Evaluation of the effectiveness of brain protection in comatose patients after circulatory arrest by command hypothermia - 2

3.3.5. Coagulation disorders 87

3.3.6. Other complications during treatment 88

CHAPTER 4. DISCUSSION 89

4.1. GENERAL CHARACTERISTICS 89

4.1.1. General characteristics of the two groups of patients studied 89

Maybe you are interested!

• Evaluation of the effectiveness of brain protection in comatose patients after circulatory arrest by command hypothermia - 25
• Evaluation of the effectiveness of selective tibial nerve resection in the treatment of lower limb muscle spasticity sequelae - 19
• The current status of diabetes and prediabetes among Khmer people in Hau Giang province and evaluation of the effectiveness of some intervention measures - 22
• Evaluation of the Effectiveness of the Program for Stabilizing Agricultural and Forestry Production Associated with Product Processing
• Study on muscle loss in patients with type 2 diabetes and initial evaluation of the effectiveness of exercise intervention - 7

4.1.2. Characteristics of hypothermic patients 99

4.2. EVALUATION OF THE RESULTS OF TARGETED HYPOTHERMIA TREATMENT OF 33°C FOR COMA PATIENTS AFTER CIRCULATORY ARREST 109

4.2.1. Survival rate 109

4.2.2. Results of neurological rehabilitation when treating hypothermia with a target of 33°C 112

4.2.3. Some factors affecting 30-day mortality in the hypothermia treatment group 115

4.2.4. Other treatment outcomes in the hypothermia treatment group 121

4.3. COMPLICATIONS DURING HYPOTHERMIA TREATMENT 122 4.3.1. Shivering 122

4.3.2. Arrhythmia 123

4.3.3. Disorders of blood potassium concentration 124

4.3.4. Hyperglycemia 125

4.3.5. Coagulation disorders 126

4.3.6. Other complications during treatment 127

CONCLUSION 133

PROPOSAL 135

LIMITATIONS OF TOPIC 136

LIST OF WORKS RELATED TO THE THESIS REFERENCES

APPENDIX

LIST OF TABLES

Table 1.1. Shivering in bed scale 20

Table 1.2. Clinical outcomes of mild hypothermia after cardiopulmonary resuscitation in dogs 25

Table 1.3. Hypothermia test results of Williams GR Jr 26

Table 1.4. Studies on hypothermia in comatose patients after CPR 29

Table 1.5. Characteristics of ThermoGuard 37 cooling catheters

Table 2.1. CPC 49 brain performance score assessment

Table 2.2. Stages of acute kidney injury 52

Table 2.3. Research variables 54

Table 3.1. Age and gender characteristics of study patients 59

Table 3.2. Characteristics of patient history 60

Table 3.3. Place of circulatory arrest 61

Table 3.4. Characteristics of circulatory arrest 61

Table 3.5. Causes of circulatory arrest 62

Table 3.6. Some clinical characteristics at admission 63

Table 3.7. Paraclinical indicators at admission 64

Table 3.8. Time to cardiac arrest in intervention group 65

Table 3.9. Time to perform hypothermia 66

Table 3.10. Temperature reduction rate of different types of hypothermia catheters 67

Table 3.11. Effect of hypothermia catheter type on 30-day mortality 67 Table 3.12. Blood magnesium concentration (mmol/L) 72

Table 3.13. Liver enzyme changes during hypothermia stages 72

Table 3.14. Development of renal function during stages of hypothermia 73

Table 3.15. Glasgow score at admission 76

Table 3.16. Glasgow score on the 3rd day of treatment 77

Table 3.17. Glasgow score before and after treatment with target hypothermia of 33°C 77

Table 3.18. EEG characteristics associated with patient outcomes 79

Table 3.19. Magnetic resonance imaging associated with patient outcomes 80

Table 3.20. Univariate analysis of factors affecting 30-day mortality. 80 Table 3.21. Multivariate analysis of factors affecting 30-day mortality. 81

Table 3.22. Interventional procedures in patients with NTH due to cardiovascular causes.. 82 Table 3.23. Some other treatment results 82

Table 3.24. Dosage of sedatives, analgesics, muscle relaxants 83

Table 3.25. Cardiac arrhythmias 83

Table 3.26. Blood potassium concentration on admission 84

Table 3.27. Changes in blood potassium at the stages of target hypothermia 33ºC 84

Table 3.28. Blood sugar at the time of admission 85

Table 3.29. Changes in blood sugar during the stages of hypothermia with a target of 33ºC. 86 Table 3.30. Use of insulin in blood sugar control 86

Table 3.31. Changes in coagulation in study 87

Table 3.32. Other complications during treatment 88

Table 3.33. Impact of ventilator-associated pneumonia 88

Figure 3.1. Heart rate evolution during hypothermia treatment 68

Figure 3.2. Evolution of mean arterial blood pressure during hypothermia treatment 69

Figure 3.3. Lactate evolution during the stages of hypothermia target 33ºC. 70 Figure 3.4. Acid-base evolution during the stages of hypothermia target 33ºC.. 71 Figure 3.5. Survival rate at the time of discharge in the two groups of patients 74

Figure 3.6. Survival rate at 30 days 75

Figure 3.7. Survival rate at 6 months 75

Figure 3.8. 1-year survival time 76

Figure 3.9. Neurological recovery results at 30 days 78

Figure 3.10. Neurological recovery results at 6 months 78

Figure 1.1. Schematic illustration of the microvascular and cellular pathological consequences occurring in primary brain injury after NTH 6

Figure 1.2. Magnetic resonance imaging of hypoxic brain damage in the hippocampus and bilateral gray matter 7

Figure 1.3. Reperfusion injury produces free oxygen radicals 8

Figure 1.4. Brain protection mechanism during hypothermia command 16

Figure 1.5. Chill threshold by age 20

Figure 1.6. Survival curve in HACA study 28

Figure 1.7. Arctic Sun cooling system with 34 patches

Figure 1.8. Blanketrol 34 system

Figure 1.9. InnerCool STx 34 cooling blanket system

Figure 1.10. InnerCool RTx 35 cooling catheter

Figure 1.11. ZOLL 35 ThermoGuard Cooling Catheter

Figure 1.12. Structure of Thermogard XP 36 hypothermia machine

Figure 1.13. Control screen of the Thermogard XP hypothermia machine. 36

Figure 1.14. Structure of ZOLL 37 hypothermia catheter

Figure 1.15. Description of how to connect the Thermoguard XP 38 system

Figure 1.16. How to cool (or warm) the blood flow in the body through a catheter. 38 Figure 2.1. Stages in the treatment of hypothermia with a target of 33°C 44

Figure 2.2. Treatment process for patients with hypothermia targeting 33°C ... 47 Figure 2.3. Study diagram 56

PROBLEM STATEMENT

Cardiac arrest (CAD) is a sudden loss of effective cardiac contractility, commonly occurring both in and out of hospital, with a high mortality rate. According to the 2016 American Heart Association report [1], there are approximately 350,000 out-of-hospital CAD patients each year, and approximately 200,000 in-hospital CAD patients, and this number is likely to increase [1]. Despite advances in cardiopulmonary resuscitation, the outcome of CAD patients remains poor, with approximately 10% of patients surviving to the time of admission and approximately 5% with good neurological recovery [1],[2]. In the PAROS study in Vietnam, the rate of patients surviving to hospital discharge was 14.1% [3].

Patients who have successfully undergone cardiopulmonary resuscitation (CPR) and have restored spontaneous circulation (ROSC) mostly suffer brain damage due to ischemia - lack of oxygen during cardiac arrest and damage during reperfusion [4], causing brain cell death. Brain damage is the main cause of death and leaves high sequelae for patients later [5]. Patients who survive and are discharged from the hospital have a high rate of coma or vegetative state, which is a burden for families and society [4], [5]. Treatment methods for patients after CPR aim to minimize these injuries.

To date, many drug and treatment trials have been conducted, but no studies have shown any improvement in neurological function or patient outcomes [6],[7],[8],[9],[10]. Meanwhile, hypothermia by various mechanisms has been shown to protect the brain from post-traumatic stress disorder (PTSD). Many studies on mild hypothermia (reducing core body temperature to 32°C - 34°C) conducted on comatose patients after PTSD have shown many positive signs, improving neurological outcomes and increasing survival rates, especially the HACA study in Europe [11] and Bernard's study in Australia [12]. These are two randomized controlled trials with a

breakthrough, bringing the patient's body temperature down to the target of 32 - 34°C within 12 - 24 hours. Research results show that comatose patients after NTH who were cooled to the target of 32 - 34°C had a much higher rate of neurological recovery and survival than the control group.

Several subsequent clinical trials comparing target hypothermia of 33°C versus target hypothermia of 36°C showed similar efficacy in terms of mortality and neurological outcomes at these 2 target temperatures [13].

In the 2015 guidelines, the American Heart Association recommended target hypothermia of 32°C - 36°C for comatose patients after VT at level IB for out-of-hospital VT due to ventricular fibrillation, and level IC for other arrhythmias and in-hospital VT [14]. In 2020, the American Heart Association further upgraded the recommendation to level IB for all VT patients regardless of rhythm [15].

Currently, many countries in the world consider hypothermia treatment for comatose patients after CPR as a standard, routine treatment method. In Vietnam, there is currently no medical facility researching this issue, so we conducted a study on " Evaluation of brain protection effectiveness in comatose patients after CPR using the command hypothermia method ". We chose the target temperature of 33°C in the study based on the physiological basis of better brain protection when the temperature is lowered [16], insignificant complications [16], as well as evidence from the results of the HACA study and Bernard's [11], [12]. The study has two objectives:

1. Evaluation of treatment outcomes and brain protection efficacy of directed hypothermia with a target of 33°C in the treatment of comatose patients after cardiac arrest.

2. Comment on complications of directed hypothermia with a target of 33°C.

CHAPTER 1. OVERVIEW OF DOCUMENTS

1.1. Circulatory arrest

1.1.1. Concept of circulatory arrest

Cardiac arrest, also known as circulatory arrest, is a sudden loss of effective myocardial contractility [17]. The two main causes are cardiac (about 65%) and non-cardiac causes (about 35%) [17]. Over time, NTH progresses through three stages [18] (although the time boundaries between the stages are only relative):

The electrical phase: is calculated from the time of NTH to about 4 minutes after NTH [18]. This is a very effective defibrillation phase, increasing the survival rate to nearly 50% [18 ].

The circulatory phase: the time is calculated from about 4 minutes to 10 minutes after NTH, while the patient is still in a state of ventricular fibrillation [18]. The most important lifesaving therapy during this phase is oxygenation techniques (external chest compressions/breathing) combined with epinephrine performed first, followed by defibrillation (delayed defibrillation for 1-3 minutes) [18],[ 19].

The metabolic phase: is calculated from 10 minutes after NTH onwards [18]. During this phase, the effectiveness of both immediate defibrillation and cardiopulmonary resuscitation followed by defibrillation decreases rapidly and the survival rate is very low [18 ].

Important milestones in cardiopulmonary resuscitation.

- No-flow time : is the time from NTH to cardiopulmonary resuscitation (external chest compression). The longer this time, the more severe the prognosis for brain damage.