High Flow, High Pain

History and Physical

An 11-year-old previously healthy girl was admitted to the emergency department with a 3-day history of moderate occipital pain associated with vomiting. There was no recent history of infections, vaccinations, head trauma, or toxic exposures. Family history was negative for migraine or chronic headache, psychiatric disorders, or early-onset stroke. Physical examination showed weight 32 kg (50th–75th percentile), height 126 cm (25th–50th percentile), head circumference 54 cm (75th–90th percentile), blood pressure 100/62 mm/Hg (50th percentile), and pulse 88 bpm.

On admission, her headache increased to 8/10. While in the hospital, she became lethargic with a marked decrease in consciousness and a Glasgow Coma scale of 13. During neurologic evaluation, she was not oriented to a person or location and had difficulty following instructions. Cranial nerve, motor exam, and deep tendon reflexes were normal.

Diagnostic Workup

Head CT performed immediately after admission revealed an acute left anterior temporal hematoma with surrounding vasogenic edema ( Fig. 27.1 ). Head CTA revealed a ruptured giant left MCA bifurcation arteriovenous malformation (AVM) measuring 2.5 cm, with superficial venous drainage via the vein of Labbé ( Fig. 27.2 ). Cerebral angiography confirmed the diagnosis of AVM ( Fig. 27.3 ). The patient underwent two angiographic embolizations with no further bleeding. Follow-up MRI showed development of parenchymal encephalomalacia and siderosis surrounding the AVM with a small residual nidus ( Fig. 27.4 ).

A photo shows two axial brain CT images displaying a dark left temporal hematoma with surrounding lighter area indicating edema. — Fig. 27.1

A photo shows three medical brain images displaying a ruptured giant arteriovenous malformation in different planes: coronal, sagittal, and coronal MIP views. — Fig. 27.2

Cerebral angiography displaying left middle carotid artery arteriovenous malformation in anteroposterior and lateral views, with white arrows indicating abnormal blood vessels. — Fig. 27.3

A photo shows brain MRI scans displaying encephalomalacia, siderosis, and a small residual nidus across three different imaging techniques. — Fig. 27.4

Clinical Differential Diagnosis

Acute severe headache is the hallmark of hemorrhagic stroke (HS). Thunderclap headache, particularly if accompanied by nausea/vomiting or other neurological symptoms, should be considered HS until otherwise proven. Underlying lesions include ruptured aneurysms or AVMs. Patients can present with nonspecific encephalopathy and altered consciousness. Progressive neurological deficits can occur with brain parenchymal or cranial nerve compression.

Systemic causes of subarachnoid hemorrhage include leukemia, idiopathic thrombocytopenic purpura, hemorrhagic disease of the newborn, hemophilia, and other bleeding diatheses. Seizures, meningeal signs, and fever can occur and can be distinguished from infectious meningitis by CSF testing.

Imaging Differential Diagnosis

Cavernous malformations (CCMs): Approximately 85% of brain CCMs are supratentorial in children (92% cerebral, 8% basal ganglia). The remainder are located infratentorially (57% brainstem, 43% cerebellar). Rarely, CCMs can also occur in the spinal cord. CT can show hyperdense areas of hemorrhage and calcification in larger lesions ( Fig. 27.5A ). Brain MRI, especially susceptibility-weighted sequences, has the greatest sensitivity for micro- and macrohemorrhages ( Fig. 27.5B ). MRI screening is recommended for first-degree relatives of patients with CCMs with two or more affected family members.