Medical Sciences

DOI: 10.26693/jmbs 04.01.118

UDK 616.831.94-005.1-036-07:616
Colonels-K
CLINICAL-PATHOGENETIC THE VALUE OF HYPONATREMIA IN THE
ARACHNOID WITH SUBARACHNOID HAEMORRHAGE OF ATTRAUMATIC
GENESIS
Of Zaporizhzhya Medical Academy of Postgraduate Education, MOH of Ukraine
kuzya.cat01121981@gmail.com
Subarachnoid hemorrhage is one of the most severe types of disorders of cerebral circulation,
characterised by prehospital leitality at primary hemorrhage due to rupture of aneurysms 10-15%.
Purpose of the study. Assess the clinical-pathogenetic value of hyponatremia as a manifestation of
SIADH syndrome in inpatient patients who have been hospitalized for subarachnoid haemorrhage
and spontaneous etiology. Materials and methods. 87 patients with subarachnoid hemorrhage have
been examined. Age distribution is typical for this disease – most patients had aged between 30
and 60 years, with a predominance of aged 40-60, elderly patients (over 60 years) – 20.7%. The
average age was 49, 97 years. Men were 44, women – 43. All patients were given a clinical
neurologic assessment of the SAC course according to the modified Fisher scale, WFNS scale,
Nunt & NEMS scale, GOSE results scale (Glasgow Outcome Scale Extended) and generalizable
classification scale for estimating the prediction of SAC result (C.S. Ogilvy et B.S. Carter).
Results of the study. The greatest number of patients with marked hyponatremia is 14 people –
correlates with the heaviest severity degrees according to the modified scale Fisher – 3-4 degree.
In 7 patients with 3-5, the degree of severity of subarachnoid hemorrhage with WFNS (3-13 on
the Glasgow scale score and presence/absence of motor and/or linguistic deficits) was diagnosed
statistically significant (P < 0.05) hyponatremia. These patients accounted for 41.18% of the total
number of patients in these groups. At 3-4 gravity stages according to the scale of the Nunt & is
statistically accurate hyponatremia (P < 0.05) is confirmed in 11 patients of this group (40.74% of
the total amount). The level of atraemia in patients 3-4 of severity of the GOSE results scale
(Glasgow Outcome Scale Extended) was 131,36 ± 1,53 mmol/L, and in 5 persons of this group
(45.45%). The easiest Pìn of gravity of subarachnoid hemorrhage in patients with a scale of the
GOSE results corresponds to the smallest number of patients with hyponatremia. Half of patients
with severe clinical status (54.55%) According to the generalized classification scale to assess the
prognosis of the result of subarachnoid hemorrhage (C.S. Ogilvy et B.S. Carter) had hyponatremia.
Conclusions. Clinical-pathogenetic values of hyponatremia as a manifestation of SIADH
syndrome in inpatient patients who have been hospitalized for subarachnoid haemorrhage and
spontaneous etiology, it testifies to the close association of expressiveness of Disorders of osmotic
homeostasis and severity of clinical course of subarachnoid hemorrhage according to the modified
scale of the Fisher, WFNS scale, Nunt & NES scale, results of GOSE scale (Glasgow Outcome
Scale Extended) and generalizing classification scale for The prognosis of the result of
subarachnoid hemorrhage (C.S. Ogilvy et B.S. Carter). In subarachnoid hemorrhage in persons
with hyponatremia sprâženìst whey level of sodium and serum copeptiin is adequately and reliably
approximated by equation of regression of logarithmic nature (based on the basis of 10), with the
values of Copeptiniv more 0.70 ng/ml in more than 50% of cases registered atraemia of medium
severity.
Keywords: aneurysmatic subarachnoid hemorrhage, SIADH syndrome, WFNS scale,
hyponatremia, Copeptin.

Communication work with scientific programs, plans, themes. The work is a fragment of the
RESEARCH Department of Nervous Diseases of the Zaporizhzhia Medical Academy of
Postgraduate Education at the Ministry of Health of Ukraine: «Comprehensive diagnosis and
forecasting algorithms of subarachnoid hemorrhage in patients of different age groups», no state.
Registration 0115U000657.
Relevance. Subarachnoid hemorrhage (SAC) – CLINICAL-PATHOGENETIC VALUES of
HYPONATREMIA with SUBARACHNOID BLEEDING in the SUBAARIDAL hemorrhage
A blood circulation characterised by prehospital leitality at primary hemorrhage due to a rupture
of aneurysms 10-15% [1]. The main cause of AKI complications is caused by repeated hemorrhage
in the presence of aneurysms, in which mortality is already reaching 70% [2]. To date, the level of
adverse effects in patients with AKI remains high enough because of the factors that affect the
course and prognosis of the disease. A wide range of AKI requires a clearer approach to keeping
these patients. Quite often, SAK is associated with electrolyte disturbances and homeostasis of
circulating blood volume. Hyponatremia occurs in 10-34% to 1% of SAC patients, degrades
prognosis. These patients present with excessive natriuresis and osmotic diuretic, resulting in a
decrease in systemic blood volume. All patients with SAC demonstrated increased urine volume
and increased sodium excretion in the urine. Adrenomedoline, a vaszelaxotic peptide secreted into
cerebrospinal fluid (CSF), has natriuretical effects in the kidneys. According to previous studies,
Adrenomedoline concentration in CSF was considerably higher in the late period compared with
the early SAC period [4].
The results of studies using logistics regression analysis showed that the concentration of
Adrenomedulina in CSF in late period correlates with hyponatremia and delayed brain ischemia.
At the very beginning, the SAC hyponatremia without reducing the volume of circulating blood
has been prevented by the infusion of sodium and water resistant to renal excretion. There are no
significant correlation between concentration of hormones and natriureosis. The purpose of
treatment of hyponatremia is to maintain positive water-electrolyte balance. The syndrome of
inadequate antidiuretic hormone secretion (ADG) (Syndrome of Inappropriate Antidiuretic
Hormone Secretion – SIADH) is a condition determined by the excessive release of antidiuretic
hormone (ADH) from the pituitary gland or other sources or its prolonged action on vasopressin
receptors. This condition was first detected in two lung cancer patients by William Schwartz and
Frederick Barter (William Schwartz and Frederic Bartter) in 1967. They developed the classic
criteria of Schwartz and barter to diagnose SIADH, which has not changed until today. SIADH is
characterised by impaired water excretion, leading to hyponatremia with Gìpervolemìêû or
Euvolemìêû [5]. Most SIADH occurs due to another primary disease of another localization.
Hereditary SIADH, also known as Nephrogenic SIADH, was caused by increased functional
mutations in vasopressin 2 (V2) in kidney receptors.
One of the common causes of this syndrome is the damage to the central nervous system: any CNS
pathology can aggravate an ADG from the pituitary gland, which will lead to SIADH. These
abnormalities include: stroke, SAC, infection, trauma, mental illnesses and psychoses. In patients
with SIADH, ADG levels are high even in the presence of decreased osmolality of plasma and/or
hyponatremia. Excess water absorption leads to an increase in blood volume [7].
An acute drop in blood pressure is perceived by receptors of volume, not osmotic receptors, this
causes the release of ADG (along with other hormones such as renin and adrenaline), generating
free absorption of water from the kidneys. This can potentially lead to hyponatremia and reduced
efficacy of extracellular osmolality. This effect is more common in patients with liver disease or
cardiac disease, and hyponatremia in these patients is a direct predictor of worse prognosis. The
clinical manifestations of SIADH can be associated with hyponatremia and a decrease in
extracellular osmolarity, resulting in water movement in the cells causing cerebral edema. Signs
and symptoms depend on the rate and severity of hyponatremia and the degree of brain swelling.
Early clinical manifestations of acute hyponatremia include nausea and malaise, which can be
observed when the serum sodium concentration decreases below 125-130 Iec/l (norm 135-145
micrograms/Liter). Vomiting is an ominous sign for patients with acute hyponatremia. With the
more serious and acute incidence of sodium concentration, there is a headache, lethargy,
obturation, and, in the end, there may be seizures. Coma and respiratory cessation may occur if the
serum sodium levels fall below 115-120 IEC/L. Acute hyponatremia encephalopathy may be
reversible but may have persistent neurological deficit or death, especially in women in
premenopausal stage [9]. Hyponatremia in SAK significantly deepens the main pathological
process, worsens the course of rehabilitation period, reduces the effectiveness of therapeutic
measures, prolongs the duration of inpatient treatment and at zapìznìlìj or irrational its correction
significantly increases the level of fatality of patients, which caused the importance and directivity
of this clinical study. The purpose of the study: to assess the clinical-pathogenetic value of the
development of hyponatremia as a manifestation of SIADH syndrome in inpatient patients who
are hospitalized over subarachnoid hemorrhage.
Materials and methods of research. 87 patients with SAC were examined, including 38 (43.68%)
With isolated SAC, 14 (16.09%) – with Subarachnoid, 29 (33.33%) – with subarachnoid-
ventricular, 6 (6.9%) – with subarachnoid-venereal-ventricular hemorrhage, the one with a
superventricular-venovascular bleeding total number of mixed hemorrhage was 56.32%. The study
was carried out in compliance with the basic provisions of the "Rules of ethical principles of
conducting scientific medical research involving human beings", approved by the Helsinki
Declaration (19642013), ICH GCP (1996), EEC Directive No 609 (from 24.11.1986), orders
Ministry of Health of Ukraine no 690 from 23.09.2009, no 944 from 14.12.2009, no 616 from
03.08.2012, each patient or his relatives signed informed consent to participate in the study. Age
distribution is typical for this disease – most patients had aged between 30 and 60 years, with a
predominance of aged 40-60, elderly patients (over 60 years) – 20.7%. The average age was 49,
97 years. Men were 44, women – 43. Receipts of more than half of patients occurred in the first
day after SAK-46 people (52.87%). A SAC due to a rupture of a mysco aneurysm (MA) is
confirmed by an angiographic method in 63 patients (72.41%), and 5 of them have been repeated
hemorrhage with a ruptured MA. In remaining cases (27.59%) The presence of MA or Artero-
venous malformation is instrumentally not verified, but angiographic examination by these
patients has been conducted once. The findings indicated that the most commonly detected anterior
cerebral artery aneurysms and the anterior connective artery of PSAIS – 25.29%, internal carotid
artery (14.94%) and middle cerebral artery (22.99%), and the most rarely-aneurysms of Vertebro-
Basillary basin (2.3%) and peripheral aneurysms. Thus, the frequency of verification of PMA-PSA
and Ma was more reliably than other localizations. A history of arterial hypertension has been
noted in 43 patients (49.43%). Various diseases and syndromes of the nervous system are marked
with a history of 5 patients. Most often there were discirculatory encephalopathy, convulsive
syndrome, and HX of SAC. "Family" aneurysms is found in 2 patients most often showed the
following symptoms, early and late complications: headache in 50 patients (57.47%), muscle tonic
symptoms in 48 people (55.17%), and 51 patients have had vasospadism (62.07%), General
Hypoesthesia, and jet pain symptoms in 41 and 40 sufferers (47.13 and 45.98%). Almost the fourth
part of patients complain
She was on nausea and vomiting (27.59%), short-term loss of consciousness (27.59%), and almost
half of the cases was diagnosed with deferred (secondary) ischemia (31.03%). Hydrocephalus had
15 people (17.24%), motor deficit-16 (18.39%), and seizures occurred in 13 patients (14.94%).
Repeated hemorrhage was diagnosed in only 3 patients (3.45%). Four patients were among the
complications of linguistic disturbances (4.6%), and cerebral edema developed in 7 people
(8.05%). The majority of patients in this sample had the easiest The severity of SAC according to
the classification of the World Organization of Neurosurgeons (WFNS) – 33 patients (37.93%),
which corresponds to 15 Balam on the Glasgow scale and the absence of motor and linguistic
deficits. The second severity of the diagnosed in the 37 people (42.53%), is 13-14 points on the
Glasgow scale and the absence of motor and linguistic deficits. The next small cohort of patients
was treated to 3 severity – 14 patients (16.09%), they had 13-14 points on the Glasgow scale and
a certain degree of Ruthenian and/or language Deficiency. Two people were attributed to 4 degrees
of severity (2.30%) With 7-12 points on the Glasgow scale and the presence/absence of motor
and/or linguistic deficits. One patient (1.15%) belonged to extreme 5 severity category with 3-6
points on Glasgow's scale and presence/absence of motor and/or linguistic deficits. According to
the classification of Nunt & НSS in a given cohort 31 patient (35.63%) There were not quite
symptoms or symptoms were minimal: headache and stiff neck, which corresponds to 1 degree of
severity. The greatest number of patients treated to 2 severity – 38 people (43.68%), with
symptoms of headache, neck stiffness, lack of neurological deficit (except cranial nerve palsy).
Drowsiness, stun or slight focal deficit, and 3 severity diagnosed in 16 patients (18.39%). Severe
state in the form of stupor, moderate to severe hemiparesis, early cerebral rigidity, vegetative
disorders has been found in 2 patients (2.30%). Extremely severe condition and 5 severity with
deep coma, decerebral rigidity, and terminal condition are not detected in any patient.
One person (1.15%), according to the GOSE results scale (Glasgow Outcome Scale Extended) Of
the 3 degrees has neuromuscular insolvency: the patient in consciousness, however, severe
neurological symptoms keep treatment in the resuscitation department. Next 10 patients (11.49%)
With 4 degrees of gravity have severe failure: is rough Neurological defect due to which patients
need third-party care. Moderate nonindependence: Mental status within the norm, while patients
are unable to perform a number of necessary actions and need outpatient observations diagnosed
in 16 patients (18.39%), which corresponds to the 5th degree. Light Non-independence: mental
status within the norm, the sick themselves serve, move themselves or with-restaurant support.
However, the need for special employment was found in 28 people (32.18%) With 6 degrees of
severity. Good recovery: Patients gradually return to their former lives, have minor neurological
abnormalities, move alone demonstrates the most numerous cohort of patients – 32 people
(36.78%) In group 7 of severity. The percentage of probability of the forecast of SAK 78 – 80%
of a successful result according to the generalized classification scale for estimation of SAC result
(C.S. Ogilvy et B.S. Carter) had 76 patients with points from 0 to 2 (87.36%), i.e. the greatest
number of patients. Three points and 65 – 67%, less successful result was demonstrated by 10
patients (11.49 1.15%) Credited 25%, poor result, and total 4 points. Operative treatment was
performed in 40 patients (46%), conservative therapy was used accordingly for 47 patients (54%).
The average duration of hospital treatment was 17.64 beds. For a total angiographic study, a
AXIOM Artis MP «Siemens» was employed. Each patient conducted a selective study of all
vascular basins through the femoral access method of Seldynger. Statistical analysis was carried
out using the application packages "Statistica 6.1" (StatSoft Inc., USA, RGXR412D674002FWC7
serial number), "Microsoft Excel 2013". For all types of analysis statistically significant
differences were considered in P. < 0.05. In examining the frequency of the meeting, the indicators
were performed using the χ ² criterion with conjugation table analysis. To assess the association
between variables expressed in the quantitative scale, conducted a procedure of binary regression
analysis using linear, logarithmic, exponential, Polìnomìnalnoï (2 and 3 degree) models reaching
the independent (according to the criterion of Darbina-Watson), the normal distribution of residues
(in accordance with the indicators of asymmetry and excesses). The final choice of regression
equations was carried out using the generalized quality criterion, which found as a weighted
amount of the generalized criterion
Accuracy and generalized adequacy criterion. As the accuracy criterion used normalized the
average relative error of approximation, and as the criterion of adequacy-normalized value
criterion Darbin-Wothson. When analyzing the regression equations, we took into account the
amount of multiple correlation coefficient, as well as the magnitude of the R2 determination
coefficient. Also, individual statistical procedures and algorithms are implemented in the form of
specially written macros in their respective programs. Results of the study. The following results
are obtained in the course of the study. In 4 persons 1 degree of severity of SAC by Fisher (minimal
SAC without evidence of intractricular hemorrhage (IVH) in any of the lateral ventricles) was
discovered hyponatremia, serum sodium levels were an average of 137,82 ± 0.75 mmol/L in this
patient group, with a relative incidence of hyponatremia from a total group of patients with a given
severity of SAK 11.76% (table 1).
Table 1 – Level of atraemia and frequency of hyponatremia in various gravity levels in patients
with SAC according to the modified scale Fisher, M ± m (95% confidence interval)
 Severity of SAC by Serum sodium Number of cases of
Fisher concentration, hyponatremia
mmol/L Abs. Relative
Number, quantity,%
persons
1 137,82±0,75 4 11.76
(136,35-139,3)
2 137,73±1,03 (135,7- 4 18.18
139,75)
3 132,82±1,25 10 58.82*
(130,38-135,27)*#
4 133,71±1,16 4 28.57*
(131,44-135,99)*#

NOTES: * – p < 0.05 compared to patients with 1 degree; # – < 0.05 compared to patients with 2
degrees of severity.

In the next group of 2nd severity in the Fisher (minimal SAC with signs of intractricular
hemorrhage (IVH) in any of the lateral ventricles), also in 4 patients diagnosed with hyponatremia
with an average sodium level of 137,73 ± 1,03 mmol/L, which means that 18.18% of patients of
the total severity of this degree were hyponatremia. The more pronounced statistically accurate (p
< 0.05) hyponatremia is detected in the third group of patients with an average serum sodium level
of 132,82 ± 1.25 mmol/L. In 10 people (58.82%) related to the 3rd degree of gravity on a scale of
Fisher (thick layer of subarachnoid)
Without signs of IVH hemorrhage in any of the lateral ventricles), laboratory hyponatremia has
been confirmed. Four patients (28.57% of the total number of patients of this group) with the most
severe condition according to the scale of the Fisher (the most massive hemorrhage – a thick layer
of SAC with signs of IVH in both side ventricoses) had also low serum sodium level statistically
significantly (p. < 0.05), the average rate of this electrolyte in the group was 133,71 ± 1,16 mmol/L.
Consequently, the greatest number of patients with severe hyponatremia correlates with the
heaviest severity degrees according to the modified scale Fisher – 3-4 degree. According to the
classification of the World Organization of Neurosurgeons (WFNS) to assess the severity of SAK
1st the easiest severity (15 points on Glasgow's scale and the absence of motor and linguistic
deficits) posted the next level of serum sodium in these patients – 138,94 ± 0,53 mmol/L, and
hyponatremia is not detected in any patient (table. 2).
Table 2-Levels of atraemia and frequency of hyponatremia according to the classification of the
World Organization of Neurosurgeons for evaluation of SAC severity (WFNS), M ± m (95%
confidence interval)
Severity of SAC by Number of cases of
WFNS hyponatremia
 Serum sodium Abs. Relative
concentration, Number, quantity,%
mmol/L persons
1 138,94±0,53 (137,91- 0 -
139,97)
2 135,49±0,86 (133,8- 15 40.54*
137,18)*
3-5 132,24±1,21 (129,86- 7 41.18*
134,61)*
NOTES: * – p < 0.05 compared to patients with 1 degree; # – < 0.05 compared to patients with 2
degrees.
In 15 patients of the second group by severity according to the classification of the World
Organization of Neurosurgeons for the assessment of SAC severity (WFNS) (40.54% of the total
number of patients of this group), which is 13-14 points on the Glasgow scale and absence of
motor and linguistic deficit, revealed statistically reliable (p < 0.05) hyponatremia. The average
sodium level in this group was 135,49 ± 0,86 mmol/L. In 7 patients with 3-5-m degree in SAC
severity WFNS (3-13 per Glasgow scale and presence/absence of motor and/or linguistic deficit)
diagnosed statistically significant (P < 0.05) hyponatremia. These patients amounted to 41.18% of
the number of patients of these groups. On average, at a given degree of severity, the SAC level
of sodium was 132,24 ± 1.21 mmol/L. The level of hyponatremia has also correlated with the
severity of the SAC's clinical course according to the Nunt & Inse Scale (table 3).

Table 3-level of atraemia and frequency of hyponatremia in patients with SAC in severity
according to the Nunt & sнs scale, M ± M (95% confidence interval)
The severity of SAC Serum sodium Number of cases of
for H-H concentration, hyponatremia
mmol/L Abs. Relative
Number, quantity,%
persons
1 138,67±0,68 0 -
(137,34-139,99)
2 136,83±0,76 11 26.19
(135,34-138,33)
3-4 133,44±1,03 (131,42- 11 40.74*
135,47) *#
NOTES: * – p < 0.05 compared to patients with 1 degree; # – < 0.05 compared to patients with 2
degrees of severity.
1-St Severity according to the UNT & scale did not have very few symptoms, or symptoms were
minimal: headache and stiff neck, and moderate serum sodium 138,67 ± 0,68 mmol/L, cases of
hyponatremia on detected. Patients presenting with headache, neck stiffness, absence of
neurological deficits (other than cranial nerve palsy) were treated as a 2nd severity according to
the & Nesses's Nunt scale, and 11 people (26.19% of the total number of patients in this group)
had hyponatremia when averaging lower than whey sodium per group of 136,83 ± 0,76 mmol/L.
At 3-4 gravity stages according to the scale of the Nunt & Inms and the presence of the following
pronounced clinical picture: drowsiness, stun or slight focal deficit, stupor, moderate or severe
hemiparesis, early decerebral rigidity, vegetative disorders, is diagnosed with serum sodium
133,44 ± 1,03 mmol/L, that is the lowest among all groups. Statistically accurate hyponatremia (P.
< 0.05) has been confirmed in 11 patients of this group (40.74% of total). The level of atraemia
in patients 3-4 of severity of the GOSE results scale (Glasgow Outcome Scale Extended) was
131,36 ± 1,53 mmol/L, and in 5 persons of this group (45.45%) Hyponatremia detected. For this
severity level, the GOSE results clinically characteristic of the scale: a patient in consciousness,
but severe neurological symptoms
Causes treatment in the resuscitation department or a coarse neurological defect due to which
patients need third-party care (table. 4).
Table 4 – Sodium levels and frequency of hyponatremia in patients with GOSE result scale
(Glasgow Outcome Scale Extended), M ± M (95% confidence interval)
Severity of SAC by Serum sodium Number of cases of
GOSE concentration, hyponatremia
mmol/L Abs. Relative
Number, quantity,%
persons
3-4 131,36±1,53 (128,37- 5 45.45
134,36)
5 134,19±1,25 (131,73- 7 43.75
136,64)
6 137,82±0,79 (136,27- 5 17.86*
139,37) * #
7 137,34±0,82 (135,73- 5 15.63*#
138,96) * #
NOTES: * – p < 0.05 compared to patients with 1 degree; # – < 0.05 compared to patients with 2
degrees.
In 7 people from the 5th degree of gravity according to the results scale GOSE (43.75%) It is
diagnosed hyponatremia, with clinically given group of patients having a mental status within the
norm, patients are unable to perform a number of necessary actions and require outpatient
observation, the median level of sodium in the group was 134,19 ± 1.25 mmol/L. In 5 patients with
statistically significant hyponatremia (P < 0.05) and 6th degree of severity according to the GOSE
results scale (17.86% of the total number of patients in this cohort) clinically prevailed the
following neurological symptoms: mental status within normal limits, Patients themselves serve,
move themselves or with-restaurant support. On average, the serum sodium group was determined
at the level of 137,82 ± 0,79 mmol/L. In the 7th degree of gravity in line with GOSE results,
patients have a good recovery: patients are gradually returning to their former lives, there are minor
neurological abnormalities move alone, serum sodium levels in these patients 137,34 ± 0,82
mmol/L. hyponatremia is also found in 5 patients, representing 15.63% of the total number of
patients of this group (p < 0.05). Thus, the easiest the severity of SAC in patients with a scale of
GOSE results (Glasgow Outcome Scale Extended) corresponds to the smallest number of patients
with hyponatremia. The level of atraemia and the frequency of hyponatremia in patients according
to the generalized classification scale to assess the prediction of the SAC result (C.S. Ogilvy et
B.S. Carter) is presented in table 5.
Table 5 – Sodium and frequency of hyponatremia in patients according to the generalized
classification scale to assess the prognosis of SAC (C.S. Ogilvy et B.S. Carter), M ± M (95%
confidence interval)
The severity of SAC Serum sodium Number of cases of
by Ogilvy concentration, hyponatremia
mmol/L Abs. Relative
Number, quantity,%
persons
0 138,83±0,66 0 -
(137,53-140,12)
1 137,36±1,02 6 24.0
(135,37-139,35)
2 134,64±0,92 10 35.71*
(132,83-136,46) * #
3-4 131,73±1,51 6 54.55*
(128,78-134,67) * #
NOTES: * – p < 0.05 compared to patients with 1 degree; # – < 0.05 compared to patients with 2
degrees.
The percentage of probability of the prognosis of AKI 78 – 80% of a successful result according
to the generalized classification scale for estimation of SAC result (C.S. Ogilvy et B.S. Carter) had
patients with scores from 0 to 2, i.e. the greatest number of patients. The severity of the SAC at
Ogilvy 0 points was consistent with the serum sodium level of 138,83 ± 0,66 mmol/L in the
absence of patients with hyponatremia. 1 point for C.S. Ogilvy et B.S. Carter and hyponatremia
had 6 patients with a second cohort of 24.0% of the total. 2 points and statistically hyponatremia
(P < 0.05) demonstrated 10 patients (35.71%). 3-4 points and 25 to 67% for less successful results
along with hyponatremia had 6 people of the last group (54.55% of the total number of patients in
this cohort), while at the same time within the statistical reliability (R < 0.05). On average, a group
of serum sodium is 131,73 ± 1, 5 mmol/L. That is, almost half of patients with severe clinical
condition according to the generalized classification scale to assess the prognosis of SAC result
(C.S. Ogilvy et B.S. Carter) was a hyponatremia. Further, the research of orientation, tightness and
character of the of connectedness between indexes and construction of functional dependence
between the investigated variables, was carried out binary regression analysis, during which as an
independent argument the level of expression Coneptina (Biommarker of a system of
neurohormonal regulation) was conducted, and as a dependent variable-the level of atraemia. The
findings testified to the fact that the correlation between numerical variables in patients with
normal serum sodium is wore unreliable in nature, whereas in individuals with hyponatremia the
resulting ratio with a high degree of accuracy and
Adequacy was approximated by a logarithmic model of nature, namely:
Na = 124.19 – 29.9 × log10 (Copeptin),
where (R = 0.83, R2 = 0.69, normalized R2 = 0.66 when F = 42.14, p < 0.001). Thus, a credible
close relationship between the level of glycosylated peptide with neuroendocrine properties,
Conepinosis, and expressiveness of the disturbance of osmotic homeostasis has been
demonstrated, and this model describes about 70% of the total variance of triemia (figure).

Rice. Regression analysis results of the correlation between the concentration of Copetin and
serum sodium levels in patients with SAC against the background of hyponatremia
Investigation of the peculiarities of the violations of osmotic homeostasis in SAK in those with
hyponatremia depending on the severity of expression neuroendothelial Biommarker, it indicates
that the Sprâženìst serum sodium and serum copetiniin is adequately and reliably approximated by
the equation of a logarithmic character regression (based on the 10 basis), which is important, the
values of the independent ancestor of the more than 0.70 ng/ml in more than 50% of cases recorded
a medium severity sodium. Discussion. The depth of neurological disorders in hyponatremia is
defined to be more at the rate of its development than the degree of reduction of sodium ions in
the blood. Chronic hyponatremia allows the brain to adapt, and patients remain without expressed
symptoms, despite the serum sodium concentration below 120 mmol/L. Chronic hyponatremia can
cause such nonspecific symptoms like nausea, vomiting, gait abnormalities, memory and thinking,
fatigue, dizziness, confusion of consciousness, and muscle cramps. Nausea and vomiting present
in approximately one third of patients with
Chronic hyponatremia that has a serum sodium concentration of less than 120 mmol/L. Idiopathic
SIADH is more common in patients older than 65 years, and mild to moderate hyponatremia in
these patients can contribute to bone fractures, and increase the risk of falls and Nordic walking
problems. Patients should be asked for a history of head injury, chronic pain, smoking, weight loss,
symptoms of lung disease, drug use, or substance abuse (especially heroin and ecstasy). Excess
fluid source should be assessed, and the duration of this state should be considered. Physical exam
should include evaluation of volume of circulating blood, as these patients are usually êuvolemìčnì.
Skin Turgor and blood pressure are within normal limits as a rule. A detailed analysis of
neurological and vascular diseases should be carried out. There is no single best test to diagnose
SIADH. Patients typically have hyponatremia with normal volume of circulating blood. Schwartz
and Barter developed a clinical criterion in 1967, which is still valid. Schwartz and Barttera clinical
criterion:
− Serum sodium less than 135 Meq/L.
− Serum osmolality is less than 275 Mosm/kg.
− Sodium urine is more than 40 micrograms/liter (via Adsorrated absorption of free water from
the renal collector kanaltsiv).
− Urine osmolality is more than 100 Mosm/kg.
− No clinical signs of circulating blood volume depletion – normal skin turgor, arterial pressure
within the control range.
− No other causes of hyponatremia
– Adrenal insufficiency, hypothyroidism, heart failure, pituitary insufficiency, renal disease with
salt loss, liver disease, medications that worsen renal water excretion.
− Correction of hyponatremia due to fluid restriction. Renal function tests and glycemic analysis
should be performed to diagnose hyperglycemia and uremia, as these are potential causes of
pseudohyponatremia. SIADH Tests: Serum osmolality and sodium, sodium concentration and
urine osmolality, test of renal function: urea and creatinine, blood sugar, thyroid profile, serum
cortisol, serum k +, bicarbonate, chloride, lipid profile, liver function. Hypothyroidism and adrenal
insufficiency should be excluded in patients with SIADH. Further tests should be made to find out
the main causes according to the history disease [12].
Patients with SIADH have a combination of ADG-induced water retention and secondary fluid
loss. Total fluid loss is more pronounced than water retention in patients with chronic SIADH.
SIADH treatment involves correction and maintenance of normal sodium levels and correction of
underlying abnormalities, such as hypothyroidism, lung disease, and CNS. The purpose of
correction of sodium level is more than 130 Iec/l [13]. The choice of treatment significantly
depends on the severity of symptoms during the debut of the disease. Moderate but rapid decline
in sodium levels can cause severe symptoms such as delusions, confusion, and seizures; Whereas
chronic but significant hyponatremia (less than 125 micrograms/liter) can cause weak or less
expressed symptoms. So, in patients with mild and medium-sized symptoms, the mainstay of
treatment is water intake restriction less than 800 ml/day. If hyponatremia is stable, you can give
sodium chloride in the form of oral salt tablets or intravenous saline. Salt tablets can also be
combined with diuretics, such as furosemide (20 mg twice daily), as this contributes to lower urine
concentration and, thus, increases the excretion of water, especially among patients who have urine
osmolality much higher than serum osmolality (more than 500 Mosm/kg) [14]. To adjust sodium
level, it should be known that urine osmolality in such patients is usually twice the serum
osmolality, i.e., more than 500 Mosm/kg. Consequently, the fluid required for the correction of
sodium levels should have osmolality exceeding the urine osmolality. Isotonic physiological
solution may not correct hyponatremia in these patients, or may even worsen hyponatremia and
symptoms. Therefore, it is necessary to use a solution with a concentration of electrolytes greater
than the concentration of electrolytes in the urine. For this purpose, 3% hypertonic saline
(osmolality of 513 Mosm/kg) is used in patients with severe symptomatic or persistent
hyponatremia. Also, the adjustment coefficient is an important factor. It should not exceed 8
micrograms/L for 24 hours or 0.5 to 1 μg/l per hour. Faster correction may lead to osmotic
deeuthelialization of the CNS, resulting in severe fatal complications such as the syndrome of
osmotic deenilization (a "closed man" syndrome) causing quadriplegia.
Patients with severe symptoms such as seizures, altered mental or delirium, require urgent initial
correction of hypertensive salt infusion for the first few hours, rather than merely limiting water
intake. Bolis 100 ml of 3% hypertonic solution are given within the first 3 to 4 hours, and the
sodium level is measured within 2 – 3 hours, so further doses can be adjusted to avoid correction
too quickly. Increasing from 3 to 4 Iec/L for the first few hours with severe symptoms can be
justified. If the patient's mental state does not improve, the following painful 100 ml of hypertonic
solution can be obtained in the same way until the symptoms are reduced. Vasopressin receptor
antagonists, such as Coniwaptan (IV) or Tolwaptan (pills), are also available and approved for
severe persistent SIADH cases. These drugs prevent free water delays by antagonizing V2
receptors and correcting hyponatremia. Tolwaptan is hepatotoxic, and should not be administered
to patients with liver disease. Intravenous Coniwaptan is very effective at correcting hyponatremia.
Other types of therapy, such as lithium and demeclocyclic drugs, are also effective in the treatment
of SIADH, but both are nephrotoxic and have other potential adverse effects; Consequently, they
should only be used when other therapy options fail [17]. Conclusions. Clinical-pathogenetic
values of hyponatremia as a manifestation of SIADH syndrome in inpatient patients who have
been hospitalized for subarachnoid haemorrhage and spontaneous etiology, the close association
demonstrates the severity of violations of osmotic homeostasis and the severity of the clinical
course of SAC according to the modified Fisher scale, WFNS scale, Nunt & NES scale, GOSE
results scale (Glasgow Outcome Scale Extended) and the generalized classification scale for
estimation of the result forecast SAC (C.S. Ogilvy et B.S. Carter). At SAK in persons with
hyponatremia sprâženìst whey level of sodium and serum copeptinii indicator is adequately and
reliably approximated by equation of regression of logarithmic nature (based on the basis of 10),
while the values of conepin more than 0.70 ng/ml in more than 50% of cases were recorded by a
medium severity sodium. The prospect of further research is to determine the dynamics of atraemia
in patients with netravmatičnìj aetiology SAC on the background of treatment.