A clinical case report published in Clinical Case Reports documents the occurrence of sudden respiratory failure and pulseless electrical activity cardiac arrest in a 25-year-old female patient with end-stage renal disease undergoing revision surgery for an upper-extremity arteriovenous fistula. The life-threatening deterioration was attributed to severe perioperative anaphylaxis occurring shortly after the administration of regional nerve blocks and procedural intravenous sedation. Following prolonged cardiopulmonary resuscitation and emergency initiation of veno-venous extracorporeal membrane oxygenation, the patient achieved physiological stabilization and completed an intensive multi-week recovery.
Respiratory failure during anesthesia represents an uncommon yet critical complication, arising in approximately 5% to 10% of high-risk surgical candidates and driving significant perioperative morbidity and mortality. Individuals presenting with end-stage renal disease carry heightened vulnerability to perioperative ventilatory compromise stemming from chronic fluid overload, uremic pulmonary dysfunction, severe anemia, and baseline metabolic derangements. Concurrently, these patients remain susceptible to perioperative anaphylactic reactions, an acute immunoglobulin E-mediated process wherein mast cells and basophils rapidly degranulate to release mediators such as histamine, tryptase, and platelet-activating factor. This physiological cascade produces severe bronchospasm, diffuse vasodilation, and widespread capillary leakage that can swiftly culminate in circulatory collapse.
The patient in the report was a 25-year-old female receiving thrice-weekly maintenance hemodialysis via a right internal jugular tunneled dialysis catheter who presented for elective revision of her right upper-extremity arteriovenous fistula. Her established medical history included type 1 diabetes mellitus, hypertension, asthma, deep venous thrombosis, peptic ulcer disease, postoperative nausea and vomiting, and documented difficulty with intravenous access. Ten months prior to the index procedure, she had suffered a perioperative cardiac arrest during anesthetic induction for access surgery. That previous episode featured immediate, severe bronchospasm with failed ventilation, leading to pulseless electrical activity arrest requiring cardiopulmonary resuscitation, multiple rounds of chest compressions, three doses of epinephrine, and emergency endotracheal intubation. At that time, treating teams suspected rocuronium-induced histamine release as the mechanism, though definitive diagnostic testing was not performed.
For the scheduled fistula revision, clinical teams opted for regional anesthesia, a modality frequently utilized for dialysis access creation because it provides superior vascular outcomes and higher primary patency rates compared to local infiltration. In the preoperative holding area, the patient received single-shot right brachial plexus and intercostobrachial nerve blocks to supply operative anesthesia and post-procedural analgesia. The brachial plexus block administered 6.5 mL of 0.5% bupivacaine, 2 mg of dexamethasone, and 50 mg of 1% lidocaine, while the intercostobrachial block comprised 3.5 mL of 0.5% bupivacaine, 2 mg of dexamethasone, and 50 mg of 1% lidocaine. In these regional preparations, bupivacaine and lidocaine served as the primary local anesthetic agents, while dexamethasone was incorporated as an adjuvant to prolong block duration.
Following transfer to the operating room, the patient was positioned supine and administered a single 1-mg intravenous dose of midazolam for procedural sedation during surgical skin preparation. Documented baseline vital signs showed a blood pressure of 130/82 mmHg, a heart rate of 81 beats per minute, an oxygen saturation of 89%, and a blood glucose level of 111 mg/dL. Approximately 40 minutes after completion of the regional nerve blocks and 10 minutes after intravenous midazolam administration, the patient acutely reported feeling hot and nauseated, with repeat blood glucose measured at 117 mg/dL. Her condition rapidly deteriorated as she became profoundly hypoxic and minimally responsive, with blood pressure dropping to 88/43 mmHg, pulse at 82 beats per minute, and oxygen saturation falling to 54%. Despite immediate two-hand bag-mask ventilation, she progressed into pulseless electrical activity arrest.
Advanced cardiac life support protocols were initiated immediately, incorporating continuous external chest compressions, intravenous vasopressors, and emergency endotracheal intubation utilizing a 7.0-mm cuffed tube. Intubation proved technically difficult due to copious airway secretions, requiring three GlideScope attempts that inadvertently caused a laceration to the right soft palate. Resuscitation teams placed right femoral arterial and venous lines, achieving intermittent return of spontaneous circulation supported by continuous epinephrine and norepinephrine infusions.
Despite regaining sustained return of spontaneous circulation, the patient experienced refractory physiological instability characterized by persistent hypoxemia with an arterial oxygen tension below 40 mmHg, extreme hypercapnia with arterial carbon dioxide tension exceeding 100 mmHg, and profound metabolic acidosis with a serum pH of 6.9. Laboratory investigation demonstrated a serum tryptase concentration of 137 μg/L, vastly exceeding the normal reference ceiling of 8.4 μg/L and providing biochemical confirmation of severe anaphylaxis. During cardiopulmonary resuscitation and subsequent stabilization, pharmacological administration totaled 5,144 μg of epinephrine administered via 0.1 mg/mL bolus injections, 1,785 μg of epinephrine via a 4 mg/250 mL saline infusion, and 737 μg of norepinephrine from a 16 mg/250 mL infusion. Because severe hypoxemia remained refractory to maximal mechanical ventilation, clinicians placed the patient on veno-venous extracorporeal membrane oxygenation through bilateral femoral cannulation, utilizing a blood flow of 2.82 L/min, a pump speed of 2,525 revolutions per minute, sweep gas flow of 4 L/min, fraction of inspired oxygen of 60%, maintaining oxygen saturations between 88% and 92% and arterial oxygen tension at 75 mmHg.
Over a 17-day inpatient admission, with the arrest designated as day zero, repeated bronchoscopic evaluations demonstrated submucosal erythema, thick cloudy secretions, and extensive mucus plugging, while bronchoalveolar lavage cultures showed no growth. The soft palate laceration sustained during emergency intubation was surgically sutured and managed with a 500-mg oral rinse of 5% tranexamic acid alongside empiric amoxicillin-clavulanate. Veno-venous extracorporeal membrane oxygenation support was successfully decannulated on day three. On day four, the patient was extubated to nasal cannula, with arterial blood gas testing confirming a pH of 7.38, arterial carbon dioxide tension of 52 mmHg, arterial oxygen tension of 109 mmHg, and serum bicarbonate of 30 mmol/L.
The patient subsequently experienced secondary respiratory decompensation, requiring escalation to a high-flow nasal cannula on day six after noninvasive ventilation failed due to severe agitation. On day seven, worsening respiratory failure with tachypnea and arterial oxygen tension of 48 mmHg necessitated emergency re-intubation, with empiric piperacillin-tazobactam and vancomycin started pending microbiology results. Transthoracic echocardiography documented preserved biventricular systolic function, showing a left ventricular ejection fraction of 60% and a normal right ventricle. Following clinical improvement, she was successfully extubated to nasal cannula on day 11 and remained stable, with thrice-weekly hemodialysis maintained through her right internal jugular tunneled catheter throughout hospitalization.
In evaluating the potential drivers of the patient’s respiratory arrest, the authors examined multiple contributing factors alongside anaphylaxis, including regional phrenic nerve blockade, central oversedation, and upper airway obstruction. Phrenic nerve involvement causing hemidiaphragmatic paralysis occurs in 34% to 70% of supraclavicular brachial plexus blocks even with ultrasound guidance, which can induce severe ventilatory compromise in baseline-vulnerable, anemic, and fluid-overloaded dialysis patients. Furthermore, midazolam depresses central hypoxic and hypercapnic ventilatory drives, creating compounded risks in individuals with preexisting asthma and renal failure, particularly in preoperative holding settings where continuous respiratory monitoring may be less rigorous. While mechanical airway obstruction from muscle relaxation can induce hypoxemia, mechanical vascular obstruction secondary to fistula thrombus mobilization was considered unlikely because the surgical revision had not yet begun prior to arrest and imaging showed no pulmonary embolism.
The clinical course and markedly elevated serum tryptase level strongly supported perioperative anaphylaxis, prompting allergy specialists to recommend temporary avoidance of all perioperative agents administered during both surgical events. However, the report highlights key diagnostic limitations: clinical details from the initial arrest were reconstructed retrospectively, and confirmatory outpatient allergy testing was not completed following discharge. Because the patient received multiple simultaneous pharmacological agents and rocuronium was not utilized during the second event, the specific causative allergen could not be definitively established. To minimize future perioperative risks in complex dialysis patients, the authors emphasize thorough preoperative risk stratification, using infraclavicular rather than supraclavicular approaches to limit phrenic nerve spread, selecting anesthetics with favorable cardiovascular profiles such as ropivacaine over bupivacaine, employing minimal effective local volumes, and executing prompt life support including extracorporeal membrane oxygenation when refractory hypoxemia occurs.
Subject of Research: Perioperative anaphylaxis, respiratory failure, and extracorporeal life support in end-stage renal disease
Article Title: Perioperative Anaphylaxis and Respiratory Failure During AVF Surgery in an End‐Stage Renal Disease Patient
Article References: Dow, M., Srinivasan, A., & Ayad, S. (2026). Perioperative Anaphylaxis and Respiratory Failure During AVF Surgery in an End‐Stage Renal Disease Patient. Clinical Case Reports, 14(11), Article e73809. https://doi.org/10.1002/ccr3.73809
Image Credits: AI Generated
DOI: 10.1002/ccr3.73809
Keywords: perioperative anaphylaxis, end-stage renal disease, arteriovenous fistula, cardiac arrest, extracorporeal membrane oxygenation, serum tryptase, regional anesthesia, respiratory failure, Perioperative, Anaphylaxis, Respiratory, Failure
News Source: Ophelia Keating. (November 6, 2026). Severe Perioperative Anaphylaxis and Cardiac Arrest Complicate Vascular Access Surgery. Scienmag.



