A 46-year-old female with a history of asthma and anxiety presents to the emergency department (ED) with progressively worsening shortness of breath for 5 days. She states that her rescue inhaler is not giving her much symptom relief. In the ED, she was given multiple nebulizer treatments. The patient was admitted to the floor but had progressing shortness of breath and anxiety. She was still hypoxic (saturating 93% on room air), hypercapnic, and, thus, was transferred to the intensive care unit. Upon arrival, the patient was tachycardic, tachypneic, and sitting up in a tripod position. Her arterial blood gas showed a pH of 7.13, PCO2 of 95, and PO2 of 166. The decision was made to intubate the patient, which was done using video laryngoscopy with a 7.5mm endotracheal tube. The post-intubation film was unremarkable.
About 2 hours after the intubation, the family felt that her stomach and face looked swollen. At that time, she was noted to have subcutaneous emphysema of her neck and chest. The ventilator showed that her peak pressures were elevated, at 60mmHg. A chest x-ray demonstrated the subcutaneous emphysema but no pneumothoraces. She was noted to have pneumomediastinum. Empiric bilateral chest tubes were placed in the patient.
Overnight, she developed further abdominal distention as well as facial and chest wall swelling. Subcutaneous emphysema also tracked to her arms and legs. Bladder pressures were checked showing a bladder pressure of 30mmHg. General Surgery was consulted for suspected abdominal compartment syndrome (ACS). She underwent computed tomography (CT) of the neck, chest, and abdomen, which showed free air in the abdominal cavity and diffuse subcutaneous emphysema in the neck, mandible, and periorbital region, as well as subcutaneous air in the chest, neck, abdomen, and thighs. Incidentally, she was noted to have cerebral edema. She was diagnosed with pneumomediastinum, pneumopericardium, and pneumoperitoneum and was immediately taken to the operating room for abdominal decompression. Per the surgeon’s report, the hypothesis was that the pneumomediastinum air tracked down from the chest to the abdomen via the falciform ligament and the flimsy peritoneal violation of the falciform ligament resulted in a pneumoperitoneum under tension.
The patient was transferred to a tertiary care center for an ENT evaluation of a suspected tracheal tear.
A tracheal tear that likely occurred during the intubation might have caused the initial injury. Emergency intubation is the primary risk factor for post-intubation tracheal rupture (Minambres 2009).
In our patient, the CT scan was unable to identify any obvious tracheal tear. However, computed tomography of the chest is only 85% sensitive in diagnosing tracheal tears post-intubation (Chen 2001). Gold standard is bronchoscopy, but this is limited to tears large enough to see using the bronchoscope. The patient was not stable enough to undergo bronchoscopy, but the clinical presentation suggested that a tracheal tear was the most likely etiology of her symptoms.
Females have a higher incidence of tracheal tears secondary to endotracheal intubation, with the theory being that the pars membranosa is weaker in women than in men, and that female tracheal diameters are usually smaller than male diameters. This in turn makes them more susceptible to injury from intubation and cuff over-inflation (Carbognani 2004). Other risk factors for tracheal tear include: short stature, underlying connective tissue disease, chronic obstructive pulmonary disease, steroid use, and difficult airway anatomy (Hofmann 2002).
The treatment of tracheal tears ranges from medical management to surgical treatment. Management depends on ventilatory status and the nature and severity of the laceration. Emergent surgical repair is indicated for patients who have rapid progression of air leaks, mediastinitis, and respiratory deterioration (Gomez 2005). In our case, surgical repair was indicated as she was having rapid progression of air leaks that eventually led to ACS, extensive emphysema, and cerebral edema.
Her ACS developed secondary to pneumoperitoneum. Pneumoperitoneum decreases abdominal compliance, leading to the syndrome. Classically, ACS is defined as development of organ dysfunction with an intra-abdominal pressure greater than 20mmHg, and has a mortality rate of 60-70% (Hunt). The treatment of ACS is resuscitative fluids along with emergent surgical decompression of the abdomen.
Our patient’s clinical condition rapidly deteriorated due to an iatrogenic cause. However, with strict monitoring of her vital signs and symptoms, early decision-making and identification of a potentially disastrous situation, she was diagnosed and treated properly, and eventually transferred to a tertiary care center.
Editor’s Note: See also “Diagnosis and Treatment of Pneumomediastinum” from Vol. 43 #6.
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