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MINISTRY OF EDUCATION AND TRAINING

MINISTRY OF DEFENSE

SCIENCE RESEARCH INSTITUTE OF CLINICAL MEDICINE AND
PHARMACY 108

============

The thesis has beeb successfully completed at :
SCIENCE RESEARCH INSTITUTE OF CLINICAL MEDICINE AND
PHARMACY 108

Science Instructor :
PGS.TS. Nguyen Phuong Dong

NGUYEN DINH DUNG

Opponent 1:
Opponent 2:

STUDYING CLINICAL, SUBCLINICAL
CHARACTERISTICS, ASSOCITATED FACTORS
AND TREATMENT RESULTS OF HYPONATREMIA
IN PATIENTS WITH CEREBRAL HEMORRHAGE
Major

: Anesthesia - Resusciation

Major code

: 62.72.01.22

Opponent 3:
Thesis has been defended at Institite- level Thesis Evaluation Council
held in Science Research Institute Of Clinical Medicine And Pharmacy
108
At
(hour),
/
/ 2019
This thesis may be found at:
1. National library
2. Library of Science Research Institute Of Clinical Medicine And
Pharmacy 108

SUMMARY OF MEDICAL DOCTORAL THESIS

HA NOI– 2019


CSWS
SIADH
CNS

1

2

LIST OF ABRREVIATION

Clinical symptoms:Patients with mild hyponatremia only exhibit anorexia,
insensitive drowsiness, nausea, vomiting. Consciousness disorders, coma,
convulsions, hypothermia, acute circulatory failure, breathing disorders,
decreased tendon reflexes may occur in patients with severe hyponatremia.
Patients with acute severe hyponatremia may have a very high risk of
neurological complications: confusion, coma, convulsions, apnea. Some
nonspecific signs, such as loss of appetite, vomiting, apathy, nausea and
fatigue, can be detected through clinical manifestations of hypotension,
delayed pinches, sunken eyes, dry mucous membranes, lack of armpits sweat,
tachycardia and orthostatic hypotension.
Subclinical:
+ Serum sodium concentration
✓ Normal: 135 - 145 mmol/l
✓ Mild: 130 - 134 mmol/l
✓ Moderate: 125 - 129 mmol/l
✓ Servere: < 125 mmol/l
+ Serum osmolality: Sodium is the main ingredient that determines the serum
osmotic pressure (90%).
+ Urinary sodium concentration:
✓ Urinary sodium concentration<20 mmol/l: Cause of hyponatremia is due to
extra-renal salt loss.
✓Urinary sodium concentration> 20 mmol/l:Cause ofhyponatremia is due to
renal salt loss.
1.2. The role and significance of sodium - osmostic pressure in the treatment of
cerebral hemorrhage
Hypotonic hyponatremia causes water to enter brain cells, leading to
cerebral edema. Because the skull surrounds the brain, the brain is limited in
dilation increasing intracranial pressure occurs, thereby aggravating the brain
damage inherent in patients with cerebral hemorrhage.
Hypovolemic hyponatremia may cause a decrease in cerebral perfusion

flow, thereby aggravating the brain lesions in patients with cerebral
hemorrhage.
Hypernatremia is always accompanied by hypertonicity, so hypernatremia
causes water to be pulled out from the brain cells, leading to brain cell atrophy.
1.3. Causes of hyponatremia in patients with cerebral bleeding
Hyponatremia in patients with cerebral stroke and CNS lesions has begun
to be studied much in the 70s of the twentieth century.
Hyponatremia in patients with brain damage is mainly attributed to two
syndromes: SIADH, CSWS, in addition to many causes such as the use of
mannitol diuretics, furosemide, multiple fluids or possibly a combination of
many causes. The differential diagnosis of these two syndromes is important

cerebral salt wasting syndrome
of inappropriate anti-diuretic hormone secretion
central nervous system

INTRODUCTION
Hyponatremia is a common electrolyte disorder in patients with cerebral
hemorrhage, accounting for 30-60%.Hyponatremia in patients with cerebral
hemorrhage increases the rate of complications, mortalityand prolongsthe
duration of treatment.
Clinical symptoms of hyponatremia are poor, especially in patients with
cerebral hemorrhage, they easily confused with symptoms of central nervous
system (CNS)damage caused by cerebral hemorrhage such as confusion,
seizure, coma…The reasons of hyponatremia and associatedfactors have not been
clearly defined, but the results of many studies often suggest that the causes of
hyponatremia are two syndromes: syndrome of inappropriate anti-diuretic hormone
secretion (SIADH) and cerebral salt wasting syndrome (CSWS). Clinically, these
two syndromes have many similar and easily confused symptoms, but the
pathogenesis mechanisms are completely different and treatment principles are also

different. Some studies suggest that it is possible to determine causes of
hyponatremia based on BNP, NT - ProBNP concentrations.
Treatment of hyponatremia in patients with cerebral hemorrhage to ensure
efficiency and safety is based not only on sodium levels even as mild but also on
clinicalcharateristics , associated factors, and causes of hyponatremia. Currently,
the consented recommendations is that3% NaCl solution is appropriate
concentration, ensure treatment goals, minimize complications. Therefore we
conducted the research:"Studying clinical and subclinical characteristics,
asociated factors and treatment results of hyponatremia in patients with
cerebral hemorrhage" with twoobjectives:
1. Comment on clinical, subclinical characteristics and factors associated
with hyponatremia in patients with cerebral hemorrhage.
2. Evaluation of the treatment results of hyponatremia in patients with
cerebral hemorrhage.
Chapter 1
LITERATURE OVERVIEW
1.1. Definition of hyponatre mia
Hyponatremia is defined as a serum sodium concentrationof less than
135 mEq/L.
While hypernatremia is always associated with increasedserum
osmolality, hyponatremia may be associated with low, normal or high blood
osmolality.


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because they differ in their nature and treatment.
SIADH syndrome is an unreasonable secretion of ADH, leading to

hyponatremia due to dilution (excess fluid volume) so treatment should limit
infusion. CSWS syndrome is hyponatremia due to an increase in loss of
sodium and water through the kidneys, so treatment needs to compensate for
sodium and water.
The syndrome of inappropriate antidiuretic hormone secretion (SIADH)
includes:
✓ Serum sodiumconcentration ≤ 135mmol/l
✓ Urinary sodiumconcentration> 20 mEq/l
✓ CVP> 6cmH2O
✓ Blood osmotic pressure <280mmol / kg
✓Urine osmotic pressure >Blood osmotic pressure
✓ Decreased A. uric, albumin, protein, Hb, Hct...
✓ Kidney function, thyroid, adrenal gland normal
✓There are no signs of peripheral edema, no signs of dehydration
Principles of treatment
Treat underlying disease.
Restrict fluid - fluid restriction is the main treatment in most SIADH patients,
with a proposed goal of less than 800 - 1000 ml /day. Fluid restriction may
promote cerebral vasoconstriction in patients with subarachnoid hemorrhage
because it is usually treated with an increase in circulating volume. As well as
related to blood pressure, intracranial pressure is a very important factor in
monitoring the treatment of patients with cerebral or subarachnoid hemorrhage.
Therefore, hyponatremia in patients with cerebral or subarachnoid
hemorrhageshould be treated with hypertonic saline (3%) to preserve
cerebrospinal fluid and prevent cerebral edema complications of hyponatremia.
Cerebral salt wasting syndrome (CSWS) includes:
✓ Serum sodium concentration ≤ 135mmol / l
✓ Urinary sodium concentration> 20 mEq / l
✓ CVP <6cmH2O
✓ Dehydration of the body: dry skin, tachycardia, increasedhematocrite,

increased blood uric acid, increased blood albumin concentration.
✓ No renal failure, hypothyroidism, hypopituitarism
Principles of treatment
Restoring circulating volume with isotonic saline is the recommended therapy
in CSWS, as it may prevent the release of ADH, thus allowing the elimination
of excess water and correction of hyponatremia. Patients can continue to
maintain 3% NaCl, depending on clinical manifestation.

1.4. Treatment of hyponatremia in patients with cerebral he morrhage
The principle of treatment of hyponatremia is based on:
➢The condition of the extracellular fluid volume
➢The occurrence of clinical symptoms
➢The length of osmotic pressure reduction
➢ Risk of neurological complications
Adjusting too quickly hyponatremia to normal values may cause myelin loss in
the pons.
Target of sodium adjustment:
➢Serum sodium concentration increase < 0.5 mmol / h, the total increase<10
mmol / 24h.
➢If the patient has seizures or other neurological symptoms, adjust the serum
sodium concentration by 2-4 mmol / h within 2-4 hours to bring the patient out
of danger.
Chapter 2
SUBJECTS AND RESEARCH METHODOLOGY
2.1. Study subjects
These
patients
diagnosed
and
treated

for
cerebral
hemorrhage(intracerebralhemorrhage, subarachnoid hemorrhage) at Stroke
Center 108 from 9/2016 to 9/2018.
2.1.1. Inclusion criteria
Diagnostic criteria for cerebral hemorrhage:
According the defination about stroke of WHO in 1989
Subclinical symptoms: brain CT image scan ...
Diagnostic criteria for hyponatremia: serumsodium concentration <135
mmol/ l.
2.1.2. Exclusion criteria
Patients with a history of heart failure, chronic renal failure, adrenal
insufficiency, hypothyroidism, pituitary disease.
Patients with brain tumors, tuberculous meningitis, cerebral infarction...
Patients did not agree to participate in the study.
2.1.3.Standards to remove from the study
The patient died within 24 hours during treatment.
2.1.4. Time and place of research
Time: September 2016 - September 2018
Place: Brain Stroke Center - Central Military Hospital 108
2.2. Study methods
A prospective descriptive study, longitudinal monitoring from admission
to discharge or death - return home.


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2.3. Research content and research criteria

2.3.1. General characteristics of the subject group in the study
Age, gender
Reasons for admission to the hospital
Characteristics of the disease onset: gradual, exertion, sudden
Time from onset of illness to admission (days)
The previous treatment
Medical history: hypertension, diabetes, stroke, hyperlipidemia, smoking,
alcoholism ...
Signs of onset: headache, vomiting, nausea, hemiplegia, coma in 2 groups of
normal and low serum sodium concentration patients and finding differences.
2.3.2. Clinical, subclinical characteristics and related factors
Describe clinical and subclinical characteristics
• Clinical characteristics of cerebral hemorrhage patients with hyponatremia
compared toa group with normal serum sodiumconcentrationat admission:
+ Headache, nausea, vomiting, dizziness, stiff neck, meningeal syndrome,
sensory disorders, swallowing disorders.
+ Cognitive disorders: calculated on a scale of Glassgow divided into 3 levels of
cognitive disorders: the severe level when Glassgow ≤8, the moderate level when
Glasgow from 9 to12, the mild level when Glassgow from 13 to15 points.
+ Evaluation of muscle strength: right and left hemiplegia.
+ Evaluation of vital signs:an average of 2 groups through indicators: pulse,
temperature, blood pressure, breathing rate.
+ Evaluation of stroke status on NISSH scale is divided into 5 levels: 0 points,
1-4 points, 5-15 points, 16-20 points, and 21 to 41 points.
• Subclinical characteristics of cerebral hemorrhage patients with hyponatremia
compared to a group with normal serum sodium concentration:
+ The average values of the indicators: erythrocytes, leukocytes, hemoglobin,
hematocrit, platelets, APTT, PT, fibrinogen, glucose, urea, creatinine, cholesterol,
triglycerides, enzymes AST, ALT, GGT, and bilirubin ...
• Clinical characteristics in patients with cerebral hemorrhage with

hyponatremia at the time of hyponatremia
+ Clinical changes when hyponatremia.
+ Classifyhyponatremia by three levels: <125 mmol / l, 125-129 mmol/l and
130- <135 mmol/l.
Causes of hyponatremia
+ Classify clinical symptoms at the time of hyponatremia by causes: CSWS,
SIADH, and other groups, and compare the differences among the groups of
the causes
+ Assess the subclinical characteristics of patients at the time of hyponatremia
according to 3 cause groups and compare the differences among them.
+ Blood osmotic pressure, assess blood osmotic pressure according to three

groups of causes and find differences.
+ Urinary osmotic pressure, assess the urinary osmotic pressure according to
three groups of causes and find differences.
+ Urinary sodium concentration of the patients, surveyurinary sodium
concentrationin 3 groups of causes and find differences.
+ Average Pro-BNP concentration by gender, age and correlation with NISSH
stroke scale
+ Average ProBNP concentration according to 3 causes groups and find
differences among these groups.
Relationships
• Relationship between hyponatremia and medical history.
• Relationship between the site of brain lesions and hyponatremia.
• Relationship between the size of brain damage and hyponatremia.
• Relationship between vascular intervention and hyponatremia.
• Relationship between treatment measures and hyponatremia.
2.3.3. Evaluate the results of treating hyponatremia in patients with cerebral
hemorrhage
• Treatment results in two patient groups with hyponatremia and nonhyponatremiainclude: living without sequel, living with sequeles and death according to mRs Score from admission to discharge, then find difference

between two groups.
• Treatment results for three causes of hyponatremia: CSWS, SIADH and
other causes. Compare the difference among them.
• Change of clinical and subclinical indicators after treatment compared to
before treatment.
• Average hospitalization duration of hyponatremia patients in 3 groups.
• Duration of treatment with 3% NaCl.
• Complications of both hyponatremia and non-hyponatremia groups
during a period of hospitalization: pneumonia, sepsis, convulsions and acute
renal failure...
• Results of hyponatremia treatment with NaCl3%: changes in blood
osmotic pressure, urinary osmotic pressure, urinary sodium concentration,
serum sodium concentration,and complications during treatment.
• Cognitive changes when treating withNaCl3% in three groups of causes
according to three levels: better, unchanged, worse.
• Post-treatment change in patients with hyponatremia.
• Effect of hyponatremia on the outcome of treatment.
• Changes in muscle strength after treatment
• Change NISSH scale after treatment.
• Rankin from admission upon discharge.
2.4. Research process


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All patients admitted and diagnosed with cerebral hemorrhage were tested
for plasma electrolyte tests; asked about the disease; exam on clinic and
subclinical according to sample medical record of 108 Central Military

Hospital. Electrolyte test was repeated at least once during treatment of patients
with cerebral hemorrhage, normally serum sodium concentration was checked
every 2 -3 days; in severe cases, hyponatremia patients were checked for serum
sodium concentration every 24 - 48 hours. Hyponatremia patients (Na + <135
mmol/l) were tested for urinary electrolyte tests(urinarysodium concentration
at a moment and/or urinary sodium concentration in the next morning), urine
osmotic pressure, blood osmotic pressure.
Hyponatremia patients with urinary sodium concentration> 20mmol/l
(renal sodium loss) were clinically monitored, placeda central venous catheter
to measure central venous pressure, tested urea, creatinine, a.uric, albumin,
protein, Hb, Hct ... to diagnose and determine the causes of hyponatremia.
The NT-proBNP test was performed on apatient at the time of
hyponatremia detection.
Patients with hyponatremia are classified, assessed for risk, and treated:
+Patients with mild hyponatremia (131 ≤ Na ≤134 mmol / l), mild clinical
manifestations, no clinical adverse events and diabetes with poor blood sugar
control, hypertension or fluctuating blood pressure,did not treat hyponatremia
and continued to be monitored and corrected based on clinical status and
subsequent blood sodium.
+ Patients with mild hyponatremia, without symptoms, risk of
complications such as worse cognitive, worse paralysis, increased headache,
vomiting, nausea ... and stable blood pressure control, were guided to increase
serum sodium concentration by a rise in solute intake with 10g of salt in the
daily diet.
+ Patients with profound hyponatremia (Na + <125mmol / l), moderate
hyponatremia (125 ≤ Na + ≤ 129 mmol / l) and mild hyponatremia (130 ≤ Na +
≤134 mmol / l) accompanied by symptoms , risk of complications such as
worse cognition, worse paralysis, more or not reduced headache, vomiting,
nausea, convulsion - epilepsy..., were used NaCl3% solution in hyponatremia
treatment.

These patients were tested for blood sodium monitoring every 24 -48 hours
during hypertonic salt treatment and checked every 6 hours for the progression
and severity of the disease.
Patients were monitored during treatment until thedisease stabilized or
death.
The procedure of intravenously infused maintenance of NaCl 3% solution in
the treatment of hyponatremia according to Carolyn W et al:
+ Patients with profound and moderate hyponatremia: starting with

intravenously infusion of 450ml ofNaCl3% solution and maintaining for 24
hours.
+ Patients with mild hyponatremia: starting with intravenously infusion of
225ml ofNaCl3% solution and maintaining for 24 hours.
Serum sodium concentration test is repeated every 24 - 48 hours and the
dose of NaCl 3% solution is adjusted
[Na +] below 130mmol/l: increase the volume of NaCl 3% solution to
650ml/24h; if currently not infused, the volume is 450ml / 24h.
[Na +] in the range of 130 - 134 mmol / l: maintaining the volume ofNaCl 3%
solution; if currently not infused, the volume is 225ml/24h.
[Na +] in the range of 135 - 150mmol / l: stop the infusion, check the sodium
concentration and adjust according to the reference scale.
* In case of severe, acute and complicated hyponatremia: quickly remove
serum sodium concentration from the danger zone before sustaining
intravenous infusion.
* When identifying the cause of hyponatremia, hyponatremia treatment is
adjusted according to the specific cause:
+ Treatment of hyponatremia in patients with cerebral bleeding when the cause
is SIADH:
NaCl 3% solution should be continued to maintain (recommended to use in
hyponatremia due to SIADH in patients with cerebral hemorrhage).

NaCl 0.9% solution is indicated for about 1000ml/24 hours with no limit of
lower fluid because of the risk of other complications such as cerebral
vasospasm, cerebral infarction ...; consider using furosemide if there are no
contraindications, the doses of furosemide and NaCl 3% solution are based on
the level of fluid excess, the level of hyponatremia.
+ Treatment of hyponatremia in patients with cerebral hemorrhage when the
cause is CSWS:
Circulating volume compensation with isotonic saline solution (NaCl
0.9%) is the recommended therapy in CSWS, as it may prevent the release of
ADH, thus allowing the elimination of excess water and adjusting
hyponatremia. The volume of NaCl 0.9% depends on the patient's lack of fluid
and is adjusted according to the course of the disease, the amount of fluid is
usually supplemented at 2000 - 3000ml / 24 hours, NaCl 3% solution is
considered further whether maintained or not, depending on the degree of
hyponatremia and clinical manifestations of the patient.
Treatment of brain bleeding according to the algorithm:


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hyponatremia from day 1 to day 4, from day 5 to day 8, and between day 9 and
from day 14 are 42.23%, 32.72% and 16.67%, respectively.
3.2.3.Clinical changes at the time of hyponatremia

2.3. Analyzing data
- Entering data and cleaning data with EpiData software 3.1
- The data after cleaning will be transferred to STATA 12.0 software to
analyze the results.

Better
50

42
31

28

24

22
17

19

20
10

Worse

40

40
30

Unchanged

7
1

1

01

5

20

1 2 01

1516

16
5

3
0 20 0 0 01 00 12

32
23
15

17
30

13

45

0

Figure 3.3. Clinical changes when hyponatremia
Comme nt:
There were 87 patients with hyponatremia from the second day after
admission in which:
40/59 patients still had headache at the moment of hyponatremia, 1 patient had
just appeareda headache and 5 patients had increased headache. 17/87 patients
(19.50%) worsened with perception, 42/87 patients (48.27%) had no
improvement in perception. 13 /51 patients (25.49%) increased paralysis.
3.2.4. Causes - The degree of hyponatremia

Chapter 3
RESULTS
3.1. General informations of the research subjects
We followed 409 patients with cerebral hemorrhage between 2016 and
2018, among them there were 180 hyponatremia patients (44%), 21
hypernatremia patients (5.1%) and 208 patients with normal serum sodium
concentration.
The average age of the study group was 58.9 years old.
The proportion of male patients (64.3%) was higher than female patients
(35.7%).
3.2.Clinical and subclinical characte ristics of cere bral he morrhage
patie nts with hyponatre mia
3.2.1. Status - The hyponatremia moment
6% (17)
100%
90%
80%
70%

60%
50%
40%
30%
20%
10%
0%

3,2% (4)

46%(58)

53%(15
0)

50,8%(6
4)

41%(11
6))
Intracerebral
(n=283)

Hypernatremia

Subarachnoid
(n=126)
Normal

Hyponatremia

Figure 3.1. Status - The hyponatremia
moment

Figure 3.5. The level of
Figure 3.4. Causes of hyponatremia
hyponatremia
Comme nt: Among 180 cerebral hemorrhage patients with hyponatremia, 14
patients (8%) had severe hyponatremia(<125 mmol / l), 59 ones (33%) had
moderate level (125-129 mmol / l) and 107 patients (59%) had mild
hyponatremia (130 - 134mmol / l). Hyponatremia caused by CSWS, SIADH
and unexplained causes accounted for 24.4%, 33.3%, and 42.3%, respectively.

Figure 3.2.The rate of hyponatremia
over time

Comme nt:
180/409 patients with hyponatremia accounted for 44%, ones with
hypernatremia accounted for 5.1%, 50.9% of total patients had normal serum
sodium concentration. The rate of hyponatremia patients with subarachnoid
hemorrhage (50.8%) was higher than hyponatremia patients with intracerebral
hemorrhage, whereas hypernatremia was more common in patients with
intracerebral hemorrhage (6% - 3.2%).
Occurrence of hyponatremia is most prevalent in the first day of the disease,
accounting for 15%, the percentages ofpatients with occurrence of


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3.2.6. Clinical characteristics of hyponatremia in the groups of causes:
CSWS, SIADH and unknown causes
Table 3.8. Clinical characteristics of the groups of hyponatremia causes
CSWS
SIADH
Unknow cause
Causes
(n=44)
(n=60)
(76)
symptoms
Headache
17(38,64%)
35(58,33%)
52(43,9%)
Dehydrated dry
12(27,27%)
0
0
skin
Dysphagia
29(65.9%)
23(38,3%)
19(25,0%)
24-hour urine (ml) 3547.95± 1161.45 2463.52 ± 974.98 2629.93 ±1086.42

p
<0.01

420,1± 285,5

107,1 ± 133,1

Hyponatremia
(n=180)

Normal
(n=208)

OR
95% CI

p

Yes

19 (67,9%)

9 (32,1%)

161 (44,7%)

199 (55,3%)

2,6
(1,1 – 5,9)

0,018

No
Yes

31 (77,5%)

9 (22,5%)

< ,001

No

149 (42,8%)

199 (57,2%)

4,6
(2,1- 9,9)

Yes

38 (58,5%)

27 (41,5%)

No

142 (44%)

181 (56%)

1,8
(1 – 3,1)

0,032

Medical history
Diabetes

0.00
<0.01
<0.01

Comme nt:
Dehydrated dry skin was only seen in patients with hyponatremia due to
CSWS (p <0.05). Dysphagia were more common in hyponatremia owning to
CSWS (p <0.05). The amount of urine of patients with hyponatremia due to
CSWS was higher than that of patients with hyponatremia due to SIADH and
other causes.
Table 3.9. Clinical symptoms of patients with hyponatremia according to
etiology groups(continued)
Hyponatre mia Hyponatre mia
Unknow
Clinic
due to CSWS
due to SIADH
cause
p
(n=44)
(n=60)
(n=76)

Glasgow
10.02 ±3.63
11.46 ±3.40
13± 2.75
<0.001
NISSH
21.21± 1.36
14.12 ±10.66
10.19 ±10.85
<0.001
Comme nt:
The Glasgow score of patients with CSWS hyponatremia was the lowest,
there was a difference in Glasgow score of 3 etiology groups (p <0.05). There
was a difference in NISSH score at admission in the 3 groups of hyponatremia
causes. The NISSH score was the highest in CSWS patients.
3.2.12. NT-proBNP concentration in causes of hyponatremia
Table 3.18. NT-proBNP concentration in causes of hyponatremia
Cause of
CSWS
SIADH
hyponatremia
p
(n=31)
(n=47)
NT-proBNP (pg/ml)

hemorrhage
3.3.3. Relationship between hyponatremia and medical history
Table 3.22. Relationship between hyponatremia and medical history

<0,005

Comme nt:NT-proBNP concentration in patients with hyponatremia due to CSWS
(420.1 ± 285.5 pg / ml) was higher than in patients with hyponatremia due to SIADH
(107.1 ± 133.1pg / ml) with statistical significance p <0.05.
3.3. Several factors associated with hyponatremia in patients with cerebral

Hypertension
with regular
treatment
Smoke

Comme nt:
Patients with diabetes had a 2.6 times higher risk of hyponatremia (p
<0.05). Patients with regularly treated hypertension had 4.6 times higher risk of
hyponatremia (p <0.001). Smoking patients had 1.8 times higher risk of
hyponatremia than non-smoking patients (p <0.05).
3.3.4. Relationship between hyponatremia and brain damage
Relationship between hyponatremia and location of the injury
Table 3.23. Relationship between hyponatremia and location of the injury
Location of injury

Hyponatremia
( n=180)

Normal
(n=208)

OR
(95% CI)

Frontal lobe
(12)

Yes

22(66.7%)

11(33.3%)

2,5(1,2-5,3)

No

158(44.5%)

197(55.5%)

1

Central gray
(94)

Yes

30 (31,9%)

64 (68,1%)

1

No

150 (51%)

144 (49%)

2,2 (1,4 – 3,6)

Ventricle
(81)

Yes

52 (64,2%)

29 (35,8%)

2,5 (1,5 – 4,2)

No

128 (41,7%)

179 (58,3%)

1

p

< 0,01

< 0,01

< 0,001

Comme nt:
Patients with frontal lobe lesions had 2.5 times higher risk of
hyponatremia than patients without frontal lobe lesions (p <0.01). Patients
without lesions in central gray were 2.2 times higher at risk hyponatremia than
patients with central gray lesions (p <0.01). Patients with ventricular
hemorrhage were 2.5 times more likely to have hyponatremia than nonhemorrhagic ventricular patients (p <0.001).
Relationship between hyponatremia and lesion size


13

14

Table 3.24.Relationship between hyponatre mia and lesion size

times higher than those without mechanical ventilation (p <0.001). Patients
with Glasgow ≤ 8 had 2.4 times higher risk of hyponatremia than Glasgow
patients with Glasgow score > 8 (p <0.01).
3.4. Treatment results
3.4.2. Change of serum sodium concentration, blood osmotic pressure before
and after treatment
Percentage of patients reaching the target of treating hyponatremia with
NaCl 3% infusion (135mmol/l ≤ Na < 150mmol/l)
Table 3.28.Percentage of patients reaching the goal of treating hyponatremia

with NaCl 3% infusion(135mmol/l ≤ Na < 150mmol/l)

Volume of
Hyponatre mia
Normal (122)
p
injury (cm3)
(91)
<30
52(35,9%)
93(64,1%)
30-60
24(54,5%)
20(45,5%)
<0,05
>60
15(57,7%)
11(42,3%)
Comme nt:There was a statistically significant relationship (p <0.05) between
hyponatremia and brain lesion size, the greater the volume of lesions, the
higher the rate of hyponatremia.
3.3.5. Relationship between vascular intervention and hyponatremia
Relationship between vascular intervention and hyponatremia
Table 3.25.Relationship between vascular intervention and hyponatremia
Vascular intervention
Non- intervention
(257)
Coil embolization (79)
Drain, open the
skull(52)

Hyponatremia
(n=180)

Normal
(n=208)

OR
(95% CI)

111(43,2%)

146 (56,8%)

1

34(43,0%)

45 (57,0%)

1(0,6-1,7)

35 (67,3%)

17(32,7%)

2,7(1,4-5,1)

p

< 0,05

Comme nt:Patients with opened or drained skulls had 2.7 times higher risk of
hyponatremia than non-intervention patients and the difference was statistically
significant with p <0.05.
3.3.6. Relationship between hyponatremia and perception, the internal treatment
Table 3.26. Relationship between hyponatremia and perception and
treatment
Method
Glasgow
Mannitol 20%
Furosemid
With oxygen
respirator

≤8
>8
Yes
No
Yes
No
Yes
No

Hyponatremia

Normal

41 (64,1%)
139 (42,9%)

144(51.8%)
35(32.1%)
98(50.0%)
81(42.4%)
54 (65,1%)
126 (41,3%)

23 (35,9%)
185 (57,1%)
134(48.2%)
74(67.9%)
98(50.0%)
110(57.6%)
29 (34,9%)
179 (58,7%)

OR
(95% CI)

p

2,4 (1,4 – 4,1)

0,002

2,3(1,4-3,6
1
1,4
1

< 0,05
>0,05

2,6 (1,6 – 4,4) <0,001

Commme nt:
The rate of patients infused 20% mannitol and having hyponatremia
(51.8%) was 2.3 times higher than patients with normal serum sodium
concentration. Patients with oxygen respirator had a risk of hyponatremia 2.6

135mmol/l ≤ Na < 150mmol/l
Na < 135 mmol/l
Na ≥ 150 mmol/l

Number of
patients (n)
69
12
2

Percentage
(%)
83.13%
14.46%
2.41%

Commets:69/83 patients (83.13%) reached the goal of treating hyponatremia
(135mmol/l ≤ Na < 150mmol/l), 12 patientshad hyponatremia (14.46%), 2
patients had hypernatremia (2.41%).
Modification of serum sodium concentration before and after treatment

with NaCl 3% solution
Table 3.30.Modification of sodium before and after treatment withNaCl 3% solution
Causes
CSWS
Na
(n=29)
Na
before treatment
128.83± 3.66
(mmol/l)
Na
after
treatment
137.13± 6.70
(mmol/l)
Delta Na per day (mmol/l)

SIADH
(n=34)

Others
(n=20)

All causes
(n=83)

129.02± 3.25

129.10 ±2.96

128.97±3.30

137.5 ±4.01

137.52±5.85

137.37±5.47
2.95 ± 3.45

Comme nt:The average serum sodium concentration was 128.97±3.30 mmol/l
at the start of using NaCl 3% the infusion and 137.25±5.53 mmol/l when
stopping infusion, the average correction of serum sodium concentrationwas
2.95 ± 3.45 mmol per day.
Increased blood sodium concentration and blood osmotic pressure during
treatment with 3% NaCl solution
Table 3.32.Complications during treatment withNaCl 3%
Number of patients
Percentage
Complications
(n=83)
(%)
Hypertonic
2
2,4%
Hypernatremia
2
2,4%
Comme nt: 2/83 patients (2,4%) had hypernatremia, 2 patients had blood
hypertonic during treatment of NaCl 3% infusion.
3.4.4. Clinical changes before and after hyponatremia treatment

16

14 (7,8%)

15

Hyponatremia (180)

Normal (n=208)

15

withNaCl3% solution
Cognitive changes (Glasgow) before and after treatment with NaCl 3% solution
19 (63.3%)

8 (4,4%)

8 (4,4%)

10
4 (1,92%)
2 (0,96%)

5

16(47%) 16(47%)

20
5 (2,78%)
3 (1,4%)

2 (0,96%)

15
10

Pneumonia

Sepsis

Chapter 4
DISCUSSION
4.1. General characteristics of the research group
4.1.1. Distribution of patients with cerebral hemorrhage by gender and age
Age and gender
From 2016 to 2018, we monitored 409 patients with cerebral hemorrhage,
including 126 patients with subarachnoid hemorrhage, 283 patients with bleeding
in the brain parenchyma,accounting for 30.8%, 69.2% respectively. The average
age of the study group was 58.9 ± 15.2. The common age is 41 - 60 years old
(45.5%) and 61 - 80 years old (39.1%).
The proportion of men (64.3%) was more than women (35.7%), this was also
characteristic of the stroke group. Males were more common than females in both
subarachnoid hemorrhage and bleeding in brain parenchyma.
4.2. Clinical and subclinical characteristics of cerebral he morrhage
patients with hyponatre mia
4.2.1. Blood sodium concentration status
180/409 patients with hyponatremia accounted for 44% and

hypernatremia patients made up 5.1%.50.9% of total patients had normal blood
sodium concentration. The rate of hyponatremia in patients with subarachnoid
bleeding (50.8%) was higher than in patients with cerebral hemorrhage (41%),
whereas hypernatremia was more common in patients with intracerebral
bleeding (6% - 3.2%).
4.2.2. The moment of hyponatremia occurence

1(9.6%)

Worse (8/83)

0

Convulsions Acute renal failure

Figure 3.13.Complications during hospitalization
Comme nt:7.8% of total hyponatremia patientshad pneumonia complications,
while this rate in patients with normal blood sodium concentration was .9%,
this difference was statistically significant. Sepsis complication - severe
infections and seizures in hyponatremia and normal groups was 4.4%, 1%,
respectivelyand this difference was statistically significant with p <0.05.Acute
renal failure in the hyponatremia group was also more common.

Better (45/83)
Unchanged (30/83)

2(5.8%)

5

0

10(52.6)%
8(42.1%)

6(20%)
5(16.6%)

CSWS (30)

SIADH (34)

Others (19)

Figure 3.9. Perception change before and after treatment with NaCl 3%
solution in the groups of hyponatremia causes
Comme nt:
42/79 patients were better about cognitionafter treatment, accounting for
53.16%, the cognition of 31/79 patients(39.24%) was unchanged. 6 patients
(7.59%) were worse aboutcognition after treatment. The average Glasgow
score was 12,84 ± 2,89 point at the starting of treatment and 13,01 ± 2,86 point
when finishing treatment
3.4.8. The general results of the research group
Table 3.35.The general results of the research group
Results

Hyponatremia
(n=180)

Normal

(n=205)

Death

13 (7,3%)

5 (2,4%)

Living without complications

51 (28,3%)

73 (35,6%)

Living with complications

116 (64,4%)

127 (62,0%)

Mild disability (mRs=0,1,2)

71(39.4%)

125(60.1%)

Moderate disability (mRs=3,4)

77(42.8%)

61(29.3%)

Serious disability, TV (mRs=5,6)

32(17.8%)

22(10.6%)

Average mRs

2.95±1.65

2.19 ±1.513

p

<0,05

<0,05

<0,05

Comme nt:
The rate of dead(7,3%) và complicated(64,4%)hyponatremia patients was
higher than patients having normal serum sodium concentration ,with 2,4%;
62,0% (p <0,05), respectively.The rate of having a moderate and serious
disability in the hyponatremia cerebral hemorrhagic patientswas higher than
those in patients with normal serum sodium concentration. The average
ranking score of hyponatremia group (2.95±1.65) was higher than that of the
group without hyponatremia (2.19 ±1.513).

3.4.12. Complications during hospitalization


17

18

Occurrence of hyponatremia is most prevalent in the first day of the
disease, accounting for 15%, the percentages of patients with the occurrence of
hyponatremia from day 1 to day 4, from day 5 to day 8, and between day 9 and
after day 14 are 42.23%, 32.72% and 16.67% , respectively (Figure. 3.3).These
results indicate that monitoring of hyponatremia should be considered at the time of
admission and continue for approximately 14 days of illness. This result is also
consistent with studies of Dang Hoc Lam (2010), Saleem S (2014), Alimohamadi
M et al. (2016): hyponatremia on the first day of 15.1%.
4.2.3. Clinical changes at the time of hyponatremia
Among 180 cerebral hemorrhage patients with hyponatremia, 87 patients
had hyponatremia from the second day after admission, we compared some
clinical symptoms at the time of hyponatremia occurrence:
Headache: 40/59 patients (67.79%) still had a headache at the time of
hyponatremia, 5/41 patients (12.19%) had an increase in head level.
Perceptual status (Glasgow): 17/87 patients (19.50%) had the cognitive
deterioration, 42/87 patients (48.27%) had the unchanged perception status;
thus worsening perception is a hyponatremia symptom in patients with cerebral
hemorrhage, especially when these patients have no change in brain lesion on
CT or MRI of the brain. Nguyen Viet Quang (2013) researched on patients
with traumatic brain injury and showed a positive correlation between Glasgow
score and blood sodium concentration. Paralysis: 13/51 patients (25.49%) had
increased paralysis, 23/51 patients (45.09%) had unchanged paralysis. The high
rate of increased paralysis may be due to the progression of cerebral bleeding,

but it is also possible that hyponatremia may contribute to this increase.
4.2.4. Causes of hyponatremia
Hyponatremia caused by CSWS, SIADH and unknown causeaccounted
for 24.4%, 33.3%, and 42.2%, respectively. Our rate is similar to that of Kao L
et al (23% - 34.5%). The rate of CSWS is very diverse, not consistent
according to each author and it is often described in cases of meningeal
tuberculosis, neurosurgery and CNS lesions. According to Natarajan K et al
(2016), the rates of hyponatremia due to CSWS, SIADH and unexplained
causes were 31%, 46%, 23%, respectively.
4.2.5. Levels of hyponatremia
Among 180 cerebral hemorrhage patients with hyponatremia, 14 patients
(8%) had severe hyponatremia (<125 mmol / l), 59 ones (33%) had moderate
level (125-129 mmol / l) and 107 patients (59%) had mild hyponatremia, thus
patients mainly hadmild hyponatremia (130 - 134 mmol / l). According to Ha
QuangBinh (2012), these percentages are 16,7%,23,8%, and 59,5%,
respectively.

CSWS, SIADH and unknown causes
Dry skin (100%), dysphagia (45.4%) were more common in patients with
hyponatremia due to CSWS (<0.05). This result is consistent with the
pathogenetic mechanism of CSWS. Hyponatremia associated with dehydration,
swallowing disorders can be confused because compared to SIADH and other
causes CSWS often occurs in more severe patients.
Glasgow score of patients with CSWS hyponatremia was the lowest, there
was a difference of Glasgow score in 3 cause groups (p <0.05). The rate of
patients having Glasgow score ≤ 8 pointsis higher than one in 2 rest causes.
There was a difference in NISSH score at admission in the three groups of
hyponatremia causes, the NISSH score was the highest in CSWS patients, and
CSWS patientshavingNISSH scores> 21 pointsaccounted for a much higher
proportion than those in the rest two causes. This result confirms our finding

above: CSWS is more common in patients with severe clinical manifestations.
The urine indices had a statistically significant difference (p <0.01) in 3 groups
of causes, in which hyponatremia due to CSWS was much higher. Thus,
polyuria is the symptom suggesting a diagnosis of hyponatremia due to CSWS.
According to Allen IArieff et al (2017), the amount of urine in CSWS patients
is more than that of SIADH patients.
Symptoms such as low urination, oliguria were not clear because a large
number of patients with cerebral hemorrhage were treated with mannitol and/
or furosemide. There were no signs of dehydration, thus we did not monitor
weight gain due to fluid retention in study patients.
4.2.7. NT-proBNP concentrations in the groups of hyponatremia causes
The concentration of NT-proBNP in CSWS patients (420.1 ± 285.5 pg / ml)
was higher than in SIADH patients (107.1 ± 133.1pg / ml), the difference was
statistically significant with p <0.05. Our results were similar to those of
Spatenkova V et al. in 2008: NT-proBNP concentration was significantly
higher in patients with CSWS (430.4 ± 706.4 pg / ml) compared to not only the
reference range (125 pg / ml, P = 0.001) but also the control group (268.3 ±
203.9, P <0.001).
According to George Tobin et al (2018), NT-proBNP> 125 pg / ml could
diagnose CSWS with 87.50% sensitivity and 93.33% specificity (P <0.001).
Positive predictive value is 93, 33% and the negative predictive value is
87.50%.
4.3. Some factors associated with hyponatremia in patients with cerebral
hemorrhage
4.3.1. Relationship between hyponatremia and medical history
Patients with diabetes are 2.6 times more likely to suffer from
hyponatremia than those without diabetes (p <0.05). Huang WY et al. (2012)
studied 925 patients with cerebral infarction. Diabetes was significantly 4.08

4.2.6. Clinical characteristics of hyponatremia in the groups of causes:

19

20

times higher in patients with hyponatremia (p <0.001). Patients with
hypertension who were regularly treated had 4.6 times higher risk of
hyponatremia and the difference was statistically significant (p <0.001).
Smoking patients had a 1.8 times higher risk of hyponatremia than nonsmokers and the difference was statistically significant (p < 0.05). We do not
understand the causes and pathogenetic mechanisms of these factors.
According to Kuramatsu JB et al (2014), a 464- patient study showed that
medical histories of hypertension, smoking, and thiazide diuretics were seen in
hyponatremia patients more than patients with normal blood sodium
concentration.
4.3.2. Relationship between hyponatremia and brain lesions
Relationship between hyponatremia and site of lesions
Patients with brain lesions in the frontal lobe were 2.5 times more likely
to have hyponatremia than patients without brain lesions in the frontal lobe and
the difference was statistically significant (p <0.01). The percentage
hyponatremia at this position was 66.7%. The rate of hyponatremia in the brain
lesion group in the periaqueductal gray was 31.9%. Patients without damage of
the central gray were 2.2 times more likely to have hyponatremia and the
difference was statistically significant (p <0.01 ) Patients with ventricular
hemorrhage were 2.5 times more likely to have hyponatremia and this is
statistically significant difference (p <0.001). The rate of hyponatremia in this
position is 64.2%. Research by Natarajan K et al. (2016) shows that
hyponatremia is more common in patients with right brain lesions.
Relationship between hyponatremia and size of the lesions
The patients with lesion size less than 30cm3 had a lower rate of

hyponatremia (35.9%), while the large size group above 60cm3 had a
significantly higher rate of hyponatremia (57.7%). There was a statistically
significant relationship (p <0.05) between hyponatremia and size of brain lesions,
the larger the volume of lesions, the higher the rate of hyponatremia. According to
Kuramatsu JB et al. (2014), patients with hyponatremia have a larger lesion size
compared to the group without hyponatremia (23.4cm3 compared to 17.7cm3).
4.3.3.Relationship between hyponatremia and cognition , treatment methods
Relationship between vascular intervention and hyponatremia
Vascular interventions are related to hyponatremia in patients with
cerebral hemorrhage. In 52 patients with opening cranial interventions and
having an external drain, more than half (67.3%) of patients had hyponatremia.
Among patients with coil embolizations, 43% of them hadhyponatremia,
43.2% of patients without interventionhad hyponatremia. Patients with opening
cranial and drainage interventions were 2.7 times more likely to have
hyponatremia, and the difference was statistically significant with p <0.05.
Relationship between hyponatremia and cognitition, treatment methods

In cerebral hemorrhage patients infusedmannitol 20% solution, the proportion
of patients with hyponatremia (51.8%) was 2.3 times higher than patients with
normal blood sodium concentration. Osmotic diuretics cause water distribution
disorders, leading to hyponatremia. A study of Carole I et al. (2009) mannitol 20%
reduced serum sodium and chloride concentration to 97.7% and 98.5%,
respectively.
Patients with mechanical ventilation had a risk of hyponatremia 2.6 times
higher than those without mechanical ventilation and the difference was
statistically significant (p <0.001). According to Truong Thi Mai Hong (2012),
the rate of intubation and mechanical ventilation in patients with hyponatremia
105/339 (31%) is significantly higher compared to patients with normal blood
sodium concentration 40/470 (8.5%).
Patients with Glasgow ≤ 8 points were 2.4 times more at risk of

hyponatremia than patients with Glasgow > 8 point and the difference was
statistically significant (p <0.01). According to Ha QuangBinh (2012): the rate
of hyponatremia in Glasgow ≤ 8 group is 90.5% and higher than that of
Glasgow> 8 point group (9.5%).
4.4. Results of treatment
4.4.1.Change of serum sodium concentration, blood osmotic pressure before
and after treatment with NaCl 3% solution
Rate of the patients reaching the goal of treatment
69 / 82 patients (83.13%) achieved the goal of treating
hyponatremia(135mmol / l ≤ Na <150mmol / l). 12 patients have low blood
sodium concentration because these patients were discharged or determined the
cause and blood sodium> 130mmol / l, we stoppedto infuse NaCl 3% solution.
2 patients had hypernatremia. In the group of patients supplemented with table
salt, 12 / 20 patients (60%) reached the goal of treating hyponatremia
(135mmol / l ≤ Na <150mmol / l), 8 patients had low blood sodium
concentration in the range 130 - 134 mmol / l, accounting for 40% , no patients
had hypernatremia. Carolyn Woo et al. (2009) studied 176 hyponatremia
patients treated with 3% NaCl solution (Na ≤ 133 mmol / l or a rapid reduction
of 6mmol / 24h) and in 49 patients who weresustantively infused NaCl3%
solution 83.8% of them reachedthe goal of treatment.
Change of serum sodium concentration before and after treatment with NaCl
3% solution
The average blood sodium concentration at the beginning of infusingNaCl
3% solution was 128.97 ± 3.30 mmol / l, and 137.37 ± 5.47 mmol / l when
stopping infusion. The rate of blood sodium correction is 2.95 ± 3.45 mmol
/day. Our blood sodium correction rate is lower than that of the study of
Carolyn Woo (0.44 ± 0.36mmol / hour). This result may be due to that in
Carolyn Woo's study, the 3% NaCl infusion rate was adjusted more frequently

21

22

every 6 hours, whereas in our study every 24 to 48 hours.
Change of Blood osmotic pressure before anđ after treatment with NaCl 3%
solution
Blood osmotic pressure increased after treatment with the most changes
in SIADH group. All SIADH patients increased osmotic pressure, while the
remaining 2 groups had some patients with decreased blood osmotic
pressureafter treatment.
Hypernatremia, blood osmotic pressure during treatment with NaCl 3%
solution
2/83 patients (2.4%) had hypernatremia (Na> 150mmol), 2 patients
increased blood osmotic pressure,at the time of hyponatremia and after
treatment: 334mosmol / kg, 342 mosmol / kg, respectively) . The reason is
that at the beginning of treatment, we did not have the result of blood
osmotic pressure, and patients with diabetes. During treatment with NaCl 3%
solution, no clinical manifestations of complications were noted. Blood sodium
concentration also quickly returned to normal when stopped using NaCl 3%
solution. 1 patient increased blood osmotic pressure due to hypernatremia (Na
= 163mmol / l), this patient also stopped infusion, adjusted to normal and the
patient was discharged from hospital with good status (Glasgow: 15 points),
our complication rate was similar to Carolyn Woo and much lower according
to Froelich M et al. This is due to that infusion NaCl3% did not have a suitable
reference and adjustment process.
4.4.2. Change of cognition before and after treating hyponatremia with NaCl 3%
solution
42/79 patients had a good improvement in perception after treatment
accounted for 53.16%, 31/79 patients (39.24%) did not have any change in

perception after treatment. Post-treatment perceptions of 6 patients (7.59%)
worsened. The average value of Glasgow at the beginning of treatment was
12.84 ± 2.89 point and 13.01 ± 2.86 point in the end . Among them, CSWS
patients have the most obvious improvement in perception Figure 3.10.
In addition to treating hyponatremia, NaCl 3% solutionhas antiedematous effect and is the most effective in hyponatremia patients in the
acute phase of brain bleeding (<7 days). According to Nguyen Anh Tuan
(2014), Le Hong Trung (2017), Kamel H et al. (2012) NaCl 3% solution is
effective in the treatment of increased intracranial pressure. The time of
control intracranial pressure of this solution is longer than mannitol. This
may also be the cause of clinical change, especially headache manifestation
when infusingNaCl 3% to treat hyponatremia.

4.4.3. The general results of the research group
The mortality rate of the hyponatremia group was 7.3%, 69.5% of the
surviving patients had complications at some levels: living without
complications at 28.3% while in the group having normal blood sodium
concentration, these rates were 2.4%, 62% and 35.6%, respectively There
was a statistically significant difference with p <0.05 of these rates. The
mortality rate in patients with hyponatremia was higher than in patients
with normal blood sodium complications while the rate of unsequeled
survival was lower. Evaluation of treatment results on 1195 patients with
cerebral hemorrhage due to hypertension at 108 Hospital Brain Stroke
Center from 2003 to 2011: the death rate was 11.3%, 68.2%. ofthe survival
lived with complication.
Evaluation of the degree of disability of the patients on a Rankin scale
when discharge showed that patients with CMN had hyponatremia, the rate of
cerebral hemorrhage patients with mild disability (39.4%) was lower than that
of patients without hyponatremia(60.1%). However, the prevalence of
moderate and severe disability was higher (42.8% - 17.8% compared to 29.3%
- 10.6%). The average Rankin score of the group with hyponatremia (2.95 ±

1.65) was higher than the group without hyponatremia (2.19 ± 1,513), these
differences were statistically significant with p <0.05. According to Ha
QuangBinh( 2012) the mortality rate in the hyponatremia group was much
higher than the group with normal blood sodium concentration, univariate
analysis showed a significant association with OR = 0.273, 95% CI 0.08 - 0.88
, p = 0.029.Corona et al. (2013): hyponatremia even mildly was associated
with a significant increase in mortality in the ICU department (RR: 2.60; 95%
CI: 2 , 31 - 2.93, p <0.0001).
4.4.4. Complications during hospitalization
The rate of pneumonia in cerebral hemorrhagic and hyponatremia patients
(7.8%) was higher than that of patients with normal blood sodium
concentration (1.9%). According to Huang WY et al. (2012) , in 925 patients
with cerebral infarction, pneumonia found in the hyponatremia group was 2.15
times higher than the group with normal blood sodium concentration (p <0.05).
Sepsis complication - severe infections and seizures in the hyponatremia group
was 4.4% while in the normal sodium group,this rate was 1%. This difference was
statistically significant with p <0.05. Acute renal failure was also found morein the
hyponatremia group (2.78% compared to 1.4%). According to Do Mai Huyen and
Nguyen Van Thong ‘s (2012) retrospective study on 6213 patients with acute brain
stroke pneumonia rate was 4.8%, convulsive complication rate was 0.94%,
secondary brain bleeding was 0.3% while in our study, two patients (1.1%) were
diagnosed with secondary brain bleeding in the hyponatremia group and nobody in
the normal blood sodium concentration group.


23

24

CONCLUSIONS

Through a study of 409 patients with cerebral hemorrhage, including
180 patients with hyponatremia at Military Central Hospital 108 from 2016 to
2018, we draw some conclusions
1, Clinical, subclinical characteristics, factors associated with hyponatremia in
patients with cerebral hemorrhage:
Hyponatremia was a common electrolyte disorder in patients with cerebral
hemorrhage at 44%; the rate of hyponatremia in patients with intracerebral
hemorrhage was 41% and in subarachnoid bleeding was 50.8%.
The most common occurrence of hyponatremia is in the first day of the
disease, accounting for 15%, hyponatremia from day 1 to 4 accounted for
(42.23%); Severe hyponatremia (blood sodium <125mmol / l) accounted for
8%, moderate and mild hyponatremia made up 33% and 59% respectively.
Cerebral hemorrhagic patients with hyponatremia have lower Glasgow
points and higher NISSH scores than those with normal sodium concentration;
the frequency of symptoms of nausea, stiff neck, meningeal syndrome,
swallowing disorders in patients with hyponatremia is higher. 25.49% of
patients showed signs of worsening perception had little improvement in
headaches and more significant paralysis.
Hyponatremia caused by CSWS accounted for 24.4%, by SIADH
accounted for 33.3%, by the unknown causes made up 42.2%; CSWS patients
are older than SIADH.
Signs of dry skin and dehydration were seen only in CSWS patients,
swallowing disorders were higher in CSWSgroup , and a headache was more
common in SIADH patients (p <0.05).
Hyponatremia due to CSWS has a lower Glasgow score and a higher
NISSH score than SIADH patients and other causes (p <0.05).
There was a statistically significant difference in the amount of urine of
patients in 3 cause groups (p <0.01) The amount of urine of CSWS patients
(3547.95 ± 1161.45ml) was much higher than that of SIADH and other
groups.

The blood osmotic pressure group (>295mosmol/kg) in CSWS patients
accounted for and was more than that in SIADH patients (15.6%), with p
<0.05.
NT-proBNP in CSWS patients (420.1 ± 285.5pg / ml) was higher than in
SIADH patients (107.1 ± 133.1pg / ml) with p <0.05.
Patients with medical histories of diabetes, hypertension, smoking had a
higher risk of hyponatremia than the group without these diseases (p <0.05).
Patients with brain lesions in the frontal lobe, ventricular hemorrhage were
at higher risk of hyponatremia, whereas lesions of central gray had a low risk
of hyponatremia with OR respectively: 2.5-2.2-2.5.\ (p <0.05).The larger the

volume of lesions is, the higher the rate of hyponatremia is.
Patients with 20% mannitol use, mechanical ventilation, Glasgow score ≤
8 point, cranial opening and cranial drainage have a higher risk of
hyponatremia with OR: 2,3-2,6-2,4-2,7, respectively.
2. Evaluation of results of hyponatremia treatment in patients with
cerebral he morrhage:
83 patientswith cerebral hemorrhage (46.11%) were selected to treat
hyponatremia with infusing NaCl 3%
63 / 83 patients (83.13%) achieved the goal of treatment (135mmol / l ≤ Na
<150mmol / l); blood sodium correction rate is 2.95 ± 3.45 mmol / day.
Treatment of hyponatremia with NaCl3% solution improves headaches,
nausea, perception, ...
The rate of hypernatremia and an increase in blood osmotic pressure during
the treatment of hyponatremia with NaCl 3% infusion was very low (2.4%, 2.4%).
There was a statistically significant improvement of hyponatremia group in
Glasgow points, muscle strength, and NISSH scores when discharge.
The group of patients with hyponatremia had a longer average hospitalization,
a longer duration of treatment at the lower health facilities and a statistically
significant difference (p <0.01). CSWS patients had a longer hospital stay than

SIADH patients (p <0.05).
The mortality rate of patients with hyponatremia was 7.3%, 69.5% of all
patients lived with complications at some levels . The mortality rate of patients with
hyponatremia (7.3%) was higher than that of patients with normal blood sodium
concentration (2.4%) with p <0.05. CSWS patients had a higher mortality rate and
complicated rate (15.91% - 83.8%) than SIADH patients (1.67% - 74.57%).
Hyponatremia patients with cerebral hemorrhage had higher rates of
pneumonia, sepsis, convulsions, acute renal failure, and secondary bleeding than
patients with normal blood sodium concentration.
RECOMMENDATIONS
Through this study we recommend:
1. Particular attention should be paid to monitor treatment of hyponatremia in
patients with cerebral hemorrhage, especially patients with changes in
perception, swallowing disorders, severe headache, increased headache,
nausea, vomiting, slowly improving paralysis, mechanical ventilation,
deep coma, open-skull surgery, using 20% mannitol, brain lessionsin the
frontal lobe, ventricular hemorrhage. Time of monitoring is in 14 days.
2. Conduct in-depth research with large sample sizes to determine the
diagnostic criteria for the causes of hyponatremia (NT-ProBNP values),
as well as the effeciency of hyponatremia treatment according to the
pathogenetic
mechanisms.


LIST OF ANNOUNCED RESEARCH PROJECTS
RELATED TO THESIS TOPIC

1.

Nguyen

DinhDung(2017).

Study

on

clinical,

subclinical

characteristics and treatment of hyponatremia in patients with
cerebral hemorrhage. Journal of Practical Medicine, 1047-2017,
page 10-13.
2.

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