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Radiological Case of the Month
Laura M. Ibsen, MD
From the Division of Pediatric Critical Care Medicine, Department of
Pediatrics, Oregon Health Sciences University, Portland.
Arch Pediatr Adolesc Med. 2002;156:293-294.
A PREVIOUSLY healthy 16-year-old boy was brought to the emergency department
with a 1-day history of fever, headache, and lethargy. On that day, he vomited
several times, was disoriented, and was incontinent. The physical examination
results were notable for confusion, meningismus, and anisocoria.
Results of a lumbar puncture showed an opening pressure of 55 cm H2O. The cerebrospinal fluid (CSF) was grossly purulent. Laboratory test
results were white blood cell count, 17 x 103/µL (59%
segmented neutrophils, 37% band forms); glucose, 20 mg/dL (1.11 mmol/L); and
protein, 5.83 g/dL. A gram stain of the CSF showed intracellular gram-negative
diplococci. Treatment was started with ceftriaxone, 75 mg/kg and mannitol,
0.5 g/kg. A computed tomogram of the brain was normal and showed unremarkable
cisterns and ventricles. On arrival after transfer to a tertiary hospital,
his blood pressure was 168/100 mm Hg and his heart rate was 80 beats per minute.
The physical examination results showed minimally responsive pupils, petechiae
of the face, hands, and feet, and decerebrate posturing in response to painful
stimuli. The left side was less responsive than the right. Because of clinical
evidence of increased intracranial pressure (ICP), an intraparenchymal catheter
was placed in the right frontal lobe and the initial ICP was greater than
80 mm Hg. He was immediately treated with intravenous mannitol, sodium pentothal,
fetanyl, and midazolam, and an external ventricular CSF drain was placed.
After drainage of approximately 10 to 20 mL of CSF, the ICP was 10 to 14 mm
Hg. A xenon-enhanced computed tomographic (CT) scan was obtained (Figure 1). Therapy consisted of dopamine to
maintain a mean arterial pressure greater than 80 mm Hg, with a goal of a
cerebral perfusion pressure of greater than 70 mm Hg, sedation with fentanyl
and midazolam, muscle relaxation with pancuronium, mannitol for ICP greater
than 20 cm H2O, mild hyperventilation to maintain arterial PCO2 of 35 to 40 mm Hg, and continuation of antibiotics. The CSF cultures
grew Neisseria meningiditis. On the fifth hospital
day, he had improved and was following commands. The ventriculostomy and the
endotracheal tube were removed. A detailed neurologic examination performed
after extubation revealed no focal deficits, and his mental status continued
to improve. At the time of discharge on the 10th hospital day, the patient
had normal neurologic examination results.
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Denouement and Discussion: Intracranial Hypertension and Reduced Cerebral Blood Flow in Meningococcal Meningitis
Figure 1. Computed tomographic
scan showing an extraventricular drain and cerebral edema. The anterior horn
of the right lateral ventricle appears smaller than the left but is within
normal limits. The xenon flow study shows the left hemisphere with normal
perfusion and flow from 30 to 60 mL/100 mg of tissue per minute. The right
frontal/parietal cortex is hypoperfused with flows of 20 mL/100 mg of tissue
per minute, with sparing of the occipital region on posterior parietal lobes,
where flows are 30 to 50 mL/100 mg of tissue per minute.
Stable xenon CT cerebral blood flow (CBF) determination is effective
to evaluate brain perfusion after traumatic brain injury. Stable (nonradioactive)
xenon gas is inhaled and acts as a tracer. The CT scan is obtained with specialized
software, and the attenuation of the signal reflects the perfusion within
the brain while the regional blood flow is quantitated. The scans are performed
when arterial PCO2 and mean arterial blood pressure are known.
Measurement of CBF coupled with information about ICP have been used to guide
clinical management of traumatic brain injury. Xenon CT has been used in the
evaluation of CBF in nontraumatic brain injury1
but its efficacy in guiding therapy is not as well established.
Neurologic injury in bacterial meningitis is due to several factors,
such as elevated ICP, vasculitis, sinus thrombosis, alterations in CBF, defective
autoregulation of CBF, or alterations in cerebral metabolism.2
Elevated ICP may be due to cerebral edema,3
increased CSF volume,4-5
or increased cerebral blood volume.6 Cerebral
blood flow is elevated, normal, or decreased during the course of bacterial
meningitis.1 Many patients with bacterial
meningitis have intact CBF/PCO2 reactivity; hence, hyperventilation
may further reduce CBF in patients whose CBF is already below normal.1 Our patient likely had cerebral edema and decreased
compliance, which was not evident on the initial CT. Since his CBF was low,
increased cerebral blood volume was not a factor in the increased ICP.
Computed tomography and magnetic resonance imaging have demonstrated
a wide variety of cerebral abnormalities in children with bacterial meningitis.
The incidence of abnormality varies among series, and recent studies have
shown a low incidence of cerebral edema without any relationship to neurologic
examination or outcome4, 7.
While CT scans are useful if they reveal specific focal abnormalities or edema
to indicate the presence of elevated ICP, a normal CT scan does not preclude
increased ICP.
If the physical examination or initial imaging study suggests that ICP
is elevated, internal ICP monitoring should be considered. If ICP is found
to be elevated, a xenon CT aids in determining the treatment strategy by delineating
the pattern of CBF. In our case, since the patient had decreased CBF, the
treatment strategy focused on improving cerebral perfusion pressure and minimizing
cerebral metabolic needs while avoiding hyperventilation (which would have
decreased already compromised blood flow). While there is no direct evidence
that this treatment strategy improves outcome, there is evidence that patients
with lower cerebral perfusion pressure (mean arterial pressure - ICP)
have poorer outcomes, and that patients with low CBF have poorer outcomes.1 The only way to manipulate CBF and cerebral perfusion
pressure is with simultaneous monitoring of arterial blood pressure and ICP,
paired with quantitative CBF to guide management.
AUTHOR INFORMATION
Accepted for publication June 15, 1999.
Corresponding author: Laura M. Ibsen, MD, Oregon Health Sciences
University, Division of Pediatric Critical Care Medicine, Department of Pediatrics,
3181 SW Sam Jackson Park Rd, Portland, OR 97201-3098.
REFERENCES
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1. Ashwal S, Stringer W, Tomasi L, et al. Cerebral blood flow and carbon dioxide reactivity in children with
bacterial meningitis. J Pediatr. 1990;117:523-530.
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2. Berkowitz I. Update: meningitis. Crit Care Med. 1993;21:S316-S318.
3. Horwitz SJ, Boxerbaum B, O'Bell J. Cerebral herniation in bacterial meningitis in childhood. Ann Neurol. 1980;7:524-528.
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4. Cabral DA, Flodmark O, Farrel K, Speert DP. Prospective study of computed tomography in acute bacterial meningitis. J Pediatr. 1987;111:201-205.
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5. Tauber MG, Khayam-Gashi H, Sande MA. Effects of ampicillin and corticosteroids on brain water content, cerebrospinal
fluid pressure, and cerebrospinal fluid lactate levels in experimental pneumococcal
meningitis. J Infect Dis. 1985;151:528-524.
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6. Tureen J. Cerebral blood flow and metabolism in experimental meningitis. Pediatr Infect Dis J. 1989;8:917-919.
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7. Kline MW, Kaplan SL. Computed tomography in bacterial meningitis of childhood. Pediatr Infect Dis J. 1988;7:855-857.
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SECTION EDITOR: BEVERLY P. WOOD, MD
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
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ABSTRACT
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