73 yo male with a PHx of HT represented to ED.
He was seen the night before with a swollen L calf following an international flight. He had no chest symptoms and was otherwise well and so he was discharged home with an US booked for the morning to investigate for DVT.
He presented the next morning: hypotensive (SBP 70/) tachycardic (Hr110-130 SR), sweaty and hypoxic (sats 85-90%), afebrile. He still had a swollen L calf. On close inspection there were 2 blisters posteriorly and bruising anteriorly. His chest had basal crackles.
If we are thinking DVT complicated by PE, this patient qualified for thrombolysis in the ED.
this is his ED cardiac ultrasound
PLAX: tachycardic, dilated LV and RV, poor LV contractility. No obvious RV>LV, no septal bowing to left: ie no features of massive PE
PSAx showing global decreased LV contractility. (note: slight D shape to LV was due to off axis view)
Other cardiac views were similar. The echo seemed to have moderate LV and RV dysfunction
associated with tachycardia. He didn't have any previous echoes for comparison. His IVC was small and collapsing >50%. None of this fit with a massive PE (which should have dilated RV>LV, septal bowing to L, dilated non collapsing IVC).
His L leg US showed a lot of subcutaneous oedema and cobblestoning with no evidence of DVT.
Cobblestoning is the presence of fluid between subcutaneous fat. It is usually seen in cellulitis or peripheral oedema. But it is not a specific sign. It can also be seen in patients with DVT if there is significant venous insufficiency.
Given all this, we went down the path of sepsis as a cause of hypotension and resuscitated him with fluids and inotropes and started broad spectrum antibiotics.
His lung US didn't show consolidation; just a few b blines bilateral bases.
The leg was further assessed for evidence of subcutaneous gas. None was palpable, seen on XR or US. However he was acutely sensitive to palpation.
If gas is present, it can be easily seen with US and is shown to be a good rule in sign of nec fasc (sens and spec 88% and 93% respectively(1))
Given the leg was the only source of sepsis, his presentation and a positive response to fluids and inotropes, he was rapidly referred to plastics with a presumptive diagnosis of necrotising fascitis.
He was taken to theatre and his leg was debrided to mid thigh.
PLAx 2 hours after presentation: worsening LV function (likely due to cardiomyopathy of sepsis). Note now a dilated LA. IVC was also now dilated and non collapsing.
Further fluid resuscitation (post 1.5L) was stopped at this point due to the risk of pulmonary oedema