Page 1 of 13
European Journal of Business &
Social Sciences
Available at https://ejbss.org/
ISSN: 2235-767X
Volume 07 Issue 05
May 2019
Available online:https://ejbss.org/ P a g e | 580
UDC: 616.831-008.918: 617.51-001-005.98: 616-085
Effects Of Mannitol And Hypertonic Solution Of Sodium Chloride On
Intracranial Pressure In Patients With Brain Injury
MurotovTemur Malik Nizomovich, Jumanazarov Farrux Fayzullaevich,
Juraev Pirnazar Bahodirovich
TashkentMedicalAcademy
The Department of Anesthesiology and Resuscitation
Uzbekistan
Purpose:study the comparative efficacy of using a 15% solution of
mannitol and a hypertonic 7% solution of sodium chloride in the complex
treatment of patients with TBI.
Material and methods:It examined 20 patients aged from 18 years to 65
years with a variety of traumatic-brain injuries, and depressed level of
consciousness from 4 to 11 points on the scale of coma Glasgow
Results:infusion ofmannitol in the indicated dosage led to a decrease in
ICP after 30 minutes by42, 3%, and after120minit remained below the initial
data by23,9%.Infusion of a7% solution ofNaClby 30 minutes led to a decrease
in ICP by 55.4%, and by the end of 120 minICPremained below the initial
data by 39.9%.
Findings:Thedecrease in ICPwithin the limits of 30 and 120 minutes after
the introduction of hyperosmolar solutions is more pronounced with IV
injection of 7%NaCl solutionrelative to 15% Mannitol in calculated dosages,
which must be borne in mind in patients with concomitant cardiac and renal
pathology.
Key words:TBI, brain edema, CPP,ICP,NaCl,mannitol,
The brain from many points of view (anatomy, cellular organization and
function) - complex organ. When it is damaged, the response is also complex
Page 2 of 13
European Journal of Business &
Social Sciences
Available at https://ejbss.org/
ISSN: 2235-767X
Volume 07 Issue 05
May 2019
Available online:https://ejbss.org/ P a g e | 581
and multifaceted [1]. Traumatic brain injury (TBI) is defined as a change in
brain function or its other structures, pathology, caused by external force [2].
General pathological effects of brain injury include
hematoma,Subarachnoidhemorrhage, contusion and diffuse axonal
damage[1,3]. They differ in severity from mild to severe TBI. Severe head
injury has a high mortality rate up to 30-60% in studies on unselected
populations [4].Survivors have a significant burdenphysical, mental,
emotional and cognitive disorders that disrupt the lives of people their families
and bearhuge costs for society[5].TBI is a growingproblem of public health in
significant proportions. More than 50 million cases of TBI are recorded at the
international level every year [6] and it is estimated that about half of the
world's population will have one or more TBI during their lifetime. In the
European Union up to 1.5 million people arehospitalized and 57,000 die each
year due to traumatic brain injury [7]. TBI is the leading cause of death among
young people and disability among of all ages [8] and accounts for 30% of all
deaths associated with injuries. [5,7,9].
TBI can be divided into primary and secondary injury [3,10]. The primary
injury is caused by direct external influence of. mechanical force, leading to
disturbances of the blood-brain barrier (BBB) and blood vessels that
contribute to edema [3,11,12,13,14]. Secondary injury refers to a cascade of
delayed pathological processes that can last for hours of days and play so
important role in morbidity and mortality and as a result of head injury and is
characterized by ischemia, disturbance of BBB and brain edema[3,8,13], what
It is associated with activation of microglia and astrocytes in the brain that
produce tons of cytokines and chemokines, and attraction of peripheral
immune cells to the brain [3,10, 12,15,16].
Page 3 of 13
European Journal of Business &
Social Sciences
Available at https://ejbss.org/
ISSN: 2235-767X
Volume 07 Issue 05
May 2019
Available online:https://ejbss.org/ P a g e | 582
Cerebral edema after TBI leads to devastating damage of brain structures.
[13]. TBI is characterized by mixed cytotoxic and vasogenic edema,
mechanism conducive to general cerebral edema [17,18].Treatment of
cerebral edema aimed at extracting excess water from brain tissue into the
intravascular space. This is usually achieved with osmolar therapy.
The severityof cerebral edema is directly proportional to the increase in
ICP. Increased intracranial pressure, reduced cerebral perfusion pressure [19].
These processes lead to impaired cerebral circulation and occurs cerebral
ischemia.
It is necessary to clearly understand the nature of the disorders of the
blood-brain barrier, brain metabolism, and cerebral bloodstream to properly
exercise adequate treatment. The blood-brain barrier restricts the flow only for
fat-soluble substances, although water can move freely [20]. Considering this
concept is crucial for understanding how mannitol and hypertonic solution
help reduce brain swelling. According to Butterworth et al. auth., "The
movement of a particular substance through the blood-brain barrier is
regulated at the same time in size, charge, lipid solubility and degree of
protein binding in the blood. ". The largemoleculsof mannitol are unable to
cross the blood-brain barrier, and sodium ions limited in their passage. When
a large amount of mannitol or hypertonic saline falls into blood, the flow of
these substances cannot cross the BBB. This creates plasma hypertonus in the
vascular network of the brain, which leads to an increase in the osmotic
gradient, which leads to the movement of water from brain parenchyma in
blood vessels [20].
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