|LETTERS TO EDITOR
|Year : 2016 | Volume
| Issue : 7 | Page : 527-528
Post-operative pneumothorax with subcutaneous emphysema in a pre-eclamptic patient
Suresh Kumar1, Ankita Kabi2, Charu Bamba2
1 Department of Anaesthesia, Apollo Spectra and Cradle Hospital, New Delhi, India
2 Department of Anaesthesia and Intensive Care, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India
|Date of Web Publication||12-Jul-2016|
D II/231, West Kidwai Nagar, New Delhi - 110 023
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Kumar S, Kabi A, Bamba C. Post-operative pneumothorax with subcutaneous emphysema in a pre-eclamptic patient. Indian J Anaesth 2016;60:527-8
|How to cite this URL:|
Kumar S, Kabi A, Bamba C. Post-operative pneumothorax with subcutaneous emphysema in a pre-eclamptic patient. Indian J Anaesth [serial online] 2016 [cited 2020 Jan 24];60:527-8. Available from: http://www.ijaweb.org/text.asp?2016/60/7/527/186024
A 30-year-old female patient presented with severe pre-eclampsia for emergency caesarean section. On the operating table, she had a blood pressure (BP) of 176/98 mm Hg, pulse rate 102/min, oxygen saturation (SpO2) 99% and air entry was equal bilaterally.
Rapid sequence induction and intubation were performed; gentle laryngoscopy was performed and cuffed endotracheal tube (ETT), 7.5 internal diameter was inserted aided by a stylet. The depth of anaesthesia was maintained with O2, nitrous oxide, isoflurane and muscle relaxant vecuronium (total dose of 6 mg) was used. The monitors used were electrocardiograph, pulse oximeter, non-invasive BP, and end-tidal carbon dioxide (CO2) monitor. The patient was ventilated on closed circuit with mechanical ventilation (volume control mode with respiratory rate [RR] 12/min, tidal volume of 450 ml, without positive end-expiratory pressure (PEEP), with mean airway pressure of 14 cm H2O). Intra-operative period was uneventful. The surgery was completed in 1 h. Postoperatively, the neuromuscular blockade was reversed with neostigmine 2.5 mg intravenous (iv), glycopyrrolate 0.5 mg iv. Due to inadequate reversal of neuromuscular blockade as suspected by poor respiratory efforts, the reversal drugs were supplemented. Arterial blood gas report showed normal partial pressure of oxygen and potential of hydrogen. However, CO2 retention was present, so we continued to manually assist her ventilation.
After 10 min, her respiratory efforts were adequate, but her protective airway reflexes were blunted and she was tolerating the ETT well. Therefore, we decided not to extubate the trachea. While shifting the patient to recovery room on T piece, she had a violent coughing and retching episode after which she became restless and developed bradycardia with SpO2 decreasing to 82%. We then noticed palpable crepitus all over the chest, face and doubtful air entry on chest auscultation. As we suspected displacement of ETT, we extubated the trachea. She was unable to maintain adequate respiratory efforts. Hence, we paralysed her and reintubated her trachea. Thereafter, her vital signs stabilised. Air entry on the left side was decreased. She was shifted to the Intensive Care Unit (ICU) for mechanical ventilation. A chest X-ray was done in the ICU, which showed left-sided pneumothorax with subcutaneous emphysema. An intercostal chest drain was inserted and patient. The patient was maintained ventilatory support without delay (volume control mode with RR 14/min, TV 450 ml, PEEP of 0 cm H2O, inspiratory to expiratory ratio (I: E ratio) of 1:2 and peak airway pressures limited to 24 cm H2O). We could not find any obvious airway rent as assessed by fibreoptic bronchoscopy. The patient's relative did not give consent for computed tomography of thorax. After 24 h of stay in the ICU, the patient's vital signs got stabilised with normal respiratory parameters. The patient's trachea was extubated. After 24 h of cessation of air column movement, the intercostal chest drain was removed.
Pneumothorax with subcutaneous emphysema in the immediate postoperative period can be spontaneous or iatrogenic. Spontaneous causes include rupture of undiagnosed bullae, spontaneous post-violent cough airway tear, alveolar rupture and post-emetic rupture of the oesophagus.,,
Iatrogenic causes include trauma to the pharynx, trachea during traumatic intubation, over inflation of ETT cuff, repeated intubation attempts, re-positioning of ETT without deflating the cuff, stylet protruding beyond ETT tip, patient movement or coughing during intubation/extubation and patient head and neck movement after intubation. In our patient, adequate precautions were taken to prevent these iatrogenic causes. Decrease in SpO2 and bradycardia did not occur in the intra-operative period during which positive pressure ventilation was provided, so the aetiology being rupture of undiagnosed bullae due to positive pressure ventilation is unlikely.
There are patient and surgical factors such as congenital tracheal anomalies, chronic use of steroids, chronic obstructive pulmonary disease, thoracic and laparoscopic surgeries. None of these factors are involved in our case.
Even though, we could not find any obvious airway rent while doing fibreoptic bronchoscopy, a possibility of airway injury cannot be completely ruled out. There is a high probability that either the violent coughing or retching episode in the post-operative period or ETT displacement due to violent head and neck movement during transfer to the recovery room could have led to an airway or oesophageal rent.
We would like to create an awareness that airway trauma can lead to pneumothorax with subcutaneous emphysema in a pregnant patient due to fragile oedematous airway mucosa. We, therefore, reemphasise the importance of gentle laryngoscopy and intubation, maintenance of cuff pressure, administration of anti-emetics, smooth reversal, extubation and care of ETT while shifting the patient.
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Conflicts of interest
There are no conflicts of interest.
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