Skip Navigation LinksHome > September 2000 - Volume 93 - Issue 3 > Pulmonary Hemorrhage Associated with Negative-pressure Pulmo...
Anesthesiology:
Case Reports

Pulmonary Hemorrhage Associated with Negative-pressure Pulmonary Edema

Dolinski, Sylvia Y. M.D.*; MacGregor, Drew A. M.D.†; Scuderi, Phillip E. M.D.†

Free Access
Article Outline
Collapse Box

Author Information

NEGATIVE-PRESSURE pulmonary edema (NPPE) is an infrequent complication of acute airway obstruction, such as what can occur with laryngospasm. Typically, this complication develops in young, healthy patients without underlying disease. We describe a case of severe endobronchial and alveolar hemorrhage that complicated postextubation laryngospasm.
Back to Top | Article Outline

Case Report

An otherwise healthy 33-yr-old woman underwent elective outpatient septoplasty at our institution for relief of chronic nasal obstructive symptoms. The patient quit smoking 2 yr before the surgery. She had previously undergone general anesthesia once, without complications. There was no family history of difficulties with anesthesia. The patient’s height was 160 cm, she weighed 70 kg, and results of her physical examination were normal.
Fig. 1
Fig. 1
Image Tools
Fig. 2
Fig. 2
Image Tools
After premedication with midazolam, anesthesia was induced with use of propofol, lidocaine, and fentanyl intravenously, followed by rocuronium to facilitate tracheal intubation. Anesthesia was maintained with sevoflurane in 70% nitrous oxide and 30% oxygen. The surgery was uneventful. As the procedure concluded, nasal packing was inserted, neostigmine and glycopyrrolate were administered, and administration of inhalational agents was discontinued. The patient initiated spontaneous ventilation but began coughing vigorously. She reached for the endotracheal tube and was extubated subsequently. Her ventilatory efforts resulted in chest wall retraction, without apparent air movement for approximately 45 s. Continuous positive airway pressure with 100% oxygen was applied using a face mask. This failed to relieve the laryngospasm, and 30 mg succinylcholine was administered intravenously. The patient was reintubated without trauma to the trachea. Neither gastric contents nor blood was present in the oropharynx. Oxygen saturation measured by pulse oximetry (Spo2), which had decreased to approximately 70% before administration of succinylcholine, improved after intubation; however, 8 cm H2O positive end-expiratory pressure (PEEP) and 100% oxygen were needed to increase Spo2 to 100%. Blood pressure decreased to 77/50 mmHg but returned to 100 mmHg systolic after administration of 5.0 mg intravenous ephedrine and a total of 900 ml crystalloid. Bilateral rhonchi were audible during auscultation and a frothy serosanguinous fluid was suctioned from the endotracheal tube. Within 5 min, this fluid became progressively more bloody. A chest roentgenogram obtained in the recovery room showed perihilar interstitial and alveolar opacification consistent with pulmonary edema, with a normal-sized heart (fig. 1). Peribronchial cuffing and air bronchograms were noted in the upper lung fields. The first arterial blood gas measurement obtained within 20 min of the initial event showed a pH of 7.34, an arterial carbon dioxide tension (Paco2) of 39 mmHg, and an arterial oxygen tension (Pao2) of 61 mmHg, with a fractional inspired oxygen tension (Fio2) of 1.0. As neuromuscular blockade regressed, the patient experienced paroxysmal coughing, which seemed to exacerbate pulmonary bleeding. She was administered 25–35 μg · kg−1 · min−1 propofol by continuous infusion, 4 mg pancuronium bromide for neuromuscular blockade, and 10 mg furosemide. Mechanical ventilation was reinitiated. She was transferred subsequently to the intensive care unit with an Fio2 of 0.6, a PEEP of 8.0 cm H2O, and a respiratory rate of 10 breaths/min. With these settings, arterial blood gas measurements showed a pH of 7.35, a Paco2 of 40 mmHg, and a Pao2 of, again, 61 mmHg. During the next 4 h, respiratory and cardiovascular conditions worsened, necessitating increased Fio2 to 1.0, a PEEP of 15 cm H2O, and vasopressor support with use of 8.0 μg · kg−1 · min−1 dopamine. The patient’s condition and course were consistent with alveolar hemorrhage (fig. 2). Pulmonary and radial arterial monitoring were performed. Initial pulmonary arterial readings included cardiac output, 4.9 l/min; pulmonary arterial pressure, 29/17 mmHg; pulmonary arterial occlusion pressure, 9 mmHg; and systemic vascular resistance, 950 dyne · s · cm−5. Transthoracic echocardiography showed an ejection fraction of 63% and normal chamber size. Empiric antibiotic coverage with alatrofloxacin was initiated. The patient continued to experience pulmonary hemorrhage. Her hemoglobin concentration decreased by 3.0 g/dl to 7.7 g/dl over 7 h. Bronchoscopy and open-lung biopsy were thought to be contraindicated because of the patient’s respiratory status, which necessitated a PEEP of 15 cm H2O and an Fio2 of 0.85 to yield a Pao2 of 61 mmHg. She continued to bleed extensively, resulting in transfusion of 2 units of packed erythrocytes. On the second day in the hospital, she continued to have extensive pulmonary bleeding. Decreasing arterial oxygenation necessitated an increase in Fio2 to 1.0. In addition to general supportive measures, administration of cyclophosphamide, corticosteroids, and plasmapheresis was started for presumed Wegener vasculitis, capillaritis, or Goodpasture syndrome. On the fourth postoperative day, the patient’s condition began to show marked improvement. Oxygenation improved dramatically, and Fio2 was reduced to 0.4. Neuromuscular blockade was discontinued, sedation was decreased, and ventilatory support was reduced. On the sixth postoperative day, she was extubated. Tests for human immunodeficiency virus, lupus anticoagulant, antinuclear antibodies, antineutrophil cytoplasmic antibodies, and anti–glomerular basement membrane antibodies all yielded negative results, and multiple blood and urine cultures had no microbial growth. Plasmapheresis and immunosuppressants were discontinued. She was discharged from the hospital after 2 weeks, with normal results of chest roentgenographt. Follow-up at 21 months showed no functional deficit, and, therefore, no pulmonary function tests were performed.
Back to Top | Article Outline

Discussion

We describe the case of a 33-yr-old woman whose routine surgery with general anesthesia was complicated by laryngospasm, followed by NPPE and alveolar hemorrhage. Aspiration, blood from the surgical site, fluid overload, and anaphylactoid reaction were ruled out as possible causes. The initial chest roentgenogram, arterial blood gas, and presentation after nasal surgery were characteristic of NPPE, except for the presence of pulmonary hemorrhage. Although a possible cause could have been disruption of bronchial vessels, which has been implicated as the cause of frank hemorrhage, 1,2 worsening oxygenation, continued hemorrhage with a decreasing hematocrit concentration, and alveolar consolidation shown by chest roentgenography indicate alveolar hemorrhage.
Laryngospasm is a common complication after tracheal extubation, occurring in as many as 8–237 of every 1,000 anesthetic procedures. 3–5 NPPE has been reported in 11% of healthy young patients who experience laryngospasm. 6 These data suggest that the incidence of NPPE may be as high as 1 in 1,000 anesthetic cases. Despite these statistics, the presence of pulmonary hemorrhage complicating NPPE has not been extensively reported.
Frank pulmonary hemorrhage associated with NPPE is rare, with only one report in the English literature. 7 Two other case reports describe bleeding from bronchial vessels. 1,2 Goldenberg et al.8 reported the development of tricuspid and pulmonary insufficiency in two of six patients with postlaryngospasm NPPE. The current patient had only isolated, mild tricuspid regurgitation shown by echocardiographic examination. This may have been the result of higher pulmonary artery pressure development secondary to hypoxemia because she required increasingly higher levels of Fio2 and PEEP.
Negative-pressure pulmonary edema is the result of three pathophysiologic processes: negative intrathoracic pressure, 6 increase of systemic vascular and pulmonary capillary hydrostatic pressure, and mechanical stress at the alveolar–capillary level. 9 First, negative intrathoracic pressure increases venous return by reduction in right atrial pressure, with a concomitant increase in pulmonary arterial and pulmonary capillary hydrostatic pressures, complicated by a reduction in perivascular interstitial hydrostatic pressure. 9 This causes an increased transcapillary pressure gradient, favoring the transudation of fluid into the interstitial space. In addition, increased central venous pressures impede passive lymphatic blood flow. 10 Second, pulmonary blood volume is augmented by increases in systemic pressure secondary to the release of norepinephrine in response to hypoxia, hypercapnia, and anxiety. 7 The effect is distention of the right ventricle, leading to interventricular septal shift and a resultant reduction in cardiac output. 7 The increase of systemic vascular resistance further increases left ventricular wall tension, which contributes to impediment of left ventricular ejection. 11 However, the classic description of NPPE includes serosanguinous or pink, frothy fluid, which implies some capillary leak of proteinaceous material. Therefore, the third invoked process indicates that this capillary leak could be a result of mechanical failure of the alveolar–capillary membrane, resulting in alveolar edema or frank hemorrhage. 12,13 The actual negative-pressure threshold for pulmonary microvasculature disruption is not known in humans. In a rabbit model, this stress failure occurs at a microvasculature pressure of approximately 40 mmHg. 14 Marked negative intrapleural pressures have caused increased capillary permeability in a rabbit model of reexpansion pulmonary edema. 15
Laryngospasm after tracheal extubation was observed in the patient described, and the subsequent development of NPPE was not unexpected. However, the dramatic and prolonged pulmonary hemorrhage forced us to consider other causes. These included Wegener granulomatosis, Goodpasture syndrome, capillaritis, vasculitis, and infection. Each of these potential causes was treated empirically in this patient, although each was ruled out subsequently by studies that yielded negative results. This patient shows that frank pulmonary hemorrhage can complicate NPPE after laryngospasm.
Back to Top | Article Outline

References

1. Koch SM, Abramson DC, Ford M, Peterson D, Katz J: Bronchoscopic findings in post-obstructive pulmonary oedema. Can J Anaesth 1996; 43: 73–6

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

3. Olsson GL, Hallen B: Laryngospasm during anaesthesia. A computer-aided incidence study in 136,929 patients. Acta Anaesthesiol Scand 1984; 28: 567–75

4. Lee CK, Chien TJ, Hsu JC, Yang CY, Hsiao JM, Huang YR, Chang CL: The effect of acupuncture on the incidence of postextubation laryngospasm in children. Anaesthesia 1998; 53: 917–20

5. Holmes JR, Hensinger RN, Wojtys EW: Postoperative pulmonary edema in young, athletic adults. Am J Sports Med 1991; 19: 365–71

6. Tami TA, Chu F, Wildes TO, Kaplan M: Pulmonary edema and acute upper airway obstruction. Laryngoscope 1986; 96: 506–9

7. Schwartz DR, Maroo A, Malhotra A, Kesselman H: Negative pressure pulmonary hemorrhage. Chest 1999; 115: 1194–7

8. Goldenberg JD, Portugal LG, Wenig BL, Weingarten RT: Negative-pressure pulmonary edema in the otolaryngology patient. Otolaryngol Head Neck Surg 1997; 117: 62–6

9. Timby J, Reed C, Zeilender S, Glauser FL: ‘Mechanical’ causes of pulmonary edema. Chest 1990; 98: 973–9

10. Allen SJ, Drake RE: Microvascular fluid exchange, Anesthesia: Biologic Foundations. Edited by Yaksh TL. Philadelphia, Lippincott–Raven, 1997, p 1427

11. Buda SJ, Pinsky MR, Ingens NB Jr, Daughters GT II, Stinson EB, Alderman EL: Effect of intrathoracic pressure on left ventricular performance. N Engl J Med 1979; 301: 453–9

12. Staub NC: The pathogenesis of pulmonary edema. Prog Cardiovasc Dis 1980; 23: 53–80

13. West JB, Mathieu-Costello O: Vulnerability of pulmonary capillaries in heart disease. Circulation 1995; 92: 622–31

14. West JB, Tsukimoto K, Mathieu-Costello O, Prediletto R: Stress failure in pulmonary capillaries. J Appl Physiol 1991; 70: 1731–42

15. Pavlin DJ, Nestle ML, Cheney FEW: Increased pulmonary vascular permeability as a cause of re-expansion edema in rabbits. Am Rev Respir Dis 1981; 124: 422–7

Cited By:

This article has been cited 17 time(s).

Jsls-Journal of the Society of Laparoendoscopic Surgeons
Negative Pressure Pulmonary Edema after Laparoscopic Donor Nephrectomy
Gupta, M; Akhavan, A; Hall, M; Palese, M
Jsls-Journal of the Society of Laparoendoscopic Surgeons, 16(4): 647-649.
10.4293/108680812X13517013316519
CrossRef
Revue De Pneumologie Clinique
Postobstructive pulmonary oedema: Unusual complication after endotracheal extubation at the recovery of general anaesthesia
Belyamani, L; Azendour, H; Elhassouni, A; Zidouh, S; Kamili, ND
Revue De Pneumologie Clinique, 64(5): 264-265.
10.1016/j.pneumo.2008.03.005
CrossRef
Oral Surgery Oral Medicine Oral Pathology Oral Radiology and Endodontics
Negative pressure pulmonary edema
Louis, PJ; Fernandes, R
Oral Surgery Oral Medicine Oral Pathology Oral Radiology and Endodontics, 93(1): 4-6.
10.1067/moe.2002.119909
CrossRef
Annales Francaises D Anesthesie Et De Reanimation
Pulmonary oedema after a knee arthroscopy
Idabouk, L; Minville, V; Salau, S; Castel, A; Franchitto, N; Pourrut, JC
Annales Francaises D Anesthesie Et De Reanimation, 25(9): 1007-1010.
10.1016/j.annfar.2006.03.043
CrossRef
Archives of Facial Plastic Surgery
Negative-pressure pulmonary edema after routine septorhinoplasty - Discussion of pathophysiology, treatment, and prevention
Westreich, R; Sampson, I; Shaari, CM; Lawson, W
Archives of Facial Plastic Surgery, 8(1): 8-15.

Orthopedics
Negative-pressure pulmonary edema in the arthroscopic patient
Messerschmitt, P; Stambough, JL
Orthopedics, 28(4): 413-415.

Journal of Anesthesia
Negative-pressure acute tracheobronchial hemorrhage and pulmonary edema
Papaioannou, V; Terzi, I; Dragoumanis, C; Pneumatikos, I
Journal of Anesthesia, 23(3): 417-420.
10.1007/s00540-009-0757-0
CrossRef
Chest
Negative pressure pulmonary edema as an unsuspected imitator of acute lung injury/ARDS
Ackland, GL; Mythen, MG
Chest, 127(5): 1867-1868.

Neurologia Medico-Chirurgica
Negative pressure pulmonary edema following foramen magnum decompression for Chiari malformation type I
Hirano, Y; Sugawara, T; Sato, Y; Sato, K; Omae, T; Sasajima, T; Mizoi, K
Neurologia Medico-Chirurgica, 48(3): 137-139.

Annales Francaises D Anesthesie Et De Reanimation
Postobstructif pulmonary oedema after endotracheal extubation at the recovery of general anaesthesia
Samet, A; Fossard, JP; Samet, H; Hirchi, M; Fuchs-Buder, T
Annales Francaises D Anesthesie Et De Reanimation, 24(): 1287-1290.
10.1016/j.annfar.2005.05.003
CrossRef
Anasthesiologie Intensivmedizin Notfallmedizin Schmerztherapie
Negative-pressure pulmonary edema (NPPE)
Alb, M; Tsagogiorgas, C; Meinhardt, JP
Anasthesiologie Intensivmedizin Notfallmedizin Schmerztherapie, 41(2): 64-78.
10.1055/s-2006-924969
CrossRef
Anesthesia and Analgesia
Nasal pack causing upper airway obstruction
Eipe, N; Choudhrie, A
Anesthesia and Analgesia, 100(6): 1861.
10.1213/01.ANE.0000151482.91599.CC
CrossRef
Journal of the Royal Society of Medicine
Pulmonary oedema induced by a piece of chicken
Ranta, M; Cain, AJ; Odutoye, B; Mountain, RE
Journal of the Royal Society of Medicine, 95(8): 404-405.

Canadian Journal of Anaesthesia-Journal Canadien D Anesthesie
Negative pressure pulmonary edema: endobronchial intubation or acute lung injury in a predisposed patient?
Garg, R
Canadian Journal of Anaesthesia-Journal Canadien D Anesthesie, 56(3): 264.
10.1007/s12630-009-9044-7
CrossRef
Journal of the Royal Army Medical Corps
Post-operative negative pressure pulmonary oedema in an athletic male
Stewart, SK; Johnston, AM
Journal of the Royal Army Medical Corps, 159(1): 56-58.
10.1136/jramc-2013-000016
CrossRef
Anesthesiology
Case Scenario: Acute Postoperative Negative Pressure Pulmonary Edema
Krodel, D; Bittner, E; Abdulnour, R; Brown, R; Eikermann, M
Anesthesiology, 113(1): 200-207.
10.1097/ALN.0b013e3181e32e68
PDF (1333) | CrossRef
Anesthesiology
Airway Bleeding in Negative-pressure Pulmonary Edema
McConkey, P
Anesthesiology, 95(1): 272.

Back to Top | Article Outline

© 2000 American Society of Anesthesiologists, Inc.

Publication of an advertisement in Anesthesiology Online does not constitute endorsement by the American Society of Anesthesiologists, Inc. or Lippincott Williams & Wilkins, Inc. of the product or service being advertised.
Login

Article Tools

Images

Share