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In diabetic ketoacidosis (DKA), breathlessness reflects the underlying respiratory alkalosis in response to metabolic acidosis. However, it can also be a manifestation of a rare respiratory complication.
A man aged 44, diagnosed with type 1 diabetes at the age of 20, was admitted as an emergency. Nausea and malaise had begun four days earlier; on the day before admission this had progressed to severe retching and vomiting and he missed his insulin injections (Human Mixtard 30/70, 40 and 20 units daily). There was a history of recurrent prolonged hypoglycaemic episodes leading to mild to moderate cognitive impairment. Clinically he was very dehydrated with Kussmaul respiration. He was afebrile, with blood pressure 148/89 mmHg and heart rate 140 per minute. Subcutaneous emphysema was palpable in the supraclavicular fossae. Biochemical investigations confirmed DKA with plasma glucose 43.5 mmol/L, arterial blood pH 7.23, bicarbonate 9 mmol/L, PaCO2 3.3 kPa and PaO2 16.8 kPa. Urine dipstix showed heavy ketonuria (3+). He also had compensatory hyponatraemia (Na+ 125 mmol/L) and mild renal impairment (K+ 4.6 mmol/L, urea 18.5 mmol/L, creatinine 141 μmol/L). A chest radiograph confirmed interstitial emphysema and pneumomediastinum. There was no pneumothorax. Treatment was with intravenous fluid, insulin and a course of antibiotics (cefuroxime and metronidazole) to cover possible oesophageal rupture. A water-soluble contrast swallow study later excluded oesophageal perforation. He gradually improved over the next 48 hours, and the interstitial emphysema resolved over four days. A chest radiograph 2 weeks after admission showed complete resolution of the pneumomediastinum.
The incidence of pneumomediastinum complicating DKA is likely to be underestimated because the resultant breathlessness tends to be overshadowed by hyperventilation due to DKA. Symptoms such as retrosternal pain are uncommon. Subcutaneous emphysema is present in about half the cases. Occasionally, a crackling or crunching sound synchronous with the heart beat (Hamman's sign) is audible over the left sternal edge1. The major differential diagnosis is oesophageal rupture (Boerhaave's syndrome), which should be excluded by contrast study or endoscopy.
In DKA, several factors may contribute to the development of pneumomediastinum2. Severe vomiting in DKA produces a Valsalva-like effect with large momentary swings in intrathoracic pressure which can lead to alveolar rupture3. This is much more likely to occur when alveoli are already susceptible due to over-distension during Kussmaul respiration. Rupture of the alveolar wall introduces air into the perivascular adventitia, leading to interstitial emphysema. Interestingly, however, pneumomediastinum in association with severe DKA has been described in the absence of cough and vomiting4. This prompts the speculation that in some instances the alveolar wall is weakened by the metabolic derangement of ketoacidosis. In the published work there are indications that rupture may be due to constitutional weakness. Males outnumber females and the typical patient is young4,5. Most are under 20, and before the present case the oldest reported was 295.
The prognosis of pneumomediastinum complicating DKA is excellent without special interventions other than management of DKA.