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Status Epilepticus: Clinical Features, Pathophysiology, and Treatment

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Presentation on theme: "Status Epilepticus: Clinical Features, Pathophysiology, and Treatment"— Presentation transcript:

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Epilepsy Case Presentation and Diagnostic Process

A key opinion leader presents the case of a 16-year-old male with epilepsy, and considers the diagnostic process to accurately determine the classification. 

Trevor Resnick, MD : The case that forms the basis for this discussion is a 16-year-old boy who presents with a convulsion while eating lunch at school. And the convulsion started with him flinging his soda up into the air. He had no prior history of any risk factors other than sensitivity to bright lights and video games.

He was seen by a neurologist. The neurologist did an examination, some blood testing, an MRI, which was normal, and then did an EEG [electroencephalogram], which demonstrated a 4-Hz generalized spike-and-wave pattern, and a photoparoxysmal response at flash rates of 12, 14, 16, and 18 Hz.

Two months after that first incident he had another convulsion, and his teachers reported that he would stare into space in class. He was ultimately diagnosed with partial seizures, with secondarily generalized tonic-clonic seizures. He was initially treated with levetiracetam, 500 mg twice a day, but soon after starting therapy he experienced fatigue and dizziness, and his parents observed that he was more aggressive, more irritable at home, and this was also being reported to the parents by his teachers.

If we put the EEG aside, because the EEG is part of the testing that takes this from a diagnosis of a seizure or 2 seizures and moves it in a direction of a classification of an epilepsy or an epilepsy syndrome. And there are various things that can do that. It can be either an EEG, it can be an imaging study, it can be a genetic mutation. It can even be family history. All these things go into the piece of the puzzle that enables us, or sometimes doesn’t enable us, to make the diagnosis of an epilepsy syndrome.

In this case we have 2 clinical seizures in a previously healthy adolescent who then has an EEG that provides additional information. If we take it a step at a time, the first piece of information is that he has a seizure that is characterized initially by him throwing a soda into the air, and then him having what is described as a generalized tonic-clonic seizure, and then a week later another similar seizure.

If we start at the top and we say, “OK, this is a seizure that clinically looks like a generalized tonic-clonic seizure, the first question is, is this a generalized seizure, or is this a focal seizure that has evolved into a generalized seizure?” And with the information that we have from the clinical story, one would have to say, “I don’t know, it could be either.”

And then the question is, “Well, how do we then look into it further?” Looking into it further to see whether it’s one or the other would require either more clinical information, which we don’t have, or additional tests like an EEG and/or an MRI. In this case the only information we have is an EEG, and the EEG shows findings that are very typical and consistent with a generalized seizure, and not a focal seizure evolving into a generalized seizure. I think that’s the first point of discussion in this case.

It’s perfectly reasonable under the circumstances to say, this adolescent had a generalized seizure, and I don’t know whether it’s A or whether it’s B. However, after you’ve done the EEG, then it would be more appropriate to say the EEG findings are more consistent with a generalized seizure, and therefore, he would have to be treated as if he had a generalized seizure.

Video EEG monitoring is a significant tool that we use in diagnosing patients with epilepsy, or in characterizing the nature of the seizure. This case that we’ve been discussing, assuming the EEG wouldn’t have shown us something that was classic for a generalized seizure, assuming it was normal and the patient was having more frequent seizures, a video EEG may have helped us to characterize the nature of the EEG because it’s a longer study. And also, to be able to capture these episodes and enable us to actually diagnose a more specific epilepsy syndrome.

The other scenario is in patients who are having events that appear to be seizures but are not clearly seizures, and under those circumstances video EEG may enable us to discriminate between one and the other.

Another question that comes up, and it comes up in this patient as well, is what tools do you use to get the maximum information from the patients to come up with a diagnosis that is as specific as possible? In many cases you can’t do that. But that’s often where you have to go back in terms of the clinical history, where if you’re suspicious that they have a specific seizure type, you are going to ask about certain things in the history that the patient may not have volunteered because they thought they weren’t important, or they’re so overwhelmed with having had a generalized tonic-clonic seizure that they don’t think to mention the other issue.

I think added clinical information is really important. Family history is significant. Especially in 2020, highly evolved genetic mutation testing that’s ever expanding has provided us with a diagnosis of a genetic mutation as the cause of the patient’s seizures that really wasn’t available to us 20 years ago. And our ability to say this patient has generalized seizures with this specific mutation is a very different way of describing epilepsy than it had been previously.

So genetic mutation testing, imaging studies, family history, clinical history, EEG, a lot of those things we already had, but being able to add these other parameters in has allowed us be much more specific with a diagnosis.

To get back to this adolescent, in this case if you weren’t sure whether the seizure was focal at onset or generalized, then doing an imaging study would be perfectly appropriate to see if there was structural pathology that was causing the patient’s seizures. Once you have an EEG that demonstrates a generalized spike wave on the EEG, the likelihood of the imaging study providing any additional information is very small. This is the kind of case though where doing genetic mutation studies, or an epilepsy panel, may provide additional information, especially if there’s a positive family history of seizures.

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Clinical Case Presentation on Absence Seizures Diagnosis and Treatment Care Services and Outcomes in an Adult Patient

M. s. umashankar.

Department of Pharmaceutics, SRM College of Pharmacy, SRM Institute of Science and Technology, Kanchipuram, Tamil Nadu, India

A. Bharath Kumar

1 Department of Pharmacy Practice, SRM College of Pharmacy, SRM Institute of Science and Technology, Kanchipuram, Tamil Nadu, India

Absence seizures are often associated with impaired or loss of consciousness clinically proved to have an impact on motor and cognitive abnormalities of the nerve cells of the brain. Seizure admits several etiopathophysiological events leading to several neurofunctional changes in the reticulothalamocortical circuitry zones of the central nervous system. This paves the episodes of absence seizure events. A clinical case report of absence seizure in a 25 years age adult patient came to the hospital with impaired consciousness. The brain magnetic resonance imaging scanning of the patient detected a small focal flair hypertensive area in the right parasellar region close to cavernous sinus with mild flair hypersensitivity in the left cavernous sinuses, right maxillary, and ethmoid sinusitis. The electroencephalogram of the brain showed normal waves with electrode artifacts was observed. The patient was confirmed with absence seizures, and he was treated with oxcarbazepine 150 mg twice daily. The patient was recovered from seizure and discharged with medications. He was called for follow-up examination once in 3-month period.

I NTRODUCTION

Seizure is a short episode of abnormal electrical activity in the brain with intense electrical signals.[ 1 ] Typically, absence seizure lasts from few seconds to minutes with the loss of consciousness and no any marked convulsions, often occur in children aged <10 years.[ 1 , 2 ] Absence seizures explicit behavioral arrest, unresponsiveness, cyclic blinking of eyelids, suddenly stopped speech and movement, mouth chewing, lip smacking, and rubbing fingers. The diagnosis includes complete blood count test, brain computerized tomography scan, magnetic resonance imaging (MRI), electroencephalogram, and cerebrospinal fluid examination which provides the evidence and demonstrates clearly the origin of seizure lesions in the brain. The prevention and management of the absence seizure can be done using phenytoin and carbamazepine with the ketogenic diet.[ 3 , 4 , 5 , 6 ]

C ASE R EPORT

Mr. VA, a 25 year old male patient with an episode of absence seizures, was presented to the general medicine with loss of consciousness lasted for 2–4 min, giddiness, and dimness of vision. The patient reported that he regained from his loss of consciousness after few minutes, however, the giddiness persisted. The patient had no vomiting, involuntary movements, headache, fever, urinary incontinence, and palpitations.

Family history

His family history had that his mother suffered from generalized tonic–clonic seizures and developed intense erythematous patch under the right eye spreading over the right cheek. She took phenobarbitone, iron, and vitamin supplements.

Past medical history details

Mr. VA is a bachelor male with no any history of head injury, neurological illness, and drug abuse. He experienced the episode of absence seizure characterized by loss of consciousness and impaired memory quite sometime in the past 2 years. He said that he remained unresponsive and unable to recall his events after retrieved from the episode and experienced baseline memory disturbances. The patient's past medical history showed no any chronic diseases include diabetes mellitus, hypertension, and cardiovascular problems. Similar to his mother, the patient had intense erythematous patch under the right eye spreading over the right cheek with no numbness or itching.

General examination reports

The patient was conscious, oriented, afebrile, pulse rate of 82 bpm, and with normal respirations. His blood pressure was normal, and the cardiovascular sounds S1 and S2 were normal. The chest X-ray revealed normal, and the electrocardiogram showed no ST-T changes with any sinus rhythm. P/A was soft, no organomegaly and no pallor/icterus/cyanosis/pedal edema were seen.

Hematology laboratory examinations exhibited hemoglobin 14.7 g/dl, packed cell volume 42%, white blood cells 10,300/cum, neutrophils 83%, eosinophils 6%, basophils 2%, lymphocytes 12%, monocytes 2%, red blood cells 4.7 × 10 6 /mm 3 , erythrocyte sedimentation rate 30/h, mean corpuscular volume 89 fl, mean corpuscular hemoglobin 31 pg/cell, mean corpuscular hemoglobin concentration 35 g/dl, and platelets of 234,000 cells/cum.

Serum electrolytes values were found to be normal. Blood sugar test reported fasting blood sugar was 107 mg/dl, random blood sugar was 170 mg/dl, postprandial blood sugar level was 150 mg/dl, and capillary blood glucose was 84 mg/dl. HbA1C was also found within normal. Liver function test reported that elevated alkaline phosphatase 71 international units/liter, and other parameters were found to be normal. Renal function test detected normal values; however, a slightly elevated uric acid level was found to be l4.3 mg/dl. His cholesterol test revealed all the parameters were found to be normal.

Neurological investigation reports

The patient's central nervous system examination revealed normal higher functions with no motor sensory deficits and bilateral plantar flexor. The electroencephalogram of the brain showed that the electrical waves remained normal with some electrode artifacts confirming the detection of absence seizure [ Figure 1 ].

Electroencephalogram of the brain

The patient's brain MRI scan revealed the presence of small focal flair hypertensive area in the right parasellar region close to cavernous sinus and mild flair hypersensitivity in the left cavernous sinus. The MRI scans also revealed right maxillary and ethmoid sinusitis and no blooming restrictions were noted[ 7 ] [ Figure 2 and Table 1 ]. Patient medications chart.

Magnetic resonance image scan of the brain

Patient medications chart

D ISCUSSION

The above clinical findings and laboratory tests reported that the patient was detected with the episodes of absence seizures. In the case, the patient was presented with absence seizures which progressively associate with temporary loss of consciousness.[ 8 ] The etiology represented that there was an increase in the cerebral blood flow, increased intracranial pressure which ultimately provokes the development of seizure; it was evident in the case of Mr. VA. The patient's pathophysiology revealed neuronal changes which led to changes in the reticulothalamocortical circuitry which may be associated with genetic liability exhibiting absence seizure.[ 9 ] Patient has not incurred any kind of symptoms in his childhood, however it was manifested recently. A study by Avanzini et al ., showed an increased oscillatory activity in the reticulothalamocortical circuitry proved to be the cause for the absence seizure which has made a promising diagnostic tool in this patient.[ 9 , 10 ]

Since the patient's mother had seizure and had not underwent any proper treatment which may be due to the economic status which may be the reason conjoined with genetic liability in this case.[ 11 ]

As reported by Thomas et al . sudden withdrawal of drugs, such as diazepines, psychotropic, antidepressant drugs, autoimmune diseases, brain accidents, and electrolyte disturbances being a factor which imposes the incidences of absence seizures.[ 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 ]

After 1 week of hospital stay, the patient was treated with the drugs as shown in Table 1 . He was thoroughly monitored and found that his vital signs were normal. He responded well to the medications, and diet intake was normal. He showed positive improvement in his conditions and showed no further seizure incidences. The patient was advised for stress management, adequate rest, and regular sleeping with healthy diet. The patient was asked for a follow-up every 3 months, and he was then discharged from the hospital.[ 2 , 13 , 14 ] On his first follow-up visit, he was quite normal and taken the discharge medications regularly, and he reported no any new episode of seizures. An effective preventive measure toward the patient's health status can prevent the risk factors which ultimately improves better quality of life, as reported by Nutthaya Vongkasamchai et al .[ 15 ]

C ONCLUSION

The pathophysiological mechanisms underlying epilepsy are autism spectrum disorder (ASD) resistance and sudden ASD dose reduction can trigger withdrawal response of seizure; hence, dose reduction or removal should be done gradually. Effective understanding of pathophysiological mechanisms, drug targeting, antiepileptogenesis, and genetics can provide a better understanding of epilepsy and its management. New molecular drug target, pharmacogenomics, and documentation of the individual patient's report can improve the treatments effectively.[ 16 , 17 ]

Clinical pharmacist should be positioned in the clinical practice to identify the risk factors for seizure origin, early diagnosis, and treatment can reduce the healthcare cost. Initiating awareness programs on disease prevention and management, regular patient follow-up care, and medication adherence can reduce the individual's disease burden and hospital revisit which can ultimately promote health-related quality of life. Regular implementation of these practices among healthcare team can reduce the individual's healthcare cost and hospital revisit.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Conflicts of interest.

There are no conflicts of interest.

Acknowledgement

We would like to thank Dr. K.S. Lakshmi, Dean, SRM College of Pharmacy, SRM Institute of Science and Technology, for her encouragement and support.

R EFERENCES

Management of Epilepsy

Oct 13, 2014

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Management of Epilepsy. Robert L. Macdonald M.D., Ph.D. Department of Neurology Vanderbilt University Medical Center Nashville, TN . Management of Epilepsy – Learning Objectives. Identify the differences between seizures and epilepsy.

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Presentation Transcript

Management of Epilepsy Robert L. Macdonald M.D., Ph.D. Department of Neurology Vanderbilt University Medical Center Nashville, TN

Management of Epilepsy – Learning Objectives • Identify the differences between seizures and epilepsy. • Describe the management of a patient after a first seizure. • Describe the management of a patient with epilepsy. • Discuss the management of epilepsy in women of child bearing age.

Epidemiology of Seizures and Epilepsy • Seizures • Incidence: approximately 80/100,000 per year • Lifetime prevalence: 9% (1/3 benign febrile convulsions) • Epilepsy • Chronic recurring, unprovoked seizures • Incidence: approximately 45/100,000 per year • Point prevalence: 0.5-1%

Seizure Classification • Partial seizures (focal or local origin) • Simple partial seizures with: • motor signs • somatosensory or special sensory symptoms • autonomic symptoms or signs • psychic symptoms (disturbance of higher cerebral function) • Complex partial seizures with: • Impaired consciousness • Presence and nature of aura (simple partial origin) • Automatisms and other motor activity • Secondary generalized seizures

Seizure Classification • Primary generalized seizures (bilateral origin) • Absence • Myoclonic • Atonic • Tonic • Tonic-clonic

Epilepsy Syndromes • Partial epilepsies • Idiopathic • Symptomatic • Cryptogenic • Generalized epilepsies • Idiopathic • Symptomatic • Cryptogenic • Undetermined epilepsies • Special syndromes

Questions Raised by a First Seizure • Seizure or not? • Partial (focal) or generalized onset? • Evidence of CNS dysfunction? • Seizure type? Syndrome type? • Metabolic or other precipitant? • Studies? • Treatment - start an antiepileptic drug (AED)?

Evaluation of a First Seizure • History, physical exam • Blood tests: CBC, electrolytes, glucose, Ca, Mg, hepatic and renal function • Lumbar puncture only if meningitis or encephalitis suspected and potential for brain herniation is ruled out • Blood or urine screen for drugs • Partial seizures are presumed to be due to a structural lesion unless proven otherwise. • Electroencephalogram if indicated • CT or MR brain scan if indicated

Evaluation of a First Seizure-Precipitants • Metabolic and Electrolyte Imbalance • Low (occ high) blood glucose, Na, Ca, Mg • Stimulant/other proconvulsant intoxication • IV drug use, cocaine, ephedrine, herbal remedies • Sedative/medication reduction • Sleep deprivation, stress • Hormonal variations • Infection

Medical Management of First Seizure Whether or not to treat a first seizure is controversial. • The risk of recurrence within 5 years is 16-62% and with a single unprovoked seizure (normal EEG and MRI) is about 40%. • Abnormal imaging, abnormal EEG or + family history of epilepsy increase recurrence risk. • Quality of life issues are important for AED Rx. • Was the seizure “precipitated”? If so, Rx with an AED is not necessary – remove the precipitant. • Treat a first seizure if there is a high likelihood of developing epilepsy (recurrence rate is reduced by AED treatment).

Medical Management of Epilepsy • First diagnose seizure type(s), epilepsy syndrome, and etiology. • Try pharmacotherapy first (unless etiology necessitates surgery). • Use monotherapy with an AED that is the most appropriate for seizure type/epilepsy syndrome (but other considerations also play a role), and safest. • Start at a low dose, increase slowly.

Medical Management of Epilepsy • Try to reach the lowest effective dose. • Target: seizure control with no side effects • We may use drug levels if needed (but we should not be bound by the drug levels) • If drug A fails, try drug B monotherapy. • Try polytherapy if monotherapy fails. • anticipate drug interactions

Choosing an AED • Seizure type • Epilepsy syndrome • Pharmacokinetic profile • Interactions/other medical conditions • Efficacy • Expected adverse effects • Useful as monotherapy - simplifies treatment and reduces adverse effects • Cost

Phenytoin (Dilantin) Carbamazepine (Tegretol, Carbatrol) Valproate (Depakote) Phenobarbital Primidone (Mysoline) Clonazepam (Klonopin) Ethosuximide (Zarontin) Methsuximide (Celontin) Felbamate (Felbatol)* Gabapentin (Neurontin)¶ Lamotrigine (Lamictal)* Topiramate (Topamax)* Tiagabine (Gabitril) Levetiracetam (Keppra)¶ Oxcarbazepine (Trileptal)* Zonisamide (Zonegran) Pregabalin (Lyrica) Antiepileptic Drugs oldnew *new drugs approved to be used in monotherapy ¶no monotherapy indication, but comparative monotherapy trial

Spectrum of Efficacy of Old AEDs AED Partial AbsenceMyoclonic Phenytoin ++ - - Carbamazepine ++ - - Valproate ++++++ Primidone + - - Phenobarbital + - - Clonazepam + + + Methsuximide + + + Ethosuximide - ++ -

Spectrum of Efficacy of New AEDs AED Partial Absence Myoclonic Felbamate (Felbatol) + + + Gabapentin (Neurontin) + - - Lamotrigine (Lamictal) + + +/- Topiramate (Topamax) + +/- + Tiagabine (Gabitril) + - - Levetiracetam (Keppra) + + + Oxcarbazepine (Trileptal) + - - Zonisamide (Zonegran) + + + Pregabalin (Lyrica) + - -

Partial Seizures- The First AED • First AED - in general: • Carbamazepine (Tegretol, Carbatrol) • Phenytoin (Dilantin) • Oxcarbazepine (Trileptal) • Topiramate (Topamax) • Valproate (Depakote) • First AED - special situations when other AEDs may be considered • Gabapentin (Neurontin) • Lamotrigine (Lamictal) • Levetiracetam (Keppra) • ?Zonisamide (Zonegran), ?Pregabalin (Lyrica)

Generalized Seizures- The First AED • Generalized onset seizures Absence: valproate* = ethosuximide Myoclonic: valproate, clonazepam Tonic-clonic: valproate = phenytoin, carbamazepine * the risk of valproate-induced hepatic failure must be carefully weighed in young children

AED Initiation and Monitoring • Discuss likely and unlikely but important adverse effects. • Discuss likelihood of success. • Discuss recording/reporting seizures (seizure calendar), adverse effects, potential precipitants. • Obtain appropriate “baseline” laboratory tests • CBC, platelets, LFTs • Initiate therapy with an appropriate dose. • Monitor AED levels when appropriate.

AED Interactions • AEDs that induce metabolism of other drugs: carbamazepine, phenytoin, phenobarbital • AEDs that inhibit metabolism of other drugs: valproate, felbamate • AEDs that are highly protein bound: valproate, phenytoin, tiagabine • Other drugs may alter metabolism or protein binding of antiepileptic drugs

AED Serum Concentrations • In general AED serum concentrations can be used as a guide for evaluating the efficacy of medication therapy for epilepsy. • Serum concentrations are useful when optimizing AED therapy, assessing compliance, or teasing out drug-drug interactions. • They should be used to monitor pharmacodynamic and pharmacokinetic interactions.

Evaluation After Seizure Recurrence • Progressive pathology? • Avoidable precipitant? • If on an AED • Problem with compliance or pharmacokinetic factor? • Increase dose? • Change medication? • If on multiple AEDs • Convert to monotherapy from polytherapy? • Eliminate sedative drugs first • Withdraw antiepileptic drugs slowly over several months • If not on AED • Start therapy?

Preconception Counseling and Teratogenicity • Preconception information should be offered to all females with childbearing potential since most major malformations occur at an early stage in pregnancy, often before the woman knows she is pregnant. • If changes in AED medication are to be made, they should be completed before conception. • If AED treatment is needed, a single agent is preferred.

Preconception Counseling and Teratogenicity • The use of phenytoin, valproate, carbamazepine, lamotrigine, and phenobarbital has been associated with an increased risk of major malformations and minor morphological anomalies. (3% with carbamazepine or lamotrigine, 7% with valproate, and 15% with two or more AEDs). • It is not known if vigabatrin, gabapentin, levetiracetam, topiramate, oxcarbazepine, pregabalin, and tiagabine are associated with a risk of fetal abnormalities in humans. • Women with epilepsy who are planning a pregnancy should take folic acid 1 mg/day in the preconception period and throughout the pregnancy; vitamin K should be used in the last month of pregnancy in women on enzyme-inducing AEDs.

Contraception and AEDs • For women on nonenzyme-inducing AEDs (valproate, benzodiazepines, vigabatrin, gabapentin, tiagabine, levetiracetam, pregabalin), all current contraceptive methods are suitable. • Hormonal forms of contraception are affected by enzyme-inducing AEDs (phenytoin, barbiturates, carbamazepine, oxcarbazepine, topiramate [>200 mg/day], and lamotrigine); women taking these forms of contraception should be counseled on their risks and benefits.

Non-Drug Treatment/Lifestyle Modifications • Adequate sleep • Avoidance of alcohol, stimulants, etc. • Avoidance of non-precipitants • Stress reduction — specific techniques • Adequate diet • Exercise

Discontinuing AEDs • Seizure free 2 years implies overall >60% chance of successful withdrawal in some epilepsy syndromes • Favorable factors • Control achieved easily on one drug at low dose • No previous unsuccessful attempts at withdrawal • Normal neurologic status and EEG? • Primarily generalized seizures except JME • “Benign” syndrome • Consider relative risks/benefits (driving, pregnancy)

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637 views • 62 slides

Management of Patients With Epilepsy

Management of Patients With Epilepsy. Definition. Seizure Single provoked/unprovoked episode Epilepsy Two or more unprovoked seizures. Numbers….Numbers. Unprovoked seizure: Risk in US ~ 1/100 Epilepsy/Recurrent unprovoked seizures 8 th leading cause of morbidity

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Epilepsy and Seizure Management. For EMS Personnel.

542 views • 36 slides

309 views • 28 slides

Definition of epilepsy

Definition of epilepsy. In 2005, a Task Force of the International League Against Epilepsy (ILAE) formulated conceptual definitions of “seizure” and “epilepsy”. The “two unprovoked seizure” definition of epilepsy has served us well, but it is inadequate in some clinical circumstances.

152 views • 14 slides

Imaging of Epilepsy

Imaging of Epilepsy. Ali Jassim Alhashli Year IV – Unit VIII (CNS) – Problem 6. Introduction. 1% of population in the world suffer from epilepsy (so it is relatively common). 8% of population in the world will experience at least 1 seizure during their lifetime. Importance of imaging:

176 views • 14 slides

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Epilepsy and Seizure Action Plan

It seems that you like this template, epilepsy and seizure action plan presentation, free google slides theme, powerpoint template, and canva presentation template.

What to do if you see someone who is having a seizure? Acting swiftly is key, and so is remaining calm. It can be a good idea to have a series of informative speeches on epilepsy, seizures and first aid. To help you with that, we have this customizable template. Its palette is ideal for topics related to healthcare, as it contains white, bluish green and dark blue. Although there are geometric shapes, they are small and close to the edges, so it's more a decorative touch than anything. There are also timelines, infographics, maps and other useful assets!

Features of this template

• 100% editable and easy to modify
• 35 different slides to impress your audience
• Contains easy-to-edit graphics such as graphs, maps, tables, timelines and mockups
• Includes 500+ icons and Flaticon’s extension for customizing your slides
• Designed to be used in Google Slides, Canva, and Microsoft PowerPoint
• 16:9 widescreen format suitable for all types of screens
• Includes information about fonts, colors, and credits of the resources used

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