A talk by Flora Bird from TBS24

1. TBI and CV dysfunction
Dr Flora Bird
LAA

3. Traumatic brain injury – Why?

4. Background – Why care?
• Traumatic brain injury (TBI)
- Worldwide global health problem; International call for further research (Rosenfeld 2012)
- Most common cause of death or disability in < 40 years-old in the UK (NICE 2014)
- Europe – 37% (95% CI 36-38) of all injury-related deaths (Majden 2016)
- USA – 50% trauma deaths assoc with Head AIS ≥ 4 (Bardes 2018)
- 2:1 (M:F) (Majden 2016)
• LAA data (2019-2020):
>5 per week severe TBI (GCS ≤ 8) (clinical interpretation)
>1 per week severe isolated TBI conveyed to MTC
• Lack of improvement in outcome in last 30 years (Patel, 2005; Stein, 2010; Cole, 2019)

5. Golden Hour
Golden seconds to minutes
‘Hyperacute phase’

7. • Early pathophysiology
• Cardiovascular sequalae
• CV dysfunction/ shock
• Clinical challenges

8. Pathophysiology of severe TBI
• Multi system effects – not limited to the brain alone
• Sequalae associated with axonal stretch
• Apnoea and dysventilation
• Systemic inflammatory response (pro-inflammatory, coagulopathy)
• Cardiovascular

9. ‘Shock does not result from isolated brain injuries’
ATLS

10. CASE
81 F, Pedestrian vs. motorbike
Immediately unconscious, breathing with dysventilation
GCS 4, Unequal pupils
IMP:
1. Significant TBI - suspected SAH, SDH, IPH.
2. Left rib fractures
3. Right scapula fracture ? Rib fractures.
4. At risk of intra abdominal injury and pelvic fracture.
5. Open left tib fib.

13. Treatment?

14. Treatment?
• Blood transfusion
• RSI
• Thoracostomies
• HTS
• Arterial line
• POCUS
• Escort to MTC – Code Red/ Code Black

15. Outcome
• Bilateral rib fractures and surgical emphysema. No flail. left and right tibial
fractures. Unstable pelvic fracture with haematomas. Grade 2 splenic lac.
• Subarachnoid blood and cerebral contusions. Right skull fracture and facial
fractures. C6/7 ?ligament injury.
• Admitted to ICU with bolt.
• 3 RBC and 2FFP given in resus.

16. Outcome
• Bilateral rib fractures and surgical emphysema. No flail. left and right tibial
fractures. Unstable pelvic fracture with haematomas. Grade 2 splenic lac.
• Subarachnoid blood and cerebral contusions. Right skull fracture and facial
fractures. C6/7 ?ligament injury.
• Admitted to ICU with bolt.
• 3 RBC and 2FFP given in resus.
• Sadly RIP

18. Data
• Observational cohort database study of severe iTBI patients (Head AIS 3+) at a Level 1 trauma
centre (2008-2019) and from a physician-led air ambulance service (2019-20)
• CV Dysfunction = HR >100 with SBP <100mmHg
• Aims: (1) determine the prevalence and phenotype of CVD after iTBI in the hyper-acute phase
(2) compare treatment and clinical outcomes in those with CVD vs non-CVD.

19. Results
• N 168
• Median 46 years (IQR 30-61)
• 77% were male
• Median ISS was 25 (IQR 17-29) (51% having Head AIS 5)
• Incident to HEMS on scene: 31 min (IQR 20-42); 1 in 4 <20 min
• 20% had physiological shock on initial assessment
• 24% of LAA cohort had CVD prior to PHEA

20. Table 1
Variable Non-CVD (n 135) CVD (n 33)
Age 46 (30 - 60) 40 (30 - 63)
Sex n (%) MALE 106 (79%) 24 (73%)
ISS 25 (17 - 29) 25 (12 - 30)
Head AIS 5 (4 - 5) 5 (3-5)
Time: Injury to pre-hospital
assessment (min)
31 (20-41) 31 (21 - 44)
Time: Injury to hospital (min) 83 (69 - 99) 88 (76 - 100)
GCS on scene 5 (3 - 7) 3 (3 - 5) **
First observation on scene:
HR
SBP
82 (68-97)
142 (137-147)
103 (50-120)
73 (0-110) **
ED arrival observations:
HR
BP
Lactate
86 (72-99)
139 (117-159)
2.4 (1.4 - 3.3)
104 (94-113) **
107 (94-119) **
6.1 (1.7 - 10.9) **
Clotting on arrival to hospital n (%)
INR >1.2 OR PT >17.4 19 (15%) 13 (43%) **

21. Table 1
Variable Non-CVD (n 135) CVD (n 33)
Age 46 (30 - 60) 40 (30 - 63)
Sex n (%) MALE 106 (79%) 24 (73%)
ISS 25 (17 - 29) 25 (12 - 30)
Head AIS 5 (4 - 5) 5 (3-5)
Time: Injury to pre-hospital
assessment (min)
31 (20-41) 31 (21 - 44)
Time: Injury to hospital (min) 83 (69 - 99) 88 (76 - 100)
GCS on scene 5 (3 - 7) 3 (3 - 5) **
First observation on scene:
HR
SBP
82 (68-97)
142 (137-147)
103 (50-120)
73 (0-110) **
ED arrival observations:
HR
BP
Lactate
86 (72-99)
139 (117-159)
2.4 (1.4 - 3.3)
104 (94-113) **
107 (94-119) **
6.1 (1.7 - 10.9) **
Clotting on arrival to hospital n (%)
INR >1.2 OR PT >17.4 19 (15%) 13 (43%) **

22. Table 2
Variable Non-CVD (n 135) CVD (n 33)
Prehospital treatment
Drug assisted intubation (%)
Hypertonic saline (NaCl 5%) n (%)
Blood products (PRBC)
Blood products (FFP)
47 (94%)
40 (30%)
0 (0)
0 (0)
17 (90%)
13 (39%)
0 (0 - 2) **
0 (0 - 1) **
24 hour blood transfusion (units) 0 (0) 3 (0 - 8) **
Neurosurgical Intervention 48 (43%) 13 (43%)
ICU LOS (days) 11 (3 - 19) 12 (2 - 25)
Vasopressor days 2 (0 - 5) 2 (0 - 4)
Total LOS (days) 28 (13 - 47) 32 (10 - 61)
Time to death (days) 2.5 (2 - 6) 2.5 (1 - 6)
28-day mortality 42 (31%) 20 (61%) **

23. Table 2
Variable Non-CVD (n 135) CVD (n 33)
Prehospital treatment
Drug assisted intubation (%)
Hypertonic saline (NaCl 5%) n (%)
Blood products (PRBC)
Blood products (FFP)
47 (94%)
40 (30%)
0 (0)
0 (0)
17 (90%)
13 (39%)
0 (0 - 2) **
0 (0 - 1) **
24 hour blood transfusion (units) 0 (0) 3 (0 - 8) **
Neurosurgical Intervention 48 (43%) 13 (43%)
ICU LOS (days) 11 (3 - 19) 12 (2 - 25)
Vasopressor days 2 (0 - 5) 2 (0 - 4)
Total LOS (days) 28 (13 - 47) 32 (10 - 61)
Time to death (days) 2.5 (2 - 6) 2.5 (1 - 6)
28-day mortality 42 (31%) 20 (61%) **

24. 0
10
20
30
40
50
60
AIS 3 AIS 4 AIS 5 AIS 6
Incidence
(%)
AIS non-CVD CVD
*
**
0
10
20
30
40
50
60
70
80
90
EDH SDH SAH/IP/IV DAI HIE
Incidence
(%)
TBI pathology non-CVD CVD
**
0
5
10
15
20
25
30
35
40
45
50
Fall >2m Fall <2m RTC Assault Other
Incidence
(%)
Mechanism of Injury non-CVD CVD
0
5
10
15
20
25
30
1
0
-
1
9
2
0
-
2
9
3
0
-
3
9
4
0
-
4
9
5
0
-
5
9
6
0
-
6
9
7
0
-
7
9
8
0
-
8
9
9
0
-
9
9
Proportion
(%)
Age (years) non-CVD CVD

25. 0
5
10
15
20
25
30
AIS 3 AIS 4 AIS 5 AIS 6
Mortality
(%)
AIS non-CVD CVD
**
*
0
10
20
30
40
50
60
70
Died Nursinghome/Hospital Home
Proportion
(%)
Destination non-CVD CVD
**

26. Pathophysiology
Cardiovascular – systemic CAs
• Animal models
- 1894 - stress response to TBI (Polis, 1894)
- 1980s - CA surge (Rosner, 1984)
• Humans
- Plasma CAs correlate with ISS, GCS (Woolf, 92)
- Elevated plasma CAs assoc with
functional outcome & mortality (Rizoli, 2017)
Rosner et al. J. Neurosurgery. 1984, 61 (1)

27. Pathophysiology
Cardiovascular – local CAs
Local myocardial effects:
• CA release from efferent cardiac sympathetic neurons
• Opens b1-A Ca channels, Ca influx, myofibril contraction,
ATP depletion, mitochondrial damage, myocyte death
• Contraction band necrosis on autopsy (normal coronary
arteries)
• ‘Neurogenic stunned myocardium’
(Karch et al. 1986)
(Mann et al. 1991)

28. A hypothesis for CV dysfunction in iTBI:
Apnoea ➜ hypoxia, hypercarbia, acidosis
+
Systemic CA surge ➜ increased SVR, afterload, myocardial demand
+
Local CA effects ➜ myocyte hypercontraction & death
+
Systemic inflammatory mediated response
• See ‘shocked state’, fluctuating BPs, changes on ECHO
• Results inadequate cerebral perfusion and oxygen delivery

29. • How to recognise?
• How to best treat?
• How to best optimise CO
and cerebral perfusion/
cerebral oxygenation?
The challenge

30. Responding to the challenge
• Importance of impact in the hyperacute phase
• Role of dispatch
• “Exquisite attention to detail from the earliest point of contact”
• Use of POCUS

31. Conclusion
• TBI a major concern and proportion of pre-hospital trauma work; Lack of
improvement in outcome over last 30 yrs
• Likely no quick fix; Improvement may come from precise pre-hospital
management in the hyperacute phase; Importance of dispatch and bystanders
• CV dysfunction in severe TBI present in 24% patients pre-PHEA
• Requires better understanding of early pathophysiology

32. Thank you