Hypercapnic cerebral edema presenting in a woman with asthma: a case report

Abstract

IntroductionCommon causes of non-traumatic acute cerebral edema include malignant hypertension, hyponatremia, anoxia, and cerebral vascular accident. The computed tomographic images and data obtained during care of the patient described in this case report provide evidence that hypercarbia can cause increased intracranial pressure and coma without permanent brain injury. Partial pressure of carbon dioxide evaluation for coma is essential to provide faster diagnosis and therapeutic correction in certain common critical disease states. We present the case of a patient in a coma associated with cerebral edema during a typical asthma exacerbation with hypercapnic respiratory failure.Case presentationAn obese 63-year-old African American woman with asthma presented to our hospital with facial swelling and shortness of breath. Immediately following intubation for hypercapnic respiratory failure, she was noted to have a dilated, unresponsive right pupil. An emergent computed tomographic head scan revealed that she had increased intracranial pressure. A neurosurgeon agreed with the computed tomography interpretation and recommended no surgical intervention. The patient's respiratory acidosis was corrected with ventilatory management over several hours in the intensive care unit. Nine and one-half hours later a follow-up head computed tomographic scan was read as normal without cerebral edema. At 12 hours, the patient's right pupil was 5 mm in diameter and reactive. By 24 hours, her pupils were symmetrically equal and reactive. Her symptoms had improved, and she was extubated. A brain magnetic resonance imaging scan revealed no abnormalities.ConclusionAlteration of consciousness related to hypercapnia during respiratory failure is not generally thought to be related to cerebral edema. Respiratory acidosis resulting from hypercarbia is known to produce carbon dioxide narcosis and coma, but no current treatment algorithm suggests that rapid hypercapnia correction can be critical to neurologic outcome. To the best of our knowledge, our case is a unique example of the physiological changes that may occur in relation to arterial carbon dioxide concentration in the normal brain in the setting of typical hypercapnic respiratory failure. Correction of respiratory acidosis reversed the neurologic symptoms and physiology causing cerebral edema and coma in our patient. Rare similar cases have been sporadically reported in the medical literature, typically in children. Our case is also unusual in that rapid deterioration and clinical status were directly observed on simultaneous computed tomographic scans. Had this patient been found unresponsive, or had she had brief respiratory or cardiac arrest, the scan could have been interpreted as global anoxic injury leading to a different therapeutic course.

Permissive hypercapnia for severe acute respiratory distress syndrome in immunocompromised children: A single center experience

“…Multiple reports of acute asthma reassure that even excessively high values of hypercapnia can be survived without sequelae [ 37 ; 38 ]. However, there are reports where acute exposure to high CO 2 was associated with cerebral vasodilation, and cerebral edema.…”

Permissive hypercapnia: Is there any upper limit?

“…Previous animal studies have reported vasogenic cerebral edema in hypercapnic acidosis and in human beings cerebral edema have been reported in severe respiratory acidosis associated with asthma. [ 3 ] Hypercapnia has a beneficial effect on brain in an optimal range. Lowering CO 2 causes cerebral vasoconstriction whereas increased CO 2 results in cerebral edema.…”

A 47‐year‐old woman with hypercapnia and altered mental status

“…As such, altered mental status in patients with severe CO 2 retention usually does not alarm clinicians to pursue neurological workups. However, it has been well documented that carbon dioxide can exert detrimental effects on the brain through several mechanisms, including acid‐base disturbance, metabolic changes, modification of cerebral blood flow, increased intracranial pressure and dysfunction of neuron membrane ion channels . In fact, scattered case reports of hypercapnic cerebral edema can be found in the literature, and was characterized by rapid and complete resolution of neurological function once CO 2 retention was corrected .…”

“…However, it has been well documented that carbon dioxide can exert detrimental effects on the brain through several mechanisms, including acid‐base disturbance, metabolic changes, modification of cerebral blood flow, increased intracranial pressure and dysfunction of neuron membrane ion channels . In fact, scattered case reports of hypercapnic cerebral edema can be found in the literature, and was characterized by rapid and complete resolution of neurological function once CO 2 retention was corrected . The true incidence of hypercapnic cerebral edema might be significantly underestimated, as the neurologic findings might frequently be overlooked by clinicians due to insufficient awareness and brain imaging is almost never pursued in this clinical setting.…”