Citation: Parul M, Gaurav V, Ajay K, Smita P.Central venous catheter insertion site infection leading to subcutaneous emphysema.Anaesth Pain & Intensive Care 2014;18(3):315-16
A 20-year-old lady presented to our hospital with pain and distension of abdomen, feculent vomiting and inability to pass faeces and flatus since 15 days. She looked sick, was febrile, and had a pulse rate of 140/min, blood pressure 76/40 mmHg, respiratory rate 34/min and SpO2 87% (room air). On auscultation, chest had bilateral crepitations. Abdominal examination revealed guarding and rigidity with absent bowel sounds. A diagnosis of intestinal obstruction with septic shock was made. Oxygen therapy, fluids and noradrenaline infusion was started. A central venous catheter (CVC) was inserted in right subclavian vein. Standard general anesthesia was administered for laparotomy. The small bowel had adhesions, stricture and a perforation for which loop ileostomy with urobag laparostomy was done. After completion of surgery, in view of her poor general condition and unstable vitals, anesthesia was not reversed and she was shifted to the ICU for further management. In the ICU, she received ventilatory support (SIMV+PS), broad spectrum antibiotics, vasopressors, parenteral nutrition and other supportive care.On tenth day, a slight swelling was noted primarily around the CVC insertion site, right upper chest and neck. On palpation there was a crackling sensation under the skin suggesting subcutaneous emphysema (SE). She had no chest pain or discomfort. No change in airway pressures and other vital parameters was noted. The chest radiograph showed evidence of SE involving the right chest wall and neck, with no evidence of pneumothorax or pneumomediastinum (Figure 1).The right subclavian vein cannulation was done ten days ago and no subsequent intervention was done. On examining the CVC insertion site, a small skin wound around the CVC was seen (Figure 2).
The CVC was removed. Blood samples, CVC tip and wound swab were sent for culture. Wound was cleaned and air tight surgical dressing was done. Left internal jugular vein was subsequently cannulated. Blood culture showed no growth. Acinetobacter species was isolated from both CVC tip and wound cultures. Antibiotics were changed according to sensitivity. There was no further increase in SE and it subsequently resolved over two weeks.
Perhaps, in our case, air was sucked in through the small skin wound around the CVC insertion point due to negative intrathoracic pressure being transmitted to the perivascular interstitial space. A large amount of air may have entered the soft tissues due to a ball-valve mechanism.1 The absence of barriers in the subcutaneous tissues throughout the body allow free movement of air under the skin.2
Cutaneous ulcers and small skin wounds can cause SE.1 There are reports of SE involving the upper limb following trivial laceration on the dorsum of hand 3 and elbow 4, air being trapped from the skin wound due to a flap valve and a ball-valve mechanism, respectively. The treatment is directed at the underlying cause; subcutaneous air eventually gets absorbed over time. However, massive SE leading to respiratory embarrassment5 and requiring insertion of subcutaneous drains has been reported. 6
To conclude, CVC insertion site infection may be a potential cause of SE and daily inspection for signs of infection should be done. Transparent bio-occlusive dressings protect from infection and allow inspection without the need to remove dressing.
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