Background
Pedicled flaps are useful for reconstructive surgery. Previously, we often used vascularized supraclavicular flaps, especially for head and neck reconstruction, but then shifted to using thoracic branch of the supraclavicular artery (TBSA) flaps. However, limited research exists on the anatomy of TBSA flaps and on the use of indocyanine green (ICG) fluorescence videoangiography for supraclavicular artery flaps. We utilized ICG fluorescence videoangiography to harvest reliable flaps in reconstructive operations, and describe the results herein.
Methods
Data were retrospectively reviewed from six patients (five men and one woman: average age, 54 years; range, 48–60 years) for whom ICG videoangiography was performed to observe the skin perfusion of a supraclavicular flap after it was raised. Areas where the flap showed good enhancement were considered to be favorable for flap survival. The observation of ICG dye indicated good skin perfusion, which is predictive of flap survival; therefore, we trimmed any areas without dye filling and used the remaining viable part of the flap.
Results
The flaps ranged in size from 13×5.5 cm to 17×6.5 cm. One patient received a conventional supraclavicular flap, four patients received a TBSA flap, and one patient received a flap that was considered to be intermediate between a supraclavicular flap and a TBSA flap. The flaps completely survived in all cases, and no flap necrosis was observed.
Conclusions
The TBSA flap is very useful in reconstructive surgery, and reliable flaps could be obtained by using ICG fluorescence videoangiography intraoperatively.
Mendonça et al reported 3 spinal muscular atrophy (SMA) type 0 cases that demonstrated progressive supratentorial brain atrophy. 1 These cases support the hypothesis that survival motor neuron (SMN), the causative gene for SMA, was expressed widely throughout the central nervous system (CNS), including cerebral cortex and cerebellum. 2 Herein, we describe 1 SMA type 0 case with severe diffuse CNS atrophy involving the supra-and infratentorial brain and the spinal cord.A 2-year-old girl was born at term with no fetal movements detected from the 3rd trimester onwards. The Apgar scores at 1 and 5 minutes after birth were 1 and 6, respectively. Absence of spontaneous breathing required immediate tracheal intubation. She had marked muscle weakness, generalized hypotonia, absent deep tendon reflexes, and tongue fasciculations. Polymerase chain reaction revealed homozygous deletion of SMN1 and neuronal apoptosis inhibitory protein (NAIP) genes. A multiplex ligation-dependent probe amplification assay detected 1 copy of SMN2; thus, she was diagnosed with SMA type 0. At 4 months of age, she developed distal necrosis (Fig). Intermittent bradycardia appeared during infancy. Eye and limb movements were absent since early infancy, but pupillary reflex was preserved. Before 2 years of age, clonic seizures with minimal limb and eyelid movement and tachycardia appeared. Seizures lasted a few minutes, and no convulsive status epilepticus was observed. Interictal electroencephalography revealed a suppression burst pattern unobserved in the neonatal period. Head magnetic resonance imaging (MRI) findings suggesting hypoxic ischemic encephalopathy were undocumented in the neonatal period. Serial MRI presented progressive atrophy of the cerebral cortex, subcortical white matter, thalamus, and basal ganglia. Although volumes of cervical cord, brainstem, and cerebellum were relatively spared at 7 months, these volumes were reduced at 2 years.The report by Mendonça et al showed sparring of the cerebellum. 1 Our case demonstrated a more severe phenotype, with brainstem and cerebellum atrophy accompanied by epilepsy.As previously reported in some severe cases, our patient had distal necrosis, probably due to autonomic dysfunction and perfusion impairment. 3 A recent study showed that concurrent homozygous deletion of SMN1 and NAIP was associated with a severe phenotype. 4 NAIP is adjacent to SMN and is known as the modifying gene of the SMA phenotype, although its direct role has not been fully investigated. The genotype in our case may explain the phenotypic severity and demonstrate SMA pathology extending to the entire CNS.
A therapeutic IVIg dose can attenuate neutrophil accumulation and regulate neutrophil apoptosis in the lung during endotoxemia. It is possible that the pathways by which IVIG induces neutrophil apoptosis may differ depending on the IVIg concentration.
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