Prehospital Management of Head Injury

Traumatic brain injury (TBI) is defined as the results of an external application of force to the skull and/or brain with primary and secondary damage. Approx. 200-300 cases of traumatic brain injury of varying degrees of severity are seen per 100,000 persons in Germany annually. In 1994, approx. 10,000 patients died because of severe traumatic brain injury. During childhood, approx. 25% of all traumatic deaths derive from traumatic brain injury. In polytraumatized patients, the prognosis is decisively influenced by an accompanying traumatic brain injury (approx. 40% lethality).

Whereas the primary damage leading to a prognosis of TBI (soft-tissue and bone injury, injury to blood vessels and dura mater, damage to cerebral substance) can only be influenced by preventive measures, subsequent secondary damage and complications of prolonged coma caused, among other things, by such primary damage can be influenced by prehospital emergency measures.

Arterial hypotension (approx. > 20 % of patients) and arterial hypoxia (approx. > 20 % of all patients), frequently accompanied by hypercapnia, result in subsequent secondary cerebral damage in most traumatic brain injury patients due to reduced tissue oxygenation, whereby it is the combination of these conditions that determines the deleterious course. That is why respiratory and circulatory resuscitation and stabilization must be the top-priority objectives of emergency prehospital medical care of the traumatic brain injury patient, continuing throughout ensuing transport.

Cerebral blood flow (CBF) is subject to physiological autoregulation with a range of approx. 50 - 150 mmHg mean arterial pressure (MAP) and is approx. 50 ml / 100 g cerebral tissue / min. Following a traumatic brain injury, this autoregulation mechanism is presumably disturbed such that CBF is determined directly by cerebral perfusion pressure (CPP) (as is otherwise the case outside the limits of physiological autoregulation). The CPP is determined by MAP and intracranial pressure (ICP) according to the formula CPP = MAP - ICP (mmHg). To ensure a sufficient CPP, the MAP should be at least > 60 mmHg at physiological ICP (approx. 5 - 15 mmHg). With increasing ICP, the MAP must also be raised. Since ICP (dependent on cerebral parenchyma, blood volume and liquor) increases rapidly in traumatic brain injury due to intracranial bleeding, oedema, vasoparalysis, contusion foci and hindrances to liquor drainage with limited compensation capacity, CPP and CBF both drop assuming a constant MAP. Unfortunately, especially in cases of raised ICP due to an arterial hypercapnia, the ICP is raised further, often resulting in a lethal vicious circle. These interrelations outline the importance of the circulatory and respiratory situation governing the MAP for avoidance of secondary damage in TBI.

In accordance with the rule "first A - B - C, then ICP", the primary examination in prehospital diagnostics (Fig. 1) should focus on the vital functions airway, breathing and cardiovascular function, followed by state of consciousness, eye opening / pupils, motor response, external injuries and potential accompanying conditions or injuries.

In addition to the clinical evaluation based on examination and auscultation, respiration should also be checked by means of pulsoxymetry (SaO₂) and end expiratory CO₂ measurement (EtCO₂) and the circulation by means of non-invasive arterial pressure measurement (NIP), preferably automatic NIP.

Textfeld: Fig. 2
Glasgow Coma Scale for Head Injury
Glasgow Coma Scale, Eye opening
Spontaneous 4
To loud voice 3
To pain 2
None 1

Verbal response
Oriented 5
Confused, disoriented 4
Inappropriate words 3
Incomprehensible sounds 2
None 1

Best motor response
Obeys 6
Localizes 5
Withdraws (flexion) 4
Abnormal flexion posturing 3
Extension posturing 2
None 1

The Glasgow Coma Scale (GCS, Fig. 2) is used to check state of consciousness, eye opening and motor response in traumatic brain injury patients simply, objectively and reproducibly for documentation in the medical emergency report.

Concerning additional injuries in traumatic brain injury, particular attention should be paid to potential concurrent injury of the cervical (thoracic, lumbar) spine (in approx. 10% of all traumatic brain injury patients) until a definitive radiological exclusion is achieved. Whereas in adults an intracranial or subgaleal haemorrhage (haematoma) is never the sole cause of a haemorrhagic shock, these injuries may have cardiovascular effects in neonates, infants and small children.

All unconscious patients with a GCS < 8 (Fig. 3) are orotracheally intubated (Fig. 4) and ventilated (Fig. 5) as soon as possible without additional risk to the patient. Since the respiratory situation in patients with a GCS > 8 may deteriorate rapidly, e.g. due to additional injuries (injuries to middle part of face or cervical spine), the indication for orotracheal intubation in these patients should be interpreted liberally. Potential cervical spine damage must be taken into account during emergency intubation of patients with a potential full stomach. The cervical spine must therefore be manually stabilized during the intubation process by an assistant to prevent lateral torsion or anteflexion.

Textfeld: Fig. 6

Volume substitution in TBI

· Isotonic crystalloids: e.g. Ringer solution, NaCl, Sterofundin
· Colloidal solutions: e.g. HAES 6%, gelatine prep.
· "Low volume resuscitation": hypertonic NaCl + HAES/dextrane ??
· No glucose 5% => cave: cerebral oedema!

Subsequent ventilation should be done with a mechanical ventilator, since manual ventilation with a manuell system often leads to an unnoticed hypoventilation. The effectiveness of respiratory resuscitation efforts is monitored in terms of oxygenation on the basis of SaO₂ (> 95%) and in terms of ventilation on the basis of EtCO₂ (35 mmHg). To avoid an additional cerebral ischaemia, a pronounced hyperventilation (EtCO₂ < 35 mmHg) should be avoided in the pre-hospital phase.

Textfeld: Fig. 5

Artificial ventilation in traumatic brain injury

· FiO2 1,0 (if SaO2>95 % => FiO2 0.5)
· RMV 100 ml / kg b.w.
· VR 10 - 12 /min
· I:E = 1:1.5 - 2
· PEEP < 10 cmH2O allowed
· Normoventilation EtCO2 35 mmHg

All primarily non-intubation patients should receive O₂ through a mask (> 6 l/min); oxygenation should be monitored closely in terms of SaO₂. In all patients with traumatic brain injury one or more peripheral venous, large-lumen catheters should be inserted and securely fixed to facilitate sufficient volume therapy (there being in most cases no indication for preclinical central venous access). The therapeutic goal of subsequent volume therapy with crystalloid / colloidal solutions (never use hypotonic crystalloid solutions, Fig. 6) should be an MAP of > 90 mmHg to facilitate a sufficient CPP with raised ICP. Potential hypertonic cardiovascular reactions should be treated primarily with a mild analgosedation. Warning: pronounced hypotension may result from administration of antihypertensives!

In accordance with the recommendations of the German Neurosurgical Association and, the German Association for Anaesthesiology and Intensive Care Medicine and the DIVI (Deutsche interdisziplinäre Vereinigung für Intensiv- und Notfallmedzin), the efficacy of "neuroprotective drugs" such as corticosteroids, calcium antagonists, barbiturates or THAM has not been confirmed, so that routine preclinical administration of these substances would not seem advisable. If state of consciousness is compromised with concurrent anisocoria as an indication of raised ICP, a brief infusion of mannitol (0.3-1.5 g / kg / 15 min.) should be considered.

Following positioning accordingly (30° elevation of upper body, neutral position) and immobilization of cervical spine with suitable collar / splint, transport patient while monitoring the haemodynamic and respiratory situation (at least cardiac frequency, NIP, SaO₂, EtCO₂, respirator parameters). Patients with GCS < 12 must be transported accompanied by a physician in an ambulance car or rescue helicopter to a suitable facility for treatment. Patients with a GCS > 13 can be transported in an ambulance car accompanied by ambulance personnel. Suitable treatment centres for patients with GCS < 12 should be equipped to make native and CT radiographs of the skull and spine at all time (24 h) and have such images evaluated by radiology specialists. Neurosurgical consultation should also be available.

24-hour neurosurgical standby is required for traumatic brain injury patients with a GCS < 8. All traumatic brain injury patients should be monitored closely in a suitable ICU for haemodynamic, respiratory and neurological vital functions with recording of time curves for these parameters.

Fig. 7 provides a summary of the main steps in "preclinical management in traumatic brain injury". For further recommendations on primary treatment of patients with traumatic brain injury are found in: "Empfehlungen der Deutschen Gesellschaft für Neurochirurgie and der Deutschen Gesellschaft für Anästhesiologie and Intensivmedizin sowie der DIVI" (Der Notarzt 13 (1997): 45-48).