䡵
CORRESPONDENCE
Anesthesiology 2005; 103:205
© 2005 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc.
Sickle Cell and Anesthesia: Do Not Abandon Well-established
Practices without Evidence
In their table 5 on page 777 (Guidelines for the use of Perioperative
Prophylactic Erythrocyte Transfusion), the foundation for this table is
not clear and certainly not evidence based. It suggests guidelines for
perioperative transfusion that are misleading given the absence of
prospective, randomized data to support a nontransfusion approach.
We acknowledge the lack of a proven causal relation between
hypoxia, dehydration, and hypothermia and sickling events in the
perioperative clinical setting (page 782). However, in the context of
sickle cell disease, we are compelled to prove that no such relation
exists before abandoning practices that have been associated with
decreased perioperative morbidity and mortality in these patients.
A conservative approach to children with sickle cell disease in the
perioperative period has been and continues to be adequate hydration
and correction of anemia. To propose a therapeutic nihilistic approach
to the treatment of these patients in the absence of substantive evidence is dangerous. Despite the best care today, the perioperative
mortality rate in patients with sickle cell disease of 1 in 100 is severalfold greater than that in nonsickle adults, approximately 1 in
300,000, and in nonsickle children, 1 in 50,000 – 80,000. Before our
current practice patterns for these children are changed, prospective
randomized studies that examine anesthetic practices in this and other
diseases should be conducted.
Salvatore R. Goodwin M.D.,* Charles Haberkern, M.D., Mark
Crawford, M.B.B.S., Jerrold Lerman, M.D., Thomas Mancuso,
Myron Yaster, M.D. * Nemours Children’s Clinic, Jacksonville,
Florida. sgoodwin@nemours.org
References
1. Firth PG, Head A: Sickle cell disease and anesthesia. ANESTHESIOLOGY 2004;
101:766–85
2. Vichinsky EP, Neumayr LD, Haberkern C, Earles AN, Eckman J, Koshy M,
Black DM: The perioperative complication rate of orthopedic surgery in sickle
cell disease: Report of the National Sickle Cell Surgery Study Group. Am J Hematol 1999; 62:129–38
3. Vichinsky EP, Haberkern CM, Neumayr L, Earles AN, Black D, Koshy M,
Pegelow C, Abboud M, Ohene-Frempong K, Iyer RV: A comparison of conservative and aggressive transfusion regimens in the perioperative management of
sickle cell disease. The Preoperative Transfusion in Sickle Cell Disease Study
Group. N Engl J Med 1995; 333:206–13
4. Haberkern CM, Neumayr LD, Orringer EP, Earles AN, Robertson SM, Black
D, Abboud MR, Koshy M, Idowu O, Vichinsky EP: Cholecystectomy in sickle cell
anemia patients: Perioperative outcome of 364 cases from the National Preoperative Transfusion Study. Preoperative Transfusion in Sickle Cell Disease Study
Group. Blood 1997; 89:1533–42
5. Griffin TC, Buchanan GR: Elective surgery in children with sickle cell
disease without preoperative blood transfusion. J Pediatr Surg 1993; 28:681–5
David C. Warltier, M.D., Ph.D., served as Handling Editor for this Correspondence.
Anesthesiology 2005; 103:205–7
(Accepted for publication March 3, 2005.)
© 2005 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc.
In Reply:—We wish to thank the correspondents for their interest in
our review1 and for correcting the typographical errors. Although a
small typographical error in the sickle genetic code has extensive
consequences, the equivalent inaccuracies in the review fortunately do
not have similarly far-reaching effects on our conclusions. Regarding
the work by Vichinsky et al.,2– 4 the fact that this was analysis of
subpopulations of the same patient group was explicitly stated in the
relevant studies. Our motivation for reviewing these new studies in detail
was the additional information provided, not ignorance of the database
from which it originated. The data from Haberkern et al.2 (Complications,
page 1534) are in fact correctly reported in table 4 of the original article,1
which is repeated now as table 1 in this reply. The correspondents are
confusing sickle-specific events with overall complications, rates that
variously included fever, transfusion reactions, and postoperative surgical
David C. Warltier, M.D., Ph.D., acted as Handling Editor for this Correspondence.
Anesthesiology, V 103, No 1, Jul 2005
205
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To the Editor:—Firth and Head11 are to be congratulated for providing
a comprehensive review of the pathophysiology of sickle cell disease
and erudite discussion of its implications for anesthesiologists. We also
appreciate their attempts to apply evidence-based knowledge to our
understanding of the perioperative care of these patients. Although
this will undoubtedly become a valuable resource for anesthesiologists,
we are compelled to provide some corrections in the text and tables as
well as provide alternative interpretations of some of the evidence.
The authors refer to a randomized no-transfusion group in their
discussion of Vichinsky et al. (reference 98, page 776).2 In fact, there
was not a randomized no-transfusion group. The authors seemed to
have missed the fact that this report and several more by the same
authors were reports of subpopulations of the work by this group. In
this and subsequent articles from the Preoperative Transfusion in
Sickle Cell Disease Study Group as initially reported by Vichinsky et
al.,3 the groups were the same (described below). Furthermore, the
second to last sentence in the third paragraph on page 776 should
read, “This [acute chest syndrome] occurred in 21% of cases in both
the aggressive transfusion and the nonrandomized nontransfusion
group, 8% in the conservative transfusion group, and 3% in the nonrandomized transfusion group,” as described in table 4.
In table 4 on page 775, regarding Haberkern et al., “1995,”4 the
numbers and percents for “cholecystectomies, complications” for the
four groups are in fact the numbers of patients in the groups and
the percents of sickle cell events, not the numbers and percents of
complications. (This study was actually published in 1997.) The percentages of total complications and acute chest syndrome in the four groups
(as listed) are in fact as follows: group 1, randomized aggressive transfusion: 36%/9%; group 2, randomized simple transfusion: 39%/11%; group 3,
nonrandomized nontransfusion: 43%/19%; and group 4, nonrandomized
transfusion: 41%/7%. These groups are the same in all of the studies
reported by the Preoperative Transfusion in Sickle Cell Disease Study
Group. These corrected data underscore concerns regarding the risk of
perioperative complications in the nontransfusion group.
In the discussion of Griffin and Buchanan,5 the authors concluded
that “any potential benefit from transfusion would therefore be low
and risks of transfusion were not justified for minor procedures.”
However, the actual conclusion from this report stated that “operative
transfusions might be avoided in children with sickle cell disease who
undergo most minor surgical procedures.” The overall complication
rate was 26%, thoracotomy/laparotomy 50%, tonsillectomy and adenoidectomy 56%, others 5%. This report neither provided evidence to
withhold transfusion in any group nor lobbied against transfusions.
CORRESPONDENCE
206
Table 1. Outcomes from Recent Studies of Perioperative Blood Transfusion*
Reference
Categories
Griffin and Buchanan
(1993)
Retrospective nonrandomized;
66 children
Koshy et al.87 (1995)
Retrospective nonrandomized;
1,079 adults, children; lowand moderate-risk surgical
procedures
Vichinsky et al.88
(1995)
Prospective randomized; 604
assorted procedures
Haberkern et al.89
(1997)
Prospective randomized,
nonrandomized; 364
patients
Prospective randomized,
nonrandomized groups; 138
procedures
Minor procedures
Complications
Other procedures
Complications
Hb SS—low risk
Complications
Hb SS—moderate risk
Complications
Hb SS—high risk
Complications
Procedures
Complications
Transfusion complications
Cholecystectomies
Complications
Transfusion complications
Orthopedic procedures
ACS
Transfusion complications
Vichinsky et al.98
(1999)
R-XTF
R-TF
NR-TF
248
4.8%
390
7.9%
12
16.7%
303
15%
14%
110
12%
15%
34
21%
24%
301
15%
7%
120
19%
8%
40
8%
15%
97
18%
9%
40
3%
NR-NTF
46
2%
20
15%
145
12.9%
43
4.7%
0
37
32%
3%
24
21%
* This table is an amended version of table 4 from the original article.
Complications refers to sickle cell disease–specific complications, such as pain crises or acute chest syndrome.
ACS ⫽ acute chest syndrome; Hb SS ⫽ patients homologous for hemoglobin S; NR-NTF ⫽ nonrandomized nontransfusion; NR-TF ⫽ nonrandomized
conservative or aggressive transfusion; R-TF ⫽ randomized conservative transfusion; R-XTF ⫽ randomized aggressive transfusion.
problems.2 These general outcomes are not the appropriate endpoints by
which to assess the need for or effect of transfusion.
With respect to the work of Griffin and Buchanan,5 the correspondents seem to have formed their opinions from the abstract summary.
We refer the correspondents to the tables, text, and prominent citations6,7 discussed by Griffin and Buchanan.5 The complications comprising the rates cited by the authors were largely atelectasis and
transient, uncomplicated postoperative pyrexia, which the investigators5 emphasized were not specific to sickle cell disease. Again, it is
misleading to cite the incidence of a heterogeneous group of complications in a heterogeneous population as motivation for an intervention against the lower occurrence of a specific subset of complications
in a specific subpopulation. The incidence of complications specific to
sickle cell disease in the relevant minor procedure subpopulation was,
as reported,1 2% (n ⫽ 1 in 46).5 The sole patient with the sickle
complication of acute chest syndrome had significant preexisting cardiopulmonary dysfunction. The researchers5 cited these facts in their
extensive discussion of the limits of any potential role for transfusion.
They concluded, “our data support the concept that preoperative
blood transfusions may be unnecessary for children with sickle cell
disease . . . undergoing most minor operations (who) might therefore
be spared the cost, inconvenience, and risks of infection, alloimmunization and transfusion reactions inherent in RBC transfusions” (page
685).5
In response to the suggestion that table 5, Guidelines for the Use of
Perioperative Prophylactic Erythrocyte Transfusion, from the original
article is not evidence based, we refer the correspondents to the text
of the review and relevant selected references.1 Some of the rationale
and evidence that simple transfusion be avoided in low-risk situations
has been reemphasized above. As the correspondents’ call for prospective randomized trials acknowledges, the evidence for the efficacy of
simple transfusion in intermediate-risk situations is incomplete, and we
cannot therefore say conclusively that transfusion is or is not indicated.
Our guidelines for high-risk cases were based on a systematic review of
the primary neuroanesthetic and cardiothoracic literature of the preceding four decades, although we limited our citations of this fragmentary evidence to a short selection at the request of the ANESTHESIOLOGY
reviewers. We concede that our guidelines for transfusion in uncomplicated pain crises are not evidence based—simply because we are
Anesthesiology, V 103, No 1, Jul 2005
unaware of conclusive evidence to support or refute the practice of
transfusion. We cannot advocate an intervention in the absence of
supportive evidence and concur with authoritative peer opinion that
transfusion is not indicated.8 A detailed critique of practice based on
the largely uncontrolled data on transfusion for acute chest syndrome
was beyond the scope of an already lengthy review.1 The guidelines on
acute chest syndrome are consequently limited to the well-documented evidence that transfusion can improve arterial hemoglobin
oxygenation, a predictable and possibly nonspecific physiologic consequence of increasing mixed venous saturation and pulmonary capillary transit time by correction of anemia in the face of pulmonary
shunting and impaired gas exchange. The guidelines are therefore
based on what data are available. Because this evidence is incomplete,
we simply provided guidelines, rather than making more proscriptive
recommendations.
The correspondents state that we are compelled to prove that no
causal relation exists between hypoxia, dehydration, and hypothermia
and acute perioperative complications before abandoning practices
associated with decreased perioperative morbidity and mortality. The
only definitive way to do this, subjecting patients to these injuries in a
well-constructed study, is practically difficult and ethically impossible.
The studies cited, including exposure to inhalational and hypobaric
hypoxia, the use of occlusive arterial tourniquets, and the coexistence
of sickle cell disease and cyanotic heart disease, strongly suggest that
hypoxia-induced sickling (and by extension acute cellular dehydration)
are not triggers of acute complications.1 The relevant practices that are
associated with an apparent decrease in morbidity and mortality are
probably the overall general improvements in basic anesthetic and
perioperative care, not specific unproven deviations from standard
practice. We do not advocate therapeutic nihilism, as the correspondents aver, but rather, we encourage adherence to these basic standards of anesthetic care.
We are surprised by the correspondents’ continued enthusiasm for
transfusion, given their familiarity with the relevant literature.2– 4 The
previously widespread adoption of a practice, exchange transfusion, in
the absence of controlled studies, was no guarantee of efficacy or lack
of harm.2– 4 Although the liberal use of transfusion may be well established in the correspondents’ practice, this is similarly not proof of
efficacy or freedom from injury. For considerations of effect, we direct
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Study Details
96
CORRESPONDENCE
Paul G. Firth, M.B., Ch.B., C. Alvin Head, M.D.* * Medical College
of Georgia, Augusta, Georgia. ahead@mcg.edu
References
1. Firth PG, Head CA: Sickle cell disease and anesthesia. ANESTHESIOLOGY 2004;
101:766–85
2. Haberkern CM, Neumayr LD, Orringer EP, Earles AN, Robertson SM, Black
D, Abboud MR, Koshy M, Idowu O, Vichinsky EP: Cholecystectomy in sickle cell
anemia patients: Perioperative outcome of 364 cases from the National Preoperative Transfusion Study. Preoperative Transfusion in Sickle Cell Disease Study
Group. Blood 1997; 89:1533–42
Anesthesiology 2005; 103:207– 8
3. Vichinsky EP, Haberkern CM, Neumayr L, Earles AN, Black D, Koshy M,
Pegelow C, Abboud M, Ohene-Frempong K, Iyer RV: A comparison of conservative and aggressive transfusion regimens in the perioperative management of
sickle cell disease. The Preoperative Transfusion in Sickle Cell Disease Study
Group. N Engl J Med 1995; 333:206–13
4. Vichinsky EP, Neumayr LD, Haberkern C, Earles AN, Eckman J, Koshy M,
Black DM: The perioperative complication rate of orthopedic surgery in sickle
cell disease: Report of the National Sickle Cell Surgery Study Group. Am J Hematol 1999; 62:129–38
5. Griffin TC, Buchanan GR: Elective surgery in children with sickle cell
disease without preoperative blood transfusion. J Pediatr Surg 1993; 28:681–5
6. Odura KA, Searle JF: Anaesthesia in sickle cell states: A plea for simplicity.
BMJ 1972; 44:596–8
7. Homi J, Reynolds J, Skinner A, Hanna W, Serjeant G: General anaesthesia in
sickle-cell disease. BMJ 1979; 1:1599–601
8. Rees DC, Olujohungbe AD, Parker NE, Stephens D, Telfer P, Wright J,
British Committee for Standards in Haematology, General Hematology Task Force
by the Sickle Cell Working Party:Guidelines for the management of acute painful
crisis in sickle cell disease. Br J Haematol 2003; 120:744–52
9. Hassan M, Hasan S, Giday S, Alamgir, L, Banks A, Fredrick W, Smoot D,
Castro O: Hepatitis C in sickle cell disease. J Natl Med Assoc 2003; 95:939–42
10. King SD, Dodd RY, Haynes G, Wynter HH, Sullivan MT, Serjeant GR,
Choo-Chang E, Michael E: Prevalence of antibodies to hepatitis C and other
markers in Jamaica. West Indian Med J 1995; 44:55–7
11. Garratty G: Severe reactions associated with transfusion of patients with
sickle cell disease. Transfusion 1997; 37:357–61
12. Firth PG, Tsuruta Y, Kamath Y, Dzik W, Ogilvy CS, Peterfreund RA:
Transfusion-related acute lung injury or acute chest syndrome of sickle cell
disease? A case report. Can J Anesth 2003; 50:895–9
(Accepted for publication March 3, 2005.)
© 2005 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc.
Circadian Influences, Low-dose Isoflurane, and the Ventilatory
Response to Hypoxia
To the Editor:—Pandit et al.1 are to be congratulated on their study on
the effects pain and audiovisual stimulation on depression of the acute
hypoxic ventilatory response by low-dose halothane. Their results are
in good correspondence with some of the key studies in this complex
field of research.2– 6 As stated by the authors, there is now ample
evidence for the existence of quantitative differences in the ability of
low-dose inhalational anesthetics to depress the ventilatory response to
acute hypoxia in humans. For example, 0.1% end-tidal halothane depresses the response by 50 – 60%, whereas the same concentration of
isoflurane has much less of an effect (reduction 30 – 40%).1– 6 The
authors discuss several explanations for the observed differences between halothane and isoflurane, such as differences in pharmacokinetics, differences in the production of reactive oxygen species, and
differences in their interaction with sites in the central nervous system
involved in behavioral control of breathing. Evenly important are issues
related to methodology.7 Often, very small differences in protocols
may cause large differences in study outcomes. I would like to give an
example of the latter. In three subjects, the ventilatory responses to
hypoxia at three time points on one single day were measured: 8:00 AM,
noon, and 4:00 PM. At 9:00 AM, one additional response during inhalation of 0.2% end-tidal isoflurane was obtained. The ventilation (Vi)
response to five end-tidal PO2 levels was analyzed using the following
equation: Vi ⫽ G exp(⫺D PETO2) ⫹ y0 (G is the hypoxic sensitivity, D
is a shape parameter, and y0 is ventilation at hyperoxia). Control and
recovery responses varied considerably by 20 –30% for parameter G
and 30 – 40% for parameter y0 (fig. 1). Consequently, the depression of
the isoflurane response relative to the control and recovery responses
was evenly variable and varied from 50 to 70%. The picture that
emerges is that the circadian rhythm has important influences on the
ventilatory response to hypoxia and consequently on the influences
Anesthesiology, V 103, No 1, Jul 2005
Fig. 1. Ventilatory response to hypoxia obtained at five oxygen
levels in a 25-yr-old woman. Nondrug studies were performed at
8:00 AM, noon, and 4:00 PM. At 9:00 AM, the effect of 0.2% endtidal isoflurane was measured. The lines through the data are
curve fits to the data using the following equation: Vi ⴝ G
exp(ⴚD PETO2) ⴙ y0. The variability among control and recovery responses is apparent. PO2 ⴝ partial pressure of oxygen.
that low-dose anesthetics have on the response. How the behavioral
control system interacts with circadian influences remains unknown.
Although I realize that the study I present here is of small sample size,
it points toward (1) an important and complex role for circadian
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them to long-established alternative approaches of avoiding perioperative transfusion.6,7 For evidence of harm, consider a recent study of
150 multiply transfused American patients that found an incidence of
hepatitis C infection of 35.3%, a sobering demonstration of iatrogenic
inury.9 By contrast, in Jamaica, where transfusion practices are far
more conservative, a study of 250 patients documented an infection
rate of 2%.10 Rather than preventing acute sickle problems, transfusion
can actually precipitate acute pain11 and pulmonary complications.12
We do not suggest that our review is the last word on management or
even that the model we outline explains all aspects of sickle cell
disease. We therefore strongly support the call for prospective randomized studies of anesthetic practice for sickle cell disease. Given the
proven potential for iatrogenic injury, we urge the correspondents to
consider the cautious methods of others1,5– 8,12 and, in the absence of
conclusive evidence, not to abandon a well-established practice: First
do no harm.
207
CORRESPONDENCE
208
influences on the interaction between anesthesia and behavioral and
chemical control of breathing and (2) the need for identical protocols
when comparing agents and studies on the influence of low-dose
anesthetic agents on ventilatory control.
Albert Dahan, M.D., Ph.D., Leiden University Medical Center,
Leiden, The Netherlands. a.dahan@lumc.nl
References
Anesthesiology 2005; 103:208
(Accepted for publication March 28, 2005.)
© 2005 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc.
In Reply:—I thank Dr. Dahan for his interest in my article.1 He presents
data from three subjects (he acknowledges that this is a very small
sample) that show some “within-day variation” in the acute hypoxic
ventilatory response (AHVR). The figure he presents for one subject
indicates that minute ventilation in euoxia is lowest in the morning,
highest at midday, and in-between in the afternoon. I do not know
whether this same pattern is the same in all subjects. The minute
ventilation in euoxia was as high as approximately 20 l/min, and this
implies either that the end-tidal partial pressure of carbon dioxide
(PCO2) of Dahan’s subject varied widely during the day or that, if
end-tidal PCO 2 was constant, the metabolic CO2 output of the lung
must have varied widely during the day. The AHVR variation must
therefore have correlated with end-tidal PCO2 and/or CO2 output in
Dahan’s small series. However, neither Sahn et al..2 nor Zhang and
Robbins3 were able to find such correlations.
Nonetheless, the within-day variation reported by Dahan may indeed
be a “circadian” influence, and I agree that the observation needs
further study. Variation in the AHVR within individuals on repeat
testing is well established,4 but it seems that between-day variation is
greater than within-day (circadian) variation.2,3 The study of Zhang
and Robbins3 sheds important light on the issue of variation. They
found that the method of inducing hypoxia (they studied square wave
hypoxic input, incremental hypoxic steps, and simulated rebreathing)
did not influence the AHVR measured. So it seems that the methodologic influences to which Dahan refers may not be as influential as we
all (intuitively) might think them to be. This is perhaps further supported by my analysis that there is no actual difference in the result of
studies using rebreathing as compared with those using step hypoxia
in assessing the reduction in AHVR by low-dose anesthetic.5
Zhang and Robbins3 also found that between-day variation was
greater than within-day (circadian) variation, so although the withinday variation found by Dahan is of interest, it is possible that betweenday variation is more important.
There are two practical questions: (1) Does this variation in AHVR
impact upon the results of the relevant studies, and (2) how can we
account for it or control for it experimentally?
With regard to the first question, if the variation in AHVR influenced
Anesthesiology 2005; 103:208 –9
the outcome of studies, it might prove difficult (because of the large
confidence intervals) to show, for example, that anesthetics blunt
AHVR. However, this is not the case, and many different studies
consistently find that halothane, enflurane, and sevoflurane reduce
AHVR. The only agent for which there is less consistency in different
studies’ results is isoflurane. Although this may be a result of inherent
variation in AHVR, it is also possible (and perhaps more likely) to be
due to some property of isoflurane that gives it a more variable effect
than other agents.
With regard to the second question, there seem to be two general
ways to control for variation. One is to conduct each experimental
period in a study at precisely the same time of day. However, this does
not control between-day variability (which seems more important).
The second way is to conduct experimental periods at random times of
day in a suitable number of different subjects, ideally using repeated
experimental periods in the same subject, and then average the results
to reduce any systematic variation. One problem is that repeated
exposure is often (ethically) undesirable in anesthetic studies, but
where possible, I prefer this second approach.
Jaideep J. Pandit, D.Phil., F.R.C.A., John Radcliffe Hospital,
Oxford, United Kingdom. jaideep.pandit@physiol.ox.ac.uk
References
1. Pandit JJ, Moreau B, Donoghue S, Robbins PA: Effect of pain and audiovisual
stimulation on the depression of acute hypoxic ventilatory response by low-dose
halothane in humans. ANESTHESIOLOGY 2004; 101:1409–16
2. Sahn SA, Zwillich CW, Dick N, McCullough RE, Lakshminarayan S, Weil JV:
Variability of ventilatory responses to hypoxia and hypercapnia. J Appl Physiol
1977; 43:1019–25
3. Zhang S, Robbins PA: Methodological and physiological variability within
the ventilatory response to hypoxia in humans. J Appl Physiol 2000; 88:1924–32
4. Hirschman CA, McCullough RE, Weil JV: Normal values for hypoxic and
hypercapnic ventilatory drives in man. J Appl Physiol 1975; 38:1095–8
5. Pandit JJ: The variable effect of low-dose volatile anaesthetics on the acute
ventilatory response to hypoxia in humans: A quantitative review. Anaesthesia
2002; 57:632–43
(Accepted for publication March 28, 2005.)
© 2005 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc.
Position of the Shoulder for Subclavian Approach
To the Editor:—We read with interest the article by Kitagawa et al.1
regarding the proper shoulder position for subclavian vein (SCV)
puncture. They are to be congratulated for performing an important
Anesthesiology, V 103, No 1, Jul 2005
study about the anatomical backgrounds of SCV catheterization. The
major finding of their article was that, when compared with neutral
and elevated positions, the lowered shoulder position is the best for
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1. Pandit JJ, Moreau B, Donoghue S, Robbins PA: Effect of pain and audiovisual
stimulation on the acute hypoxic ventilatory responseby low dose halothane.
ANESTHESIOLOGY 2004; 101:1409–16
2. Knill RL, Gelb AW: Ventilatory response to hypoxia and hypercapnia during
halothane sedation and anesthesia in man. ANESTHESIOLOGY 1978; 49:244–51
3. Knill RL, Kieraszewicz HT, Dodgson BG: Chemical regulation of ventilation
during isoflurane sedation and anesthesia in humans. Can Anaesth Soc J 1983;
30:607–14
4. Dahan A, van den Elsen MJLJ, Berkenbosch A, DeGoede J, van Kleef JW,
Bovill JG: Effects of subanesthetic halothane on the ventilatory response to
hypercapnia and acute hypoxia in healthy volunteers. ANESTHESIOLOGY 1994; 80:
727–38
5. van den Elsen M, Dahan A, DeGoede J, Berkenbosch A, van Kleef J:
Influences of subanesthetic isoflurane on ventilatory control in humans. ANESTHESIOLOGY 1995; 83:478–90
6. Sarton E, Dahan A, Teppema L, van den Elsen M, Olofsen E, Berkenbosch A,
van Kleef J: Acute pain and central nervous system arousal do not restore
impaired hypoxic ventilatory response during sevoflurane sedation. ANESTHESIOLOGY 1996; 85:295–303
7. Robotham JL: Do low-dose inhalational anesthetic agents alter ventilatory
control? (editorial). ANESTHESIOLOGY 1994; 80:723–6
CORRESPONDENCE
Anesthesiology 2005; 103:209 –10
In Reply:—We thank Drs. Bahk and Ryu for their interest in our article1
and valuable comments. We would like to take the opportunity to
address the issues raised by their insights, point by point.
First, the longest overlap length between the lower border of the
clavicle and the subclavian vein (SCV) in the inner third of the clavicle
was cited as one of the principal reasons for recommending a lowered
shoulder position. Drs. Bahk and Ryu describe concern about cases in
which a needle may cross the lower border between the midclavicular
line and inner third of clavicle. However, a lowered shoulder seems to
offer a more appropriate position than other shoulder positions, because overlap increases with extension to the lateral side from the
inner third of the clavicle, as described in our article. The lowered
shoulder also increases the proximity of the SCV to the undersurface of
the clavicle. This allows reliable SCV puncture and reduces the risk of
complications such as pneumothorax during the use of basic SCV
puncture technique (needle advancement contacting the undersurface
of the clavicle), because the needle is not advanced beyond the necessary depth. The shaded area in figure 2 of our article1 extends from
the SCV to the innominate vein because we were using the definition
of overlap described by Land2 as the area of clavicle overlapping with
the SCV, including the innominate vein.
Second, although we assessed probability of contact between the
needle and the SCV using the longest and shortest diameters of the
vein, assessment using SCV cross-sectional area may be more suitable,
as indicated by Drs. Bahk and Ryu. We therefore reevaluated contact
probabilities using the products of both halves of the longest and
shortest diameters and the circular constant, expressing the area of an
ellipsoid, and then compared values among the three shoulder positions, because the cross-sectional area of the SCV can be regarded as
an ellipsoid, as indicated in figure 2 of our article.1 The result was
Areadown ⬇ Areaneutral ⬇ Areaupl, being consistent with the results as
Anesthesiology, V 103, No 1, Jul 2005
SCV and the innominate vein is more acute,2 there seems to be a risk of
directing the SCV catheter into the IJV when the shoulder is lowered.
Last, changing the shoulder position after successful venipuncture,
as suggested in the article,1 carries the risk of withdrawing the puncture needle out of the vein. Even changing the shoulder position after
advancing the guide wire may not be helpful, because a guide wire may
already be directed to the IJV because of the short distance between
the SCV puncture point and the confluence of the IJV and the SCV. If
SCV catheterization is attempted with the shoulder lowered, tilting the
head toward the catheterization side without movement of the shoulder may be more helpful in reducing the incidence of catheter malposition into the IJV.3
All the above-mentioned concerns should be clarified before deciding whether we should adopt the lowered shoulder position during
SCV catheterization.
Jae-Hyon Bahk, M.D.,* Ho-Geol Ryu, M.D. * Seoul National
University Hospital, Seoul National University College of Medicine,
Seoul, Korea. bahkjh@snu.ac.kr
References
1. Kitagawa N, Oda M, Totoki T, Miyazaki N, Nagasawa I, Nakazono T, Tamai
T, Morimoto M: Proper shoulder position for subclavian venipuncture: A prospective randomized clinical trial and anatomical perspectives using multislice
computed tomography. ANESTHESIOLOGY 2004; 101:1306–12
2. Cobb LM, Vinocur CD, Wagner CW, Weintraub WH: The central venous
anatomy in infants. Surg Gynecol Obstet 1987; 165:230–4
3. Jung CW, Bahk JH, Kim MW, Lee KH, Ko H: Head position for facilitating
the superior vena caval localization of catheter during the right subclavian
catheterization in children. Crit Care Med 2002; 30:297–9
(Accepted for publication March 28, 2005.)
© 2005 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc.
assessed using SCV diameters, resulting in being substantially comparable in the contact probability among the three shoulder positions.
Although we assessed overlap using the same methods described by
Land2 and Tan et al.3 as mentioned before, we agree with the proposal
by Drs. Bahk and Ryu that overlap length of the SCV on an imaginary line
drawn between the needle entry point and the midportion of the clavicular head is more relevant than using a point on the lower border of the
clavicle. We are grateful to both doctors for making this recommendation.
Regarding the third and fourth comments made by Drs. Bahk and
Ryu, the small number of patients participating in this clinical trial
limited comparisons of SCV cannulation success rates between elevated and lowered positions only, where comparisons were expected
to identify the most marked differences. From our experience, we
believe that a clinical trial with a sufficient sample population will
confirm the superiority of a lowered shoulder position over a neutral
position in terms of success rates for SCV puncture. However, this
issue must be clarified in a randomized clinical trial in the future. All
catheterizations performed in the present trial were inserted into the
right SCV, and no catheters were directed into the internal jugular vein.
With our procedure inserting a catheter or guide wire into the SCV,
advancement after a change in shoulder position from lowered to
neutral may contribute to leading the catheter or guide wire toward
the innominate vein. In addition, although Drs. Bahk and Ryu express
concern regarding the risk of withdrawing the puncture needle from
the SCV during the change in shoulder position after successful venipuncture, we believe that the risks associated with the procedure in
actual practice are not as large as they suggest. Even if shoulder
position changes from a lowered to a neutral or even a slightly elevated
position, we have experienced minimal movement of the puncture
needle. This is due to movement of the needle and syringe in an
integrated manner along with the clavicle and surrounding tissue and
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the SCV approach. However, we would like to make a few comments
regarding the article.
First, the longest overlap length between the lower border of the
clavicle and the SCV in the inner third of the clavicle was one of the
main reasons for quoting the lowered shoulder position. However, a
needle path aiming at the suprasternal notch may cross the lower
border of the clavicle somewhere between the midclavicular line and
the inner third of the clavicle. In addition, the shaded overlap area in
figure 1 of the article1 extends out of the SCV, even to the innominate
vein.
Second, one of the most important factors for successful catheterization is probability of contact between the puncture needle and the
SCV. Because the cross-sectional area rather than the diameter on a
plane is more important for the probability of contact, the crosssectional area of the SCV beneath the inner third of the clavicle should
be regarded as a major factor. If the cross-sectional area is not available,
there may be another way of analyzing the probability of contact.
Overlap length of the SCV on an imaginary line drawn between the
needle entry point and the midportion of the clavicular head seems to
be more relevant than that on the lower border of the clavicle. In figure
1 of the article,1 we can realize that the neutral and lowered positions
are comparable, but the elevated position has the shortest overlap
length on the imaginary line.
Third, with regard to the small clinical trial, why were the neutral
and lowered positions not compared? Where was the catheter tip
located? Were there any catheters directed to the internal jugular vein
(IJV)? As explained in figure 4 of the article,1 the angle formed between
the SCV and the innominate vein becomes narrower with the shoulder
lowered. Considering the fact that, in children, a right SCV catheter is
frequently positioned in the IJV because the angle formed between the
209
CORRESPONDENCE
210
due to the motionless area of the sternoclavicular joint, resulting in the
needle remaining relatively still in the region of insertion. However, we
do not recommend marked shoulder elevation. Shoulder movement
after SCV puncture in infant cases may also increase the risks associated with withdrawing the needle. We think that our procedure can be
applied to school-aged children and older patients, but not to children
younger than school age, and infants in particular. In the case of
infants, tilting the head toward the side of catheterization may help to
reduce the incidence of catheter malposition into the internal jugular
vein, as recommended by Drs. Bahk and Ryu.4
Anesthesiology 2005; 103:210
1. Kitagawa N, Oda M, Totoki T, Miyazaki N, Nagasawa I, Nakazono T, Tamai
T, Morimoto M: Proper shoulder position for subclavian venipuncture: A prospective randomized clinical trial and anatomical perspectives using multislice
computed tomography. ANESTHESIOLOGY 2004; 101:1306–12
2. Land RE: Anatomic relationships of the right subclavian vein. Arch Surg
1971; 102:178–80
3. Tan B-K, Hong S-W, Huang MHS, Lee S-T: Anatomic basis of safe percutaneous subclavian venous catheterization. J Trauma 2000; 48:82–6
4. Jung CW, Bahk JH, Kim MW, Lee KH, Ko H: Head position for facilitating
the superior vena caval localization of catheter during the right subclavian
catheterization in children. Crit Care Med 2002; 30:297–9
(Accepted for publication March 28, 2005.)
© 2005 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc.
Myocardial Performance Index and Tissue Doppler Systolic Wave
Velocity Are Preload Dependent
To the Editor:—We read with great interest the article about myocardial performance index and tissue Doppler imaging in patients with
single ventricles, comparing two anesthetic regimens, sevoflurane and
fentanyl–midazolam.1
The authors found no change in myocardial performance index,
which is a global index of both systolic and diastolic function. However, they describe a significant decrease of both myocardial Doppler
imaging systolic (Sm) and early diastolic (Em) wave velocities from
baseline to dose 1 and dose 2 with fentanyl–midazolam (table 3 in their
article). Nevertheless, both (neo)aortic flow and time–velocity integral
decreased significantly.
An important limitation of this study, the preload dependency of
both parameters used, was not fully discussed. It has to be speculated
that anesthetics, in a setting as used in this study, although not shown,
induce major changes in loading conditions.2 Assessment of ventricular
function implies that load-independent methods should be used. It has
been indirectly suggested in the literature that myocardial performance
is preload dependent: Broberg et al.3 described a close relation between this index and dP/dtmax, the latter being strongly preload
dependent.4 Recently, this preload dependency was also suggested by
our group when we described a close relation between myocardial
performance index and preload adjusted maximal power.5
In addition, the same problem arises with the systolic flow wave
velocity of the tissue Doppler imaging. Our group recently showed
clearly that this flow wave velocity is load dependent.6 Therefore, a
decrease in the length of the myocardial fibers due to a decrease in
EDV will lead to decreases in stroke volume, the velocity of shortening,
and systolic tissue velocity obtained with tissue Doppler imaging.
Anesthesiology 2005; 103:210 –1
In Reply:—The load dependence of the myocardial performance index
in congenital heart disease has been evaluated. No significant change
was found before or after surgical correction of atrial septal defect
(right ventricular preload), pulmonic stenosis (right ventricular afterload), or congenitally corrected transposition of the great vessels (right
ventricular preload and afterload).1 Acute changes in myocardial performance index with manipulation of preload/afterload have been
demonstrated in adult volunteers with healthy hearts—to Valsalva
maneuver, leg lifting, and nitroglycerine administration. However, the
patients in this study with previous myocardial infarction and abnormal
Anesthesiology, V 103, No 1, Jul 2005
Echocardiographic parameters as myocardial performance indexes
and systolic Doppler myocardial velocity must be used cautiously in
view of various physiologic and pathophysiologic interfering factors, in
particular when one is assessing hemodynamics in conjunction with
various dose regimens of anesthetics.
Jan Poelaert, M.D., Ph.D., * Amà Ruggero, M.D. * Ghent
University Hospital, Gent, Belgium. jan.poelaert@ugent.be
References
1. Ikemba CM, Su JT, Stayer SA, Miller-Hance WC, Eidem BW, Bezold LI, Hall
SR, Havemann LM, Andropoulos DB: Myocardial performance index with sevoflurane–pancuronium versus fentanyl–midazolam–pancuroniumin infants with a
functional single ventricle. ANESTHESIOLOGY 2004; 101:1298–305
2. Pagel P, Lowe D, Hettrick D, Jamali I, Kersten J, Tessmer J, Warltier D:
Isoflurane, but not halothane, improves indices of diastolic performance in dogs
with rapid ventricular, pacing-induced cardiomyopathy. ANESTHESIOLOGY 1996;
85:644–54
3. Broberg CS, Pantely GA, Barber BJ, Mack GK, Lee K, Thigpen T, Davis LE,
Sahn D, Hohimer AR: Validation of the myocardial performance index by echocardiography in mice: A noninvasive measure of left ventricular function. J Am
Soc Echocardiogr 2003; 16:814–23
4. Little WC: The left ventricular dP/dtmax-end-diastolic volume relation in
closed-chest dogs. Circ Res 1985; 56:808–15
5. Poelaert J, Heerman J, Schupfer G, Moerman A, Reyntjens K, Roosens C:
Estimation of myocardial performance in CABG patients. Acta Anaesthesiol Scand
2004; 48:973–9
6. Amà R, Segers P, Roosens C, Claessens T, Verdonck P, Poelaert J: Effects of
load on systolic mitral annular velocity by tissue Doppler imaging. Anesth Analg
2004; 99:332–8
(Accepted for publication March 28, 2005.)
© 2005 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc.
ventricular function did not exhibit any changes in myocardial performance index.2
Doppler tissue imaging has load dependence3,4 but has been demonstrated to be more independent of preload than conventional Doppler measures of mitral inflow.5,6 In addition, in patients with ventricular
dysfunction, changes in preload affect Doppler tissue imaging velocities much less and correlate well with invasive measures of left ventricular diastolic pressure.6 Significant increases in afterload seen in
patients with aortic stenosis do decrease Doppler tissue imaging velocity.7 However, no significant impact on Doppler tissue imaging
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Norihito Kitagawa, M.D.,* Mayuko Oda, M.D., Masatoshi
Morimoto, M.D., Noriaki Miyazaki, M.D. * Tsuruta Hospital,
Ushizu, Saga, Japan. kitagawa@mail.anes.saga-med.ac.jp
References
CORRESPONDENCE
211
Table 1. Combined Systemic and Pulmonary Vascular
Resistance Index
Group
Baseline
Dose 1
Dose 2
Sevoflurane (n ⫽ 16)
Fentanyl–midazolam
(n ⫽ 14)
597 ⫾ 260
621 ⫾ 344
484 ⫾ 228*
575 ⫾ 343
494 ⫾ 223*
598 ⫾ 344
Results are presented as mean ⫾ SD; combined systemic and pulmonary
vascular resistance index units are dyn 䡠 s 䡠 cm⫺5 䡠 m2.
* P ⬍ 0.05, different from baseline by one-way repeated-measures analysis of
variance.
Anesthesiology 2005; 103:211–2
Dean B. Andropoulos, M.D.,* Benjamin W. Eidem, M.D.,
Wanda C. Miller-Hance, M.D., Louis I. Bezold, M.D. * Baylor
College of Medicine/Texas Children’s Hospital, Houston, Texas.
dra@bcm.tmc.edu
References
1. Eidem BW, O’Leary PW, Tei C, Seward JB: Usefulness of the myocardial
performance index for assessing right ventricular function in congenital heart
disease. Am J Cardiol 2000; 86:654–8
2. Moller JE, Poulsen SH, Egstrup K: Effect of preload alterations on a new
Doppler echocardiographic index of combined systolic and diastolic performance. J Am Soc Echocardiogr 1999; 12:1065–72
3. Firstenberg MS, Greenberg NL, Main ML, Drinko KJ, Odabashian JA, Thomas
JD, Garcia MJ: Determinants of diastolic myocardial tissue Doppler velocities:
influences of relaxation and preload. J Appl Physiol 2001; 90:299–307
4. Dincer I, Kumbasar D, Nergisoglu G, Atmack Y, Kutlay S, Akyurek O, Sayin
T, Erol C, Oral D: Assessment of left ventricular diastolic function with Doppler
tissue imaging: effects of preload and place of measurements. Int J Cardiovasc
Imaging 2002; 18:155–60
5. Sohn DW, Chai IH, Lee DJ, Kim HC, Kim HS, Oh BH, Lee MM, Park YB, Choi
YS, Seo JD, Lee YW: Assessment of mitral annulus velocity by Doppler tissue
imaging in the evaluation of left ventricular diastolic function. J Am Coll Cardiol
1997; 30:474–80
6. Nagueh SF, Sun H, Kopelen HA, Middleton KJ, Khoury DS: Hemodynamic
determinants of the mitral annulus diastolic velocities by tissue Doppler. J Am
Coll Cardiol 2001; 37:278–85
7. Eidem BW, McMahon CJ, Ayres NA, Kovalchin JP, Denfield SJ, Altman CA,
Bezold LI, Pignatelli RH: Clinical impact of altered left ventricular loading conditions on Doppler tissue imaging velocities: A study in congenital heart disease.
J Am Soc Echo 2005; (in press)
8. Ikemba CM, Su JT, Stayer SA, Miller-Hance WC, Eidem BW, Bezold LI, Hall
SR, Havemann LM, Andropoulos DB: Myocardial performance index with sevoflurane–pancuronium versus fentanyl–midazolam–pancuronium in infants with a
functional single ventricle. ANESTHESIOLOGY 2004; 101:1298–305
9. Rivenes SM, Lewin MB, Stayer SA, Bent ST, Schoenig HM, McKenzie ED,
Fraser CD, Andropoulos DB: Cardiovascular effects of sevoflurane, isoflurane,
halothane, and fentanyl–midazolam in children with congenital heart disease: An
echocardiographic study of myocardial contractility and hemodynamics. ANESTHESIOLOGY 2001; 94:223–9
(Accepted for publication March 28, 2005.)
© 2005 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc.
Transsacrococcygeal Ganglion Impar Block for Postherpetic
Neuralgia
To the Editor:—I read with interest the case report about sacral
postherpetic neuralgia and the excellent results in its treatment using
the paramedial approach to the ganglion impar.1 The authors included
in their discussion the different approaches that have been undertaken
in the past to block the ganglion impar. It was also impressive to see
the double-bent needle used to achieve this block. Many practitioners
have elected not to perform this block because of their impression of
its complexity and technical difficulty. Unfortunately, this has led to a
decrease in popularity of this effective block in pain medicine.
In the past, I described a case in which coccydynia was controlled
with the blockage of the ganglion impar through the sacrococcygeal
junction.2 The authors briefly mentioned this technique, but I am
afraid their description could be interpreted to mean that this approach is of minimal value. They state, “This approach can be useful in
Anesthesiology, V 103, No 1, Jul 2005
patients with normal anatomy but may prove challenging in patients
with arthritic changes in the bones and calcification of the ligaments of
the sacrum and coccyx.” I have to disagree with the authors and would
like to clarify that this approach is quite simple, straightforward, and
equally effective. Minimal arthritic changes occur in this area, and, if
any, the bone changes seldom are major challenges with this approach.
de Leon-Casasola3 described the transsacrococcygeal approach as the
easiest way of performing the ganglion impar block. Over the years,
many practitioners have tried to simplify the approach, and many
reports have been published advocating the transsacrococcygeal route
for its simplicity and effectiveness.4,5
I believe that the message we should be sending to practitioners is
that ganglion impar block could be performed through an easily
achieved technique under fluoroscopy and that it is effective in the
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velocities of increased left ventricular preload with ventricular septal
defects was noted.
With regard to the loading conditions for the patients in our current
study,8 preload was not specifically assessed, largely because of the
inability to use conventional methods to compute left ventricular
end-diastolic volume, because of the irregular geometry of the functional single ventricle. Central venous pressure, a rough estimate of
preload, was not changed with either of the two anesthetic levels with
the two regimens we studied. In a previous study of two-ventricle
patients with congenital heart disease, we demonstrated that neither
fentanyl–midazolam nor sevoflurane, in doses similar to those used in
the current study, had any effect on left ventricular end-diastolic
volume measured by the biplane method of Simpson.9 In the same
previous study, neither fentanyl–midazolam nor sevoflurane changed
systemic vascular resistance index, calculated echocardiographically.
In the current study, we did not specifically calculate systemic vascular
resistance index because the patients had a functional single ventricle,
and systemic and pulmonary blood flow both occurred in the aorta of
most patients, so the conventional concept of systemic vascular resistance did not apply. However, if one was to calculate a combined
systemic and pulmonary vascular resistance index in the patients of our
current study, by dividing the difference between mean arterial pressure and central venous pressure (assuming no change in central
venous pressure from baseline) by the aortic or neoaortic outflow,
there is no change in systemic and pulmonary vascular resistance index
with fentanyl–midazolam but a significant decrease with sevoflurane at
both anesthetic levels (table 1).
Therefore, the changes in loading conditions induced by the anesthetic regimens for congenital heart disease can be estimated to be no
change with fentanyl–midazolam and a 17% decrease in afterload with
sevoflurane.
Although we agree with the caution of Drs. Poelaert and Amà to
consider changes in loading conditions and other pathophysiologic
factors when performing and interpreting echocardiographic studies
assessing response to anesthetics, we believe our conclusions are valid
for single-ventricle infants. Myocardial performance index in particular
represents an appropriate method to assess myocardial function in
patients with abnormal ventricular geometry, such as those with a
functional single ventricle.
CORRESPONDENCE
212
management of sacral pathologies, including postherpetic neuralgia. It
is discouraging to see a good intervention fade into disfavor because of
the complexity of the technical aspect of its performance when a
technically simple alternative is present and equally effective.
Abdallah I. Kabbara, M.D., Louis Stoke VA Hospital of Cleveland, Case
Western Reserve University, Cleveland, Ohio. draikabbara@yahoo.com
References
1. McAllister RK, Carpentier BW, Malkuch G: Sacral postherpetic neuralgia
and successful treatment using a paramedical approach to the ganglion impar.
ANESTHESIOLOGY 2004; 101:1472–4
(Accepted for publication March 30, 2005.)
© 2005 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc.
Ganglion Impar Block in Noncancer Perineal Pain: What Drugs,
What Strategy?
To the Editor:—We read2 with great interest the recently published
case report by McAllister et al. 1 describing the successful management
of postherpetic neuralgia in the perineal area using repeated ganglion
impar blockade by a local anesthetic solution. This is one of the first
case reports describing the efficacy of blockade of the terminal part of
the sympathetic chain in non– cancer-related pain. We congratulate the
authors on their therapeutic success, but several questions remain to
be answered.
Ganglion impar blockade is not a routinely used analgesic procedure. Initial articles have reported chemical neurolysis of the ganglion
impar as adjuvant therapy of cancer-related pain in the perineal region.
In their overview, De Medicis and de Leon-Casasola provide a summary
of studies evaluating the efficacy and complication rate of ganglion
impar blockade.2 They conclude there have been only two studies
reporting good efficacy of neurolytic blockade using 6% phenol for
visceral perineal pain of cancer origin in a total of 36 patients. There is
only one study addressing the efficacy of ganglion impar inhibition in
noncancer pain. The procedure was found to be ineffective in 20
patients with coccygodynia.3 In addition to this study, there have been
only a couple of case reports on the successful management of perineal
pain of noncancer etiology using this technique of blockade.1,4
In their patient with postherpetic neuralgia, McAllister et al. used a
corticosteroid as an additive to a local anesthetic, administering it to
the presacral area. The analgesic efficacy of corticosteroids to sacral
sympathetic structures has not been demonstrated to date, and the
mechanism of its analgesic activity remains unclear.
Another thing we found surprising was the long-term analgesic
effect of local anesthetic solution (3–5 months). The common duration
of the analgesic effect of local anesthetics administered to that area in
diagnostic/prognostic blockade is 2–7 days.2
† Michalek P, Dutka J: The efficacy of ganglion impar block in chronic
non-malignant perineal pain. World Congress of Anaesthesiologists; April 2,
2004; Paris, France. Abstract PO336. Available at: www.wca2004.com. Accessed
March 28, 2005.
Anesthesiology 2005; 103:212–3
In Reply:—I would like to thank Dr. Kabbara for his further information and clarification of the ease of the transsacrococcygeal approach
to the ganglion impar. It was not my intent to impugn the utility of this
approach, but to highlight the ease of the paramedial approach to the
ganglion impar as a useful alternative. It is my hope that this potentially
Anesthesiology, V 103, No 1, Jul 2005
In our experience with the management of noncancer perineal pain
in 26 patients with chronic pain after perineal surgery, vulvodynia, and
vulvar pruritus to date, we are able to make a preliminary outcome
determination using the ganglion impar procedure: A testing blockade
with a local anesthetic has an analgesic efficacy of 2–5 days. Multiple
blockade was accomplished in these patients using a mixture of a local
anesthetic with clonidine (10 ml bupivacaine, 0.375%, plus 75 g
clonidine). In this pilot study, clonidine extended the analgesic effect
to as long as 14 days. Clonidine administered to the sympathetic
nervous system presumably prolongs the duration of blockade, as
demonstrated by Kimura et al.5 Still, to achieve long-term analgesic
effect in this cohort, most patients required chemical ganglion impar
neurolysis or radiofrequency thermolesion.†
Further larger and randomized clinical studies are needed to confirm
the acceptability of ganglion impar blockade and destruction in noncancer perineal pain.
Pavel Michalek, M.D., Ph.D.,* Libor Dolecek, M.D., Petr Stadler,
M.D. * Na Homolce Hospital, Prague, Czech Republic.
pafkam@seznam.cz
References
1. McAllister RK, Carpentier BW, Malkuch G: Sacral postherpetic neuralgia
and successful treatment using a paramedial approach to the ganglion impar.
ANESTHESIOLOGY 2004; 101:1472–4
2. DeMedicis E, de Leon-Casasola O: Ganglion impar block: Critical evaluation.
Tech Reg Anesth Pain Manage 2001; 5:120–2
3. Vranken JH, Bannink IMJ, Zuurmond WWA, Sassen AM, de Lange JJ: Invasive procedures in patients with coccygodynia: Caudal epidural infiltration,
pudendal nerve block and blockade of the ganglion impar (abstract). Reg Anesth
Pain Med 2002; 25:S25
4. Kamalam DR, Freedman GM, Kreitzer JM: Radiofrequency ablation of ganglion impar for intractable coccydynia (abstract). Anesth Analg 2002; 94:S228
5. Kimura Y, Hamaguchi S, Okuda Y, Kitajima T: Addition of clonidine increases duration and magnitude of vasodilative effect induced by sympathetic
block with mepivacaine in dogs. Reg Anesth Pain Med 2001; 26:329–32
(Accepted for publication March 30, 2005.)
© 2005 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc.
useful sympathetic block will find favor with clinicians, by either
approach, and that many patients will benefit from it.
The interest and comments of Michalek et al. are appreciated. They
note that the duration of efficacy of sympathetic block of the ganglion
impar with local anesthetics and steroids in my case report does not
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Anesthesiology 2005; 1:212
2. Kuthuru M, Kabbara AI, Oldenburg P, Rosenberg SK: Coccygeal pain relief
after transsacrococcygeal block of the ganglion impar under fluoroscopy: A case
report. Arch Phys Med Rehabil 2003; 84:E24
3. de Leon-Casasola OA: Critical evaluation of chemical neurolysis of the
sympathetic axis for cancer pain. Cancer Control 2000; 7:142–8
4. Basagan Mogol E, Turker G, Kelebek Girgin N, Uckunkaya N, Sahin S:
Blockade of ganglion impar through sacrococcygeal junction for cancer-related
pelvic pain. Agri 2004; 16:48–53
5. Munir MA, Zhang J, Ahmad M: Modified needle-inside-needle technique for
the ganglion impar block. Can J Anaesth 2004; 51:915–7
CORRESPONDENCE
Anesthesiology 2005; 103:213
Therefore, the experience of Michalek et al. with duration of efficacy may not necessarily apply to PHN due to complex and differing
mechanisms of pain. I agree that further investigation is warranted.
However, because PHN in the sacral dermatomes is uncommon, it will
be difficult to conduct a well-controlled study to find more definitive
answers.
Russell McAllister, M.D., Scott & White Memorial Hospital and
Clinic; Scott, Sherwood, and Brindley Foundation; the Texas A&M
University Health Science Center College of Medicine; Temple,
Texas. rmcallister@swmail.sw.org
References
1. Forrest JB: Management of chronic dorsal root pain with epidural steroid.
Can Anaesth Soc J 1978; 25:218–25
2. Forrest JB: The response to epidural steroid injections in chronic dorsal root
pain. Can Anaesth Soc J 1980; 27:40–6
3. Milligan NS, Nash TP: Treatment of post-herpetic neuralgia: A review of 77
consecutive cases. Pain 1985; 23:381–95
4. Hetherington RG: Herpes zoster and post-herpetic neuralgia, The Management of Pain. Edited by Ashburn MA, Rice LJ. New York, Churchill Livingstone,
1998, pp 351–62
(Accepted for publication March 30, 2005.)
© 2005 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc.
Valve Leaks with New Disposable Extraglottic Airway Devices
Fig. 1. Arrow indicates where leak exists between cuff valve
deflator and surroundings of the pilot balloon cuff of the
CobraPLA®.
To the Editor:—We would like to report six cases of spontaneous cuff
deflation that occurred during a clinical trial of a new disposable
extraglottic airway device, the CobraPLA® (Engineered Medical Systems, Inc., Indianapolis, IN).1 The cuff pressure decreased to almost
zero during maintenance of anesthesia. These events were detected by
continuous cuff pressure monitoring using a transducer attached to a
monitor (S/5 AM; Datex-Ohmeda, Helsinki, Finland) during the maintenance phase of anesthesia and did not influence the clinical performance of the device, primarily because the patients were breathing
spontaneously. The patients were not moved during surgery, with the
Supported by the Catharina Foundation, Eindhoven, The Netherlands, and
Engineered Medical Systems, Indianapolis, Indiana, who provided the study
samples.
† Laryngeal Airway Device Recall Notice UK MDA/2003/027. Available at: http://
www.medicaldevices.gov.uk/mda/mdawebsitev2.nsf/webvwSearchResults/
FDE3B3C0A919083280256D8E004946A0. Accessed August 27, 2003.
Anesthesiology, V 103, No 1, Jul 2005
transducer positioned on the patient’s shoulder throughout the duration of the procedure. The devices’ cuffs were checked for leaks before
use as recommended by the manufacturers. When checked after removal of the device, the cuff itself did not show any defect, but
submersion in water revealed tiny bubbles of air escaping from the
pilot balloon valve, showing a continuous leak at the cuff deflator
valves with their surroundings (fig. 1).
A similar problem has been reported with another new extraglottic
airway mask, the Marshall Laryngeal Airway Device (Marshall Products
Ltd., Bath, United Kingdom). In the United Kingdom, the Medical
Devices Regulatory Agency issued a Medical Device Alert† in 2003
regarding cuff failure due to a small number of pilot balloon valves
leaking. This led to the manufacturer’s recall of the product.
Cuff deflation is undesirable because it can lead to a loss of seal with
the respiratory/gastrointestinal tracts and put the patient at risk of
ventilatory failure, aspiration, and gastric insufflation.2
We urge the manufacturers of new extraglottic devices to ensure
better quality control of their products, including the cuff deflator
valves. However, because one cannot guarantee 100% quality control
at all times, we also urge clinicians to incorporate cuff pressure monitoring into their routine practice.
André van Zundert, M.D., Ph.D., F.R.C.A., * Al-Shaikh Baha,
F.R.C.A., Joseph Brimacombe, M.D., F.C.A.R.C.S.I., F.R.C.A.,
Ch.B., M.B., Eric Mortier M.D., Ph.D. * Catharina Hospital–Brabant
Medical School, Eindhoven, The Netherlands. zundert@iae.nl
References
1. Akca O, Wadhwa A, Sengupta P, Durrani J, Hanni K, Wenke M, Yucel Y,
Lenhardt R, Doufas AG, Sessler DI: The new perilaryngeal airway (CobraPLA) is
as efficient as the laryngeal mask airway (LMA) but provides better airway sealing
pressures. Anesth Analg 2004; 99:272–8
2. Brimacombe J: Problems, Laryngeal Mask Anesthesia: Principles and Practice, 2nd edition. London, WB Saunders, 2004, pp 551–76
(Accepted for publication January 11, 2005.)
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match the duration of relief that they have seen in treating patients
with perineal pain of noncancer etiology (chronic postoperative perineal pain, vulvodynia, and vulvar pruritus). However, the mechanism
of pain in postherpetic neuralgic (PHN), although not completely
understood, seems to be quite different from that in the patient population treated by Michalek et al.
Treatment of PHN with sympathetic blocks, with or without steroids, is controversial but has been described in several studies with
favorable results far outlasting the normal duration of action of the
local anesthetic or steroid. Forrest1 injected 1–2 ml bupivacaine, 0.5%,
with 60 –120 mg methylprednisolone once a week for 3 weeks. At 1
month, 57% of patients were pain free, and 6 months later, 86% of
these patients continued to be pain free. Forrest also reported on 37
patients with longstanding PHN who were treated with three epidural
steroid injections given at 1-week intervals. Significant reductions in
visual analog scale ratings were noted at 1 month, and 89% of the
patients were pain free at 1 yr.2 Milligan and Nash3 also reported
favorable long-lasting relief of PHN after stellate ganglion blocks. The
mechanism of the prolonged effect is unclear. Hetherington4 advocated consideration of sympathetic blocks as a major adjunctive therapy for all PHN patients, although it is recognized that there are no
guidelines as to how many to perform or how often to perform them.
213
CORRESPONDENCE
214
Anesthesiology 2005; 103:214
Anesthesiology 2005; 103:214 –5
units distributed worldwide, we might assume that a very limited
number of devices (the ones used by Dr. van Zundert et al.) had a
minimal leak that could not be identified at preoperative check. Alternatively, we have been notified by another investigator that in some
units, during continuous cuff pressure monitoring, a small leak can
occur at the monitoring connection site and not from the device
itself; that clinician did not think that the valve was malfunctioning.
Finally, damage to the devices in question could have also occurred
during forceful cleaning before the postuse submersion test. It is
reassuring to Engineered Medical Systems that the deflated cuff did not
influence the clinical performance of the device or the end-tidal carbon
dioxide measurement during the study of Dr. van Zundert et al., which
speaks highly to the performance of the CobraPLA®.
Although we cannot state with certainty that the experience of Dr.
van Zundert et al. was unique, it seems that it was isolated and that
valve failure has not posed a significant clinical problem for clinicians.
We are confident that the CobraPLA® meets the rigorous quality
standards clinicians and patients deserve in their medical products.
Brad Quinn, Engineered Medical Systems, Indianapolis, Indiana.
bquinn@engmedsys.com
(Accepted for publication January 11, 2005.)
© 2005 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc.
Life-threatening Ventilatory Obstruction due to a Defective
Tracheal Tube during Spinal Surgery in the Prone Position
To the Editor:—In the current days of high-tech equipment and welldefined safety regulations, technical failures are less likely to occur,
and so are we to consider them when clinical complications happen.
Endotracheal tube defects are probably seen by today’s anesthesiologists as a thing of the past. A review of the literature showed that all of
the cases reported in relation to defective tubes occurred when tubes
were submitted to repeated sterilizations.
A 39-yr-old woman, with insignificant past medical history, was
scheduled to undergo lumbar discectomy. General anesthesia was
induced with thiopental (450 mg), fentanyl (150 g), and vecuronium
(8 mg). Tracheal intubation was performed with a 7-mm reinforced
endotracheal tube (Safety Flex; Mallinckrodt Medical, Athlone, Ireland;
expiration date 2006-09). The patient was positioned in prone position. Normal breath sounds were heard equally in both lungs. Anesthesia was maintained with sevoflurane (1.0 –1.5%) and nitrous oxide
(67%) in oxygen, and muscle relaxation was achieved with vecuronium
bolus. Approximately 2 h after induction, we started to experience
difficulties in ventilating the patient’s lungs. Peak inspiratory pressure
started to increase while compliance and tidal volume decreased.
Pulmonary auscultation remained normal. The capnograph showed a
positive deflection on the inspiratory phase; it was assumed that
relaxation was insufficient, and a 4-mg bolus of vecuronium was
administered. A suction catheter was used to remove possible airway
secretions. It was noted that the catheter did not pass through the
tube. Tube obstruction was then suspected. Ventilation became very
difficult, even using bag ventilation. The patient was quickly returned
to the supine position. The face, neck, and upper trunk showed
congested veins. Bradycardia with bigeminism occurred and ventilation became impossible, but oxygen saturation did not decrease below
98%. The endotracheal tube was replaced with a new one. All abnor-
Support was provided solely from institutional and/or departmental sources.
Anesthesiology, V 103, No 1, Jul 2005
mal variables returned to baseline. The patient was repositioned for
surgery, and the procedure was completed without further complications. Recovery and the postoperative period were uneventful.
Later inspection of the tube showed a transparent halo on the
outside surface. The inner view showed an intramural bubble that
completely occluded the lumen. The 3-cm-long bubble was located
11.5 cm from the distal end. A fiberscope was used to obtain a photo
of the bubble from the inside of the tube.
Ventilatory distress in the prone position may be a serious complication. The differential diagnosis included consideration of pneumothorax and bronchospasm, but auscultation of both lungs remained
possible and was normal. In the case reported, ventilatory distress was
due to a bubble protruding into the lumen of the tube. This bubble
most probably was not due to any sort of extrinsic damage to the tube
during its use. The inclusion of tiny air bubbles in the wall of a
reinforced tube can be a result of the production procedure of this
kind of tube.1 Most certainly, nitrous oxide exposure and diffusion was
the cause of expansion of the tube defect.2– 4 This would explain the
fact that during the initial 2 h of the procedure, no problems were
noted. The electrocardiographic changes observed were probably due
to increased intrathoracic pressure caused during manual ventilation.
This is reinforced by the striking congestion of the neck veins. It is
possible that manual ventilation forced gases into the lungs but that
some valve mechanism due to the presence of the bubble prevented
expiration. This, combined with the 100% oxygen used, would also
explain why the oxygen saturation did not decrease. It is interesting to
note that oxygen saturation may not be an indicator of severe airway
problems. To our knowledge, this is the first report of this kind of
endotracheal tube obstruction with a disposable armored tube. It
shows that even in modern days of increased attention to quality
control, simple technical defects may occur. The manufacturer was
notified about the incident.
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In Reply:—We fully agree with Dr. van Zundert et al. that manufacturers of extraglottic devices (and all other medical devices) should assure
quality control of their products.
Since the CobraPLA® (Engineered Medical Systems, Inc., Indianapolis, IN) was introduced into clinical practice in 2003, Engineered
Medical Systems has ensured the quality of the cuff deflator valve with
a comprehensive validation and production procedure of every product made, which includes a pressure test of the deflator valve and a full
16-h inflation test of the deflator valve/cuff assembly, with no leakage
allowed.
For a manufacturer to fully assess and address a valve issue such as
Dr. van Zundert et al. describe, it is imperative that the products in
question be promptly returned to the producer (in its original condition at the time of use) for evaluation. Unfortunately, Engineered
Medical Systems never received the six devices in question back at our
facility for a proper inspection to be conducted. When we visited Dr.
van Zundert in the Netherlands after receiving a copy of his correspondence to ANESTHESIOLOGY, we were presented with a bundle of more
than 30 CobraPLAs®, which had been used and then cleaned. There
was no documentation as to which ones had been used in his report.
As a result, we cannot be certain as to the cause of the failures.
Considering the fact that Engineered Medical Systems has not received a single other report of a cuff deflator valve failure from all the
© 2005 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc.
CORRESPONDENCE
Isabel A. Santos, M.D.,* Carla A. Oliveira, M.D., Leónia
Ferreira, M.D. * Hospital Geral de Santo António, Porto, Portugal.
ialex@mail.telepac.pt
References
1. Paul M, Dueck M, Kampe S, Petzke F: Failure to detect an unusual obstruction in a reinforced endotracheal tube with fiberoptic examination. Anesth Analg
2003; 97:909–10
Anesthesiology 2005; 103:215
Anesthesiology 2005; 103:215– 6
2. Populaire C, Robard S, Souron R: An armoured endotracheal tube obstruction in a child. Can J Anaesth 1989; 36:331–2
3. Ohn K, Wu W: Another complication of armored endotracheal tubes.
Anesth Analg 1980; 59:215–6
4. Munson ES, Stevens DS, Redfern RE: Endotracheal tube obstruction by
nitrous oxide. ANESTHESIOLOGY 1980; 52:275–76
(Accepted for publication February 2, 2005.)
© 2005 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc.
this product range are met before release of the product from the
plant.
We would like to draw the reader’s attention to our Instructions for
Use leaflet that is supplied with this product. These instructions clearly
specify all warnings/precautions to be taken with this product and
suggested directions for use.
We regret that the customer experienced problems using one of our
products. We do, however, appreciate their bringing this matter to our
attention. Feedback is very important because we strive to maintain a
high-quality product and a high level of customer communication and
satisfaction.
Deirdre Kennedy, B.Sc., Gregor Bertaggia* * Tyco Healthcare,
Hennef, Germany. gregor.bertaggia@emea.tycohealthcare.com
(Accepted for publication February 2, 2005.)
© 2005 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc.
Fatal Thrombosis in an Adult after Thoracoabdominal Aneurysm
Repair with Aprotinin and Deep Hypothermic Circulatory Arrest
To the Editor:—We report a case of fatal aortic thrombosis after
aprotinin exposure in an adult undergoing repair of a thoracoabdominal aneurysm using cardiopulmonary bypass and deep hypothermic
circulatory arrest (DHCA).
A 78-yr-old woman presented with a ruptured thoracoabdominal
aortic aneurysm involving the aortic arch (Crawford type I). The
patient was taken emergently to the operating room for repair using
our DHCA protocol that has been previously described.1– 6
Anesthetic induction was with titrated fentanyl and midazolam.
Neuromuscular blockade was achieved and maintained with titrated
pancuronium. The trachea was intubated with a left-sided doublelumen tube (Tyco Healthcare/Mallinckrodt, St. Louis, MO). Correct
endotracheal position was confirmed by serial fiberoptic bronchoscopy. Intraoperative monitoring included American Society of Anesthesiologists routine monitors as well as indwelling radial arterial and
pulmonary arterial catheters. Because of the emergent nature of the
procedure, a lumbar cerebrospinal fluid drain was not placed. Anesthesia was maintained with isoflurane in oxygen, as well as titrated
fentanyl and midazolam.
The patient was given aprotinin (Bayer Corporation, Pittsburgh, PA)
as follows: 2 million kallikrein inhibitory units intravenously as a load,
followed by an infusion of 0.5 million kallikrein inhibitory units per
hour. The cardiopulmonary bypass crystalloid prime was also loaded
with aprotinin (2 million kallikrein inhibitory units).
The patient was positioned in the right lateral decubitus position.
Support was provided solely from institutional and/or departmental sources.
Anesthesiology, V 103, No 1, Jul 2005
Surgical incision, dissection, and initiation of cardiopulmonary bypass
were uneventful. Heparinization for cardiopulmonary bypass was titrated to maintain the activated coagulation time (kaolin activator) of
greater than 600 s. The surgical repair was technically uncomplicated;
the aorta was replaced with a Hemashield vascular graft (Boston Scientific, Natick, MA). The cardiopulmonary bypass time was 212 min,
with a deep hypothermic circulatory arrest time of 38 min.
After successful separation from cardiopulmonary bypass, protamine
was administered in a titrated fashion without adverse reaction. Despite aprotinin and adequate protamine (calculated to neutralize the
full dose of heparin), hemostasis in the surgical field was not achieved.
There was significant microvascular bleeding. No overt vascular bleeding was detected despite careful surgical inspection. Platelet infusion
was begun. Ten minutes after initiation of the platelet infusion, the
patient experienced cardiac arrest that was refractory to pharmacologic resuscitation. Transesophageal echocardiography revealed diffuse intraaortic thrombosis (figs. 1 and 2). The patient did not respond
to further resuscitative efforts. The family declined a postmortem
examination.
Catastrophic thrombosis with aprotinin in DHCA was first noted in
the early 1990s.7 The most likely explanation for these observations
was inadequate heparinization because it was only appreciated in the
mid-1990s that aprotinin exposure prolongs the activated clotting
time.8 At our institution, we perform 70 – 80 thoracic aortic procedures
with DHCA per year. Our DHCA protocol includes routine application
of an antifibrinolytic, either aminocaproic acid or aprotinin. Aprotinin
is reserved for the high-risk DHCA population.1– 4
Inadequate heparinization as the cause of the prothrombotic state in
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In Reply:—Tyco Mallinckrodt (Athlone, Ireland) would like to point
out that unfortunately, in this instance, the Safety Flex product involved in the complaint was not returned to the manufacturer. Therefore, a comprehensive evaluation could not be conducted relating to
potential root cause of this problem.
In the absence of the sample in question, we have attempted to
simulate the problem described in the letter by Santos et al. We have
been unable to do so under normal simulated use conditions. However, we were able to create an occlusion in a Safety Flex product by
subjecting it to sterilization cycles that are different than those used at
our manufacturing site. Using a moist heat sterilization cycle or a
high-pressure gas cycle, we managed to create occlusions and other
disfigurations in the product.
Mallinckrodt manufactures Safety Flex tracheal tubes with defined
validated processes, and the product is checked at several key intervals
during manufacture to ensure that all quality criteria associated with
215
CORRESPONDENCE
216
John G. T. Augoustides, M.D.,* Judy Lin, B.A., Andrew J.
Gambone, B.A., Albert T. Cheung, M.D. * Hospital of the University
of Pennsylvania, Philadelphia, Pennsylvania. yiandoc@hotmail.com
Fig. 1. Short axis view of descending aorta with transesophageal
echocardiography, showing aortic graft lumen filled with
thrombus.
this case is extremely unlikely, given that our standard DHCA protocol
was followed and given the DHCA experience at our institution. It is
more likely that the prothrombotic state was multifactorial in etiology:
disseminated intravascular coagulation triggered by hypothermic cardiopulmonary bypass, the antifibrinolytic action of aprotinin, neutralization of heparin, and the presence of transfused functional platelets.
The presence of hemostatic aortic graft material in this case was
Hemashield (Boston Scientific), which, although hemostatic, has not
Fig. 2. Long axis view of descending aorta with transesophageal
echocardiography, showing aortic graft lumen filled with
thrombus.
Anesthesiology, V 103, No 1, Jul 2005
References
1. Augoustides JGT, Weiner J, Pinchasik D, Bavaria JE, Ochroch EA: Clinical
predictors for mortality in adults after thoracic aortic surgery requiring deep
hypothermic circulatory arrest (abstract). ANESTHESIOLOGY 2003; 99:A-138
2. Augoustides JGT, Gambone AJ, Floyd TF, Bavaria JE, Cheung AT: Perioperative outcome after adult deep hypothermic circulatory arrest for elective repair
of the ascending aorta and aortic arch (abstract). ANESTHESIOLOGY 2004; 101:A222
3. Bavaria JE, Brinster DR, Gorman RC, Woo YJ, Gleason T, Pochettino A:
Advances in the treatment of acute type A dissection: An integrated approach.
Ann Thorac Surg 2002; 74:1848–52
4. Stecker MM, Cheung AT, Pochettino A, Kent GP, Patterson T, Weiss SJ,
Bavaria JE: Deep hypothermic circulatory arrest: I. Effects of cooling on electroencephalogram and evoked potentials. Ann Thorac Surg 2001; 71:14–21
5. Stecker MM, Cheung AT, Pochettino A, Kent GP, Patterson T, Weiss SJ,
Bavaria JE: Deep hypothermic circulatory arrest: II. Changes in electroencephalogram and evoked potentials during rewarming. Ann Thorac Surg 2001; 71:22–8
6. Cheung AT, Bavaria JE, Pochettino A, Weiss SJ, Barclay DK, Stecker MM:
Oxygen delivery during retrograde cerebral perfusion in humans. Anesth Analg
1999; 88:8–15
7. Sundt III, TM Kouchoukos NT, Saffitz JE, Murphy SF, Wareing TH, Stahl DJ:
Renal dysfunction and intravascular coagulation with aprotinin and hypothermic
circulatory arrest. Ann Thorac Surg 1993; 55:1418–24
8. Despotis GJ, Filos KS, Levine V, Alsoufiev A, Spitznagel E: Aprotinin prolongs activated and nonactivated whole blood clotting time and potentiates the
effect of heparin in vitro Anesth Analg 1996; 82:1126–31
9. Mohamed MS, Mukherjee M, Kakkar VV: Thrombogenicity of heparin and
non-heparin bound arterial prostheses: An in vitro evaluation. J R Coll Surg Edinb
1998; 43:155–7
10. Hirt SW, Dosis D, Siclari F, Rohde R, Haverich A: Collagen presealed or
uncoated aortic bifurcation Dacron prosthesis: A 5 year clinical follow-up study.
Thorac Cardiovasc Surg 1991; 39:365–70
11. Fanashawe MP, Shore-Lesserson L, Reich D: Two cases of fatal thrombosis
after aminocaproic acid therapy and deep hypothermic circulatory arrest. ANESTHESIOLOGY 2001; 95:1525–27
12. Heindel SW, Mill MR, Freid E, Valley RD, White GC, Norfleet EA: Fatal
thrombosis associated with a hemi-Fontan procedure, heparin-protamine reversal, and aprotinin. ANESTHESIOLOGY 2001; 94:369–71
(Accepted for publication February 16, 2005.)
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been associated with acute intravascular thrombosis.9,10 The mechanism of this fatal thoracic aortic thrombosis is unclear.
Fatal thrombosis has been reported in adult DHCA; the antifibrinolytic, however, was not aprotinin but aminocaproic acid.11 This syndrome has also been reported in pediatric cardiopulmonary bypass; the
antifibrinolytic was aprotinin.12
Therefore, our case is the first reported case of fatal thrombosis in an
adult undergoing DHCA in the presence of aprotinin despite adequate
heparinization. Despite adequate heparinization, this syndrome is still
possible in cardiovascular surgery necessitating cardiopulmonary bypass, regardless of antifibrinolytic or patient age. Further hypothesisdriven perioperative research is required to understand and prevent
this uncommon but important complication associated with antifibrinolytic therapy.