Revista Adolescência e Saúde

Revista Oficial do Núcleo de Estudos da Saúde do Adolescente / UERJ

NESA Publicação oficial
ISSN: 2177-5281 (Online)

Vol. 9 nº 1 - Jan/Mar - 2012

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Páginas 46 a 53

Pediatric Stroke: Diagnostic Reminders, Case Studies and Guidelines

Acidente vascular pediátrico: lembrar para diagnosticar. Casos clínicos e linhas de orientaçao

Autores: Marta Filipa Ferreira Santalha1; Ana Cristina Gonçalves Ribeiro Ferreira Barros1; Diana Manuela Gonçalves Baptista1; Armandina Moreira da Silva Neto2; Maria Isolina Pedroso Ramos dos Santos Aguiar2; Cristina Maria Gonçalves Ferreira2; Maria de Lurdes Rodrigues3

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How to cite this article

Keywords: Stroke, adolescent, adolescent health, ischemic stroke, hemorrhagic stroke, pediatric.
Descritores: Acidente cerebral vascular, adolescente, saúde do adolescente, pediátrico, AVC hemorrágico, AVC isquêmico.

OBJECTIVE: Pediatric stroke affects an estimated 2 to 13/100 000 children each year, with difficulties in diagnosis, treatment and etiological investigation. This paper describes two cases of pediatric stroke with different etiologies (ischemic and hemorrhagic) that illustrate these difficulties.
DATA SOURCE AND SYNTHESIS: The first case study presents a healthy thirteen year old Caucasian girl with sudden-onset aphasia where the MRI showed an ischemic stroke near the cortical branch of the left middle cerebral artery. The investigation did not allow a conclusive etiological diagnosis of stroke. Her progress was favorable, with full recovery from the neurological deficits, taking acetylsalicylic acid (AAS). The second case study presents a sixteen year old girl with right parietal headache, vomiting and acute left hemiparesis. The computed tomographic (CT) scan showed acute intraparenchymal hematoma in the right front insular temporal subcortical area, with cerebral angiography revealing arteriovenous malformation (AVM) in the right insular region and several aneurysmal formations. Treatment included embolization and subsequent decompressive craniotomy, with neurological sequelae still persisting. Diagnosis is hampered by the non-specific symptomology that is inherent to complaints presented by adolescents.
CONCLUSION: As the pediatric age bracket has expanded, it is important to raise awareness among healthcare practitioners in order to recognize these vascular events, allowing early targeted intervention and minimizing the sequelae. A theoretical review of pediatric stroke is presented, suggesting guidelines for diagnosis, approaches and treatment.

OBJETIVO: O acidente vascular cerebral (AVC) pediátrico tem uma incidência estimada de 2-13/100 000 crianças/ano e apresenta dificuldades no diagnóstico, investigaçao etiológica e terapêutica. Descrevem-se dois casos clínicos de AVC em idade pediátrica, com etiologia diferente (isquêmico e hemorrágico) que ilustram essas dificuldades.
FONTE E SINTESE DOS DADOS: O primeiro caso refere-se a uma adolescente, sexo feminino de 13 anos de idade, raça caucasiana e saudável, com afasia de instalaçao súbita em que a RMN CE revelou enfarte isquêmico no território do ramo cortical da artéria cerebral média esquerda. A investigaçao nao permitiu um diagnóstico etiológico do AVC conclusivo. A evoluçao foi favorável com recuperaçao completa dos déficits neurológicos, estando medicada com ácido acetilsalicílico (AAS). O segundo caso referese a uma adolescente do sexo feminino, 16 anos, com cefaleia parietal direita, vómitos e hemiparesia esquerda de instalaçao aguda. A tomografia computadorizada cerebral (TC CE) revelou hematoma agudo intraparenquimatoso fronto-insulo-temporal subcortical à direita e a angiografia cerebral revelou uma malformaçao arteriovenosa (MAV) na regiao insular direita e várias formaçoes aneurismáticas. O tratamento incluiu embolizaçao e posteriormente craniotomia descompressiva, com sequelas neurológicas persistentes à data atual. A inespecificidade da sintomatologia, inerente à abordagem das queixas dos adolescentes, dificulta o diagnóstico.
CONCLUSAO: Face ao alargamento da idade pediátrica é importante sensibilizar os profissionais de saúde para o reconhecimento atempado deste evento vascular, permitindo uma intervençao precoce e dirigida, minorando sequelas. Elabora-se em seguida, uma revisao teórica sobre acidente vascular cerebral pediátrico, sugerindo-se orientaçoes no diagnóstico, abordagem e tratamento.


Pediatric stroke is caused by a tightly-located interruption of the cerebral blood flow 1.2 confirmed through neuro-imaging, 2 which encompasses ischemic and hemorrhagic strokes, resulting in neurological deficits that persist for more than 24 hours.1,2 Ischemic pediatric stroke may also be divided into arterial and venous sinus thrombosis, while hemorrhagic stroke includes intracerebral and subarachnoid hemorrhages. 3,4,5

It appears at an annual rate of 2-13/100,000 children, 3,5 with 60% to 75% being ischemic and 25% - 40% being hemorrhagic. 3

Several studies have disclosed that pediatric stroke is more common among boys, although there is no known explanation for this fact. 1, 2,5,6,7,8 Among black children, the risk of vascular events is twice as high as among white children.3

The predisposing factors are complex and varied, ranging from cardiac and hematological causes, in addition to vascular, metabolic and infectious diseases, as well as traumas and neoplasias (Chart 1).2,4

The presentation varies by age, etiology and the area of the cerebral parenchyma affected. 4,9

Hemiparesia is the most common type of presentation.4,5 Other neurological signs may be present, such as: aphasia, 4,5 visual alterations,,2,5 ataxia,4,5 dizziness, 4,5, convulsions 1,2 and alterations in consciousness 4. The younger the child, the higher the possibility of encephalopathy.

Two clinical case studies are presented:

Case Study 1

Adolescent, 13 year old, girl, white, with no material pathological antecedents. Family history of renal pathology and hypertension in both parents.

Taken to the emergency room due to the sudden onset of alterations in language, denying ingestion of medications or poison, or cranial-encephalic trauma.

On admission, she was confused, polypneic, with tachycardia and normal blood pressure, with difficulties in naming and repeating, in the neurological examination although with preserved understanding but completely unable to write.

An analytical study was conducted in the ER, with a clotting test and cerebral computed tomography not revealing any alterations. As the neurological deficits persisted, she was hospitalized, starting with acetylsalicylic acid (AAS) (2 mg/kg/day).

Cerebral nuclear magnetic resonance imaging performed on D3 of hospitalization showed: left cortical frontal opercular lesion suggestive of acute / sub-acute ischemic stroke (area of the cortical branch of the left middle cerebral artery)".

The cerebral angiography showed no alterations. The rest of the study continued: cardiac, carotid, vascular, immunological autoimmunity metabolic and genetic mutations of thrombophilia, in which anticardiolipin and anti-β2-glycoprotein antibodies were noteworthy, an IgM+ fraction and thermolability for methylenetetrahydrofolate reductase (MTHFR) (C677T) homozygous mutant, although with normal homocysteine and folic acid levels.

During hospitalization, she continued on AAS and began speech therapy on the fourth day, with a gradual complete reduction in the neurological deficits. She was released from hospital on D19, with advice on making appointments with the Development, Neurology and Speech Therapy units.

Three months after the acute phase, the autoimmunity study was repeated and a prothrombotic study was conducted, indicating the normalization of the anticardiolipin and anti-β2-glycoprotein 1 antibody titers.

Case Study 2

Adolescent girl, 16 years old, white, with no family history or material personal antecedents. She went to the emergency room after vomiting up food for two days, together with headache, initially right parietal, subsequently holocranial, becoming steadily worse. The ingestion of medications or poison was denied, or cranial-encephalic trauma.

On admission, she presented a coma of 14/15 on the Glasgow scale (O3/4 V5 M6), apyretic, with normal blood pressure and a heartbeat appropriate for her age, presenting prostration, a stiff neck and a slight reduction in the muscle strength of the upper left limb (Level 4), during the objective examination.

An analytical study was conducted in the emergency room, including a clotting test that did not reveal any alterations, and cerebral computed tomography that showed: "acute frontal insulo-temporal subcortical intraparenchymal hematoma on the right measuring some 48x26x35 cm, resulting in the disappearance of nearby cortical grooves and part of the homolateral ventricle, with contralateral deviation of the middle structures. Presence of right sylvian / perisylvian vascular malformation, containing several aneurismatic dilations...".

The adolescent was transferred to a hospital center with neurological care, where a cerebral angiography showed: "pial arteriovenous malformation in the right insular region. several aneurismatic formations".

She underwent embolization, which increased the intracranial pressure, requiring an urgent decompression craniotomy with surgical removal of the intracerebral hematoma and complete dissection of the arteriovenous malformation. Subsequently, she was transferred to the pediatric intensive care unit, where she maintained good intracranial pressure and adequate blood pressure.

The set of cerebral computed tomographies showed the progressive reduction of the hematoma and post surgical edema. As inter-occurrences, pneumonia was recorded due to H. influenzae with complete atelectasis of the left lung and pneumothorax on the right. She was then transferred to the hospital of origin on D55 for ongoing care, being released seven days later. At the moment, she presents the following sequelae: left hemiparesia, predominantly brachial (Level 3/4), secondary epilepsy (controlled with sodium valproate and carbamazepine), depression and difficulties in returning to school. She is being monitored through consultations by the Development, Pediatric Psychiatry, and Speech Therapy Units, as well as Physical and Rehabilitation Medicine.


In the first case study, the non-specific nature of the clinical presentation is stressed, particularly the psychomotor agitation of the adolescent, which resulted in difficulties in perceiving the aphasia among the general practitioners. The investigation did not allow the establishment of a conclusive etiological diagnosis of stroke. Although initially positive IgM fraction antiphospholipid antibodies were noted, raising the possibility of a probable diagnosis of antiphospholipid syndrome, they returned to normal twelve weeks later. In fact, the presence of these antibodies does not always reflect a pathology, and may be positive in between 1% to 5% of healthy people.10 Temporary increases are noted in the presence of infections (bacterial, viral or parasite). 11,12, medications (phenothyazides, phenitoin, hydralazine, quinine, amoxicillin, propranolol, oral contraceptives, etc.)12,13,14 and neoplasias (neoplasia of the lung, colon, ovary, lymphomas, etc)10,13.

The presence of a MTHFR (C677T) mutation has been associated with ischemic stroke in some studies, but not in others, 15,16,17,18,19 with further investigation required in order to establish a causal link.

Thus, this adolescent continued with no etiological diagnosis. In some series, almost 30% of patients continue with no etiology.20,21

The second case study reflects the need for greater awareness among healthcare practitioners, in order to recognize this vascular event, through making full neurological and physical examinations mandatory, when addressing symptoms as frequent as headaches and vomiting, which may reflect some severe neurological pathology.

In view of the expansion of the pediatric age, it has become crucial to standardize attitudes in order to ensure early, correct diagnoses. Some guidelines are thus presented below.


When a child presents with suspected stroke, a detailed description of current diseases must be drawn up, investigating signs of infection, unexplained fever, drug ingestion, headaches, cranial-encephalic trauma 4, 22, and the personal history of cardiac, hematological, vascular and metabolic pathologies. In the family history, antecedents must be sought for early onset atherosclerotic disease, hereditary cerebrovascular disease such as cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), cardiac and hematological diseases and earlier embolic episodes.

When approaching the child, it is important to conduct a detailed physical and neurological examination, including an assessment of the vital signs and fundoscopy, in addition to checking for signs of head or neck injury. If possible, the patient must be assessed by the Neurology or Neuropediatrics unit.

Supplementary diagnostic examinations

It is suggested that a laboratory study be conducted, with a full hemogram, 4, 6 glycemia, 3 hepatic function, thyroid, iron kinetics, sedimentation speed and clotting study 4,6 (TP, aPTT, fibrinogen), although at times the role of these examinations in diagnosis may not be too clear.4

A full thrombophilic evaluation is indicated 4, 23 in the acute phase for all children with homocysteine dosing, vitamin B12, folic acid, plasminogen, Von Willebrand Factor, antiphospholipid antibodies, Factor VIII, Factor XII, prothrombin 20210, MTHFR C677T, Factor V Leiden Mutation G1619A, with a study being completed over a period of at least thirty days, with dosing for protein C, protein S, antithrombin III and lipoprotein (a).

Hemoglobin electrophoresis, toxicology urine examination and viral marker tests may be indicated for some children, 4 depending on their clinical histories.

Lumbar punctures must be considered when infection or subarachnoid hemorrhaging 1,24 is suspected, when the cerebral computed tomography is normal 24 and if the child is thermodynamically stable.

The cerebral computed tomography neuro-imaging examination is usually available, allowing rapid diagnosis of cerebral hemorrhage. Nevertheless, it is less sensitive than the cerebral nuclear magnetic resonance imaging, particularly for acute lesions and in the posterior cranial fossa 5 whereby, after excluding cerebral computed tomography hemorrhage, a nuclear magnetic resonance imaging diffusion, dissemination and perfusion study must be conducted, as this allows ischemias to be detected minutes after the event.

Computed angiotomography is a non-invasive method for evaluating intra and extra-cranial circulation, with the disadvantages of exposure to radiation, the use of endovenous contrast and difficulties in timing the administration of the contrast bolus in small children.4,5

Magnetic resonance angiography of the intracranial and cervical arteries is a non-invasive, sensitive approach that does not require exposure to radiation or endovenous access. Comparative studies show that magnetic resonance angiography is as sensitive as conventional angiography for detecting vasculopathy in the internal carotid artery and the middle cerebral artery, although less sensitive for detecting small blood vessel disease. 5, 25

Transthoracic echocardiograms and electrocardiograms must be conducted for small children with ischemic stroke or patients with known or suspected congenital cardiopathies.4

A transesophagal echocardiogram must be performed when the transthoracic echocardiogram does not offer a diagnosis, or if there is marked suspicion of a cardio-embolic source.24

Should arrhythmia be suspected, particularly fibrillation, Holter monitoring is indicated. 24 Should convulsions be present, an electroencephalogram must be performed 24 and, should metabolic disease be suspected, a metabolic study must be conducted (dosing amino acids in the blood and urine, ammonia, lactate, pyruvate, and organic acids in the urine).


The initial treatment for stroke is support, 3 with high priority assigned to airway stabilization, avoiding hypoxia, placing endovenous accesses, immediately correcting deficits in volemia and hydro-electrolyte imbalances, clotting and hematological problems. 4 Blood sugar levels must be kept at between 60 and 120 mg/dl.1 Fever must be treated aggressively in order to maintain a body temperature between 36.5°C and 37.5°C, which helps limit the range of the stroke, with better outcomes for patients.1

Ischemic stroke

With regard to antithrombotic treatment, there are no controlled randomized studies for assessing the effectiveness of anticoagulant or antiplatelet therapy for the treatment of cerebral ischemic stroke at pediatric ages, with therapeutic strategies having been extrapolated for studies of adults.5,8,23

There are some differences among the various guidelines, in terms of ischemic stroke treatment, although none of them recommend the use of thrombolytics.1,23

The American Academy of Chest Physicians recommends non-fractioned heparin, low molecular weight heparin or aspirin (1 to 5 mg/kg/day) as an initial treatment for children without sickle cell anemia, until excluding dissection or embolic causes (Level 1B). After exclusion, daily prophylaxis with AAS is required for at least two years. 26

In the presence of arterial dissection or a cardioembolic event, anticoagulant treatment with low molecular weight heparin is indicated, or vitamin K antagonists, for a period of at least six weeks, depending on the treatment subsequent to the imaging evaluation (Level 2C). 26

For children with venous sinus thrombosis, and no material intracranial hemorrhage, initial anti-clotting treatment is recommended with non-fractioned heparin or low molecular weight heparin, and subsequently with low molecular weight heparin or vitamin K antagonists, for a period of at least three months (Level 1B). If incomplete radiological recanalization is noted after three months of treatment, or persistent, worsening symptoms, anticlotting treatment must be administered for a further three months (Level 2C).26

For children with venous sinus thrombosis and significant intracranial hemorrhaging, radiological monitoring of the thrombosis is recommended between the fifth and seventh days; should the thrombus spread, anticlotting treatment is suggested (Level 2C).26

Thrombolysis, thrombectomy or surgical decompression is suggested only for children with severe venous sinus thrombosis and no improvement when treated with non-fractioned heparin. 26

For children with sickle cell anemia and stroke, endovenous hydration is recommended, and exchange transfusion, in order to reduce the Hemoglobin S levels to values below 30% of the total hemoglobin (Level 1B). Subsequently, a long term transfusion program is recommended (Level 1B) and, if the transcranial Doppler speed exceeds 200 cm/s, regular blood transfusions are recommended indefinitely (Level 1B)26.

For children taking AAS and with stroke or recurrent transient ischemic attacks, it is suggested that the treatment be altered to clopidogrel or an anticoagulant (low molecular weight heparin or vitamin K antagonists) (Level 2C).26

Hemorrhagic Stroke

When treating hemorrhagic stroke, the use of mannitol and steroids has been recommended in order to reduce intracranial pressure.1

Surgical intervention to remove the hematoma, decompression craniotomy, embolization or repair of the vascular anomaly may also be necessary. However, treatment will depend on the cause and status of the patient.1

Surgical treatment of arteriovenous malformations will depend on the size, vein drainage pattern (surface, deep) and location.27

Treatment recommendations and guidelines for arteriovenous malformations were published in 2001 by the American Stroke Association (ASA). 28

Severe thrombocytopenia must be corrected rapidly with patients with intracranial hemorrhage (Level 1B) administering vitamin K to patients with vitamin K dependent clotting disorders (Level 1B).29


The risk of recurrence after an ischemic stroke is 10% to 25 % in children undergoing treatment, and up to 50% among those who are not treated.23 Above all, the presence of risk factors is higher during the first six months after the initial event. 23 The pediatric stroke mortality rate varies between 7% and 28% 20.


The prognosis depends on the clinical presentation, etiology, type of vascular event and its dimensions.1,2

Some studies indicate that 55% of children develop sense, motor or cognitive deficits, convulsions or delayed development, 15% die and 35% remain neurologically normal.4


It is crucial to enhance awareness among healthcare practitioners of the importance of recognizing cerebral vascular events at pediatric ages, as this posts significant morbidity and mobility rates. It is even more important to conduct further studies on the evidence and safety of treatments during the acute phase, particularly thrombolytics, which may alter the progression and prognosis for the disease.

Thus, when attending any child with a new neurological deficit, the possibility of stroke must be investigated, in order to allow early directed intervention in order to minimize long term sequelae.


The authors thank Dr Inês Carrilho (neuropediatrician at the Oporto Hospital Center) for her contribution in reviewing the paper.


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1. Student, Medical Pediatrics. Centro Hospitalar do Alto Ave. Guimaraes, Portugal.
2. Hospital Assistant in Pediatrics. Centro Hospitalar do Alto Ave. Guimaraes, Portugal.
3. Assistant in Neurology. Centro Hospitalar do Alto Ave. Guimaraes, Portugal.

Marta Filipa Ferreira Santalha
Rua de Sao Miguel 320
Lousada, Portugal

Received: November 18, 2011
Approved: January 10, 2012
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