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any other gaboon viper bite survivors out there?

gaboon_survivor Oct 08, 2003 07:13 PM

just found this site...wouldnt mind hearing anyone else's experience...I was unlucky enough to be zapped by one on the ankle,in Zambia, in 93, while working on a farm, was scaring wild pigeons from around a field with an air rifle!! Was stalking quietly in 18" high grass, so must have surprized it. I grew up there till 18, and was back visiting much later for a few months. gaboons were rare in the area. we mostly ran into mambas, spitting cobras, puff adders.

It was a miracle that I survived the first hrs, and first week.. the first dr treating me assumed it was a puff adder, so did not give anti-venon till the 4th day when it was obvious something serious was wrong..internal bleeding, no clotting, renal failure, gang-green, septiceemia etc. ended up being rushed to Johanessburg ($10 grand for that ticket) and spent a week in icu..most of which i dont remember, they saved my leg (which I was very happy about since am an avid squash player), after 4 or 5 operations, ended up with some nice scars from faciotomy/skin grafts up to my knee. have ended up with a fused ankle in the side direction (no tendons), and lousy circulation..but am otherwize fine...thanks to God who answered many prayers on my behalf.

I was told by the Dr in joburg, that only a gaboon could have caused the damage i recieved...and that I was very luckey to survive and keep my leg. will post some picture if anyone is interested.

Replies (27)

budman 1st Oct 08, 2003 09:12 PM

to show my m8s what can happen
plus bites are my hoby thanks in advance
bud
email them to me if you want ok thanks

WW Oct 09, 2003 11:05 AM

Glad you are OK - sounds like a truly terrifying ordeal.

Can you just clarify one thing: did you see the snake yourself and identify it as a gaboon viper, or are you just assuming it was a gaboon viper from the symptoms and from what the doctor was saying?

Thanks,

Wolfgang
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WW Home

gaboon_survivor Oct 09, 2003 07:58 PM

I never did see the snake...afrer the zap from the side/behind I had jumped forward a few steps and spent maybe 10 secs still hoping to hear or see something move..and then went for help. The dr who did the surgury in johannesburg said it had to be a gaboon viper.

BGF Oct 09, 2003 10:51 PM

What did he base this diagnosis off of? Statistically speaking it would be more likely to be a puffer adder. The envenomation profile of the two snakes is largely similar and without a specific test (which does not exist) it would be impossible to tell the two apart from the symptoms alone. As the same antivenom is given for either snake, its more of an academic rather than clinical issue.

All the best
Bryan

------------------

Dr. Bryan Grieg Fry
Deputy Director
Australian Venom Research Unit
University of Melbourne

gaboon_survivor Oct 10, 2003 08:15 PM

all I can offer is the surgeon in Joburg was experienced with snake bites...and was convinced it was a gaboon viper..based on the symptons i arrived with...I guess. I am not a medical professional, or snake expert...but I do personnaly know quite a few that were bitten in zambia by puff adders, with much less severe consequences then I experienced, I thought the gaboon is much more deadly because of the volume of venom it can deliver in a bite..has killed elephants I have heard.

WW Oct 10, 2003 04:58 AM

>>I never did see the snake...afrer the zap from the side/behind I had jumped forward a few steps and spent maybe 10 secs still hoping to hear or see something move..and then went for help. The dr who did the surgury in johannesburg said it had to be a gaboon viper.

With all due respect to him, there is no way the doctor could have told from the symptoms what you got bitten by. What you decribe is perfectly typical for a severe puff adder bite. In fact, from what meagre information is available, gaboon vipers cause LESS local tissue damage than puff adders. However, gabby bites often lead to rapid shock and collapse within minutes after the bite (somewhat similar to what Dean Ripa describes for bushmasters).

Moreover, again with all due respect to the Dr. in Joburg, I rather doubt he would have had much experience of gaboon viper bites. Gaboons are very rare and localised in S. Africa, and bites are very rare - if he had ever seen one before at all, then he would have been very lucky. He certainly won't have seen a representative sample.

Chances are you were bitten by a puff adder. Let's not kid ourselves that puff adders can't cause any particular severity of bite: they are the main mankilling snake in much of Sub-Saharan Africa, at least where Echis does not occur.

Cheers,

Wolfgang
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WW Home

Jeremy G Oct 10, 2003 06:39 AM

Although admitingly I am rather lay with regards to Bitis natural history, it would seem that the enviroment you were in would not be suitable for a gaboon but perfect for a puff adder. I have always belived them (gaboons) to be more of a forest, humid loving snake sp and being in the middle of a feild does not sound like typical Bitis gabonica habitat. I have read accounts of them hanging around the forest edge but most discribe them as being camoflouged within the dense leaf litter of a forest, usualy were water is near by. Again, I have no formal experince with the sp or even the genus at all so everything I say is based on some very breif readings.

Thank you very much for your account and I am very glad you recoved from this most tragic encounter.

Best Regards,
Jeremy

GaboonKeeper Oct 10, 2003 03:04 PM

Jeremy,
I will have to say you are absolutly correct in your statement..... Gaboon an puff adder habitats do not generaly cross..... But do boarder eachother..... The puff adder was most likely the culprit in this situation...... The syptoms of a bite just about mirror eachother between the two species...... Gaboons for the most part do not inhabit tall dry grassy areas...... Infact they can dehydrate rather fast...... They need humidity and generaly do not drink from standing pools of water...... Instead they use their heads as a chanel to funnel water from rain or condensation to their mouths...... So tall grassy fields would not be the habitat of choice for a gaboon but would be a prime location for a puff adder......

gaboon_survivor Oct 10, 2003 08:01 PM

fyi, the northwest part of Zambia is forest land, interspirsed with plains..Gaboon vipers are in that area, I saw many dead and alive, when I lived there, and my dad ran over over one a few months after I was bitten..sent me the fangs for a souvenir.

I was bitten in a forested area near the edge of a farm field, but the grass was thick (18" as it was the middle of the rainy season...December.

WW Oct 13, 2003 03:16 AM

>>fyi, the northwest part of Zambia is forest land, interspirsed with plains..Gaboon vipers are in that area, I saw many dead and alive, when I lived there, and my dad ran over over one a few months after I was bitten..sent me the fangs for a souvenir.
>>
>>I was bitten in a forested area near the edge of a farm field, but the grass was thick (18" as it was the middle of the rainy season...December.

That habitat would certainly be consistent with B. gabonica as well as puff adders. Contrary to expectations, gaboons usually found near forest edges, often around villages, as much as in the dense forest itself. This has even been confirmed with radiotracking studies.

Cheers,

Wolfgang
-----
WW Home

gaboon_survivor Oct 10, 2003 08:32 PM

all i can offer is the surgeon was experienced with many snake bites, it was the 'best' private hospital that treated people from outside S. Africa as well..as myself

do puff adders cause your blood to stop clotting, and your entire right side of your body turn to a bruise from the internal bleeding?...i know quite a few who were reportedly bitten by them in Zambia, and had nothing like that.

bottom line is I guess I will never know for sure...should have got done on my hand and knees in the grass!!

any other gaboon bite survivors out there? heard an elephant at a zoo in the us was killed by one in 4 hrs..heard that from a reptile zoo owner in Ottawa, Can.

WK Oct 11, 2003 12:05 PM

do puff adders cause your blood to stop clotting, and your entire right side of your body turn to a bruise from the internal bleeding?...i know quite a few who were reportedly bitten by them in Zambia, and had nothing like that.

The inability to clot effectively and the bruising may have been due to something other than the direct effect of the venom. Damaged tissue releases a substance called "tissue factor" that initiates clotting of blood. Bacteria can also release substances that do this. This means that tissue damage (like that seen following a bite by a gaboon or puff) or infection / sepsis can result in activation of the clotting cascade. If this is prolonged, the raw materials for forming clots are depleted and the ability to form clots is lost. This increases the risk of hemorrhage (bruising is visible evidence of hemorrhage into superficial tissue). Venom can also initiate this process, but the fact that these problems developed several days following the bite makes me thing infection / worsening tissue damage were likely contributing to the clotting problems.

I am glad you survived intact. What were your symptoms when you first presented to a doctor? I’m curious as to why antivenom administration was delayed?

Regards,
WK

gaboon_survivor Oct 13, 2003 09:01 PM

the dr flew to where I was...had to leave very quickly as daylight was running out for landing on a grass strip, and cleaned out his hospital fridge, and ended up with only mamba av in his bag, which he gave me approx 1.5 hrs after the bite hoping it would have some effect. when he arrived 1.5 hr after, I was in shock, had been dry-heaving for an hr, fair pain and ankle starting to swell. before the dr arrived, a nurse had me on drip after 1 hr and administered adrenalin to keep my blood pressure up. The first night was hell, as Dr had no pain medication with him, until a supply arrived by road at 1 am.

the dr flew me back to a hospital the next morning fearing having to cut my leg to relieve the swelling. there was a mix up as there was a private supply of polyvalent at the hospital, but the dr was not told about it till day 4 when he administered it...hazzards of an accident in Africa I guess.

I appreciate the info you have all shared with me!

WK Oct 16, 2003 02:32 PM

The Univ. of California@San Diego site you referenced below is good one. It gives information on quite a few snakes. I have some time so I’ll take the opportunity to eat a late sandwich and expand on your posted excerpt. Hopefully, you and other interested forum readers may gain greater appreciation & respect for venomous herps and their venoms through closer consideration of what they do. It helps me, too, to review this stuff now and then. Your UCSD website excerpts are italicized:

Hematological signs and symptoms:

The blood is a fascinating organ that is made up of formed elements (blood cells, platelets) and plasma (a.k.a. serum). Blood serves to carry vital substances like oxygen and nutrients to the body’s tissues. It also carries waste products from these tissues to other organs like the liver, lungs, and kidneys for disposal. Blood is essential for fighting infection because it carries antibodies, complement, and white blood cells (essential components of the immune system) to areas where they are needed. The vascular system is made up of blood vessels and lymphatic vessels. These serve as the "roadway" along which blood and blood components travel while carrying out their duties. Blood contains the raw materials for clot formation, which is one of the essential first steps, along with platelet aggregation, in repairing vascular damage like that seen during normal wear and tear (analogous to pot holes in a road) or trauma. These clotting materials or "factors" circulate in an inactive state in blood, but activate upon encountering evidence of vascular damage or tissue damage, directing clot formation to areas where it is needed and thereby, hopefully, decreasing loss of blood from the vascular system.

We often hear that viperid venoms "attack the blood" or are "tissue destructive". Thinking about this as disruption of the processes / systems I mentioned in the above paragraph might give you some idea of the clinical potential of such venoms.

Gabbon Viper venom has a thrombin-like enzyme which quickly depletes serum fibrin levels thus rendering the blood incoagulable.

I’m not tremendously knowledgeable about the contents of Gaboon venom. But, if you have a look at the diagram below outlining the events in clot formation, you will see that thrombin (the red TH) or thrombin-like action would deplete fibrinogen (fibrin precursor) by converting it to fibrin (and therefore actually increase fibrin!). This point is of academic interest only, however, since the result is the same: fibrinogen used up = can’t make more fibrin = can’t make a clot = "blood incoagulable".

In addition the venom has hemorrhagic activity as it causes widespread damage to the microvasculature.

In other words, not only does it disrupt the ability to patch holes in the road, it also blows holes in the road. This translates into unstoppable leakage of blood into tissue, producing severe swelling and discoloration / blistering at the bite site (imagine filling a water balloon from a blood-delivering faucet). If the swelling becomes extremely severe, pressures inside a bitten extremity can become high enough to directly damage tissue as well as impede flow of blood in and out of the area, which, as you recall, is carrying tissue-sustaining oxygen (imagine the water balloon is actually a leather sac that is eventually stretched to its limit with blood – the pressure inside will eventually exceed the line pressure pushing blood out of he faucet, halting forward blood flow). This represents a "compartment syndrome", requiring fasciotomy to relieve the pressure and restore the flow of blood.

Of note, the lungs and gastrointestinal tract are extremely sensitive to this hemorrhagic activity.

This reflects the relatively large size of the vascular bed supplying these organs. You will often find that organs serving to exchange substances with the environment (lungs-oxygen and carbon dioxide / gastrointestinal – nutrients, waste / kidneys – waste) are "vasculary endowed". This makes sense since blood and blood vessels are responsible for transporting these substances to their destinations.

Finally, disseminated intravascular coagulopathy and anemia may also occur.

I prefer the words disseminated intravascular coagulation because tihs is more reflective of the underlying process. This is the entity I described in my previous post that results in depletion of clotting factors (represented by green Roman numerals in the above diagram), platelets, and fibrinogen. Again, this process involves inappropriate activation of the clotting cascade, and usually primarily occurs the smaller blood vessels. The widespread precipitation of tiny clots in these small vessels not only uses up platelets and clotting factors, but also causes damage to tissues supplied by these now blocked vessels. This can be a very bad situation resulting, at the same time (and somewhat paradoxically), in ischemic organ damage and hemorrhage. Severe DIC has at least a 50% associated mortality. As I said in my previous post, causes of DIC are varied, including things like infection, tissue damage, cancer, and yes, venom. Clues to the cause are provided by timing / onset and associated medical history.

The patient should be monitored closely and blood products including whole blood, packed RBC's platelets, cryoprecipitate, and fresh frozen plasma should be given when indicated.

It is interesting to consider each of these treatments and when / why one would be more appropriate than the next. Whole blood is rarely used nowadays. The individual components of blood store much better when separated from one another, but if WB is all you have, that’s what you have to use. "Packed" red blood cells are red blood cells minus plasma and minus most of the white blood cells. Red cells carry oxygen and carbon dioxide. Without these, blood cannot supply oxygen to or remove CO2 from tissues. PRBC’s are used to treat significant blood loss or anemia. In the context of snakebite, PRBC’s would be indicated for significant (shock-producing) internal hemorrhage. Platelets are formed elements of blood that, along with fibrin, provide the structural building blocks for clot formation. They also represent the first "finger in the dike" when a hole appears in a vessel wall. If platelet numbers are decreased significantly, clot formation is hindered. Spontaneous hemorrhage is a real risk if platelet numbers are extremely low. Giving platelets is indicated for thrombocytopenia (low platelet count) accompanied by evidence of hemorrhage like that which might occur in the setting of venomous snakebite (from direct platelet destruction, consumption through clotting activation, DIC etc.). In addition to decreasing platelet number, venoms also can affect platelet function, but this is a lengthy discussion topic in itself and one I can’t get into during my lunch break. Fresh frozen plasma and cryoprecipitate are used to replace coagulation factors and fibrinogen (cryo is better for fibrinogen) so they would be useful in countering the effects of a thrombin-like venom component or severe DIC + hemorrhage.

Thanks for providing the additional information about your bite. You are lucky to have your life and limbs! One more question, if you don’t mind - when you eventually received the right AV (one vial day 4 post bite?!), did you or your doctor note any change in your status? If so, what changed, exactly?

Well, back to work.

Cheers,
WK

gaboon_survivor Oct 17, 2003 12:34 PM

>>Thanks for providing the additional information about your bite. You are lucky to have your life and limbs! One more question, if you don’t mind - when you eventually received the right AV (one vial day 4 post bite?!), did you or your doctor note any change in your status? If so, what changed, exactly?
>>
>>Well, back to work.
>>
>>Cheers,
>>WK
>>

thanks also for expanding on that...cant say I understood it all being a civil engineer..but it does help.
to try answer your question, I dont think my status changed much with the AV, but it definitely improved temporarily day 5 when they lined up all they could trust not being hiv and matching, to donate whole blood for me. I stopped hilucinating and felt better, took food/water for maybe 12 hrs, then deteriorated again, lungs started filling etc...day 6 (i think) was when they decided to medivac me to joburg, and they said I was within hrs of my life when I arrived there.

reading that site I referred to earlier, looks like the gaboon and puff adder bites are treated very similar, which is what you pointed out ealier that the venoms are very close...do any distinct differences jump out for you that would make you lean gaboon vs puff adder in my case? given the further info I have provided, and given that gaboons were sighted in the area by trustworthy sources - my Dad others close to the time of my bite.

My understanding and experience growing up in Zambia was that puff adders where rarely fatal even if not treated with AV (which is often the case in africa)...which i guess is why i still lean towards the opinion of the experienced surgeon who said only a gaboon could cause the degree of damage i had.

I could follow this up with the first Dr in zambia that treated me, he has retired since, but worked there as a missionary dr for 37 yrs I recall (delivered me also)...and treated many snake bites. one thing he mentioned after i returned from joburg was that he was so used to treating black skinned people, the colouration of my ankle (black - I am caucasian) did not clue him earlier that i had more serious complications developing.

Another exlanation for the lack of antivenom supply at a rural mission hospital (or any hosp. in Zambia), is that it was a struggle to keep stock up to date, refridgerated etc. with numerouse power outages, AV not available in the country, except importing privately from S africa, and also the problem with getting correct id of snake, most done hang around to clober it.

cheers

WK Oct 18, 2003 01:34 AM

Either snake could have produced the problems you experienced so, obviously, there is no way to know for sure which it was. However, from scanning the handful of case reports in the medical literature, it seems to me that severe coagulation problems are less common following envenomation by puff adders vs. gaboon vipers. There was one gaboon case in which clotting problems developed 3 days post, similar to what you described if I’m reading your history correctly. The rapid hypotension you experienced also seems to be more associated with gaboon bites, as is the lung edema / effusion.

As people more knowledgeable than I have said here, puffs are more commonly the culprit in bites occurring in areas inhabited by both species, but I can see no compelling reason for you to change your moniker to “Puff Survivor”.

Best of luck,
WK

WW Oct 19, 2003 05:29 AM

After all that was written, I have to say I see no reasn to discount a gaboon bite.

To those critical of the guy and his action with spitting cobras, all I will say is that when you are living in the rural tropics, where snakes are a common and omnipresent danger, one's feelings about them and interactions with them tend to look just a shade different from our rose-tinted spectacles view from the comfort of our first world living rooms.

Cheers,

Wolfgang

>>Either snake could have produced the problems you experienced so, obviously, there is no way to know for sure which it was. However, from scanning the handful of case reports in the medical literature, it seems to me that severe coagulation problems are less common following envenomation by puff adders vs. gaboon vipers. There was one gaboon case in which clotting problems developed 3 days post, similar to what you described if I’m reading your history correctly. The rapid hypotension you experienced also seems to be more associated with gaboon bites, as is the lung edema / effusion.
>>
>>As people more knowledgeable than I have said here, puffs are more commonly the culprit in bites occurring in areas inhabited by both species, but I can see no compelling reason for you to change your moniker to “Puff Survivor”.
>>
>>Best of luck,
>>WK
>>
-----
WW Home

gaboon_survivor Oct 20, 2003 09:26 PM

thanks...one other thing I remember, when I was bitten I was stalking quietly and did not hear the 'typical' warning hiss or puff of a puff adder, and am pretty sure I did not step on the snake (unless it was the tip of its tail), though i'm sure it could have been as surprised also due to me stalking.

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.

cheers

>>After all that was written, I have to say I see no reasn to discount a gaboon bite.
>>
>>To those critical of the guy and his action with spitting cobras, all I will say is that when you are living in the rural tropics, where snakes are a common and omnipresent danger, one's feelings about them and interactions with them tend to look just a shade different from our rose-tinted spectacles view from the comfort of our first world living rooms.
>>
>>Cheers,
>>
>>Wolfgang
>>
>>
>>>>Either snake could have produced the problems you experienced so, obviously, there is no way to know for sure which it was. However, from scanning the handful of case reports in the medical literature, it seems to me that severe coagulation problems are less common following envenomation by puff adders vs. gaboon vipers. There was one gaboon case in which clotting problems developed 3 days post, similar to what you described if I’m reading your history correctly. The rapid hypotension you experienced also seems to be more associated with gaboon bites, as is the lung edema / effusion.
>>>>
>>>>As people more knowledgeable than I have said here, puffs are more commonly the culprit in bites occurring in areas inhabited by both species, but I can see no compelling reason for you to change your moniker to “Puff Survivor”.
>>>>
>>>>Best of luck,
>>>>WK
>>>>
>>-----
>> WW Home

WK Oct 21, 2003 11:37 AM

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

gaboon_survivor Oct 22, 2003 08:03 PM

I am sure I was on oxygen when the blood was taken, as I had been on the flight down and in the ambulance. dont see FiO2 anywhere in report. the following was also in the report for the date of my admitance:
arterial blood gasses PO2 - 4.3kpa minimum 9.3
PCO2- 5.3 kpa rang 4.5 to 6
oxygen saturation - 63% perferable rate 90 to 99
PH - 7.338 lower than acceptable asidosis
blood gas repeat on 40%oxygen mask 6 l/min
PO2 - 11.5 kpa range 9.3 to 11
PCO2 3.2 kpa range 5.42 to 6
PH - 7.53

6 days later on 7/1/94
PI - "had drop to 79%"
patient time - 17 sec pt
control time - 13.5 sec pt range 11 to 16
ptt at this time - 41 sec control 33 sec
bleeding time - 2.5 range 2.5 to 8 min normal
cheers

>>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
>>

WK Oct 23, 2003 01:32 PM

I am sure I was on oxygen when the blood was taken, as I had been on the flight down and in the ambulance. dont see FiO2 anywhere in report. the following was also in the report for the date of my admitance:
arterial blood gasses PO2 - 4.3kpa minimum 9.3
PCO2- 5.3 kpa rang 4.5 to 6
oxygen saturation - 63% perferable rate 90 to 99
PH - 7.338 lower than acceptable asidosis
blood gas repeat on 40%oxygen mask 6 l/min
PO2 - 11.5 kpa range 9.3 to 11
PCO2 3.2 kpa range 5.42 to 6
PH - 7.53

6 days later on 7/1/94
PI - "had drop to 79%"
patient time - 17 sec pt
control time - 13.5 sec pt range 11 to 16
ptt at this time - 41 sec control 33 sec
bleeding time - 2.5 range 2.5 to 8 min normal

I’m not accustomed to seeing ABG’s in KiloPascals so I converted these to Torrs. Your first ABG was pH 7.338 (slightly low) / pC02 40 (normal) / pO2 32 (extremely low). It is somewhat surprising that 40% O2 at 6 liters per minute via mask alone would bring your second ABG to 7.53 (too high) / pCO2 24 (low) / pO2 86 (normal). These latest data also cast some doubt on ARDS as the cause your respiratory problem. I’d be happy to expand on things if you or anyone else is interested.

I still can not sort out what PI represents in your reports. Is it possible that it is PL with L in lower case instead of an I? If that’s so, Pl could represent platelets. However, these are not usually expressed as percentages like you are reporting. Anyway, your PT and PTT on Jan. 7 were elevated which could be consistent with a DIC picture. Since this is several days after the bite, I’m not sure that venom was a contributing factor (what’s the usual half-life of venom components in a bite recipient’s body? Anyone know? Bryan?). You did say you were septicemic and this is a common cause of DIC in ICU patients.

The bleeding time is a reflection of platelet number and function. Yours was normal, indicating an adequate number of functionally intact platelets.

Cheers,
WK

gaboon_survivor Oct 15, 2003 08:21 PM

>>do puff adders cause your blood to stop clotting, and your entire right side of your body turn to a bruise from the internal bleeding?...i know quite a few who were reportedly bitten by them in Zambia, and had nothing like that.
>>
>>
>>The inability to clot effectively and the bruising may have been due to something other than the direct effect of the venom. Damaged tissue releases a substance called "tissue factor" that initiates clotting of blood. Bacteria can also release substances that do this. This means that tissue damage (like that seen following a bite by a gaboon or puff) or infection / sepsis can result in activation of the clotting cascade. If this is prolonged, the raw materials for forming clots are depleted and the ability to form clots is lost. This increases the risk of hemorrhage (bruising is visible evidence of hemorrhage into superficial tissue). Venom can also initiate this process, but the fact that these problems developed several days following the bite makes me thing infection / worsening tissue damage were likely contributing to the clotting problems.
>>
>>I am glad you survived intact. What were your symptoms when you first presented to a doctor? I’m curious as to why antivenom administration was delayed?
>>
>>Regards,
>>WK
>>
found this info at:
http://www-surgery.ucsd.edu/ent/DAVIDSON/Snake/Gabonica.htm

Hematological signs and symptoms: Gabbon Viper venom has a thrombin-like enzyme which quickly depletes serum fibrin levels thus rendering the blood incoagulable. In addition the venom has hemorrhagic activity as it causes widespread damage to the microvasculature. Of note, the lungs and gastrointestinal tract are extremely sensitive to this hemorrhagic activity. Finally, disseminated intravascular coagulopathy and anemia may also occur. The patient should be monitored closely and blood products including whole blood, packed RBC's platelets, cryoprecipitate, and fresh frozen plasma should be given when indicated.

they recommend upto 10 vials of AV for a servere envenomation, i think i got only 1!

BGF Oct 11, 2003 03:19 PM

G'day mate

The best way to describe a puff adder bite is imagine a limb being put into a vice and crushed. The tissue damage and bruising can be absolutely shocking. From what you've said, that should sound awfully familiar.

As for the killing of an elephant, its quite possible that a large species of either one could do that in the wild but I somehow suspect it never happened to a captive elephant in a US zoo unless they made their safari park truly authentic and let a heap of venomous snakes loose (which wouldn't seem to be terribly likely).

Yes blood clotting can also be dramatically affected by fibrinolytic enzymes which destroy all the 'glue' that would normally hold a blood clot together.

Cheers
Bryan
Venomdoc Homepage

vvvddd Oct 11, 2003 01:49 AM

Any large Bitis bite will surely ruin your day, if not your life. Why is it that many doctors wait to give AV in these situations? It really boggles my mind.

Van

gaboon_survivor Oct 17, 2003 08:14 PM

>>Any large Bitis bite will surely ruin your day, if not your life. Why is it that many doctors wait to give AV in these situations? It really boggles my mind.
>>
>>Van

thanks...the hospital that fist treated me was one of the best equiped and staffed in the country, founded and run by a mission organization for 50 yrs, my understanding is they have a hard time stocking many drugs including antivenonms, as they keep expiring or getting damaged when there are extended power outages, and all medication must be brought in from outside the country (south africa)...challenges of serving a 3rd world country. the government hospitals almost always have no power or water!!!

gaboon_survivor Oct 17, 2003 07:49 PM

...hopefully it will help keep all you viper cuddlers extra vigilent! if url below doesnt work they're at: http://ca.f1.pg.photos.yahoo.com/er_structural

this wasnt the culprit but was found nearby by my Dad - Dec 93
Image

gaboon_survivor Oct 17, 2003 08:06 PM

>>...hopefully it will help keep all you viper cuddlers extra vigilent! if url below doesnt work they're at: http://ca.f1.pg.photos.yahoo.com/er_structural
>>
>>this wasnt the culprit but was found nearby by my Dad - Dec 93
>>

sorry that image link did not work..it was a mile long, if interested go to the above and open gaboon_survivor folder
cheers

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