This case study is
based on a 27-year-old gentleman that was attended by an ambulance crew in an
amusement arcade. The information from this case study has been used to
formulate a clinical diagnosis and possible differential diagnoses. This
assignment will discuss the pathophysiology behind the clinical diagnosis, followed
by a treatment plan tailored to this case study. Furthermore, a critical
analysis will be conducted on whether the current ‘gold standard’ line of
treatment is best in comparison to other evidence-based literature.
Case Presentation and Clinical Impression
The patient is a
27-year-old male, who was said to be playing on the fruit machines when a
friend witnessed him drop to the floor and begin shaking and jerking. Upon initial
examination the patient was still convulsing, had frothy red sputum coming from
his mouth and was incontinent of urine. On gaining the patients past medical history
(PMH), the patient had
a diagnosis of the seizure disorder epilepsy. The patient is prescribed
Lamotrigine medication, an anticonvulsant treatment for epilepsy and bipolar
disorder (Excellent, 2017). The first clinical
impression at present is an epileptic seizure. It is important to consider other
potential causes, differential diagnoses and explore them.
Seizures are not unique
to the neurological disorder epilepsy; they can happen in most serious
illnesses or injuries affecting the brain (Porth, 2009;
Falvo, 2014). These include metabolic derangements, infections (sepsis),
tumours, hypoglycaemia, hypoxia, CVA (acronym but not been written in full prior), drug/
alcohol abuse or withdrawal, vascular lesions, congenital deformities and traumatic
brain injury (Porth, 2009; Hauser & Beghi, 2008).
From the PMH, examination of current signs and symptoms as well as discussing events
pre-seizure, you can begin to deduce or exclude possible potential diagnoses.
At this stage of
the medical investigation, his presenting state is not down to a traumatic occurrence
that we are aware of. After speaking with his friend and getting a comprehending
the events leading up to the seizure and by visibly assessing the environment, there
appears to be no indication the seizure caused traumatic injury.
At least 40% of
type 1 diabetic patients will have at least one hypoglycaemic seizure (Jacobson et al., 2007 cited in Steinhoff, 2011). Hypoglycaemia
and non-kenotic hyperglycaemia are metabolic errors that cause epileptic seizures
(Wolf et al., 2005 cited in Steinhoff, 2011). Diabetes
is not mentioned in his PMH, yet a routine blood glucose reading was taken as
part of basic observations. The BM reading came out at 5.1, which falls within
normal clinical ranges. A diabetic seizure cannot be ruled out. A research
project carried out by Umpierrez et al (2002)
discussed that hyperglycaemia was present in 38% of patients admitted to a
hospital in Atlanta, GA in 1998 and only 26% of them had known diabetes, and
the remaining 12% had no history of diabetes. The patients’ BM will be monitored, especially if he was to show
signs of another seizure, to use as a comparison.
The development of
seizures can be associated with cerebral haemorrhage (Delanty,
2002). This is associated with spontaneous intracerebral or subarachnoid
haemorrhages correlating with hypertension (Delanty,
2002). In regards to this case study, the
patient is not hypertensive, so at this stage in my assessment there is nothing
to lead me to believe this could be causing the seizure. Furthermore, he is not
on any prescribed blood pressure medications.
Mobbs (2001) state that there is a strong link between hypertension and strokes,
with hypertensives being at increased risk. It is said that strokes occur more
often in men than women, so in regards to this case study this patient is at
greater risk (Hof & Mobbs, 2001). A patient
experiencing a stroke, whether it’s a TIA or a CVA can present with a seizure,
due to structural changes in the brain (Delanty, 2002).
According to Ford, Kelson and Rigge (1999) people
who have epilepsy are more prone to strokes. Research carried out by Koubeissi, Alshekhell & Mehndiratta (2015) states
that seizures in strokes are very common and can happen after 2 weeks of the
onset of haemorrhage. Approximately 1-35% of patients develop late seizures
after having a stroke (Koubeissi, Alshekhell &
Mehndiratta, 2015). A FAST test carried out during the basic assessment,
once recovered from the current seizure will determine if this was a cause. However,
further tests will need to be carried out in hospital to rule out a stroke indefinitely.
and Froscher (2004) cited in Steinhoff (2011) and Delanty (2002)
both state that the most common causes of an acute symptomatic seizure in
adulthood can be influenced and triggered by alcohol or drug abuse. Delanty (2002) lead on to say that alcohol withdrawal
seizures refer to seizures that happened secondary to the withdrawal of alcohol
post a period of persistent administration and abuse. With regards to this
gentleman there are no significant signs of substance abuse.
Large doses of
penicillin can cause seizures (Delanty, 2002) again
at this time it cannot be rule out that the patient had taken a large dose of
penicillin. Cocaine, phencyclidine and amphetamines are all recreational drugs
strongly associated with seizures (Delanty, 2002),
this cannot be ruled out without various blood tests or confirmation from the
patient that he hasn’t taken such drugs.
Once the patient is
capable of verbal conversation, questions will be asked about his seizure
history and what happened prior to this episode. This conversation will not be
able to rule anything out but it could inform further investigations/ examinations.
It is important to be aware of all potential differential diagnoses and
constantly reassess the patient because nothing can be indefinitely ruled out.
Considering all the
presenting symptoms, a working diagnosis of an epileptic seizure has been
formulated. This leads on to the discussion of the pathophysiology of epileptic
seizures in section 2.
Epilepsy is a
condition that affects people of all ages, with more than 45,000 in the UK
living with the condition (Scott, 2012). It is
possible to have good seizure control with strict prescribed treatment following
diagnosis this is the case for about 80% of diagnosed patients (Scott, 2012). Epilepsy is a seizure disorder and is
the second most common neurologic disorder, represented as a syndrome not as a
specific disease (McCance, 2010). Epileptic
seizures are unique to every individual, not one epileptic patient is the same,
the signs and symptoms, post and pre-seizure are different (Shorvon, 2010). The term epilepsy is applied where
there is no underlying and correctable solution for the random abnormalities in
brain activity, resulting in seizures (McCance, 2010).
Epilepsy is a broad
term of the primary condition that causes seizures (McCance,
2010). It is important to note that a seizure is only one feature of the
epileptic syndrome (Book, 2009). Epilepsy starts when a group of neurons
lose conductivity stimulation (impulses conveying from the periphery towards
the central nervous system) and function as an epileptogenic focus (Scott, 2012). The neurons in this process are
hypersensitive and easily activated so the sudden change in cellular
environment causes the neurones to react and fire abnormally (Scott, 2012). This process of the neurones firing abnormally
is exacerbated by the increased permeability of the cytoplasmic membranes increasing
the hypersensitivity of the neurons (Scott, 2009).
when neurons are synchronously active resulting in neurons firing and sending
messages using electrical signals (Albert et al., 2002).
A resting membrane potential is determined by the gradients of ions and by the
permeability of each type of ion, so in the event of primary abnormality leads to the membrane weakness
resulting insatiability excess of the resting potential (Scharfman, 2007). Each signal that passes through a
neuron represents ions flowing in and out, via protein channels. This is
controlled by neurotransmitters, a type of signalling molecule (Cooper, 2000). Neurotransmitters bind to their
receptors to relay messages about opening or closing the ion channels (Bromfield, Cavazos & Sirven, 2006).
Neurotransmitters are either excitatory, opening the protein channels, making
the neurons more likely to execute an action potential or inhibitory, closing
the protein channels, making the neurons less likely to fire (Bromfield, et al., 2006).
Seizures are the
outcome of paroxysmal events associated with abnormal electrical discharges of
neurones in the brain (Scott, 2012). This is the
result of clusters of neurons in the brain becoming impaired; therefore sending
out sudden excitatory signals, repeatedly (Albert et
al., 2002). The paroxysmal discharge is when there is too much or too
little of inhibition or excitation, a disturbance in the mechanism where there
should be a balance (Scharfman, 2007). The
principal excitatory neurotransmitter is Glutamate and GABA is the principal
inhibitory neurotransmitter within the brain (Book,
2009; Bromfield, et al., 2006). Glutamate and NMDA receptors are for
fast long synaptic activation of the sodium channels compared to the GABA
receptor that is mediated via the potassium channels (Book,
This excess firing
is characterised into two simultaneous events in a group of neurons (Albert et al., 2002); high frequency bursts of action
potentials and hyper-synchronisation (Bromfield, et
al., 2006). The increase of extracellular calcium opens the sodium
channel following the sudden burst in activity produced by the long-lasting
depolarisation of neurons (Boss & Huether, 2013),
generating repetitive action potentials and increasing the frequency of the
neurons involved (Albert et al., 2002). Tumours,
brain injuries or infections can affect these channels. Once the intensity of
seizure discharge has reached its optimum and successfully progressed to
adjacent brain areas then it will become epileptogenic and the excitement
messages will feed back to other parts of the brain (Scott,
2009). Finally the discharge will eventually become less frequent once
the messages have been passed around the brain, the seizure will stop (Scott, 2009).
The physical signs
a patient will present during their seizure are dependent on which channels are
simultaneously firing and which neurons. There are two types of seizures; focal
seizures (aka partial seizures) or generalised seizures (Scott, 2012). A seizure is classified by clinical
manifestations, site of origin, EEG correlates, or response to therapy (McCance, 2010).
A focal seizure is limited to one
hemisphere or lobe of the brain, involving individual neurons associated with
structural abnormalities in the cortical brain tissue (McCance,
2010). Some seizures might start of as a partial seizure, localised to
one hemisphere of the brain but the activity may spread to the entire brain,
leading to a generalised seizure (Scott, 2012).
Partial seizures are categorised into four sub types; Jacksonian seizure,
sensory seizure, complex partial seizure and secondarily generalised seizure (Scott, 2012).
seizures involve a group of neurons acting together, do not have a focal onset
and originate from a subcortical or deeper brain focus opposed to happening in
cortical tissue (McCance, 2010). The widespread
nature of these seizures means that both hemispheres of the brain are affected
as a result of cellular, biochemical or structural abnormalities (McCance, 2010). Compared to partial seizures
consciousness is always impaired or lost (McCance, 2010).
This type of seizure is spilt into four sub types; absence or petit mal,
myoclonic, generalised tonic-clonic and akinetic (Scott,
In regards to this
case study the patient is having a tonic-clonic seizure. A tonic- clonic
seizures present as the most dramatic of seizures in epileptics (Bruni, 2004). These epileptic outbursts generally
happen without warning (Shovon, 1993). The
seizure is made up of 2 phases; the seizure is initiated by loss of
consciousness; the patient will drop to the floor, followed by the body
becoming stiff (tonic phase) and then interchangeable episodes of muscle spasms
and relaxation (clonic phase) (Scott, 2012; Bruni, 2004).
Consciousness is regained slowly in the postictal period (Bruni, 2004).
The acute anatomical
changes that may be specifically present in a tonic- clonic seizure include;
increase in blood pressure and heart rate, apnoea, mydriasis, urinary
incontinence, cyanosis and diaphoresis (Bodhankar &
Vyawahare, 2008; Bruni, 2004).
From the onset,
seizure activity greatly increases cerebral metabolism due to physiological
mechanisms compensating for this perturbation. Cerebral blood flow is greatly
increased so massive cardiovascular and autonomic changes begin to occur. When
blood pressure rises, so does cardiac output and rate, resulting in hydrosis,
hyperpyrexia, salivation and emesis.
As the seizure
progresses the compensatory physiological mechanisms fail. Fatigue happens when
the body struggles to compensate. Systemic and cerebral hypoxia is common,
there is increased oxygen demand required due to the convulsions and later
pulmonary hypertension occurs. As the chest muscles tighten from the convulsions
the patients respiratory rate increases due to ventilation difficulties. Hence
oxygen is indicated in the treatment of seizures.
with convulsions can be a medical emergency, if the following features present
then the patient is classed as time critical; major problems with ABC, serious
head injury, failed treatment of epileptics or underlying infection (JRCALC, 2016). It is importation to stress that JRCALC
are UK ambulance guidelines. The primary assessment tool for any medical or
traumatic emergency follows the same stepwise ABCDE approach, which is taught
as standard (Bonner, Carpenter & Garcia, 2007).
This patients’ treatment can be sub-divided; primary survey (ABC), secondary/
disability survey, treatment and then the decision on what care pathway to take
whether the patient needs to be transported to the most appropriate healthcare
department or if a safeguarding referral needs to be made. Each stage is made
in the best interest of the patient.
The first goal of
treatment, before administering anticonvulsants is the stepwise approach of
airway, breathing and circulation (ABCDE). Only once ABCDE has been assessed
and corrected (need to be stabilised or resolved even if it’s a short-term
intervention), only at that point the clinician should move onto a thorough
assessment (Bonner, Carpenter & Garcia, 2007).
The patient is still
fitting on the crew’s arrival so maintaining the airway is vital. JRCALC (2016) states
that a nasopharyngeal airway is the most effective airway adjunct in a
convulsing patient, however cautions need to be taken if you suspect basal
skull fracture or facial injuries. In this case the risks have been eliminated,
therefore a nasopharyngeal airway is indicated. An oropharyngeal airway should
not be used if the patient is still convulsing (JRCALC,
2016). At present, there is no research indicating that during
a seizure an airway adjunct should be used and if it is beneficial to use one
during a seizure or not (Osborne et al., 2014).
This patient is
still actively fitting so putting in an airway could be extremely hard and
could be unsafe for the clinician to do so, in the events of a violent seizure
the patient in unpredictable. If an OPA cannot be put in on the first attempt
it is important to move on and not waste time.The main focus at the moment is
to stop the patient fitting, once this is done successfully all other aspects
will resolve without airway interventions.
This patient is
fitting in a public area, so it is hard to position the patient in a comfortable
position with adequate support. JRCALC (2016)
states that a convulsing patient need to be positioned in a comfortable position
whilst protecting them from any dangers, especially their head. Injuries to the
mouth and tongue are common sequelae of epileptic convulsions (JRCALC, 2016), so this needs to be closely monitored
because you do not want the patient to occlude their airway with their tongue
or other bodily fluids (Brigo, Nardone &
Bongiovanni, 2012). The likelihood of the patient staying in one
position is unlikely, due to the sudden bursts of jerking movements.
In 2001, DeToldedo and Lowe carried out some research into the
best position to place a patient having a seizure. It is noted in the study
that patients often aspirate during a seizure and are often prone to
dislocating their shoulders. DeToldedo and Lowe (2001)
concluded that placing a fitting patient in the lateral decubitus position is
more beneficial to minimise harm and further injury during the seizure episode
(DeToldedo & Lowe, 2001). The main outcome
of this position is it minimises the risk of aspiration (DeToldedo & Lowe, 2001). The ambulance guidelines (JRCALC, 2016) do not state what position to put the
patient in; it states that it should be comfortable.
During an active convulsion,
it is hard to gain an accurate SpO2 measurement due to rapid movement. Therefore,
it is always assumed safe and best practice to administer 15 litres per minute
of oxygen until a suitable, reliable SpO2 measurement can be obtained (JRCALC, 2016). Only once an SpO2 level has been
achieved can the clinician suitably alter the oxygen flow to the patient, to
try and achieve the target saturation. The reason behind this process and
assumption of oxygen needed is because during a convulsion the brain is acutely
being starved of oxygen (JRCALC, 2016). The
patient’s oxygen saturation levels need to be constantly monitored and if required
corrected accordingly even in the post- ictal stages. Once again research
carried out by Osborne et al., (2014), states that the use of oxygen
supplement and what dose should be administrated is a grey area because there
is uncertainty about its value to the patient.
It is important to
note that the aforementioned interventions do not resolve the seizure but help
prevent the patient from deteriorating and causing other problems, primary to
the seizure. Drug interventions help solve seizures or at least stop epileptic
episodes. Thus, it is important not to spend too much time correcting ABCDE.
Everything needs to be weighed up in regards to how long clinicians stay on
scene to administer drugs, which is more beneficial to the patient and time
Once the primary
ABCDE survey has been done, anticonvulsants should be given before doing a full
diagnostic work-up (Chen & Wasterlain, 2006).
If substantial changes were to occur especially after drug treatment has been
undertaken then these changes should be treated appropriately (Chen & Wasterlain, 2006).
JRCALC (2016) guidelines state that most tonic-clonic
convulsions are self-contained and do not require an anticonvulsant or any drug
treatment to resolve them. JRCALC (2016) states
that drugs should only be administered if convulsions last longer than 5 minutes
or are reoccurring without the patient making a full recovery from the first.
et al. (2014), suggest that the first line of treatment in a confirmed fitting
patient is the patient’s own midazolam, if it is available to hand it should be
administered via the buccal or intranasal route. This is supported in JRCALC (2016), which states that the clinician should
refer to the patient’s own midazolam guidelines and if the patient does not
have this medication then resort to diazepam. Midazolam is the preferred drug
of choice when treating a convulsion compared to diazepam because of the faster
onset (Osborne et al., 2014). Diazepam’s delay
in onset is due to the clinician needing to gain intravenous access or by the
rectal route (PR), which is seen to have slower absorption (Osborne et al., 2014).
JRCALC (2016), states that the
intravenous (IV) route is preferred for terminating fits, and should be the
first choice. Attempting to gain IV access in a fitting patient can be
extremely hard due to jerking movements. Osborne et al.
(2014) states that attempting IV access can delay the timely
administration of emergency medications and delay hospital transfer.
Only upon early
recognition should diazepam be considered when using the PR route, where IV
access cannot be obtained (JRCALC, 2016). If IV
access is gained after PR diazepam has been administered then a single dose of
IV diazepam can be administered but only if necessary (JRCALC,
2016). There is no value in giving a drug as a preventive; it only works
during an active, on-going seizure (JRCALC, 2016).
The PR route,
specifically for this patient is not appropriate. This patient is having a
seizure in a public place so to keep his dignity, the IV route is most
appropriate then the PR route. If we were treating this patient in his own home
or in a private location then this route could be used in the best interest of
the patient. Rectal diazepam is safe and most effective drug treatment, in the
pre-hospital environment (JRCALC, 2016).
Wasterlain (2006) carried out a literature review critically analysing
different drug treatments for fitting patients. In their research they found
that phenytoin, lorazepam, diazepam and phenobarbital were the top
anticonvulsant drugs to compare. Most of the literature compared in the Chen and Wasterlain (2006) study found no significant
differences in using any of the drugs mentioned. They were all seen acceptable
in initial treatment for epileptics (Chen &
In regards to
whether this patient needs to be transported to an emergency department (ED) or
not, it is dependent upon whether the patient has reacted to the treatment. If
the patient has recovered to normal state then a conversation can be had, as to
whether this has happened before and if anything was acutely different.
Patient’s known to have seizure disorders know how their bodies react and
recover, if nothing was acutely different or worrying to the patient or if his
observations are normal then they do not need transporting to the nearest ED (Osborne et al., 2014). If this patient has recovered
well and there was nothing abnormal in his observations then he would not have
to travel in, what the crew would do is advise and treat on scene. A
conversation will be had to advise the patient to seek medical support if these
seizure episodes started to happen more often.