Respiratory Medicine CME
Volume 2, Issue 2 , Pages 92-98, 2009

High-frequency oscillatory ventilation in severe lung haemorrhage: A case study of three centres

  • Elisabeth L.I.M. Duval

      Affiliations

    • Paediatric Intensive Care Unit, University Medical Centre Utrecht, P.O. Box 85090, 3508 AB Utrecht, the Netherlands
    • Corresponding Author InformationCorresponding author. present address: Paediatric Intensive Care Unit, Q. Paola Children's Hospital, Lindendreef 1, 2020 Antwerp, Belgium. Tel.: +32 3 280 2090; fax: +32 3 281 3471.
    • ,
  • Dick G. Markhorst

      Affiliations

    • Paediatric Intensive Care Unit, University Medical Centre Utrecht, P.O. Box 85090, 3508 AB Utrecht, the Netherlands
    • Paediatric Intensive Care Unit, VU University Medical Centre, P.O. Box 7057, 1007 MB Amsterdam, the Netherlands
    • ,
  • José Ramet

      Affiliations

    • Department of Paediatrics, Queen Paola Children's Hospital, Lindendreef 1, 2020 Antwerp, Belgium
    • ,
  • Adrianus J. van Vught

      Affiliations

    • Paediatric Intensive Care Unit, University Medical Centre Utrecht, P.O. Box 85090, 3508 AB Utrecht, the Netherlands

Received 8 August 2008; accepted 15 October 2008.

Article Outline

Summary 

Aim

To describe the safety and efficacy of HFOV as a rescue therapy for lung haemorrhage.

Methods

We conducted a retrospective case study of nine children. Lung haemorrhage was defined as large amounts of blood-stained effluent not attributable to a cardiovascular malformation or trauma, with bilateral opacities on chest X-ray. HFOV was started when conventional ventilation was ineffective in controlling the haemorrhage resulting in hypoxaemia or hypercarbia. A strategy was used aiming at tamponading transudation of oedema and decreasing blood flow from ruptured vessels.

Results

Seven infants improved significantly on HFOV. Two infants died, both showing an increasing oxygenation index.

Conclusions

HFOV therapy can be life-saving in massive lung haemorrhage in children, using a strategy with high pressures to tamponade transudation of haemorrhagic oedema, and to decrease blood flow from ruptured arterioles by reducing blood flow and increasing intrathoracic pressure. Similar to previous trials, an increasing oxygenation index was a sign of imminent death.

Keywords: Paediatrics, Lung haemorrhage, High-frequency oscillatory ventilation, Respiratory failure

Abbreviations: HFOV, high-frequency oscillatory ventilation, CMV, conventional mechanical ventilation, HPO, haemorrhagic pulmonary oedema, ECMO, extracorporeal membrane oxygenation, AVSD, atrioventricular septum defect, BiPAP, biphasic positive airway pressure, Paw, mean airway pressure, CDP, continuous distending pressure, OI, oxygenation index, MVI, modified ventilatory index, CMV-pneumonia, cytomegalovirus pneumonia, DIC, disseminated intravascular coagulation, HFV, high-frequency ventilatory

 

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Introduction 

Haemorrhagic pulmonary oedema (HPO) is a relatively uncommon but potentially life threatening event in children. In general it is a presenting symptom of an underlying condition, often with heterogeneous causes beyond the neonatal period. In most instances pulmonary haemorrhage is a reflection of advanced pulmonary oedema, although true traumatic haemorrhage can occur as well.1, 2 Accumulation of the haemorrhagic fluid in the alveoli will result in both airway obstruction and ventilation–perfusion mismatch with acute gas exchange failure. These gas exchange disturbances are often refractory to conventional mechanical ventilation (CMV) even with high peak and end-expiratory pressures with consequently a substantial mortality and morbidity due to barotrauma or volutrauma.1 Although mortality is high (up to 50%), HPO does not significantly increase the risk of later pulmonary or neurodevelopmental disabilities among those who survive, justifying the use of invasive and aggressive therapies such as extracorporeal membrane oxygenation (ECMO).3, 4 Although high-frequency oscillatory ventilation (HFOV) has previously been shown to be effective in severe respiratory failure, data on the use of HFOV for HPO in childhood are scant.5, 6, 7, 8 We report our experience with HFOV in nine patients with lung haemorrhage who deteriorated on CMV.

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Methods 

A retrospective case study was performed to identify all children who developed HPO at the University Medical Centre, Utrecht, the VU University Medical Centre, Amsterdam, the Netherlands, and Queen Paola Children's Hospital, Antwerp, Belgium. All three facilities are regional referral centres for paediatric intensive care, caring for approximately 700–1000 new paediatric intensive care patients annually. Acute pulmonary haemorrhage was defined as the presence of a large amount of blood-stained lung effluent which could not be attributed to a cardiac or vascular malformation or known extrinsic trauma, with bilateral opacities on chest X-ray.

All patients were initially ventilated with either pressure regulated volume controlled or biphasic positive airway pressure (BiPAP) controlled ventilation (Servo 300, Siemens, or Evita 2 Dura, Dräger). To control pulmonary haemorrhage, mean airway pressure (Paw) was increased and patients were put in prone position to improve oxygenation. All patients had indwelling catheters for pressure monitoring, analysis of arterial blood gases and infusion of medication and fluids. HFOV (SensorMedics 3100A, Yorba Linda, CA) was started when CMV was not effective in controlling the pulmonary haemorrhage, resulting in ongoing efflux of blood-stained fluid with progressive hypoxaemia, hypercarbia and/or severe atelectasis. The “open-lung strategy” was employed during HFOV, with high continuous distending pressure (CDP), designed primarily to rapidly recruit and maintain lung volume in diffuse alveolar disease.5, 6 The haemorrhage was deemed under control when arterial oxygen saturation (SaO2) was above 90% with an FiO2 of less than 0.6, arterial pH was above 7.25 irrespective of PaCO2 and there was no longer blood obtained from the endotracheal tube. General supportive care remained unchanged during transition. In children less than 10kg, we started with a frequency of 10–15Hz and above 10kg, 8Hz. Whenever respiratory acidosis persisted, frequency was decreased. Proximal pressure amplitude was adjusted according to chest wall vibrations and PaCO2. Inspiratory time was set at 33%. Bias gas flow was 20– 40l/min as necessary to maintain CDP. We use inline suction catheters. Suctioning usually is not necessary for the first 24h after transition to HFOV. If needed, CDP is routinely set 2–3cm higher during suctioning with return to baseline values within 20min afterwards.

We started with an FiO2 of 1.0 and CDP 4cm above Paw during CMV. Subsequently CDP was increased rapidly with steps of 2–3cmH2O, until pulmonary haemorrhage was macroscopically controlled with visual cessation of bleeding, and oxygenation targets were reached. The Institutional Review Board of our hospital approved the report of these cases. A waiver of informed consent was granted for retrospective data analysis.

Statistics 

Values are reported as median and quartiles (Q1–Q3). They were compared to baseline values on CMV, using Wilcoxon's signed ranks test (SPSS 11.5 for Windows, SPSS Software, Chicago, IL, USA). Statistical significance was assumed when p-value was less than 0.05.

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Results 

Conventional mechanical ventilation 

Table 1 shows patient characteristics and CMV values prior to translation. In five children HPO presented within 24h after initiation of CMV. Three children suffered from pneumonia, three showed massive bleeding after thoracic surgery and two showed idiopathic pulmonary haemorrhage. One child, a 4-week-old Down patient, with atrioventricular septum defect and severe tracheomalacia, had been on CMV for more than 3weeks, requiring high ventilatory support due to sepsis and severe recurrent atelectasis of the lung. On day 22 she developed HPO, probably due to barotrauma.

Table 1. Patient characteristics with CMV characteristics prior to translation.
PatientSexWeightAgeHistoryDiagnosisPIPPEEPpHPaCO2MVIPaO2/FiO2OI
kg cmH2OcmH2O torr
1M3.03wkBilateral CDH, Di George syndromePost correction CDH5077.24581169120.9
2F3.05wkTGAPost switch operation2177.37463913510.4
3F8.518mAgranulocytosisPost lung biopsy2857.2743366127.8
4F55.812yPost renal TXCMV-pneumonia40157.07928120314.7
5F5.44mOmenn syndromeIdiopathic38107.2263965339.6
6F34.010yANLL, post bone marrow TXPneumonia34207.2657396043.3
7F4.26mDown, AVSD, duodenal web, tracheo-bronchomalaciaChronic lung disease18107.3849262156.5
8M7.68mDown, ex-premature, BPDVaricella pneumonia30147.3364588324.1
9F1323mMitochondrial enzymopathyIdiopathic30167.2668418127.1

wk, weeks; m, months; y, years; CDH, congenital diaphragmatic hernia; TGA, transposition of great arteries; TX, transplantation; CMV-pneumonia, cytomegalovirus; ANLL, acute non-lymphatic leukaemia; AVSD, atrio-ventriculum septum defect; BPD, bronchopulmonary dysplasia; MVI, modified ventilatory index, respiratory rate×PaCO2 (torr)×PIP (cmH2O)/1000; OI, oxygenation index FiO2×100×CDP (cmH2O)/PaO2 (torr).

Most of the children were on CMV for a very short period with a median period (Q1–Q3) of 1 (0.6–6). Just before transition to HFOV, seven of the children showed progressive hypoxemia (Oxygenation Index (OI) >13), five of them in combination with respiratory acidosis (pH <7.25, modified ventilatory index (MVI) >40). Two had ongoing visual bleeding with atelectasis. All except two (patients 4 and 6) showed a normal coagulation status.

High-frequency oscillatory ventilation 

Nine children were treated with HFOV for HPO. Median duration (Q1–Q3) on HFOV was 9days (3–15). Median maximum CDP was 28cmH2O (22–41). HFOV improved oxygenation in seven of nine infants. Figure 1 shows the OI on CMV and during the first 72h on HFOV of all responders. Compared to baseline values there is a significant decrease in OI on t2 (p=0.028) and t3 (p=0.046). OI after 72h decreased to 6.8 (4.8–9.5). Patients 4 and 6, who died from respiratory failure, are represented separately, showing an increasing OI (Figure 2). Figure 3 shows the PaCO2 (torr) of all patients. Statistical significance was reached after 48 and 72h with a decrease from 58mmHg (48–66) pre-HFOV to 50mmHg (p=0.046) and 41mmHg (p=0.042) respectively. Figure 4 shows the PaO2/FiO2 ratio: at baseline the median was 113 (82–206); after 24 and 48h of HFOV the PaO2/FIO2 ratio had increased significantly to 214 (p=0.012) and 210 (p=0.018) respectively.

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  • Figure 1 

    Boxplot of OI values of all patients prior to and during the first 72h on HFOV. TCMV represents the PaCO2 on CMV prior to HFOV, T1, T2, T3 and T4 after stabilisation, 24, 48 and 72h on HFOV, respectively. *p<0.05.

  • View full-size image.
  • Figure 2 

    OI values of non-responders prior to and during the first 72h on HFOV. TCMV represents the PaCO2 on CMV prior to HFOV, T1, T2, T3 and T4 after stabilisation, 24, 48 and 72h on HFOV, respectively.

  • View full-size image.
  • Figure 3 

    Boxplot of PaCO2 values (torr) of all patients prior to and during the first 72h on HFOV. TCMV represents the PaCO2 on CMV prior to HFOV, T1, T2, T3 and T4 after stabilisation, 24, 48 and 72h on HFOV respectively. *p<0.05.

  • View full-size image.
  • Figure 4 

    Boxplot of PaO2/FiO2 ratio of all responders prior to and during the first 72h on HFOV. TCMV represents the PaCO2 on CMV prior to HFOV, T1, T2, T3 and T4 after stabilisation, 24, 48 and 72h on HFOV respectively. *p<0.05.

One patient developed a new airleak during HFOV (isolated pneumomediastinum). Three needed additional circulatory support during transition (one fluid resuscitation, two also inotrope support), there were no other signs of cardiac compromise in the remaining patients. Prone position was used also during HFOV to improve oxygenation. No other additional therapies were used.

Two of the patients died due to respiratory failure. The first patient was a 10-year-old girl with acute leukaemia, whose post bone marrow transplantation course was complicated with sepsis and HPO, uncontrollable with PEEP levels up to 20cmH2O. HFOV was initiated 2h after admission to our unit, but the bleeding could not be stopped with a maximum CDP of 45cmH2O, and she died within a few hours. The second patient was a 13-year-old girl who acquired CMV-pneumonia after renal transplantation. After 4days of ventilation she had a profuse bleeding, successfully treated with HFOV. A second episode of HPO on the third day appeared untreatable even with a CDP of 45cmH2O, an inspiratory time up to 50% and prone position. Both of these two non-responders showed severe disseminated intravascular coagulation (DIC). Two other patients died because of therapy withdrawal due to non-pulmonary causes; they were responding well on the oscillator, with a decrease of the OI from 28 to 7 for patient 3 and from 40 to 7 for patient 5, respectively.

All but one survivor were weaned directly from HFOV to CPAP and extubated 1day later. Two patients needed oxygen after 28days, one with pre-existent bronchopulmonary dysplasia. All were discharged home without supplemental oxygen.

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Discussion 

Our findings suggest that HFOV could be a safe rescue therapy in treating children with massive pulmonary haemorrhage. Although a rare event in childhood, pulmonary haemorrhage might be life threatening, requiring immediate intervention.1, 3, 4, 10, 16 In 1922, Browne reported six cases of what he called “acute haemorrhagic pneumonia” characterised by lung haemorrhage.11 Cole et al. in 1973 suggested that the term haemorrhagic pulmonary oedema might more accurately describe this condition. They demonstrated that the effluent was almost always haemorrhagic oedema rather than whole blood and suggested that increased pulmonary capillary pressures due to acute left ventricular failure after asphyxia, acidosis and bradycardia were the main factors in the pathogenesis.2 Nowadays, HPO is considered to be hemorrhagic oedema resulting from shear stress of pulmonary capillaries associated with lung overdistension, inadequate protective surface tension and fragility of the pulmonary capillary wall.12

HPO in childhood results from a wide aetiologic spectrum: cardiovascular malformations, infectious processes, mycotoxins, milk protein allergy and immune vasculitis.13 It has recently been revised to include those conditions with and without pulmonary capillaritis.14 It may occur in the setting of vasculitis syndromes (Wegener's granulomatosis, systemic lupus erythematosus and Goodpasture's syndrome). In this setting, a therapeutic role has been suggested for high-dose steroids. Coagulopathies and tracheobronchial trauma may lead to true haemorrhage.

This is different in the neonatal period, where the underlying cause is most likely an increase in the pulmonary blood flow through a patent ductus arteriosus, which could be potentiated by other disorders like asphyxia, infection and coagulopathy.15, 16, 17 Since exogenous surfactant was introduced, frequency of HPO in premature respiratory distress syndrome has increased.17, 18, 19 It is postulated that after surfactant exposure, pulmonary vascular resistance decreases and that the increase in left to right shunting and lung compliance results in an acute rise in lung capillary pressure, leading to pulmonary haemorrhage.4, 20

Data on incidence in children is lacking. In neonates occurrence of HPO has been estimated at 0.7– 3.8 events per 1000 living births.16, 17, 18, 19 In the 1990s, the incidence in children was increased in several Midwestern U.S. cities. Although no obvious cause was established, the toxigenic fungus Stachybotrys atra was found in almost all of the case homes studied. These spores carry several classes of toxins, which could lead to formation of fragile capillaries, subsequently at risk for stress haemorrhage.15, 20, 21

The poor prognosis of HPO was finally challenged when Cole and Entress,22 and in the late 1970s Trompeter et al.23 and Castile and Kleinber,24 described survival after treatment with mechanical ventilation. Currently, approximately 50% of infants who suffer from HPO survive.4

The first step in the treatment of HPO is to assess and ensure an adequate airway and ventilation: life threatening to these patients is asphyxia, rather than massive blood loss. The source of bleeding is usually difficult to detect. Selective intubation may be attempted but is often difficult in children, especially when the right upper lobe is involved.25, 26 Emergency bronchoscopy may be performed to localise the focus which may be controlled with pressure or topical therapy. If the bleeding persists, arteriography with selective embolisation or surgical resection of the bleeding focus may be required.27

The use of high-frequency ventilation (HFV) in HPO has not been extensively described in the literature. Table 2 shows an overview of all the reports in English on the use of HFV in children and adults with HPO.1, 10, 26, 28, 29, 30, 31, 32 There was a total of 49 patients, 5 treated with high-frequency jet ventilation, 25 with HFOV, 17 with high-frequency flow interrupter and in two patients the HFV mode is not specified. Thirty-five patients survived (71.4%) and 12 died. The cause of death was uncontrollable haemorrhage in two and severe airleak syndrome in three patients. It was unspecified in seven patients; they all died within 24h after initiation of HFOV. Similar to our report, OI was significantly decreased in the survivors. In our patients the “open-lung strategy” was employed during HFOV, with high CDP, designed primarily to rapidly recruit and maintain lung volume in diffuse alveolar disease. However, during lung haemorrhage the high CDP tamponades the transudation of haemorrhagic oedema and cells from engorged capillaries, and decreases blood flow from ruptured vessels by increasing intrathoracic pressure and reducing pulmonary blood flow.33

Table 2. Overview of the literature.
Baden et al.28De Jongh et al.29Pappas et al.30Cheng et al.31Ko et al.1Chavez et al.10Haselton et al.32Al Kharfy17Chalak et al.26
No. of cases22611811171
Age (range)InfantsAdults0.9–6m60yNeonates (gest. age 25–41wk)1m6yrNeonates (gest. age 24–29wk)Neonate (gest. age 24wk)
Cause of HPOPost arterial switch operationDuring ECMOIdiopathic (Stachybotrys atra?)Perioperatively for aortic dissection repairPDA (n=11), surfactant (n=7) MAS (n=2) asphyxia (n=1)Idiopathic (cow milk?)Post BMTxPDA (n=10), coagulopathy (n=3), unknown (n=5)Persistent pulmonary hypertension, PDA
Prior mode of CMVCMV, PIP 50cmH2O PEEP 10–15cmH2O CMV, PC-modeSeparate CMV with double lumen tubeCMV, PC-mode CMV, PC-modeCMV, Paw >12cmH2O, FiO2 0.8+pH <7.28Was already on HFV with CDP of 9cmH2O and amplitude of 28
Duration on CMV (range)<1h 1–10days<1h2h–6d1d7h42–91h3d
Mode of HFVHFOVHFJVHFJV+CMV (n=2)HFJV for the affected lungHFOV HFOVFlow interrupter HFV
HFOV (n=4)
OI on CMV (range) 10–49 Survivors: 10–20 Survivors: 26±12
Non-survivors: 8–11 Non-survivors: 59±27
Initial settings on HFVCDP 24–30cmH2O HFJV (PIP=PIP CMV)+CMV (PEEP 5cmH2O)Driving pressure 30PSI, fr 150bpm, PEEP 24cmH2OCDP=Paw on CMV+2–3cmH2O CDP of 32cmH2O
HFOV (CDP=Paw on CMV)
Days on HFV (range)2–8 0.8–5.1<1Survivors:0.5–8.138Survivors 1–512d
Non-survivors 0.4–1.3
Additional therapyNoneNone SteroidsSteroids Tracheal epinephrine
Outcome2/2 survived2/2 survived6/6 survived1/1 survived13/18 survived1/1 survived1/1 survived10/17 survived1/1 survived
Cause of death Uncontrollable airleak (n=3), uncontrollable haemorrhage (n=2) Not specified

d, days; wk, weeks; m, months; y, years; HPO, haemorrhagic pulmonary oedema; ECMO, extracorporeal membrane oxygenation; PDA, persistent ductus arteriosus; MAS, meconuium aspiration syndrome; BMTx, bone marrow transplantation; CMV, conventional mechanical ventilation; PC-mode, pressure control mode; HFV, high-frequency ventilation; HFOV, high-frequency oscillatory ventilation; HFJV, high-frequency jet ventilation; OI, oxygenation index; CDP, continuous distending pressure.

In addition, increases in intrathoracic pressure decrease intrathoracic blood volume and venous return and indirectly help to reduce the transmural intrathoracic vascular pressure. Respiratory mortality rate was two out of nine patients (22%), comparable to overall mortality of HPO on HFV. Similar to previous trials, an increasing OI was specific for imminent death.5, 6, 7, 9, 17 Our two non-responders represented true haemorrhages with severe DIC. Since the underlying conditions causing DIC and pulmonary haemorrhage could not be successfully treated, mechanical ventilation did not influence their outcome. When they were transferred to HFOV, the more powerful SensorMedics 3100B, enabling the use of higher CDP and bias flow, was not yet available. The 3100A with a maximal CDP of 45cmH2O proved to be insufficient for both children with weights of 34kg and 56kg respectively. Our data include only nine patients, a sample too small to make any conclusive result. Further research should focus on trying to determine which patient would benefit from rescuing therapy with HFOV and/or which subgroup will need additional therapy.

To conclude, HFOV can be effective in massive pulmonary haemorrhage with rapid improvement in oxygenation and ultimately life-saving effects in this often fatal condition. The use of high distending pressures aims at tamponading transudation of oedema and cells from capillaries, and decreasing blood flow from ruptured pre-capillary arterioles by reducing pulmonary blood flow and increasing intrathoracic pressure.

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Conflict of interest statement 

None of the authors has a conflict of interest to declare in relation to this work.

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References 

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PII: S1755-0017(08)00093-6

doi:10.1016/j.rmedc.2008.10.008

Respiratory Medicine CME
Volume 2, Issue 2 , Pages 92-98, 2009

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