Pneumomediastinum complicating diabetic ketoacidosis

BACKGROUND

Pneumomediastinum is an uncommon finding in which air occupies the mediastinal space.1 Air may enter the mediastinum secondary to disruption of the skin, airway or oesophagus or may be produced by gas-forming bacteria spreading inferiorly from the oral cavity or neck.2 Alternatively, it may occur ‘spontaneously’, following alveolar rupture through straining, vomiting, coughing or an increased respiratory effort.1 2 Spontaneous pneumomediastinum is a diagnosis of exclusion and is made only after ruling out traumatic injury, oesophageal perforation and infection.1

Depending on its aetiology, pneumomediastinum can be a benign condition or life-threatening emergency. Its presence in Boerhaave syndrome, a transmural oesophageal rupture caused by severe straining or vomiting, is associated with a mortality risk of 15% to 43%.3 4 Death may result from an infectious mediastinitis or compression of the great vessels by an increased mediastinal pressure.5 6 Spontaneous pneumomediastinum, on the other hand, generally has a good prognosis and is self-limiting.7

Patients with diabetic ketoacidosis (DKA) often experience retching and vomiting, which can lead to both alveolar and oesophageal rupture, making differentiating between spontaneous and secondary pneumomediastinum a challenge.8 Although fluoroscopic oesophagography is considered the imaging study of choice for diagnosing oesophageal rupture, its use in emergencies is limited by the inability of critically ill patients to change positions and swallow contrast medium.9 Alternatively, upper endoscopy may be performed but could enlarge a perforation’s size and risks the need for surgery.10 Despite these difficulties, every effort has to be made to exclude oesophageal rupture because if surgery is required, its delay beyond 24 hours increases morbidity and mortality.10

Here, we present a case of DKA complicated by pneumomediastinum, in which fluoroscopic oesophagography was unavailable and feasible.

Case presentation

A man in his 20s, with a body weight of 84 kg, presented late in the evening to the emergency department with vomiting and reduced consciousness. Four years prior, he was diagnosed with type 1 diabetes. According to his family, he had been ill for 3 days, complaining of nausea, abdominal pain and having diarrhoea. While feeling unwell, had not been using insulin therapy. Since 1 day, he had vomited repeatedly, developed laboured breathing and became increasingly lethargic. He had not experienced fever, coughing or haematemesis, or reported of chest pain or pain when swallowing. He had no other medical history or history of trauma.

Investigations

Physical examination revealed a Glasgow Coma Scale of 13 (E3M6V4). Kussmaul breathing pattern was present with a frequency of 35 bpm. He was tachycardic and had a systolic blood pressure of 79 mm Hg and a diastolic pressure of 60 mm Hg. In the chest and neck region, subcutaneous emphysema was felt. Thoracic excursions were symmetric and no tracheal deviation was detected. Breathing sounds were heard bilaterally with inspiratory crepitations on the right lower side of the chest. Heart sounds were normal and no distended jugular veins or Kussmaul’s sign were observed.

Laboratory analysis of his blood showed a glucose of 48 mmol/L (864 mg/dL), Na+ 117 mmol/L, K+ 6.0 mmol/L, Cl− 86 mmol/L, creatinine 196 umol/L, albumin 41.8 g/L, c-reactive protein 296 mg/L, white cell count of 37×10^9/L and an arterial blood gas with a pH of 6.84, pO2 of 8.1 kPa (61 mm Hg), pCO2 of 2.2 kPa (17 mm Hg), HCO3− of 2.9 mmol/L and lactate of 1.5 mmol/L. The effective osmolality was calculated to be 282 mOsm/L. The anion gap was 28 mEq/L, providing a delta anion gap/delta HCO3- ratio approximating one. Urine analysis confirmed ketonuria. His ECG showed a sinus tachycardia without ST-segment deviations or T-wave alterations. Respiratory virus PCR testing of COVID-19 and influenza were negative.

A chest X-ray showed subcutaneous emphysema at the upper chest and radiolucent streaks outlining the heart and aortic arch, indicating a pneumomediastinum (figure 1). Additionally, there were consolidations in the right lower lobe and behind the heart. A CT scan without intravenous contrast material of his chest and neck was made to evaluate the extent of the pneumomediastinum and whether airway or oesophageal injury was present (figures 2 and 3). Pneumomediastinum and pneumopericardium were seen without evidence of rib fractures, tracheal or oesophageal injury. Air extended superiorly from between the clavicles to the cranial base and was also visible in the epidural space of the spinal canal. No pneumothorax was present. Aspiration pneumonia was suggested by the combined findings of gastric dilatation, stasis of gastric content in the lower half of the oesophagus and consolidations in the lower lobes of both lungs.

Figure 1

Anteroposterior chest X-ray (upper image) with a corresponding coronal CT image (lower left image) and illustration (lower right image). Air demarcates the right cardiac border and surrounds the aortic arc. A pneumopericardium is visible, with air seperating the left cardiac border from the pericardium and mediastinal parietal pleura.

Figure 2

Axial chest CT image (upper image) and illustration (lower image) displaying the heart and lower mediastinum at the level of the seventh thoracic vertebra. Air surrounds the heart and right lower pulmonary vein. Air is also seen in the posterior mediastinum, covering the anterior surface of oesophagus and descending aorta.

Figure 3

Axial chest CT image (upper image) and illustration (lower image) displaying the upper mediastinum at the level of the third thoracic vertebra. Air covers the great vessels and trachea. Subcutaneous emphysema is seen anterior to the sternum. A small amount of air is visible in the spinal canal.

Differential diagnosis

Our patient was diagnosed with DKA complicated by a pneumomediastinum and an aspiration pneumonia. The DKA may have been precipitated by a (viral) gastroenteritis or respiratory infection and worsened by discontinuation of insulin therapy.

The pneumomediastinum resulted from his laboured breathing, retching and vomiting, increasing alveolar pressure and causing alveolar rupture. Oesophageal rupture was unlikely as the patient did not experience fever, had no history of chest pain or pain when swallowing and had a CT-scan without oesophageal wall thickening, periesophageal fat stranding and effusions. Although the lower posterior mediastinum contained air, we regarded this to be of alveolar origin spreading diffusely into all mediastinal compartments, rather than originating from the oesophageal lumen.

We considered using fluoroscopic oesophagography to rule out oesophageal rupture, but at the time of presentation the fluoroscopy suite and qualified technologist were unavailable. Also, due to his reduced consciousness and gastroparesis, drinking contrast material would have risked further aspiration. CT oesophagography was not performed, as there were no standardised protocols in place.

Treatment

Treatment of his pneumomediastinum was supportive with antiemetics and close monitoring for complications. The DKA was treated according to national protocols.11 We initiated intravenous antibiotics for aspiration pneumonia and placed a nasogastric tube to resolve gastric retention. This tube was seen to be positioned correctly on X-ray imaging and no bloody gastric content was aspirated.

Outcome and follow-up

After 2 days of insulin therapy, the blood pH and anion gap had normalised. He remained haemodynamically stable without the use of vasopressors, seemingly confirming the absence of an oesophageal rupture.

Despite high-flow oxygen therapy, blood oxygen levels deteriorated and work of breathing increased. Intubation was performed and mechanical ventilation was started. A chest CT with intravenous contrast material was repeated to evaluate the presence of mediastinal abscesses and the extent of the pneumomediastinum. It showed a clear reduction of mediastinal air and subcutaneous emphysema (figure 4). New consolidations had developed in the apical segments. Our patient was later diagnosed with bronchopulmonary aspergillosis and treated with voriconazole. His stool culture was negative for bacterial, viral and parasitic pathogens.

Figure 4

Axial chest CT images without intravenous contrast from admission (left two images) and with intravenous contrast after 7 days (right two images). Air surrounding the heart and great vessels diminishes over time.

He was discharged to a rehabilitation centre 2 months after admission to recover from ICU-acquired weakness. After 3 months, he returned to his daily routine. He currently attends the outpatient diabetic clinic every 2 weeks.