Basilar Predominant Emphysema: Thinking beyond Alpha-1-Antitrypsin Deficiency.

Basilar predominant emphysema, or disproportionate emphysematous involvement of the lung bases compared to the apices, is an uncommon radiographic pattern of emphysema traditionally associated with alpha-1-antitrypsin deficiency (AATD). We present a case of a 59-year-old female with 41 pack-year tobacco use, Stage IV COPD with supplemental oxygen, and bibasilar predominant emphysema who successfully underwent bronchoscopic lung volume reduction. She presented with recurrent hospitalizations for frequent exacerbations. After lung reduction, the patient displayed improvement in functional status without hospitalizations at the 15-month follow-up. Careful history taking is essential for any patients diagnosed with lower lobe emphysema to elucidate the underlying etiology. This case challenges the notion that basilar emphysema is sensitive or specific for AATD and emphasizes that this pattern of emphysema has a broad differential diagnosis and alternative etiologies should be considered. Our patient was ultimately diagnosed with smoking-related emphysema, with atypical bibasilar involvement. Furthermore, basilar predominant emphysema should be considered a separate entity from its apical predominant counterpart.

Lumbar osteomyelitis and knee septic arthritis caused by Streptococcus agalactiae bacteraemia.

A man in his late 70s presented to the emergency department endorsing a week of malaise. He was recently hospitalised for 2 days for new back pain and was discharged with non-opioid pain medications but continued to seek care as he felt unwell. On presentation, he was afebrile with a leukocytosis. Physical examination revealed a painful left knee with no evidence of trauma. Arthrocentesis revealed purulent fluid with elevated white blood cell consistent with septic arthritis. He was started on broad-spectrum antibiotics and underwent irrigation and synovectomy of the left knee. Aspirate and blood cultures grew Streptococcus agalactiae Transthoracic echocardiogram showed no vegetations; however, an MRI of lumbar spine showed L2-L3 and L4-L5 osteomyelitis. He was treated with intravenous ceftriaxone for 3 weeks and then oral levofloxacin for 3 weeks, for a total 6 week course of antibiotics.

Cognitive functioning following traumatic brain injury: A five-year follow-up.

OBJECTIVE: To describe the long-term prevalence and severity of cognitive deficits following significant (i.e., ventilation required for >24 hours) traumatic brain injury. To assess a comprehensive range of cognitive functions using psychometric measures with established normative, reliability, and validity data. METHODS: A group of 71 adults was assessed at approximately five years (mean = 66 months) following injury. Assessment of cognitive functioning covered the domains of intelligence, attention, verbal and visual memory, visual-spatial construction, and executive functions. RESULTS: Impairment was evident across all domains but prevalence varied both within and between domains. Across aspects of intelligence clinical impairment ranged from 8-25% , attention 39-62% , verbal memory 16-46% , visual memory 23-51% , visual-spatial construction 38% , and executive functions (verbal fluency) 13% . In addition, 3-23% of performances across the measures were in the borderline range, suggesting a high prevalence of subclinical deficit. CONCLUSIONS: Although the prevalence of impairment may vary across cognitive domains, long-term follow-up documented deficits in all six domains. These findings provide further evidence that while improvement of cognitive functioning following significant traumatic brain injury may be possible, recovery of function is unlikely.