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ACAD-AE-MED  August 2008

ACAD-AE-MED August 2008

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Subject:

Re: Interesting Case

From:

Coats Tim - Professor of Emergency Medicine <[log in to unmask]>

Reply-To:

Accident and Emergency Academic List <[log in to unmask]>

Date:

Fri, 15 Aug 2008 09:49:00 +0100

Content-Type:

text/plain

Parts/Attachments:

Parts/Attachments

text/plain (145 lines)

D-Dimer is a sensitive but not specific test.

It is a SNOUT - SeNsitive Negative rules OUT (see Sackett's excellent
EBM handbook). It is definitely not a SPIN (SPecific Positive rules IN).

You may be making the error of thinking that just because the absence of
D-dimer means something (no D-dimer = rule out dvt etc) then the
presence fo D-dimer must also mean something. As Andrew points out a
raised D-dimer is meaningless, as it will be up in just about every sick
patient (my guess is that poor tissue perfusion increases microvascular
coagulation and so activates local thrombolysis).

So I think tha the answer to your question is that you should not be
worrying about the question! You do not need to reconcile a massively
raised D-dimer with a negative CTPA, as a massively raised D-dimer is
not a useful diagnostic indicator of thrombo-embolism.

Any diagnostic test that you do is either a SPIN or a SNOUT (very few do
both). I find this a very useful concept when thinking of the meaning of
a test result in an individual patient.

Tim. Coats.

-----Original Message-----
From: Accident and Emergency Academic List
[mailto:[log in to unmask]] On Behalf Of Andrew Webster
Sent: 15 August 2008 07:05
To: [log in to unmask]
Subject: Re: Interesting Case

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

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