|LETTER TO THE EDITOR
|Year : 2014 | Volume
| Issue : 4 | Page : 473-474
Negative pressure pulmonary edema on induction with face mask
Nita Hazarika, Namita Saraswat, Rajesh Sood
Department of Anesthesiology, Dr Ram Manohar Lohia Hospital, New Delhi, India
|Date of Submission||24-May-2014|
|Date of Acceptance||12-Jun-2014|
|Date of Web Publication||28-Nov-2014|
Post Graduate Student, Department of Anesthesiology, Dr. Ram Manohar Lohia Hospital, New Delhi
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Hazarika N, Saraswat N, Sood R. Negative pressure pulmonary edema on induction with face mask. Ain-Shams J Anaesthesiol 2014;7:473-4
|How to cite this URL:|
Hazarika N, Saraswat N, Sood R. Negative pressure pulmonary edema on induction with face mask. Ain-Shams J Anaesthesiol [serial online] 2014 [cited 2020 May 29];7:473-4. Available from: http://www.asja.eg.net/text.asp?2014/7/4/473/145661
Pulmonary edema is defined as abnormal accumulation of fluid in the extravascular compartment of the lung. Negative pressure pulmonary edema (NPPE) represents a pure form of hydrostatic edema.
The incidence of NPPE, as a complication of all anesthetics, is said to be 0.05-0.1% . The morbidity and mortality of an unrecognized event of NPPE is as high as 40% .
Laryngospasm, bilateral vocal cord paralysis, aspirated foreign body, epiglottitis, kinking or biting of the laryngeal mask or endotracheal tube at emergence from general anesthesia, tumor, strangulation, interrupted hanging, premature administration of muscle relaxants , and even vigorous hiccups  are reported as causes. Of these, laryngospasm remains the most common cause, accounting for ~50% of the reported cases .
A 10-year-old girl weighing 40 kg with bilateral congenital tallipes equino varus was scheduled for bilateral tendo-Achillis lengthening. There was no associated congenital anomaly. After ensuring adequate preoperative fasting, she was shifted to the operating table. General anesthesia was planned and the child was premedicated with 1 mg midazolam and 80 µg of fentanyl. Propofol (80 mg) was given for induction. Attempts for check ventilation before giving muscle relaxant landed the patient to vigorous hiccups. Anesthesia deepened with propofol and 4 mg vecuronium was given. Hiccups lasted for 1 min; suddenly after 2 min, peripheral oxygen saturation (SpO 2 ) started decreasing requiring 100% oxygen to maintain it near 90%. EtCO 2 and airway pressures also rose to 55 and 43 mmHg, respectively. Auscultation revealed bilateral diffuse rales. Patient was immediately intubated with a 5.5 cuffed endotracheal tube and put on pressure-controlled ventilation with positive end expiratory pressure (PEEP) of 5 mmHg. Arterial blood gas showed respiratory acidosis with pH of 7.25, PO 2 of 60 mmHg, and PCO 2 of 58 mmHg. Simultaneously, her blood pressure rose to 150/90 mmHg and heart rate was 138/min. Suctioning of the endotracheal tube revealed pink frothy secretions. A diagnosis of NPPE was made and furosemide (10 mg) and morphine (2 mg) were given. Patient was then transferred to ICU where controlled ventilation with PEEP continued. She made a marked recovery within 2 h with improvement in saturation and lowering of EtCO 2 . Auscultation revealed almost a clear chest. She was extubated successfully after 4 h.
The pathogenesis of this pulmonary disorder is still heavily debated. It is widely accepted that the cause is multifactorial with a central mechanism involving the generation of a large inspiratory force against an obstructed upper airway, which triggers an accumulation of high negative intrapleural pressure in the range of -50 to −100 cmH 2O [1,4]. This high negative intrapleural pressure creates a pressure gradient allowing for the extravasation of fluid from the pulmonary capillaries into the interstitial and alveolar spaces, as well as a large increase in venous return resulting in increased preload. Concomitantly, hypoxia and sympathetic stimulation from laryngospasm increase mean arterial pressure and after load, causing decreased forward stroke volume. Once obstruction relieves, evidence of NPPE can occur anywhere from minutes to hours later with signs of respiratory distress. The hallmark sign of NPPE is pink, frothy sputum. Physical examination of the patient may reveal rales, coarse rhonchi, and occasional wheezes and diaphoresis. Chest radiograph findings can be positive for diffuse bilateral interstitial and alveolar infiltrates appearing as 'whited out' areas. Arterial blood gas samples can be normal or show an acute respiratory acidosis. Because of this relatively nonspecific clinical picture, a differential diagnosis must be carefully considered before diagnosing the patient with NPPE, which include pulmonary aspiration, acute respiratory distress syndrome, pulmonary embolization, intravascular volume overload, etc. .
Treatment is focused on improving respiratory function and avoiding further damage to the lung. Resolution of the clinical and radiological features is rapid, usually within 24 h . It is important to apply positive pressure to the airway early. Nasal bilevel positive airway pressure, mask continuous positive airway pressure (CPAP), and intubation and ventilation with PEEP have been used successfully .
NPPE has been described without any clinical evidence of airway obstruction, which suggests that obstructive events can be subtle . Our patient had vigorous hiccups during induction. Hiccups are brief, powerful inspiratory efforts synchronous with glottic closure . Studies in cats have shown that hiccups can cause negative intrathoracic pressures that are four times greater than during normal inspiration . In our patient, the continuous, forceful hiccups were sufficient to cause NPPE.
Most of the cases of NPPE occur during emergence from anesthesia. This is the first case of NPPE that we encountered during induction of anesthesia on mask. Hence, we conclude that prolonged vigorous hiccups in anesthetized, spontaneously breathing patients who are not intubated may precipitate NPPE.
| Acknowledgements|| |
| References|| |
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