Presentation and management of traumatic occipital spur fracture

Occipital spur is an abnormal bony outgrowth of the external occipital protuberance (EOP). We describe an interesting and previously unreported case of fracture of an occipital spur following trauma. Our 20-year-old male patient was treated in the emergency department (ED) and discharged home without complication. Neurosurgical consultation was obtained but is not requisite for these injuries. Greater awareness of this unique presentation may help to expedite future emergency department treatment.     

Carbon dioxide recruitment threshold as a predictor of successful weaning in chronic obstructive pulmonary disease patients: A pilot study

Abstract Several methods have been used to predict successful weaning and extubation among chronic obstructive pulmonary disease (COPD) patients. The objective of this study is to determine whether carbon dioxide recruitment threshold (PCO₂RT) can be used as adjunct to conventional weaning parameters to predict early weaning and successful extubation. Twelve COPD patients who were ready to be extubated based on conventional weaning parameters were divided into group A ( n = 7) and group B ( n = 5). Group A were those patients with better weaning parameters and hence a higher probability of successful extubation as compared to group B. Carbon dioxide apnoeic threshold (PCO₂AT) was obtained by hyperventilating the patient using an increment of two breaths per min until apnoea occurs. At this point, the PCO₂AT or the PaCO₂ during said apnoeic period was recorded. A dead space of 150 cc is then added to the circuit until the patient starts to breathe as evidenced by the sensitivity trigger indicator. The PCO₂ obtained at this period is termed PCO₂RT. After weaning for 30 min on a T-tube, another arterial blood gas is determined and this is called the PCO₂SB or the CO₂ level after 30 min on spontaneous breathing. If the PCO₂SB-PCO₂RT difference is high with a sensitivity of 85.71% and specificity of 100% vs sensitivity of 57.14% and specificity of 60% using the conventional weaning parameters. Thus an increase in PCO₂SB at 30 min T-tube is indicative of impending respiratory pump failure and that other causes of failure to wean must be investigated.     

Government advice on peanut avoidance during pregnancy – is it followed correctly and what is the impact on sensitization?

BACKGROUND: In 1998, the UK government issued precautionary advice that pregnant or breast-feeding women with a family history of atopy, may wish to avoid eating peanuts during pregnancy and lactation. This study aimed to assess the compliance with this recommendation and investigate its impact upon peanut sensitization. METHODS: A total of 858 children born immediately after the advice were followed for 2 years and assessed for peanut sensitization. A standardized questionnaire was used to ascertain history of atopy and maternal exposure to peanuts during pregnancy. Following parental consent children were skin prick tested to assess sensitization to peanuts. RESULTS: Sixty-five per cent of mothers had avoided peanuts during pregnancy. Forty-two per cent of the mothers had heard about the government advice, and half modified their diet as a consequence. Neither maternal nor family history of atopy had any significant effect on peanut consumption. Parity did play a role, and mothers having their first child were twice as likely to change their diet (P<0.001). Mothers of 77% of the children sensitized to peanuts had avoided peanuts during pregnancy. In this cohort study maternal consumption of peanut during pregnancy was not associated with peanut sensitization in the infant. CONCLUSIONS: The majority of mothers in this cohort avoided peanut consumption during pregnancy. It is likely that either the government advice is misunderstood by mothers, or that those who communicate the advice have not fully explained who it is targeted at.     

Additive effects of CD59 expression in Gal knockout mice in vitro but not in an ex vivo model

Abstract: Transgenic expression of the human complement regulatory molecule CD59 in mice and genetic deletion of the major xenoantigen galactose α 1,3 galactose (Gal KO) each resulted in partial protection of spleen cells from lysis by human serum. These protective effects were additive when the two genetic modifications were combined. However, when the effects of these genetic modifications were examined in an ex vivo model in which mouse hearts were perfused with human plasma, it was Gal KO which was the modification which determined protection. CD59 expression alone was not protective and CD59 expression in combination with Gal knockout did not result in a significant additional increase in protection over and above that provided by Gal knockout alone. The likely explanation for this discrepancy between the in vitro and ex vivo data is that the H2-K^b promoter used to drive CD59 expression results I in substantially less expression on endothelium than on spleen cells.