Tension Pneumothorax

Recognize it on the monitor, not from the textbook - decreased breath sounds, distended neck veins, and a non-midline trachea are uncommon and late. Under anesthesia what you actually see is a rising peak airway pressure with hypotension, tachycardia, a narrowing pulse pressure, and desaturation.

Confirm with ultrasound, do not wait for the film - absent lung sliding, loss of the comet-tail artifact, and a lung point make the diagnosis, and in skilled hands sensitivity reaches 94% with 100% specificity, better than chest radiograph. If the patient is unstable, decompress first and image after.

Decompress immediately - a 14 to 16 gauge, 4.5 cm angiocatheter into the second intercostal space at the midclavicular line, passing just superior to the rib. Follow with a thoracostomy tube in the fifth intercostal space just anterior to the midaxillary line, again above the rib.

Turn off the nitrous - N2O can drive the pneumothorax itself. If the collection came from N2O or insufflated CO2, there is no associated pulmonary trauma, and the patient is hemodynamically stable, spontaneous resolution is possible and watching is reasonable; PEEP has been used to treat a capnothorax after laparoscopy.

Oxygen buys time - high FiO2 speeds reabsorption of pleural gas up to fourfold compared with the 1% to 2% of volume per day that resolves on room air.

Know who is at risk in your room - central line placement carries a 1% to 13% pneumothorax rate, up to 30% in some settings, and the risk rises with a subclavian approach, a failed first pass at the initial vein, and positive-pressure ventilation, and falls with ultrasound guidance. Barotrauma, insufflation, and even colonoscopic perforation have all produced tension physiology on the table.

Positive pressure feeds the valve - once tension is suspected, every delivered breath makes it worse. Hold positive-pressure ventilation in a suspected pneumothorax until it is decompressed unless respiratory failure forces your hand.

It comes back - recurrence runs over 15%, ipsilateral or contralateral. A pneumothorax on the preop history changes your index of suspicion for every subsequent anesthetic.

Air enters the pleural space through a one-way valve — a lacerated visceral pleura, a ruptured alveolus, a needle track — and cannot get back out. Intrapleural pressure climbs with every breath, the ipsilateral lung collapses, and the mediastinum shifts contralaterally, compressing the heart, the great vessels, and the remaining lung. Venous return and cardiac filling fall, producing obstructive shock; hypoxemia triggers pulmonary vasoconstriction and raises pulmonary vascular resistance, and the combination of hypoxemia, acidosis, and falling cardiac output ends in arrest. Most in-hospital cases are iatrogenic — barotrauma from positive-pressure ventilation accounts for the majority, with central venous catheterization next. Positive pressure is what converts a simple pneumothorax into a tension one.