Felis ISSN 2398-2950

Head trauma: assessment of patient

Contributor(s): Peter Dickinson, Simon Platt, Laurent Garosi

Introduction

Clinical examination

  • Initial physical assessment of the severely brain-injured patient focuses on imminently life-threatening abnormalities.
  • It is important not to focus initially on the patient's neurological status as many patients will be in a state of hypovolemic shock following a head injury, which can exacerbate a depressed mentation.
  • Hypovolemia will need to be recognized and addressed immediately.
  • As with all types of acute injury, the "ABCs" (airway, breathing, cardiovascular status) aspects of emergency care are extremely important.

Systemic blood pressure

  • Cerebral perfusion pressure (CPP) is the pressure gradient driving cerebral blood flow (CBF), including delivery of oxygen and metabolites. 
  • CPP is defined as the mean arterial pressure (MAP) minus the intracranial pressure (ICP):  CPP = MAP – ICP. 
  • CBF is a function of CPP and cerebral vascular resistance (CVR): CBF = CPP/CVR.  CVR dependent on blood viscosity and vessel diameter.
  • A major mechanism controlling CVR is pressure autoregulation, the intrinsic ability of the vasculature to maintain a constant CBF and ICP over a wide range of pressure (MAP of 50 – 150 mmHg). 
  • With severe head trauma, blood pressure autoregulation can be lost focally or globally as well as partially or completely. A partial loss resets the lower MAP extreme to a higher value (eg from 50 mm Hg to 80 mm Hg). Without pressure autoregulation, CBF becomes directly proportional to systemic blood pressure.
  • ICP is the pressure inside the skull exerted by the intracranial contents.
  • Intracranial hypertension perpetuates secondary injury.
  • An initial hyperdynamic cardiovascular response to severe head trauma, leads to elevations in blood pressure, heart rate, and cardiac output which is sympathetically mediated.
  • In some cases an elevated systemic arterial pressure may benefit ischemic areas, but in others it may cause increased hydrostatic pressures resulting in cerebral edema.
  • Systemic hypertension Hypertension elicits bradycardia; bradycardia together with hypertension (eg Cushing reflex) in a stuporous or comatose animal may indicate rising ICP and the necessity for therapeutic intervention aimed at decreasing the ICP.
  • Protracted hypotension is an ominous predictor of poor outcome and therefore should be promptly addressed and its causes treated. Similar to the hypertensive situation, lowered arterial pressures may aggravate localized ischemia and also promote cerebral edema.
  • The systemic or mean arterial blood pressure (MABP) is a valuable monitoring parameter for the management of head-injured cats because it is closely related to cerebral blood flow and brain perfusion: cerebral perfusion pressure = MABP-ICP.
  • As MABP decreases to < 50 mm Hg, vasodilatation ensues, and cerebral blood flow decreases and becomes dependent on MABP, in head trauma patients.
  • Blood pressure can also be checked regularly and easily with the aid of indirect blood pressure monitors Blood pressure: Doppler ultrasound.
  • Ideally, the above assessment should be made in combination with ICP monitoring (see below) Intracranial pressure measurement.

Patient ventilation

  • Respiratory system dysfunction can be common after head injury.

It is important to differentiate respiratory dysfunction as a result of pulmonary damage from that due to brain injury.

  • Respiratory compromise may result from pneumothorax Pneumothorax, pulmonary contusion Lung: pulmonary hemorrhage, aspiration pneumonia Pneumonia, or an abnormal respiratory drive.
  • It is extremely important to monitor patient respiratory function, ensuring adequacy of the airway, noting the rate and depth of breathing
  • Consider objectively assessing the function with pulse oximetry, capnography and arterial blood gas analysis.
  • The most dramatic respiratory abnormality seen following head injury can be neurogenic pulmonary edema (NPO).
  • Neurogenic pulmonary edema Lung: pulmonary edema is usually self-limiting if the patient survives, and will resolve in a matter of hours to days, but can cause severe dyspnea, tachypnea and hypoxemia.
  • Hypoxemia Hypoxemia is usually associated with hyperventilation and may be due in part to the abnormal breathing patterns seen after head trauma.
  • Hyperventilation may be caused by midbrain injury or compression (as a result for example of transtentorial herniation Brain: tentorial herniation) and as such represents a poor prognosis. It can also be a rsult of central mediation secondary to cerebral acidosis or cerebral hypoxemia.
  • Apneustic, ataxic and Cheyne-Stokes respirations indicate brain-stem disease.
  • Cheynes-Stokes respiration is a period of hyperventilation followed by apnea and is usually secondary to diencephalic injury and reduced responsiveness to partial pressure of arterial carbon dioxide.
  • The head injured patient may have also sustained chest trauma which in itself may cause hypoxia, which reinforces the need for thoracic radiographs Radiography: thorax close to the time of patient admission.
  • The patient should be thoroughly assessed for traumatic injuries Trauma: overview; these include skull, vertebral and long bone fractures as well as splenic torsions and ruptured ureters.

Neurological assessment

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Further Reading

Publications

Refereed papers

  • Recent references from VetMed Resource and PubMed.
  • Kuo K W, Bacek L M, Taylor A R (2018) Head traumaVet Clin North Am Small Anim Pract 48, 111-128 PubMed.
  • Oliveira K M, Fukushima F B, Oliveira C M et al (2013) Head trauma as a possible cause of central diabetes insipidus in a cat. J Feline Med Surg 15, 155-159 PubMed.
  • Grohman K, Schmidt M J, Moritz A et al (2012) Prevalence of seizures in cats after head trauma. JAVMA 241, 1467-1470 PubMed.
  • Sande A, West C (2010) Traumatic brain injury: a review of pathophysiology and management. J Vet Emerg Crit Care (San Antonio) 20, 177-190 PubMed.
  • Platt S R, Radaelli S T & McDonnell J J (2001) The prognostic value of the modified Glasgow coma score in canine head trauma. JVIM 15(6), 581-584.
  • Dewey C W (2000) Emergency management of the head trauma patient. Vet Clin North Am: Sm Anim Pract 30, 207-225.
  • Ghajar J (2000) Traumatic brain injury. Lancet 356, 923-929.

Other sources of information

  • Shores A (1983) Craniocerebral trauma. In: Current Vet Therapy X: Small Anim Pract Philadelphia: W B Saunders. pp 847-854.


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