Anesth Analg 2004;99:687-688
© 2004 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000133003.50366.1A
CARDIOVASCULAR ANESTHESIA
The Absence of Arterial Oxygen Desaturation During Massive Oxygen Embolism After Hydrogen Peroxide Irrigation
Wei-Zen Sun, MD*,
Chin-Shuang Lin, MD*,
Andy A. Lee, MD
, and
Wei-Hung Chan, MD*
*Department of Anesthesiology, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan; and
Department of Anesthesiology, University of Washington, Seattle, Washington
Address correspondence and reprint requests to Wei-Zen Sun, MD, Department of Anesthesiology, National Taiwan University Hospital, No. 7, Chung-Shan South Rd., Taipei 10016, Taiwan. Address e-mail to wzsun{at}ntu.edu.tw
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Abstract
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For decades, water-mill murmur, decrease in end-tidal CO2 (PETCO2), hypotension, and hypoxemia have been accepted as diagnostic criteria for gas embolism. In this case report, a 19-yr-old male patient developed a sudden reduction in PETCO2 and profound circulatory collapse 15 min after intramedullary irrigation with H2O2. However, arterial oxygen desaturation never developed throughout the entire course of resuscitation from presumed massive oxygen embolism.
IMPLICATIONS: We describe a young patient who developed circulatory collapse after intramedullary irrigation with H2O2. Notably, arterial oxygen saturation did not substantially change throughout the resuscitation from presumed oxygen embolization.
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Introduction
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Hydrogen peroxide (H2O2) can be hazardous when irrigated into the stomach (1,2), subcutaneous tissue (3), or open wounds (4). Catabolism of H2O2 produces oxygen and water; 1 mL of 3% H2O2 releases approximately 10 mL of oxygen (5). When the amount of oxygen exceeds its maximal blood solubility, venous embolization occurs. For decades, water-mill murmur, decreases in end-tidal CO2 (PETCO2), hypotension, and hypoxemia have been accepted as standard diagnostic criteria for gas embolism (6–8) and have occurred in previous reports after H2O2 irrigation (1–4). In this case report, we present a young, healthy patient who developed a sudden reduction in PETCO2, murmurs, and profound circulatory collapse 15 min after intramedullary irrigation with H2O2. However, arterial oxygen desaturation never developed throughout the entire course of resuscitation. This novel observation is discussed and reviewed.
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Case Report
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A 19-yr-old 51-kg male patient, ASA physical status I, who sustained an open, comminuted fracture of the left femur, was scheduled for removal of an infected intramedullary nail and wound debridement. He did not take any premedication before arrival in the operating room. Standard routine monitoring included electrocardiography, noninvasive arterial blood pressure, pulse oximeter, and capnography. Anesthesia was induced uneventfully and was maintained by an atracurium, desflurane, oxygen, and air mixture with a fraction of inspired oxygen of 0.5. The patient was placed in the right lateral decubitus position and maintained a stable hemodynamic status. After the intramedullary nail was removed, the surgeon inserted a 50-cm rubber tube into the femoral shaft for thorough manual irrigation by syringe. A total of 300 mL of 1% H2O2 was continuously injected through the tube. As the solution was being infused, vigorous bubbling was noted at the entry site, and very little solution was draining back out. Approximately 15 min after the irrigation, we noticed a rapid decline of PETCO2 from 32 to 15 mm Hg. Meanwhile, the arterial blood pressure was 138/80 mm Hg, heart rate was 65 bpm, and SpO2 remained at 97%. Three minutes later, sinus bradycardia with a heart rate 42 bpm and arterial blood pressure of 56/19 mm Hg suddenly developed, with marked ST segment elevation. Ventricular tachycardia and fibrillation immediately followed. Precordial compression was initiated immediately after resumption of the supine position. Defibrillation effectively converted the ventricular fibrillation to sinus arrhythmia after the first attempt with 50 J. Grade III cardiac murmurs were auscultated in both the systolic and diastolic phases. Coarse bruit pulsation was continuously felt during palpation of the common carotid artery. A few minutes later, ventricular fibrillation recurred despite further administration of epinephrine, bicarbonate, lidocaine, and calcium chloride. He was then defibrillated two more times, with success at the third attempt using 100 joules. Intermittent ST segment elevation and ventricular premature contraction were noticed, without hemodynamic derangement thereafter. The patient was then transferred to surgical intensive care unit for further monitoring and workup. Pulse oximetry values never declined to less than 94% during the resuscitation or thereafter.
For the first 8 h in the intensive care unit, the patient experienced persistent seizures that required aggressive treatment with diazepam 20 mg and a propofol 150 mg/h infusion. No axillary or subconjunctival petechiae were found. Neurological findings revealed a semicomatose status with profound decerebrate spasticity. Computed tomography showed diffuse brain swelling. Transcranial Doppler imaging demonstrated a generalized hypoperfusion pattern with an estimated intracranial pressure of 30 cm H2O. Transthoracic echocardiographic examination revealed impaired left ventricle (LV) contractility (ejection fraction, 36%) with a dilated left atrium and LV. Neither gas bubble nor intracardiac shunting was visible. Cardiac-specific enzymes mildly increased during resuscitation (troponin T, 0.5 ng/mL [<0.2 ng/mL]; troponin I, 1.5 ng/mL [<2 ng/mL]) and modestly increased 24 h later (troponin T, 1.2 ng/mL; troponin I, 10.4 ng/mL). At 48 h postresuscitation, the patient became fully alert and oriented. He was then tracheally extubated and withdrawn from anticonvulsant and inotropic drug therapy. Three months later, computed tomography and electroencephalogram were performed for follow-up and demonstrated recovery with no permanent neurological deficit.
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Discussion
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We describe a young healthy patient with a near-fatal catastrophe after H2O2 irrigation. These clinical manifestations suggest an episode of profound pulmonary, coronary, and cerebral embolism secondary to liberation of oxygen from H2O2. Because of the onset time, fat embolism syndrome is unlikely. The H2O2 solution rapidly decomposes to oxygen and water in contact with blood and tissue within the medullary space. As the tissue-born peroxidase was gradually washed away through irrigation, excessive H2O2 could gain access into the vasculature without being catalyzed. These events are consistent with a delay of 15 minutes from the time of H2O2 irrigation to the time of cardiovascular collapse. In air embolism, decreased SpO2 and PETCO2 simultaneously occur as a result of extensive intrapulmonary shunt (6,9,10). In our case, however, the development of reduced PETCO2 did not accompany hypoxemia, and SpO2 remained more than 94%. The pulse oximeter detected each arterial pulse waveform throughout the operation and before cardiac arrest, and we did not change any setting or move the patient.
Dissociation between oxygen exchange and carbon dioxide elimination is a unique finding during intrapulmonary shunting caused by profound cardiovascular collapse and gas embolism. Although ventilation to perfusion mismatch explains the reduced PETCO2 (6), it cannot explain why hypoxemia did not occur in our case. We hypothesize that excessive oxygen microbubbles, though mechanically obstructing the major vessels, could thoroughly mix with the venous blood within the right atrium and ventricle. The mechanism of oxygen exchange is similar to the bubble-type oxygenator of the cardiopulmonary bypass machine (11). As a result, the arterial blood becomes fully saturated with oxygen after traversing the pulmonary circulation. Oxygen microbubbles can provide an extrapulmonary pathway for oxygenation but have very little, if any, effect on carbon dioxide elimination. In contrast, poorly soluble gas both obstructs the vessels and fails to oxygenate the arterial blood under the circumstance of air embolism.
In summary, we report the interesting finding that oxygen embolism may not cause oxygen desaturation. This implies that a decrease in PETCO2 may be the first and only indicator of oxygen embolism prior to cardiovascular collapse. This case also reemphasizes the potential hazard of the application of H2O2 to semiclosed spaces. Therefore, the injection of H2O2 under pressure into a closed or partially closed cavity should be avoided.
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References
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Accepted for publication March 16, 2004.
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Abstract
Introduction
