Bernhard Panning

Acute apnea caused by an epiglottic cyst.

A life threatening complication in the course of routine sedation in a 5 year old child is reported in a case study. A retention cyst of the epiglottis was found to be responsible for obstruction of the larynx leading to acute apnea. The patient history revealed recurrent episodes of stridor previously diagnosed and treated as acute laryngotracheobronchitis as well as border line psychomotoric retardation. Cerebral magnetic resonance imaging was performed for neuroradiological evaluation. After administration of sedation the child presented with stridor and acute apnea. Emergency orotracheal intubation could prevent tracheotomy but was complicated by the unexpected presence of a tumor at the base of the tongue. Further evaluation revealed a large epiglottic cyst. After endoscopic removal of the cyst no further episodes of apnea or stridor were noted.

Cardioverter-defibrillator implantation in the catheterization laboratory: Initial experiences in 48 patients

The exponential increase in cardioverter-defibrillator implantations has resulted in a need for safe implantations that do not require long waiting periods. We report intraoperative and follow-up results in 48 patients with ventricular tachyarrhythmias who underwent cardioverter-defibrillator implantation in the catheterization laboratory. Twenty-six (54%) patients had their first cardioverter-defibrillator implant (group 1), and 22 (46%) patients underwent pulse-generator replacement (group 2). In all patients, cardioverter-defibrillator implant or pulse-generator replacement was performed with the patient under general anesthesia. In 25 (96%) of 26 patients in group 1, cardioverter-defibrillator implantation was possible with a mean defibrillation threshold of 13 +/- 8 J. One patient had a defibrillation threshold of > 25 J, and therefore cardioverter-defibrillator implant was not achieved. This patient underwent epicardial device implantation 1 day later. Another patient in group 1 had vessel rupture (vena subclavia) intraoperatively. During a mean follow-up of 2 +/- 1 months, two patients died from congestive heart failure 2 and 4 months after device implantation. An infection occurred in one patient in group 2, 3 months after generator replacement. In conclusion, these data show that in the majority of patients cardioverter-defibrillator implantation in the catheterization laboratory is safe and has a low complication rate and therefore can generally be recommended.

Multicenter experiences with a single lead electrode for dual chamber ICD systems.

NIEHAUS, M., et al.: Multicenter Experiences with a Single Lead Electrode for Dual Chamber ICD Systems. Monitoring of atrial signals improves the accuracy in identifying supraventricular tachyarrhythmias to prevent inappropriate therapies in patients with implantable ICDs. Since difficulties due to the additional atrial lead were found in dual chamber ICD systems with two leads, the authors designed a single pass VDD lead for use with dual chamber ICDs. After a successful animal study, the prototype VDD lead (single coil defibrillation lead with two additional fractally coated rings for bipolar sensing in the atrium) was temporarily used in 30 patients during a German multicenter study. Atrial and ventricular signals were recorded during sinus rhythm (SR), atrial flutter, AF, and VT or VF. The implantation of the lead was successful in 27 of 30 patients. Mean atrial pacing threshold was 2.5 ± 0.9 V/0.5 ms, mean atrial impedance was 213 ± 31Ω. Atrial amplitudes were greater during SR (2.7 ± 1.6 mV) than during atrial flutter (1.46 ± 0.3 mV, P < 0.05) or AF (0.93 ± 0.37 mV, P < 0.01). During VF atrial “sinus” signals had significantly (P < 0.01) lower amplitudes (1.4 ± 0.52 mV) than during SR. The mean ventricular sensing was 13.3 ± 7.9 mV and mean ventricular impedance was 577 ± 64Ω. Defibrillation was successful with a 20‐J shock in all patients. In addition, 99.6% of P waves could be detected in SR and 84.4% of flutter waves during atrial flutter. During AF, 56.6% of atrial signals could be detected without modification of the signal amplifier. In conclusion, a new designed VDD dual chamber lead provides stable detection of atrial and ventricular signals during SR and atrial flutter. Reliable detection of atrial signals is possible without modification of the ICD amplifier.

Zerebrale Hämodynamik während der Implantation von Kardioverter-Defibrillator-Systemen

Zusammenfassung□ GrundproblematikBei der Implantation von automatischen implantierbaren Kardioverter-Defibrillatoren (ICD) muß zur Ermittlung der Funktion und der optimalen Reizschwelle Kammerflimmern induziert werden, das einen Kreislaufstillstand und somit auch ein Sistieren der Hirndurchblutung verursacht. Ziel der vorliegenden Studie war es, bei induziertem Kammerflimmern die Veränderungen der zerebralen Blutflußgeschwindigkeit (CBFV(MCA)) in Abhängigkeit von der Länge der Fibrillationszeit und der Ausgangshöhe der CBFV(MCA) zu untersuchen.□ Patienten und Methodik60 induzierte Episoden von Kammerflimmern wurden bei neun Patienten (53,5±8 Jahre alt) während der ICD-Implantation untersucht. Zusätzlich zum anästhesiologischen Monitoring wurde zur Messung der zerebralen Blutflußgeschwindigkeit die transkranielle Doppler-Sonographie (TCD) in der Arteria cerebri media (MCA) eingesetzt. Die Dauer der Fibrillation sowie die Höhe und Dauer der CBFV(MCA)-Erhöhung in der postdefibrillatorischen Phase wurde einer Korrelationsrechnung und linearen Regression unterzogen. Außerdem wurde untersucht, ob systematische Unterschiede zwischen den verschiedenen Episoden eines Patienten bestehen (Zeittrend), wozu jeweils fünf aufeinanderfolgende Episoden verglichen wurden.□ ErgebnisseWir fanden bei allen Episoden in der postdefibrillatorischen Phase eine Hyperperfusion, das heißt ein Zeitintervall, in dem die Meßwerte der CBFV über dem vor der Fibrillation gemessenen Ausgangswert lagen. Für die Hyperperfusionsdauer ergab sich eine signifikante Abhängigkeit von der Fibrillationszeit (r=0,57; p<0,001). Die Regressionsgleichung lautet: Hyperperfusionsdauer=11,1+1,22×Fibrillationszeit. Die Hyperperfusionshöhe, das heißt die maximale CBFV nach Defibrillation, steigt mit der CBFV(MCA) vor der Fibrillation signifikant an (r=0,88; p<0,001), wobei die Regressionsgleichung lautet: Hyperperfusionshöhe=6,11+1,22×CBFV vor Fibrillation. Die Hyperperfusionsdauer wird nicht von der maximalen CBFV(MCA) nach der Defibrillation beeinflußt (r=0,08; p=0,52). Es ergaben sich keine signifikanten Unterschiede zwischen den verschiedenen Episoden eines Patienten hinsichtlich der Hyperperfusionsdauer und der maximalen CBFV nach Defibrillation.□ SchlußfolgerungNach einer induzierten ventrikulären Fibrillation ist immer eine reaktive zerebrale Hyperperfusion zu erwarten. Die Höhe der CBFV nach Defibrillation ist von der Höhe der CBFV vor der Fibrillation abhängig und verhält sich annähernd proportional zu dieser. Die Hyperperfusionsdauer (im Mittel 25,8±10,4 s) zeigt bei den von uns gemessenen Fibrillationszeiten (12±4,8 s) eine lineare Abhängigkeit von der Fibrillationsdauer. Dies gibt einen Hinweis darauf, daß es sich hier um Fibrillationszeiten handelt, bei denen sich die zerebrale Autoregulation und andere zerebrale Regulationsmechanismen reaktiv kompensierend auf die zerebrale Blutflußgeschwindigkeit auswirken. Ob der Hirnstoffwechsel ein ähnliches Verhalten zeigt wie die CBFV, ist Gegenstand weiterer Untersuchungen.Abstract□ ObjectiveDuring ICD-implantation it is necessary to prove the function and to determine the optimal threshold by means of induced ventricular fibrillation (VF). Provoked cardiac arrests cause a circulatory stop of the cerebral perfusion. Our aim was to examine the changes of cerebral blood flow velocity (CBFV(MCA)) after induced VF depending on the duration of fibrillation and prior values of CBFV(MCA).□ Patients and MethodsSixty induced episodes of VF in 9 patients (mean age±SD 53.5±8 years) were examined during ICD-implantation. Beside the standardized anaesthesiological monitoring, transcranial Doppler sonography was used to record the cerebral blood flow velocity in the middle cerebri artery CBFV(MCA). The duration of the fibrillation-period and the range and duration of the CBFV increase during the post defibrillation-period were correlated. Additionally, we examined whether systematic differences existed between the episodes of each patient (time-trend) by means of 5 following episodes of a patient.□ ResultsDuring all episodes of VF a hyperperfusion was present, that means a time intervall showing increased values of CBFV(MCA), compared to the values present before VF. The duration of hyperperfusion depended significantly on the fibrillation time (r=0,57; p<0,001). The equation of regression is: hyperperfusion time =11,1+1,22×fibrillation time. The amount of hyperperfusion, that means the maximal CBFV after defibrillation, increased significantly with CBFV(MCA) before VF (correlation=0,88; p<0,001). The equation of regression is: hyperperfusion height=6,11+1,22×CBFV(MCA) before VF. The duration of hyperperfusion is not influenced by the maximal CBFV(MCA) after defibrillation (r=0,08; p=0,52). In the examined patients no significant differences in the hyperperfusion time and maximal CBFV(MCA) after defibrillation between the episodes were found.□ ConclusionAfter induced VF you always have to expect a reactive cerebral hyperperfusion. The amount of increase of CBFV after defibrillation depends on the prior values of CBFV before fibrillation and shows a nearly proportional relation to these. The duration of hyperperfusion shows a linear dependency on VF-times. This may show that we had VF-times, in which the cerebral autoregulation and other cerebral physiological reactions compensate the drop of the CBFV(MCA) during VF in the postfibrillation time. In further studies will be examined if there are similar changes in the cerebral metabolism as in CBFV(MCA).

Tracheal adrenaline in infants

Sir, The paper of Jonmarker and coworkers (1) demonstrates that tracheal instillation of 3 pg/kg adrenaline in infants with congenital heart anomalies causes a marked increase of the mean arterial blood pressure in some infants whereas no effects at all were seen in others. The authors mention the differences between their findings in some infants and the results reported by McCrirrick and colleagues (2) who do not find any effects after tracheal administration of 10 pg/kg adrenaline in patients after coronary bypass surgery. McCrirrick et al. used a fine-bore catheter with multiple spray holes at the tip (Trache-0-Jet, International Medication Systems Ltd.) that was positioned 1-2 cm beyond the end of the tracheal tube (2). This was indicated by the marks at the proximal end of the catheter. Furthermore, the authors noted that the hemodynamic effects observed in some infants are consistent with the course of adrenaline plasma values reported by Schuttler and coworkers, who used a central venous catheter (45 cm) for deep endobronchial adrenaline administration during cardiopulmonary resuscitation (3). Finally, Jonmarker and coworkers conclude that adrenaline adsorption from the airways is unreliable, and suggest that more than 10 times the intravenous dose is needed during cardiac arrest (1). The authors diluted adrenaline to 10 pg/ml and used a 10-ml syringe to instill 9.9 to 19.8 pg “through a thin (6 Ch) suction catheter placed with its tip below the opening of the endotracheal tube”. Unfortunately, no information is given as to whether the deadspace of the suction catheter was considered. Furthermore, no information is given about the exact placement method of the suction catheter. How did the authors know that adrenaline was instilled into the trachea and not into smaller conductive airways? A peripheral catheter position would cause an instillation of adrenaline into a much smaller lung volume compared with a tracheal catheter position. The great variability of the hemodynamic effects observed in this study may depend on different instilled adrenaline doses/ kg (deadspace) and, especially, on different instillation sites. This may be the reason for the postulated unreliable adsorption from the airways. In any case, the authors’ suggestion to use a higher adrenaline dose with the described technique should be regarded with great caution. As the authors obviously demonstrate that positioning of a catheter into the airways of infants appears to be unreliable under study conditions, we agree with the authors’ final conclusion that possibly the intraosseous route is a better alternative for adrenaline administration during cardiopulmonay resuscitation of infants. Konstantinos Haymondo Bernhard Panning Siegfried Piepenbrock

Anaesthetic management during invasive and non-invasive neuroradiologic procedures

Neurodiagnostic invasive and non-invasive procedures may be performed under sedation or general anaesthesia. Both have to meet the demands of patients with neurological pathology or elevated intracranial pressure (ICP). Paediatric patients are particularly difficult to monitor, especially in nuclear magnetic resonance imaging (NMRI).