Free and pedicle flaps in lower extremity trauma

Improvements in microsurgical techniques and perioperative management have led to more attempts at limb salvage surgery after severe extremity trauma. Although some microsurgery-trained orthopedic surgeons will perform extremity soft tissue reconstruction, many rely on plastic surgeons or hand surgeons. However, the orthopedic trauma surgeon often remains the principle decision maker in the follow-up of these patients. Therefore, orthopedic surgeons should have a clear understanding of the planning and execution of flap reconstruction of the traumatized extremities. Collaboration with the microsurgery team will also improve planning of orthopedic procedures and facilitate a better understanding of the expected outcomes after tissue transfer. This becomes especially important when considering, debridement, early amputation versus extensive soft tissue reconstruction and when discussing these alternatives with patients and family as well as postoperative course. The goals of this article are to provide orthopedic trauma surgeons with an understanding of the selection, planning, and execution of tissue transfers for posttraumatic extremity reconstruction and to review their successes and outcomes in the literature. Communication between teams involved in reconstruction of the traumatized extremity and an understanding of limitations are paramount to successful outcomes after reconstruction.Level of Evidence: Not ratable.     

Cloning and sequencing of CATR1.3, a human gene associated with tumorigenic conversion.

The human squamous cell carcinoma cell line SCC83-01-82 (SCC) contains mutations in both the H-ras and p53 genes, but it exhibits a nontumorigenic phenotype in nude mice. This cell line can be converted into a cell line with a tumorigenic phenotype, SCC83-01-82CA (CA), by treatment with the mutagen methyl methanesulfonate (MMS). This indicates that additional genetic events leading to expression of a cooperating tumor susceptibility gene(s) may be required for tumorigenicity. To identify the cooperating gene(s), an expression cDNA library was made from tumorigenic Ca cells. The library DNA was transfected into nontumorigenic SCC cells and the transfected SCC cells were then injected into nude mice for the selection of a tumorigenic phenotype. Tumors developed in 3 of the 18 mice after injection. Several new cell lines were established from these transfected cell-induced tumors and designated as CATR cells. Tumor histology and karyotype analysis of these cells indicated that they were of human epithelial cell origin. All the CATR cells have the library vector sequence integrated in their genome. Cell line CATR1 expressed a single message from the integrated library representing a 1.3-kb cDNA insert that was absent from untransfected SCC cells or MMS-converted CA cells. This 1.3-kb cDNA insert was cloned by PCR amplification of reverse-transcribed CATR1 total RNA and was designated CATR1.3. The nucleotide sequence of CATR1.3 encodes a peptide of 79 amino acids, has a long 3' untranslated region, and represents an unknown gene product that was associated with the tumorigenic conversion due to the transfected expression library.     

Symptoms of advanced heart failure—A case for radiofrequency catheter ablation?

A sixty-year-old man with previous history of coronary artery disease was admitted due to progressive worsening of dyspnoea at exertion (NYHA III functional class) and no angina. Coronary angiography confirmed occlusion of the right coronary artery which was naturally bypassed by homocollaterals with TIMI 3 flow to the peripheral branches. The lesion was not technically suitable for percutaneous angioplasty. The left coronary artery was without stenosis. On echocardiography, both the left ventricle and the left atrium were dilated and hemodynamically significant mitral regurgitation was present. Surface ECG showed a left bundle branch block with repeated runs of monomorphic ventricular ectopic beats (PVC). Radiofrequency catheter ablation of the focus in the posteroseptal region of the left ventricle underneath the mitral valve was performed using electroanatomical mapping system. After the procedure, mitral regurgitation decreased and reverse remodeling of the left ventricle and the left atrium occurred with concomitant significant clinical improvement of the patient. The authors discuss several treatment strategies: mitral valve repair surgery combined with revascularization, implantation of a biventricular ICD system or elimination of the focus of monomorphic VT runs by radiofrequency catheter ablation as a possible causal approach in the treatment of PVC-induced cardiomyopathy.     

Comparison of sublingual isosorbide dinitrate and Valsalva maneuver for detection of obstruction in hypertrophic cardiomyopathy

Introduction

A left ventricular outflow tract (LVOT) obstruction assessment with a provoking test should be a routine part of the evaluation of patients with hypertrophic cardiomyopathy (HCM). The aim of this study was to compare the utility of the Valsalva maneuver (VM) and sublingual spray application of isosorbide dinitrate (ISDN) for detection of an obstruction.

Material and methods

We prospectively evaluated 81 consecutive HCM patients without severe rest LVOT obstruction (defined as peak rest pressure gradient (PG) ≥ 50 mm Hg). We measured PG at rest, during the VM, after sublingual ISDN spray, and during the VM after ISDN. An obstruction was defined as a PG ≥ 30 mm Hg.

Results

An obstruction was present in 15 patients (19%) at rest (median and interquartile range of PG 16 (7–26) mm Hg), in 38 patients (47%) during the VM (PG 28 (12–49) mm Hg), in 50 (62%) patients after ISDN (PG 50 (12–79) mm Hg), and in 55 patients (68%) during the VM after ISDN (PG 59 (20–87) mm Hg). The difference in occurrence of obstruction among different provoking tests was statistically significant for all comparisons (p < 0.001, except for the comparison of the ISDN test with the VM during ISDN, p = 0.025).

Conclusions

The ISDN test and the VM are useful screening methods for the detection of an HCM obstruction. Although ISDN appears to be more precise than the VM, the best option is a combination of both methods, which maximizes inducement of LVOT obstruction in patients with HCM.     

ABCB4 mutations underlie hormonal cholestasis but not pediatric idiopathic gallstones

AIM:To investigate the contribution of ABCB4 mutations to pediatric idiopathic gallstone disease and the potential of hormonal contraceptives to prompt clinical manifestations of multidrug resistance protein 3 deficiency.METHODS:Mutational analysis of ABCB4,screening for copy number variations by multiplex ligation-dependent probe amplification,genotyping for low expression allele c.1331T>C of ABCB11 and genotyping for variation c.55G>C in ABCG8 previously associated with cholesterol gallstones in adults was performed in 35 pediatric subjects with idiopathic gallstones who fulfilled the clinical criteria for low phospholipid-associated cholelithiasis syndrome(LPAC,OMIM#600803)and in 5young females with suspected LPAC and their families(5 probands,15 additional family members).The probands came to medical attention for contraceptiveassociated intrahepatic cholestasis.RESULTS:A possibly pathogenic variant of ABCB4was found only in one of the 35 pediatric subjects with idiopathic cholesterol gallstones whereas 15 members of the studied 5 LPAC kindreds were confirmed and another one was highly suspected to carry predictably pathogenic mutations in ABCB4.Among these 16,however,none developed gallstones in childhood.In 5index patients,all young females carrying at least one pathogenic mutation in one allele of ABCB4,manifestation of LPAC as intrahepatic cholestasis with elevated serum activity of gamma-glutamyltransferase was induced by hormonal contraceptives.Variants ABCB11c.1331T>C and ABCG8 c.55G>C were not significantly overrepresented in the 35 examined patients with suspect LPAC.CONCLUSION:Clinical criteria for LPAC syndrome caused by mutations in ABCB4 cannot be applied topediatric patients with idiopathic gallstones.Sexual immaturity even prevents manifestation of LPAC.