Transcript Presented by Yasser Yamed MD Neurology

‫بسم اللة الرحمن الرحيم‬
‫ّللا َو ُي َعلِّ ُم ُك ُم ُه‬
‫َوا َّتقُو ْا َه‬
‫ّللا‬
‫َو ه‬
‫ّللا ُ ِب ُكل ِّ َ‬
‫ش ْي ٍء َعلِي ٌم‬
‫صدق اهلل العظيم‬
‫سورةالبقرة – اآلية ‪282‬‬
Stroke In Children
Presented by
Yasser Hamed
MD Neurology

Pediatrics is the branch of medicine that deals
with the medical care of infants, children, and
adolescents, and the age limit up to 18 (in some
places until age 21 as in the United States)

Pediatric stroke is an important cause of long-term
disability, with children often living for many years
with significant neurological deficits.

In children, 55% of strokes are ischemic, in contrast
to adults in whom 80–85% of all strokes are
ischemic.
Strokes in children differ from those in adults
in three important ways:

Predisposing factors (In children, congenital and acquired heart
disorders, hematologic conditions are common causes. In contrast,
hypertension, smoking and hypercholesterolemia are more common
predispositions in adults..

Clinical evolution (children often improve much more than an adult
with a comparable lesion because of the abundant collateral circulation or
because of the differences in response of the immature brain to the
lesion).

Anatomic site of pathology (children commonly show occlusion of the
intracranial portion of the internal carotid artery, whereas adults more
frequently show extracranial occlusions of the internal carotid).
Epidemiology

The reported incidence of pediatric stroke ranges from 1.2 to 13 cases
per 100,000 children under 18 years of age.

In Egypt (Al kharga District), the incidence of pediatric stroke was
4/100,000 and prevalence was 26/100,000 children under 20 years of age..

However, pediatric stroke is likely more common than that reported as it
is thought to be frequently undiagnosed or misdiagnosed.

In one report, 19 out of 45 children with a stroke did not receive a
correct diagnosis until 15 hours to 3 months after initial presentation.

Stroke is more common in boys than girls.

Stroke is appear to be more predominant in
black children.

This difference may be attributed to sickle
cell anemia.
Risk Factors and Causes

Cardiac (CCHD, VSD, ASD and RHD) are the most
common cause of stroke in childhood, accounting for up to a
third of all AIS.

Hematologic
◦ Sickle cell disease (SCD) is a very common cause of
stroke.
◦ AIS is more common in the younger age whereas
hemorrhagic strokes occurs more frequently in older
children and adults.
◦ Children with SCD develop all types of ICH
◦
Hypercoagulable disorder including antithrombin III, protein C & S
deficiencies, factor V Leiden mutation, elevated levels of lipoprotein
(a) and antiphospholipid antibody syndrome.
◦
It is suspected in individuals with recurrent DVT, recurrent
pulmonary emboli, or a family history of thrombotic events or if
thrombotic events occur during childhood or adolescence.
◦
Hemophilia A (factor VIII deficiency) and B (factor IX deficiency)
are the two most common hereditary bleeding disorders that
cause intracranial hemorrhage.
◦
Vitamin K deficiency results in decreased factors II, VII, IX, and X.
◦
Thrombocytopenia results from either immune thrombocytopenic
purpura (ITP) or the combined effects of leukemia or its treatment.
Nontraumatic brain hemorrhage does not usually occur with
platelets counts above 20,000 to 30,000,

Infection
 Varicella infection within the past year can result in basal ganglia
infarction.
 HIV infection can cause stroke secondary to HIV-induced vasculitis,
vasculopathy with subsequent aneurysms, or hemorrhage in the
context of immune thrombocytopenia

Vascular
 Arteriovenous malformations (AVM) are the most common cause of
hemorrhagic stroke, but can also cause thrombotic stroke. AVM may
be associated with neurocutaneous syndromes such as Sturge-Weber
disease, tuberous sclerosis and neurofibromatosis.
 Moyamoya is another important vascular cause of childhood stroke
and is associated with conditions such as Down syndrome,
neurofibromatosis, and sickle cell disease.

Syndromes and Metabolic Disorders
 Marfan syndrome are at risk of ischemic stroke.
 Homocysteinuria can cause AIS and should be
suspected in the presence of mental retardation
associated with lens dislocation and occasionally
pectus excavatum.

Vasculitis
 Cerebral vasculitis is a less common cause of
stroke in children, and is more common in children
older than 14 years of age. Although idiopathic
vasculitis is most often diagnosed, signs and
symptoms of systemic vasculitides with Kawasaki
disease,
Henoch-Schnlein
Purpura
(HSP),
polyarteritis nodosa, Takayasu’s arteritis, juvenile
rheumatoid arthritis, systemic lupus erythematosus,
inflammatory bowel disease, sarcoidosis, Sjogren
syndrome, or Behcet disease should be considered

Oncologic
 Children with cancer are at increased risk for AIS as a result
of their disease, subsequent treatment, and susceptibility to
infection.
 Intracranial hemorrhage may complicate an intracranial
tumor.
 Leukemia and lymphoma create a hypercoagulable state.
 L-asparaginase decreases antithrombin levels, and may trigger
venous thrombosis.
 Radiation therapy for brain tumours can cause vasculopathies.

Trauma
 Dissection of the carotid or vertebral arteries resulting from
hyperextension or rotational injuries of the neck.
 Symptoms of traumatic arterial dissection can be delayed by 24 hours, and
the risk is greatest within a few days of the vascular injury.

Drugs
 Cerebral infarcts and hemorrhage have been reported in patients abusing
drugs such as amphetamines, cocaine and glue sniffing.
 Stimulants and heroin can also cause vasculopathies.
 Adolescent girls using oral contraceptives are at higher risk of cerebral
venous thrombosis.
 Overuse of ergot alkaloids are also associated with increased risk of
ischemic events.
Clinical Presentation

AIS most often presents as a focal neurologic
deficit. Hemiplegia is the most common focal
manifestation, occurring in up to 94% of cases.

Hemorrhagic
strokes
most
commonly
present as headaches or altered level of
consciousness.

Seizures are common in both ischemic and
hemorrhagic strokes.

There can be significant differences in the clinical presentation
based on the child’s age.

Neonatal strokes present with focal seizures or lethargy.

Infants present with lethargy, apnea spells, or hypotonia.

Toddlers present with deterioration of their general condition,
increased crying and sleepiness, irritability, feeding difficulty,
vomiting, and sepsis-like symptoms with cold extremities.

Older children demonstrate more specific neurological defects
similar to adults.
Differential Diagnosis

Hemiplagic migraine.

Focal seizures associated postictal hemiparesis
(Todd’s Paresis).

Intracranial neoplasms.

Trauma as extradural, subdural, SA and intracerebral
haematoma.

Intracranial infections such as meningitis, brain
abscess, and herpes simplex encephalitis.

Metabolic abnormalities like hypoglycemia, CADASIL
and MELAS syndrome.
Diagnostic Evaluation Ischemic Stroke:
A- Imaging

Noncontrast head CT to exclude a hemorrhagic stroke.

Diffusion-weighted MRI of the brain is the most sensitive
method to diagnose acute AIS.

MRA head, neck.

MR Venogram (especially consider with sickle cell disease).

CT angiography. MRA may be preferable to CTA

Other investigations as ultrasound to evaluate the extracranial
carotid circulation, ECG, chest radiograph, and transthoracic or
transesophageal echocardiography.
B- Laboratory:

Prothrombin time and concentration, INR.

Antithrombin, factor V Leiden, protein C&S.

Lipid profile, CBC and C-reactive protein levels.

Tests for vasculitis (ESR, antinuclear antibodies,
antidouble strand antibodies, lupus anticoagulant
and anticardiolipin antibodies).
A- Recommended universal supportive measures

Fever control (hypothermia should not be
used in children with stroke);

Normalization of serum glucose;

Maintenance of normal oxygenation;

Ameliorate increased intracranial pressure;

Treat dehydration;

Correct anemia;
B- Blood pressure management

The AHA guidelines suggest “control of
systemic hypertension” in children with AIS
and hemorrhagic stroke.

Specific guidelines for blood pressure values
are absent.
C- Anticonvulsants and EEG monitoring

Seizures are a common complication of pediatric stroke, affecting
up to 25% with AIS and up to 20% with ICH. When they occur,
seizures should be treated aggressively.

Prophylactic anticonvulsants are often used in the setting of
intraparenchymal
or
subarachnoid
hemorrhage
in
adults,
although this approach is not evidence-based practice.

The AHA pediatric stroke guidelines recommend against
prophylactic anticonvulsant use in ischemic stroke but do not
make recommendations in the setting of hemorrhagic stroke.
D- Management of intracranial pressure
Nonsurgical methods

Keeping the head of a patient’s bed at 30°.

Hyperventilation to a pCO2 of 25–30 mmHg.

Hyperosmolar therapy—with either mannitol or hypertonic
saline.

In some cases, sedation may be required to help manage
elevated ICP.

Corticosteroids should be avoided.
Surgical

An intraventricular catheter (IVC) providing both a
means
to
measure
ICP
and, via
drainage
of
cerebrospinal fluid.

Hemicraniectomy may be both life-saving and functionsparing in adults with a large AIS who progress to signs
and symptoms of impending herniation.

In children, study of 10 children with malignant middle
cerebral
artery
infarction,
seven
underwent
hemicraniectomy, all of whom survived and had
moderately good recovery.
AIS-specific treatments
A- Antiplatelet
I- Aspirin

For all older children with ischemic stroke except kids with sickle cell disease

Typical dose is 3-5 mg/kg/day. This dose can be reduced to 1 to 3 mg/kg for
long-term prophylaxis.

Risk of Reye’s syndrome is very low. It recommend to discontinue or reduce
dose to half during febrile illness.

It recommend to vaccinate for varicella and give an annual influenza vaccine.
II- Clopidogrel

For children unable to take aspirin.

Typical dose is 1mg/kg/day.
B- Anticoagulant
I - UH with loading dose 75 units/kg IV followed
by 20 units/kg/hour for children over 1 year of
age or 28 units/kg/hour below 1 year of age.
The target APTT is 60 to 85 seconds.
II- LMWH doses of 1 mg/kg every 12 hours or in
neonates, 1.5 mg/kg every 12 hours.
III- Warfarin with target of INR 2.5 to 3.5.

Consider if suspicion high for cardioembolic stroke,
arterial dissection, posterior circulation stroke.

According to the Australian AIS treatment guideline, for
children
with
confirmed AIS, UH
or
LMWH
is
recommended in the first 5 to 7 days until the evaluation
for underlying etiologies and risk factors is completed.

Children are continued on either oral or subcutaneous
anticoagulants for 3-6 months and then switched to an
antiplatelet agent, usually aspirin.

Platelet count should be monitored
C- Thrombolytic therapy

Use of thrombolytic therapy for patients aged <18 years is much more
controversial. The current AHA guidelines recommend that tPA use in
young children is limited to a clinical trial.

Evidence for the safety and efficacy of thrombolysis in children with
stroke is extremely limited. The existing studies of this treatment
suggest a high risk of hemorrhagic complications.
Recommendations for stroke and heart disease

Therapy for congestive heart failure is indicated.

When
feasible,
congenital
heart
lesions,
especially complex heart lesions with a high
stroke risk, should be repaired.

Resection of an atrial myxoma is indicated.

Surgical repair or transcatheter closure is
reasonable in individuals with a major atrial
septal defect.

In children with a risk of cardiac embolism, it
is reasonable to continue either LMWH or
warfarin for at least 1 year or until the lesion
responsible for the risk has been corrected.

Anticoagulant therapy is not recommended
for individuals with native valve endocarditis

Surgical removal of a cardiac rhabdomyoma
is not necessary in asymptomatic individuals.
Recommendations for children with SCD

Risk factors for stroke include high blood flow velocity
on TCD, low hemoglobin value, high white cell count,
hypertension, silent brain infarction, and history of chest
crisis.

Acute management of ischemic stroke resulting from
SCD should include optimal hydration, correction of
hypoxemia, and correction of systemic hypotension.

Periodic transfusions to reduce the percentage of sickle
hemoglobin are effective for reducing the risk of stroke in
children 2 to 16 years of age.

For acute cerebral infarction, exchange transfusion
designed to reduce sickle hemoglobin to <30% total
hemoglobin.

Hydroxyurea may be considered in children and young
adults with SCD and stroke who cannot continue on longterm transfusion.

Bone marrow transplantation.

Surgical revascularization procedures.
Recommendations for treatment of
coagulation disorders

Antithrombin deficiency is resistant to heparin.

After a thrombotic event, lifelong warfarin is
indicated.

Patients with protein C or S deficiency or
factor V Leiden mutation and stroke are treated
with anticoagulation.

The
prophylactic
anticoagulation
asymptomatic patients is controversal.
for
Sinus thrombosis

The antithrombotic therapy is aimed at preventing the clot
propagation and recurrence within the cerebral venous system.

For
children
without
evidence
of
significant
intracranial
haemorrhage, anticoagulation for 3-6 months is recommended,
with reassessment of re-canalization at 3-months.

With significant intracranial haemorrhage, monitoring with serial
neuroimaging is advised.

In case of clot propagation, treatment with anticoagulation is
advised.
Recommendations for treatment of hemorrhage in
Children

Children with brain hemorrhage should undergo a thorough risk factor
evaluation, including cerebral angiography when noninvasive tests have
failed to establish an origin.

Children with a severe coagulation factor deficiency should receive
appropriate factor replacement therapy, and children with less severe
factor deficiency should receive factor replacement after trauma.

Given the risk of repeat hemorrhage from congenital vascular anomalies,
these lesions should be identified and corrected whenever it is clinically
feasible.

Stabilizing all supportive measures.

Individuals with SAH may benefit from measures to
control cerebral vasospasm.

Surgical evacuation of a supratentorial intracerebral
hematoma is not recommended. However, surgery may
help selected individuals with developing brain herniation
or extremely elevated intracranial pressure.

There are no data to indicate that periodic transfusions
reduce the risk of ICH caused by SCD.
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