Two probable anaphylactic events during consecutive cranial surgeries: case report/Dos probables eventos de anafilaxia durante cirugias craneales consecutivas. Reporte de caso.
Anaphylaxis is a systemic life-threatening hypersensitivity reaction (HR). (1) Perioperative anaphylaxis is among the main causes of anesthetic complications, with an incidence rate of 1/1250 to 1/18,600 procedures and a mortality rate between 4% and 4.7% (pharmacological anaphylaxis). (2) It is caused by the stimulus of bioactive mediators releasing mast cells and basophils, in 2 or more body systems, resulting in increased capillary permeability, vasodilatation, bronchoconstriction, and hypotension. (3)
Intraoperative anaphylaxis is a complex diagnosis as several symptoms cannot be evaluated in a sedated or unconscious patient, the cutaneous signs are hidden under the surgical drapes, and several drugs are administered simultaneously. (3,4) A total of 90% of the cases develop during induction, although there are late reactions as well, and the symptoms exhibit varying intensities, ranging from mild HRs with a preponderance of cutaneous manifestations (grade I) to cardiac and/or respiratory arrest (grade IV). (3,5,6) In thepresenceofonly1 symptom, intraoperative anaphylaxis may be misdiagnosed, in addition to the lack of an evaluation by the allergy clinic, and the risk of a new--potentially lethal--exposure to the agent involved. (6)
The most frequent signs in the presence of adverse reactions are the absence of pulse, difficult ventilation from bronchospasm, desaturation, and even cardiovascular collapse or cardiac arrest as the primary manifestation. (3,5) The reduction in end-tidal C[O.sub.2] (ETC[O.sub.2]) below 20 mm Hg has also been considered a valuable marker. (6,7)
A 44-year-old male patient from a rural area, admitted to the intermediate care unit following his discharge from the intensive care unit (ICU), as a result of supraventricular tachycardia (SVT) over an elective cranial surgery which led to the interruption of the procedure (Table 1). A mild right hemiparesis was identified in the patient on clinical examination. The cardiology evaluation failed to identify any alteration and concluded that the SVT was the result of surgical manipulation or autonomic reflex. An amount of 10 mg of propanolol b.i.d. were prescribed, with a Goldman 2 index classification. No allergies (neither food nor drugs) were reported during the anesthetic evaluation and the patient was classified as American Society of Anesthesiologists (ASA) class 2 and was rescheduled.
The patient was admitted to the OR with normal vital signs and 95 kg of body weight. Balanced anesthesia was administered for induction (Tables 1 and 2) and endotracheal intubation was performed with a No. 8.5 endotracheal intubation tube (ETT). The surgical procedure began with a 99% oxygen saturation ([SpO.sub.2]) and 30mm Hg of ETC[O.sub.2]. Vital signs were normal during maintenance. One hour after induction, suddenly and with no previous blood pressure (hypotension) or heart rate (bradycardia) alterations, sustained and progressive declines in ETC[O.sub.2] and [SpO.sub.2] (down to 24mm Hg and 92%, respectively) were recorded.
Due to the alterations in ETC[O.sub.2] and [SpO.sub.2], malfunction of the ETT device was ruled out initially. Immediately after, the absence of palpable pulse and SVT was identified in the multiparameter monitor, with signs of pulseless electrical activity (PEA). Furthermore, when removing the surgical drapes, generalized edema was evidenced and consequently the patient was diagnosed with probable grade IV anaphylaxis.
Advanced cardiopulmonary resuscitation (CPR) was initiated with continuous chest compressions, IV administration of 1mg of adrenalin and manual ventilation. Two minutes later, return of spontaneous circulation (ROSC) developed and the compressions were discontinued. However, they had to be reinitiated 1 minute later because of ventricular fibrillation (VF) requiring a 200 joules biphasic shock. A second dose of adrenaline was administered. The VF relapsed on 3 occasions and the same treatment was repeated. After 2 minutes, ROSC was confirmed and a subclavian venous catheter and a radial arterial catheter were placed.
Follow-up and results
The patient was admitted to the postanesthesia care unit with 70/50 mm Hg of invasive arterial pressure, 130 bpm, 90% [SpO.sub.2], central venous pressure of 10 cm[H.sub.2]O, under volume controlled mechanical ventilation and dopamine at adjustable dose. 250 mg of hydrocortisone t.i.d. were administered 10 hours after PEA, and the patient was extubated without any complications with a Glasgow score of 14 points, 15 hours later. The patient was then transferred to the intermediate care unit where dopamine was then withdrawn after 3 days and 6 days later was transferred to the general hospitalization floor from where he was finally discharged.
The intermediate care unit evaluation focused on the SVT that led to the interruption of surgery because of an initial suspicion of cardiac pathology. However, the medical record indicated that the patient was admitted to the ICU following distributive shock resulting from anaphylaxis secondary to an adverse drug reaction (ADR), with hypotension and generalized erythema. Consequently, this first event was probably consistent with grade III anaphylaxis.
The primary cause of perioperative HRs is neuromuscular relaxants (NMRs) (50% to 70%), followed by latex (12% to 16.7%), and antibiotics (15%). (2,6) Reviewing the role of the various drugs administered over surgery in the case of immediate HRs (Table 2), sodium thiopental is often involved (incidence 1:30,000), although propofol may also be the culprit. Midazolam (administered in 2 surgeries) and fentanyl (administered in all of them) rarely trigger these reactions. (8)
Two steroid monoquaternary compounds were used (Rocuronium and Vecuronium), with replaced ammonia ions. These ions represent allergenic sites involved in the specific immunoglobulin E (IgE) recognition which could explain the crossed reactivity (CR) in skin tests of 60% to 70% of patients allergic to NMRs. CR to all relaxants is more frequent when a steroid compound triggered the initial reaction. There were also HRs in NMRs-naive patients because there is CR with cosmetics, foods, and disinfectants. (9)
Other late intraoperative anaphylaxis-causing agents are iodine povidone and chlorhexidine. (10) In a previous report (11) Naranjo's algorithm was used to assess the causality of an ADR. This algorithm enabled the analysis of a second HR, with a score of 5 for the relaxant and povidone, which makes them potential ADR agents. (12) Considering that few cases were reported in response to topical povidone, the NMR would then be the causal agent. (13)
Investigating the cause of anaphylaxis may be complex, since there may be several agents involved. (8) 3 necessary evidences have been described: medical record, biological evaluation, and skin tests. (14) The biological evaluation identifies the presence of an allergic mechanism in the reaction through early laboratory tests (total tryptase blood test and plasma histamine) and late laboratory tests (prick test, basophil activation, challenge tests, and specific IgE immunoassays). (1,3,5,8,14) In this 2 potential anaphylactic events, only clinical evidence was available. Moreover, the availability of the other tests required in our setting at the time of presentation is unclear.
The critical situation was neglecting the first HR since the patient should have been evaluated by the allergy clinic and the procedure rescheduled, once the agent involved was identified. Failure to do so led to a new exposure to the agent, resulting in a more severe preventable reaction. (6,15) Actually, every perioperative reaction must be investigated to ensure safe anesthetic procedures in the future, because even a mild reaction may be due to hypersensitivity and hence be neglected or attributed to unspecificreactions. (8,16,17)
Some therapeutic approaches to these potential HRs may be optimized; for instance, administering IV fluid challenges, Chlorphenamine and Amiodarone (to avoid the relapse of atrial fibrillation) (1,18) (Table 3). The value of the acronym dislodgement, obstruction, suspected pneumothorax and equipment or operator problem (DOPE) has been recognized to address the deterioration of the patient in mechanical ventilation. (20)
Following a HR, the anesthesiologist shall request laboratory tests that contribute to a clinical diagnosis, in addition to interconsulting with the allergy clinic to investigate the causal agent. Furthermore, all the Peruvian anesthesiology services nowadays have a mandatory record of adverse events. Finally, the early identification of the disruption in ETC[O.sub.2] y [SaO.sub.2] enabled the introduction of timely CPR measures to avoid a fatal outcome.
There were no follow-up anesthesia visits to give the patient a detailed written pharmacological report, and the result of the patient's allergy evaluation is unknown.
The Hospital Ethics Committee approved the publication of this case report because the patient is not a resident of the hospital jurisdiction to be able to obtain a written consent.
Protection of persons and animals: The authors declare that the procedures followed were consistent with the ethical standards of the responsible human experimentation committee and pursuant to World Medical Association and the Declaration of Helsinki.
Confidentiality of the information: The authors state that they have followed the institutional protocols regarding the publication of patient information.
Right to privacy and informed consent: The authors have obtained the informed consents of the patients and/or individuals mentioned herein. The custodian of this document is the corresponding author.
The authors did not receive any financial contributions for this article.
Conflicts of interest
The authors have no conflict of interest to disclose.
(1.) Chapman J, Lalkhen AG. Anaphylaxis. Anaesth Intensive Care Med 2017;18:16-21.
(2.) Mertes PM, Volcheck GW, Garvey LH, et al. Epidemiology of perioperative anaphylaxis. Presse Med 2016;45:758-767.
(3.) Kannan JA, Bernstein JA. Perioperative anaphylaxis: diagnosis, evaluation and management. Immunol Allergy Clin North Am 2015;35:321-334.
(4.) Peroni DG, Sansotta N, Bernardini R, et al. Perioperative allergy: clinical manifestations. Int J Immunopathol Pharmacol 2011;24 (3 suppl):S69-S74.
(5.) Moneret-Vautrin DA, Mertes PM. Anaphylaxis to general anesthetics. Chem Immunol Allergy 2010;95:180-189.
(6.) Mertes PM, Tajima K, Regnier-Kimmoun MA, et al. Perioperative anaphylaxis. Med Clin N Am 2010;94:761-789.
(7.) Gouel-Cheron A, de Cahisemartin L, Jonsson F, et al. Low end-tidal CO2 as a real-time severity marker of intra-anaesthetic acute hypersensitivity reactions. Br J Anaesth 2017;119:908-917.
(8.) Volcheck GW, Mertes PM. Local and general anesthetics immediate hypersensitivity reactions. Immunol Allergy Clin North Am 2014;34:525-546.
(9.) Naguib M, Lien CA, Meistelman C. Miller RD. Pharmacology of neuromuscular blocking drugs. Miller's anesthesia 8th ed. Elsevier, Canada:2015.
(10.) Ewan PW, Dugue P, Mirakian R, et al. BSACI guidelines for the investigation of suspected anaphylaxis during general anaesthesia. Clin Exp Allergy 2010;40:15-31.
(11.) Aguilera-Castro F. Intraoperative recurrence of probable allergic reaction to remifentanil. Case report. Rev Colomb Anestesiol 2017;45 (s1):31-35.
(12.) Holloway K, Green T. Comites de Farmacoterapia. Guia Practica. OMS. Departamento de Medicamentos Esenciales y Politica Farmaceutica, Francia:2003.
(13.) Caimmi S, Caimmi D, Cardinale F, et al. Perioperative allergy: uncommon agents. Int J Immunopathol Pharmacol 2011;24 (3 suppl):S61-S68.
(14.) Dewachter P, Mouton-Faivre C, Emala CW. Anaphylaxis and anesthesia: controversies and new insights. Anesthesiology 2009;111:1141-1150.
(15.) Pedersen AF, Green S, Rose MA. Failure to investigate anaesthetic anaphylaxis resulting in a preventable second anaphylactic reaction. Anaesth Intensive Care 2012;40:1053-1055.
(16.) Berroa F, Lafuente A, Javaloyes G, et al. The incidence of perioperative hypersensitivity reactions: a single-center, prospective, cohort study. Anesth Analg 2015;121:117-123.
(17.) Bevilacqua-Alen E, Illodo-Miramontes G, Lopez-Gonzalez JM, et al. Anesthetic management of muscle relaxant allergy. Rev Argent Anestesiol 2017;75:7-12.
(18.) Callaway CW, Soar J, Aibiki M, et al. Part 4: advanced life support: 2015 international consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations. Circulation 2015;132 (16 suppl 1):S84-S145.
(19.) McEvoy MD, Thies KC, Einav S, et al. Cardiac arrest in the operating room: Part 2-Special situations in the perioperative period. Anesth Analg 2018;126:889-903.
(20.) Johnson KM, Lehman RE. Acute management of the obstructed endotracheal tube. Respir Care 2012;57:1342-1344.
Rafael Ramirez-Gonzales (a), Roman Augusto Del-Castillo-Gervasi (a), Carlos Javier Shiraishi-Zapata (b), John Neper Laurencio-Ambrosio (a)
(a) Department of Anesthesiology and Surgical Center, Hospital Maria Auxiliadora, Ministry of Health, Lima, Peru
(b) Surgical Center and Anesthesiology Service, Hospital EsSalud, Talara, Peru.
How to cite this article: Ramirez-Gonzales R, Del-Castillo-Gervasi RA, Shiraishi-Zapata CJ, Laurencio-Ambrosio JN. Two probable anaphylactic events during consecutive cranial surgeries: case report. Colombian Journal of Anesthesiology. 2018;46:322-326.
Read the Spanish version of this article at: http://links.lww.com/RCA/A358.
Correspondence: Servicio de Centro Quirurgico y Anestesiologia, Hospital EsSalud, Avenida Panamericana s/n Parinas, Talara, Peru. E-mail: Shiraishi52@hotmail.com
Table 1. Timeline. Date Surgical and medical therapy events 02/19/2007 Emergency surgery: DC to remove the acute subdural hematoma secondary to severe TBI. Position: ventral decubitus. Balanced general anesthesia. Monitoring: noninvasive blood pressure, electrocardiography (3 bipolar electrodes), capnography and pulse oximetry 11/7/2007 1st elective surgery: CP with autologous cranial bone flap. Position: dorsal decubitus. Balanced general anesthesia. The same monitoring 11/8/2007-11/12/2007 IMCU admission evaluation. Surgery rescheduled 11/22/2007 2nd elective programing: DC with autologous cranial bone flap. Position: dorsal decubitus. Balanced general anesthesia. The same monitoring Date Adverse reaction Management 02/19/2007 None ICU monitoring 11/7/2007 SVT Surgery was interrupted. The patient was cardioverted in the OR and admitted to the ICU 11/8/2007-11/12/2007 None Cardiology and anesthesia 11/22/2007 PEA due to probable Advanced CPR. PACU management anaphylaxis during the immediate postoperative period CP=cranioplasty, CPR=cardiopulmonary resuscitation, DC = decompressive craniotomy, ICU=intensive care unit, IMCU=intermediate care unit, PACU= postanesthesia care unit, PEA=pulseless electrical activity, SVT = supraventricular tachycardia, TBI=traumatic brain injury. Source: Authors. Table 2. Detailed list of drugs used in the 3 surgical procedures. Date Surgical procedure Preinduction medication 02/19/2007 Emergency DC 5mg of Midazolam and 8 mg of Dexamethasone 11/07/2007 1st elective CP 8mg of Dexamethasone, (interrupted because 10mg of of SVT) Metoclopramide, 5 mg of Midazolam 11/22/2007 2nd elective CP 80 mg of Lidocaine (PEA event) Operative asepsis: iodine povidone in the 3 surgeries Date Induction 02/19/2007 Fentanyl 200 [micro]g and Vecuronium 8 mg 11/07/2007 160 mg of propofol, 250 [micro]g of fentanyl, 70 mg of rocuronium 11/22/2007 Fentanyl 250 [micro]g, 400mg of sodium thiopental and 8 mg of Vecuronium Operative asepsis: iodine povidone in the 3 surgeries Date Maintenance 02/19/2007 Sevoflurane 100% 2.5% to 2% in 2L of [O.sub.2] at 100%. Two additional doses of 100 [micro]g of fentanyl 11/07/2007 Sevoflurane 100% 2.5% in 21 of [O.sub.2] at 100% 11/22/2007 Sevoflurane 100% 2.5% in 2 L of [O.sub.2] at 100%. Additional doses: 50 [micro]g of fentanyl and 2 mg of Vecuronium Operative asepsis: iodine povidone in the 3 surgeries CP=cranioplasty, DC = decompressive craniotomy, PEA=pulseless electrical activity, SVT = supraventricular tachycardia. Source: Authors. Table 3. Differential diagnosis and management of perioperative anaphylaxis in the adult. Differential diagnosis Management of severe anaphylaxis Always keep in mind Bronchial asthma Airway (A), breathing (B), circulation (C), disability (D), and exposure (E) Cardiac arrhythmia Ask for help Myocardial infarction Position the patient on a flat surface Pericardial tamponade Raise the patient's legs Pulmonary edema Evaluate any life-threatening issues for the patient: airway (laryngeal Pulmonary embolism edema, hoarseness, stridor), breathing (dyspnea, tachypnea, wheezing, Tension pneumothorax fatigue, cyanosis, [SpO.sub.2] <92%), circulation (paleness, cold and humid Venous embolism skin, hypotension, lipothymia) Sepsis Assess mental health disorders: confusion, somnolence, comma Hereditary angioedema Pre-cardiac arrest management Mastocytosis Discontinue or remove the causal agent (relaxants, antibiotics, blood Drug overdose products, contrast media or latex). Stop the surgical procedure if Malignant hyperthermia (secondary to possible. succinylcholine) In the presence of respiratory distress, intubate immediately; use [FIO.sub.2] Myotonia and masseter spasm (secondary to 100%. If sever bronchospasm develops, monitor auto-PEEP succinylcholine) Repeated doses of adrenaline (100-300 [micro]g) every 5 minutes and Hyperpotassemia (secondary to increase the dose if no improvement is identified (in the absence of an succinylcholine) IV line, 300-500 [micro]g IM) (+ or -) 2 UI of IV Vasopressin Start the adrenalin infusion (0.05-0.3 [micro]g/kg/minute IV) for maintaining a SBP [greater than or equal to] 90 mm Hg under constant monitoring (check for myocardial ischemia) Vasopressin or norepinephrine infusion in cases of hypotension refractory to a dose of >2mg of adrenalin IV fluid challenge, IV access using a large catheter: 500-1000 mL (20 mL/kg) of crystalloid. Discontinue the colloid infusion when this could be the causal agent H1 blockers: 50 mg of diphenhydramine, 10 mg of chlorphenamine H2 blockers: 20 mg of famotidine IV Corticosteroid: 50-200 mg of hydrocortisone or 1-2 mg/kg of methylprednisolone Cardiac arrest management Start CPR in the absence of carotid pulse in 10seconds Adrenalin 100-1000 [micro]g IV; you may repeat the dose administration every 3-5 minutes, or replace for a dose of 40U of IV vasopressin Briefly disconnect the ventilator if auto-PEEP is suspected Administer H1 and H2 blockers and steroids at the above-mentioned doses Consider extracorporeal support in patients with good CPR without ROSC CPR=cardiopulmonary resuscitation, [FIO.sub.2]=fraction of inspired oxygen, PEEP=positive end-expiratory pressure, ROSC=return of spontaneous circulation. Adapted from Chapman and Lalkhen, (1) Mertes et al, (6) and McEvoy et al. (19) Source: Authors.
|Printer friendly Cite/link Email Feedback|
|Title Annotation:||CASE REPORT|
|Author:||Ramirez-Gonzales, Rafael; Del-Castillo-Gervasi, Roman Augusto; Shiraishi-Zapata, Carlos Javier; Laur|
|Publication:||Revista Colombiana de Anestesiologia|
|Date:||Oct 1, 2018|
|Previous Article:||How drug companies manipulate prescribing behavior/Como las empresas farmaceuticas manipulan la conducta para formular los medicamentos.|
|Next Article:||Dipyrone-related granulocytopenia. Case report/Granulocitopenia por dipirona: reporte de caso.|