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Head trauma: assessment of patient

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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

Neurological examination

  • Repeated neurological examination Neurological examination is important to detect changes in condition.
  • May be difficult to examine if the cat is in shock or pain post-trauma.

Modified Glasgow coma score (MGCS)

  • This scoring system enables grading of the initial neurological status and serial monitoring of the patient Small animal coma score.
  • Such a system can facilitate assessment of prognosis, which is crucial information for both the veterinarian and owner.
  • Each of 3 categories of the examination (ie level of consciousness, motor activities, brainstem reflexes are assigned to a score from 1 to 6 (see Table Head trauma: Modified Glasgow coma scale ).
  • The scores from each categories are added together to determine a patient's coma score, ranging from 3 to 8, and may be used to guide treatment decisions and prognosis.
  • The level of consciousness provides information about the functional capabilities of the cerebral cortex and the ascending reticular activating system (ARAS) in the brainstem.
It is important to note that the patient's blood pressure, oxygenation status and temperature may all affect the animal's level of consciousness and so the latter should be re-evaluated after correction of the former vital parameters.
  • Levels of consciousness range from normal, depressed, or delirious to stuporous or comatose.
  • A patient in a coma is unconscious and cannot be roused with noxious stimuli while a patient in a stupor is partially or completely unconscious, but will respond to noxious stimuli.
  • Patients presenting in a state of coma generally have bilateral or global cerebral abnormalities or severe brainstem injury and have a guarded prognosis.
  • Motor activity may be affected by the animal's level of consciousness.
  • Voluntary motor activity is characterized as normal, paretic or recumbent.
  • Abnormal motor function usually reflects either brainstem injury or spinal cord injury; the latter may complicate the assessment of head trauma.
  • Opisthotonus with hyperextension of all 4 limbs is suggestive of decerebrate rigidity whereas variable flexion and extension of the hindlimbs is seen in rigidity with cerebellar injury.
  • In head trauma without spinal involvement, segmental spinal reflexes are normal to exaggerated, but postural reactions may be diminished.
  • Neuro-ophthalmologic examination is the basis of the brainstem reflexes category.
  • Pupils that respond appropriately to light, even if miotic, indicate adequate function of the rostral brainstem, optic chiasm, optic nerves, and retinae.
  • In the absence of concurrent ocular trauma, miosis may indicate a diencephalic lesion, particularly in the hypothalamus, as this area represents the origin of the sympathetic pathway.
  • Pupils that are initially miotic and then become mydriatic are indicative of a progressive brainstem lesion.
  • Bilateral mydriasis with no response to light usually is indicative of irreversible midbrain damage or herniation of the cerebellum through the foramen magnum, or both.
  • Unilateral mydriasis may indicate unilateral cerebellar herniation or brainstem hemorrhage.
  • Oculocephalic reflexes (ie physiologic nystagmus) also may be impaired with brainstem lesions as a result of either involvement of cranial nerve nuclei that innervate the extraocular muscles or the interconnecting ascending medial longitudinal fasciculus.

Other investigations

Imaging

  • Computed tomography (CT) and magnetic resonance imaging (MRI) are the mainstays of visualizing cerebral damage, hemorrhage and obstructive hydrocephalus Hydrocephalus.
  • Advanced imaging should be reserved for patients that do not respond to initial treatment or for patients that deteriorate despite aggressive therapy.
  • It may be performed to evaluate for fractures, hemorrhages or parenchymal lesions.
  • Both of these imaging modalities require anesthesia (unless the animal is comatose or stuporous) which can destabilize the head trauma patient.

Laboratory tests

  • Total protein Blood chemistry: total protein and packed cell volume Hematology: packed cell volume analysis may be useful indicators of the dehydration status of the patient as well as assess oxygen carrying capacity which may be affected by concurrent bleeding (spleen rupture, pelvic fracture...)
  • Hyponatremia Blood biochemistry: sodium can be the most common electrolyte abnormality following head trauma in humans and therefore should be monitored in veterinary patients q2-4 hrs initially.
  • In response to the stress of the trauma, there is increased release of antidiuretic hormone (ADH) Anti-diuretic hormone (ADH) test and aldosterone. This promotes renal tubular water absorption, resulting in relative water excess.
  • In addition, the syndrome of inappropriate secretion of ADH may also result in profound levels of hyponatremia.
  • Hypernatremia Hypernatremia can result from the therapeutic use of mannitol Mannitol and potentially from traumatic diabetes insipidus Diabetes insipidus, which we may rarely recognize.
  • If phenobarbitone Phenobarbital is used to control seizure activity in these patients, it can inhibit ADH, which may exacerbate the hypernatremia.
  • Hypokalemia Hypokalemia is the most frequent potassium derangement resulting from head trauma.
  • It may be due to stress-induced aldosterone secretion. Also, increased renal excretion of potassium may occur from the therapeutic use of corticosteroids or diuretics (furosemide) Furosemide.

Intracranial Pressure (ICP) monitoring

  • ICP monitoring Intracranial pressure measurement has been investigated in cats for many years but its use is limited to a few specialist centers due to its cost.
  • ICP can be measured from various intracranial compartments.
  • Cerebrospinal fluid pressure, as a reflection of ICP, can be measured within the ventricles of the brain, at the cisterna magna, in the subarachnoid space overlying the brain, or in the lumbar area.
  • However, such monitoring cannot be continuous and requires anesthesia and CSF pressure may not always truly reflect the situation in the parenchyma.
  • A fiberoptic ICP monitoring device has been shown to be reliable in cats.
  • ICP can be measured directly from the brain tissue itself.
  • Unfortunately, the extremely high cost of the fiberoptic system is likely to limit its use.

Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Kuo K W, Bacek L M, Taylor A R (2018) Head traumaVet Clin North Am Small Anim Pract 48 (1), 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 (2), 155-159 PubMed.
  • Grohmann K, Schmidt M J, Moritz A et al (2012) Prevalence of seizures in cats after head trauma. JAVMA 241 (11), 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 (2), 177-190 PubMed.
  • Platt S R, Radaelli S T & McDonnell J J (2001) The prognostic value of the modified Glasgow Coma Scale in head trauma in dogs.​ JVIM 15 (6), 581-584 PubMed.
  • Dewey C W (2000) Emergency management of the head trauma patient. Principles and practice. Vet Clin North Am Sm Anim Pract 30 (1), 207-225 PubMed.
  • Ghajar J (2000) Traumatic brain injury. Lancet 356 (9233), 923-929 PubMed.

Other sources of information

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