Decreased Activity Level - Case 2-5: 9-Year-Old Boy
Decreased Activity Level - Case 2-5: 9-Year-Old Boy: Excerpt from Pediatric Complaints and Diagnostic Dilemmas
I. History of Present Illness
A 9-year-old boy developed emesis about 5:00 p.m. one evening and afterward went
to sleep. A few hours later, the parents had a difficult time arousing him, and
subsequently brought him to an emergency department. In the emergency
department, the child was able to relate that he fell at school and hit his
head against the wall. He did not lose consciousness at the time. He complained
of a headache. He denied any potential ingestion.
II. Past Medical History
He was a healthy child with no significant past medical history. He did not take
any medications and was not allergic to any medications. His immunizations were
appropriate for age.
III. Physical Examination
T, 37.5°C; RR, 26/min; HR, 86 bpm; BP, 120/70 mm Hg; SpO2, 97% in room air
On examination he was asleep but was easily arousable. His head was atraumatic,
but he had occipital pain with forward neck flexion. His occiput was diffusely
tender, but no bony defects were palpated. Pupils were 4 mm and reactive to 2
mm. A funduscopic examination was attempted but was unsuccessful. Kernig
's and Bruzinski's tests were negative. The remainder of his head and neck examination was
normal. His lungs, cardiac, and abdominal examination findings were normal as
well. His neurologic examination revealed that the cranial nerves were intact.
He was able to follow commands and to respond appropriately.
IV. Diagnostic Studies
A head computed tomographic (CT) study was obtained and revealed a left-sided
parietal intracranial hemorrhage, mild hydrocephalus, asymmetric ventricles
with the left ventricle being larger than the right, and blood in the fourth
ventricle. A complete blood count and serum electrolytes were normal. Serum and
urine toxicology screens were negative.
V. Course of Illness
Shortly after his CT scan results were returned, the patient had a 5-minute
generalized tonic-clonic seizure. He was loaded with phenytoin intravenously
after the seizure activity ceased. An angiogram was performed after the patient
was stable and revealed the diagnosis (Fig. 2-3).
Discussion: Case 2-5
I. Differential Diagnosis
This case illustrates a patient who has an intracranial hemorrhage. Although
these lesions are not as common in children as in adults, they can occur,
particularly after head trauma. The differential diagnosis includes any cause
of intracranial hemorrhage, including accidental and nonaccidental trauma and
nontraumatic causes such as an aneurysm, arteriovenous malformation (AVM),
bleeding disorders, arachnoid cysts, hypernatremia, galactosemia, glutaric
aciduria, and meningitis.
II. Diagnosis
Magnetic resonance imaging (MRI) scan of the head revealed a left-sided medial
parieto-occipital hemorrhage with significant intraventricular extension. The
findings suggested an AVM, but no AVM was detected on the MRI.
The patient was then sent for cranial angiography, which revealed an AVM that
arose from the left posterior cerebral artery and the superior cerebellar
artery (see Fig. 2-3).
He subsequently underwent operative drainage of the hematoma and resection of
the AVM.
III. Incidence and Epidemiology
Cerebral AVMs are congenital vascular malformations. They most likely result
from failed differentiation of the embryonic vessels into separate arterial and
venous systems, which occurs between 3 and 12 weeks of fetal age. AVMs are
arteriovenous shunts that consist of feeding arteries, a mass of coiled vessels
(the nidus), and draining veins without a capillary network. Usually, there is
no brain tissue between the two sides of the AVM, which allows a high-flow
shunt from the arterial side to the venous side. The AVM, in essence, is
stealing blood from the neighboring parts of the brain. Spontaneous thrombosis
and subsequent recanalization may occur and may account for the change in size
of an AVM over time. Ten percent of cerebral AVMs are in the posterior fossa,
10% in the midline, and the remainder in the cortex. They may be located
superficially or deep. The incidence of cerebral AVMs is 1 per 100,000 persons.
Fewer than 12% of cerebral AVMs are symptomatic. They are frequently diagnosed
between the ages of 20 and 40 years. About one fifth of AVMs that become
symptomatic do so before 15 years of age. Hemorrhage is the most frequent
complication associated with AVMs, and it is more commonly seen in children
than in adults.
IV. Clinical Presentation
Hemorrhage is the initial manifestation in up to 80% of cases of cerebral AVMs.
Seizures, which occur in about one third of the cases, may result from an acute
hemorrhage or from an epileptogenic focus from a previous hemorrhage. Infants
may present with congestive heart failure and hydrocephalus. Stroke and
seizures are more commonly seen in older children. Intracranial hemorrhage may
occur after an episode of trivial head trauma. Headache is a frequent symptom
in patients with AVMs, although it is not a very specific clinical sign.
Patients with untreated AVM who have had previous hemorrhages are at a higher
risk for rebleeding. The presentation varies with the location of the AVM:
superficial AVMs cause seizures more frequently, and deep AVMs tend to manifest
with hemorrhage.
AVMs usually continue to increase in size, with increasing risk of hemorrhage
and ischemia, resulting in seizures, gliosis, and neurologic deficits. However,
some AVMs remain the same size, and some even regress.
Two thirds of adults with AVMs have documented learning disorders. The
implication is that there are functional brain deficits that may arise before
other signs and symptoms that ultimately lead to the diagnosis of a cerebral
AVM.
V. Diagnostic Approach
Brain imaging. The diagnosis of an AVM can be made with CT, MRI, or cerebral angiography. CT
frequently is obtained after the first hemorrhage and reveals only that a
hemorrhage has occurred. If an intravenous contrast agent is administered for
the CT, the AVM nidus typically can be seen; however, if it is a small AVM, it
may be missed on CT scanning. MRI is very helpful in diagnosing AVMs.
Additionally, MRI is useful in the planning of the surgical correction of the
AVM. MRI and magnetic resonance angiography (MRA) are also used to monitor
patients after their AVM has been treated. Angiography provides an excellent
view of the vascular anatomy of the AVM.
VI. Treatment
The aim of treatment is complete removal of the AVM, because there is a high
mortality rate from untreated AVMs. The options for removal include
neurosurgical excision, embolization of the AVM, and radiotherapy obliteration
using the gamma knife, proton beam, or linear accelerator. The therapeutic
option that is most appropriate for the patient depends on the location and
size of the AVM. If the location of the AVM is deep within the brain or on the
motor cortex, excision might not be the best option. The effect of radiotherapy
takes months or years to manifest, whereas surgical excision and embolization
are immediately effective.
VII. References
1. Di Rocci C, Tamburrini G, Rollo, M. Cerebral arteriovenous malformations in
children.
Acta Neurochirurgica 2000;142:142–158.
2. Hofmeister C, Stapf C, Hartmann A, et al. Demographic, morphological, and
clinical characteristics of 1289 patients with brain arteriovenous
malformation.
Stroke 2000;31:1307–1310.
3. Menovsky T, van Overbeeke JJ. Cerebral arteriovenous malformations in
childhood: state of the art with special reference to treatment.
Eur J Pediatr 1997;156:741–746.
4. The Arteriovenous Malformation Study Group. Arteriovenous malformations of
the brain in adults.
N Engl J Med 1999;340:1812–1818.
Pictures
Book Source Details
- Book Title: Pediatric Complaints and Diagnostic Dilemmas
- Author(s): Samir S Shah MD; Stephen Ludwig MD
- Year of Publication: 2003
- Copyright Details: Pediatric Complaints and Diagnostic Dilemmas, Copyright © 2003 Lippincott Williams & Wilkins.
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