SciELO - Scientific Electronic Library Online

vol.52 issue3Meningitis after combined spinal-epidural analgesia for labor: case reportMoyamoya disease and sevoflurane anesthesia outside the surgery center: case report author indexsubject indexarticles search
Home Pagealphabetic serial listing  

Services on Demand




Related links


Revista Brasileira de Anestesiologia

Print version ISSN 0034-7094On-line version ISSN 1806-907X

Rev. Bras. Anestesiol. vol.52 no.3 Campinas May/June 2002 



Asymmetric negative pressure pulmonary edema after  acute upper airway obstruction. Case report *


Edema pulmonar asimétrico por presión negativa pós-obstrucción aguda de vía aérea superior. Relato de caso



Aldo José Peixoto, TSA, M.D.

Chefe do Departamento de Anestesiologia do Hospital de Caridade de Erechim





BACKGROUND AND OBJECTIVES: Negative pressure pulmonary edema after acute upper airway obstruction is a well-described event, though infrequently diagnosed and reported. This report aimed at presenting a case of upper airway obstruction negative pressure pulmonary edema following acute upper airway obstruction characterized by pulmonary edema asymmetry, being more prominent in the right lung.
CASE REPORT: A 4-year-old boy, 17 kg, phisical status ASA I submitted to combined tonsillectomy, adenoidectomy and turbinate cauterization under general anesthesia with sevoflurane/nitrous oxide/O2. Surgery duration was 90 minutes without complications. During anesthetic recovery and spontaneously breathing, patient reacted to tracheal tube, which was removed. Following, ventilatory efforts resulted in chest wall retraction without apparent air movement, being impossible to ventilate him with facial mask. Symptoms evolved to severe hypoxemia (50% SpO2) requiring reintubation. At this point, it was observed that the lung was stiffer and there were bilateral rales characterizing pulmonary edema. A chest X-ray showed diffuse bilateral infiltrates, right upper lobe atelectasis and marked pulmonary edema asymmetry (right greater than left). Patient was mechanically ventilated with PEEP for 20 hours when he was extubated. There was a progressive pulmonary edema improvement and patient was discharged 48 hours later.
CONCLUSIONS: Negative pressure pulmonary edema (NPPE) is a rare event with high morbidity risk. It is often not diagnosed and requires from the anesthesiologist an updated knowledge and adequate management. It is usually bilateral, rarely unilateral, and exceptionally asymmetric as in this case. Most cases are treated by mechanical ventilation with PEEP or CPAP without any other therapy. The prognosis is favorable, with most cases recovering within the first 24 hours.

Key words: COMPLICATIONS: acute pulmonary edema, laringospasm


JUSTIFICATIVA Y OBJETIVOS: Edema pulmonar por presión negativa pós-obstrucción de vía aérea actualmente es una entidad bien descrita, no obstante, probablemente poco diagnosticada y los casos poco publicados. El objetivo de este relato es presentar un caso de edema pulmonar por presión negativa pós-obstrucción de vía aérea superior, cuya principal característica fue la asimetría de edema pulmonar, siendo mucho más acentuado en el pulmón derecho.
RELATO DEL CASO: Niño de 4 años, 17 kg, ASA I, fue sometido a adenoamigdalectomia y cauterización de cornetes, bajo anestesia general con sevoflurano/óxido nitroso/O2. La cirugía duró 1 hora y 30 minutos sin cualquier interocurrencia. Con la superficialización de la anestesia y el paciente, ventilando espontáneamente, reaccionó al tubo, que fue retirado. Después de esto, los esfuerzos ventilatorios resultaron en retracción de la pared torácica, sin aparente movimiento de aire siendo imposible ventilarlo con máscara facial, ocurriendo hipoxemia grave (SpO2 de 50%) necesitando ser reintubado. En este momento fue verificado que el pulmón se encontraba más duro y había estertores bilateralmente, caracterizando edema pulmonar. Una radiografía de tórax mostró infiltración pulmonar difuso bilateralmente, no obstante, con atelectasia del lobo superior derecho, mostrando acentuada asimetría de edema pulmonar. El paciente tuvo que ser ventilado mecánicamente con PEEP durante 20 horas, cuando fue extubado. Hubo mejoría progresiva del edema pulmonar, recibiendo alta en 48 horas.
CONCLUSIONES: El edema pulmonar por presión negativa es una entidad rara con alto grado de morbidad, poco diagnosticada y exige del anestesiologista conocimiento actualizado y tratamiento adecuado. Normalmente es bilateral, raramente unilateral y excepcionalmente con expresiva asimetría como en nuestro relato. La mayoría de los casos es tratada con soporte ventilatorio con PEEP o CPAP, no necesitando de cualquier otra terapia. El pronóstico es bueno, con mejoría en la mayoría de los casos en las primeras 24 horas.




Negative pressure pulmonary edema after acute airway obstruction is a well described event, though infrequently diagnosed and reported 1,2. Little more than 100 cases are reported in the international literature under several names, such as, “post-obstructive pulmonary edema”, “negative pressure pulmonary edema”, or “laryngospasm-induced pulmonary edema” 1. There are only 11 cases reported in the Brazilian literature 3-11.

This report aimed at describing a case of negative pressure pulmonary edema after acute upper airway obstruction characterized by asymmetric edema, more prominent in the right lung.



A 4-year-old boy, 17 kg, physical status ASA I, without other diseases, allergies or previous anesthesias, submitted to combined tonsillectomy, adenoidectomy and turbinate cauterization. Monitoring consisted of precordial stethoscope, ECG, pulse oximetry, capnography and non-invasive blood pressure. Patient was not premedicated and inhalational anesthesia was induced in the presence of the parents with facial mask and sevoflurane/nitrous oxide/O2, using a Bain circuit. A catheter was then inserted in a peripheral vein and 10 µg fentanyl and 20 mg lidocaine were injected. Anesthesia was maintained with 5% sevoflurane and nitrous oxide/O2 in a 2:1 ratio. Tracheal intubation was performed with a 5.5 tube without cuff or neuromuscular blockers and ventilation was manually controlled. Rectal 25 mg diclofenac were administered for postoperative analgesia and 2 mg dexametasone were administered aiming at nausea and vomiting prevention. Immediately before surgery, 10 µg fentanyl were administered and anesthesia was maintained with 2% to 4% sevoflurane with 60% nitrous oxide and 40% oxygen. One hour after beginning of surgery, additional 10 µg fentanyl were administered. Surgery duration was 1 hour and 30 minutes and there were no complications.

During anesthetic recovery and spontaneously breathing, patient reacted to the tracheal tube which was then removed. Following, ventilatory efforts resulted in chest wall retraction without apparent air movement. We tried to ventilate him with a facial mask, however without success and with a progressive saturation decrease which reached 50%. Patient was reintubated without neuromuscular blockers and was manually ventilated with Bain’s circuit. There was an immediate improvement in saturation which reached 98% with FiO2 of 1. At this point, it was observed that the lung was stiffer for ventilation, and auscultation revealed diffuse bilateral rales, more prominent to the right. Since the patient would not tolerate oxygen inspired fraction decrease, was desaturating below 85% and presented high respiratory rate, we decided to sedate him with midazolam. Repeated 1 mg doses were administered to maintain sedation and 2 mg morphine were associated. Surgery was being performed in a clinic without Intensive Care Unit (ICU) and this demanded some time for us to prepare patient’s safe transfer to a hospital with more resources to confirm diagnosis and start treatment.

It took approximately 90 minutes to get to the ICU. Meanwhile, the patient was ventilated with Bain or Rees-Baraka circuits with FiO2 of 1, maintaining 90% to 96% saturation. In the ICU, patient was placed in mechanical ventilation with inspiratory pressure = 20 cmH2O, HR = 20, PEEP = 10 cmH2O, SIMV modality with supporting pressure = 10 cmH2O and FiO2 = 1. Chest X-ray, made 2 hours after beginning of symptoms, showed wide parenchymal consolidation with right lung upper lobe atelectasis, while a bilateral diffuse, interstitial infiltrate was observed, together with a mild left lung vicarious hyperexpansion (Figure 1). X-ray showed that there was no selective intubation justifying right lung atelectasis and we decided for a fibrobronchoscopy which showed patent bronchi, without foreign bodies, with small bronchial mucosa hemorrhages and abundant pinkish right lung secretion. The conclusion was right lung upper lobe consolidation due to the large amount of fluid to the right.

Patient was sedated with 50 to 70 µ propofol continuous infusion and 1 mg bolus morphine every 3 hours. Rectal 25 mg diclofenac was also maintained at 8-hour intervals.

Respiratory prosthesis was progressively adjusted to obtain SpO2 above 90% with FiO2 below 0.6. Approximately 6 hours after starting positive pressure ventilation patient presented with saturation above 90% with FiO2 = 0.5 and PEEP = 10 cmH2O. Arterial blood gases were analyzed and showed pH = 7.44, PaO2 = 166 cmH2O, PaCO2 = 32 mmHg and HCO3 = 19 mEq.L-1. Another chest X-ray, 4 hours after the first, showed the disappearance of right lung atelectasis and evidenced lung diffuse infiltrates, more prominent to the right. After 6 hours of ventilatory support, saturation was maintained at 96% with FiO2 = 0.4 and PEEP = 8 cmH2O. After 12 hours of ventilatory support, saturation was maintained at 96% with FiO2 = 0.35 and PEEP = 5 cmH2O, showing significant improvement, but mechanical ventilation was maintained for 20 hours when patient was weaned and extubated. Patient’s conditions were good, with normal respiratory rate, without respiratory effort and 96% O2 saturation by nasal catheter (1 L.min-1). A chest X-ray after extubation and approximately 24 hours after the event has shown marked improvement, however with persistent residual interstitial infiltrate with minor alveolar consolidations to the right and with the left lung virtually clean, characterizing pulmonary edema asymmetry resolution (Figure 2).

Ten hours after extubation, that is, 30 hours after beginning of complication, saturation was 96% in room air and nasal catheter was removed. Patient satisfactorily ventilated both lungs with normal auscultation and was discharged from ICU.

The following day (48 hours after the event) patient was in good conditions, with normal pulmonary auscultation, with 96% SpO2 in room air and was discharged.

A chest X-ray performed 72 hours after beginning of pulmonary edema was almost normal, but there were still minor right lung upper lobe infiltrates (Figure 3).



A review of the international literature resulted in 108 cases of negative pressure pulmonary edema after airway obstruction. The first case was reported in 1977 by Oswalt et al. 12, however none of the three cases reported were caused by upper airway obstruction during anesthesia. The first cases of negative pressure pulmonary edema after airway obstruction (laryngospasm) during anesthesia were published in the 80s 13. In Brazil, Doval 3 published the first report in 1987 and from then on, only 11 cases were reported 3-11. A broader retrospective study was performed by Deepika et al. 2 in 1997, who studied the records of 31,826 surgeries performed from 1992 to 1995 in the Jackson Memorial Hospital, University of Miami, and have found 30 cases of negative pressure pulmonary edema (NPPE). The incidence of NPPE was 0.094% and complications have occurred few minutes after airway obstruction. This obstruction was more common after extubation (73.4%) and in all cases was caused by laryngospasm. In the remaining 26.6%, acute airway obstruction occurred during airway manipulation. These preoperative obstructions were caused by tumors, Ludwig’s angina and laryngospasm. Intubation and end expiratory positive pressure ventilation were performed in 83.3% of cases and only 20% needed mechanical ventilation for more than 24 hours. All patients survived. Literature suggests an incidence of 0.5 to 1/1000 anesthesias 1,2,10, with an incidence of 5% to 10% of upper airway obstruction 1, being more common in young and healthy males who are more predisposed to major negative pressure differences 2,14.

Laryngospasm is defined as glottic occlusion, secondary to laryngeal constrictor muscles contraction (interarytenoids, lateral cricoarytenoids, and internal and external thyroary- tenoids), in response to a stimulation. Laryngospasm and bronchospasm are manifestations of upper airways and lungs defensive reflex system. During laryngospasm, spasm is a response to mechanical or chemical stimulation intrinsic or extrinsic to painful stimulation, involving all laryngeal and chest wall muscles, and tracheobronchial tree smooth muscles. This protective reflex is mediated by the vagus nerve 2,15.

Laryngospasm is more often seen in anesthetic emergence during extubation 2, both with tracheal tubes and laryngeal mask 16. However, it may be less frequent when there is a major noxious stimulation in the surgical site during anesthesia recovery. This may generate high intrapleural negative pressure levels and cause pulmonary edema 17,18.

Pathophysiology of pulmonary edema after laryngospasm and upper airway obstruction seems to be multifactorial 2. Major mechanism is the generation of significant intrapleural negative pressure 19,20, which may vary from -50 to -100 mmHg 21,22. This pressure is then transmitted to the pulmonary interstitium increasing venous return to the right side of the heart and causing an increase in pulmonary capillary hydrostatic pressure. This is the initial pulmonary edema event 19-23. Due to ventricular interdependence, right ventricular distension may decrease left ventricular compliance by emptying the septum to the left and increasing left ventricle end diastolic pressure and pulmonary capillary pressure 2,23.

Intrapleural negative pressure is the primary pathological event in the genesis of pulmonary edema, but hypoxia, hypercapnia, acidosis and hyperadrenergic states also contribute to its development 2. Hypoxemia increases more pre-capillary than post-capillary pulmonary vascular resistance 24, resulting in an increase in wedge pressure. Hypoxemia changes capillary integrity and triggers adrenergic activation. A higher catecholamine release associated to hypercarbia leads to increased systemic circulation blood redistribution to the pulmonary circuit, leading to an increase in pulmonary vascular resistance. In addition, hypoxemia and acidosis are known for their myocardial depressing action, which contributes to pulmonary edema development 2.

A recent study with rats has shown a worsening in alveolar fluid clearance by volatile anesthetics (halothane and isoflurane) 25, increasing the possibility of anesthetics involvement in the pathogenesis. Postoperative myocardial depression caused by residual anesthetic agents may make this moment especially susceptible for pulmonary edema development 1.

Pulmonary edema presents with stertors and bulbous rales at auscultation, dyspnea, cyanosis and airy pinkish secretion 26. Differential diagnosis includes gastric content aspiration, hidden heart disease, fluid overload and anaphylaxis 1,26. There has been no gastric content regurgitation in our case because bronchoscopy, chest X-ray and case evolution have not shown any evidence of aspirative pneumonitis. Fluid overload was ruled out because only 250 ml lactated Ringer’s solution were infused during surgery. Our patient had no signs of cardiovascular disease. Anaphylaxis would present with erythema, shock, tissue edema or any other sign of histamine release, but none of these signs were present in our patient.

A simple chest X-ray showing edema with diffuse, probably bilateral, alveolar-interstitial pattern, more centralized with enlarged pulmonary pedicle and normal heart is a very important exam for the diagnosis of NPPE 27. Unilateral pulmonary edema reports are infrequent in the literature and causes have been patients’ position when gravitational effects could explain the presentation due to the increased blood volume and pulmonary pressure in the pending lung 28,29 and diaphragm paralysis due to interscalenic block 30. Our patient had a pulmonary edema more pronounced in the right lung without any relationship with position since the patient remained all the time in the supine position. This made us think about a difference in negative pressure between both hemithorax with a higher negative pressure in the right hemithorax, thus justifying a marked pulmonary edema to the right, even with upper lobe atelectasis. This pronounced pulmonary edema asymmetry in our patient, without being unilateral, is what makes this case peculiar.

A bronchoscopy to rule out the presence of foreign bodies revealed the absence of any obstructive factor with just a large amount of serum-bloody secretion. The large right pulmonary edema has markedly decreased this lung’s compliance, resulting in upper lobe atelectasis and consequent left lung inflation (Figure 1).

Frequent NPPE bronchoscopic findings are diffuse hemorrhages in tracheal and bronchial mucosa, suggesting that they were caused by bronchial vessels rupture. This may probably contribute to the pinkish aspect of the secretion 31.

In most publications, 85% of patients were reintubated and ventilated with PEEP 2. Some cases, however, may be treated with CPAP under facial mask or nasal prong. Recently, McConkey 1 has reported 6 pulmonary edemas after airway obstruction of which only one was reintubated.

Early laryngospasm relief with neuromuscular blockers has been suggested as a preventive measure. This would prevent intrathoracic negative pressure, adrenergic discharge and hypoxia implied in post-obstructive pulmonary edema pathogenesis 1. Maybe patients should not be reintubated without neuromuscular blockers since this mechanical and painful stimulation without relaxation could worsen pulmonary edema ethiopathogenic factors 2. For its fast onset, succynilcholine would be the drug of choice 1. Sometimes, low 5 to 10 mg succynilcholine doses are enough to treat laryngospasm 22.

Diuretics have been used in some reports, but it does not seem to be an indication for such therapy 1,2,10. Similarly, steroid therapy is not indicated 2,10,32.

NPPE prevention is difficult, but one should think about this pathology in susceptible patients (young, obese, with airway hyper-reactivity, sleep apnea and difficult intubation) 10. One could think that extubation in a deeper anesthesia plane could avoid laryngospasm, but some studies have shown that the incidence of laryngospasm in children is higher in the anesthetized group as compared to the awaken group 33. In most post-obstructive pulmonary edema reports in children, tracheal tube had been removed before emergence 34,35.

For what has been described, and according to the literature, one may conclude that:

a) NPPE is an infrequent event with high morbidity rate. It is not always diagnosed and requires updated knowledge and adequate treatment;
b) Ideally, patients should be extubated awaken since especially pediatric patients have a higher NPPE incidence when extubated before emergence;
c) Prevention and early airway obstruction relief avoiding severe prolonged hypoxemia (SpO2 below 80%) will decrease NPPE incidence. For such, neuromuscular blockers should be used for reintubation or to allow ventilation under facial mask;
d) Pulmonary edema is often bilateral, may be asymmetric and is seldom unilateral;
e) Therapy in most cases is based on PEEP or CPAP ventilation, intubated or not, and no other drug therapy is necessary;
f) Prognosis is favorable with most improvements occurring during the first 24 hours.



01. McConkey PP- Postobstructive pulmonary oedema. A case series and review. Anesth Intensive Care, 2000;28:72-76.        [ Links ]

02. Deepika K, Kenaan CA, Barrocas MS et al - Negative pressure pulmonary edema after acute upper airway obstruction. J Clin Anesth, 1997;9:403-408.        [ Links ]

03. Doval JLS - Edema pulmonar secundário a laringoespasmo. Relato de caso. Rev Bras Anestesiol, 1987;37:417-419.        [ Links ]

04. Palmieri JTS, Benigno Jr OT, Fonte EBJ - Edema pulmonar pós laringoespasmo. Relato de caso e revisão da literatura. Rev Bras Anestesiol, 1994;44:(Supl18):CBA013        [ Links ]

05. Gomes DL, Amarante G, Arturo L et al - Edema pulmonar por pressão negativa: Relato de caso. Rev Bras Anestesiol, 1997;47:(Supl 22):CBA131A.        [ Links ]

06. Grando TA, Silva ES, Santos OBAF - Edema pulmonar por pressão negativa. Relato de caso. Rev Bras Anestesiol, 1997; 47:(Supl 22):CBA131B.        [ Links ]

07. Marques MB, Borges ZDO, Castro CHV - Edema agudo de pulmão pós-extubação. Relato de caso. Rev Bras Anestesiol, 1997;47:(Supl22):CBA132A.        [ Links ]

08. Souto AFP, Silva CR, Souza LF et al - Edema agudo pulmonar associado a obstrução de vias aéreas. Apresentação de caso. Rev Bras Anestesiol, 1997;47:(Supl 22):CBA132B.        [ Links ]

09. Reascos CLA, Nishima MH, Bello CN - Edema agudo pulmonar após tentativa de intubação com anestesia tópica. Relato de caso. Rev Bras Anestesiol, 1997;47:(Supl 22):CBA133A.        [ Links ]

10. Silva ES, Santos OBAF, Grando TA - Edema pulmonar por pressão negativa. Relato de casos. Rev Bras Anestesiol, 1999; 49:343-348        [ Links ]

11. Fortis E, Meller K, Nora FS et al - Edema pulmonar por pressão negativa após laringoespasmo. Relato de caso. Rev Bras Anestesiol, 2000;50:(Supl 25):CBA105A.        [ Links ]

12. Oswalt CE, Gates GA, Holmstrom FMG - Pulmonary edema as a complication of acute airway obstruction. JAMA, 1977;238: 1833-1835.        [ Links ]

13. Lorch DG, Sahn AS - Post-extubation pulmonary edema following anesthesia induced upper airway obstruction. Are certain patients at increased risk? Chest, 1986;90:802-805.        [ Links ]

14. Calkin M, Kiim KC, Price C et al - Risk factors for negative pressure pulmonary edema. Anesth Analg, 1993;76:S32.        [ Links ]

15. Leroy DV - Clinically Relevant Anatomy, em: Kirb RR, Gravenstein N - Clinical Anesthesia Practice. Philadelphia: WB Saunders, 1994:439-457.        [ Links ]

16. Devys JM, Balleau C, Jayr C et al - Biting the laryngeal mask: an unusual cause of negative pressure pulmonary edema. Can J Anaesth, 2000;47:176-178.        [ Links ]

17. Sadraoui A, Benslama A, Miguil M et al - Pulmonary edema following laryngospasm in a child. Ann Fr Anesth Reanim, 1994; 13:865-867.        [ Links ]

18. Bhavani-Shankar K, Hart NS, Mushlin PS - Negative pressure induced airway and pulmonary injury. Can J Anaesth, 1997;44: 78-81.        [ Links ]

19. Lang SA, Duncan PG, Shephard DA et al - Pulmonary oedema associated with airway obstruction. Can J Anaesth, 1990;37: 210-218.        [ Links ]

20. Umbrain V, Camu F - Acute pulmonary edema after laryngospasm. Acta Anaesthesiol Belg, 1993;44:149-153.        [ Links ]

21. Timby J, Reed C, Zeilender S et al - “Mechanical” causes of pulmonary edema. Chest, 1990;98:973-979.        [ Links ]

22. Lathan SR, Silverman ME, Thomas BL et al - Postoperative pulmonary edema. South Med J, 1999;92:313-315.        [ Links ]

23. Salem MR, Heyman HJ - Laryngospasm and negative pressure pulmonary edema. Curr Rev Clin Anesthesiol, 1995;15: 125-132.        [ Links ]

24. Siegel LC, Pearl RG, August DA - Pulmonary capillary pressure measurement during global hypoxia in sheep. Anesth Analg, 1993;76:149-155.        [ Links ]

25. Rezaiguia-Delcaux S, Jayr C, Luo DF et al - Halothane and isoflurane decrease alveolar epithelial fluid clearance in rats. Anesthesiology, 1998;88:751-760.        [ Links ]

26. Sulek CA - Negative Pressure Pulmonary Edema, em: Gravenstein N, Kirbb RR - Complications in Anesthesiology, 2nd Ed, Philadelphia, Lippincott Raven, 1996;191-197.        [ Links ]

27. Cascade PN, Alexander GD, Mackie DS - Negative pressure pulmonary edema after endotracheal intubation. Radiology, 1993;186:671-675.        [ Links ]

28. Bourke, AM - Unilateral pulmonary oedema following postextubation laryngospasm. Anaesthesia, 1997;52:928.        [ Links ]

29. Sullivan, M - Unilateral negative pressure pulmonary edema during anesthesia with a laryngeal mask airway. Can J Anaesth, 1999;46:1053-1056.        [ Links ]

30. Betts A, Eggan JR - Unilateral pulmonary edema with interscalene block. Case report. Anesthesiology, 1998;88: 1113-1114.        [ Links ]

31. Koch SM, Abramson DC, Ford M et al - Bronchoscopic findings in post-obstructive pulmonary oedema. Can J Anaesth, 1996;43:73-76.        [ Links ]

32. Ho LI, Haarn HJ, Lien TC et al - Postextubation laryngeal edema in adults. Risc factor evaluation and prevention by hydrocortisone. Intensive Care Med, 1996;22:933-936.        [ Links ]

33. Tenório SB, Oliveira SG, Floriano MSK et al - Laringoespasmo e extubação traqueal em plano anestésico: estudo comparativo em crianças. Rev Bras Anestesiol, 1993;43:293-296.        [ Links ]

34. Brandom BW - Pulmonary edema after airway obstruction. Int Anesthesiol Clin, 1997;35:75-84.        [ Links ]

35. Lee KWT, Downes JJ - Pulmonary edema secondary to laryngospasm in children. Anesthesiology, 1983;59:695-697.        [ Links ]



Correspondence to
Dr. Aldo José Peixoto
Address: Rua São Paulo, 256/101
ZIP: 99700-000 City: Erechim, Brazil

Submitted for publication October 9, 2001
Accepted for publication December 5, 2001



* Received from Departamento de Anestesiologia do Hospital de Caridade de Erechim, RS

Creative Commons License All the contents of this journal, except where otherwise noted, is licensed under a Creative Commons Attribution License