Table 1.
Principal features to consider when treating unhealthy pregnant women
Disease | Features and/or indications |
Asthma [15] | Recommended use of corticosteroids to prevent critical illness |
Oral corticosteroids associated with a two-fold increase in pre-eclampsia and with a minimal incidence (0.4%) +of oral clefts (if taken in the first trimester) | |
Pulmonary oedema [15] | Cardiogenic basis secondary to haemodynamic factors occurring during pregnancy: |
↑ cardiac output | |
↑ heart rate | |
↓ systemic vascular resistance | |
↓ colloid osmotic pressure | |
A consequence of tocolytic therapy and of pre-eclampsia | |
If no improvement within 24 h after diuresis, invasive haemodynamic monitoring and/or rapid antihypertensive therapy are required | |
Severe restrictive lung disease [10] | Risk of hypoxic and hypercapnic respiratory failure because the ability to increase ventilation is limited |
Severely reduced vital capacity but pregnancy can be well tolerated | |
Minimal complication: preterm delivery with newborn needing high-dependency support | |
Lung function and oxygen saturation should be monitored | |
Supplemental oxygen and noninvasive ventilation may be required | |
Pre-eclampsia [16] | The most common obstetric disorder, with multisystem ramifications |
↑ minute ventilation because of ↑ concentration of blood leptin (a ventilation-stimulating hormone) | |
↓ vital capacity secondary to lower transverse section area of the upper airways, pharyngeal oedema and excessive weight gain with higher adipose deposition around the neck | |
↓ exercise tolerance | |
Respiratory muscle function is not affected | |
Heart and lung transplantation [17] | Better to avoid conception within the first 1–2 years after transplantation |
Potential pregnancy-related complications: prematurity, low weight at birth and postpartum graft loss | |
Maintenance of immunosuppression with close monitoring of cyclosporine blood levels during gestation | |
Accurately diagnose signs of pre-eclampsia, as it is a multi-organ disease | |
Hereditary neuromuscular disorders [18] | Identify the highest risk group according to the diaphragmatic and/or bulbar involvement of the disease |
↑ respiratory muscle load by higher airway resistance and impaired bulbar load, leading to overwhelmed respiratory muscle capacity | |
Hypoventilation | |
Monitor the respiratory and cough function | |
Maximise airway clearance | |
High aspiration risk in the third trimester because of ↑ abdominal pressure and ↓ gastro-oesophageal sphincter tone | |
ARDS [19] | Non-obstetric causes: sepsis, pneumonia, intracerebral haemorrhage, blood transfusion and trauma |
Obstetric causes: amniotic fluid embolism, pre-eclampsia, septic abortion, retained products of conception and complication from tocolytic therapy | |
Management includes: prompt antibiotic therapy, conservative fluid strategy, use of mechanical ventilation and extracorporeal life support in case of refractory ARDS | |
Mechanical ventilation [20] | Similar indications to those for non-pregnant patients, with some exceptions: |
Oxygen therapy may also help fetal distress | |
Consider that PCO2 in pregnancy is about 30 mmHg when interpreting arterial blood gases | |
Airways are narrow (consequence of mucosal surface hyperaemia), so it is preferable to perform endotracheal intubation via oral route using a smaller tube | |
↓ oxygen reserve of the mother, so use pre-oxygenation with 100% oxygen during intubation to avoid arterial desaturation after a short period of apnoea | |
Better to avoid respiratory alkalosis as it leads to problems in uterine blood flow and fetal oxygenation | |
Treat respiratory acidosis with bicarbonate |
ARDS: acute respiratory distress syndrome; ↑: increased; ↓: decreased.