Thats the problem with D-dimer it goes up in most critically ill patients,
used appropriately in the right conditions and patient populations can help
exclude disease, but also very non-specific and lots of things elevate. For
dissection I think to be useful in excluding dissection the cut off needs to
be less than 100 ng/ml so very low.
-----Original Message-----
From: Accident and Emergency Academic List
[mailto:[log in to unmask]] On Behalf Of John Ryan
Sent: 15 August 2008 06:09
To: [log in to unmask]
Subject: Re: Interesting Case
Has she bled somewhere to give the raised D dimer ? Was there CPR with
fractured ribs ?
I have read a paper recently on elevated d-dimer in Aortic dissection.
Whats with the 'possible transient PEA' ?. Was there no ambulance rythm
strip ? She has an abnormal heart, previous MI, on ACE inhibitor. Could
this not have been an arrythmia ?
Did she have glycosuria ? I suspect its not DKA. Maybe she decomepnsated
because of VT and the resultant cardiac failure cleared with positive
pressure ventilation and the normalisation of her rythm. What was her intial
CVP ? Perhaps the decompensation caused a NSTEMI. After all if she had a MI
10 yars ago (and she is in your catchment area David ;-) ) then her
coronary arteries are unlikely to have actually got better in the last 10
years, presuming she had no post MI intervention such as angioplasty
John Ryan
----- Original Message -----
From: "David Menzies" <[log in to unmask]>
To: <[log in to unmask]>
Sent: Friday, August 15, 2008 12:22 AM
Subject: Interesting Case
I wonder could I pick the collective brains of this list with a recent case?
58 year old woman calls an ambulance for acute dyspnoea at 4am. On arrival
of ambulance she is tachypnoeic 40/min, cyanotic with SpO2 60% on room
air. Minutes after ambulance arrival she collapses with respiratory arrest
and
possible transient PEA.
On arrival at ED she is GCS 5/15 tolerating an OPA with agonal resps. Pulse
50bpm, sinus rhythm, BP 194/80mmHg. SpO2 89% with assisted ventilations -
very little air movement bilaterally. Temp 34.4.
She undergoes RSI with propofol and sux. Very tight lungs immediately post
intubation but responded well to salbutamol via ETT.
Initial ABG is Ph: 6.77, PCO2: 15.4, PO2 47.8, Base Xs: -19.3, HCO3: 10.6,
Lactate: 12, Blood Sugar: 19.2.
Portable CXR is clear. Clinically, the olnly finding is MR. Myocardium
clearly
very irritable, multiple ectopics and runs of tachycardia and bradycardia.
She is treated as a DKA with insulin, fluids and NaHCO3.
CT Brain shows no bleed or infarct. D-dimers are raised at 3036 ng/ml
(normal
0-200). CTPA shows no PE.
FBC, UEC, LFTs, TNI are all near normal.
ABG normalised within 2 hours of intubation. She did not require further
bronchodilators. No evidence of pulmonary oedema. Blood sugars stabilised
without further insulin.
ECHO reveals severe MR and some LVH. TNI has risen to 0.06. She has no
evidence of infection and was extubated the next day. Urine and blood
toxicology are negative. The patient denies any ingestion. No preceeding
symptoms reported.
She had an MI 10 years ago and takes Ramipril, Betaloc and Aspirin.
She is now well but d-dimers have risen to 7000.
Cardiology feel this is a NSTEMI with Mitral Regurgitation as a consequence.
Medics are unsure.
I wonder can anyone reconcile the massively elevated d-dimers with a
negative CTPA and the original ABG which improved rapidly following
ventilation? I have not seen the scan myself, but I imagine an embolus
large
enough to cause this degree of compromise would not be missed?
I do not have the final answer yet!
Thanks,
David Menzies,
SpR Emergency Medcine,
Dublin
|