Objective:To summarize the clinical characteristics of focal cerebral arteriopathy (FCA) in children, and to analyze its influencing factor of prognosis.Methods:A retrospective cohort study was conducted. Clinical data from 40 children with FCA who were hospitalized at the Department of Neurology, Beijing Children′s Hospital, Capital Medical University, from September 2015 to August 2024 were collected. A centralized follow-up was conducted in October 2024 via outpatient clinics or the internet. The pediatric stroke outcome measure (PSOM) was used to evaluate their outcomes. Based on the PSOM, the children were further divided into a group with normal neurological function and another group with abnormal neurological function. Differences between groups were analyzed using the Mann-Whitney U test and Fisher exact test. Univariate Logistic regression analysis was performed to identify the influencing factors for neurological outcomes in children with FCA. Results:A total of 40 children were included, with 20 males and 20 females, and the onset age of 9.2 (6.8, 12.5) years. Among them, 12 cases (30%) had a history of varicella within 1 year before onset. There were 23 cases (58%) presenting with transient ischemic attack (TIA) or recurrent fluctuating symptoms of onset, while 3 cases (8%) developed progressive stroke within the first month of onset. The M1 segment of the middle cerebral artery was the most commonly affected vascular site, with a total of 16 cases (40%). Arterial occlusion occurred in 8 cases (20%). Lumbar puncture was completed in 36 children, and white blood cell counts in cerebrospinal fluid was increased in 6 cases. All 23 patients who completed magnetic resonance vessel wall imaging (VWI) showed circular enhancement of the arterial wall. A total of 28 patients (70%) received antiplatelet or anticoagulation therapy, and 16 patients (40%) received hormone therapy. At admission, the pediatric National Institute of Health Stroke Scale (PedNIHSS) score was 6.0 (2.0, 8.8) points, which decreased to 0.5 (0, 3.0) points at discharge. The follow-up duration was 1.6 (0.8, 4.9) years, with 1 case lost to follow-up. There was 1 case presenting with recurrence course manifesting as TIA. Among the 39 cases who completed the follow-up, 23 cases (59%) were assessed as neurologically normal by PSOM, while 16 cases (41%) were assessed as neurologically abnormal. Among the 29 cases who completed the imaging review, magnetic resonance angiography (MRA) review in 23 cases indicated stability or improvement in the original arterial stenosis, with 6 cases experiencing transient worsening of arterial stenosis early in the disease course (within 2 months), which later improved. Arterial stenosis progression occurred in 6 cases at the final review of 29 cases who completed the imaging review, with 1 case developing progressive cerebral arteriopathy. The proportion of patients with headache, altered consciousness, and aphasia in the abnormal neurological function group, as well as the PedNISS scores at admission and discharge, were all higher than those in the normal neurological function group (all P<0.05). Univariate Logistic regression analysis revealed that only a PedNISS score>6 points at onset was an influencing factor for abnormal neurological function ( OR=20.58, 95% CI 3.93-107.70, P<0.001). Conclusions:Childhood FCA often presents with fluctuating onset, and the proximal segment of the middle cerebral artery is frequently affected. Progression of arterial stenosis is common within 2 months of the disease course, but clinical progression and new ischemic lesions are uncommon. Most patients have a favorable long-term prognosis. PedNIHSS score>6 points at admission is related to abnormal neurological function outcomes.

Objective:To summarize the clinical characteristics of focal cerebral arteriopathy (FCA) in children, and to analyze its influencing factor of prognosis.Methods:A retrospective cohort study was conducted. Clinical data from 40 children with FCA who were hospitalized at the Department of Neurology, Beijing Children′s Hospital, Capital Medical University, from September 2015 to August 2024 were collected. A centralized follow-up was conducted in October 2024 via outpatient clinics or the internet. The pediatric stroke outcome measure (PSOM) was used to evaluate their outcomes. Based on the PSOM, the children were further divided into a group with normal neurological function and another group with abnormal neurological function. Differences between groups were analyzed using the Mann-Whitney U test and Fisher exact test. Univariate Logistic regression analysis was performed to identify the influencing factors for neurological outcomes in children with FCA. Results:A total of 40 children were included, with 20 males and 20 females, and the onset age of 9.2 (6.8, 12.5) years. Among them, 12 cases (30%) had a history of varicella within 1 year before onset. There were 23 cases (58%) presenting with transient ischemic attack (TIA) or recurrent fluctuating symptoms of onset, while 3 cases (8%) developed progressive stroke within the first month of onset. The M1 segment of the middle cerebral artery was the most commonly affected vascular site, with a total of 16 cases (40%). Arterial occlusion occurred in 8 cases (20%). Lumbar puncture was completed in 36 children, and white blood cell counts in cerebrospinal fluid was increased in 6 cases. All 23 patients who completed magnetic resonance vessel wall imaging (VWI) showed circular enhancement of the arterial wall. A total of 28 patients (70%) received antiplatelet or anticoagulation therapy, and 16 patients (40%) received hormone therapy. At admission, the pediatric National Institute of Health Stroke Scale (PedNIHSS) score was 6.0 (2.0, 8.8) points, which decreased to 0.5 (0, 3.0) points at discharge. The follow-up duration was 1.6 (0.8, 4.9) years, with 1 case lost to follow-up. There was 1 case presenting with recurrence course manifesting as TIA. Among the 39 cases who completed the follow-up, 23 cases (59%) were assessed as neurologically normal by PSOM, while 16 cases (41%) were assessed as neurologically abnormal. Among the 29 cases who completed the imaging review, magnetic resonance angiography (MRA) review in 23 cases indicated stability or improvement in the original arterial stenosis, with 6 cases experiencing transient worsening of arterial stenosis early in the disease course (within 2 months), which later improved. Arterial stenosis progression occurred in 6 cases at the final review of 29 cases who completed the imaging review, with 1 case developing progressive cerebral arteriopathy. The proportion of patients with headache, altered consciousness, and aphasia in the abnormal neurological function group, as well as the PedNISS scores at admission and discharge, were all higher than those in the normal neurological function group (all P<0.05). Univariate Logistic regression analysis revealed that only a PedNISS score>6 points at onset was an influencing factor for abnormal neurological function ( OR=20.58, 95% CI 3.93-107.70, P<0.001). Conclusions:Childhood FCA often presents with fluctuating onset, and the proximal segment of the middle cerebral artery is frequently affected. Progression of arterial stenosis is common within 2 months of the disease course, but clinical progression and new ischemic lesions are uncommon. Most patients have a favorable long-term prognosis. PedNIHSS score>6 points at admission is related to abnormal neurological function outcomes.

OBJECTIVE To explore the effects of different concentrations of aconitine on the ventricular electrophysiology of the rat heart when applied to the heart. METHODS By optical mapping technology, the effects of different concentrations of aconitine on ventricular action potential and calcium signal in rats before and 15 min after administration were observed by in vitro administration of aconitine 0.3, 1, 3 ng·mL−1. RESULTS Compared with the blank group, aconitine could be concentration-dependent to delay the conduction of action potentials under both spontaneous and 6 Hz stimulation rhythms, and there was a significant difference at a concentration of 3 ng·mL−1(P<0.05 or P<0.01). Compared with blank group, when the concentration of aconitine was 1 and 3 ng·mL−1, the action potential duration(APD) of the ventricle was significantly prolonged(P<0.01). Aconitine could also increase the dispersion of action potential conduction(P<0.05) and reduce the ratio of effective refractory period(ERP) to APD90(P<0.01). In addition, aconitine could also be concentration-dependent delay of calcium signal conduction, reduce the speed of calcium conduction(P<0.05 or P<0.01), increase the dispersion of calcium conduction and calcium transient duration(P<0.05 or P<0.01), and reduce the amplitude of calcium signal(P<0.01). CONCLUSION Using the optical labeling technique, it can be visualized that aconitine induces arrhythmia by concentration-dependent delay of ventricular action potential and calcium signaling in rats.To explore the effects of different concentrations of aconitine on the ventricular electrophysiology of the rat heart when applied to the heart. METHODS By optical mapping technology, the effects of different concentrations of aconitine on ventricular action potential and calcium signal in rats before and 15 min after administration were observed by in vitro administration of aconitine 0.3, 1, 3 ng·mL−1. RESULTS Compared with the blank group, aconitine could be concentration-dependent to delay the conduction of action potentials under both spontaneous and 6 Hz stimulation rhythms, and there was a significant difference at a concentration of 3 ng·mL−1(P<0.05 or P<0.01). Compared with blank group, when the concentration of aconitine was 1 and 3 ng·mL−1, the action potential duration(APD) of the ventricle was significantly prolonged(P<0.01). Aconitine could also increase the dispersion of action potential conduction(P<0.05) and reduce the ratio of effective refractory period(ERP) to APD90(P<0.01). In addition, aconitine could also be concentration-dependent delay of calcium signal conduction, reduce the speed of calcium conduction(P<0.05 or P<0.01), increase the dispersion of calcium conduction and calcium transient duration(P<0.05 or P<0.01), and reduce the amplitude of calcium signal(P<0.01). CONCLUSION Using the optical labeling technique, it can be visualized that aconitine induces arrhythmia by concentration-dependent delay of ventricular action potential and calcium signaling in rats.

Objective:To summarize the clinical characteristics and genetic features of tyrosine hydroxylase deficiency(THD) caused by TH gene variants for the improvement of the understanding of the disease. Methods:The clinical and genetic data of 33 children with THD caused by TH gene variants were diagnosed in the Department of Neurology of Beijing Children′s Hospital, Capital Medical University from May 2011 to January 2020 and their data were retrospectively collected and analyzed. Results:There were 19 females and 14 males.The age at onset was ranged from 0 to 6.3 years.13 patients developed diseases, accompanied with fever after infection, and 1 patient suffered from hypoxia, 19 patients suffered from no predisposing factors.There were 7 mild TH-deficient dopa-responsive dystonia cases, 16 severe TH-deficient infantile parkinsonism with motor delay cases and 10 very severe TH-deficient progressive infantile encephalopathy cases.Clinical symptoms were fluctuating, including 26 cases of diurnal fluctuation, 22 cases of infection aggravation, and 30 cases of fatigue aggravation.The initial symptoms included tiptoeing and numbness in the limbs(7 cases), motor development retardation or degression (26 cases), fremitus (8 cases), ptosis (2 cases), and status dystonicus (3 cases). Other clinical features had hypermyotonia (23 cases), hypomyotonia (27 cases), decreased movement (27 cases), decreased facial expression (24 cases), fremitus (18 cases), tiptoeing (20 cases), talipes equinovarus (7 cases), ptosis (8 cases), oculogyric crisis (10 cases), salivation (21 cases), dysphagia (12 cases), dysarthria (16 cases), dyspnea (3 cases), increased sleep (10 cases), decreased sleep (5 cases), irritable mood (15 cases), apathetic mood (2 cases), profuse sweating (8 cases), and status dystonicus (6 cases). A total of 6 patients′ right limbs were more severe, and 14 patients′ lower limbs were more severe.Eight patients had family history, and Levodopa treatment was effective for all patients.Ten patients suffered side effects, including dyskinesia and irritability.Four patients were lost follow-up, and 29 patients were followed up between 0.8 and 13.2 years old until Ja-nuary 2020.Totally, 22 patients almost had no such symptoms.Twenty-five TH gene pathogenic variants were discovered in 33 patients.There were 13 novel variants (c.1160T>C, c.1303T>C, c.887G>A, c.1084G>A, c.1097A>T, c.734G>T, c.907C>G, c.588G>T, c.992T>G, c.755G>A, c.184-6C>T, c.1510C>T, c.910G>A) and 2 patients had c. 910G>A variant.Meanwhile, there were 5 hot variants [c.698G>A(13 cases), c.457C>T(9 cases), c.739G>A(6 cases), c.1481C>T(4 cases), c.694C>T(3 cases)]. c.910G>A(2 cases) may be the foun-der variant of Chinese population. Conclusions:THD caused by TH gene variant mostly onsets from infant, with complex clinical features.Most of these patients were severe, and only a few were very severe and mild.Very severe and mild symptoms were easily misdiagnosed.Levodopa treatment was obviously effective.A possible founder variant of Chinese population (c.910G>A) was found.c.698G>A and c. 457C>T mutations mainly appeared in patients with severe and extremely severe THD, while c. 739G>A mainly appeared in patients with mild THD.

Objective:To summarize the clinical data of patients with acute pandysautonomia (APD) and discuss the treatment and prognosis of them.Methods:A total of 13 patients with APD in the Department of Neurology, Beijing Children′s Hospital, Capital Medical University, from January 2010 to December 2019, were investigated retrospectively.The general data, clinical symptoms, autonomic nerve examination and function test, laboratory examination, treatment and follow-up were collected and analyzed.Results:There were 4 males and 9 females in 13 patients with APD, with an average age was 8 years and 5 months (3 years and 8 months to 12 years and 5 months ). The average course of disease was 94.5 d (14-410 d). The common initial symptoms were gastrointestinal motility disorder (11 cases), dysuria (3 cases), and upright syncope/vertigo (3 cases). During the course of the disease, all the patients manifested with gastrointestinal motility disfunction and dyshidrosis, glands involvement and orthostatic hypotension in 12 cases, abnormal pupil in 9 case and urinary retention in 7 case.Other symptoms included fatigue in 9 cases, emotional disorder in 4 cases, limb weakness in 2 cases, and sensory disturbance in 2 cases.All the patients were treated with intravenous immunoglobulin (IVIG), and 3 cases combined with glucocorticoid.Six patients with severe gastrointestinal symptoms were treated with intravenous nutrition; 4 patients were fed with jejunum, 3 cases of whom returned to normal diet within 1-12 months, and 1 patient was followed up for 5 years and 2 months.Hyponatremia was found in 7 cases, which recovered in 2-30 d. Nine cases were followed up for 1 month to 9 years.Seven cases were normal in daily work and study, with satisfactory nutritional status, stable mood and no relapse.Conclusions:The clinical manifestations of APD are varied.The initial symptoms are gastrointestinal motility disorders, orthostatic hypotension, urinary retention and hyponatremia.Individualized multi-disciplinary comprehensive management for symptoms, especially the comprehensive treatment of gastrointestinal motility disorders, management of postural hypotension, and the urinary system diagnosis and individualized treatment of can shorten the length of hospital stay and improve the prognosis effectively.

Objective To explore the phenotype and genotype of mitochondrial DNA depletion syndromes (MDS) in Chinese children.Methods The clinical and genetic data of 12 MDS patients (8 were boys and 4 were girls) diagnosed in the Department of Neurology in Beijing Children's Hospital,Capital Medical University from October 2010 to April 2018 were retrospectively collected and analyzed.Results The developmental milestones were normal or mildly retardated before disease onset.The age of onset ranged from 0 to 2.9-year-old.Most cases developed postnatal or after infection.The most common initial symptoms were feeding difficulty,seizure,muscle weakness,psychomotor regression and hepatic dysfunction.At the last evaluation,all the patients had developmental retardation,failure to thrive,muscle weakness,and dysphagia.Other clinical features were weight loss (9 cases),hearing impairment (7 cases),ptosis (6 cases),seizure (5 cases),dyspnea (4 cases),visual impairment (1 case),hirsutism (1 case),lactic acidosis (7 cases),elevated hepatic enzymes (4 cases) and creatine kinase (2 cases),elevated protein in cerebrospinal fluid (3 cases),abnormalities on screening for inborn error of metabolism (10 cases) and brain magnetic resonance imaging (MRI) (10 cases),abnormal electromyogram (including neurogenic or myogenic injury) (5 cases).Five patients died of infection or multiple organ failure.A total of 18 novel mutations presented below were detected in these patients.Among the 6 cases of encephalomyopathy,there were 3 with SUCLG1 mutation (c.916G＞T,c.619T＞C,c.980dupT were novel),2 with SUCLA2 mutation (c.851G＞A,c.971G＞A were novel),and one with RRM2B mutation (c.456-2A＞G,c.212T＞C were novel).All the cases of hepatic encephalopathy all had POLG mutations (c.3151G＞A,c.2294C＞T,c.2858G＞C,c.680G＞A and c.150_158delGCAGCAGCA were novel).Two cases of infantile-onset spinocerebellar ataxia had TWNK mutations (c.1163C＞T,c.1319T＞C,c.1388G＞A and e.257_258delAG were novel).One case of myopathy had TK2 mutations (c.557C＞G and c.341A＞T were novel).Conclusions The clinical and genetic features of MDS were heterogeneous.Eighteen novel mutations in six MDS related genes were reported,which expanded the genetic spectrum of MDS in Chinese children.

Objective To discuss the clinical manifestations,imaging features and prognosis of children with mild encephalitis/encephalopathy with a reversible splenial lesion(MERS).Methods Twenty-five patients with MERS admitted to Beijing Children′s Hospital,Capital Medical University,between November 2013 and March 2016 were enrolled and their clinical and imaging data were retrospectively analyzed.Ages of onset of these 25 cases were from 6 months to 13 years old.Because of different clinical manifestations in different onset ages,these 25 cases were divided into 2 groups:≤6 years old group (20 cases),with the onset age of 6 months to 3 years and 9 months old(average 2 years and 2 months);>6 years old group(5 cases),with the onset age of 9 years 3 months to 13 years old (average 10 years and 10 months).Results Nineteen cases among the 25 patients had infection history before onset,including 10 cases of digestive tract infection(all were ≤6 years old children),9 cases of respiratory tract infection(6 children ≤6 years old and 3 children >6 years old).The main clinical manifestations included convulsion (18/25 cases,72.0%),fever (17/25 cases,68.0%),vomiting (11/25 cases,44.0%),and disturbance of consciousness (11/25 cases,44.0%).The main clinical manifestation of ≤6 years old group was convulsion (18/20 cases,90.0%),while the main clinical manifestations of the>6 years old group were fever(3/5 cases,60.0%),headache and dizziness(2/5 cases,40.0%),and none of the patients in >6 years old group had convulsion.Eight cases had liver function injury,myocardial enzymes increased in 10 cases,and hyponatremia occurred in 9 cases.Magnetic resonance imaging (MRI) showed 21 cases were type Ⅰ MERS(only involving corpus callosum),and 4 cases of type Ⅱ MERS which involved corpus callosum as well as deep brain white matter,subcortical white matter (centrum semiovale).MRI lesions disappeared after 8-56 days (average 16.5 days) of anti-infection and reducing intracranial pressure treatment.Conclusion MERS is more common in ≤6 years old children,and digestive tract infection is common in ≤6 years old children,while respiratory tract infection is common in >6 years old children.The symptoms in children are mainly manifested as fever,convulsion,vomiting,conscious disturbance,and so on.Infection and hyponatremia are the main causes of MERS in children.MRI is the first choice of imaging examination methods.

Objective: To investigate the clinically and genetic characteristics of children with Leigh syndrome. Method: Patients with clinically diagnosed Leigh syndrome(LS)in the department of Neurology, Beijing Children′s Hospital from January 2013 to February 2016 underwent the mitochondrial DNA (mtDNA) and nuclear DNA (nDNA) detecting with next generation sequencing (NGS) technology. The clinical data of gene confirmed cases were retrospectively collected and analyzed. The differences in the onset age, clinical manifestations, lactic acid level and MRI results between the mtDNA variation and nDNA variation were compared and analyzed.t test, Chi-square test and Fisher′s exact test were used for statistical analysis. Result: Thirty-five cases were diagnosed by gene detection, including 20 males and 15 females. The median onset age was 1 year (ranging from the neonatal period to 4.4 years old). The age of onset within 2 years accounted for 74%(26 cases). The onset age of initial symptoms, including developmental delay, developmental regression, and seizures, were 6 (4, 12) months, 12 (8, 14) months, and 6 (1, 23) months respectively. The onset age of ptosis, extrapyramidal symptoms and ataxia were 26 (18, 44) months, 28 (23, 40) months and 28 (19, 35) months, respectively. There were significant differences in the onset age between the three groups (H=21.919, P=0.01). Within the 35 cases, 29 were manifested with developmental delay (83%), 26 with dystonia (74%), 18 with growth retardation, 15 with myasthenia, 13 with developmental regression, 11 with dysphagia, 10 with feeding difficulties, 4 with skeletal dysplasia, and 2 with digestive tract symptoms; nystagmus and respiratory abnormalities were observed in 9 cases respectively; extrapyramidal symptoms, peripheral nerve injury, ptosis, seizures were observed in 8 cases respectively; and ataxia, ophthalmoplegia and hypertrichiasis were found in 5 cases respectively.The blood lactic acid was measured in 32 LS patients, within which 23 cases (72%) had increased results; 8 out of 11 cases who underwent were cerebrospinal fluid lactic acid test had increased results. The results of neuroimaging revealed that all the patients were involved in the brainstem and (or) basal ganglia, of whom 27 (77%) had brainstem involvement, 24 (69%) had basal ganglia involvement. Thirteen out of 14 patients who had medulla oblongata involvement had nDNA variation; while 7 out of 8 patients with cerebellar involvement had nDNA variation. Genetic etiology was confirmed in all patients, among whom there were 17 cases (49%) with mtDNA mutation, including 8993T>C/G (n=5), 14487T>C (n=4), 13513G>A (n=2), 9176T>C, 10158T>C, 3697G>A, 10191T>C, 14459A>G and 11777C>A (n=1) respectively. Remaining 18 cases(51%) had nDNA mutation, including SURF1 gene(n=10), PDHA1 gene(n=3) and one case each of NDUFV1, NDUFAF6, NDUFAF5, NDUFS1 and COQ7 genes. In this study, 27 types of mutations were founded, 15 of which had not been previously reported. Respiratory chain gene mutations have been found in 31 cases(89%); 3 cases had PDHc gene mutations, and 1 case had other mutation. Conclusion LS usually occurs in infants. The most common primary symptoms are age-dependent abnormal movements, ocular symptoms, and seizures. Respiratory chain defects is the most common causes of LS.SURF1 is the most common variation, followed by 8993T>C/G, 14487 T>C and 13513G>A mutation.

Objective: To analyze the clinical and genetic features of progressive cavitating leukoencephalopathy (PCL). Method: The data of clinical and genetic features of 4 PCL patients diagnosed by Beijing Children′s Hospital between January 2015 and January 2016 were analyzed. The cases with complete clinical data retrieved on literature search at China National Knowledge Infrastructure, Wanfang Data Knowledge Service Platform and PubMed (up to August 2016) by using search terms of"NDUFV1" ,"NDUFS1" , or"leukoencephalopathy" , were summarized. Result: There were three females and one male, two of which were compatriots. The age of onset ranged from 6 months to 15 months. All four children′s first symptoms were motor development regression, and the developmental milestones were almost normal before the onset. Of the 4 patients, 3 had cognitive impairment, 1 had seizures, 4 had dystonia and pyramidal impairment, 2 had emaciation, and 1 had nystagmus. The lactate concentrations of 4 patients were normal in blood. One patient had lactaciduria in the urinary organic acid analysis. Cranial magnetic resonance imaging (MRI) of all patients showed leukoencephalopathy, involved in the corpus callosum, and three patients accompanied by cystic lesions. Follow up for 2-13 years showed that the physical and language development were improved. Genetic analysis revealed that mutations in NDUFS1 were found in three patients and NDUFV1 mutation was found in one patient. All six mutations (p.Arg377Cys and p. Arg377His in NDUFV1; p. Arg482Glyfs^*5, p.Thr368Pro, p.Tyr454X and p. Asp565Gly in NDUFS1) are novel. Five English case reports including 10 PCL patients were collected. Together with this group of 4 cases, a total of 14 cases were involved. All 14 children patients had motor development regression, 11 cases had cognitive impairment and dystonia, 6 cases had pyramidal impairment, 5 cases had irritability, 4 cases had epilepsy and nystagmus, 3 cases had strabismus and swallowing difficulty. Cranial MRI showed patchy leukoencephalopathy with cavities, involved in the corpus callosum. Follow up for 19 months-15 years that the neurology development were improved slowly in all patients. Conclusion NDUFS1 and NDUFV1 gene mutation screening should be performed firstly in patients with PCL clinical and imaging feature.

Background and purpose:Perioperative anesthetic management is thought to be critical to the success of free flap breast reconstruction. The purpose of this study was to discuss intraoperative fluid, hemodynamic and temperature management in patients undergoing deep inferior epigastric perforator (DIEP) flap breast reconstruction.Methods:From Jun. 2011 to Dec. 2015, 126 patients underwent DIEP lfap breast reconstruction. Postoperative complications were reviewed. Intraoperative fluid infusion rate was analyzed. Mean arterial blood pressure (MAP) and core temperature were measured before induction (T0), after lfap elevation but before lfap transfer (T1), 15 min after flap revascularization (T2), and at the end of surgery (T3).Results:Nine patients developed flap compromised: 7 were salvaged and 2 failed. The mean intraoperative lfuid infusion rate was (5.44±1.66) (mL?kg-1)/h. MAP at T0, T1, T2 and T3 were (87.45±8.90), (74.19±8.63), (74.60±8.71) and (79.62±7.88) mmHg, respectively. Core temperature at T0, T1, T2 and T3 were (36.69±0.14), (36.36±0.18), (36.27±0.14) and (36.21±0.15)℃, respectively. Conclusion:Standard practice focusing on intraoperative lfuid management, hemodynamic adjustment and temperature control in microsurgical reconstruction of the breast should be established to further improve free lfap outcome.