164 LETTERS TO THE EDITOR

intravenous or inhalation anesthetics (eg, sevoflurane) of an opioid-based anesthesia. Therefore, in this retrospective case series, we
compared myocardial damage, measured by the time course of cardiac troponin T (cTnT), between a sevoflurane/sufentanil and a
midazolam/remifentanil technique in patients undergoing CABG surgery with CPB and blood cardioplegic solution.
Data of 26 (12 in group 1 and 14 in group 2) consecutive patients were evaluated according to the German data protection acts.
All patients were premedicated with intramuscular morphine/flunitrazepam. Two experienced anesthetists performed anesthesia
with either a continuous infusion of sufentanil (median total dose, 400 ␮g) supplemented with 0.8 to 1.5% end-tidal sevoflurane
before and after CPB and with 2 to 4 mg/kg/h of propofol during CPB (group 1) or a continuous infusion of remifentanil (median
total dose, 21.5 mg) supplemented with midazolam (median total dose, 15 mg) (group 2) depending on clinical demands.
Rocuronium was used as the muscle relaxant in both groups, and patients in group 2 were given 100 ␮g of sufentanil intravenously
before transfer to the intensive care unit. There, all patients were treated in the same way. A standard CPB technique (cannulation
of the right atrium and the ascending aorta, cooling to a temperature of 32°C, and Calafiore cardioplegic solution after
cross-clamping of the aorta and thereafter at regular intervals until unclamping) was used. Nominal data were compared by
chi-square analysis and ordinal data by Mann-Whitney U tests. A p value ⬍0.05 was considered statistically significant.
Demographic (sex, age, height, and weight), preoperative (New York Heart Association classification, left-ventricular ejection
fraction, left-ventricular end-diastolic pressure, and creatinine), operation-related (time of operation, CPB, and aortic cross-
clamping) and hemodynamic data (heart rate, mean arterial pressure, central venous pressure, mean pulmonary arterial pressure,
pulmonary capillary wedge pressure and cardiac index before and after CPB, and need for inotropic support or vasopressors) did
not differ between groups (Table 1). The perioperative cTnT concentrations did not differ as well (Fig 1).
In this case series, sevoflurane was not superior to midazolam with regard to myocardial damage measured by postoperative cTnT. Data
on cardioprotective effects of benzodiazepines are scarce and similar results to ours were recently published for isoflurane3 and in pediatric
cardiac surgery.4 Despite methodologic weaknesses (retrospective study, small number of cases, 2 different opioids, and propofol during
CPB in group 1), we recommend further studies to elucidate the clinical circumstances in which sevoflurane exerts its cardioprotective
effects, especially in cardiac surgery patients on CPB with the use of cardioplegic solutions.

Gunther Wiesner, MD*

Andreas Barankay, MD*
Siegmund Braun, MD†
Peter Tassani-Prell, MD*
*Department of Anesthesiology and †Institute of Laboratory Medicine
German Heart Centre
Munich, Germany

REFERENCES
1. De Hert SG, ten Broecke PW, Mertens E, et al: Sevoflurane but not propofol preserves myocardial function in coronary surgery patients.
Anesthesiology 97:42-49, 2002
2. Julier K, da Silva R, Garcia C, et al: Preconditioning by sevoflurane decreases biochemical markers for myocardial and renal dysfunction in
coronary artery bypass graft surgery: A double-blinded, placebo-controlled, multicenter study. Anesthesiology 98:1315-1327, 2003
3. Fellahi JL, Gue X, Philippe E, et al: Isoflurane may not influence postoperative cardiac troponin I release and clinical outcome in adult cardiac
surgery. Eur J Anaesthesiol 21:688-693, 2004
4. Malagon I, Hogenbirk K, van Pelt J, et al: Effect of three different anaesthetic agents on the postoperative production of cardiac troponin T
in paediatric cardiac surgery. Br J Anaesth 94:805-809, 2005

doi:10.1053/j.jvca.2006.02.019

Diaphragm Paralysis in Children After Cardiac Surgery

To the Editor:

We read with great interest the article by Moideen and associates entitled “Bilateral Phrenic Nerve Palsy in a Neonate Following
Complex Congenital Cardiac Surgery.”1 Although we appreciate their excellent result and presentation, we have some comments
about their diagnosis and treatment strategies. Also, we would like to share our experience about diaphragm paralysis (DP) after
cardiac surgery.
We have performed 3,464 cardiac operations between 1996 and 2006 and DP was noted in 174 patients (5%). Eleven patients
had bilateral DP. Sixty-four patients (1.8%) among them were surgically treated with transthoracic diaphragm plication. We found
that plication after 10 days from the surgery and pneumonia are major risk factors for mortality in patients less than 1 year of age.
In the presented case, it was surprising that the patient was free from infection during hospitalization or the authors did not mention
the pathogens and the antibiotic therapy against intensive care unit pathogens, since the patient was followed with open chest for
3 days and reoperated, then was discharged on postoperative day 73. Even in plicated patients, antibiotic therapy lasts weeks until
LETTERS TO THE EDITOR 165

full recovery, and this is one of the most significant portions of treatment expenses. In addition, it must be considered that thymus
gland resection and dissection with electrocautery even in tissues far from the phrenic nerve, and the use of topical cooling devices
to prevent ice slush injury,2 are possible reasons for DP that the authors did not state.
In diagnosis of DP, suspicion is the first major step, especially in bilateral DP. Echocardiography shows diaphragm movements
well. Routine fluoroscopy must be performed because segmental movements of the diaphragm are shown best using it in the
follow-up period.
We found high incidences of DP in arterial switch (19%), Blalock-Tausig shunts (23%), and tetralogy of Fallot (27%) procedures.
All arterial switch patients with DP were plicated (12 patients), and all survived. In 11 bilateral DP patients, we performed bilateral
diaphragm plication for all of them, and all have survived; 3 of them were under the age of 1 year.
It is more important to prevent DP than to treat it. All surgical risk factors in neonates must be eliminated. Particularly in bilateral
DP, early and complete surgical management must be performed to prevent mortality and high treatment costs. We would like to
congratulate the authors again for handling such a challenging case with success.

Suleyman Ozkan, MD
Tankut Akay, MD
Department of Cardiovascular Surgery
Baskent University Hospital
Ankara, Turkey

REFERENCES
1. Moideen I, Nair SG, Shivaprakasha K, et al: Bilateral phrenic nerve palsy in a neonate following complex congenital cardiac surgery.
J Cardiothorac Vasc Anesth 20:76-79, 2006
2. Efthimiou J, Butler J, Woodham C, et al: Diaphragm paralysis following cardiac surgery: Role of the phrenic nerve cold injury. Ann Thorac
Surg 52:1005-1008, 1991

doi:10.1053/j.jvca.2006.04.008

Reply

To the Editor:

The authors appreciate the comments of Drs Ozkan and Akay regarding the incidence of infection and pneumonia in infants after
bilateral phrenic nerve palsy (PNP).
The primary intention of this case report was to highlight the conservative management of bilateral PNP in neonates. Surprisingly,
this infant, despite spending 72 days in the intensive care unit, did not develop any pneumonia. However, she developed systemic
sepsis (which was not mentioned in the case report), which was suspected on the sixth postoperative day, because of rising white
cell counts (increased to 23.6 K/␮L with neutrophil counts of 91%) and falling platelet counts (reduced to 13,000 K/␮L). A blood
culture at this time returned positive for a gram-negative organism (Acenatobacter species). Our routine antibiotic prophylaxis is
a combination of cefazolin (25 mg/kg/dose every eight hours) and ofloxacin (6 mg/kg/dose every twelve hours). After the onset of
sepsis, this was changed to piperacillin/Tazobactum (50 mg/kg/dose every eight hours) with ofloxacin (same dose) and later
narrowed down to a single antibiotic (Piperacillin/Tazobactum) after receiving the sensitivity pattern. This was continued for 10
days. All central and arterial catheters were removed 2 days after the tracheostomy was performed.
Probably one of the reasons why this infant did not develop pneumonia is related to our practice of doing an “open-lung
maneuver” in all our pediatric patients. There is very limited literature available on the use of open lung in children and probably
none related to pediatric cardiac surgery. What we practice is that after every endotracheal suction, we increase the positive
end-expiratory pressure to 20 to 25 cmH2O for 30 to 40 seconds. This maneuver can be easily performed in a well-sedated child
without the need for muscle paralysis. It does not lead to any hemodynamic disturbances. In this institute, this is a routine practice,
and we have noticed a reduction in the incidence of lung collapse and pneumonia in the postoperative period.
I fully agree with Drs Ozkan and Akay that the crux of the matter lies in the prevention of PNP and having a high degree of
suspicion in the intensive care unit, particularly in children who fail weaning for no particular reason.

Suresh G. Nair, MD
Department of Anaesthesiology
Division of Cardiac Anesthesia
Amrita Institute of Medical Sciences and Research Center
Kerala, India

doi:10.1053/j.jvca.2006.04.006