Anaesthetics Department, Royal Free Hospital, Pond Street, London NW3 2QG, UKE-mail: clarehayesbradley@yahoo.com
Accepted for publication: December 12, 2003
![]() |
Abstract |
---|
![]() ![]() ![]() ![]() ![]() ![]() |
---|
Br J Anaesth 2004; 92: 7547
Keywords: blood, haemoptysis; complications, pulmonary haemorrhage; complications, vasculitis; position, prone; ventilation, oxygenation
![]() |
Introduction |
---|
![]() ![]() ![]() ![]() ![]() ![]() |
---|
![]() |
Case report |
---|
![]() ![]() ![]() ![]() ![]() ![]() |
---|
|
Despite one plasma exchange and cyclophosphamide, gas exchange worsened. Ventilation was with pressure control mode, FIO2 1.0, positive end-expiratory pressure (PEEP) 18 cm H2O and an inspiration:expiration ratio of 2:1. Oxygen saturations were 7080% (PaO2 6.3 kPa), and tracheal suction gave only brief improvement. On turning into the prone position, copious, heavily bloodied tracheal secretions were obtained and oxygen saturation improved (Fig. 2). In the prone position, minute ventilation (MV) increased from 9.2 litre min1 to 13.2 litre min1, and PaCO2 decreased from 9.1 kPa to 7.0 kPa. With airway pressure set at 22 cm H2O, tidal volume increased from 420 ml to 590 ml. After 10 h he was returned to the supine position and the improvement in oxygenation was initially maintained (Fig. 2). MV remained increased at 14.1 litre min1 and PaCO2 6.4 kPa. On the two subsequent days he was placed in the prone position for 14 and 15 h, respectively because of further impairment of oxygenation. Similar but less dramatic improvements occurred. No complications were encountered.
|
Ventilation was weaned as his respiratory function improved, but he remained oliguric and needed haemofiltration. After removal of the tracheal tube (day 10) he was transferred to the renal unit for further management.
![]() |
Discussion |
---|
![]() ![]() ![]() ![]() ![]() ![]() |
---|
The ANCA-associated vasculitides are syndromes previously subdivided into Wegeners, Churg Strauss and microscopic polyangiitis.1 Pulmonary haemorrhage occurs from alveolar capillaritis.1 2 Alveolar capillaries rupture into alveoli, rapidly filling them with blood.1 If patients survive the initial massive haemoptysis and respiratory failure they may secondarily develop pulmonary fibrosis or ARDS.1 At presentation, patients with vasculitic pulmonary haemorrhage may fulfil ARDS criteria, however, haemorrhage into alveoli is a specific pathology, not common to all ARDS patients, warranting separate consideration.
Management of the vasculitis includes immunosuppression and plasma exchange. Methylprednisolone and cyclophosphamide are well established therapies (sometimes with prophylaxis for cyclophosphamide-induced haemorrhagic cystitis). Pulmonary haemorrhage typically stops within 37 days of starting steroid therapy, although it can last longer.1 Plasma exchange/pheresis in ANCA-positive vasculitides is as yet unproven but often used. Evidence for improved outcome with plasma exchange in vasculitic pulmonary haemorrhage comes from Goodpastures syndrome (a similar clinical picture to the ANCA-positive vasculitides but caused by circulating anti-basement membrane antibodies). Other treatment considerations are intravenous immunoglobulin and prophylaxis against Pneumocystis carinii pneumonia.1
Serious pulmonary haemorrhage from causes other than trauma has a mortality of 3085%.3 Identification and tamponade of bleeding from a large vessel by flexible/rigid bronchoscopy may be possible, or a bleeding lung can be isolated by double lumen endotracheal tube.4 A single bleeding source can then be embolized. Intrabronchial iced saline lavage, epinephrine and tranexamic acid can be effective with a localized bleeding source, either for temporary or permanent relief,4 but are not useful in diffuse haemorrhage.
Diffuse lung haemorrhage from vasculitis may respond to activated factor VII.5 Despite normal coagulation studies, patients with systemic vasculitis can have increased tissue factor pathway inhibition, which can inhibit endogenous tissue factor/VIIa complex. By giving factor VIIa, this inhibition is bypassed and vessel coagulation improves. One such report of factor VIIa reducing vasculitic pulmonary haemorrhage has been published.5 Systemic desmopressin and tranexamic acid can also be considered.
In refractory hypoxia, inhaled nitric oxide can selectively vasodilate ventilated lung and improve oxygenation. In pulmonary haemorrhage, free haemoglobin in the airways could bind nitric oxide and thereby inhibit its effect. The anti-platelet effect of nitric oxide could be disadvantageous in acute haemorrhage.3 In a case of refractory hypoxia from diffuse lung haemorrhage caused by leptospirosis, oxygenation improved when nitric oxide was started on day 6 of intensive care admission,3 suggesting that residual blood in the airways does not contraindicate the use of nitric oxide.
A clinical trial of prone ventilation in ARDS6 found that oxygenation improved in 70% of instances, most improvement occurring in the first hour. The trial involved patients who fulfilled criteria for ARDS/acute lung injury to be placed prone for 6 h for 10 days. Overall mortality was not reduced, but patients with the lowest PaO2:FIO2 ratio had lower mortality at the end of the 10 day study, suggesting that ventilation in the prone position may be useful for severe hypoxaemia.6 The prone position may improve ventilationperfusion (V/Q) matching by changes in inflation, ventilation, recruitment and perfusion of alveoli, both in normal patients and those with ARDS.79
Ventilation in the prone position may help conditions other than ARDS. Oxygenation improved in a patient with neurogenic pulmonary oedema when the patient was kept prone for 21 h without complication.10 The improved oxygenation often persists when the patient returns to the supine position, possibly because different pressures are required to open rather than keep open airways.8
Two case reports of acute large vessel pulmonary haemorrhage managed by placing the patient in the prone position emphasize the importance of the prone position in removing secretions and/or blood. These patients had haemorrhage from a main bronchus resulting in hypoxia with and without hypoventilation. In the supine position, secretions and blood will drain posteriorly blocking dependent airways and cause hypoventilation of dorsal lung units. Drainage of blood is encouraged by the prone positionthe natural drainage position of the superior segments of the lower lobes.11 12 Clearing the airways to these lobes will allow greater ventilation and higher tidal volumes. Blood in the alveoli may be a barrier to gas diffusion. Drainage of this blood by the prone position may improve oxygenation.13
The patient reported here developed widespread alveolar haemorrhage from vasculitis, and prone ventilation improved oxygenation and ventilation dramatically. These responses were at least partially sustained in supine position. A review of the mechanisms for improvements in V/Q matching suggest why this may be so.69 Copious bloody secretions were noted each time the patient was placed prone, and the effectiveness of being turned prone to obtain drainage of the airways cannot be ignored.1113 There may be a tendency to ignore prone positioning for treatment after a study showing no mortality benefit in ARDS patients.6 This may be wrong. It may be inappropriate to extrapolate clinical findings from one conditionARDS, to anotherdiffuse pulmonary haemorrhage. No studies exist of prone ventilation for pulmonary haemorrhage. The study of patients with ARDS may have failed to show benefit because the prone position was only used for short periods. Nitric oxide has been used to treat hypoxia from pulmonary haemorrhage,3 but was not considered for this patient. Other treatments for alveolar capillaritis such as factor VIIa may be considered in the future.5 Experience from this patient suggests that prone ventilation should be considered for severe hypoxia from diffuse pulmonary haemorrhage.
![]() |
References |
---|
![]() ![]() ![]() ![]() ![]() ![]() |
---|
2 Rodriguez W, Hanama N, Guy E, Guntupalli J. Pulmonaryrenal syndromes in the intensive care unit. Crit Care Clin 2002; 18: 88195[ISI][Medline]
3 Borer A, Metz I, Gilad J, et al. Massive pulmonary haemorrhage caused by leptospirosis successfully treated by nitric oxide inhalation and haemofiltration. J Infection 1999; 38: 425[CrossRef][ISI][Medline]
4 Hakanson E, Konstantinov IE, Fransson S-G, Svedjeholm R. Management of life threatening haemoptysis. Br J Anaesth 2002; 88: 2915
5 Bettensley AD, Yankaskas JR. Factor VIIa for alveolar haemorrhage in microscopic polyangiitis. Am J Resp Crit Care Med 2002; 166: 12912[CrossRef]
6 Gattinoni L, Tognini G, Pesenti A, et al. Effect of prone positioning on the survival of patients with acute respiratory failure. N Engl J Med 2001; 345: 56873
7 Pelosi P, Brazzi L, Gatinoni L. Prone position in acute respiratory distress syndrome. Eur Respir J 2002; 20: 101728
8 Tobin A, Kelly W. Prone ventilationits time. Anaesth Intensive Care 1999; 27: 194201[ISI][Medline]
9 Mure M, Lindahl SGE. Prone position improves gas exchangebut how? Act Anaesthesiol Scand 2001; 45: 1509[CrossRef][ISI]
10 Fletcher SJ, Atkinson JD. Use of prone ventilation in neurogenic pulmonary oedema. Br J Anaesth 2003; 90: 23840
11 Savage R. Prone position as a life saving measure for acute pulmonary haemorrhage in a young adult with cystic fibrosis. Anaesth Intensive Care 2002; 30: 2235[ISI][Medline]
12 MacKenzie CF. Anatomy, physiology, and pathology of the prone position and postural drainage. Crit Care Med 2001; 29: 10845[CrossRef][ISI][Medline]
13 Savage R. Prone, head down for pulmonary haemorrhage. Br J Anaesth 2002; 89: 1856