Negative pressure pulmonary edema in the prone position: a case report

Cases Journal, Jul 2009

Acute airway obstruction can result in life - threatening pulmonary edema. It can develop rapidly, without warning, in otherwise healthy patients. Negative pressure pulmonary edema has been described after acute airway obstruction in situations when a patient is breathing against an obstructed airway such as croup, epiglottitis or laryngospasm. In the following case, we observed a rare occurrence of pulmonary edema in a female following sedation in the prone position.

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Negative pressure pulmonary edema in the prone position: a case report

Hesham Omar 2 Jaya Kolla 1 Amrat Anand 0 Willem Nel 0 Devanand Mangar 1 Enrico Camporesi 3 0 Florida Gulf to Bay Anesthesiology Associates , PA, Tampa, Florida , USA 1 Research Associate, Tampa General Hospital, Florida Gulf to Bay Anesthesiology Associates , PA, Tampa, Florida , USA 2 Department of Cardiovascular Medicine, Cairo University Hospital, Cairo, Egypt, Visiting Scholar at Tampa General Hospital, Florida Gulf to Bay Anesthesiology Associates , PA, Tampa, Florida , USA 3 Department of Surgery/Anesthesiology, University of South Florida, Tampa, FL and Florida Gulf to Bay Anesthesiology Associates , PA, Tampa, Florida , USA Acute airway obstruction can result in life - threatening pulmonary edema. It can develop rapidly, without warning, in otherwise healthy patients. Negative pressure pulmonary edema has been described after acute airway obstruction in situations when a patient is breathing against an obstructed airway such as croup, epiglottitis or laryngospasm. In the following case, we observed a rare occurrence of pulmonary edema in a female following sedation in the prone position. - Case presentation A 49-year-old Caucasian female, with a long history of heavy cigarette smoking and a previous diagnosis of supraventricular tachycardia, for which cardiac ablation was performed 2 years ago, was admitted to the hospital for an elective sacral neuromodulator lead change to treat urinary incontinence. In the operating room, the patient received monitored anesthesia care (MAC) in the prone position. During the procedure she required increasing sedation (IV propofol infusion) and after thirty minutes the patient showed progressive hypercapnia from the nasal cannula sample line, while receiving supplemental oxygen (4 L/min). An oral airway was placed, but end-tidal CO2 ranged from 65 to 75 mmHg and did not improve. It was then decided to place a laryngeal mask and to supply positive pressure ventilation; however no improvement of the hypercapnia ensued and we could not provide adequate ventilation. The patient was then emergently intubated to secure an airway and provide adequate ventilation. This required interruption of surgery, turning the patient supine, ventilating oxygen by mask and a succinylcholine bolus. During the intubation process, marked edema above the vocal cords was noticed by an experienced anesthesiologist, allowing only for a smaller sized endotracheal tube to be inserted (6 mm with difficulty, but not a 7 mm tube). The patient was given dexamethasone 8 mg and diphenhydramine 25 mg for the airway edema. Following intubation and after securing the tube in place, we started positive pressure ventilation and returned the patient to the prone position, and the end tidal CO2 returned within normal range. However, within a few minutes, the patient developed bibasilar rales, with abundant frothy, blood tinged secretions appearing in the tube. We maintained the patient prone while the surgical procedure was concluded. The edema fluid was adequately suctioned and abated after 10 minutes of positive pressure ventilation. Postoperatively the patient remained intubated and sedated on a propofol infusion. While in recovery, an arterial blood gas obtained on Synchronized Intermittent Mechanical Ventilation (SIMV) and FiO2 of 30%, showed a PO2 of 92 mmHg, PCO2 of 46 mmHg, pH of 7.34 and HCO3 of 25 mEq/L with a SaO2 of 97%. Chest X-ray performed after surgery indicated clear lung fields with normal size heart and no evidence of pulmonary edema. The patients condition steadily improved and she was subsequently extubated two hours later but continued to be closely monitored overnight and was discharged the following day without requiring an ICU stay. Discussion In this case report we describe a case of NPPE following supraglottic obstruction with deepening sedation in the prone position. Supraglottic obstruction was possibly induced by intense inspiratory effort in a patient who was sedated and hypoventilating leading to airway obstruction and subsequently pulmonary edema. Another possibility is malpositioning (or biting) of the LMA causing inspiratory efforts against an obstructed airway, which could be the cause for the observed supraglottic swelling. The apparent absence of gastric contents in the pulmonary edema fluid, the absence of left ventricular dysfunction in a previously performed echocardiogram and the sequence of the described symptoms make the diagnosis of acute NPPE likely. NPPE is a relatively uncommon intra-operative and postoperative complication and is still a diagnosis by exclusion of other factors. Generally, NPPE occurs when inspiratory effort against an obstruction creates a large intrapulmonary negative pressure which can increase venous return with subsequent increase in the pulmonary capillary hydrostatic pressure. The transudation of fluid from the pulmonary vasculature causes edema formation into the alveolar space [1,2]. Normal inspiratory pleural pressure rang (...truncated)


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Hesham Omar, Jaya Kolla, Amrat Anand, Willem Nel, Devanand Mangar, Enrico Camporesi. Negative pressure pulmonary edema in the prone position: a case report, Cases Journal, 2009, pp. 8594, 2, DOI: 10.4076/1757-1626-2-8594