24 Seizures
Seizure disorders represent a relatively common reason for emergency consultation and presentation. Seizures are classified as generalized or partial/focal, and the tonic–clonic form of generalized seizures forms the basis of the following discussion. In some animals with generalized seizures, the inciting cause is transient or rapidly reversible (e.g. intoxication, hypoglycaemia), while in others seizures occur due to a more long-term abnormality (e.g. chronic brain disorder resulting in epilepsy). The causes of seizures are typically divided into primary intracranial or extracranial causes and are summarized in Box 24.1.
Nursing Aspect
Owners quite commonly ring for advice with respect to cats and especially dogs that have suffered one or more seizures and the duty nurse is often the person from whom this initial advice is obtained. In the author’s opinion, not all animals that have suffered a seizure need to be examined. The recommendation to examine the animal at the clinic should be guided by the owner’s wishes but also after obtaining adequate information with respect to:
In animals that have suffered only one self-limiting (isolated) seizure, that appear to have recovered satisfactorily, and in which an obvious inciting cause has not been identified, it may be appropriate for the animal to remain at home for close monitoring. However, owners must be advised to ensure that the animal is not able to harm him/herself should another seizure occur. They should also contact the practice again either if another seizure occurs or if behavioural signs suggestive of prodrome or aura (pre-seizure behaviour) are observed.
It is recommended that animals with cluster seizures (two or more seizures within 24 hours) are examined as soon as possible, and animals in status epilepticus must be presented to the clinic immediately.
Signalment is important when considering the possible aetiology of a seizure disorder. For example, young animals are more likely to suffer intoxication from dietary indiscretion or to seizure as a result of congenital anomalies. Hypoglycaemia-induced seizures are more common in puppies, especially of toy breeds, while older animals are more likely to seizure as a result of intracranial neoplasia. Idiopathic epilepsy is more common in certain breeds (e.g. German shepherd dogs) and affected animals usually seizure for the first time at 1–5 years of age. Intracranial tumours are more common in certain breeds (e.g. Boxers), as are the range of inflammatory central nervous system diseases (e.g. Maltese terriers, Yorkshire terriers, Pugs). True idiopathic epilepsy is much less common in cats than it is in dogs.
Clinical Tip
A thorough history is mandatory for all animals with seizures, although the timing should be governed by the patient’s clinical status on presentation. Owners should be asked to describe the seizure episode(s) as thoroughly as possible, including pre-, intra- and postictal phases. It is important to establish the number of seizures that have occurred and their timing, the nature and duration of the seizure(s), any known or possible exposure to inciting factors (e.g. intoxication; recent feeding with portosystemic shunt), previous seizure history and previous medical history. If the patient is already on anticonvulsive therapy, the drugs, dosages and timing of last administration should be established. Details of any monitoring of serum anticonvulsant levels should be obtained if the owner knows this information.
Major body system examination may need to be delayed in an animal that presents actively seizuring. Neurological examination may be normal or severely abnormal in animals with seizure disorders. Some animals present in the middle of a seizure, some with postictal abnormalities, while others have fully recovered. A full neurological examination is warranted in any animal with a seizure history but it is sometimes necessary to wait for postictal abnormalities to resolve before a reliable examination can be performed. In addition, anticonvulsive medications that may need to be administered in an emergency will also potentially alter the findings of a neurological examination.
Cardiovascular examination may be abnormal in animals that have seizured. True seizures are unlikely to occur as a result of a primary cardiovascular disorder although cerebrovascular abnormalities may cause other neurological signs. Cardiovascular abnormalities that may occur secondary to seizures include tachycardia, hyperaemic mucous membranes and rapid capillary refill time. Furthermore, in some cases the cause of the seizure may also have direct effects on the cardiovascular system; this is especially common with certain poisons. In general, seizures should not cause systemic hypoperfusion but perfusion abnormalities may be seen following severe sustained seizure activity. In addition, the author has anecdotally noted a variety of cardiovascular abnormalities in animals with primary brain disease that have been presumed to be a direct result of the cerebral disorder (a brain–heart connection has been documented in people). Finally, depending on the cause of the seizures and their severity and duration, some animals may present with intracranial hypertension that may be detectable clinically as bradycardia and systemic hypertension (Cushing’s reflex – see Ch. 28). If facilities allow, systemic blood pressure should be measured in all animals presenting with active seizures or marked postictal abnormalities.
Respiratory examination may or may not be normal in animals with seizures. Seizures are unlikely to occur as a result of a primary respiratory disorder and the most common respiratory abnormalities identified are panting and tachypnoea. Aspiration may occur as a consequence of seizuring and other abnormal respiratory findings are possible in such cases. Neurogenic (noncardiogenic) pulmonary oedema may also cause respiratory abnormalities.
Rectal temperature may be normal, decreased or increased in animals with seizures depending on the timing of presentation. Severe seizure activity, in particular status epilepticus (see below), may result in marked hyperthermia which may need to be managed specifically (see Ch. 16).
Clinical Tip
The need to perform an emergency database in an animal with a seizure disorder should be governed by the patient’s clinical status at the time of presentation. Blood glucose should be checked as a minimum in all animals that present either seizuring or with marked neurological abnormalities. In middle-aged to older dogs that present with clinically significant hypoglycaemia, a blood sample should be collected for measurement of serum insulin concentration prior to therapeutic administration of intravenous glucose if possible. Insulinomas are seen most commonly in medium to large breed dogs and have been identified in dogs as young as 3 years old.
Checking for hyper- or hyponatraemia and hypocalcaemia is also recommended if possible although these abnormalities are much less frequently implicated than hypoglycaemia as a cause of seizures in small animals.
In animals that are already receiving anticonvulsive therapy, it is recommended to obtain samples as early on as possible for measurement of serum drug concentrations.
Clinical Tip
Routine diagnostic imaging is rarely a priority in patients with seizures but may be required following initial stabilization. For example, respiratory abnormalities may need to be investigated with thoracic radiography that may show evidence of aspiration pneumonia (alveolar pattern in right middle lung lobe and ventral parts of other lobes) or neurogenic (noncardiogenic) oedema (caudodorsal interstitial to alveolar lung pattern). Abdominal radiography may occasionally be of use for example in some types of intoxication. Referral for more specialist and/or advanced diagnostic imaging may be indicated in patients thought to be suffering from an on-going seizure disorder (e.g. abdominal ultrasonography for portosystemic shunt, cerebral magnetic resonance imaging (MRI) for primary brain disorder).
Animals presenting in the postictal phase of a generalized seizure do not require any treatment if physical examination is normal. Patients with persistent postictal abnormalities may need to be hospitalized for on-going monitoring. This is often determined as much by owner preference as it is by the patient’s clinical status.
Diazepam should be administered per rectum (1 mg/kg; 2 mg/kg if receiving concurrent phenobarbital) in an animal that presents actively seizuring to facilitate intravenous catheter placement. Proprietary rectal diazepam tubes may be used, or injectable diazepam may be diluted with water or saline to increase the volume to be administered and then infused per rectum. Using injectable diazepam allows more accurate dosing but involves a greater time delay in preparation. Depending on the size of the animal, the use of a well-lubricated long intravenous catheter (with stylet removed), urinary catheter or nasooesophageal feeding tube will allow the diazepam to be administered more proximally in the rectum. This should minimize spillage from the anus and maximize drug absorption. The rectal mucosa has an extensive blood supply and drug absorption should occur readily so long as the solution is in contact with the mucosa and not mixed into faecal material. Flow-by oxygen supplementation should also be provided initially.
An intravenous catheter should be placed into a peripheral vein and a sample obtained via the catheter for blood glucose and serum electrolyte measurement and potentially a more extensive emergency database. Additional diazepam (0.5 mg/kg i.v.) should then be administered and additional anticonvulsive therapy employed (see Status epilepticus, below) if necessary. On-going maintenance fluid therapy (see Ch. 4) and close monitoring should be provided; glucose supplementation may be required in some cases.
The decision to start oral anticonvulsive therapy should be made on an individual case basis and will depend on factors such as:
Oral anticonvulsive therapy is likely to be indicated in animals suspected of having an on-going seizure focus or those that have suffered severe or sustained seizure activity necessitating aggressive parenteral treatment. Although completely normal previously, animals that have suffered severe seizures secondary to intoxication may require short-term (months) tapered oral anticonvulsive therapy due to seizure-induced neuronal damage.
Head trauma may rarely be associated with seizures in the short term. In addition, animals occasionally develop seizures some time after the traumatic incident and it is presumed that the seizures are a result of a seizure focus resulting from the prior traumatic brain injury. On-going oral anticonvulsive therapy is likely to be indicated in these cases.
Although older texts describe a longer period of time, the current definition of status epilepticus is sustained generalized seizure activity for more than 5 minutes, or multiple consecutive seizures without return of consciousness in between. Status epilepticus can cause severe hyperthermia which can have marked and potentially life-threatening consequences (see Ch. 38), and may be associated with significant cardiovascular abnormalities (often tachycardia and hypertension early on, followed by bradycardia and hypotension). Hypoglycaemia and hypoxaemia may also occur. There is a significant risk of permanent neuronal damage due to sustained seizure activity and timely and aggressive intervention is warranted. Neurogenic pulmonary oedema may develop rapidly following status epilepticus.
Management of status epilepticus typically starts with rectal diazepam administration (1 mg/kg; 2 mg/kg if receiving concurrent phenobarbital) as above to facilitate intravenous catheter placement, and flow-by oxygen supplementation is provided. Further diazepam administration (0.5 mg/kg i.v.) is then performed in an attempt to control the clinical signs. However, typically no more than three boluses are administered before the use of an additional drug is considered. In general, this involves heavily sedating or anaesthetizing the patient for a variable period of time in order to stop or minimize motor activity associated with seizuring.
If financial constraints do not exist, a constant rate infusion of propofol is used. The appropriate dose is administered (2 mg/kg aliquots slowly i.v. to effect), followed by a constant rate infusion starting at 6 mg/kg/hr and titrating upwards (or downwards) to effect. The use of a syringe driver here is preferred although a solution of propofol in normal saline can be made and administered via a fluid administration set using an infusion pump. These patients are recumbent and immobile, and although not ideal, it may therefore be possible to manage them adequately without the use of an infusion pump if one is not available. In cases in which high rates of propofol infusion prove necessary, additional agents should be considered in a propofol-sparing capacity. In particular, midazolam has been used either as intermittent boluses (0.1–0.5 mg/kg i.v.) or preferably as a constant rate infusion (0.1–0.8 mg/kg/hr). The dose of propofol generally starts to be tapered after 24 hours (e.g. reducing by 25% every 2–4 hours).
If financial or practical constraints preclude the use of a propofol infusion, pentobarbital boluses may be a viable alternative. However, to the author’s knowledge, a sterile formulation of this agent for injectable use is no longer readily available and the risks associated with using nonsterile preparations available for euthanasia must clearly be borne in mind and discussed with the owner. The recommended dose is 5–20 mg/kg slowly i.v. to effect (e.g. 3 mg/kg aliquots q 90 s). The use of thiopentone and inhalational anaesthesia may also be considered.
Endotracheal intubation should be performed in all anaesthetized patients to protect the airway and prevent aspiration. Oxygen supplementation is not mandatory unless specific indications exist. Vital parameters should be monitored and recorded regularly, and fluid therapy administered to maintain hydration and electrolyte concentrations. In some cases general anaesthesia or heavy sedation is required for 48 hours or more.
Phenobarbital loading should be performed in all animals presenting in status epilepticus. The most aggressive intravenous protocols (e.g. 3 mg/kg slow i.v. q 30–60 min, up to total dose of 18–24 mg/kg in 24 hours) are typically reserved for those cases requiring anaesthesia. The delay in onset of action of phenobarbital means that it is generally not helpful in controlling signs very early on but its sedative effects are likely to facilitate propofol dose reduction. Blood for serum drug concentration measurement should be obtained prior to loading if possible in animals already on phenobarbital therapy. Following loading, patients are usually maintained on 3–5 mg/kg slow i.v. q 12 hr for 24–48 hours before changing to enteral therapy.
The approach to status epilepticus is summarized in Box 24.2.
BOX 24.2 Management of status epilepticus
Nursing Aspect
Standard nursing measures for recumbent patients should be implemented in animals anaesthetized or heavily sedated to control seizures. These measures include: