Elsevier

Resuscitation

Volume 68, Issue 1, January 2006, Pages 155-159
Resuscitation

CASE REPORT
Cardiac arrest and resuscitation with an automatic mechanical chest compression device (LUCAS) due to anaphylaxis of a woman receiving caesarean section because of pre-eclampsia

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Summary

We report a case of anaphylaxis with pulseless electrical activity (PEA)(verified by ECG and a radial intra-arterial line) in a 30-year-old woman who received 3G Promiten (dextran-1) and a prophylactic intra-venous infusion of Macrodex (dextran) for postoperative thromboembolism during caesarean section for pre-eclampsia in the 24th week of gestation. Manual chest compressions, followed by mechanical chest compressions (LUCAS, Jolife, Lund, Sweden), were performed for 50 min before restoration of spontaneous circulation (ROSC). She awoke the next day with no sequelae. She had some suction cup marks on the sternum but otherwise no complications of the chest compressions. At follow up by phone 1 month later, she and her baby were doing well.

Introduction

The annual international incidence of fatal anaphylactic reactions seems to be in the region of 154 per 1 million hospitalised patients per year [1]. Ljungstrom et al. reported in 1983 that the incidence of fatal dextran-induced anaphylactoid/anaphylactic reactions was 0.003% for dextran 40, and 0.004% for dextran 70 [2], and that reactions had occurred after infusion of only 0.5–1.0 ml of dextran [2]. Schoning et al. describe a clinical prospective study (randomised, single blind, n = 300) on the incidence of adverse reactions to colloidal polysaccharides [3]. Bronchospasm followed by cardiac arrest occurred during dextran infusion even after hapten blockage with monovalent dextran-1 [3]. The Schoning et al. study was stopped prematurely when 116 patients were included due to cardiac arrest [3]. This gives an incidence of about 0.9% with a confidence interval ranging from 0.02 to 4.96%. Laxenaire et al. reported similar incidence (1%) without pre-treatment with dextran-1 [4].

The haemodynamic pattern in anaphylactic shock with cardiac arrest was reported by Nicolas et al. in 1984 [5]. They documented a fall in mean arterial pressure (MAP) and systemic vascular resistance index (SVRI), an increase in cardiac index (CI) and stroke index (SI) with a rapid fall in wedge pressure and cardiac arrest without any arrhythmia or other ECG anomaly [5]. This demonstrates the importance of maintaining the left ventricular filling pressure at a normal level in the course of anaphylactic shock [5].

The present Guidelines on how to perform CPR during anaphylaxis and circulatory collapse (with or without PEA, asystole, or VF) are not based on double-blinded randomised studies, but on experience with nonfatal cases [6]. It is important to provide airway control, oxygenation, ventilation and support of circulation. Airway control may be a challenge; upper or lower airway obstruction due to angioneurotic oedema may cause bag-mask ventilation and tracheal intubation to fail. Cricothyrotomy may be difficult or impossible because severe swelling will obliterate landmarks. Alternative airway techniques should be considered: fiberoptic tracheal intubation, digital tracheal intubation, needle cricothyrotomy followed by transtracheal ventilation [6]. Support of circulation requires rapid volume resuscitation (2–4 l of isotonic crystalloid) and administration of vasopressors, adrenaline (epinephrine) 1–3 mg i.v. the first 3 min, 3–5 mg the next 3 min, then 4–10 μg/min) [6]. There is little data about the value of antihistamines and steroids in anaphylactic cardiac arrest, but it is reasonable to assume that little additional harm could result. Since the arrest rhythm in anaphylactic cardiac arrest is often PEA or asystole, atropine and transcutaneous pacing are recommended. Prolonged CPR is indicated in order to maintain sufficient oxygen delivery until the catastrophic effects of the anaphylactic reactions are resolved [6]. Manual chest compression for such a long time may be difficult and fail to provide sufficient blood flow, and therefore mechanical chest compression should be considered.

A review article by Wik has described most of the manual and mechanical automatic chest compression devices that have been introduced [7]. It has been reported previously that CPR in hypothermic patients, and in certain intoxication or poisoning cases may have to be continued for several hours before they respond to treatment [8], [9]. Cardiopulmonary bypass (CPB) may be preferred, but it is not available in all hospitals. Mechanical external chest compressions (ECC) may also be used as a bridge to CPB [9], [11], open-heart surgery, percutaneous intervention (PCI) [10], or organ perfusion until donation/transplantation is possible. In these cases mechanical ECC can sustain organ perfusion until more sophisticated support is available.

The present case report is the first to describe the use of a new gas powered mechanical ECC device (LUCAS, Jolife, Lund, Sweden) [9] during resuscitation from cardiac arrest caused by anaphylactic shock. A 30-year-old woman who experienced cardiac arrest after administration of Promiten (hapten, dextran-1) and Macrodex (dextran) during induction of anaesthesia for caesarean section of a 24-week baby is reported.

Section snippets

The patient

A 30-year-old woman (weight 101 kg, height 167 cm) with no previous history of allergy or diseases arrived at the operating room to have a caesarean section of a 24-week baby due to severe pre-eclamsia. Her intra-arterial blood pressure was 190/100 mmHg, pulse 76, and SaO2 97% on air, Na 134 mmol/l, K 3.8 mmol/l, thrombocytes 95 × 109 l−1, albumin 25 g/l, creatinine 69 μmol/l, and urea 6.1 μmol/l. The caesarean section was planned to be done under spinal anaesthesia.

The incident

When arriving at the operating room she received Ringers acetate 1000 ml and 2 l O2 by a nasal cannula. At 2045, 3 grams of Promiten (hapten, dextran-1) was given i.v., followed by an infusion of 500 ml Macrodex (dextran). Shortly thereafter, her blood pressure fell to 90/50 mmHg. Simultaneously she rapidly developed bronchospasm. She received ketamine 150 mg and Nimbex 10 mg for intubation. It was impossible to ventilate her due to the extremely high resistance to airway flow caused by bronchospasm.

The post resuscitation period

During the post resuscitation period, she was kept asleep and ventilated with a ventilator. She received an infusion of noradrenaline for 6 h. It was decided not to induce hypothermia due to bleeding from the vagina and nose. Serum tryptase was 95.3 μg/l (reference < 24 μg/l). All other blood samples were normal. At 30 h post cardiac arrest, anaesthesia was stopped and she woke up and was extubated at 32 h post arrest. At that time, she was able to talk and had no neurological sequelae. Her baby was

The period after hospital discharge

At follow-up, 32 days after the cardiac arrest, she had no pareses and her mental function was excellent. The baby had gained weight (640 g) and was also doing well.

Discussion

The present case report is the first published report on the use of a mechanical chest compression device (LUCAS) during resuscitation of a patient who had suffered cardiac arrest caused by anaphylactic shock. During anaphylactic reactions, antibody/antigen reaction causes agglutination of plasma protein and aggregates of immune complexes plasma protein, and blood cells obstruct the capillaries [12]. The volume of circulating plasma falls [13]. The remaining blood may not pass capillary

Conclusion

Victims of anaphylaxis with circulatory arrest should be seen as potentially resuscitable with a prospect of full recovery if prolonged manual and mechanical CPR, epinephrine and infusion of isotonic solutions are delivered.

References (25)

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    Anaphylactoid complications related to the use of 40,000 molecular weight dextran

    Annals de l’Anesthesiologie Francaise

    (1976)
  • F. Nicolas et al.

    Hemodynamic pattern in anaphylactic shock with cardiac arrest

    Crit Care Med

    (1984)
  • Cited by (0)

    A Spanish and Portuguese translated version of the summary of this article appears in the online version, at 10.1016/j.resuscitation.2005.06.001.

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