Nghiên cứu sự biến đổi một số chỉ số sinh học và tác dụng của điều trị tái tăng áp trong bệnh giảm áp cấp tính thực nghiệm

MINISTRY OF EDUCATION AND TRAINING MINISTRY OF DEFENCE
VIETNAM MILITARY MEDICAL UNIVERSITY

CAO HONG PHUC

RESEARCH ON SOME OF BIOLOGICAL CHANGES AND
EFFECTS OF RECOMPRESSION TREAMENT IN
EXPERIMENTAL DECOMPRESSION SICKNESS

MEDICAL DORTOR PHILOSOPHY THESIS

HA NOI-2018


MINISTRY OF EDUCATION AND TRAINING MINISTRY OF DEFENCE
VIETNAM MILITARY MEDICAL UNIVERSITY

CAO HONG PHUC

RESEARCH ON SOME OF BIOLOGICAL CHANGES AND
EFFECTS OF RECOMPRESSION TREAMENT IN
EXPERIMENTAL DECOMPRESSION SICKNESS

Branch: Bio - Medicine Sciense
Code: 972 01 01

MEDICAL DORTOR PHILOSOPHY THESIS
SUPERVISORS:
1. Assoc.Prof. Nguyen Tung Linh, PhD

2. Assoc.Prof. Dang Quoc Bao, PhD

HA NOI-2018


i

COMMITMENT
I declare that this is my onw thesis which was carried out by scientific
supports of superviors.
All results that were presented in this thesis have been authentic and
published in scientific articles. The thesis is not repeated to previous thesises
or projects. If there is something wrong, I will take my responsibility.
Author

Cao Hong Phuc


ii

ACKNOWLEGEMEND
After years of in-depth research, this thesis has been completed. I would
like to show my sincerely thanks to the Party Committee, Broad of Directors:
Vietnam Military Medical University, Military Hospital No 103, National
Institute Of Hygiene And Epidemiology for their facilitation.
I would also like to thank: Department of Medicine of Arms, Department
of Medical Physiology, Department of Experimental Operation, Department
of Medical Physics (Vietnam Military Medical University), Departemt of
Hematology and Tranfusion, Patho-Histology and Judical Medicine (Military
Medical No 103), Laboratory of Micro-Structure (Virus Department, National
Institute Of Hygiene And Epidemiology), Department of Post - Graduate

Training for their technical help in my study.
In addition, I am completely grateful to my suppervisors: Asscoc.Prof
Nguyen Tung Linh, PhD (first suppervios), Asscoc.Prof Dang Quoc Bao, PhD
(second suppervios). The doors of their offices were always open whenever I
ran into a trouble spot about my reseach. They consistently allowed this paper
to be my own work, steered me in the right direction in experimental period.
They also set good examples for me to follow in doing all scientific tasks.
Besides, I would like to express my heartfelt gratitude to my parents and
parents - in - law for their bringing up and supporting me to make this work
possible. Last but not least, I am deeply indebted to my wife and my son for
being on my side, encouraging me a lots throughout my years of study.
AUTHOR

Cao Hong Phuc


iii

CONTENT
SUBTITLE PAGE
COMMITMENT................................................................................................i
ACKNOWLEGEMEND..................................................................................ii
CONTENT.......................................................................................................iii
ABBREVIATIONS AND DEFINITIONS....................................................viii
LIST OF TABLES..........................................................................................xii
LIST OF FIGURES.......................................................................................xvi
INTRODUTION............................................................................................... 1
CHAPTER 1. OVERVIEW.............................................................................. 3
1.1. CLINICAL, INVESTIGATING CHARACTERISTICS OF
ACUTE DECOMPRESSION SICKNESS 3

1.1.1. Causes and risk factors................................................................3
1.1.2. Clinical characteristics................................................................ 7
1.1.3. Investigating characteristics......................................................12
1.1.4. Diagnosis and classification......................................................14
1.1.5. Treatment.................................................................................. 16
1.2. INFLUENCES OF THE BUBBLES IN DECOMPRESSION
SICKNESS 20
1.2.1. Bubble formation in the decompression sickness.....................21
1.2.2. Influences of the bubbles in decompression sickness...............22
1.3. STUDIES ON ANIMAL MODELS AND BIOLOGICAL
CHANGES IN ACUTE DECOMPRESSION SICKNESS

24


iv

1.3.1. Studies on animal models in decompression sickness..............24
1.3.2. Some studies of peripheral blood cell changes in acute
decompression sickness 26
1.3.3. Some studies of coagulation changes in decompression
sickness

28

1.3.4. Some studies of biochemical changes in acute decompression
sickness

30

CHAPTER 2. SUBJECTS AND METHODS.................................................34
2.1. SUBJIECTS......................................................................................34
2.1.1. Subjects..................................................................................... 34
2.1.2. Laboratories.............................................................................. 34
2.1.3. Period........................................................................................ 35
2.2. METHODS.......................................................................................35
2.2.1. Study design..............................................................................35
2.2.2. Study Issues...............................................................................40
2.2.3. Study equipments......................................................................40
2.2.4. Research indexes and methods................................................. 42
2.2.5. Data Analysis............................................................................ 53
CHAPTER 3. RESULTS................................................................................ 55
3.1. ETABLISHING THE EXPERIMENTAL ACUTE
DECOMPRESSION SICKNESS MODEL

55

3.1.1. Influence of some diving factors on acute decompression
sickness

55


v

3.1.2. Comparision the efficacy of models to cause the
decompression sickness 60
3.2. CHANGES IN HEMATOLOGICAL, BIOCHEMICAL AND
PATHOHISTOLOGICAL INDEXES IN ACUTE
DECOMPRESSION SICKNESS

62

3.2.1. Changes in hematological indexes in acute decompression
sickness rabbits

62

3.2.2. Changes in some of biochemical indexes in acute
decompression sickness rabbits 72
3.2.4. Some of pathohistological characteristics in acute
decompression sickness rabbits 73
3.3. EFFECTS OF RECOMPRESSION TREATMENT IN
ACUTE DECOMPRESSION SICKNESS 83
3.3.1. Effects on clinical symptoms in acute decompression
sickness rabbits

83

3.3.2. Effects on hematological index in acute decompression
sickness rabbits

85

3.3.3. Effects of recompression treatment on some biochemical
indexes in in acute decompression sickness rabbits 94
CHAPTER 4. DISCUSSION..........................................................................97
4.1. ANIMAL MODEL OF EXPERIMENTAL ACUTE
DECOMPRESSION SICKNESS

97

4.1.1. Influence of some diving factors on experimental acute
decompression sickness 97


vi

4.1.2. Effecting comparison of experimental acute
decompression sickness of models

101

4.2. CHANGES IN SOME HEMATOLOGICAL,
BIOCHEMICAL, AND PATHOHISTOLOGICAL
INDEXES IN EXPERIMENTAL ACUTE
DECOMPRESSION SICKNESS

104

4.2.1. Changes of some hematological indexes in experimental
acute decompression sickness rabbits 104
4.2.2. Platelet activation in experimental acute decompression
sickness

114

4.2.3. Changes of some biochemical indexes in acute
decompression sickness rabbits 118
4.2.4. Changes of pathohistological indexes in experimental

acute decompression sickness rabbit 120
4.3. EFFECTS OF RECOMPRESSION TREATMENT ON
EXPERIMENTAL ACUTE DECOMPRESSION
SICKNESS 123
4.3.1. Effects of recompression treatment on clinical symptoms
in experimental acute decompression sickness rabbits

123

4.3.2. Effects of the recompression treatment on haematological
indexes in acute decompression sickness rabbits

128

4.3.3. Effect of recompression treatment on biochemical indices
in acute decompression sickness rabbit

134

CONCLUSION.............................................................................................137


vii

SUGGESSTIONS.........................................................................................139

LIST OF PUBLISHED ARTICLES RELATED TO
RESULTS OF THESIS.................................................................................140
REFFERENCES........................................................................................... 141
APPENDIXES..............................................................................................158

viii

ABBREVIATIONS AND DEFINITIONS

Num

Abbre

Deffinition

Vietnamese Meaning

1. 2D
2. ADP

Two Dimension
Adenosine diphosphate

Hai chiều

3. ALT

Alanine transaminase

Enzym chuyển amin
Alanine

4. APTT

Activated Partial

Thời gian thromboplastin

Thromboplastin Time

hoạt hóa từng phần

5. Ar

Argon

Khí argon

6. ARN

Acid Ribonucleic

A-xít Ribonucleic

7. AST

Aspartate transaminase

Enzym chuyển amin
Aspartate

8. ATA

Atmospheres Absolute

9. ATP

Adenosine triphosphate

10. Aβ

β-amyloid

11. BTG

Beta thromboglobulin

12. Conc

Concentration

13. CPK

Creatine phosphokinase

14. CSF

Cerebrospinal fluid T-Tau

T-tau
15. CT

Áp suất khí quyển tuyệt đối

Nồng độ
Protein T-Tau trong dịch
não tủy

Computerized

Chụp cắt lớp vi tính

Tomography
16. DCS

Decompression sickness

Bệnh giảm áp


ix

Num Abbre
17. DWI

Deffinition

Vietnamese Meaning

Diffusion Weighted
Imaging

18. EDTA

Ethylene diamine tetra

Chất chống đông EDTA

acetic acid
19. ET-1

Endothelin 1

20. Fib

Fibrinogen

21. FSF

Fibrin Stabilizing Factor

Yếu tố ổn định Fibrin

22. G

Group

Nhóm

23. GFAP

Glial fibrillary acidic
protein

24. Hb

Hemoglobin

25. HCl

Hydrochloric acid

26. Hct

Hematocrit

27. HE

Hematoxylin-Eosin

A-xit Clohydric
Thuốc nhuộm
Hematoxylin-Eosin

28. HMWK

High Molecular Weight

Kininogen khối lượng

Kininogen

phân tử cao

29. HRP

Horseradish peroxidase

30. HSP 70

Heat Shock Protein 70

Protein sốc nhiệt 70

31. ICAM-1

Intercellular Cell Adhesion

Chất liên kết tế bào 1

Mollecular - 1
32. IL-1β

Interleukin 1 beta

33. IL-6

Interleukin 6

34. KLPT

Khối lượng phân tử

x

Num Abbre

Deffinition

Vietnamese Meaning

35. LDH

Lactate dehydrogenase

36. MCH

Mean corpuscular

Hàm lượng hemoglobin

hemoglobin

trung bình hồng cầu

Mean corpuscular

Nồng độ hemoglobin

hemoglobin concentration

trung bình hồng cầu

Mean corpuscular volume

Thể tích trung bình hồng

37. MCHC
38. MCV

cầu
39. MDA

Malodialdehyde

40. MH

Mơ hình

41. MPV

Mean platelet volume

Thể tích trung bình tiểu
cầu

42. NSE

Neuron-Specific Enolase

43. OR

Odd Ratio

Tỷ suất chênh

44. Para

Paralysis

Liệt

45. PF4

Platelet Factor 4

Yếu tố 4 tiểu cầu

46. Post

Post-experiment

Sau gây bệnh

47. Pre

Pre-experiment

Trước gây bệnh

48. PT

Prothrombin Time

Thời gian prothrombin

49. RR

Relative risk

Nguy cơ tương đối

50. sGPV

Soluble Glycoprotein V

Glycoprotein V hòa tan

51. T2WI

T2 Weighted Image

52. TAT

Thrombin-Antithrombin

Phức hợp thrombin -

Complex

antithrombin

Tumor necrosis factor

Yếu tố hoại tử u alpha

53. TNF-α

alpha


xi

Num Abbre
54. TT
55. TTR

Deffinition
Thrombin Time
Transthyretin

Vietnamese Meaning
Thời gian thrombin


xii

LIST OF TABLES
Num
2.1.

Table

Page

Classification of clinical severity in experimental acute
decompression sickness rabbits..................................................44

2.2.
rabbits

Paralysis classification in acute decompression sickness
44

2.3.

Classification of post-treatment response............................... 44

2.4.

Bubble grade in experimental decompression sickness.........52

3.1.

The rabbit number of decompression sickness with variable

bottom time.................................................................................55
3.2.

Clinical severity of rabbits after experiment..........................56

3.3.

The number of death rabbit after experiment with variable
bottom time.................................................................................56

3.4.

The rabbit number of decompression sickness with variable

ascent rate................................................................................... 57
3.5.

Clinical severity of decompression sickness............................57

3.6.

The number of death rabbits after decompression................58

3.7.

The rabbit number of decompression sickness......................58

3.8.

Clinical severity and consecutive compression......................59

3.9.

The number of death rabbit and consecutive compression..59

3.10.

Influence of some diving factors on decompression sickness
60

3.11.

The rate of decompression sickness and survival of rabbits

after compressing as four models............................................... 61
3.12.

Clinical severity of rabbit after compressing as four models 61

3.13.

Bubble grade of rabbit after compressing as four models.....62


xiii

Num
3.14.

Table

Page

Changes in red blood cell count according to clinical

severity in acute decompression sickness

3.15.

Changes in hemoglobin concentration according to
clinical severity in acute decompression sickness

3.16.

65

Changes in platelet count according to clinical severity
in acute decompression sickness

3.21.

65

Changes in white blood cell percentage according to
clinical severity in acute decompression sickness

3.20.

64

Changes in white blood cell count according to clinical
severity in acute decompression sickness

3.19.

63

Changes in MCV, MCH, MCHC according to clinical
severity in acute decompression sickness

3.18.

63

Changes in hematocrit according to clinical severity
in acute decompression sickness

3.17.

62

66

Change in MPV according to clinical severity in acute
decompression sickness 67

3.22.

PT change according to clinical severity.................................68

3.23.

APTT change according to clinical severity............................69

3.24.

Plasma fibrinogen concentration according to clinical

severity in acute decompression sickness

3.25.

71

Changes in plasma platelet markers between pre and
post acute decompression sickness

71

3.26.

Changes in liver enzyme activity..............................................72

3.27.

Changes in plasma concentration of ure and creatinin.........73

3.28.

The rabbit number of bubbles in micro pathohistological
images after acute decompression sickness in 1st phase

78


xiv

Num

Table

Page

3.29.

Distribution of rabbits according to bubble grade and
paralysis grade in acute decompression sickness rabbits 80

3.30.

Rabbit number of platelet activation after acute
decompression sickness 83

3.31.

Changes in clinical symptoms between pre and post

treatment in acute decompression sickness rabbits 83
3.32.

Changes in clinical severity between pre and post treatment
in acute decompression sickness rabbits

84

3.33.

Treatment responding rabbits according to clinical category

84

3.34.

Treatment responding rabbits according to clinical severity 85

3.35.

Effects of recompression treatment on red blood

count in acute decompression sickness rabbits
3.36.

Effects of recompression treatment on hemoglobin

concentration in acute decompression sickness rabbits
3.37.

85
86

Effects of recompression treatment on hematocrit in acute

decompression sickness rabbits 87
3.38.

Effects of recompression treatment on MCV, MCH
and MCHC in acute decompression sickness rabbits

3.39.

Effects of recompression treatment on white blood
count in acute decompression sickness rabbits

3.40.

87
88

Effects of recompression treatment on leukocyte

percentage in acute decompression sickness rabbits 89
3.41.

Effects of recompression treatment on platelet

count in acute decompression sickness rabbits
3.42.

91

Effects of recompression treatment on MPV in acute
decompression sickness rabbits 91


xv

Num
3.43.

Table

Page

Effects of recompression treatment on PT in acute
decompression sickness rabbits 92

3.44.

Effects of recompression treatment on APPT in acute
decompression sickness rabbits 93

3.45.

Effects of recompression treatment on plasma
concentration of fibrinogen in acute decompression
sickness rabbits

3.46.

93

Effects of recompression treatment on liver enzyme
activities in acute decompression sickness rabbits 94

3.47.

Effects of recompression treatment on plasma ure
and creatinin concentration in acute decompression
sickness rabbits

95


xvi

LIST OF FIGURES
Num

Figure

Page

1.1.

Cutis mamorata..........................................................................9

1.2.

Nitrogen bubbles in the left atrial chamber..........................13

1.3.

Nitrogen bubble in spinal cord of decompression sickness dog ..

14

1.4.

Liver injury caused by the bubbles........................................23

1.5.

Platelet ultrastructure.............................................................27

2.1.

Diagram of 1st phase of study.................................................36

2.2.

Diagram of 2st phase of study.................................................37

2.3.

Recompression treatment protocol....................................... 39

2.4.

Experimental recompression chamber.................................41

2.5.

Gold coating on electromicroscope specimen........................53

3.1.

The relation between platelet count and survival time

post experiment...........................................................................66

3.2.

Change in platelet count between pre and post
decompression sickness according to paralysis degree..............67

3.3.

Relation between PT and survival of rabbits after acute
decompression sickness..............................................................68

3.4.

Relation between PT and platelet count..................................69

3.5.

Relation between APPT and survival time of rabbits............70

3.6.

Relation between APTT and platelet count in rabbits

after acute decompression sickness............................................ 70
3.7.

Vessels in normal and acute decompression sickness rabbit..74

3.8.

Adominal muscle vessels in normal and acute

decompression sickness rabbit....................................................74

3.9.

Lumbar branch of vena cava in normal and acute
decompression sickness rabbit....................................................75


xvii

Num
3.10.

Figure

Page

Mesenteric veins in normal and acute decompression

sickness rabbit

75

3.11.

Vena cava in normal and acute decompression......................76

3.12.

Abdomincal aorta in normal and acute decompression........76

3.13.

Bubbles in the blood drained out from the incised organs....77

3.14.

Abdominal muscle in acute decompression sickness rabbits. 77

3.15.

Vein of abdominal muscle in acute decompression sickness

rabbits (HE x100) 77
3.16.

Liver tissue in in acute decompression sickness rabbits........78

3.17.

Lung tissue in acute decompression sickness rabbits.............78

3.18.

Kidney cappilary in acute decompression sickness rabbits...78

3.19.

Kidney tissue in acute decompression sickness rabbits.........78

3.20.

Inside heart in acute decompression sickness rabbits............78

3.21.

Coronary vessles in acute decompression sickness rabbits.. .78

3.22.

Distribution of clinical severity according to bubble grade
in acute decompression sickness rabbits

3.23.

80

Survival time of rabbits and bubble grade in acute
decompression sickness rabbits 81

3.24.

Platele shape in normal rabbits.............................................. 82

3.25.

Pseudopods and oblong shape of platelet in acute

decompression sickness rabbits 82
3.26.

Platelet deformation and degeneration in acute
decompression sickness rabbits 82


1

INTRODUTION
Decompression sickness is a occupational disease of divers, causes
noticeable economic harmfulness, a lot of complication and may cause death.
Although patients were treated completely, some worse patients could still
bare seriously outcomes [1].
The number of decompression sickness patients has been a not - small
number in occupational disease group. According to British Diving Coucil,
the death patients were 98 cases in 2010 [2]. In Denmark, Svendsen J.C. et al
realised that there were 205 decompression sickness patients from 1993 to
2013, average 14 patients/year [3]. In Vietnam, Nguyen Van Non et al
reported that the rate of decompression sickness was 22% of fishery
population in Northern Bay [4]. It is clear that decompression sickness should
be put in high consideration.
So far, most reseachers presumed that bubble is a mainly factor causing
disorders of this desease [5], [6]. Looking at ultrasound images, bubbles were
seen at vein, heart chambers, arteriole, thigh artery [6], [7]. When applied
recompression treatment to minimise the bubbles, it was seen that clinical
symtomes were improved [8]. Therefore they played an importanted role in
machenism of decompession sickness. The relation, however, between
bubbles and risk, severity and prognosis of this desease has not been studied
in detail.
In reality, some patients were applied by recompression treatment did not
recover completely [9], [10]. Moreover, a small number of patients got mild

improvement by using antiplatetet drugs (the drugs could not decrease bubble
grade ) [11]. Hence, a part form bubble role, there were other biological
disorders which contributed to the disease machenism.


2
Some previous studies also found out investigational changes in this
disease [1], [6], including hematological, biochemical and immunological
changes. Nevertheless, there was disagreement among these changes and they
developed in different trends. Their role in decompression sickness was not
evaluated fully and the changes in about mentioned factors in treatment period
have not been described in detail. The correlation between those changes and
risk, severity, prognosis as well as their roles in early dignosis of
decompresion sickness have had unclear points.
Untill now, decompresion sickness studíe in Vietnam have been limited.
A few authors studied the proportion of decompression sickness in some
areas, others assessed the effect of treatment at shore and in hospital on
clinical symtoms [4], [12]. There have not been any reseacher who set up the
experimental decompression sickness model in animal. And there have not
been

anyone

looking

deeply

into

hematological,

biochemical,

pathohisological changes in acute decompression sickness. The study that
surveys the drug effects have been few bacause there are not the
decompression sickness model in animal.
Due to above reasons, we carried out this study “Research on some of
biological changes and effects of recompression treament in experimental
decompression sickness” which aims following 3 objectives:
1. Establishing up the decopression sickenss model in animal.
2. Determining some of hematological, biochemical, pathohistological
changes in experimental decompresion sickness.
3. Evaluating the effects of recompression treatment in experimental
decompression sickness.


3
CHAPTER 1
OVERVIEW
1.1. CLINICAL, INVESTIGATING CHARACTERISTICS OF ACUTE
DECOMPRESSION SICKNESS
1.1.1. Causes and risk factors
* Rate of decompression sickness
Decompression sickness is an occupational disease of divers and persons
working in environments with variable pressure, which is shown by the
symptom of pathological disorders, caused by a rapid drop in pressure
resulting in excessive satuproportionn of inert gas in the body, forming
bubbles in the blood and in the tissues of organs [5], [13].
Clinically, decompression sickness is divided into 2 types: acute and
chronic type [1], [13]. Acute decompression sickness has symptoms which is

directly related to a rapid drop in pressure occuring within 24 hours after the
time of drop in pressure [13]. Chronic decompression sickness occurs later,
normally from several months to several years, because of micro bubbles
formed in a long time or unthorough treatment in the acute stage [13].
Chronic decompression sickness includes 2 categories: primary category and
secondary category, in which primary category often causes injuries of
avascular necrosis at the head of long bones, and secondary category often
causes injuries in spinal marrow and inner ear [13].
Decompression sickness usually occurs in fishermen who dive to catch
aquatic species, professional divers, unprofessional divers, and submarine
sailors in the process of escape. The disease can also be found in aviation and
is often referred to as high-altitude decompression illness which only occurs
with a small proportion.


4
Decompression sickness has many different names: the bends,
decompression illness, Caisson disease. In Vietnam, nowadays it is known as
decompression sickness [1].
Gempp E. et al showed that about 13% of catastrophes at sea in France is
caused by decompression sickness [14]. Dardeau M.R. et al found there were
33/95 cases of decompression sickness injury from diving catastrophes in
North America [15]. Svendsen J.C. et al indicated that there were 205 patients
engaged in decompression sickness from 1999 to 2013 in Denmark, averagely
14 patients/year [3]. Among potentially fatal disease groups, decompression
sickness falls on the group of average risk [16].
In Vietnam, Pham Huy Nang et al showed that decompression sickness
in the North was 49.64% of total civil diving catastrophes [12]. Nguyen Van
Non et al reported the rate of patients engaged in decompression sickness in
the Gulf of Tonkin was 22% of total diving fishary men [4]. Phung Thi Thanh

Tu et al showed that the proportion of persons engaged in diving catastrophes
among fishermen of Khanh Hoa was 78.8%, and the rate of fishermen
engaged in polio (mainly caused by acute decompression sickness) was 5.3%
(21 persons) [17].
Therefore, the quantity of patients engaged in decompression sickness is
still significant, appearing in a lot of places in the world, including Vietnam.
* Causes
Decompression sickness is caused by rapid drop in pressure in the procss
of diving or during the dive or the airplane cockpit uncovered while flying
[1], [5], [6].
* Risk and mitigating factors
- Risk factors:
+ Non-compliance with diving steps in the process of diving and
working underwater [1].


5
+ Movement intensity: The more movement intensity at the bottom is,
the higher decompression sickness risk is [1].
+ Temperature of water environment: The higher the water temperature
is, the higher decompression sickness risk is [1]. The water surface
temperature is less than 100C, the decompression sickness risk is high.
+ Components of breathing gas: The higher the nitrogen proportion is,
the higher decompression sickness risk. Connolly D.M. et al find if the
breathing gas contains 21% nitrogen proportion (21% N2, 75% O2, 4% Ar),
the decompression sickness risk is lower than gas mixtures with a nitrogen
proportion 42% (42% N2, 56% O2, 2% Ar) [18]
+ Age: The older the person was, the higher decompression sickness risk
was and the less recovery from disease was [1]. The experimental data by
Buzzacott P. et al on rats showed that the proportion of 13 week-old rats

engaged in decompression sickness (70%) was higher than the proportion of
11 week-old rats (18%) [19].
+ Mannitol: The consumption of mannitol increases decompression
sickness risk. The study by Maistre S. et al shows that the proportion of
decompression sickness on rats increases from 40% for rats fed with normal
food to 80% for rats fed with mannitol [20].
+

Movement

after

diving:

Movement

after

diving

increased

decompression sickness risk. Madden D. et al assumed that movement after
diving increased the bubble risk of pulse and increases decompression
sickness risk [21].
+ Disease genes: Some genes related to decompression sickness such as
thyroid hormone regulatory genes and production of TNF-α necrotic factors.
Liu X. et al found that spinal cord decompression sickness contained 2/9
expression genes as thyroid hormone regulatory genes and TNF-α necrotic

6
factors; 2/7 expression reducing genes was the acyl-coA gene and membrane
potential protein [22].
+ High-intensity sounds: High-intensity sounds (204dB, 8kHz) causes
decompression sickness risk and a mortality rate higher than moderateintensity sounds or merely repeated sounds [23].
+ Atrial septal defect: Causes the increase of decompression sickness
risk. Furthermore, the size of atrial septal defect at 10mm or more can result
in the increase of decompression sickness severity [24], [25].
+ Obesity: increases decompression sickness risk [1].
+ Dehydration: Increases decompression sickness risk, especially
dehydration over 24 hours [1].
+ Alcohol: Drinking alcohol just before diving increases decompression
sickness risk [1]. However, Buzzacott P. et al found chronic alcoholism might
not cause decompression sickness risk [26].
+ Repetitive diving in many times within 24 hours increases
decompression sickness risk [1].
+ Other factors: coming to the surface in many times, spinal cord
surgery, former patients engaged in decompression sickness increase
decompression sickness risk [1].
- Reductive factors:
+ Thermal contact: Thermal contact within 30 minutes (dry sauna)
before diving may mitigate bubble level and reduce decompression sickness
risk [27].
+ Whole-body vibration: Whole-body vibration at a frequency of 3540Hz within 30 minutes before diving reduces bubble level, the quantity of
cellular debris, decompression sickness risk [28].