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ABSTRACT
A new emergency method is proposed for determining the degree of microcirculation disorders in critical conditions
in patients with acute cerebrovascular accident and severe traumatic brain injury, based on the capillary-venous
difference in blood hemoglobin. The technical method is simple and convenient for any clinical laboratory and allows
you to control the dynamics of the effectiveness of ongoing intensive care.
KEYWORDS
Capillary, venous hemoglobin, brain, trauma.
INTRODUCTION
Traumatic brain injury (TBI) is the leading cause of
death and morbidity among people under 45
worldwide and remains one of the most common types
of injury to this day. In the general structure of injuries,
it accounts for about 40-50% of all types of injuries, and
Research Article
DIAGNOSTICS OF MICROCIRCULATION DISTURBANCES IN CRITICAL
CONDITIONS IN PATIENTS WITH ACUTE CEREMONIAL CIRCULATION
DISORDER AND SEVERE CRANIO-BRAIN INJURY
Submission Date:
January 15, 2023,
Accepted Date:
January 20, 2023,
Published Date:
January 25, 2023
Crossref doi:
https://doi.org/10.37547/ijmscr/Volume03Issue01-04
Eshonov Olim Shoyimqulovich
Phd, Head Of The Course Of Anesthesiology And Resuscitation, Associate Professor Of The Department Of
Surgical Diseases And Resuscitation, Bukhara State Medical Institute, Uzbekistan
Yarashev Akmal Rustamovich
Phd, Head Of The Department Of “Neuroresuscitation” Of The Bukhara Branch Of The Republican Scientific
Center For Emergency Medical Care, Uzbekistan
Journal
Website:
https://theusajournals.
com/index.php/ijmscr
Copyright:
Original
content from this work
may be used under the
terms of the creative
commons
attributes
4.0 licence.
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the number of patients with TBI in recent decades has
only been growing [5,11,17,23].
Among the causes of TBI, domestic and road traffic
injuries are leading. TBI is a huge global health
problem. The cost of neurorehabilitation after TBI is
more than $35 billion a year. The total loss to society
from disability and the cost of providing medical care
to the victims is about $100 billion a year. The overall
mortality in severe TBI reaches 65
–
70%, and 50% of
victims who have had TBI lose their ability to work to
some extent [9].
The study of neuronal damage and the mechanisms of
their protection in critical conditions is an urgent
problem in resuscitation. In patients with TBI, factors
contributing to the development of secondary brain
damage include: arterial hypotension, hypoxia,
excessive formation of reactive oxygen species,
anemia, endotoxemia, hyper- and hypocapnia,
disorders of water-electrolyte and energy metabolism
[1,16,17].
Modern ideas about the pathogenesis of TBI are based
on the identification of primary and secondary factors
of brain damage [11,18].
The action of the primary traumatic agent triggers the
development of biochemical and immunological
reactions that lead to destructive processes. Oxidative
phosphorylation in mitochondria is disturbed, the
concentration of intracellular calcium increases, free
oxygen radicals and vasoactive metabolites of
arachidonic acid are released, and the mechanisms of
the complement cascade and lipid peroxidation are
activated [11].
The action of factors of secondary brain damage leads
to a disruption in the delivery of oxygen and nutrients
to brain cells and causes their insufficient utilization.
There are disorders of cerebral microcirculation,
oxygenation and metabolism of neurons, brain edema
and its ischemia develop [12]. Secondary ischemic brain
damage, according to different authors, develops in
36.0
–
42.6% of patients with TBI, the severity of which
corresponds to an average degree, and in 81.0
–
86.4%
of patients with severe TBI [4]. A number of modern
studies consider microcirculatory dysfunction as the
central mechanism for the formation of multiple organ
failure in critical conditions [24,28].
Among the extracranial factors of secondary brain
damage that contribute to the development and
maintenance of intracranial hypertension, there are:
arterial
hypotension,
hypoxemia,
hypo-
and
hypercapnia, hyperthermia, disturbances in electrolyte
homeostasis and water-energy metabolism. All these
factors trigger a chain of pathological reactions that
lead to impaired oxygenation and metabolism of nerve
cells and the development of cerebral ischemia.
Increasing ischemia causes cerebral edema with an
increase in its intracranial volume, which, in turn, leads
to a further increase in ICP. Due to intracranial
hypertension, cerebral blood flow decreases and brain
perfusion is disturbed [28, 30].
Cerebral
hemodynamic
disorders
leading
to
insufficient brain perfusion and the development of its
ischemia are considered to be the main factors causing
secondary brain damage in TBI [29].
The death of neurons in TBI also occurs due to the
initiation of apoptosis processes, which can be
triggered both directly by the action of a traumatic
agent on the cell genome, and due to the damaging
effect of inflammatory mediators. At the moment of
injury, a sharp inhibition of the autonomic system of
cerebral blood flow regulation develops, which leads
to a significant decrease in volumetric cerebral blood
flow in the area of injury and adjacent brain tissue [21].
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When autoregulation of cerebral blood flow is
disturbed in the acute period of TBI, the ability of
cerebral capillaries to compensatory changes in tone in
response to changes in blood pressure and carbon
dioxide levels in arterial blood is impaired, which leads
to an increase in the sensitivity of the brain to ischemic
damage. Under conditions of reduced cerebral blood
flow, even a slight decrease in cerebral perfusion
pressure can lead to the development of secondary
ischemic brain damage. This position is also confirmed
by the fact that arterial hypotension in the acute period
of TBI, leading to a decrease in cerebral perfusion,
becomes a statistically significant prognostic factor for
the development of an unfavorable outcome [25].
In addition, there is evidence that with an increase in
the duration of episodes of arterial hypotension, the
risk of developing such outcomes increases by more
than 2.5 times [8].
One of the earliest extracranial factors of secondary
brain damage, which begins to act immediately after
injury, is arterial hypotension (a decrease in systolic
blood pressure less than 90 mm Hg). As a result of a
decrease in blood pressure, brain perfusion decreases
and its ischemia develops. The most common causes of
arterial hypotension in patients with severe TBI include
hypovolemia and violations of the central regulation of
hemodynamics. Hypovolemia - a discrepancy between
the volume of circulating blood (BCV) and the capacity
of the vascular bed - may be due to shock and blood
loss in patients with TBI and severe extracranial injuries
(fractures of large bones of the skeleton, damage to
internal organs, extensive wounds of the skin), as well
as insufficient fluid intake from - for violations of the
level of wakefulness, fluid loss during hyperthermia,
diarrhea, vomiting, polyuria. Sometimes a number of
patients have a sufficient fluid content in the div, but
a decrease in BCV is associated with vasodilation or
increased capillary permeability. Violations of the
central regulation of hemodynamics occur as a result
of the spread of the dislocation syndrome to the level
of the medulla oblongata with involvement of the
vasomotor center in the pathological process or with
primary contusion of the brainstem [13,26,27].
The significance of the problem of acute
cerebrovascular accident (ACV) is determined by its
prevalence,
high
mortality
and
disability.
Vasoconstriction in ischemic stroke leads to the
development of circulatory hypoxia. In the early stages
of ischemic stroke, there is a decrease in the oxygen
delivery index due to the development of a
hypodynamic type of blood circulation. In the future,
against this background, pulmonary complications and
microcirculation disorders join. One of the reasons for
the development of hemodynamic disorders, and
consequently the oxygen transport system, is a
dysfunction of the stem structures as a result of their
damage,
which
is
confirmed
by
clinical,
neurophysiological, radiological and pathoanatomical
data [2,3,10].
The features of microcirculation disorders established
in ischemic stroke make it possible to recommend
active use of drugs that improve arterial blood flow
and relieve vascular spasm to patients with ischemic
stroke both in the early and late recovery periods.
Detection of microcirculatory disorders in patients
with ischemic stroke and their timely correction at the
early stages of neurorehabilitation will improve the
quality of life and optimize early rehabilitation in this
category of patients [6].
Against the background of acute focal cerebral
ischemia, a microcirculatory-cellular cascade of
reactions is realized. Medical science has advanced in
the systematization of microcirculatory and cellular
reactions that occur in IS [2,22], but their pathogenetic
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mechanisms and clinical significance have not been
studied enough.
An urgent problem is the search for technologies for
studying microcirculation not only in patients with
acute ischemic stroke, but also with chronic disorders
of cerebral circulation.
Laboratory signs of hypoxemia include a decrease in
the partial pressure of oxygen in arterial blood (PaO2)
less than 60 mm Hg. and a decrease in arterial oxygen
saturation (SaO2) of less than 90%.
Direct assessment of microcirculatory blood flow using
instrumental research methods has a number of
advantages over indirect methods. Thanks to modern
technical advances, it has become possible to promote
modern methods for studying microcirculation in
clinical practice [14,19].
Despite the existing limitations, a set of facts indicates
the effectiveness of microcirculation monitoring and
may be the rationale for choosing therapies. There is a
proven relationship between low cardiac output,
inadequate
oxygen
delivery,
reduced
venous
hemoglobin oxygen saturation (SvO2), central venous
hemoglobin oxygen saturation (ScvO2), and poor
outcome in critically ill patients. The use of these
variables as endpoints for intensive care was
associated with favorable disease outcomes. It was
assumed that this leads to an improvement in tissue
perfusion and saturation with oxygen, a decrease in
the level of complications and organ dysfunction
[7,20].
At the same time, as some authors note, there is no
objective and reliable method of dynamic control of
microcirculatory blood flow in critical conditions in the
practice of intensive care units.
The development of secondary brain damage
significantly aggravates the condition of patients with
TBI, impairs the recovery of mental and motor activity,
and increases the risk of developing an unfavorable
outcome. In this regard, prevention and timely
correction of factors of secondary brain damage
remain the most important task in the treatment of
patients with severe TBI and ischemic stroke.
Thus, by preventing and limiting the action of
secondary ischemic factors of brain damage, it is
possible to significantly improve the prognosis of
ischemic stroke in severe TBI.
The purpose of the study: to develop a method for
diagnosing microcirculation disorders and to evaluate
its information content in patients with acute
cerebrovascular accidents and severe TBI.
Material and methods. 37 patients aged 32 to 65 years
(mean age 56.3 ± 3 years) were examined in the neuro-
reanimation department of the Bukhara regional
branch of the Republican Scientific Center for
Emergency Medical Care. Hemoglobin in capillary
blood and from the subclavian vein was studied in 11
patients with acute cerebrovascular accident and in 14
patients with severe TBI.
Based on the opposite effect of Fareus Lindqvist, that
in pathological conditions with a decrease in the
diameter of the vessel, blood viscosity increases
slightly, and therefore the red blood indices (Hb and
Ht) in the central and peripheral vessels should be
different, we proposed a simple method for
determining microcirculation disorders based on the
difference in capillary - venous hemoglobin
(Hbcapillary-Hbvenous) blood. As is known, in healthy
people, in the study of hemoglobin, the values of
capillary and venous blood do not have a significantly
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significant difference. The control group consisted of
12 patients.
Method for emergency diagnosis of disorders of blood
microcirculation in patients is carried out as follows.
Upon admission to the clinic, before the start of
infusion therapy, the patient is simultaneously taking
capillary blood from the finger and venous blood from
the subclavian vein. Blood for hemoglobin content is
examined with an MKMF-1 microcalorimeter. At the
same time, saturation is measured on the finger with a
pulse oximeter. The values of capillary and venous
hemoglobin obtained from the general blood test are
compared. According to the ratio of the difference in
capillary-venous hemoglobin (HbcapillaryHbvenous,
g/l) to the blood saturation index (SpO2,%), from the
proposed formula:
KDDBM = (Hbcap-Hbvein) / SpO2
determine the coefficient of the degree of disturbance
of blood microcirculation (KDDBM, conventional
units). The directly proportional dependence of the
coefficient of the degree of disturbance of blood
microcirculation on the comparative value of the
obtained difference in capillary-venous hemoglobin
and the inversely proportional dependence on the
index of blood saturation, shows that the greater the
difference in capillary-venous hemoglobin of the
blood, the more disturbed microcirculation and the
lower the value of oxygen saturation of arterial blood.
With an increase in the coefficient of the degree of
disturbance of blood microcirculation from 0.1 and
more conventional units. the degree of disturbance of
blood microcirculation is diagnosed. Normally, this
ratio is 0.01-0.09 conventional units. units, (Patent UZ
FAP No. 02139).
RESULTS AND DISCUSSION
Our studies have shown a significant difference in
capillary-
venous hemoglobin (from 7 to 12 g/l. Р<0.05)
in patients with severe TBI and acute cerebrovascular
accident, while in patients in the control group this
difference was 2-3 g/l. l., (see table 1).
The difference in capillary-venous hemoglobin (Hb) in patients control and main groups (g/l). Table 1.
Patients
Number
of patients
Hb
capillary
Нb
venous
Difference
(Нb
capillary
- Нb
venous
)
SpO
2
KDDBM,
conventional
units
Р
Control gr.
12
114±2,4 112±1,6
2 ±1,2
96±1,4
0,02
Р
>
001
Severe
TBI
14
119±2,3 107±2,1 12±2,2 79±3,2
0,15
Р<005
Strokes
11
122±1,2 115±1,1
7±1,3
82±1,3
0,1
Р<005
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At the same time, it was found that the largest
difference in capillary-venous hemoglobin was in
patients with severe TBI. Loss of central regulation of
vascular tone and hypovolemia due to blood loss in
severe TBI seem to exacerbate changes in the
rheological properties of blood, which leads to severe
microcirculation disorders.
Thus, the results of emergency diagnostics obtained by
the proposed method indicate that the more severe
the patient's condition, the higher the index of the
degree of disturbance of blood microcirculation (from
0.1 and more standard units), which means that
microcirculation is disturbed more and more deeply,
and the level of saturation of arterial blood decreases
accordingly. The method for emergency diagnosis of
blood microcirculation disorders in these patients is
convenient, simple and accessible to all emergency
clinical laboratories. EFFECT: method makes it possible
to provide a fast reliable result of the analysis of blood
microcirculation disorders, control the effectiveness
and timely correction of the ongoing infusion therapy,
reduce the time of research and reduce their cost.
CONCLUSION
The proposed method for emergency diagnosis of
blood microcirculation disorders in patients with acute
cerebrovascular accidents and severe TBI allows you to
quickly determine microcirculation disorders, select
the composition of infusion therapy and ensure
effective monitoring of the results obtained from it in
dynamics.
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