Severe acute respiratory distress syndrome in pregnancy. Caesarean section in the second trimester to improve maternal ventilation.
|Article Type:||Case study|
Acute respiratory distress syndrome
Cesarean section (Case studies)
|Publication:||Name: Anaesthesia and Intensive Care Publisher: Australian Society of Anaesthetists Audience: Academic Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2007 Australian Society of Anaesthetists ISSN: 0310-057X|
|Issue:||Date: Dec, 2007 Source Volume: 35 Source Issue: 6|
|Geographic:||Geographic Scope: United Kingdom Geographic Code: 4EUUK United Kingdom|
We report the case of a 25-year-old woman in the second trimester of pregnancy with acute respiratory distress syndrome associated with miliary tuberculosis. Delivery of the baby by caesarean section at 24 weeks gestation resulted in an immediate and sustained improvement in respiratory function and maternal survival. We believe this to be the first report suggesting a role for caesarean section, performed with the aim of an improvement in maternal respiratory function, at such an early point in pregnancy.
Key Words: ARDS, pregnancy, tuberculosis
The patient was a pregnant 25-year-old, previously fit female of Indian origin. Her antenatal clinic booking weight was 63 kg at eight weeks gestation. She presented at 20 weeks gestation with a three-week history of dyspnoea, cough productive of purulent sputum and recurrent fever. Investigation over the subsequent four weeks as an inpatient failed to reveal the cause, but she was treated for presumed community-acquired pneumonia. Of note her chest X-ray on admission was unremarkable; extensive microbiological investigation failed to identify an infecting organism; a transthoracic echocardiogram was normal and all tests for a malignant or immunological cause were negative. After four weeks of fluctuating pyrexia, a repeat chest X-ray showed new nodular shadowing throughout the mid and lower lung zones bilaterally, consistent with a diagnosis of miliary tuberculosis. She was commenced on anti-tuberculous therapy with rifampicin, isoniazid, ethambutol and pyrizinamide and was subsequently admitted to the intensive care unit (ICU) because of deteriorating respiratory function. Her chest X-ray now demonstrated bilateral pulmonary infiltrates consistent with acute respiratory distress syndrome (ARDS). Because of increasing exhaustion she was sedated with propofol and alfentanil, her trachea was intubated and her lungs ventilated with pressure controlled (BiLevel[TM]) ventilation via a Puritan Bennett[R] 840[TM] (Tyco Healthcare, U.K.). Intermittent boluses of atracurium were required to improve ventilator synchrony and chest wall compliance. A 30 to 45 degree head-up posture was maintained, with a 15 degree left lateral tilt to limit the effects of aortocaval compression.
Her condition deteriorated with the development of presumed septic shock and multiple organ dysfunction, manifesting as persistent pyrexia, a serum lactate of 6 mmol/l, oliguria and hypotension requiring escalating doses of noradrenaline to 0.6 [micro]g/kg/minute. A transthoracic echocardiogram demonstrated a hyperdynamic left ventricle, moderate tricuspid regurgitation, an estimated pulmonary artery systolic blood pressure of 51 mmHg and a normal right ventricle. Her coagulation profile became deranged with a prothrombin time of 22 seconds (normal range 11 to 14 seconds). Respiratory compliance deteriorated to the point where ventilator pressures of 32/15 cm[H.sub.2]O (peak/PEEP) were necessary to achieve a tidal volume ([V.sub.T]) of approximately 280 ml. Inverse ratio ventilation (IRV) was employed with an inspiratory: expiratory time ratio of 1.5:1 with no evidence of gas trapping. An Fi[O.sub.2] of 1.0 was required to achieve a [P.sub.a][O.sub.2] of 8 to 9 kPa. The [P.sub.a]C[O.sub.2] was maintained in the range of 8 to 10 kPa, resulting in a mixed metabolic and respiratory acidosis of pH 7.04 to 7.1. In an attempt to improve maternal lung function, at 24 weeks and three days gestation, a classical caesarean section was performed in the ICU after correction of the coagulopathy with fresh frozen plasma. Anaesthesia was maintained with propofol and alfentanil infusions and muscle relaxation was achieved with a bolus of atracurium 50 mg. Immediately prior to the skin incision the [V.sub.T] had fallen to 200 ml, with an oxygen saturation (Sp[O.sub.2]) of 90% on the ventilator settings described above. Immediately following delivery of the baby the [V.sub.T] rose to 380 ml with no change in ventilator settings. Within five minutes her oxygenation improved markedly, allowing the Fi[O.sub.2] to be reduced to 0.65, while achieving an Sp[O.sub.2] of 96%. The baby was immediately intubated and transferred to the neonatal ICU but died at nine days of age due to sepsis. The improvements in maternal physiology seen on delivery were maintained after closure of the abdomen. Her urine output improved and there was no subsequent rise in serum creatinine. Noradrenaline requirement gradually decreased until discontinuation 36 hours after the caesarean section. The prothrombin time returned to normal over three days, although the platelet count fell to 59 x [10.sup.9]/l on the first postoperative day, recovering over the following week. Full enteral nutrition was re-established within 12 hours and there was no hepatic dysfunction. A tracheostomy was performed on day seven after intubation to facilitate ventilatory weaning and this was subsequently decannulated on day 35.
Two weeks following the caesarean section microbiological culture results became available, identifying Mycobacterium tuberculosis in maternal sputum, urine and the placenta. She was discharged to the ward on day 38 and to home with ongoing anti-tuberculous therapy 19 days later, having no residual physical impairment.
The patient provided written consent for the publication of this case report.
Acute respiratory distress syndrome describes a condition characterised by the acute onset of bilateral infiltrates on chest radiography, hypoxaemia (defined as a [P.sub.a][O.sub.2]/Fi[O.sub.2] ratio <200 mmHg) and no evidence of left atrial hypertension (1). This case describes ARDS due to miliary tuberculous in the second trimester of pregnancy. Caesarean section and delivery of the baby was associated with an immediate and sustained improvement in respiratory function and subsequent maternal survival. While unusual in the western world, tuberculous is a well described cause of ARDS (2). Acute respiratory distress syndrome is uncommon in pregnancy. In a retrospective cohort study of over 2.5 million deliveries in Canada between 1991 and 2000, ARDS occurred in 205 cases (0.08 cases per 1000 deliveries) and had a mortality rate of 5.4% (3). The syndrome may occur coincidentally (e.g. due to sepsis, trauma, burns etc) or as a consequence of a pregnancy-related complication (e.g. pre-eclampsia or amniotic fluid embolism).
Pregnancy has physiological effects on the maternal respiratory system that are likely to be deleterious to a patient with ARDS. The expanding uterus pushes the diaphragm up, reducing functional residual capacity and decreasing total respiratory compliance, due to a reduction in chest wall compliance (4). Lung compliance remains unchanged in normal pregnancy but is characteristically reduced in ARDS. Fetal oxygenation is clearly dependent on maternal oxygenation, requiring a gradient of partial pressure across the placenta for oxygen transfer. While the effects of maternal ARDS and hypoxia on the fetus have not been well studied, high rates of fetal death, spontaneous labour and perinatal asphyxia are reported (5-7). In addition to the effects on the lungs, pregnancy also increases oxygen consumption by approximately 20 to 30% by the third trimester6. For a recent, detailed review of ARDS in pregnancy the reader is directed to the article by Cole (8).
In the non-pregnant patient with critical respiratory failure, the therapeutic options available to improve lung function are few and are based upon limited evidence of clinically significant outcome benefit. In most clinical trials in patients with ARDS, pregnancy is an exclusion criterion, further reducing the evidence available on which to base treatment decisions in this patient group.
We were already ventilating our patient's lungs in a manner approximating to the low tidal volume regimen described by the ARDS network study (9) with the exception of our target [P.sub.a][O.sub.2] (55 to 80 mmHg in the trial). We were arbitrarily attempting to maintain the Sp[O.sub.2] >95% due to the uncertain effects of maternal hypoxia on fetal oxygenation. Delivery of the baby removes fetal well-being as a consideration when deciding on the options for ventilatory targets, including accepting lower maternal [P.sub.a][O.sub.2] values and allowing permissive hypercapnia.
Inverse ratio ventilation (which was of some benefit in this patient) can increase [P.sub.a][O.sub.2] by increasing mean airway pressure and lung recruitment, however it has not been shown to increase survival from ARDS. Inverse ratio ventilation may however reduce cardiac output, potentially compromising placental blood flow.
Prone ventilation has been shown to improve oxygenation, although not mortality, in ARDS (10). Avoiding abdominal splinting of the diaphragm is essential while ventilating a patient in the prone position; this is likely to be more difficult in the patient with a gravid uterus. Prone positioning may also result in aortocaval compression, with deleterious effects on haemodynamic status. We considered the use of a kinetic turning bed, but felt that patient rotation would be contraindicated because of the risk of intermittent aortocaval compression.
A recent study has shown that a conservative approach to fluid balance, as opposed to a liberal strategy, has been shown to improve oxygenation and shorten duration of ventilation (11). Although that trial showed no evidence of an increase in non-pulmonary organ failures in the group undergoing fluid restriction, concerns about placental perfusion led us to avoid fluid restriction and/or diuresis (6).
Other treatment modalities which may improve oxygenation in ARDS, such as inhaled nitric oxide (12), high frequency oscillatory ventilation and extracorporeal membrane oxygenation have not been shown to improve survival, have not been described in ARDS in pregnancy (8) and were not available to us. We considered that the patient was unlikely to survive a transfer to another institution offering these services.
The key decision in this patient's management was whether delivery of the fetus would improve the respiratory function in a rapidly deteriorating situation. As is often the case in the management of critically ill pregnant women, difficult decisions have to be taken in circumstances when optimal management of the mother may reduce the chance of a good fetal outcome. At 24 weeks gestation, the fetal outcome from delivery was likely to be poor, with reported mortalities of around 50% (13) and a high incidence of morbidity in survivors. Had the baby not been delivered, prolonged and probably worsening oxygen delivery to the placenta may well have led to fetal death or disability. The evidence base available to guide decision-making in this instance consists of a few small case series and isolated case reports. The published cases differ from ours in that maternal benefit from delivery is not a consistent finding; most cases occurred in the third trimester of pregnancy and very few reports included objective measures of lung mechanics. Catanzarite et al described 28 pregnant women with ARDS and recommended delivery after 28 weeks gestation for fetal wellbeing, but did not describe the maternal outcome (5). Daily et al described a 31-week gestation pregnant patient with ARDS secondary to appendicitis. Spontaneous delivery resulted in an immediate improvement in [P.sub.a][O.sub.2]/Fi[O.sub.2] ratio, from 62 to 165 mmHg, with no change in PEEP requirement (14). Tomlinson et al reported 10 patients requiring intubation (nine of whom had pneumonia) who delivered while receiving ventilatory support (15). Seven delivered vaginally and three by caesarean section. Only two patients were in the second trimester and both died. Overall there was a mean reduction in Fi[O.sub.2] of 28% but no improvement in other ventilatory indices such as tidal volume, PEEP, peak inspiratory pressure or static compliance. Tomlinson et al commented that only three patients showed dramatic improvement in all respiratory characteristics and they concluded that their data did not support a benefit of emptying the uterus in an attempt to improve maternal oxygenation. Collop and Sahn described five patients who delivered by caesarean section during ventilation, only one of whom showed dramatic improvement in oxygenation, although further details were not supplied (7). De Rooij et al reported a patient in the third trimester with amniotic fluid embolism. Caesarean section resulted in a "quick and uneventful recovery with complete resolution of the pulmonary oedema" but precise details of respiratory function were not provided (16).
In summary, we describe a 24-week gestation pregnant woman with severe ARDS who underwent caesarean section with the intention of improving maternal respiratory function. This intervention resulted in an immediate and sustained improvement in both oxygenation and respiratory system compliance. Delivery of the baby also eliminated concerns about the effects of the maternal ventilatory strategy on the developing fetus. We believe that delivery of the fetus should be considered in the management of the pregnant patient with life-threatening respiratory failure, even as early as 24 weeks gestation.
Accepted for publication on July 11, 2007.
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M. P. ORAM *, P. SEAL [[dagger]], C. E. McKINSTRY [[double dagger]]
Critical Care Unit, Cheltenham General Hospital, Cheltenham, United Kingdom
* M.B., B.Ch., F.R.C.A., D.I.C.M., Consultant.
[[dagger]] M.B., B.S., F.R.C.A., Specialist Registrar.
[[double dagger]] M.B., B.Ch., M.R.C.P., F.R.C.A., D.I.C.M., Consultant.
Address for reprints: Dr M. P. Oram, Department of Anaesthesia, Cheltenham General Hospital, Sandford Road, Cheltenham, Gloucestershire GL53 7AN, U.K.
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