Veterinarni Medicina, 63, 2018 (08): 345–357

Review Article

https://doi.org/10.17221/20/2017-VETMED

Traumatic brain injury in dogs and cats:

a systematic review
L.O. Dos Santos1, G.G. Caldas2, C.R.O. Santos2*, D.B. Junior2
1
Metropolitan Union for Education and Culture, UNIME, Salvador, Brazil
2
Veterinary Hospital of the Federal University San Francisco Valley, Petrolina, Brazil
*Corresponding author: cassiareginavet@yahoo.com.br

ABSTRACT: Traumatic brain injury occurs frequently in dogs and cats due to motor vehicle accidents, falls and
crush injuries. The primary lesion occurs at the time of injury and causes direct, irreversible damage to the brain
parenchyma and vasculature. Secondary lesions occur in the minutes following the trauma due to a combination of
physical and biochemical changes that lead to intracranial hypertension. Therefore, knowing the pathophysiology
of the cranioencephalic trauma is essential for treatment directed at minimising secondary damage. The approach
to the patient affected by traumatic brain injury is based on the ABCD of trauma, guided by the neurological
examination with the aid of imaging exams and adequate therapeutic measures. The treatment of patients with
cranioencephalic trauma is still in many ways controversial. For that reason, this literature review aims to address
the main points regarding the pathophysiology of this disease and to describe the clinical and surgical therapeutic
options currently available.

Keywords: head injury; small animals; pathophysiology; treatment

Contents
3.4 Osmotic diuretics
1. Pathophysiology 3.5 Hypothermia
1.1 Primary injury 3.6 Hyperventilation
1.2 Secondary injury 3.7 Glucocorticoids
2. Patient assessment 3.8 Anticonvulsants
3. Treatment 3.9 Pain management
3.1 Intracranial pressure control 3.10 Decompressive surgery
3.2 Fluid therapy 4. Prognosis
3.3 Oxygenation 5. References

1. Pathophysiology are a determinant for cerebral oedema (Helmy et al.

2007). The damage resulting from this injury can
An understanding of the pathophysiology is es- be separated into two categories, chronologically
sential in guiding and evaluating treatment success divided into primary and secondary injury.
in traumatic brain injury (TBI). High-speed injuries
involving rapid acceleration and deceleration, espe-
cially when there is no rotating element, result in 1.1 Primary injury
shear forces at the border between the white matter
and the grey neocortical matter. This shear force The primary injury occurs immediately after
can cause generalised lesions in the axonal struc- trauma as a direct consequence of the physical in-
ture, known as diffuse axonal lesions (DAL), which sult. Its extent depends on the type and intensity of

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the impact force and can involve inevitable and in- Hernandez et al. 2002). From a physiological and
tractable damage to the cerebral parenchyma, such morphological point of view, this accumulation of
as surface contusions (i.e. bruising where the pia is fluid in the encephalon can generate a vasogenic
intact; O’Connor et al. 2011), bruises, haemorrhage, oedema (Klatzo 1994). Vasogenic oedema occurs
lacerations (i.e. where the pia is torn; O’Connor et due to direct vascular damage, causing an increase
al. 2011) and DAL, (Czosnyka and Pickard 2004; in vascular permeability and consequent extrava-
Portella et al. 2005; Helmy et al. 2007). The most sation of plasma fluids and proteins out into the
severe forms of primary brain injury are lacera- intravascular space, which then accumulate in the
tions, and vasogenic oedema may also occur if there cerebral parenchyma, causing an increase in vol-
is a direct vascular injury followed by intracranial ume (Varella-Hernandez et al. 2002).
haemorrhage. The occurrence of cranial fractures Physical insults can trigger an inflammatory pro-
can generate cerebral trauma that damages the pa- cess in the central nervous system due to the loss of
renchyma and blood vessels, making clinical man- stability of the blood-brain barrier, which is essen-
agement impossible and increasing the odds that tial in regulating the access of cells and macromol-
the patient will die (Sande and West 2010; Dewey ecules from the periphery to the central nervous
and Fletcher 2015). Hence, the professional must system. Lymphocytes, macrophages and microglia
be able to adequately prevent, recognise and treat cells are potent generators of reactive molecules
secondary injuries (Sande and West 2010) since and mediators of inflammation such as adhesion
primary injury is essentially an irreversible event molecules, metalloproteinases, chemokines and cy-
(O’Connor et al. 2011). tokines. The combination of systemic insults, such
as pneumothorax, haemothorax, rib fractures, pul-
monary contusions and intracranial physical and
1.2 Secondary injury biochemical changes are responsible for the genesis
of secondary lesions such as haematomas, intracra-
Secondary lesions occur in the minutes or even nial hypertension, infection, hypoxia, oedema and
days following trauma and involve the activation of cerebral ischaemia. Axial haematomas within the
several biomechanical mechanisms that together cerebral parenchyma and extra-axial subarachnoid,
act to perpetuate brain lesions and whose course subdural and epidural haematomas lead to com-
is a determining factor for the patient’s prognosis pression of the brain with subsequent neurological
(Sande and West 2010). The main determinants of dysfunction (Vandevelde 2004).
high mortality in TBI are the severity of the pri- Physical trauma triggers biochemical pathways
mary lesions and complications from the second- that work together to perpetuate damage to brain
ary lesions that cause cerebral ischaemia triggering tissue. Secondary intracranial injury is mediated
intracranial hypertension, systemic hypotension, by increased activity of excitatory neurotransmit-
hypoxia, hyperpyrexia, hypercapnia, hypoglycae- ters such as glutamate and aspartate, which are
mia and a focal lesion, such as subdural haema- released in large quantities immediately after
toma, that is an indicative of a lesion in the brain trauma, accelerating metabolic activity and sub-
parenchyma (Helmy et al. 2007). Another aggravat- sequently leading to depletion of ATP (adenosine
ing factor is multiple trauma with haemorrhage and triphosphate), with consequent failure of the so-
brain oedema that are responsible for the appear- dium and potassium (Na/K) pump and intracellular
ance of secondary autolytic processes that eventu- calcium and sodium accumulation in the neurons.
ally lead to death (Rabelo et al. 2010). Depolarisation leads to a greater release of the
Cerebral oedema may be due to a non-specific aforementioned neurotransmitters which mediate
response to brain insults such as trauma, cell dam- further increases in intracellular calcium through
age and ischaemia that can disturb Starling’s law. secondary messengers and proteolytic enzymes,
Starling’s law states that the greater the volume of creating an osmotic gradient and promoting water
blood received by the ventricle during diastole, the diffusion. This event is called cytotoxic oedema.
greater the blood volume ejected into the arter- Other factors responsible for the genesis of second-
ies during systole. Thus, imbalances in Starling’s ary lesions are the generation of reactive oxygen
law can lead to accumulation of fluid in the brain species and the release of inflammatory cytokines.
parenchyma, worsening the oedema (Varella- Reactive oxygen species arise due to local tissue

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acidosis and hypoperfusion and are detrimental intracranial volume balance. CPP can be defined
to cell membranes; particularly destructive are in the following formula:
hydroxyl radicals, which have a great capacity to
remove hydrogen atoms from the methylene group CPP = MAP – ICP
of polyunsaturated fatty acids, thereby initiating
where: CPP = cerebral perfusion pressure; MAP = mean arte-
lipid peroxidation. The resulting oxidation of li-
rial pressure; ICP = intracranial pressure
pids in the cell membrane alters permeability and
leads to dysfunction. As brain tissue is rich in li- Thus, blood pressure is important to maintain
pids, it is particularly susceptible and sensitive to CBF, especially in circumstances where cerebro-
oxidative injury. The release of cytokines activates vascular autoregulation has been impaired, such as
the arachidonic acid cascade and the coagulation after TBI. However, even if autoregulation is intact,
cascade, destabilising the blood-brain barrier and changes in blood pressure and intracranial pressure
inducing nitric oxide production. This is respon- may alter blood volume as a result of dilation or
sible for excessive vasodilatation, leading to loss of constriction of cerebral blood vessels (Dunn 2002;
pressure autoregulation (Varella-Hernandez et al. Rabelo et al. 2010; Cooper et al. 2011). CPP is the
2002; Sande and West 2010). main determinant of cerebral blood flow and thus,
The relationship between volume and intrac- brain oxygenation and nutritional support depend
ranial pressure is non-linear. The Monro-Kellie on it (Vandevelde 2004).
doctrine states that the skull is a closed, inelastic Although the brain constitutes only 2% of the
compartment containing three components, cer- body weight, it consumes 15% of cardiac output,
ebral parenchyma (80%), arterial and venous blood 20% of inhaled oxygen and more than 25% of glu-
(10%) and cerebrospinal fluid (10%), that under cose. There are two phases in CBF autoregulation
normal circumstances exist in a state of dynamic which together ensure the constancy required for
equilibrium. An increase in the volume of any of the fulfilment of the oxygen and glucose require-
these components should be compensated for by a ments of brain tissue. The first one, related to au-
decrease in one or more of the others; otherwise, toregulation of blood pressure, allows maintenance
an increase in intracranial pressure is unavoid- of CBF during constant variations of MAP between
able (Sande and West 2010). When compensatory 50 and 120 mm Hg. Thus, increases in MAP leads to
mechanisms fail to maintain the equilibrium be- vasoconstriction and decreased vasodilation in the
tween these components, there is an increase in brain. These changes occur due to logarithmic vas-
intracranial volume, which causes compression of oreactivity to changes in CPP. The second phase is
the cerebral vasculature with consequent intracra- metabolic autoregulation in response to hypercap-
nial hypertension and reduced cerebral blood flow nia, which causes vasodilation, decreased cerebral
(CBF). There is then an increase in carbon dioxide, vascular resistance and hypoxia. Levels of O2 lower
which is locally detected at the vasomotor centre, than 60 mm Hg induce vasodilation, thus increas-
and which then initiates a sympathetic nervous ing CBF (Yates and Roberts 2000). CBF increases
system response that results in increased ejection with vasodilation and decreases with constriction
volume and heart rate. This results in increased of cerebral arterioles, termed cerebral resistance
mean arterial pressure (MAP) in an attempt to in- vessels. These vessels respond to changes in sys-
crease cerebral perfusion pressure (CPP). Systemic temic blood pressure (autoregulation of pressure),
hypertension is detected by baroreceptors, located blood viscosity (autoregulation of viscosity) and
in the walls of the carotid arteries and aortic arch, metabolic demand, keeping CBF levels within the
resulting in a reflex bradycardia. This mechanism limits that are appropriate to meet the metabolic
is known as the cerebral ischaemic response or the demands of brain tissue (Varella-Hernandez et al.
Cushing reflex (Dunn 2002; Laffey and Kavanagh 2002).
2002; Portella et al. 2005; Stocchetti et al. 2005; The intravascular pressure and its effect on cer-
Sande and West 2010). ebral blood volume not only affects intracranial
The mechanism behind cerebral compliance is pressure, but also the mechanical properties of the
essential to avoid an increase in intracranial pres- brain and the capacity of the intracranial space to
sure. Cerebral perfusion pressure should be kept “fit” in its place, and low levels of blood can be det-
close to normal since low levels are detrimental to rimental to the intracranial volume balance (Rabelo

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et al. 2010). The CPP acts as the pressure gradient avoiding excessive manipulation of the head, neck
that acts on the cerebrovascular circulation, and and vertebral column because the patient may
so it is important in the regulation of the CBF and have lesions and/or fractures that have not been
required to keep it at constant levels (Dunn 2002). detected. The examination should be initially car-
ried out using an otoscope, in order to verify the
integrity of the tympanic membrane. The presence
2. Patient assessment of a clear fluid, hyaline, often mixed with blood,
can be determined by investigating flow in the
Due to the scarcity of prospective or retrospective external acoustic meatus or through the nostrils,
clinical data in the veterinary literature, treatment which characterise otoliquorrhea and rhinoliquor-
recommendations for dogs and cats with TBI are rhea, respectively. These are associated with violent
mainly based on human and experimental studies. trauma that affect the bone at the base of the skull
Also, trauma patients are usually polytraumatised and are suggestive of fracture with formation of
and the initial approach to trauma should be based cerebrospinal fluid fistula due to simultaneous rup-
on ABCD (airway, breathing, cardiovascular con- ture of the meninges. Also, hemotympanum may
dition and neurological dysfunctions) and clinical be found associated with fracture of the temporal
approach (anamnesis, physical examination, neu- bone. Ophthalmoscopy should also be performed
rological examination, stabilising the patient and to diagnose scleral bleeding, an important find-
complementary exams). For this reason, emergency ing in patients with TBI, since it may reflect cer-
management is critical to stabilise the patient and ebral and/or meningeal haemorrhage (Laffey and
should be directed towards optimising cerebral per- Kavanagh 2002; Stocchetti et al. 2005).
fusion and oxygenation and avoiding secondary in- Animals with TBI may exhibit clinical signs
jury (Menon 1999; Platt and Olby 2004; Assis 2005; similar to those with a multifocal neurological
Dewey and Fletcher 2008; Gomes and Neutel 2008). syndrome, as there may be lesions in various com-
The modified Glasgow coma scale (da Costa and partments of the brain. These types of lesions can
Dewey 2015) was adapted to veterinary medicine in generate different behavioural states, ranging from
order to classify the neurological status of a patient completely normal appearance after a short period
with TBI and perform serial monitoring over a 72- of unconsciousness to coma, stupor, delirium or
hour period (Platt 2008). This scale is divided into depression (Syring et al. 2001; Braund 2003). The
three categories of neurological examination con- neurological evaluation of the patient should con-
sisting of level of consciousness, motor activity and sist of a cautious evaluation of the patient’s state of
brainstem reflexes, and each category can receive a consciousness (AVPU Scale), respiratory pattern,
score of one to six points, giving a total of three to pupil size and responsiveness, ocular position and
18 points. The best prognosis is associated with the movement, muscle tone, proprioceptive tests when
highest score, and low scores are associated with a possible, evaluation of cranial nerves and the search
high mortality rate, with less than 50% chance of for a possible pain focus (Bagley 2005; Sande and
survival in a 72-hour period (Platt and Olby 2004). West 2010). The AVPU scale (Table 1) has fewer
This scoring system provides an estimate of the ini- variables than the Glasgow coma scale and consists
tial assessment, response to treatment, evaluates of assessing the patient’s state of consciousness by
therapeutic choices and provides a prognosis. classifying their clinical status using scores from
After the initial approach focusing on the trauma, 1 to 4: the patient is alert, the patient responds to
patient stabilisation and initial evaluation using the verbal stimulation, the patient responds to pain-
modified Glasgow coma scale, anamnesis should be ful stimuli, the patient does not respond (Rabelo
performed, consisting of logical and direct ques-
tions aiming at finding the cause of the trauma, the Table 1. AVPU Scale (Adapted from Rabelo 2008)
mental state soon after injury, whether seizures are
Score State of consciousness
present, whether there was emesis and whether the
A-1 the patient is alert
patient was able to walk immediately after trauma.
V-2 the patient responds to verbal stimulation
Once these questions have been answered, the cli-
nician must start the physical examination. This P-3 the patient responds to painful stimuli
should be done methodically and meticulously, U-4 the patient does not respond

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2008). The modified Glasgow coma scale, however, 3. Treatment

not only evaluates the patient’s state of conscious-
ness, but also takes into account motor activity Treatment for traumatic brain injury is still
and brainstem reflexes. A neurological evalua- controversial and also still based on human and
tion should be performed, preferably before ad- experimental studies as well as on the personal
ministration of any drugs with a sedative effect, experiences of professionals. The Brain Trauma
to determine the location of the lesion as well as Foundation (BTF), in collaboration with the
its severity and evolution. Imaging may also help American Association of Neurological Surgeons,
in this stage, especially in animals that are not re- has established that insufficient data does not per-
sponsive to drug treatment (Siqueira et al. 2013; mit standardisation of treatment for TBI or a single
Dewey and Fletcher 2015). treatment guideline in terms of initial patient as-
Computed tomography (CT) is the diagnostic sessment. It is based, however, on resuscitation and
method of choice for patients with TBI, since images quick stabilisation of the patient, which should fol-
are obtained faster compared to magnetic resonance low five principles: normocapnia, normoxia, nor-
imaging (MRI) and there is better visualization of motension, normothermia and normoglycaemia
acute haemorrhages and bone structures, providing (Braund 2003; Girling 2004; Platt and Olby 2004;
fundamental information to determine the progno- Dewey and Fletcher 2008; Sande and West 2010;
sis (da Costa and Dewey 2015). On CT, haemor- Dewey and Fletcher 2015).
rhage appears as hyperattenuating (hyperdense) in
the acute stages, and over time, its density decreases
with clot resorption, creating a hypoattenuating le- 3.1 Intracranial pressure control
sion which could be confused with brain oedema
(Platt et al. 2016). Conversely, CT might present The most frequent cause of death and disability
some disadvantages, such as exposure to ionising in animals with traumatic brain injury is elevated
radiation, poor soft tissue detail and poor visualisa- intracranial pressure, as this leads to dysfunction
tion of brain and subtle parenchymal lesions that of blood flow in the brain, causing hypoxia and
are better observed on MRI (da Costa and Dewey ischaemia (Lubillo et al. 2009; Cecil et al. 2011).
2015). The identification of haematomas or haem- A simple but effective procedure to aid the control
orrhage, parenchymal contusions and oedema are of intracranial pressure is to position the patient’s
easily identified on MRI. This diagnostic method head at a 30-degree angle to the body, which pro-
provides better visualisation of subtle parenchymal vides a greater arterial supply to the brain, as well
changes and provides valuable information to facili- as greater venous drainage (Figure 1). Care must
tate the prognosis (Platt et al. 2016). be taken to not compress the jugular vein since
Radiographic examination is also important in this leads to an immediate increase in intracranial
the diagnosis of TBI, since pulmonary haemor- pressure (Platt 2008). Care should also be taken to
rhage, pulmonary contusion and pneumothorax position the head properly by placing a support just
may be present in the thorax, but it is not useful below the head in order to decrease the chances of
in the identification of brain lesions and may only aspiration into the lower airways leading to com-
reveal the presence of fractures with depression plications, since these patients are predisposed to
of the calvaria (Branco 2011; Siqueira et al. 2013). regurgitation. Therefore, it is preferable to elevate
Spinal radiographs may also be essential in patients the head of the animal by placing a support under
with TBI, as it aids in the detection of spinal injuries its shoulders, so in case of reflux, the contents may
(Silva 2013). be expelled out of the mouth (Opperman 2014).
Laboratory analyses include haematological and
biochemical analyses that vary with clinical pres-
entation of the patient, blood gas analysis, serum 3.2 Fluid therapy
electrolytes and serum osmolarity (Silva 2013).
Collection of cerebrospinal fluid is contraindicated Fluid therapy has the objective of creating a state
because if the patient has an elevated intracranial of normovolemia or a mild state of hypervolemia
pressure, puncture favours encephalic herniation since the restoration of the blood volume is es-
(Branco 2011). sential in the control of the tension and pressure of

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Figure 1. Stray cat with traumatic brain injury caused by car accident
https://doi.org/10.17221/20/2017-VETMED

Figure 1. Stray cat with traumatic

brain injury caused by car accident
Reproduced with permission from the
University Veterinary Hospital of the
Federal University of San Francisco
Valley. The patient was in an incuba-
tor to maintain body temperature and
oxygen therapy. The head was ele-
vated to a 30-degree angle, providing
greater arterial supply to the brain as
well as greater venous drainage

cerebral perfusion. There is usually concern about quiring a greater volume to restore blood volume,
the aggressive use of fluid therapy in hypotensive which may exacerbate the patient’s cerebral oedema
patients on the basis that this could worsen the cer- (Platt 2008). However, isotonic crystalloids can be
ebral oedema; however, studies refute this theory used to replace diuresis caused by some drugs, such
and state that the use of fluid therapy in the patient as mannitol, and to tackle the dehydration caused
with brain injury is beneficial for the oedematous by the use of hypertonic solutions, with doses of at
brain, even if high volumes of crystalloids are used most 90 ml/kg/h for dogs and 40 to 60 ml/kg/h for
(Dewey and Fletcher 2015). cats (Verneau 2005). The use of solutions contain-
Initial resuscitation is performed with the use of ing glucose is contraindicated since the patient with
hypertonic saline solutions or synthetic colloids, as cranioencephalic trauma presents deficient tissue
they allow a rapid return to normal blood volume oxygenation and this could lead to the formation
and blood pressure while limiting the volume of of lactic acid by anaerobic glycolysis in turn caus-
fluid administered. Hypertonic saline solution has ing metabolic acidosis (Fernandez and Bernardino
shown excellent results in the initial resuscitation 2010).
of patients with TBI, and its recommended dose is
4 to 6 ml/kg of 7.5% NaCl for 10 to 15 minutes. If
an artificial colloid is added, the effect of the hy- 3.3 Oxygenation
pertonic saline solution is prolonged for hours. In
cases of shock, synthetic colloids should be given Oxygenation is a highly recommended thera-
at a dose of 10–20 ml/kg, to effect (Dewey and peutic method in patients with TBI to maintain
Fletcher 2008; Sande and West 2010; Rainey and the partial pressure of oxygen (PO 2) in arterial
Odunayo 2015). If the patient presents severe anae- blood as close as possible to normal (80 mm Hg).
mia, it is recommended to transfuse with whole Oxygen can initially be offered to the patient via
blood or packed red blood cells, so that blood vol- a mask, but this may subject the animal to stress
ume is maintained and tissue hypoxia is prevented. and is inefficient for patient monitoring. It should
The haematocrit should be increased from 25 to be replaced by a nasal catheter that may only be
30% in order to achieve the purpose of this therapy placed close to the nostrils and not introduced, or
(Dewey and Fletcher 2008; Sande and West 2010; a transtracheal tube, through which oxygen at 40%
Lorenz et al. 2011). concentration is provided at flow rates of 100 ml/
The use of isotonic crystalloids is less efficient kg/min and 50 ml/kg/min, respectively. If in a co-
when compared to the hypertonic ones, since they matose state, the patient should be immediately
rapidly suffer extravasation to the interstitium, re- intubated and ventilated according to the needs

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indicated by blood gas analysis (Platt 2008; Dewey exclusively intravenously, and it is excreted by the
and Fletcher 2015). kidneys without being metabolised or resorbed in
Although hyperoxygenation is recommended the tubules. Its administration dose is 0.5 to 2 g/kg
for patients with TBI, caution should be taken, as in bolus, but slowly, in a range of 15 to 20 minutes,
studies have reported adverse effects that include every 3 to 6 hours, with a maximum of three bo-
changes in non-damaged tissues, cerebral hyper- luses in 24 hours, at room temperature, preferably
oxic vasoconstriction, inhibition of metabolic using a filter to prevent the formation of crystals
enzymes and formation of free oxygen radicals (Gomes 2011; Dewey and Fletcher 2015; Rainey
(Floyd et al. 2003; Magnoni et al. 2003; McLeod et 2015).
al. 2003). Recent studies have demonstrated that Complications associated with the use of man-
extreme hyperoxaemia in a patient with head injury nitol in the treatment of TBI involve renal and neu-
is inefficient in accelerating the recovery process rological impairment. When it is used repeatedly
and may, through several mechanisms, increase at osmolarity values that exceed 320 mOsm/l, it
brain injury (Davis et al. 2009). increases the diuresis and can lead to dehydration,
Hyperbaric oxygen therapy is a therapy that is which may lead to systemic hypotension, ischaemia
currently gaining in popularity for the treatment and hyperkalaemia. Prolonged use may also lead to
of neurologic diseases; it consists of inhaling 100% osmotic flow reversal due to increased extravascu-
oxygen under pressures greater than 1 absolute at- lar concentration, exacerbating intracranial oede-
mosphere (ATM). Studies in experimental models ma and elevating intracranial pressure (Bullock
have shown that this procedure is capable of inhib- 1995; BTF 2007a; Dewey and Fletcher 2008).
iting apoptosis and suppressing inflammation, thus The use of furosemide in patients with TBI is
protecting the integrity of the blood-brain barrier controversial. It was believed that this drug used
and promoting angiogenesis and neurogenesis with in combination with mannitol could help increase
pressures below 3 ATM, but its clinical efficacy is diuresis and decrease hypertension. However, it
still controversial in humans because of the hetero- has now been reported that the combination of
geneity of TBI (Braswell and Crowe 2012; Sanchez furosemide and mannitol, or furosemide alone, did
2013; Hu et al. 2016). not result in any benefit to the patient, and may
cause greater depletion of the intravascular vol-
ume, altering parameters such as heart rate, mean
3.4 Osmotic diuretics arterial pressure, central venous pressure, potas-
sium, urea, haematocrit or base deficit (Sande and
Hyperosmotic therapy consists of the administra- West 2010; DiFazio and Fletcher 2013; Dewey and
tion of a substance that can create an osmotic gra- Fletcher 2015).
dient that makes the water from the extracellular
and intracellular compartments move into the ves-
sels. This osmotic gradient will therefore promote 3.5 Hypothermia
a reduction in intracranial pressure by reducing
intracranial volume and improving complacency Therapeutic hypothermia is also a treatment
(Raslan and Bhardwaj 2007). method that can be used in patients who have suf-
Mannitol is classified as an osmotic diuretic. Its fered traumatic brain injury, since the development
main and most efficient mechanism of action is the of several secondary lesions is temperature-de-
promotion of the vasoconstriction reflex through pendent. The mechanism of action for hypother-
a reduction in blood viscosity, which reduces in- mia is based on a decrease of body temperature
tracranial pressure. Another mechanism of action to 32–34 °C in order to reduce the release of ex-
of mannitol is a decrease in the production of cer- citotoxic amino acids and the production of pro-
ebrospinal fluid, and the difference in osmolarity inflammatory cytokines as well as a decrease in
leads to drainage of extravascular fluid into the excitatory signals that can result in cell death. As
intravascular space, reducing oedema (Dewey and such, it would prevent necrosis and cell apoptosis,
Fletcher 2015). The vasoconstriction reflex occurs and reduce the formation of cerebral oedema and
in a few minutes and is faster than the osmotic ef- rupture of the blood-brain barrier (Hayes 2009;
fect caused by mannitol. This drug is administered Sadaka and Veremakis 2012; McCarthy et al. 2013).

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There have been studies in humans that have also injured neurons was also noted (Platt 2008; Sande
revealed the efficacy of therapeutic hypothermia as and West 2010; Gaitero 2011).
a neuroprotectant after intracranial haemorrhage, The functional mechanisms of corticosteroids are
and it has been reported to decrease the formation increasingly well understood and it is now known
of oedema (MacLellan et al. 2006; Fingas et al. 2007; that these drugs are more efficacious in the treat-
Kawanishi et al. 2008). ment of the vasogenic type of oedema when com-
A decrease in body temperature involves adverse pared to the cytotoxic one. Recent studies have
effects. Studies in human adults and children have shown that, despite the being effective in vitro,
shown that there was no improvement in the neuro- corticosteroids were not effective when used in
logical status of patients undergoing this treatment, vivo. Therefore, due to the lack of a complete un-
but comparative studies have shown some efficacy derstanding of the functional mechanisms of cor-
in reducing intracranial pressure in children; there- ticosteroids in cerebral metabolism in TBI and of
fore, this treatment may be considered (Clifton et a specific diagnostic test to determine the type of
al. 2001; Hutchison et al. 2008). oedema present in such patients, their use is not
yet recommended (Hoshide et al. 2016).

3.6 Hyperventilation
3.8 Anticonvulsants
Hyperventilation is used to reduce intracra-
nial pressure by reducing the partial pressure Seizures are common in patients who have suf-
of CO 2 (PaCO 2), which consequently promotes fered TBI. They can be divided into three catego-
brain vasoconstriction and subsequent reduction ries: immediate, occurring up to 24 hours after the
of brain blood volume. However, the use of this trauma; early, from 24 hours to seven days after the
therapy is controversial as it can cause severe re- trauma; and late, after seven days, depending on
duction of the cerebral circulation when values of the severity of the lesion, the presence of cranial
PaCO 2 are smaller than 30–35 mm Hg. The pa- fractures, epidural, subdural, parenchymal haema-
tient should be ventilated to maintain PaCO 2 be- toma and penetrating wounds (Bratton et al. 2007;
tween 30–40 mm Hg, avoiding hypoventilation. Platt 2008; Sande and West 2010). The occurrence
Hyperventilation by itself can have deleterious ef- of seizures in patients with TBI should be treated
fects related to cerebral vasculature dilatation in aggressively as they lead to an elevation of intrac-
patients with high intracranial pressure, secondary ranial pressure, worsening the patient’s clinical
to induced hypercapnia (White et al. 2001; Platt condition. Diazepam is the drug of choice for the
2008; Dewey and Fletcher 2015). treatment of seizures, since it has a fast action and
reliable efficacy at doses of 0.5 to 1.0 mg/kg which
can be repeated in intervals of 5 to 10 minutes for
3.7 Glucocorticoids three to four doses (Sande and West 2010; Lorenz
et al. 2011).
Currently, the use of glucocorticoids (GC) in the Other drugs can be used in persistent convulsive
treatment of patients with cranioencephalic trau- episodes. Since diazepam (0.5 to 2 mg/kg) (Platt et
ma is not recommended in human or veterinary al. 2016) does not have a prolonged effect, pheno-
medicine. Despite contributing to a reduction in barbital can be used. Phenobarbital is classified as
cerebral oedema secondary to other causes, such a sedative and antiepileptic, it has antiapoptotic
as neoplasia, in patients with TBI, GCs lead to an effects and does not promote changes in cerebral
increase in mortality. This was evaluated mainly by blood flow; therefore, it promotes neuroprotec-
the use of methylprednisolone, which led to hyper- tion. Phenobarbital has a latency period of 15 to
glycaemia, immunosuppression, wound healing de- 20 minutes (Neves et al. 2010) and can be used
lay, gastric ulcers and acceleration of the catabolic in doses of 2 to 3 mg/kg i.v. followed by a loading
state. It was further associated with a worsening of dose of 18 to 24 mg/kg parenterally, over a period
neuronal damage in the presence of ischaemia due of 24 to 48 hours. Recently, the use of levetiracetam
to increased exposure to metabolic insults, and its has shown success in the treatment of emergency
association with inhibition of the remyelination of seizures due to its rapid effect and efficacy for up

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to 8 hours, with low sedative effect. The recom- of fentanyl, a potent analgesic with short duration
mended doses of levetiracetam range from 20 to and fast action, is preferable. It is used in continu-
60 mg/kg (Platt et al. 2016). The use of prophylactic ous infusion at a dose of 2–5 μg/kg/h or cutaneous
anticonvulsants may also be indicated in patients adhesives supplying 2–5 μg/kg. Caution should be
with TBI even if there are no seizures, in order to taken because its use may lead to a slight increase
avoid elevation of intracranial pressure. The rec- in intracranial pressure (Raslan and Bhardwaj
ommended dose of phenobarbital is 2 mg/kg i.m. 2007). If there are side effects, naloxone can be
every 6 to 8 hours for three to six months after used as an antagonist, reversing the effect of this
trauma, followed by gradual reduction of the dose drug (Armitage-Chan et al. 2006; Sande and West
down to complete cessation if there are no further 2010; Opperman 2014).
seizures (Platt 2008). The opioid agonist-antagonist butorphanol and
Thiopental and propofol, both classified as an- the partial agonist buprenorphine may be used
aesthetics, are also used. They exert anticonvulsant in the treatment of mild to moderate pain; they
and neuroprotective effects similar to phenobar- cause minor respiratory and cardiovascular chang-
bital. Thiopental has a rapid action and is used at es and are preferably used in cases where the pa-
a dose of 10 mg/kg at 2.5% (Harman et al. 2012). tient already presents with respiratory depression.
Propofol should be slowly administered intrave- However, side effects are more difficult to reverse
nously in small animals in a bolus dose of 1 to 6 mg/ using naloxone compared to opioids (Armitage-
kg to control seizures, followed by a dose of 0.1– Chan et al. 2006; BTF 2007c; Sande and West 2010;
0.6 mg/kg/min (Thomas 2003). Studies in humans Opperman 2014).
have confirmed the efficacy of prophylactic therapy
with anticonvulsants following TBI, which reduces
the risk of immediate seizures, but without effects 3.10 Decompressive surgery
on late convulsions. Therefore, treatment with
anticonvulsants in patients with TBI who develop Decompressive craniectomy consists of a surgi-
immediate or early seizures should always be used, cal technique where a bone flap is removed to be
and prophylactic therapy should be administered housed for a period in the abdominal subcutane-
for seven days after the initial trauma (Dewey and ous tissue, kept in a bone bank or prepared for
Fletcher 2015). later cranioplasty with heterologous materials.
Durotomy and expansion duroplasty techniques
may be associated to reduce ICP, using an au-
3.9 Pain management tologousaponeurotic galea graft. Decompressive
craniectomy promotes a decrease in intracranial
Pain management is crucial in the treatment of pressure and accommodation of the tumefied brain,
TBI, as it assists in controlling blood pressure, preventing the onset of intracranial brain hernias
perfusion and cerebral oxygenation and ultimately and is indicated for patients with cranial fractures,
in reducing intracranial pressure. Care should be depressed cranial fractures with neurological im-
taken to control analgesia, since the depression of pairment and recovery of potentially contaminated
these parameters with the elevation of intracranial bone fragments or foreign material housed in the
pressure may result in the worsening of second- cerebral parenchyma. According to the European
ary lesions. Opioids are the drugs of choice in the Brain Injury Consortium (EBIC) and the Brain
treatment of TBI pain, since their effects are easily Trauma Foundation guidelines, decompressive
reversible and they do not have adverse cardio- craniectomy is classified as a second level for the
vascular effects, making them safer. However, one treatment of refractory intracranial hypertension
should always take into account their side effects, (BTF 2007c; Hutchinson et al. 2007; Cooper et al.
which include bradycardia, respiratory depression 2011).
and hypotension, especially when used in high dos- In general, surgical intervention is well defined
es (BTF 2007b; Roberts et al. 2012). in human head-trauma management, whereas it
The use of morphine should be avoided because has played a relatively minor role for canines and
it causes emesis as a side effect, which could lead felines. It is believed that for these animals, sig-
to an elevation in intracranial pressure. The use nificant intracranial haemorrhage is rare, although,

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similar to humans, they may experience intracra- lepsy, behavioural changes, visual deficits and late
nial haemorrhage manageable via surgery. The in- hydrocephalus. The prognosis in TBI varies from
creasing availability of CT as a diagnostic method reserved to bad, although dogs and cats have a re-
might lead to surgery assuming a larger role in the markable ability to regenerate brain tissue (Murray
treatment of traumatic brain injury (da Costa and et al. 2007; Sande and West 2010).
Dewey 2015). Traumatic brain injury occurs frequently in dogs
The aim of surgery is to increase intracranial vol- and cats with a high mortality rate, mainly due to
ume, improve brain compliance, reduce intracrani- the secondary lesions that occur within minutes
al pressure and elevate cerebral perfusion pressure, of the injury. Many therapeutic measures are pro-
thereby elevating cerebral blood flow and cerebral posed; however, most are inconsistent as they lack
microvascular perfusion. When bone fragments randomised clinical trials that proving their efficacy.
are present and the skull sinking is greater than its The relevant literature reveals some disagree-
thickness, it is recommended to perform decom- ments regarding the treatment of TBI; however, the
pression via fracture reduction or removal of bone authors of published papers are unanimous among
fragments. In the case of acute extra-axial haemato- that treatment should be multimodal, and there is
mas, craniotomy can be performed. Caution should an intense search to discover new pathways for its
be taken in the case of excessive bleeding when treatment. It is clear that the management of TBI
haematoma is secondary to a venous sinus fracture should be directed towards restoring cerebral per-
(Seim 2007; Platt 2008; Siqueira et al. 2013). fusion pressure, thus maintaining blood flow and
However, surgical decompression is controversial, oxygenation, avoiding an increase in intracranial
since studies show that decompressive craniectomy pressure and minimising elevations in the cerebral
may worsen the patient’s clinical condition due to metabolic rate.
increased cerebral oedema and may be associated
with cerebral hyperaemia due to an increase in cer-
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Received: February 9, 2017
Accepted after corrections: June 1, 2018

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