IntroductionThis case study isbased on a 27-year-old gentleman that was attended by an ambulance crew in anamusement arcade. The information from this case study has been used toformulate a clinical diagnosis and possible differential diagnoses. Thisassignment will discuss the pathophysiology behind the clinical diagnosis, followedby a treatment plan tailored to this case study. Furthermore, a criticalanalysis will be conducted on whether the current ‘gold standard’ line oftreatment is best in comparison to other evidence-based literature. Section 1:Case Presentation and Clinical ImpressionThe patient is a27-year-old male, who was said to be playing on the fruit machines when afriend witnessed him drop to the floor and begin shaking and jerking.
Upon initialexamination the patient was still convulsing, had frothy red sputum coming fromhis mouth and was incontinent of urine. On gaining the patients past medical history(PMH), the patient hada diagnosis of the seizure disorder epilepsy. The patient is prescribedLamotrigine medication, an anticonvulsant treatment for epilepsy and bipolardisorder (Excellent, 2017).
The first clinicalimpression at present is an epileptic seizure. It is important to consider otherpotential causes, differential diagnoses and explore them. Seizures are not uniqueto the neurological disorder epilepsy; they can happen in most seriousillnesses 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 traumaticbrain injury (Porth, 2009; Hauser & Beghi, 2008).From the PMH, examination of current signs and symptoms as well as discussing eventspre-seizure, you can begin to deduce or exclude possible potential diagnoses.
At this stage ofthe medical investigation, his presenting state is not down to a traumatic occurrencethat we are aware of. After speaking with his friend and getting a comprehendingthe events leading up to the seizure and by visibly assessing the environment, thereappears to be no indication the seizure caused traumatic injury. At least 40% oftype 1 diabetic patients will have at least one hypoglycaemic seizure (Jacobson et al., 2007 cited in Steinhoff, 2011). Hypoglycaemiaand non-kenotic hyperglycaemia are metabolic errors that cause epileptic seizures(Wolf et al., 2005 cited in Steinhoff, 2011). Diabetesis not mentioned in his PMH, yet a routine blood glucose reading was taken aspart of basic observations. The BM reading came out at 5.
1, which falls withinnormal clinical ranges. A diabetic seizure cannot be ruled out. A researchproject carried out by Umpierrez et al (2002)discussed that hyperglycaemia was present in 38% of patients admitted to ahospital in Atlanta, GA in 1998 and only 26% of them had known diabetes, andthe remaining 12% had no history of diabetes.
The patients’ BM will be monitored, especially if he was to showsigns of another seizure, to use as a comparison. The development ofseizures can be associated with cerebral haemorrhage (Delanty,2002). This is associated with spontaneous intracerebral or subarachnoidhaemorrhages correlating with hypertension (Delanty,2002). In regards to this case study, thepatient is not hypertensive, so at this stage in my assessment there is nothingto lead me to believe this could be causing the seizure. Furthermore, he is noton any prescribed blood pressure medications. Hof andMobbs (2001) state that there is a strong link between hypertension and strokes,with hypertensives being at increased risk. It is said that strokes occur moreoften in men than women, so in regards to this case study this patient is atgreater risk (Hof & Mobbs, 2001). A patientexperiencing 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) peoplewho have epilepsy are more prone to strokes. Research carried out by Koubeissi, Alshekhell & Mehndiratta (2015) statesthat seizures in strokes are very common and can happen after 2 weeks of theonset of haemorrhage. Approximately 1-35% of patients develop late seizuresafter 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.Vassellaand Froscher (2004) cited in Steinhoff (2011) and Delanty (2002)both state that the most common causes of an acute symptomatic seizure inadulthood can be influenced and triggered by alcohol or drug abuse. Delanty (2002) lead on to say that alcohol withdrawalseizures refer to seizures that happened secondary to the withdrawal of alcoholpost a period of persistent administration and abuse.
With regards to thisgentleman there are no significant signs of substance abuse. Large doses ofpenicillin can cause seizures (Delanty, 2002) againat this time it cannot be rule out that the patient had taken a large dose ofpenicillin. Cocaine, phencyclidine and amphetamines are all recreational drugsstrongly associated with seizures (Delanty, 2002),this cannot be ruled out without various blood tests or confirmation from thepatient that he hasn’t taken such drugs. Once the patient iscapable of verbal conversation, questions will be asked about his seizurehistory and what happened prior to this episode.
This conversation will not beable to rule anything out but it could inform further investigations/ examinations.It is important to be aware of all potential differential diagnoses andconstantly reassess the patient because nothing can be indefinitely ruled out. Considering all thepresenting symptoms, a working diagnosis of an epileptic seizure has beenformulated.
This leads on to the discussion of the pathophysiology of epilepticseizures in section 2.Section2: PATHOPHYSIOLOGYEpilepsy is acondition that affects people of all ages, with more than 45,000 in the UKliving with the condition (Scott, 2012). It ispossible to have good seizure control with strict prescribed treatment followingdiagnosis this is the case for about 80% of diagnosed patients (Scott, 2012). Epilepsy is a seizure disorder and isthe second most common neurologic disorder, represented as a syndrome not as aspecific disease (McCance, 2010). Epilepticseizures 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 wherethere is no underlying and correctable solution for the random abnormalities inbrain activity, resulting in seizures (McCance, 2010).
Epilepsy is a broadterm of the primary condition that causes seizures (McCance,2010). It is important to note that a seizure is only one feature of theepileptic syndrome (Book, 2009). Epilepsy starts when a group of neuronslose conductivity stimulation (impulses conveying from the periphery towardsthe central nervous system) and function as an epileptogenic focus (Scott, 2012). The neurons in this process arehypersensitive and easily activated so the sudden change in cellularenvironment causes the neurones to react and fire abnormally (Scott, 2012). This process of the neurones firing abnormallyis exacerbated by the increased permeability of the cytoplasmic membranes increasingthe hypersensitivity of the neurons (Scott, 2009).
Seizures happenwhen neurons are synchronously active resulting in neurons firing and sendingmessages using electrical signals (Albert et al., 2002).A resting membrane potential is determined by the gradients of ions and by thepermeability of each type of ion, so in the event of primary abnormality leads to the membrane weaknessresulting insatiability excess of the resting potential (Scharfman, 2007). Each signal that passes through aneuron represents ions flowing in and out, via protein channels. This iscontrolled by neurotransmitters, a type of signalling molecule (Cooper, 2000). Neurotransmitters bind to theirreceptors to relay messages about opening or closing the ion channels (Bromfield, Cavazos & Sirven, 2006).Neurotransmitters are either excitatory, opening the protein channels, makingthe neurons more likely to execute an action potential or inhibitory, closingthe protein channels, making the neurons less likely to fire (Bromfield, et al., 2006).
Seizures are theoutcome of paroxysmal events associated with abnormal electrical discharges ofneurones in the brain (Scott, 2012). This is theresult of clusters of neurons in the brain becoming impaired; therefore sendingout sudden excitatory signals, repeatedly (Albert etal., 2002). The paroxysmal discharge is when there is too much or toolittle of inhibition or excitation, a disturbance in the mechanism where thereshould be a balance (Scharfman, 2007). Theprincipal excitatory neurotransmitter is Glutamate and GABA is the principalinhibitory neurotransmitter within the brain (Book,2009; Bromfield, et al.
, 2006). Glutamate and NMDA receptors are forfast long synaptic activation of the sodium channels compared to the GABAreceptor that is mediated via the potassium channels (Book,2009). This excess firingis characterised into two simultaneous events in a group of neurons (Albert et al., 2002); high frequency bursts of actionpotentials and hyper-synchronisation (Bromfield, etal., 2006). The increase of extracellular calcium opens the sodiumchannel following the sudden burst in activity produced by the long-lastingdepolarisation of neurons (Boss & Huether, 2013),generating repetitive action potentials and increasing the frequency of theneurons involved (Albert et al.
, 2002). Tumours,brain injuries or infections can affect these channels. Once the intensity ofseizure discharge has reached its optimum and successfully progressed toadjacent brain areas then it will become epileptogenic and the excitementmessages will feed back to other parts of the brain (Scott,2009). Finally the discharge will eventually become less frequent oncethe messages have been passed around the brain, the seizure will stop (Scott, 2009).
The physical signsa patient will present during their seizure are dependent on which channels aresimultaneously firing and which neurons. There are two types of seizures; focalseizures (aka partial seizures) or generalised seizures (Scott, 2012). A seizure is classified by clinicalmanifestations, site of origin, EEG correlates, or response to therapy (McCance, 2010). A focal seizure is limited to onehemisphere or lobe of the brain, involving individual neurons associated withstructural abnormalities in the cortical brain tissue (McCance,2010).
Some seizures might start of as a partial seizure, localised toone 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). Generalisedseizures involve a group of neurons acting together, do not have a focal onsetand originate from a subcortical or deeper brain focus opposed to happening incortical tissue (McCance, 2010). The widespreadnature of these seizures means that both hemispheres of the brain are affectedas a result of cellular, biochemical or structural abnormalities (McCance, 2010).
Compared to partial seizuresconsciousness 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,2012). In regards to thiscase study the patient is having a tonic-clonic seizure. A tonic- clonicseizures present as the most dramatic of seizures in epileptics (Bruni, 2004). These epileptic outbursts generallyhappen without warning (Shovon, 1993). Theseizure is made up of 2 phases; the seizure is initiated by loss ofconsciousness; the patient will drop to the floor, followed by the bodybecoming stiff (tonic phase) and then interchangeable episodes of muscle spasmsand relaxation (clonic phase) (Scott, 2012; Bruni, 2004).Consciousness is regained slowly in the postictal period (Bruni, 2004).
The acute anatomicalchanges that may be specifically present in a tonic- clonic seizure include;increase in blood pressure and heart rate, apnoea, mydriasis, urinaryincontinence, cyanosis and diaphoresis (Bodhankar , 2008; Bruni, 2004). From the onset,seizure activity greatly increases cerebral metabolism due to physiologicalmechanisms compensating for this perturbation. Cerebral blood flow is greatlyincreased so massive cardiovascular and autonomic changes begin to occur. Whenblood pressure rises, so does cardiac output and rate, resulting in hydrosis,hyperpyrexia, salivation and emesis. As the seizureprogresses the compensatory physiological mechanisms fail. Fatigue happens whenthe body struggles to compensate.
Systemic and cerebral hypoxia is common,there is increased oxygen demand required due to the convulsions and laterpulmonary hypertension occurs. As the chest muscles tighten from the convulsionsthe patients respiratory rate increases due to ventilation difficulties. Henceoxygen is indicated in the treatment of seizures. Section3: TREATMENTPatients presentingwith convulsions can be a medical emergency, if the following features presentthen the patient is classed as time critical; major problems with ABC, serioushead injury, failed treatment of epileptics or underlying infection (JRCALC, 2016). It is importation to stress that JRCALCare UK ambulance guidelines. The primary assessment tool for any medical ortraumatic emergency follows the same stepwise ABCDE approach, which is taughtas 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 takewhether the patient needs to be transported to the most appropriate healthcaredepartment or if a safeguarding referral needs to be made. Each stage is madein the best interest of the patient. The first goal oftreatment, before administering anticonvulsants is the stepwise approach ofairway, breathing and circulation (ABCDE). Only once ABCDE has been assessedand corrected (need to be stabilised or resolved even if it’s a short-termintervention), only at that point the clinician should move onto a thoroughassessment (Bonner, Carpenter & Garcia, 2007). The patient is stillfitting on the crew’s arrival so maintaining the airway is vital. JRCALC (2016) statesthat a nasopharyngeal airway is the most effective airway adjunct in aconvulsing patient, however cautions need to be taken if you suspect basalskull fracture or facial injuries.
In this case the risks have been eliminated,therefore a nasopharyngeal airway is indicated. An oropharyngeal airway shouldnot be used if the patient is still convulsing (JRCALC,2016). At present, there is no research indicating that duringa seizure an airway adjunct should be used and if it is beneficial to use oneduring a seizure or not (Osborne et al., 2014).
This patient isstill actively fitting so putting in an airway could be extremely hard andcould be unsafe for the clinician to do so, in the events of a violent seizurethe patient in unpredictable. If an OPA cannot be put in on the first attemptit is important to move on and not waste time.The main focus at the moment isto stop the patient fitting, once this is done successfully all other aspectswill resolve without airway interventions. This patient isfitting in a public area, so it is hard to position the patient in a comfortableposition with adequate support. JRCALC (2016)states that a convulsing patient need to be positioned in a comfortable positionwhilst protecting them from any dangers, especially their head. Injuries to themouth and tongue are common sequelae of epileptic convulsions (JRCALC, 2016), so this needs to be closely monitoredbecause you do not want the patient to occlude their airway with their tongueor other bodily fluids (Brigo, Nardone &Bongiovanni, 2012). The likelihood of the patient staying in oneposition is unlikely, due to the sudden bursts of jerking movements. In 2001, DeToldedo and Lowe carried out some research into thebest position to place a patient having a seizure.
It is noted in the studythat patients often aspirate during a seizure and are often prone todislocating their shoulders. DeToldedo and Lowe (2001)concluded that placing a fitting patient in the lateral decubitus position ismore beneficial to minimise harm and further injury during the seizure episode(DeToldedo & Lowe, 2001). The main outcomeof this position is it minimises the risk of aspiration (DeToldedo & Lowe, 2001). The ambulance guidelines (JRCALC, 2016) do not state what position to put thepatient 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 minuteof oxygen until a suitable, reliable SpO2 measurement can be obtained (JRCALC, 2016). Only once an SpO2 level has beenachieved can the clinician suitably alter the oxygen flow to the patient, totry and achieve the target saturation. The reason behind this process andassumption of oxygen needed is because during a convulsion the brain is acutelybeing starved of oxygen (JRCALC, 2016).
Thepatient’s oxygen saturation levels need to be constantly monitored and if requiredcorrected accordingly even in the post- ictal stages. Once again researchcarried out by Osborne et al., (2014), states that the use of oxygensupplement and what dose should be administrated is a grey area because thereis uncertainty about its value to the patient. It is important tonote that the aforementioned interventions do not resolve the seizure but helpprevent the patient from deteriorating and causing other problems, primary tothe seizure.
Drug interventions help solve seizures or at least stop epilepticepisodes. 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 onscene to administer drugs, which is more beneficial to the patient and timeeffective.
Once the primaryABCDE survey has been done, anticonvulsants should be given before doing a fulldiagnostic work-up (Chen & Wasterlain, 2006).If substantial changes were to occur especially after drug treatment has beenundertaken then these changes should be treated appropriately (Chen & Wasterlain, 2006).JRCALC (2016) guidelines state that most tonic-clonicconvulsions are self-contained and do not require an anticonvulsant or any drugtreatment to resolve them. JRCALC (2016) statesthat drugs should only be administered if convulsions last longer than 5 minutesor are reoccurring without the patient making a full recovery from the first. Osborneet al. (2014), suggest that the first line of treatment in a confirmed fittingpatient is the patient’s own midazolam, if it is available to hand it should beadministered via the buccal or intranasal route. This is supported in JRCALC (2016), which states that the clinician shouldrefer to the patient’s own midazolam guidelines and if the patient does nothave this medication then resort to diazepam. Midazolam is the preferred drugof choice when treating a convulsion compared to diazepam because of the fasteronset (Osborne et al.
, 2014). Diazepam’s delayin onset is due to the clinician needing to gain intravenous access or by therectal route (PR), which is seen to have slower absorption (Osborne et al., 2014). JRCALC (2016), states that theintravenous (IV) route is preferred for terminating fits, and should be thefirst choice. Attempting to gain IV access in a fitting patient can beextremely hard due to jerking movements.
Osborne et al.(2014) states that attempting IV access can delay the timelyadministration of emergency medications and delay hospital transfer. Only upon earlyrecognition should diazepam be considered when using the PR route, where IVaccess cannot be obtained (JRCALC, 2016). If IVaccess is gained after PR diazepam has been administered then a single dose ofIV diazepam can be administered but only if necessary (JRCALC,2016).
There is no value in giving a drug as a preventive; it only worksduring an active, on-going seizure (JRCALC, 2016). The PR route,specifically for this patient is not appropriate. This patient is having aseizure in a public place so to keep his dignity, the IV route is mostappropriate then the PR route.
If we were treating this patient in his own homeor in a private location then this route could be used in the best interest ofthe patient. Rectal diazepam is safe and most effective drug treatment, in thepre-hospital environment (JRCALC, 2016). Chen andWasterlain (2006) carried out a literature review critically analysingdifferent drug treatments for fitting patients. In their research they foundthat phenytoin, lorazepam, diazepam and phenobarbital were the topanticonvulsant drugs to compare.
Most of the literature compared in the Chen and Wasterlain (2006) study found no significantdifferences in using any of the drugs mentioned. They were all seen acceptablein initial treatment for epileptics (Chen &Wasterlain, 2006). In regards towhether this patient needs to be transported to an emergency department (ED) ornot, it is dependent upon whether the patient has reacted to the treatment. Ifthe patient has recovered to normal state then a conversation can be had, as towhether this has happened before and if anything was acutely different.Patient’s known to have seizure disorders know how their bodies react andrecover, if nothing was acutely different or worrying to the patient or if hisobservations are normal then they do not need transporting to the nearest ED (Osborne et al.
, 2014). If this patient has recoveredwell and there was nothing abnormal in his observations then he would not haveto travel in, what the crew would do is advise and treat on scene. Aconversation will be had to advise the patient to seek medical support if theseseizure episodes started to happen more often.