53
Igor Bokarev, Ludmila Popova
I. M. Sechenov Moscow Medical Academy, Moscow, Russia
IS IT EASY TO DEFINE DIC SYNDROME?
The possibility of intravascular blood coagulation existence in the microvascular vessels-capillaries without
the presence of a large thrombus in the arteries and
veins is known from the middle of 19th century. Selye
[1] thinks that the first description of that phenomenon was made in a German journal written by the
Russian doctor S. Botkin, who was working with R.
Virhov at that time. This phenomenon became wellknown after being entitled disseminated intravascular
coagulation (DIC) or DIC syndrome. For the lßast
40 years there were a lot of published works about it.
This problem is very interesting, because it presents
danger for human life.
It is impossible to know exactly about the prevalence of this pathology, because there is a jumble in
terminology that does not help statistics to be exact.
However, some authors suppose they have this information. So, Мüller-Веrghaus [2] wrote that we can
diagnose DIC in each of the 1,000 patients arriving
at hospital. Zilbut [3] revealed the presence of this
pathology in 1 of 867 persons who arrived to hospital.
Patients with acute leukaemia have higher rates. DIC
is revealed in 15-20% of cases [3]. In septicaemia,
with Gram-negative or Gram-positive bacteria, the
rate of DIC increases up to 30-50%, and for persons
with severe injury up to 50-70% [4]. It is difficult to
treat patients whose illness is diagnosed as DIC and
more than 50% of patients die [4].
One of the reasons of so high mortality from DIC
is due to impossibility to make exact diagnosis, and
as Levi et al. [4] think, it is provoked in the absence of
generally accepted idea of DIC syndrome. Until now,
there have been leading debates on how to define DIC
syndrome. There were several approaches to this idea.
Among them, compensated and decompensated DIC
[5], chronic DIC [6], evident and latent DIC [7], and
pre-DIC. One more reason of such a high mortality
from DIC is the presence of misunderstanding regarding
the early diagnosis of this life-theatening clinical
phenomenon, and also in the choice of treatment of
these patients after making this menacing diagnosis.
Why is it so difficult to make such a simple decision
as the formulation of the determination of DIC? We can
answer this question by observing the metamorphoses
in the process of study of DIC syndrome. This term
was proposed in the USA by a young American pathologist Donald McKay [8] in 1950, when he performed
autopsy. МсKау discovered numerous thrombi in the
vessels of a female who had died in obstetric hospital,
because of hemorrhagic diathesis. He proposed the
term „disseminated intravascular coagulation”. His
senior colleagues Seegers and Schneider [9] carried on
and made this term public. The term DIC syndrome
became widely used in medicine after 4th American
Congress of Obstetricians in 1951, where Seegers and
Schneider reported the case of McKay [9, 10]. The
phenomena began to be actively studied by many
scientists, and each of them tried to give it different
names. So Lasch [11] named it consumtion coagulopathy, Selye [1] and Machabeli [12] “thrombo-hemorrhagic syndrome”, and Оwen and Воwie [13] proposed
to name “intravascular blood coagulation and fibrinolysis“. However, the suggestion of McKay [8] was
preserved and has continued to be most popular and
recognized until the present time.
Biochemists, physiologists and clinicians paid great
attention to DIC syndrome. This made it possible to
study the facts of biochemical transformation of blood
in the course of fibrin and platelet thrombus formation and to create new methods of identification of the
SUMMARY
The possibility of intravascular blood coagulation existence in the microvascular vessels and capillaries without the
presence of a large thrombus in the arteries and veins has been known from the middle of 19th century. It is impossible to know exactly about the prevalence of this pathology, because there is a jumble in terminology that does not
help statistics to be exact. One of the reasons of so high mortality from disseminated intravascular coagulation (DIC) is
due to the impossibility to always make exact diagnosis, and as М. Levi thinks it is provoked in the absence of generally
accepted idea of DIC syndrome. We investigated these markers and the intensity of intravascular blood coagulation in a
number of patients. Our understanding of the problems of DIC was formulated on the grounds of a thirty-year study of
the problem involving over 1,500 patients. Thereby, the conception of constant intravascular microcoagulation (CIMC)
was developed with the following aims: to report the existing material and bring to researchers and doctors in practice information about the presence of the phenomenon of CIMC and to resolve debatable questions of definitions and
practical usage of up-to-date information about DIC with the help of CIMC conception.
Keywords: disseminated intravascular coagulation; diagnosis; constant intravascular microcoagulation
Srp Arh Celok Lek. 2010 Jan;138(Suppl 1):53-58
ПРЕГЛЕД ЛИТЕРАТУРЕ / REVIEW ARTICLE
54 СРПСКИ АРХИВ ЗА ЦЕЛОКУПНО ЛЕКАРСТВО
intravasclar blood coagulation markers. Today, we consider
them to be the products of fibrinogen and fibrin degradation,
which are: fibrin-monomer, D-dimer, β-thromboglobulin,
platelet factor 4 and etc. Many clinicians began to use the
above-listed methods in their researches and discovered
that sometimes patients had a higher level of these symptoms than healthy persons. In this situation they also began
to use the term „disseminated intravascular coagulation”.
Оwen and Bowie [13] proposed to name such phenomena
chronic DIC syndrome. However, this made problems to
doctors in practice, because they often could not exactly
differentiate acute from chronic DIC, and did not know
how to manage such patients.
IS IT EASY TO DETECT DIC SYNDROME?
Indeed, it is very difficult, even theoretically, to draw a
borderline between compensated undiscovered DIC and
pre-DIC, and decompensated discovered DIC and its undiscovered variants. We devoted our attention to this question
from the beginning of the 1970s. When we studied some
features of hemocoagulation in patients, we revealed important rippling of separate performances of both different
and identical patients when blood sampling was investigated separately. This enabled us to make some suppositions about the constant activity of intravascular blood
coagulation in the human body and even suggest that we
can interfere in pathologic process through purposeful
pharmacological regulation of blood coagulation (1974)
[14]. The work, which was done at the laboratory of Paul
Didishaim (1977) [15], where we studied the adhesion
of platelets to the artificial surface – cuprophen, gave us
the reason to suggest a possibility of quantitative determination of the intensity of formation of the platelet clot
in the bloodstream on the ground of measuring the level
of the platelet factor 4 in plasma. The possibility of determination of procoagulant markers and platelet components of hemocoagulation made it possible to note differences in their intensity and suggested that they are relatively independent from each other. Investigations that
we performed on a large group of patients with chronic
pathology gave the reason to reveal different importance
of separate components of hemocoagulation in different
diseases [16, 17, 18].
We also investigated the markers of the intensity of
intravascular blood coagulation in a number of patients.
It was discovered that patients who had CHD (coronary
heart disease) and diabetes mellitus, had a higher activity
of platelet part of hemocoagulation than fibrin formation
[18, 19]. Patients who had rheumatoid arthritis revealed
increased intensity of fibrin formation, which was termed
as a part of procoagulation, and it was noted that the intensity of platelet clot formation was less intensive [20, 21]. In
patients who had acute leukaemia the intensity of platelet
section of hemocoagulation was almost identical to the
increase of intensity of procoagulation. A section on the
evidence of increased blood fibrinolytic activity compared
with increased hemocoagulation also showed the absence
of strict parallelism between them (1980) [22].
We also studied the more accurate state of intravascular
clot formation with the help of TTP (thrombus protein
precursor), which helped us to detect the fibrin-monomer
without fibrin peptids А and В [23, 24]. The level of TPP
was measured in patients with acute coronary syndrome
and in haemophiliac, when there was the presence of
different clinical states, thrombosis and bleedings. In the
course of this study we revealed the following interesting
fact. In the blood of persons with haemophilia we expected
to find low coagulation and accordingly a low level of
TPP-fibrin-monomer. However, it was found that the level
of TPP was higher than that in healthy persons (Table 1).
The disclosed information made us to look more carefully
into the marker level of intravascular blood coagulation of
healthy persons [23, 24]. The results of our research were
compared with the information that we had received from
researchers from all over the world. All this has made it
possible to draw a conclusion that the process of intravascular blood microcoagulation exists permanently, considerably modifying in its intensity, and that is why some definite corrections in the interpretation of DIC were made.
CONCEPT OF CIMC
Our understanding of the problems of DIC was formulated
on the grounds of a thirty-year study of this problem and
on having studied more than 1,500 patients. It is possible
to summarise the results of our work published in domestic
and foreign journals as follows [25]:
• Constant presence of the markers of intravascular coagulation in plasma of healthy and sick persons gives us
the basis to think that intravascular microclotting of
blood is constantly present, and that there is the need
to underline its existence by the term constant microvascular microcoagulation (CIMC).
• Intensity of CIMC may be different. The level of the
markers of intravascular microcoagulation of blood,
which is measured in the plasma of healthy persons,
must be adopted as “normal”. The increasing of the intensity of intravascular microcoagulation may be seen in
some transient disorders and following intensive physical stress (exercise). After such situations have passed,
the intensity of intravascular microclotting can return
back to the “normal” level. Investigated patients with
some chronic diseases exhibit a constant increase of
the intensity of intravascular microcoagulation. They
usually do not show any special clinical traits except of
the usual clinical picture of the main disease. Previously,
these states were named “chronic intravascular microTable 1. Level of fibrin monomers, deprived fibrinopeptide a and b
in patients with coronary heart disease and haemophilia
Disease Number of patients Data
Coronary heart disease
(myocardial infarction) 19 6.99±2.85
Unstable angina 8 7.84+ 2.77
Stable angina 21 11.1±2.4
Haemophilia A 8 1.57±0.56
Healthy persons 23 0.99±0.26
SERBIAN ARCHIVES OF MEDICINE 55
coagulation” .It is possible that special regulation of
this stage of the constant intravascular microcoagulation can improve the prognosis of the disease. When
CIMC is sufficiently intensive it is possible to cause a
change in the clinical picture and organ dysfunction.
In such situations it must be considered as the highest
stage of CIMC. This and only this stage of CIMC must
be named DIC syndrome (Table 2).
• DIC syndrome is the only stage of CIMC, where the
increase of its intensity is an independent cause of the
damage of body organs and body tissues, such as bleeding, multiple organ damage, hypotony, micro- and macrothrombosis and their different combinations.
• Differences in the degree of the intensity of intravascular microcoagulation of blood can be changed, and only
in the definite stage it leads to the progress of the apparent clinical picture of DIC. At that time the manifestation of clinical picture of the syndrome may come true
very quickly. In connection with the above priorities in
diagnostics requires a combination of laboratory analyses with the obtained findings subjected to characteristics and clinical picture of the disease.
Thus, after the suggestion of the conception of CIMC
the idea of DIC and its place in the variety of intravascular blood coagulation can become more concrete and
definite (Table 2).
DIC AS A STAGE OF CIMC
We think that the identification of the idea of DIC should
be guided by МсKау’s [8] observations, with the addition of
something new that can help to include it into the idea of
greater accuracy and clarity. This should be defined more
exactly and help to understand the nature of clinical manifestations which should be expected by the doctors who
make the diagnosis of this phenomenon. It is needed to get
information about the structure of intravascular microclots.
But the term DIC should be mentioned only in the situation when the phenomenon is characterized by the intensive formation of intravascular microclots that are generated at the microvascular level, which can have different
morphologic structure, different forms of clinical manifestation leading to acute dysfunction of organs and tissues,
with life-threatening outcome.
Of course, such situations must produce the evidence of
degradation of fibrin and fibrinogen and platelets activity.
The level of fibrynopeptide A, D-dimer, soluble complexes
of fibrin-monomer, fibrin-monomer without fibrynopeptides, β-tromboglobylin and platelet factor 4 that are
circulating in the human blood, make it possible to have
the information about the intensity of intravascular microcoagulation of blood. However, the wide level of fluctuation of these rates in both healthy and ill persons present
a difficult task for the practitioner.
Many researchers have tried to identify the threat of DIC
progress by taking stock of different clinical and laboratory
parameters. Japanese researchers suggested estimating the
danger of DIC progress by scoring systems (APACHE II
and MOD). The International Subcommittee for DIC is also
actively studying this question. It suggested the following:
the diagnostic criteria of DIC are submitted in Table 3. In
addition, the following algorithm of action is proposed:
the algorithm of open DIC diagnostics, which includes the
following stages of occupation (Scheme 1) [7]. In the first
stage the risk evaluation of DIC onset is put into effect. It is
necessary to detect the presence of such diseases happening
to such patients which are associated with the possibility
of phenomenon progress. It is accepted to consider such
diseases as the following: infections, tumours, obstetric
problems, injuries and burns, immune conflicts, etc. When
they are present, the continuation of algorithm passage is
recommended. In the second stage the performance of coagulation tests is proposed, which could make it possible to
specify the condition of intravascular hemocoagulation. It
is proposed to consider such tests as the following: quantification of platelets, the level of fibrinogen, indication of
prothrombin time, and also the determination of soluble
Table 2. Levels of constant intravascular microcoagulation (CIMC) of blood intensity
Grade CIMC Features
1st Normal CIMC Levels of CIMC markers are “normal”
2nd Transient
increased CIMC
Levels of CIMC markers are increased, but they are unstable and do not produce special clinical
changes in the main disease picture
3rd Sustained
increased CIMC
Levels of CIMC markers are increased. This state is stable, but does not have special clinical
manifestations. Its regulation could be important and may increase the positive outcome of the disease
4th CIMC-DIC-Syndrome Increase of constant intravascular coagulation is rapid and produces impact on organ function,
threatening the life of patients (DIC syndrome)
Table 3. Diagnostic criteria of DIC [7]
Classification Definition Diagnostic criteria
Biological DIC Haemostatic defect without
clinical presentations
Increase of D-dimer level and 1 large criterion* of platelets
consumption or coagulation factors or 2 small criteria* of
platelets consumption or coagulation factors
Clinical DIC Haemostatic defect with hemorrhagic or ischemic
manifestations
All is identical with biological and signs of microvascular
bleeding and/or thrombosis
Complicated DIC Haemostatic defect with hemorrhagic or ischemic
manifestations which lead to organ dysfunction All is identical with clinical and signs of organ involvement
* Laboratory criteria for disseminated intravascular coagulation: D-dimer more than 500 mg/l; consumption of platelets – low (platelet count 50-100,000/mm3)
and higher (platelet count is less than 50,000/mm3), consumption of coagulation factors is low (INR=1.2-1.5) and higher (INR>1.5).
56 СРПСКИ АРХИВ ЗА ЦЕЛОКУПНО ЛЕКАРСТВО
fibrin monomer or D-dimer level. The level of increasing of
each index is marked by appointed scoring scale. Then the
calculation of organ function is performed, which is more
frequently involved in the course of syndrome development.
They are central nervous system (CNS), cardiovascular
system, lungs, liver and kidneys. Their functioning is also
estimated in the scoring scale. The analysis of hemorrhagic
manifestations takes stock of their presence or absence,
which is also fixed in the scoring scale, and total calculation of points, and this, to the author’s opinion, makes
it possible to speak about DIC presence or absence to an
even greater degree of probability. The quantity of points,
which is higher then 7, must be adopted as a great probability of this phenomenon and determines the necessity of
repeated analysis of these rates on the next day. Thereby,
based on the total score diagnostics conclusion is made.
Considering these attempts positively we should look at
them critically. Indeed, the number 1 value could not resolve
the question about confirmation or negation of DIC diagnosis. We have received evidence that such a term of the
biological DIC stage 1-3 of our CIMC only confuses the
doctor’s mind. Indeed, when we reveal that the patient has
a high level of D-dimer and other signs of fibrin formation
and the reduction of the quantity of platelets and fibrinogen (non-metering their dynamics) will lead to the situation when the doctor will decide that the patient has DIC.
In doctor’s practice the term DIC is usually associated
with a condition which is life-threatening for the patient.
That is why the diagnostics of this disease cals for active
actions, which could be unjustified, because the increase
of mark level of fibrin formation is not specific only in the
extreme stage 4 of CIMC (acute DIC), while platelet count
of the patient could be low for many other reasons. Besides,
initially the patient may have a high platelet count and/or
fibrinogen rate and having DIC, with reduced platelet and
and/or fibrinogen, not to mentioned the level. So it turns
out that there is no DIC. In such cases the doctor could
start the necessary therapy too late.
Scheme 1. Diagnostics of DIC [7]
Step 1
Risk of origination
Do patient has such diseases which are accompanied by high risk of DIC progress?
No Yes
Step 2
Fulfilment of laboratory tests
Platelet quantity, prothrombin time,
products of fibrin degradation,
soluble complexes of fibrin –monomer
Step 4
Calculation of points
Step 5
Mark 5 or over
DIC is possible It is presumably DIC
Less than 5
Step 3
Estimate of laboratory tests in points
• Platelet quantity: >100×109/L = 0 points; <100×109/L = 1 point, <50×109/L = 2 points
• Increase of mark of fibrin formation (soluble complexes of fibrin–monomer) / products of fibrin degradation:
no rise = 0 points; mean rise = 2 points; considerable rise = 3 points
• Prolongation of prothrombin time: <3 s = 0 point; 3<6 s = 1 point; >6 s = 2 points
• The level of fibrinogen: >1 g/L = 0 points; <1 g/L = 1 point
Stop
Repeat the next day Repeat in 1-2 days
SERBIAN ARCHIVES OF MEDICINE 57
At present the International Subcommittee of DIC
continues to work out refinements of DIC with different
types of diseases (injuries, obstetrical pathology, sepsis)
and search or new subtle markers – the predictors of DIC.
It seems to us that the identification of subtle marks
level of intravascular blood coagulation could not help us
to predict the progress of extreme stage of CIMC (acute
DIC according to ISTH), because they would only reproduce the intensity of CIMC, which could arise in different
diseases, as well as in healthy persons and would not lead
to DIC. Because we understand this problem well enough
we dare say that the transition of the intensity of intravascular blood coagulation to the stage of DIC can be specified, not on the ground of point calculation, but in the
following way: morbid events characterized by a high risk
of DIC progress (sepsis and other infections, neoplasm,
traumatic and surgical tissue involvement, obstetrical
pathology, vascular lesions and vascular anomaly, autoimmune diseases, allergic reactions); for timely and early
recognition of DIC progress it is recommend to do case
monitoring of the rates of fibrinogen and platelet levels.
Progressive reduction of these rates in combination with
clinical picture should be the reason for the diagnosis and
the beginning of therapy.
Thereby, the conception of CIMC was developed with
the following aims:
a) To reproduce existing material and bring to researchers
and practitioners information about the presence of the
phenomenon of CIMC in humans;
b) To resolve debatable questions of definitions and practical usage of up-to-date information about DIC with
help of CIMC conception.
CONCLUSION
We hope that further conception design of CIMС could
give us a definite answer about the role and place of
purposeful regulation of blood coagulation in therapy of
many human diseases.
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58 СРПСКИ АРХИВ ЗА ЦЕЛОКУПНО ЛЕКАРСТВО
Igor BOKAREV
I.M. Sechenov Moscow Medical Academy, 8-2 Trubetskaya Street, 119991 Moscow, Russia
Email: bokarev@online.ru
KRATAK SADRŽAJ
Mogućnost intravaskularne koagulacije krvi u krvnim sudovima i kapilarima, bez velikog tromba u arterijama i venama, poznata je od sredine devetnaestog veka. Nije moguće tačno saznati preovlađivawe ove patologije s obzirom na mnoštvo različite terminologije koja ometa izrađivawe precizne statističke analize. Jedan od razloga visoke stope smrtnosti od diseminovane intravaskularne koagulacije (DIK)
leži u nemogućnosti da se uvek postavi tačna dijagnoza. Prema mišqewu Marsela Levija (Marcel M. Levi), to je rezultat nepostojawa opšteprihvaćene ideje o DIK. Mi smo istraživali ove pokazateqe i intenzitet intravaskularne koagulacije u krvi kod velikog broja bolesnika. Naše razumevawe problema diseminovane mikrokoagulacije formulisano je na
osnovu tridesetogodišweg istraživawa ovog problema kod
više od 1.500 bolesnika. Na taj način razvili smo koncepciju konstantne intravaskularne mikrokoagulacije (KIMK),
imajući u vidu sledeće ciqeve: a) davawe izveštaja o sakupqenom materijalu; b) pružawe istraživačima i lekarima
informacije o zastupqenosti fenomena KIMK; i v) rešavawe diskutabilnih pitawa definisawa i primene u praksi
najnovijih informacija o DIK pomoću koncepcije KIMK.
Kqučne reči: diseminovana intravaskularna koagulacija;
dijagnoza; konstantna intravaskularna koagulacija
Откривање дисеминоване интраваскуларне коагулације помоћу
концепције константне интраваскуларне микрокоагулације
Игор Бокарев, Лудмила Попова
И.М. Московска медицинска академија „Сеченов”, Москва, Русија
