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

<p>Abstract</p> <p>Introduction</p> <p>Common 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.</p> <p>Case presentation</p> <p>An 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.</p> <p>Conclusion</p> <p>Alteration 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.</p

De novo design of protein cages to accommodate metal cofactors

This chapter, by reviewing the papers appeared in the literature in the last 10 years, illustrates the different strategies used for the development of de novo-designed protein cages housing mononuclear and dinuclear metal-binding sites, as well as hemes and metalloporphyrins. This chapter mainly focuses on α-helical coiled-coil and bundle structures, which self-assemble with the metal cofactors. Fewer examples of artificial metalloproteins based on β-sheet structures have appeared in the literature and they are also described in the chapter. The artificial metalloproteins reviewed in the chapter clearly show that de novo protein design provides an attractive approach for the construction of models, which appeared valuable to probe the features required for the function of complex metalloproteins. In this context, the computational procedure may allow to identify the best possible sequence library, rather than the best possible sequence