Open access

Introductory Chapter: Concomitant Traumatic Brain Injury and Haemorrhagic Shock

Written By

Sri Rama Ananta Nagabhushanam Padala, Vaishali Waindeskar, Ved Prakash Maurya, Rakesh Mishra and Amit Agrawal

Published: 27 April 2023

DOI: 10.5772/intechopen.108275

From the Edited Volume

Management of Shock - Recent Advances

Edited by Amit Agrawal and Vaishali Waindeskar

Chapter metrics overview

93 Chapter Downloads

View Full Metrics

1. Introduction

Younger people in developing countries are more frequently affected by head injuries, which have substantial economic and social effects. In patients with traumatic brain injury (TBI), external or internal haemorrhages have the potential to cause systemic hypotension [1, 2]. They can be associated with poorer outcomes (increased morbidity and mortality) compared to patients with TBI alone [3, 4]. Even brief episodes of hypotension have been shown to cause both systemic and cerebral hypoperfusion and secondary brain injury [5]. This systemic hypertension can be further complicated by raised intracranial pressure (due to TBI-related lesions), which can further compound the treatment protocols [6]. In trauma patients, the occurrence of haemorrhagic shock is associated with high mortality (as high as 50%) [7], and the reported incidence ranges from 6-16% [8]. These cases need to be differentiated from those in the paediatric population, where the isolated TBI can lead to severe shock (in the absence of apparent haemorrhage) [9, 10]. Understanding the interaction of the simultaneous presence of TBI and haemorrhagic shock is essential to implement the optimal resuscitation strategy [11] and, thus, developing strategies to improve outcomes in this subgroup of patients [5]. Investigators have used animal models to define the optimal post-resuscitation mean arterial pressure levels to ensure organ perfusion and, thus, maintain good organ functions and survival patterns [2]. The present article discusses the concepts and controversies associated with concurrent TBI and haemorrhagic shock, the clinical approach, and the management of this subgroup of patients.

Advertisement

2. Clinical examination

The clinical examination of a patient with suspected haemorrhagic shock and TBI is aimed at determining the source of the bleeding from any systemic external or internal injuries and understanding the severity of the head injury. The cursory examination of the neurological status involves the evaluation of the Glasgow Coma Scale (GCS) and pupils, which will help assess the need for further radiological evaluation or urgent surgical intervention. One should be mindful that haemorrhagic shock is one of the confounding factors in the assessment of GCS. The detailed examination of the patient must include an assessment of the airway, breathing, circulation, and disability. While the patient is being stabilized, the neurological examination and examination to rule out other injuries like haemothorax, hemoperitoneum, or long bone fractures will continue, and appropriate measures can be taken to control the ongoing haemorrhage, if any. It is important to remember that the scalp can be a significant source of bleeding in children and should be scrutinized. In a patient with TBI and shock, bilaterally dilated and fixed pupils (in the absence of local injury and any drug overdose) can be an ominous sign that signifies a poorer outcome [12].

Advertisement

3. Diagnosis

Haemorrhagic shock in a patient with traumatic brain injury must be defined using a standard definition in the given setting [13, 14]. The diagnosis of traumatic brain injury and haemorrhagic shock will be evident in most cases. However, a careful clinical evaluation, including a detailed clinical history that can be supplemented with appropriate investigations, is needed to assess the extent of brain injury and haemorrhagic shock [14]. The detailed laboratory investigations shall include complete blood counts (including haemoglobin levels), a coagulation profile, and imaging of the brain or approximate regions to find the cause of haemorrhagic shock.

Advertisement

4. Management

Management of TBI with haemorrhagic shock remains a challenge [13] which is further compounded by the fact that there is wide variability in clinical practices. Various parameters must be kept in mind while managing this patient population, including intracranial pressure monitoring, a coagulation profile, an optimum blood pressure target, and the issue of performing combined surgical procedures for a combination of injuries [13]. In addition to the standard management protocol, the objective of management in these cases is “hemodynamic and haemostatic resuscitation” [13]. An optimal blood pressure management strategy will be necessary as there may be a combination of systemic hypotension and intracranial hypertension. It will be better to maintain the systemic blood pressure on the higher side [15]. The management strategy in these patients is debatable; however, the management should focus on the management of hypotension, cerebral oedema, coagulopathy (if present), judicious use of antiepileptics, and blood replacement [13]. As recommended, tranexamic acid can be given to reduce the mortality rate in these patients [16]. A few words of caution: aggressive fluid resuscitation in these patients must be avoided as it may have deleterious effects and increase short-term mortality [17]. Although head-end elevation is a standard practice in managing patients with TBI and raised intracranial pressure, its role in managing these patients is controversial [18]. Similarly, the role of the Trendelenburg position, which has been suggested to improve transient hypotension in haemorrhagic shock [19], is doubtful [20]. Maintain a neutral head and neck position to prevent jugular compression which would further impede venous return to the heart in the background of haemorrhagic shock.

Advertisement

5. Outcome

The outcome of patients who sustain TBI and concomitant haemorrhagic shock is unfavourable. It has been reported that 33-50% of patients die before they can reach the hospital [21]. These patients’ significant causes of mortality are exsanguination and its sequelae, multi-organ dysfunction and coagulopathy [13]. Brain injury-related insults aggravate cardiovascular dysfunction and result in poorer outcomes [22]. TBI can cause cerebral oedema, requiring a higher systemic blood pressure to maintain cerebral perfusion. On the other hand, systemic hypotension in haemorrhagic shock results in decreased mean arterial pressure and subsequent decreased cerebral perfusion pressure. This interdependent impairment of haemodynamic regulatory mechanisms in a vicious cycle further leads to unfavourable outcomes [22].

Advertisement

6. Conclusions

In summary, patients with concomitant TBI and haemorrhagic shock usually sustain multisystem injuries that need an urgent and comprehensive team approach and may receive excellent pre-hospital care wherever possible. Although in most patients with TBI, shock is caused by haemorrhage, TBI can cause shock, particularly in the paediatric population. In either circumstance, the main objective is early identification of the underlying pathology and comprehensive management of responsible pathologies to improve outcomes. In traumatic intracranial pathologies, there may be a mismatch between systemic blood pressure and intracranial pressure that needs to be closely monitored to maintain optimal cerebral perfusion pressure.

Advertisement

Conflict of interest

The authors have NO conflict of interest to declare.

References

  1. 1. Gennarelli TA et al. Comparison of mortality, morbidity, and severity of 59,713 head injured patients with 114,447 patients with extracranial injuries. The Journal of Trauma. 1994;37(6):962-968
  2. 2. Hu Y et al. Identification of ideal resuscitation pressure with concurrent traumatic brain injury in a rat model of hemorrhagic shock. The Journal of Surgical Research. 2015;195(1):284-293
  3. 3. Matsushita Y et al. Delayed hemorrhagic hypotension exacerbates the hemodynamic and histopathologic consequences of traumatic brain injury in rats. Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism. 2001;21(7):847-856
  4. 4. Wald SL, Shackford SR, Fenwick J. The effect of secondary insults on mortality and long-term disability after severe head injury in a rural region without a trauma system. The Journal of Trauma. 1993;34(3):377-381
  5. 5. Doyle JA, Davis DP, Hoyt DB. The use of hypertonic saline in the treatment of traumatic brain injury. The Journal of Trauma. 2001;50(2):367-383
  6. 6. Hariri RJ et al. Traumatic brain injury, hemorrhagic shock, and fluid resuscitation: Effects on intracranial pressure and brain compliance. Journal of Neurosurgery. 1993;79(3):421-427
  7. 7. Sauaia A et al. Epidemiology of trauma deaths: A reassessment. The Journal of Trauma. 1995;38(2):185-193
  8. 8. Kauvar DS, Lefering R, Wade CE. Impact of hemorrhage on trauma outcome: An overview of epidemiology, clinical presentations, and therapeutic considerations. The Journal of Trauma. 2006;60(6 Suppl):S3-S11
  9. 9. Gardner A et al. Isolated head injury is a cause of shock in pediatric trauma patients. Pediatric Emergency Care. 2013;29(8):879-883
  10. 10. Partrick DA et al. Is hypotension a reliable indicator of blood loss from traumatic injury in children? American Journal of Surgery. 2002;184(6):555-559
  11. 11. Investigators SS et al. Saline or albumin for fluid resuscitation in patients with traumatic brain injury. The New England Journal of Medicine. 2007;357(9):874-884
  12. 12. Youmans JR. Causes of shock with head injury. Journal of Trauma and Acute Care Surgery. 1964;4(2):204-209
  13. 13. Chico-Fernández M et al. Concomitant traumatic brain injury and hemorrhagic shock: Outcomes using the Spanish Trauma ICU Registry (RETRAUCI). The American Surgeon. 2021;87(3):370-375
  14. 14. Galvagno SM et al. Outcomes after concomitant traumatic brain injury and hemorrhagic shock: A secondary analysis from the Pragmatic, Randomized Optimal Platelets and Plasma Ratios trial. The Journal of Trauma and Acute Care Surgery. 2017;83(4):668-674
  15. 15. Spahn DR et al. The European guideline on management of major bleeding and coagulopathy following trauma: Fifth edition. Critical Care (London, England). 2019;23(1):98
  16. 16. Collaborators, C.-T et al. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): A randomised, placebo-controlled trial. Lancet (London, England). 2010;376(9734):23-32
  17. 17. Stern SA et al. Effect of initially limited resuscitation in a combined model of fluid-percussion brain injury and severe uncontrolled hemorrhagic shock. Journal of Neurosurgery. 2000;93(2):305-314
  18. 18. Choi DS et al. Effects of position on intracranial pressure management in porcine traumatic brain injury with hemorrhagic shock. Emergency Medicine, Trauma and Surgical Care. 2021;8(1):1-7
  19. 19. Martin JT. The Trendelenburg position: A review of current slants about head down tilt. AANA Journal. 1995;63(1):29-36
  20. 20. Bridges N, Jarquin-Valdivia AA. Use of the Trendelenburg position as the resuscitation position: To T or not to T? American Journal of Critical Care: An Official Publication, American Association of Critical-Care Nurses. 2005;14(5):364-368
  21. 21. Ling G et al. Explosive blast neurotrauma. Journal of Neurotrauma. 2009;26(6):815-825
  22. 22. Yuan XQ, Wade CE. Traumatic brain injury attenuates the effectiveness of lactated Ringer’s solution resuscitation of hemorrhagic shock in rats. Surgery, Gynecology & Obstetrics. 1992;174(4):305-312

Written By

Sri Rama Ananta Nagabhushanam Padala, Vaishali Waindeskar, Ved Prakash Maurya, Rakesh Mishra and Amit Agrawal

Published: 27 April 2023