have the data regarding the patient’s previous
renal function or current creatinine levels. It however seems that the
patient was severely hypotensive with sepsis possibly from the chest. The
critical question regarding lactic acidos...
Thank you for the interesting case of metformin-associated lactic
acidosis. It is a very rare complication of the most widely used drug
treatment for Type 2 diabetes.
In this case, we do not have the data regarding the patient’s previous
renal function or current creatinine levels. It however seems that the
patient was severely hypotensive with sepsis possibly from the chest. The
critical question regarding lactic acidosis here is what proportion was
contributed by metformin and what proportion from the co-existing acute
critical illnesses. Lactic acidosis is a common feature in critically ill
patients with multiple pathologies. Metformin-associated lactic acidosis
is not necessarily due to metformin accumulation; true type B (aerobic)
lactic acidosis, i.e., without an apparent associated hypoxic factor,
seems exceptional (1). often the co-existing conditions cause lactic
acidosis rather than metformin itself. The metformin is an incidental
factor in many cases. We know that metformin inhibits hepatic
gluconeogenesis without altering lactate turnover or lactate oxidation,
unlike Phenformin. The lactic acidosis has been reported in type 2
diabetes patients not treated with metformin, in conditions where there is
tissue hypoxia or hypoperfusion (2).
In 2003, A Cochrane systematic review and meta-analysis of pooled data
from 194 studies (36893 patient- years in the metformin group) showed no
excess risk of fatal or non-fatal cases of lactic acidosis due to
metformin when compared to other anti-hyperglycemic therapy (3)
In the recently published Fremantle Diabetes study, Metformin did not
increase the risk of lactic acidosis, even when risk factors were present
(4). It is well known that metformin is widely prescribed even in patients
with known contra-indications. Even in this group, metformin associated
lactic acidosis is rare.
So in summary, cases of metformin-associated lactic acidosis have been
reported widely. However most of them have associated severe critical-
illnesses, which may be the major contributing factor causing
hyperlactataemia. Nevertheless metformin should be stopped in all cases of
lactic acidosis.
References.:-
1.Lalau JD, Lacroix C, Compagnon P, de Cagny B, Rigaud JP, Bleichner
G, et al. Role of Metformin Accumulation in metformin-associated lactic
acidosis. Diabetes Care 1995; 18:779-84
2. Aguilar C, Reza A, Garcia JE, Rull JA. Biguanide related lactic
acidosis: incidence and risk factors. Arch Med Res. 1992; 23:19-24
3. Salpeter SR, Greyber E, Pasternak GA, Salpeter EE. Risk of fatal
and nonfatal lactic acidosis with metformin use in type 2 diabetes
mellitus. Arch Intern Med 2003; 163:2594-602.
4.Kamber N, Davis WA, Bruce DG, Davis TM. Metformin and lactic
acidosis in an Australian community setting: the Fremantle Diabetes
Study. Med J Aust. 2008 Apr 21; 188(8):446-9
We read with interest the case report recently published by Agarwal R
and colleagues(1). The authors concluded, "a trial of NIV in acute asthma
may be justified in carefully selected and monitored patients who do not
respond to initial medical therapy. However, as it role is not clear and
as the condition of an asthmatic patient may deteriorate abruptly, extreme
caution is advisable to recognize failure...
We read with interest the case report recently published by Agarwal R
and colleagues(1). The authors concluded, "a trial of NIV in acute asthma
may be justified in carefully selected and monitored patients who do not
respond to initial medical therapy. However, as it role is not clear and
as the condition of an asthmatic patient may deteriorate abruptly, extreme
caution is advisable to recognize failure of NIV... Facilities for
immediate endotracheal intubation and next level of treatment should be
readily available.”
We approved these conclusions and we proposed several comments on this
case and on this management approach in accordance with our local
experience and with current state of knowledge (2-4).
In the case presented, patient was initially more hypoxemic (PaO2 8.4 kPa)
as hypercapnic (PaCO2 4.9 kPa) with a grade I of severity in first
arterial blood gas measurement. An initial chest X-ray was not described in
this case. We can postulated that NIV failed because patient was also in
acute respiratory failure secondary to a added complication (atelectasia,
pneumonia).
In our experience, NIV for patients with severe status asthmaticus not
improving under conventional medical therapy and on the edge of intubation
is the only possibility of decreasing morbidity and mortality of this
acute illness. We will try in this letter to explain our opinion.
The severity of an acute asthmatic exacerbation may be assessed using a
variety of signs like major dyspnea, tachypnea, the use of accessory
respiratory muscles, the presence of a pulsus paradoxus, a quiet chest on
auscultation and the decrease of the PEFR below 120 L/min. The appearance
of these signs and the increase of the dead space lead to an acute
respiratory failure with respiratory acidosis. This clinical condition is
not a priory an absolute indication for intubation and mechanical
ventilation. Indeed, only 8% of this population of patients needs in fine
endotracheal intubation (5). The absence of response to the optimal
medical treatment and especially the alteration of conscience are the
absolute indications of intubation. Patients with status asthmaticus have
a significant increase in both inspiratory and expiratory indexes of
airways obstruction. They have also a considerable dynamic hyperinflation.
Inspiratory muscle fatigue and increased physiologic dead space lead to
ventilatory failure and respiratory acidosis. In fact, hypercapnia does
not occur, however, unless the FEV1 is less than 25 % of predicted. The
pathophysiology of status asthmaticus includes airflow obstruction of both
large and small airways, inhomogeneous lung inflation, dynamic
hyperinflation, ventilation/perfusion mismatch and respiratory muscle
fatigue. Airway wall inflammation, smooth muscle-mediated
bronchoconstriction and intraluminal mucus explain airway obstruction.
Lung hyperinflation is primarily related to the fact that the highly
increased airway expiratory resistance, the high ventilatory needs, the
relative short expiratory time and the increased post-inspiratory activity
of inspiratory muscles do not permit the respiratory system to reach
static equilibrium volume at the end of expiration. Therefore, inspiration
begins at a volume in which the respiratory system exhibits a positive
recoil pressure. This pressure is called intrinsic positive-end expiratory
pressure (PEEPI) or auto-PEEP. At each respiratory cycle, this inflation
can increase and compromise the respiratory function. This phenomenon is
called dynamic hyperinflation and is directly proportional to minute
ventilation and to the degree of airflow obstruction. This phenomenon
causes substantial shortening of the diaphragm and the inspiratory
intercostal and accessory muscles, thereby reducing their mechanical
efficiency and endurance and increasing the risk for fatigue. As airway
obstruction becomes more serious and the work of breathing becomes
excessive, carbon dioxide production is greater than what can be
eliminated by alveolar ventilation. Therefore, PaCO2 increases and a
respiratory acidosis appears. Moreover, in asthma, large negative swings
in intrapleural pressure can significantly impair right ventricular
function.
The pathophysiologic condition of acute respiratory failure in asthma is
in many ways similar to that of acute respiratory failure in patients with
COPD. Although a large body of literature has clearly proved the efficacy
and advantages of NPPV in patients with COPD with ARF, only a few reports
had described this modality in patients with status asthmaticus. In our
experience, we found NIV simple to implement and well tolerated by our
patients with severe clinical conditions. Since many years, we known that
application of CPAP causes bronchodilatation and decreases airway
resistances, reexpands atelectasis and promotes elimination of secretions,
rests the diaphragm and inspiratory muscles and may offset PEEPI, and also
decreases the adverse hemodynamic effects of large peak and mean
inspiratory pleural pressures. CPAP is also available for reexpanding
atelectasis by increasing collateral flow (through collateral channels "
Kohn channels") to obstructed lung region. But in patients with acute
respiratory failure secondary to COPD, similar to patients with asthma,
short-term application of CPAP does not improve gas exchange. However,
when IPPV is added to CPAP, minute ventilation and gas exchange improve in
proportion to the amount of pressure applied. In our clinical experience,
when NPPV was used, the respiratory muscles appeared to be rapidly
unloaded, dyspnea was resolved and respiratory rate was reduced. The
effect on gases exchange was also rapidly observed. In our experience, the
mechanical effect of an early application of NPPV seems faster than the
pharmacological action.
Currently, many experts find that there is insufficient evidence to
recommend NIV in acute asthma. For these reasons, in our opinion, NIV for
patients with severe status asthmaticus not improving under conventional
medical therapy and on the edge of intubation is the only possibility of
decreasing morbidity and mortality of this acute situation. However, it is
mandatory to comply with the rules of maximal security in term of staff,
rapid access to endotracheal intubation and monitoring.
References
1. Agarwal R, Malhotra P, Gupta D. Failure of NIV in acute asthma :
case report and a word of caution. Emerg. Med. J. 2006;23: 9-10.
2.Thys F, Roeseler J, Marion E, El Gariani A, Meert P, Danse E et al.
Non invasive ventilation in severe status asthmaticus, a new therapeutic
approach ? Two case reports. Réan Urg 1998; 7: 423-6.
3. Thys F, Roeseler J, Reynaert M.S, Liistro G, Rodenstein D.O. Non
invasive ventilation for acute respiratory failure: a prospective
randomized placebo-controlled trial. Eur Respir J 2002; 20: 545-555.
4. Ram FS, Wellington S, Rowe B, Wedzicha JA. Non-invasive positive
pressure ventilation for treatment of respiratory failure due to severe
acute exacerbations of asthma. Cochrane Database Syst Rev 2005; 1:
CD004360.
5. Finfer SR, Garrard CS. Ventilatory support in asthma. Br J Hosp
Med 1993; 49:357-60
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