Both ischemic and hemorrhagic strokes occur in children. The incidence varies across countries but ranges from 1 to 5 per 100,000 per year. Approximately 55% are ischemic strokes and 45% hemorrhagic.
Ischemic strokes are caused by vascular occlusion of an artery, usually because of thromboembolism (arterial ischemic stroke [AIS]) or occlusion of venous sinuses or cerebral veins (cerebral venous sinus thrombosis [CSVT]).
Strokes that can result from vascular rupture are classified as hemorrhagic. The two main types are intracerebral hemorrhage and subarachnoid hemorrhage (SAH).
A history of complex congenital heart disease, prosthetic heart valve, recent cardiac surgery, or extracorporeal membrane oxygenation (ECMO) should raise suspicion of an embolic phenomenon.
Magnetic resonance imaging (MRI) with diffusion-weighted imaging is more sensitive in detecting small infarcts, infarcts of the brain stem and cerebellum, and infarcts that become hemorrhagic, and is more sensitive for acute ischemia than a computed tomography (CT) scan.
A CT scan will show a tumor, large bleed, or abscess, and may show loss of gray/white differentiation and dense triangle sign (hyperdense thrombus in the posterior part of superior sagittal sinus), but may not detect some acute hemorrhages.
Magnetic resonance angiography (MRA) can be done at the time of the MRI to visualize the flow through the cerebral arteries. MRI can also be used with magnetic resonance venography (MRV) to diagnose sinovenous thrombosis.
For patients in whom a hemorrhagic stroke is suspected and in whom the CT scan is negative, a lumbar puncture is indicated. Particularly with a small subarachnoid hemorrhage, the CT scan may not reveal blood.
The key function of the emergency department (ED) is stabilization of the patient’s respiratory and cardiovascular status, especially the blood pressure. In the event of an ischemic infarct, a precipitous decline in blood pressure should be avoided, since it can worsen cerebral ischemia, but if hypotension is present, careful fluid resuscitation and inotropic support may be needed.
Serum glucose should be monitored closely, as hypoglycemia can worsen the effect of the stroke, and hyperglycemia can increase infarct size.
Specific therapy is directed at the etiology of the stroke, such as correction of clotting abnormalities, antibiotics for infections, antiepileptic medication for seizures, transfusion for anemia, and surgery for evacuation of a hematoma. For patients with sickle cell disease, exchange transfusion is indicated for ischemic stroke.
Although they are uncommon in children when compared to adults, both ischemic and hemorrhagic strokes occur. The incidence varies across countries but ranges from 1 to 5 per 100,000 per year.1,2 Approximately 55% are ischemic strokes and 45% hemorrhagic.1,3 Ischemic strokes can be categorized as arterial ischemic strokes (AIS) and cerebral venous sinus thrombosis (CSVT). AIS accounts for 75% of ischemic strokes, while CSVT accounts for 25%.2 In the pediatric population, AIS usually results from a thromboembolism. Occlusion of venous sinuses or cerebral veins can result in CSVT. The majority of ischemic and hemorrhagic strokes occur in the neonatal period, but both occur in older children and adolescents, so this chapter focuses on those from 29 days to adolescence.1,4
The signs of AIS vary with age and the area of the brain affected by ischemia; they include focal neurologic findings such as hemiparesis, cranial nerve palsies, visual field deficits, and speech disturbance.1,5 Other signs and symptoms may include headache, confusion, behavioral changes, and irritability in infants.1
Children with CSVT may present with diffuse neurologic signs and seizures, but symptoms vary with age and etiology. Infants present with seizures or lethargy, while older children have headaches, vomiting, altered level of consciousness, seizures, papilledema, and focal neurologic deficits.1,6
Strokes that can result from vascular rupture are classified as hemorrhagic. The two main types are intracerebral and subarachnoid hemorrhage (SAH). Intracerebral hemorrhage is more common in children younger than 10 years, while SAH is more common in adolescents.3 Signs of hemorrhagic stroke include severe headache, decreased level of consciousness, vomiting, focal neurologic signs, and seizures.1,5
The arterial circulation to the brain is via the anterior carotids and the posterior vertebral and basilar arteries, which link via communicating arteries to form the circle of Willis. Cerebral arteries can thrombose due to damage to the arterial wall, vasculopathy, emboli, or prothrombotic conditions. Infarction occurs when loss of blood supply to cerebral tissue results in ischemia, hypoxia, and depletion of energy and carbohydrate stores. The extent of neuronal damage depends on the severity and length of time of ischemia, the availability of collateral circulation, and the metabolic needs of the brain.1
In children, risk factors are associated with 90% of AIS and include cardiac disease, prothrombotic states, arteriopathy, vasculitis, acute head and neck infections and trauma, metabolic disorders, moyamoya syndrome, chronic medical disorders (sickle cell disease, iron deficiency, cancer), and indwelling central lines.2,7,8 In some cases, no risk factor is defined, whereas in others there may actually be multiple risk factors. This is in stark contrast to adults, in whom arteriosclerosis is the leading risk factor for AIS, along with hypertension, smoking, diabetes, and hypercholesterolemia.1,9
Sinovenous thrombosis can occur due to thrombophlebitis, hemoconcentration, or coagulation disorders. Occlusion of the sinuses or other cerebral vessels results in increased venous pressure and blood–brain barrier disruption, which leads to vasogenic edema. As pressure continues to increase, cerebral edema and decreased cerebral perfusion result. In some cases, the vessels leak and the infarcts become hemorrhagic. In addition, there is a risk of developing communicating hydrocephalus after sinovenous thrombosis of the sagittal sinus or with sinus hypertension, because the arachnoid granulations, which absorb cerebrospinal fluid (CSF), become nonfunctional.1,6
Risk factors associated with CSVT are prothrombotic disorders, dehydration, systemic infection, head and neck infections (otitis media, mastoiditis, sinusitis), hematologic disorders (sickle cell disease, thalassemia), drugs (L-asparaginase), cardiac disease, cancer, systemic lupus erythematosus, diabetic ketoacidosis, pregnancy, and perinatal complications.1,2,4,6,7
The underlying diseases that cause AIS and CSVT are listed in Tables 58-1 and 58-2, respectively.
Cardiac Congenital heart disease (s/p Fontan, ECMO) S/P cardiac surgery Rheumatic heart disease Bacterial endocarditis Arrhythmias (atrial fibrillation, SVT) Cardiomyopathy Myocarditis Prosthetic heart valves Ventriculoseptal defect/atrial septal defect Patent foramen ovale |
Infection Meningitis Encephalitis Pharyngitis Necrotizing fasciitis HIV |
Arteriopathy Focal cerebral arteriopathy of childhood Moyamoya disease Postvaricella angiopathy Postradiation vasculopathy Sickle cell arteriopathy Arterial dissection Transient cerebral arteriopathy |
Systemic disorders Systemic lupus erythematosus Polyarteritis nodosa Nephrotic syndrome Inflammatory bowel disease Takayasu arteritis Dermatomyositis Rheumatoid arthritis Diabetes mellitus |
Hematologic disorders Sickle cell disease Leukemia Iron deficiency anemia Polycythemia Thrombocytosis Thrombotic thrombocytopenic purpura Idiopathic thrombocytopenic purpura |
Acquired prothrombotic states Lupus anticoagulant Anticardiolipin antibodies Protein S deficiency Protein C deficiency Antithrombin III deficiency Lipoprotein (a) abnormalities Pregnancy Indwelling catheters |
Congenital prothrombotic disorders Factor V Leiden gene defect Prothrombin gene G20210A mutation Methylenetetrahydrofolate reductase (MTHFR mutation) Antithrombin III deficiency |
Trauma Head injury Neck injury Intraoral trauma Child abuse |
Drugs Cocaine Oral contraceptives Antineoplastic agents (e.g., L-asparaginase) Steroids Amphetamines |
Metabolic disorders Hyperhomocysteinuria Mitochondrial encephalomyopathy (MELAS) Hyperlipidemia Cerebral autosomal dominant arteriopathy with subcortical infarct and leukoencephalopathy (CADASIL) |
Neurocutaneous syndromes Neurofibromatosis type 1 Sturge–Weber syndrome Tuberous sclerosis |
Hereditary disorders Ehlers–Danlos syndrome Fabry’s disease |
Vasospastic disorders Migraine |
Septic Otitis media Mastoiditis Sinusitis Lemierre syndrome Pharyngitis Parapharyngeal infections Meningitis |
| Indwelling central lines |
Prothrombotic Protein S deficiency Protein C deficiency Antiphospholipid antibodies Antithrombin III deficiency Factor V Leiden gene defect Prothrombin G20 210A mutation Hyperhomocysteinemia |
Dehydration |
Systemic diseases Systemic lupus erythematosus Nephrotic syndrome Inflammatory bowel disease |
Hematologic disorders Sickle cell disease Iron deficiency anemia Polycythemia |
Cardiac disease Cyanotic heart disease Postoperative repair |
Drugs Oral contraceptives Corticosteroids L-asparaginase |
Malignancy (and treatment) Leukemia (L-asparaginase) Brain tumor |
Head and neck injury |
| Pregnancy |
Hemorrhagic strokes involve the rupture of cerebral blood vessels with leakage of blood into the brain parenchyma, subarachnoid space, or ventricular system. The location of the hemorrhage defines the two major types of stroke as intracerebral/intraparenchymal or subarachnoid, and determines the pathophysiology, risk factors, and clinical findings.1
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