Respiratory Management for Traumatic Brain Injury

Introduction[edit | edit source]

There is a reciprocal relationship between lung function and brain function: the brain needs sufficient oxygen supply in order to operate, and the respiratory system needs instructions from the brain in order to operate.

In cases of Traumatic Brain Injury, respiratory dysfunction is the most common medical complication which occurs.[1][2] Up to one-third of patients with severe traumatic brain injury develop Acute Respiratory Distress Syndrome [ARDS][3][4]. In this syndrome, there is inflammation of the alveolar-capillary interface, which leads to fluid and proteins entering the interstitial space and alveoli. Between 20 and 30% of individuals who develop ARDS die as a result of the pulmonary infiltrate leading to respiratory failure[5].

Respiration Control within the Central Nervous System[edit | edit source]

Respiration is controlled by respiratory centres: the inspiratory and expiratory centres are located in the medulla oblongata; the pneumatic and apneustic centres are located in the pons. Together they are known as the Respiratory Control Centres [RCCs].

Neurones in the medulla trigger inspiration (sending signals to the phrenic and intercostal nerves). Frequency of respiration is controlled by the pneumatic centre, and the intensity of breathing is controlled by the apneustic centre.

Pathophysiology[edit | edit source]

There are several possible mechanisms which are thought to contribute to the respiratory complications seen in cases of brain injury:

Sympathetic Storm[edit | edit source]

There is an immediate [within seconds] sympathetic discharge when an injury occurs which raises plasma adrenaline levels to approximately 1,200 times the normal value. The adrenaline levels do then fall, but they remain at 3 times higher than normal for approximately ten days.[6][7] This results in elevated intravascular pressure, which damages the endothelium and produces pulmonary oedema (due to disruption on the alveolar-capillary barrier). Pulmonary oedema becomes protein-rich and goes into interstitial and alveolar spaces.[6][7]

Inflammatory Theory[edit | edit source]

As a direct result of the brain damage, a systemic inflammatory reaction occurs, which in turn brings about an alteration in blood-brain barrier permeability and infiltration of neutrophils and activation of macrophages in the alveolar spaces causing secondary damage to the lung tissue.[8][9]

Respiratory Assessment of Traumatic Brain Injury Patient[edit | edit source]

Medical Information[edit | edit source]

The respiratory physiotherapist should pay close attention to the following information when assessing a patient with traumatic brain injury in the acute situation:

Past Respiratory History[edit | edit source]

This will frequently be provided by family members in cases of acute and severe traumatic brain injury. The therapist should inquire about any previous respiratory conditions, as well as smoking history.

General Observation[edit | edit source]

The therapist will watch the patient and note the general respiratory pattern and posture; whether there is any cyanosis or accessory muscle use, as well as noting speech patterns if appropriate.

A respiratory pattern assessment includes;

  • breathing rate,
  • depth of breaths,
  • the symmetry of air intake/lung expansion,
  • the regularity of breaths.

Other Assessment Techniques may include:

  • Percussion - Percussion is used to detect chest resonance. Percussion applied to the patient's chest produces audible sounds which can be interpreted by a skilled examiner to discern fluid, air or solid material within the chest cavity.[10] Please see the Respiratory Assessment - Percussion page for further information, including a description of technique.
  • Auscultation - Auscultation involves using a stethoscope to listen to lung sounds. Abnormal lung sounds include wheezes, crackles, rhonchi and pleural rub. More information can be found on the Auscultation page.

Respiratory Management[edit | edit source]

In the acute stages of traumatic brain injury, the aims of management in the Intensive Care Unit are to maintain oxygen delivery in order to limit secondary neurological damage. Mechanical ventilation is commonly used with 3 aims:

  1. To prevent/minimise hypoxia
  2. To prevent/minimise hypercapnia
  3. To protect the airway from the risk of aspiration. It is acknowledged that difficulties are frequently encountered when weaning these patients from mechanical ventilation.[11]

A number of recent studies have investigated the use of protective ventilation in the early stages following traumatic brain injury.[12][13]

During mechanical ventilation, the aim of physiotherapy is to optimise respiratory function while maintaining the neuromusculoskeletal system.

Physiotherapy interventions include:[14]

References[edit | edit source]

  1. Solenski NJ, Haley EC, Kassell NF, Kongable G, Germanson T, Truskowski L, et al. Medical complications of aneurysmal subarachnoid hemorrhage: a report of the multicenter, cooperative aneurysm study. Participants of the Multicenter Cooperative Aneurysm Study. Crit Care Med. 1995;23:1007–1017.
  2. Plötz FB, Slutsky AS, van Vught AJ, Heijnen CJ. Ventilator-induced lung injury and multiple system organ failure: a critical review of facts and hypotheses. Intensive Care Med. 2004;30:1865–1872.
  3. Holland MC, Mackersie RC, Morabito D, Campbell AR, Kivett VA, Patel R, et al. The development of acute lung injury is associated with worse neurologic outcome in patients with severe traumatic brain injury. J Trauma. 2003;55:106–111. 
  4. Kahn JM, Caldwell EC, Deem S, Newell DW, Heckbert SR, Rubenfeld GD. Acute lung injury in patients with subarachnoid hemorrhage: incidence, risk factors, and outcome. Crit Care Med. 2006;34:196–202.
  5. Hough A. Physiotherapy in respiratory and cardiac care: an evidence-based approach. 4th edition. Andover: Cengage Learning, 2014.
  6. 6.0 6.1 Schirme-Mikalsen K, Vik A, Gisvold SE, Skandsen T, Hynne H, Klepstad P. Severe head injury: control of physiological variables, organ failure and complications in the intensive care unit. Acta Anaesthesiol Scand. 2007; 51: 1194-1201.
  7. 7.0 7.1 Mascia L. Acute lung injury in patients with severe brain injury: A double hit model. Neurocrit Care. 2009; 11: 417-426.
  8. Kelley BJ, Lifshitz J, Povlishock JT. Neuroinflamatory responses after experimental diffuse traumatic brain injury. J Neuropathol Exp Neurol. 2007; 66(11): 989-1001.
  9. Fremont R, Koyama T, Calfee C, Wu W, Dossett LA, Bossert FR, et al. Acute lung injury in patient s with traumatic injuries: Utility of a panel of biomarkers for diagnosis and pathogenesis. J. Trauma. 2010; 68(5): 1121-1127.
  10. Hough A. Physiotherapy in Respiratory Care. 2nd edition. London: Chapman and Hall, 1996.
  11. Coplin WM, Pierson DJ, Cooley KD, Newell DW, Rubenfeld GD. Implications of extubation delay in brain-injured patients meeting standard weaning criteria. Am J Respir Crit Care Med. 2000;161:1530–1536.
  12. Asehnoune K, Seguin P, Lasocki S, Roquilly A, Delater A, Gros A, et al. Extubation success prediction in a multicentric cohort of patients with severe brain injury. Anesthesiology. 2017;127:338–46.
  13. Godet T, Chabanne R, Marin J, Kauffmann S, Futier E, Pereira B, et al. Extubation failure in brain-injured patients: risk factors and development of a prediction score in a preliminary prospective cohort study. Anesthesiology. 2017;126:104–114.
  14. Denehy L, Berney S. Physiotherapy in the intensive care unit. Physical Therapy Reviews. 2006;11(1):49-56