46yo peritoneal dialysis patient presented with 2/12 of progressive SOB which had become acutely worse in the last 4/7. The last 2 nights she had had orthopnoea and PND. Exercise tolerance had decreased to walking to the toilet from her bed. PD had been ongoing as normal, nil abdominal pain. She still produced 1L of urine per day. No recent change to meds. No infective Sx.
OE dyspneic, accessory muscle use, unable to lie flat, sats 100% RA, decreased AE at bases, bibasal creps, no wheeze, JVPNE, no SOA.
The working diagnosis at this point was fluid overload secondary to inadequate PD.
EDUS showed no pericardial effusion and bilateral pleural effusions.
CXR: unhelpful and ambiguous as usual:
supine: difficult to interpret: heart looks enlarged ?due to AP projection, probable L pleural effusion. But nothing else dramatic.
The report by the radiology fellow reads
"AP erect mobile projection. The radiograph is under inflated and, allowing these limitations, no definitive features to suggest pulmonary oedema. The pleural spaces are clear."
It didn't make sense, so when all else fails redo the US.
R PLAPs view showing R pleural effusion and collapsed lung (annotated image below). Also note a small amount of peritoneal FF consistent with hx of PD.
L PLAP showing a L pleural effusion (annotated image below)
Cine loops of her anterior lung US didn't save: but they looked like this: extensive B lines bilaterally: consistent with APO. And now for the why:
PLAX view showing a severely dilated LV with severe systolic dysfunction. Note anterior mitral leaflet doesn't go anywhere within 5mm of the IV septum. Severely dilated LA (should be the same size as the aorta). Normal RV size. No pericardial effusion. (Annotated image below)
PLAX showing severe MR ?due to dilated LA
PSAX view showing global LV dysfunction. No RWMA (Annotated image below)
Further questioning revealed that she had had a normal echo at Melbourne Private 1 year ago as work-up for transplant. She had had a flu like illness prior to onset of SOB 2/12 ago. Cardiac enzyme testing revealed a troponin of 145. Troponin peaked at 183.
The patient was admitted to CCU with ?myocarditis causing APO. GTN lasix and spirolactone and PD started in ED improved her Sx.
She had a coronary angiogram during her admission which showed normal vessels. Formal echo confirmed the findings above. At the moment she is in CCU awaiting cardiac MRI.