The influence of preoperative risk stratification on fast-tracking patients after pulmonary resection

Fast-tracking protocols or postoperative care computerized algorithms have been shown to reduce hospital length of stay and reduce costs; however, not all patients can be fast-tracked. Certain patient characteristics may put patients at increased risk to fail fast-tracking. Additionally some patients have multiple risk factors that have an additive effect that puts them at an even increased risk to fail fast-tracking, and more importantly, to significant morbidity. It is a mistake to force these protocols on all patients because it can lead to increased complications, readmissions, and low patient and family satisfaction. By carefully analyzing surgical results via accurate prospective databases, the types of patients who fail fast-tracking and the reasons they fail can be identified. Once these characteristics are pinpointed, specific changes to the postoperative algorithm can be implemented, and these alterations can lead to improved outcomes. The authors have shown that by using pain pumps instead of epidurals in elderly patients we can improve outcomes and still fast-track octogenarians with minimal morbidity and high-patient satisfaction. We have also shown that the increased use of physical therapy and respiratory treatments (important parts of the care of all patients after pulmonary resection, but a limited resource in most hospitals) may also lead to improved surgical results for those who have low FEV1% and DLco%. Further studies are needed. Although fast-tracking protocols cannot be applied to all, the vast majority of patients who undergo elective pulmonary resection, even those at high risk, can undergo safe, efficient, and cost-saving care via preset postoperative algorithms. When the typical daily events are convened each morning and the planned date of discharge is frequently communicated with the patient and family before surgery and each day in the hospital, most patients can be safely fast-tracked with high satisfaction and outstanding results.     

The factor V B-domain provides two functions to facilitate thrombin cleavage and release of the light chain

Blood coagulation factors V and VIII are homologous proteins that have the domain organization A1-A2-B-A3-C1-C2. Upon thrombin activation, the B-domains of both molecules are released. Previous studies on factor VIII showed that the B-domain was not required for thrombin cleavage or activity. In contrast, deletion of the factor V B-domain (residues 709 to 1545) yielded a molecule with sevenfold reduced procoagulant activity that was not cleaved by thrombin. However, this factor V B- domain deletion molecule was activated by factor Xa, although the fold- activation was 85% that of wild-type factor V. Thrombin cleavage of factor V occurs initially after residue 709 and subsequently after residues 1018 and 1545. The requirement for thrombin cleavage within the B-domain at residue 1018 was evaluated by mutagenesis of Arg1018 to Ile. In the resultant R1018I mutant, the rate of thrombin activation and appearance of maximal cofactor activity was delayed and was consistent with delayed cleavage of the light chain at residue 1545. In contrast, the rate of factor Xa activation in the R1018I mutant was not altered. This finding suggests that thrombin cleavage at 1018 facilitates subsequent thrombin cleavage at 1545. Further mutagenesis was used to study the requirement for sequences within the factor V B- domain for thrombin cleavage at residue 1545. Whereas the factor V deletion molecule removing residues 709 to 1545 was not cleaved by thrombin, a smaller B-domain deletion molecule (residues 709 to 1476) containing an acidic amino acid-rich region (residues 1490 to 1520) was effectively cleaved by thrombin. These results show that residues 1476 to 1545, which contain an acidic amino acid-rich region, were required for thrombin cleavage of the light chain. Introduction of an acidic amino acid-rich region from factor VIII (residues 337 to 372) into the factor V 709 to 1545 deletion also restored thrombin cleavage of the light chain. In contrast, similar replacement with the acidic region from the factor VIII light chain (residues 1649 to 1689) was significantly less effective in promoting thrombin cleavage of the light chain. This finding suggests that the different acidic regions in factors V and VIII are not functionally equivalent in their interaction with thrombin.(ABSTRACT TRUNCATED AT 400 WORDS)     

Vasodilator agents and supracollicular transection fail to inhibit cortical spreading depression in the cat

It remains an open question as to whether cortical spreading depression (CSD) is the pathophysiological correlate of the neurological symptoms in migraine with aura. In the experimental animal, CSD is an electrophysiological phenomenon mainly mediated via NMDA receptors. However, according to case reports in humans, visual aura in migraine can be alleviated by vasodilator substances, such as amyl nitrite and isoprenaline. There is also circumstantial evidence that brainstem nuclei (dorsal raphe nucleus and locus coeruleus) may play a pivotal role in the initiation of aura. In this study, CSD was elicited in alpha-chloralose anesthetized cats by cortical needle stab injury and monitored by means of laser Doppler flowmetry. Topical application of isoprenaline (0.1-1%) and amyl nitrite (0.05%) onto the exposed cortex had no effect on the elicitation or propagation of CSD. Also, after supracollicular transection, subsequent CSDs showed no differences in the speed of propagation and associated flow changes. We conclude from these data that--given CSD probably exists in humans during migraine--spreading neurological deficits during migraine aura are independent of brainstem influence and have a primarily neuronal rather than vascular mechanism of generation.     

Transesophageal echocardiographic findings of an intracavitary cardiac metastasis from a neuroendocrine thymic carcinoma

This case report presents the unusual characteristics of a neuroendocrine thymic carcinoma that probably has metastasized to the left side of the interatrial septum from a primary thymic site.