AJR 2004; 183:865-866
© American Roentgen Ray Society
Severe Hypercapnia Mimicking Hypoxic Brain Edema on Cerebral CT
Stephan J. Schreiber,
Florian Doepp,
Georg Bohner and
José M. Valducza
University Hospital Charity Berlin 10117, Germany
A 35-year-old woman was admitted to our hospital with a subacute
deteriorating level of consciousness. She was known to have a congenital
myasthenic syndrome, clinically manifesting as a chronic hypercapnic state.
Recurrent hypoxic events required continuous oxygen insufflation (1 L/min)
during the previous 2 years. On admission, the patient had a Glasgow Coma
Scale score of 10, a blood pressure measurement of 105/60 mm Hg, and a
peripheral oxygen saturation level of 94% under 16 L/min of O2.
Arterial blood gas analysis showed severe hypercapnia
(PCO2, 81 mm Hg; PO2, 89.8 mm Hg;
base excess, 28; bicarbonate [HCO3], 57.1 mmol/L; pH, 7.473), but
other laboratory values (electrolyte levels, renal and liver function tests,
and blood count) were in the normal range. The physical examination revealed
no focal neurologic deficits. In the hospital, the global respiratory
insufficiency rapidly worsened (increasing somnolence and peripheral oxygen
saturation of 85%) leading to emergency intubation and mechanical ventilation.
A cerebral CT scan obtained on admission revealed effacement of cortical sulci
and decrease in the size of ventricles and basal cisterns similar to the
radiologic findings seen with hypoxic brain edema
(Fig. 3A). The acute
respiratory failure was found to be caused by a small pulmonary embolism.
Because our patient was not hypoxic, cerebral CT scan changes were presumed to
be related to the marked hypercapnia, and treatment was confined to mild
hyperventilation (no barbiturates or hypothermia). Follow-up cerebral CT after
24 hr showed a nearly complete normalization (pCO2, 35.2 mm Hg)
(Fig. 3B). The patient was
weaned from the ventilator, successfully extubated, and transferred to a
regular ward 5 days later. Our case was remarkable because of the triggering
mechanism and the near-complete resolution of severe brain swelling in 24
hr.
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Fig. 3A. —35-year-old woman with congenital myasthenic syndrome with presumed
acute brain edema caused by severe hypercapnia. Cerebral CT scans obtained on
admission show diffuse brain edema with effacement of sulci, diffusely
hypodense white matter, and decrease in size of lateral ventricles and basal
cisterns.
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Fig. 3B. —35-year-old woman with congenital myasthenic syndrome with presumed
acute brain edema caused by severe hypercapnia. Follow-up CT scans obtained
after 24 hr of mild hyperventilation show nearly complete resolution of signs
of brain edema.
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In general, brain edema can be caused by either intra- or extracellular
water accumulation, commonly referred to cytotoxic and vasogenic edema
[1]. The former is the result
of a loss of cell-volume regulation caused by ischemic, anoxic, or toxic
stimuli leading to swelling of cellular elements.
The latter, in which triggering events such as trauma, stroke, hemorrhage,
or hypertension lead to a disrupted blood–brain barrier show an
interstitial edema predominantly affecting the white matter
[1]. Both mechanisms often
coexist.
Brain edema caused by global hypoxia is known to be associated with a poor
clinical outcome [2]. In
contrast, our patient showed complete clinical recovery in a short time.
Therefore, a different mechanism had to be considered. Metabolic and toxic
causes were excluded by laboratory analysis. However, because of her
congenital myasthenic syndrome, the patient had a chronic hypercapnic state,
which severely decompensated because of a small acute pulmonary embolism.
Hypercapnia is known to increase the global cerebral blood flow (i.e., to
cause hyperemia and also to raise the global cerebral blood volume)
[3]. This mechanism, possibly
in combination with a disturbed blood–brain barrier
[4], is the most likely cause
of the observed CT changes in the present case because the only therapeutic
measure used, a quick normalization of CO2 values by mechanical
ventilation, led to a rapid and complete recovery.
In conclusion, cerebral CT does not allow the differentiation of diffuse
brain edema and massive blood volume increase caused by severe hypercapnia.
The values for PO2 at the time of the CT scan should be
taken into consideration if diffuse brain swelling is detected.
References
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- Morimoto Y, Kemmotsu O, Kitami K, Matsubara I, Tedo I. Acute brain
swelling after out-of-hospital cardiac arrest: pathogenesis and outcome.
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- Ito H, Kanno I, Ibaraki M, Hatazawa J, Miura S. Changes in human
cerebral blood flow and cerebral blood volume during hypercapnia and
hypocapnia measured by positron emission tomography. J Cereb Blood
Flow Metab 2003;23:665
-670[Medline]
- Knudsen GM, Paulson OB, Hertz MM. Kinetic analysis of the human
blood-brain barrier transport of lactate and its influence by hypercapnia.
J Cereb Blood Flow Metab1991; 11:581
-586[Medline]
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