Intraoperative Tissue Perfusion Measurement by Laser Speckle Imaging: A Potential Aid for Reducing Postoperative Complications in Free Flap Breast Reconstruction.

Adequate tissue perfusion is essential to minimize postoperative complications following microsurgery. Intraoperative knowledge of tissue perfusion could aid surgical decision-making and result in reduced complications. Laser speckle imaging is a new, noninvasive technique for mapping tissue perfusion. This article discusses the feasibility of using laser speckle imaging during free flap breast reconstruction and its potential to identify areas of inadequate perfusion, thus reducing surgical complications. Adult patients scheduled to undergo free flap breast reconstruction were recruited into the study. Laser speckle images were obtained from the abdominal and breast areas at different stages intraoperatively. Zonal perfusion was compared with the Holm classification and clinical observations. Twenty patients scheduled to undergo free flap breast reconstruction were recruited (23 reconstructed breasts) (mean age, 50 years; range, 32 to 68 years). Flap zonal perfusion was 238 (187 to 313), 222 (120 to 265), 206 (120 to 265), and 125 (102 to 220) perfusion units for zones I, II, III, and IV, respectively (analysis of variance, p < 0.0001). Zonal area with perfusion below an arbitrary perfusion threshold were 20 (0.3 to 75), 41 (3 to 99), 49 (9 to 97), and 99 (25 to 100) percent, respectively (analysis of variance, p < 0.0001). One example is presented to illustrate potential intraoperative uses for laser speckle imaging. This study shows that laser speckle imaging is a feasible, noninvasive technique for intraoperative mapping of tissue perfusion during free flap breast reconstruction. Zonal tissue perfusion was reduced across the Holm classification. Observations indicated the potential for laser speckle imaging to provide additional information to augment surgical decision-making by detection of inadequate tissue perfusion. This highlights the opportunity for surgeons to consider additional aids for intraoperative tissue perfusion assessment to help reduce perfusion-related complications. CLINICAL QUESTION/LEVEL OF EVIDENCE:: Diagnostic, IV.

Acetyl-l-carnitine increases nerve regeneration and target organ reinnervation - a morphological study.

Peripheral nerve injury frequently results in functional morbidity since standard management fails to adequately address many of the neurobiological hurdles to optimal regeneration. Neuronal survival and regeneration are neurotrophin dependent and require increased aerobic capacity. Acetyl-l-carnitine (ALCAR) facilitates this need and prevents neuronal loss. ALCAR is clinically safe and is shown here to significantly improve nerve regeneration and target organ reinnervation. Two groups of five rats underwent sciatic nerve division followed by immediate repair. One group received parenteral ALCAR (50mg/kg/day) from time of operation until termination at 12 weeks. A 'sham treatment' group received normal saline. A third group was left unoperated and did not receive any treatment. A segment of nerve was harvested between 5mm proximal and 10mm distal to the repair in operated groups, and at the corresponding level in the unoperated group. Mean axonal count in normal, non-axotomised nerve was 14,720 (SD 2378). That of the saline group (17,217 SD 1808) was not significantly different from normal nerve (P=0.0985). Mean number of myelinated axons in the ALCAR group (24,460 SD 3750) was significantly greater than both sham group (P<0.01) and normal nerve (P=0.0012). Mean myelin thickness in the saline treated group (0.408 microm SD 0.067 microm) was less than normal nerve (0.770 microm SD 0.143 microm) (P<0.001). Mean myelin thickness in the ALCAR group (0.627 microm SD 0.052 microm) was greater than the sham (saline) group (P<0.01) and not statistically different from normal nerve (P=0.07). ALCAR increased dermal PGP9.5 staining by 210% compared to sham treatment (P<0.0001) and significantly reduced the mean percentage weight loss in gastrocnemius muscle (ALCAR group 0.203% vs. 0.312% in sham group P=0.015). ALCAR not only increases the number of regenerating nerve fibres but also morphologically improves the quality of regeneration and target organ reinnervation. Adjuvant ALCAR treatment may improve both sensory and motor outcomes and merits further investigation.

Dermabond tissue adhesive versus Steri-Strips in unilateral cleft lip repair: an audit of infection and hypertrophic scar rates.

OBJECTIVE: The purpose of this study was to compare the infection and hypertrophic scar rates in unilateral cleft lip repairs, having had Steri-Strips or Dermabond tissue glue applied across the repair as the final stage. DESIGN: Retrospective study over 13 years of 307 unilateral cleft lip repairs by a single surgeon. The application of either Steri-Strips from 1992 to 1998 (121 patients) or Dermabond tissue adhesive from 1998 to 2006 (186 patients) was used in the final stage of the repair. SETTING: Regional Centre for Cleft Lip and Palate Care, South West of England. PARTICIPANTS: 307 consecutive unilateral cleft lip patients seen from 1992 to 2006. MAIN OUTCOME MEASURES AND RESULTS: There were five (4%) infections in the Steri-Strip group. All infections were with Staphylococcus aureus. No infections occurred in the Dermabond group (p< .001). There were 15 (12%) hypertrophic scars in the Steri-Strip group and 33 (18%) hypertrophic scars in the Dermabond group (p= .142). Revision surgery was required in a total of seven (6%) patients in the Steri-Strip group. No revisions were required in the Dermabond group (p. 1). CONCLUSION: We found a lower infection and revision rate and a similar hypertrophic scar rate when Dermabond was used instead of Steri-Strips in the final stage of unilateral cleft lip repair and suggest this study further supports the use of octyl-2-cyanoacrylate tissue adhesive in unilateral cleft lip repair.

Atypical cellular neurothekeoma--a diagnosis to be aware of.

We present a rare case of atypical cellular neurothekeoma arising in the area of a previous nose piercing on the ala of a 34-year-old female. Neurothekeoma is a benign tumour of probable nerve sheath origin. The cell of origin for neurothekeoma is still unknown but most ultrastructural and immunohistochemical studies have favoured the Schwann cell perineurium or fibroblasts. A similar but distinct, more cellular variant with a less prominent myxoid component, was termed cellular neurothekeoma and, unlike myxoid neurothekeoma, the cellular variety generally lacks immunoreactivity to most neuronal markers. Atypical cellular neurothekeoma is characterised by the following features: large size of up to 6 cm, penetration into subcutaneous fat and or muscle, diffusely infiltrating borders, vascular invasion, a high mitotic rate and marked cytological pleomorphism. In this report we provide a review of the relevant literature and describe the clinical, histological and immunohistochemical features of an atypical cellular neurothekeoma excised from the ala nasi of a 34-year-old female, a hitherto unreported lesion in the plastic surgery literature.

Delayed acetyl-L-carnitine administration and its effect on sensory neuronal rescue after peripheral nerve injury.

Protection of sensory neurons after peripheral nerve injury is clinically crucial since inadequate sensory recovery is seriously affected by the death of up to 40% of sensory neurons. Immediate acetyl-L-carnitine (ALCAR) treatment eliminates this cell loss, but may not always be clinically feasible, hence we studied the effect of delaying the initiation of ALCAR treatment. Five groups of rats (n=5 per group) underwent unilateral sciatic nerve axotomy. ALCAR treatment (50 mg/kg/day) was initiated immediately, or after delays of 6 h, 24 h or 7 days after injury. A sham-treated group served as control. L4 and L5 dorsal root ganglia were harvested bilaterally 2 weeks after injury and stereological sensory neuron counts were obtained. Immediate sham treatment provided no neuroprotection (25% loss). Cell loss was eliminated when ALCAR was commenced within

Acetyl-l-carnitine: a pathogenesis based treatment for HIV-associated antiretroviral toxic neuropathy.

BACKGROUND: Nucleoside analogue reverse transcriptase inhibitors (NRTI) disrupt neuronal mitochondrial DNA synthesis, impairing energy metabolism and resulting in a distal symmetrical polyneuropathy (DSP), an antiretroviral toxic neuropathy (ATN) that causes significant morbidity in HIV disease. Serum acetyl-l-carnitine (ALCAR) levels are decreased in neuropathy associated with NRTI therapy. ALCAR enhances neurotrophic support of sensory neurons and promotes energy metabolism, potentially causing nerve regeneration and symptom relief. OBJECTIVE: To assess the efficacy of oral ALCAR (1500 mg twice daily) for up to 33 months in an open cohort of 21 HIV-positive patients with established ATN. METHODS: Skin biopsies were excised from the leg before ALCAR treatment, at 6-12 month intervals thereafter and from HIV-negative non-neuropathic controls. Fibre types in epidermal, dermal and sweat gland innervation were quantified immunohistochemically. RESULTS: After 6 month's treatment, mean immunostaining area for small sensory fibres increased (epidermis 100%, P = 0.006; dermis 133%, P < 0.05) by more than that for all fibre types (epidermis 16%, P = 0.04; dermis 49%, P < 0.05; sweat glands 60%, P < 0.001) or for sympathetic fibres (sweat glands 41%, P < 0.0003). Compared with controls, epidermal, dermal and sweat gland innervation reached 92%, 80% and 69%, respectively, after 6 month's treatment. Innervation improvements continued (epidermis and dermis) or stabilized (sweat glands) after 24 month's treatment. Neuropathic grade improved in 76% of patients and remained unchanged in 19%. HIV RNA load, CD4 and CD8 cell counts did not alter significantly throughout the study. CONCLUSIONS: ALCAR treatment improves symptoms, causes peripheral nerve regeneration and is proposed as a pathogenesis-based treatment for DSP.

Reverse digital artery island flap in the elderly.

The following case report illustrates the successful use of the reverse digital artery island flap in elderly patients. The reverse digital artery island flap is a recognised method of providing good quality soft tissue cover to the amputated fingertip. First described in 1986 by Kojima, Lai and Han have reported their experience of 52 and 120 of these flaps, respectively. The majority of patients in the literature are less than 50 years old, with ages ranging from 3 to 62 years. The flap is based upon reversed flow in the digital artery via a communicating branch from the contralateral artery at a point 5mm proximal to the distal interphalangeal joint crease. In the two cases reported below, we have shown that the indications for this type of homodigital flap reconstruction for fingertip amputations can be safely extended to elderly patients.

Primary sensory neuronal rescue with systemic acetyl-L-carnitine following peripheral axotomy. A dose-response analysis.

The loss of a large proportion of primary sensory neurons after peripheral nerve axotomy is well documented. As a consequence of this loss, the innervation density attained on completion of regeneration will never be normal, regardless of how well the individual surviving neurons regenerate. Acetyl-L-carnitine (ALCAR), an endogenous peptide in man, has been demonstrated to protect sensory neurons, thereby avoiding loss after peripheral nerve injury. In this study we examined the dose-response effect of ALCAR on the primary sensory neurons in the rat dorsal root ganglia (DRG) 2 weeks after sciatic nerve axotomy. Six groups of adult rats (n=5) underwent unilateral sciatic nerve axotomy, without repair, followed by 2 weeks systemic treatment with one of five doses of ALCAR (range 0.5-50 mg/kg/day), or normal saline. L4 and L5 dorsal root ganglia were then harvested bilaterally and sensory neuronal cell counts obtained using the optical disector technique. ALCAR eliminated neuronal loss at higher doses (50 and 10 mg/kg/day), while lower doses did result in loss (12% at 5 mg/kg/day, p<0.05; 19% at 1 mg/kg/day, p<0.001; 23% at 0.5 mg/kg/day, p<0.001) compared to contralateral control ganglia. Treatment with normal saline resulted in a 25% (p<0.001) loss, demonstrating no protective effect in accordance with previous studies.ALCAR preserves the sensory neuronal cell population after axotomy in a dose-responsive manner and as such, has potential for improving the clinical outcome following peripheral nerve trauma when doses in excess of 10 mg/kg/day are employed.