Anaesthetic management of dogs and cats with intracranial pathology (brain injury, tumours, seizures)
MeSH keywords:anaesthesia, dog, cat, intracranial hypertension
The stabilization of intracranial volume and therefore cerebral blood flow (CBF) is crucial in patients with intracranial pathology during anesthesia. Even though intracranial hypertension is not monitored, it can be manifested through clinical symptoms. Seizures, brain traumas and tumors are the most common reasons for patients with intracranial hypertension to be anesthetized. In the preanesthetic period, patients should be systemically assessed after they are triaged. Hypotension and hypovolemia should be prevented through isotonic crystalloids, while oxygenation and ventilation should be performed. Hyperventilation can be established in urgent situations. The mitigation of intracranial hypertension can be performed through slight head elevation combined with avoidance of any increase in central venous pressure. Mannitol administrated in slow boluses or hypertonic saline (3, 5%-7, 5%) are both efficient in intracranial pressure (ICP) reduction. Hyperglycemia is a measure of damage in these patients so it should not be exacerbated. Induced hypothermia can be utilized in emergency situations. Seizures manifested after brain traumas must be treated with benzodiazepines while phenobarbital or levetiracetam can be used for maintenance. Benzodiazepines and opiods are a good choice for sedation and analgesia of such patients as they have a low impact in cardiovascular function. Acepromazine is not contraindicated anymore but still must be used with caution. Alpha 2-agonists are not preferred due to the cardiovascular depression and the emesis they cause. Injectable anesthetics such as propofol and etomidate are a good choice as they reduce CBF and protect cerebral autoregulation while volatile anesthetics may easily lead to cerebral vasodilation and therefore ICP increase. Ketamine is not prohibited anymore but should be used with caution. Total intravenous anesthesia is usually preferred than using volatile agents but in any case close monitoring, dose titration and mechanical ventilation are appropriate.
In clinical practice, veterinarians occasionally have to deal with animals with intracranial disease that should be anaesthetised, either to apply diagnostic techniques e.g., magnetic resonance imaging (MRI) or for surgical treatment of other co-existing conditions (e.g., intrathoracic and intra-abdominal injuries or fracture stabilization) or even for the neurological condition itself (e.g., craniotomy).The aim of this review is to analyse the perioperative management and anaesthetic options being available for patients with brain injury, tumours or seizures.
The brain is enclosed in the intracranial cavity and consists of three components: cerebral parenchyma, cerebrospinal fluid and blood (arterial and venous). In order to keep the intracranial pressure at normal levels, these components need to be constant. According to Monro-Kellie Doctrine, any increase in one of these factors should be followed by a decrease in either one or both of the other two, in order for intracranial volume to remain stable (Mokri 2001). The preservation of the cerebral blood flow (CBF) is one of the most important aims during anaesthesia. In fact, there is a relation among CBF, cerebral perfusion pressure (CPP) and cerebral vascular resistance (CVR): CBF = CPP / CVR. In addition, CPP results from the subtraction of the intracranial pressure (ICP) from the mean arterial pressure (MAP): CPP = MAP - ICP. As a consequence, maintaining CPP demands the appropriate control of the cardiovascular function, blood pressure and systemic vascular resistance during anaesthesia (Ghanbari et al. 2017). Thus, keeping CPP to a range between 50-70 mmHg is mandatory for patients experiencing intracranial disease (Smith 2015, Depreitere et al. 2018). Furthermore, autoregulation of CBF occurs when systemic MAP is maintained in a range between 60-160 mmHg. This mechanism is preserved by cerebral vascular responses to the changes in systemic arterial pressure (vasodilation in decrease and constriction in increase). Intracranial damage (e.g., tumours or injury), hypercapnia, hypoxia, serious changes in blood pressure and the use of volatile anaesthetics eliminate this protective mechanism and as such they should be avoided (Dagal & Lam 2009, Armstead 2016).
CBF is proportional to cerebral oxygen and metabolic requirements (CMRO2). As a result, any brain activity that increases CMRO2, is followed by an increase in CBF. This is known as the CMRO2/CBF coupling. During anaesthesia volatile agents induce changes in this relationship. They may cause a decrease in CMRO2 which is followed by an equivalent decrease in CBF. However, in the meantime the vasodilatation induced by volatile agents increases CBF. Therefore, CBF remains either stable or it is slightly decreased (Shardlow & Jackson 2011). CBF is also affected by arterial oxygen partial pressure (PaO2), when the latter is below 50 mmHg. Cerebral vasodilation caused by hypoxemia (levels below 50 mmHg), results in CBF increase and it should be avoided during anaesthesia. On the other hand, hyperoxaemia followed by vasoconstriction is not clinically important (Czosnyka et al. 2017). In contrast, the effect of arterial partial pressure of carbon dioxide (PaCO2) on CBF is more rapid. Hypercapnia causes cerebral vasodilation and an increase in CBF and ICP. In fact, for every 1 mmHg PaCO2 increase, CBF increases by 10-15 ml min−1 100 g−1 of brain tissue. On the other hand, severe hypocapnia results in intense cerebral constriction and as a result less oxygen is provided to the brain. Controlling PaCO2 is a critical point during anaesthesia in patients with intracranial disease. To avoid cerebral vasodilatation caused by hypercapnia, normocapnia or mild hypocapnia should be maintained during anaesthesia with mechanical ventilation (Tameem & Krovvidi 2013). Normally, ICP in dogs and cats ranges between 7-12 mmHg (Armitage-Chan et al. 2007). Traumatic brain injury, ischemic stroke, brain haemorrhage or neoplasms and brain oedema are some of the main causes of intracranial hypertension (Freeman 2015). In clinical practice, ICP is not usually monitored due to the difficulty and the cost of the required technique, which includes the placement of a probe into the skull (Ghanbari et al. 2017, Kuo et al 2018). However, raised ICP may be diagnosed by clinical findings such as depression, nausea, vomiting and respiratory and cardiovascular abnormalities. Some patients may manifest papillary oedema within a few hours after the increase of ICP. Patients presented with coma or stupor should be stabilized immediately. Brain imaging is mandatory in order to identify the damage, especially when there are obvious neurological signs. As ICP increases, complications such as decrease in CBF or even herniation (translocation brain parts to areas with less intracranial resistance) and ischemia may occur (Freeman 2015). Intracranial hypertension is responsible for a response of the nervous system known as Cushing’s effect. It involves increased systolic arterial blood pressure, decreased diastolic arterial blood pressure, bradycardia and respiratory abnormalities, in an attempt to prevent further ischemic damage (Freeman 2015). Raised ICP and its consequences, can be life-threatening and they should be avoided or treated as soon as possible.
In clinical practice, veterinarians sometimes have to anesthetise patients that have a history of seizures and are on treatment. Seizures are caused by temporary, sudden, synchronous irregular electrical activity of brain neurons, with variable aetiology. They are distinguished in primary and secondary seizures (Lane& Bunch 1990). Primary seizures include genetic factors and idiopathic epilepsy, while secondary seizures may be caused by metabolic disorders, more often hypoglycaemia, or intoxications such as lead poisoning and ethylene glycol toxicity. Neoplastic, inflammatory, vascular, traumatic and infectious conditions can lead to brain damage, manifested with seizures. Anticonvulsant therapy depends on the frequency and severity of seizures and is usually life-long (De Risio et al. 2015). Some of the antiepileptic drugs affect hepatic function and must be taken into consideration during anaesthesia (Lane & Bunch 1990).
Traumatic Brain injury (TBI) is a common problem caused by external forces exerted to the head from accidents, falls, kicks or even bites. Primary injury occurs right after the initial traumatic event leading to irreversible damage. On the other hand, secondary injury caused by the increase of neurotransmitters such as glutamate that raises sodium and calcium, or even from nitric oxide increase, lactic oxidosis, reactive oxygen species and reduction of adenosine triphosphate, occur later and aggravate the damage of the neuronal tissue. Increased ICP, hypotension, hypoxia, decreased CPP, inflammatory responses, hyperglycemia or hypoglycemia, hyperthermia, hypocapnia or hypercapnia are some of the secondary injuries that a clinician has to deal with in order to reduce the mortality rate (Kuo et al. 2018).
Primary brain tumours are observed in 2-4.5% of dogs admitted to post-mortem examination. The most common of them are meningiomas (50%), gliomas (35%), and choroid plexus tumours (7%). As for the secondary brain tumours in dogs, hemangiosarcoma (29-35%), lymphoma (12-20%), and metastatic carcinomas (11-20%) are the most frequently found (Miller et al. 2019). Meningioma is the most common intracranial tumour in cats too (Motta 2012). While intracranial tumours may appear at any age or breed, middle aged dogs and cats are mostly affected. Golden retrievers, Boxers, Miniature Schnauzers, English and French bulldogs, Boston terriers, Bull Mastiffs and domestic shorthaired cats are at high risk of developing brain tumours (Miller et al. 2019, Motta 2012). Except from pressing and invading in brain tissue, intracranial tumours may also cause cerebral oedema, intracranial haemorrhage, inflammation of neurons or even hydrocephalus. Therefore, these animals manifest a variety of clinical signs (Miller et al. 2019). Some non-specific signs that may appear are anorexia, weight loss and lethargy (Miller et al. 2019). Moreover, dogs with brain tumours usually have seizures. Vestibular syndrome, behavioural changes and ataxia are also frequent (Motta 2012, Troxel et al. 2003). Cats with brain tumours usually are presented with altered consciousness, cycling, seizures and lethargy. As tumours increase in volume, the pressure autoregulation mechanism is abolished and, as a result, intracranial hypertension occurs. Raised ICP induced by tumours, followed by decreased CPP are mainly responsible for the brain damage (Troxel et al. 2003).
Preanesthetic considerations of patients with increased ICP
Patients with intracranial pathology need to be triaged in order to stabilize both the cardiovascular and the respiratory system. Triage is required to identify and address life-threatening situations, such as post traumatic pneumothorax, haemothorax or rib fractures. A minimum baseline would be necessary to provide information concerning the patient’s general condition. More specifically, blood and urine samples should be collected in order to assume some basic indicators, such as serum glucose level, packed cell volume, total proteins, electrolytes and urine specific gravity. When the patient is stable (oxygenation, ventilation, normovolaemia), radiographs of the abdomen and the thorax can be performed in order to investigate for possible traumas, space occupying lesions, effusions etc. (Sande &West 2010). Neurological assessment must be done without administering anaesthesia when feasible. The Modified Glasgow Coma Scale (MGCS) system is one of the most usable prognostic tools in order to evaluate the neurological condition of the patient. It includes 3 stages of examination (level of consciousness, motor abilities and brainstem reflexes). A total score of 18 indicates a normal animal. A MGCS of 8 in the first 48 hours is a good prognostic indicator for survival (Table 1). As for the brain, computer tomography scanning does not always require general anaesthesia to identify head trauma while magnetic resonance imaging takes more time and demands anaesthesia. Neurological monitoring and evaluation every 30-60 min are mandatory for these patients in order to estimate treatment effectiveness (Kuo et al. 2018).
|Score||Motor activity||Brain stem reflexes||Level of consciousness|
|6||Normal gait, normal spinal reﬂexes||Normal pupillary light reﬂexes and oculocephalic reﬂexes||Occasional periods of alertness and responsive to environment|
|5||Hemiparesis, tetraparesis, or decerebrate activity||Slow pupillary light reﬂexes and normal to reduced oculocephalic reﬂexes||Depression or delirium, capable of responding but response may be inappropriate|
|4||Recumbent, intermittent extensor rigidity||Bilateral unresponsive miosis with normal to reduced oculocephalic reﬂexes||Semicomatose, responsive to visual stimuli|
|3||Recumbent, constant extensor rigidity||Pinpoint pupils with reduced to absent oculocephalic reﬂexes||Semicomatose, responsive to auditory stimuli|
|2||Recumbent, constant extensor rigidity with opisthotonus||Unilateral, unresponsive mydriasis with reduced to absent oculocephalic reﬂexes||Semicomatose, responsive only to repeated noxious stimuli|
|1||Recumbent, hypotonia of muscles, depressed or absent spinal reﬂexes||Bilateral, unresponsive mydriasis with reduced to absent oculocephalic reﬂexes||Comatose, unresponsive to repeated noxious stimuli|
Intravenous fluids in patients with raised ICP and traumatic brain injury are used to prevent secondary brain damage by improving CPP and oxygenation (Van der Jagt 2016). The goals of fluid therapy include instant correction of hypovolemia and hypotension, while avoiding a raised ICP. A systolic blood pressure lower than 90 mmHg is critical in humans and it should be avoided in animals too. In the beginning, isotonic crystalloids are recommended in 25% of the shock dose (20 ml kg-1 in dogs and 10 ml kg-1 in cats) over 10-15 min. Hypotension should be strictly avoided. Hypertonic saline is preferred for its rapid action and its influence on intracranial pressure (see below), although, like isotonic crystalloids, it has a limited duration of action (less than 75 min). It is administered in dosages of 4 ml kg-1 as 7.5% NaCl and 5.3 ml kg-1 3% NaCl, with a slow intravenous injection (over 10-15 min). Albumin administration should be avoided as it seems to increase the mortality rate (Kuo et al. 2018).
Normoxaemia (PaO2 > 80 mmHg and pulse haemoglobin oxygen saturation - SpO2 > 94%) and normoventilation (PaCO2 35-40 mmHg) are recommended in TBI patients, in order to stabilize the respiratory system. For oxygenation, flow-by oxygen administration is tolerated by most patients. Nasal cannulas should be avoided as they may evoke sneezing and increase ICP. Continuous monitoring is usually required; thus, oxygen cages would not be a practical option. Patients in coma or stupor without gag reflex are intubated. Temporary tracheostomy may also be a treatment option (Kuo et al. 2018). Prophylactic hyperventilation should be avoided as it induces vasoconstriction, followed by cerebral ischemia and secondary injury. The effect of hyperventilation in patients with raised ICP is rapid and effective in life-threatening situations. Thus, it is suggested in urgent cases, as well as neurosurgery in order to minimize brain swelling, while normocapnia should be restored, as soon as possible in order to avoid any side effects (Oertel et al. 2002, Curley et al. 2010).
Management of intracranial hypertension
It has been shown that a slight head elevation at a 30 degrees angle is effective in patients with raised ICP, facilitating cerebral venous outflow (Ng et al. 2004). Any increase in central venous pressure may cause an ICP increase. As a result, jugular occlusion (e.g., for blood sampling), coughing, sneezing, and the use of collars should be avoided (Dayrell-Hart & Klide 1989).
Mannitol is an osmotic diuretic that causes water to move from interstitial and intracellular areas of brain tissue to intravascular compartments, and finally to systemic circulation. It also increases CBF by blood dilution (reduced blood viscosity) and as a result more oxygen is delivered to the brain. Therefore, cerebral vasoconstriction occurs. All these mechanisms contribute to the decrease of the elevated ICP (Rosner & Coley 1987). Mannitol has an onset of action of 15-30 minutes after its infusion and it lasts for 1.5-6 h or even more (Bratton et al. 2007). The side effects may include hypovolaemia, hypotension and a reduction of CPP after excessive diuresis, pulmonary oedema from plasma expansion in patients with heart diseases and nephrotoxicity. It is preferred to be given in slow boluses of 0.2-1.0 gr kg-1 over 20-30 min (Grape & Ravussin 2012). Nevertheless, patients with elevated ICP sometimes have compromised blood-brain barrier and mannitol leaks into brain parenchyma, which leads to an increase ICP, known as rebound effect. Despite this concern, the guidelines for hyperosmotic therapy in traumatic brain injury support its use (Palma et al. 2006, Balloco et al. 2019).
Hypertonic saline (3.5%-7.5%) is also used to decrease ICP in a way similar to mannitol. Actually, it makes water move through blood-brain barrier and reduces brain water volume. Moreover, it causes plasma volume expansion, so it facilitates blood flow. In patients with hyponatremia, hypertonic saline may cause central pontine myelinolysis, so normonatraemia should be established before the infusion (Bratton et al. 2007). Hypertonic saline is efficient either given by boluses or by continuous infusion over 48-72 h (Grapes & Ravissin 2012). It is believed to be more effective than mannitol, as it has a stronger and longer effect on ICP, so it is preferred by some clinicians in patients with traumatic brain injury, but this matter is still controversial (Mangat et al. 2019).
In cerebral vasogenic oedema caused by brain tumours, glucocorticoids such as dexamethasone are a good choice in order to deal with both the oedema and the raised ICP. However, their use is harmful to patients with traumatic brain injury and should be avoided (Czosnyka et al. 2017).
Hyperglycaemia after head trauma is common in animals and is assumed to be caused by the sympatho-adrenal response following trauma. Increased glucose levels are associated with a worse neurological damage. Cerebral ischemia causing anaerobic glycolysis leading to cerebral acidosis is exaggerated by hyperglycaemia (Syring et al. 2001). Measurement of glucose levels as soon as possible after the trauma is an indicator of the damage that happened but not for its outcome (Syring et al. 2001, Sharma & Holowaychuk 2015). A clinician has to avoid ways and medications that may exacerbate hyperglycaemia, such as corticosteroids administration and dextrose solutions. On the other hand, insulin administration in order to decrease glucose levels is not yet recommended in veterinary medicine (Syring et al. 2001).
Installing mild hypothermia (32°C-35°C) decreases brain metabolism, CBF and ICP as well. It also reduces neurotransmitters, such as glutamate, it minimizes inflammatory cytokines, and it preserves blood-brain barrier. Therapeutic hypothermia can be induced by cooling devices such as blankets or even nasogastric lavage (Sande & West 2010). It is not the first choice for these patients, as it has side effects such as pneumonia, electrolyte disorders, arrhythmias, hypovolaemia and thrombocytopenia (Hayes 2009). Hypothermia is a solution to situations in which any other measure has been proven inefficient and should not be used prophylactically. Patients in hypothermia must be monitored to prevent and treat any side effect that may occur. Maintaining hypothermia for 24 hours is beneficial, but the patient should be rewarmed after that period. During that time, shivering is better to be avoided by opioids, benzodiazepines or propofol. In any way, fever must be avoided in these patients as it worsens the neurological condition (Sande & West 2010).
Seizures occurring after traumatic brain injury or because of epilepsy are a common phenomenon in both dogs and cats. They may occur even immediately after the injury (within 7 days) or later (after 7 days) (Kuo et al. 2018). They should be treated as soon as possible, as their side effects such as hyperthermia, hypoxemia, cerebral oedema and increased metabolic consumption increase ICP. These patients need to be observed and treated aggressively whenever they develop seizure activity (Sande & West 2010). Benzodiazepines are a good choice for rapid treatment of ongoing seizures, while a maintenance medication should be started after that (Kuo et al. 2018). The standard dosage of diazepam when given intravenously is 0.5 mg kg-1 (or higher if phenobarbital is already used) and its efficiency usually lasts 30 min. After that, the same dosage may be repeated. The standard dose of midazolam is about 0.2 mg kg-1 intravenously (Barnes Heller 2020). Phenobarbital can be used in an initial total daily dose of 16-20 mg kg-1 intravenously to reach stable plasma levels, as soon as possible. After that, a dose of 2-3 mg kg-1 twice daily can be used. Respiratory depression from phenobarbital should be considered, so these patients need to be monitored (Sande & West 2010). Levetiracetam administered after benzodiazepines at 30-60 mg kg-1 intravenously may be another option (Kuo et al. 2018).
Sedation and analgesia
Acepromazine is a phenothiazine with long action used for premedication or sedation in animals. Historically and anecdotally, it was strictly contraindicated in animals with seizure history, as it was assumed to decrease seizure threshold. However, according to recent studies, acepromazine was proven not to exacerbate seizure activity while in some cases it may even stop their occurrence (Tobias et al. 2006). On the other hand, acepromazine can lead to hypotension which is critical for patients with raised ICP and thus monitoring is mandatory (Bolaji-Alabi et al. 2018).
Benzodiazepines are frequently used for their anxiolytic and sedative action, while they have little effect on the respiratory system, cardiovascular system and ICP. In combination with propofol, they reduce its dose, so they prevent propofol-caused side effects, such as hypotension and hypοventilation (Kuo et al. 2018). In dogs, midazolam (0.1-0.5 mg kg-1) decreases CBF by reducing brain oxygen consumption and it protects the brain from hypoxia through this mechanism (Nugen et al. 1982, Robinson & Borer-Weir 2013). In cats, both midazolam and diazepam are used in conjunction with propofol, so as to decrease its dose (Robinson & Borer-Weir 2015).
Alpha-2 agonists are known for their sedative, anxiolytic and analgesic action, while they do not depress the respiratory system. Their reversible action is one of their benefits too. They are not a common choice in TBI, as they may lead to significant cardiovascular depression and reduce CBF. Dexmedetomidine (0.5-3 μg kg-1 h-1, followed by 0.5-1 μg kg-1 h-1) should be avoided and should be only used if there is no other choice (Kuo et al. 2018). Moreover, alpha-2 agonists may induce nausea and emesis, which is undesirable, and it needs to be controlled (Sinclair 2003). Due to the fact that the alpha-2 agonists affect the locus coeruleus and not the cortex, they can be used in patients with a history of seizures (Greene 2010).
Analgesia is important in the management of such patients, because pain and stress increase ICP. Opioids are mostly preferred as they have a low cardiovascular impact and their action may be reversible. They may induce depression of the respiratory system and they should be given with caution. Gag reflex and the ability to swallow need to be checked frequently, so as to avoid aspiration pneumonia. Continuous infusion of fentanyl in dose of 2-6 μg kg-1 h-1 is suggested to provide analgesia and avoid high blood levels of opioids (Kuo et al. 2018). Buprenorphine can be used at the dose of 0.01-0.02 mg kg-1 every 8 h intramuscularly (Kuo et al. 2018), but poor response to naloxone reversal should be considered. Butorphanol can be administered at 0.2-0.5 mg kg-1 intramuscularly (Leece 2016), repeated every 2 hours or more frequently (Sande & West 2010). Morphine is an opioid agonist used for analgesia with the side effect of emesis. Emesis in patients with intracranial pathology can aggravate raised ICP and it can be life threatening (Leece 2016).
Propofol and etomidate both reduce CMR and CBF and they preserve a good relationship between blood flow and metabolism (Greene 2010). More specifically, propofol (0.1-0.4 mg kg-1 min-1) is a good choice as it optimises CPP, it maintains cerebral autoregulation and it has both neuroprotective and antioxidant action. Side-effects, such as hypotension and hypoventilation, should be avoided by continuous monitoring, titrating doses and cardiovascular or respiratory support (Kuo et al. 2018). When given in conjunction with opioids such as fentanyl constant rate infusion, propofol overdose must be prevented (Greene 2010).
Barbiturate use may have side effects such as hypoventilation and hypotension, which can be prevented by monitoring, mechanical ventilation and cardiovascular support (Sande & West 2010). They are also known for their prolonged recovery time, which is not desirable for patients with head trauma (Armitage-Chan et al. 2007).
Ketamine (2-10 μg kg-1 min-1) (Kuo et al. 2018) was restricted for years in such patients, as it was assumed to increase ICP, despite its effects in cardiovascular and respiratory system. Nowadays, its use in TBI is reconsidered, because it may not be as dangerous as it was supposed to. Its use along with mechanical ventilation in order to preserve normocapnia and in combination with other sedative agents may be useful in neuroanaesthesia (Chang et al. 2013).
In general, total intravenous anaesthesia is a good option for patients with intracranial pathology.
Volatile anaesthetics such as isoflurane and sevoflurane have a dose-dependent effect on CBF and ICP. When used in concentrations below the minimal alveolar concentration (MAC), CBF is minimally affected (Greene 2010). However, ICP increases, while CPP decreases, when doses are over 1.5 MAC. Specifically, above MAC, cerebral vasodilation occurs and increases CBF and ICP, while hyperventilation and hypocapnia from anaesthesia enhance this effect. Volatile anaesthetics in high doses lead to the abolishment of cerebral perfusion autoregulation; as a result, perfusion depends on systemic pressure. Isoflurane disrupts autoregulation at 1 MAC, while sevoflurane at 1.5 MAC. In addition, sevoflurane is more water-soluble, and thus recover from anaesthesia is more rapid compared to isoflurane (Armitage-Chan et al. 2007).
In patients with increased ICP, inhalant anaesthetics should be kept in low concentrations in conjunction with appropriate ventilatory and cardiovascular support. When ICP is not increased, the vasodilation caused may even facilitate cerebral perfusion. Protocols including volatile anaesthetics in animals with intracranial pathology should better be avoided (Armitage-Chan 2007).
Anaesthetic considerations for specific conditions
Choosing the appropriate anaesthetic protocol for patients with traumatic brain injury demands a combination of anaesthetic agents that can preserve the cardiovascular and the respiratory function, maintain cerebral hemodynamic factors and have neuroprotective abilities so as to prevent brain ischemia. Opioids in conjunction with benzodiazepines are a good preanesthetic combination for patients with head trauma, with or without increased ICP (Armitage-Chan et al. 2007). Their use decreases the required dose for maintenance of anaesthesia (Covey-Crump & Murison 2008). Specifically, in patients with intracranial hypertension, opioids should be used in low doses, in order to avoid side effects, such as respiratory depression and hypotension (Sande & West 2010). For anaesthesia induction, thiopental or propofol are preferred (Greene 2010). Propofol has a more rapid recovery than barbiturates, but in high doses it may lead to brain ischemia. Dosage titration and arterial blood pressure monitoring should be applied during their use. Maintenance of anaesthesia may include a combination of propofol with fentanyl or even barbiturates (Armitage-Chan et al. 2007). Isoflurane and sevoflurane in low doses, along with blood pressure and ventilation support have minimal effects in cerebral hemodynamic factors. However, they are not the first choice for patients with increased ICP, as they may aggravate it (Kuo et al 2018).
When managing a patient with head trauma, continuous monitoring especially capnometry and arterial blood pressure measurement, cardiovascular support with fluids and inotropes and respiratory support with mechanical ventilation are deemed necessary (Armitage-Chan et al. 2007).
As mentioned above, the use corticosteroids in patients with brain tumours is beneficial as it restricts cerebral oedema and reduce increased ICP. The peri-operative use of prednisolone may help control CPP and ICP during surgery (Czosnyka et al. 2017). Opioids seem to be a good option for sedation of such patients, and they can be combined with benzodiazepines, decreasing the doses of the anaesthetic agents (Abelson et al. 2008). Propofol can be administered “to effect” until the jaw is relaxed, and endotracheal intubation is feasible. For the maintenance of anaesthesia, propofol in conjunction with an opioid is a safe approach, especially for patients with signs indicated intracranial hypertension. Their dose depends on changes in heart rate and MAP. MAP needs to be maintained in the range of 80-100 mmHg (Raisis et al. 2007). Volatile anaesthetics used in concentrations needed to maintain adequate anaesthesia depth can easily lead to an increased ICP and a decreased CPP due to their dose-dependent effect on ICP (Abelson et al. 2008).
Acepromazine is not contraindicated anymore to such patients so it can be used for sedation (Tobias et al. 2006).
Dexmedetomidine has neuroprotective properties, causing cerebral vasoconstriction and reducing brain oedema. It can also reduce cerebral excitatory neurotransmitters by decreasing sympathetic action and releasing noradrenaline (Gioeni et al. 2018). There is one study indicating that alpha-2 agonists, such as dexmetomidine, can be used for controlling the status epilepticus in both dogs and cats (Rusbridge et al. 2014). Dexmedetomidine infusion can be used for sedation and muscle relaxation in dose rates 3-7 μg kg-1 h-1. However, more research has to be done in order to use them as a routine protocol for controlling seizures (Gioeni D et al. 2018).
Benzodiazepines are a good sedative choice in patients with a history of seizures, as they are known for suppressing seizure activity. They should be given in case of ongoing seizures (Kuo et al. 2018).
Anaesthesia may be induced with propofol or even thiopental if available in the market, as they both are beneficial in increasing seizure threshold (Ilkiw 1992, Bergamasco et al. 2003). Total intravenous anaesthesia with propofol is a common and safe choice for the maintenance of such patients (Bergamasco et al. 2003). For patients in status epilepticus unresponsive to benzodiazepines, anaesthesia with propofol may be effective temporarily, but seizures may reappear at recovery. Ketamine is usually contraindicated in patients with intracranial pathology. However, its use can be beneficial in cases of refractory status epilepticus. It has neuroprotective properties by preventing cell death and it also decreases glutamate activity which is released excessively during refractory status epilepticus. Ketamine in conjunction with dexmedetomidine seemed to be a useful combination for three patients with refractory status epilepticus (Gioeni et al.2018). Ketamine (1 mg kg-1) with dexmedetomidine (3 μg kg-1 h-1) can be given over a 5-minute period. Their combination can be given as a continuous infusion for a period of 12 hours (Gioeni D et al. 2018).
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