Negative pressure pulmonary oedema after rhinoplasty

Indian Journal of Anaesthesia | Vol. 54| Issue 4 | Jul-Aug 2010 inspiratory mouth pressures (PIMAX) in healthy subjects--what is the lower limit of normal? Respir Med 2000;94:689-93. 3. Kiyan E, Aktas S, Toklu AS. Hemoptysis provoked by voluntary diaphragmatic contractions in breath-hold divers. Chest 2001;120:2098-100. 4. Schwartz DR, Maroo A, Malhotra A, Kesselman H. Negative pressure pulmonary hemorrhage. Chest 1999;115:1194-7. 5. Gluecker T, Capasso P, Schnyder P, Gudinchet F, Schaller MD, Revelly JP, et al. Clinical and radiologic features of pulmonary edema. Radiographics 1999;19:1507-31.

Postextubation, the patient became restless, tachypnoeic and started desaturating. 100% O 2 delivery was tried with anatomical face mask but because of inadequate seal, the continuous positive airway pressure could not be achieved. So, the plaster of nose was removed. On auscultation, there were fine crepitations in most of the lung zones and there was drooling of pink frothy sputum from the angle of the mouth. As she was haemodynamically stable, pulmonary oedema was the obvious diagnosis. Furosemide 40 mg and morphine 6 mg were given intravenously. SpO 2 improved to 94%. Portable chest radiograph was taken, which revealed bilateral fluffy shadows with normal cardiothoracic ratio. ECG and arterial blood gas analysis were normal. Gradually, the secretions decreased and SpO 2 progressed to 100%. Head end of the bed was elevated and fluid restriction was implemented. The patient was observed for another hour in the operation theatre and was shifted to recovery room after that as she remained stable. Repeat roentgenogram was normal and she was discharged on the fifth postoperative day.
Negative pressure pulmonary oedema (NPPE) is noncardiogenic and is of two types. Type I is of sudden onset following upper airway obstruction and Type II develops after surgical relief of chronic upper airway obstruction. This is called NPPE because the laryngeal spasm, or other obstructive process in which the patient can inspire against the closed glottis (modified Müeller maneuver), is capable of generating an extremely negative intrapleural pressure (peaks of sustained inspiratory pressure between −50 cm H 2 O and −100 cm H 2 O, though the mean basal pressure is around −4 cm H 2 O) [1] which can trigger pulmonary oedema. The hydrostatic forces are the primary mechanism behind postobstructive pulmonary oedema and that the alveolar epithelium remains functionally intact in acute postobstructive pulmonary oedema. [2] In Type II NPPE, it appears that the obstructive lesion produces a modest level of PEEP (positive end expiratory pressure) and increases end expiratory lung volume. Relief of the obstruction removes the PEEP and return lung volumes are preserved to normal. The sudden removal of PEEP leads to interstitial fluid transudation and pulmonary oedema. [3] On radiological evaluation, NPPE is characterised by bilateral centralised pulmonary oedema, a wide

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week earlier he had undergone a posterior medial soft tissue release surgery for neglected CTEV, the perioperative period being uneventful. After securing an intravenous access he was administered inj. midazolam 1 mg, inj. ketamine 15 mg, inj. glycopyrrolate 0.16 mg along with supplemental oxygen. He went into laryngospasm even before the procedure was started, which was broken easily with positive pressure ventilation (PPV) with 100% O 2 . The rest of the intraoperative period was uneventful. But as soon as the child was shifted on transport trolley, he went into laryngospasm again which was broken by succinylcholine (5 mg) along with PPV. As soon as the effect of succinylcholine wore off, the child went into laryngospasm for the third time. This episode resolved with forward displacement of mandible and PPV. An oral suctioning was done to remove any collected secretions along with intravenous lidocaine. Within the next few minutes, he went into laryngospasm again. We decided to intubate the trachea after giving propofol and succinylcholine. The child was extubated only when fully awake. Shockingly, he went into complete laryngospasm, again, with falling SpO 2 , for the fifth time. Auscultation now revealed fine crepitations all over the chest. Fearing negative pressure pulmonary oedema, he was intubated and given lasix (10 mg) and morphine (2.0 mg). Direct laryngoscopy showed an oedematous epiglottis and vocal cords. He was given adrenaline 0.25 mg diluted in normal saline intravenously along with dexamethasone 2 mg iv. Crepitations disappeared within the next 10 minutes. A repeat direct laryngoscopy revealed a reduction in the epiglottic oedema. IV lidocaine 20 mg and nebulisation with adrenaline were given. The trachea was extubated after gentle suctioning.
He was shifted to PACU where subsequent follow ups for the next 24 hours did not reveal any fresh episode of desaturation.
The incidence of laryngospasm in children undergoing general anaesthesia has been reported to be between 0.78% and 5%. [2] Common precipitating factors include insufficient depth of anaesthesia on intubation or extubation, or the presence of an airway irritant such as blood, mucus, surgical debris or any foreign body, prior history of active respiratory tract infection, allergies, airway anomaly or pre existing gastro oesophageal reflux disease. In our patient, pre operative assessment ruled out any pre-existing factors. Though the movement of the patient while shifting could have precipitated laryngospasm. vascular pedicle and a normal cardiothoracic ratio when the radiograph was obtained 15-165 min after the symptoms developed. [4] To conclude, acute pulmonary oedema associated with obstruction of the upper airways can aggravate low morbidity surgeries, affecting mainly young patients. The knowledge of this complication and, most importantly, its prevention are crucial.
Recurrent episodes of intractable laryngospasm followed by laryngeal and pulmonary oedema during dissociative anaesthesia with intravenous ketamine DOI: 10.4103/0019-5049.68395 Sir, Ketamine is commonly used to provide analgesia, amnesia and sedation for painful paediatric procedures. Its most dangerous side effects include: laryngospasm and apneic spells. [1] We report a case of recurrent intractable laryngospasm, followed by laryngeal and pulmonary oedema with intravenous ketamine.
A seven-year-old, 16 kg, ASA grade I child was admitted for change of Plaster of Paris cast. One