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RE: WK,WW...

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Posted by: WK at Tue Oct 21 11:37:01 2003   [ Email Message ] [ Show All Posts by WK ]  
   

I recently dug out my medical report from the joburg H to review, it is very similar to what you describe, here is a summary if interested: snake bite dec 27/93, admitted jan 2/94 with septicemia, haemolysis and early DIC, ARDS with PO2=57%, sever swelling and early compartment syndrom of lower rt leg, liver enzym abnormalities, Blood: PI=100%, INR=1.02%, patient ptt=24.9 sec, control ptt=30.3 sec, fibrin monomera=abnormal,D-dimer less than 0.5 mg/l, fibrinogen 2.62 g/l normal?

had 3 'debridement' surgeries on the 3rd,5th,10th, and skin graft on 14th.




Thanks for the additional information. ARDS stands for Acute Respiratory Distress Syndrome. This involves acute lung injury characterized by leaky blood vessesls throughout both lungs. The leaking fluid produces an impressive and fairly specific appearance on chest x-ray. One of the defining characteristics of ARDS is a PO2 to FiO2 ratio of 200 or less. PO2 is the partial pressure of oxygen expressed in millimeters of mercury (mmHg) and FiO2 is the fraction of inspired oxygen (FiO2 of air is .21, FiO2 of pure oxygen gas is 1.00). I'm not sure what "PI" is in your medical report. If your PO2 was 57 (which is much too low), the "PI" value of 100% could be FiO2=100%. Were you wearing an oxygen mask or perhaps even on a ventilator (also called respirator) when these labs were drawn? If PI is indeed FiO2, your ratio would have been 57, placing you well within the range of severe ARDS.



Your coagulation studies are interesting. The INR (stands for international normalized ratio) is an attempt to standardize prothrombin time measurement across different labs and assay systems. The prothrombin time is an assessment of the extrinsic arm of the coagulation cascade as well as the common final pathway (refer to the horrific graphic I posted in the rambling post above LOL!) An INR of 1.02 is normal. The PTT or partial thromboplastin time is an assessment of the intrinsic arm of the cascade, as well as the final common pathway. These coag tests are most useful when they are prolonged (elevated INR indicates an extrinsic pathway problem, elevated PTT indicates an intrinsic pathway problem, both elevated suggests common pathway problem - makes sense!). Your PTT was actually shortened (control or normal PTT was 30, yours was 25). This can be seen in the setting of early DIC because clotting is already activated in the sample before exposure to the assay clotting stimulus.



Your fibrinogen, fibrin monomer, and D-dimer profile is also very interesting. The relationship of these is as follows: fibrinogen is cleaved by thrombin to form --> fibrin monomer that is crosslinked by coag factor 13 to form --> fibrin polymer / clot --> that in turn is digested by plasmin to release fibrin degradation products including --> D-dimers. The only abnormal value among these that you gave was fibrin monomer. Remember that DIC involves widespread and inappropriate activation of this process, so the abnormally elevated fibrin monomers in the context of normal fibrinogen and D-dimer level is consistent with (but not specific for) early DIC. Another (and perhaps more interesting) possibility is that something in the venom is preventing fibrin polymerization or clot formation, effectively putting a block after fibrin monomer formation. This would also give elevated F monomers with normal D-dimers.



Elevation of liver enzymes is not uncommon in people that have prolonged low blood pressures. Very low blood pressure produces decreased blood flow to the liver which results in damage to liver cells through oxygen deprivation (remember O2 carried by blood). Damaged liver cells release their enzymes into circulation resulting in "liver enzyme abnormalities" (increased levels).



Thanks again for relating your bite history here. Chances are that I will never meet someone that has experienced a bite from one of these snakes, and I've learned quite a bit from the discussions prompted by your posts.



Cheers,

WK


   

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