Hyperperfusion Injury Research Articles

The small-for-size syndrome in living donor liver transplantation: current management.

Small-for-size syndrome poses a significant challenge in living donor liver transplantation, with potentially severe consequences including liver failure and death. This review explores the management strategies for SFSS, starting from the pathophysiology of the disease. SFSS arises from insufficient liver mass in the graft and hyperdynamic circulation in cirrhotic recipients, leading to portal hyperperfusion and subsequent liver injury. Risk factors include graft size, quality, recipient factors, and hemodynamic changes during transplantation.Hemodynamic monitoring is crucial during living donor liver transplantation to optimize portal vein and hepatic artery flow. Prevention strategies focus on donor-recipient matching and intraoperative graft inflow modulation. Optimizing venous outflow and avoiding portal hyperperfusion is essential. Management of established small-for-size syndrome involves supportive care, pharmacologic interventions, and radiological and surgical options. Pharmacotherapy includes somatostatin analogues, beta-blockers, and vasopressin analogues to reduce portal flow and pressure. Surgical interventions aim to modulate portal flow and mitigate complications. Retransplantation may be necessary in severe cases, guided by persistent graft dysfunction despite liver flow modulations. In conclusion, preventing and managing small-for-size syndrome in living donor liver transplantation requires comprehensive assessment and tailored interventions. Advancements in graft/recipient matching, hemodynamic monitoring, pharmacologic and surgical techniques aiming to inflow modulation have improved outcomes, enabling successful transplantation even with ultra-small grafts.

Transcranial Doppler ultrasound to evaluate the risk of hyperperfusion after endovascular stroke thrombectomy.

Hemorrhagic transformation (HT) has been reported in up to 50% of acute ischemic stroke (AIS) patients with a large vessel occlusion (LVO) treated with endovascular thrombectomy (EVT). HT may be driven by postrecanalization hyperperfusion injury and is independently associated with worse functional outcomes. Strategies to identify patients at risk for HT may assist in developing preventive therapies. We prospectively included adult AIS patients with an anterior circulation LVO achieving successful recanalization after EVT. Consenting participants received transcranial Doppler ultrasound (TCD) within 18 hours of procedure completion. We compared flow velocities according to the presence of HT on the computed tomography scan performed within the first 24±12 hours from the end of EVT. We also evaluated the association of flow velocities with systemic blood pressure (BP) readings at the time of insonation. A total of 48 patients consented to participate in the study. Six (12%) were excluded due to the absence of temporal windows. HT was detected in 20 participants (48%). Those with HT had higher peak systolic velocities on the middle cerebral arteries compared to those without HT for both the symptomatic (107±42vs. 82±25cm/second, p = .024) and asymptomatic (97±21vs. 81±25cm/second, p = .040) sides. No correlation of flow velocities on either the symptomatic or asymptomatic side and BP measurements at the time of insonation was detected. TCD can identify patients at risk of HT following successful EVT. TCD could serve as an inexpensive ancillary test to guide participant selection for clinical trials targeting postprocedural reperfusion injury.

Secondary hyperperfusion injury following surgical evacuation for acute isolated epidural hematoma with concurrent cerebral herniation.

Hemispherical cerebral swelling or even encephalocele after head trauma is a common complication and has been well elucidated previously. However, few studies have focused on the secondary brain hemorrhage or edema occurring regionally but not hemispherically in the cerebral parenchyma just underneath the surgically evacuated hematoma during or at a very early stage post-surgery. In order to explore the characteristics, hemodynamic mechanisms, and optimized treatment of a novel peri-operative complication in patients with isolated acute epidural hematoma (EDH), clinical data of 157 patients with acute-isolated EDH who underwent surgical intervention were reviewed retrospectively. Risk factors including demographic characteristics, admission Glasgow Coma Score, preoperative hemorrhagic shock, anatomical location, and morphological parameters of epidural hematoma, as well as the extent and duration of cerebral herniation on physical examination and radiographic evaluation were considered. It suggested that secondary intracerebral hemorrhage or edema was determined in 12 of 157 patients within 6 h after surgical hematoma evacuation. It was featured by remarkable, regional hyperperfusion on the computed tomography (CT) perfusion images and associated with a relatively poor neurological prognosis. In addition to concurrent cerebral herniation, which was found to be a prerequisite for the development of this novel complication, multivariate logistic regression further showed four independent risk factors contributing to this type of secondary hyperperfusion injury: cerebral herniation that lasted longer than 2 h, hematomas that were located in the non-temporal region, hematomas that were thicker than 40 mm, and hematomas occurring in pediatric and elderly patients. Secondary brain hemorrhage or edema occurring within an early perioperative period of hematoma-evacuation craniotomy for acute-isolated EDH is a rarely described hyperperfusion injury. Because it plays an important prognostic influence on patients' neurological recovery, optimized treatment should be given to block or reduce the consequent secondary brain injuries.

Treatment for Subdural Hematoma in Infants

This chapter will discuss the treatment for infant subdural hematoma. In adult cases, treatment focused on intracranial pressure(ICP)management alone is generally sufficient, but in infant cases, special ingenuity is required. First, there are some points to keep in mind regarding surgical procedures. It is important to perform blood transfusion from an early stage, avoid exposure of bleeding points, and reduce ICP by floating the bone flap that preserves blood flow. Next, it is necessary to understand the pathophysiology peculiar to infants. Extensive lower density changes seen on head computed tomography can have a profound effect on clinical outcome. This phenomenon should not be considered as simple cerebral ischemia, but is representative of the brain damage caused by status epilepticus and hyper perfusion injury. Therefore, not only ICP management, but also treatment for status epilepticus is extremely important for postoperative management. Further, cases where abuse is the cause of subdural hematoma often display poor outcomes due to a variety of medico social factors.

P9.30: Salvaging Small for Size Grafts With Splenic Artery Embolization in Living Donor Liver Transplant: Older Liver May Not Recover

Introduction: Small for size (SFS) is a dreaded problem after LDLT. Portal hyperfperfusion (large spleen) or outflow issues can cause functional SFS despite adequate GRWR (> 0.8). SAE (Splenic Artery Embolization) reduces portal flow allowing the graft to recover and regenerate. However,despite SAE, older grafts may not recover from the hyperperfusion injury. We report 3 cases which required SAE and discuss the outcomes. Method: Medical records of 3 male patients with right lobe LDLT (donors - spouses) who underwent SAE with a diagnosis of SFS were reviewed. Median MELD was 25 and donor age were 39, 40 and 59 years. Two presented with functional SFS; GRWR 0.83 and 0.82 (RIHV thrombosis leading to hyperperfusion); 1 patient (hyperperfusion due to enlarged spleen;GRWR 0.89) also had Splenic arterial steal on Doppler (patent artery on CT angiography). All 3 had initial reduction of bilirubin and INR till POD4 followed by worsening LFT and ascites.SAE was done after Doppler findings/Triphasic CT/MRI and no suspicion of biliary issues.Results: SAE was successful in reducing portal flow in all 3.The patients with younger grafts(Donor age<45)showed rapid improvement; normalization of bilirubin and disappearance of ascites over next 2 weeks. However, the patient with older graft after showing initial reduction of bilirubin and ascites (Doppler showed continuous >30 % reduced portal flow) had worsening jaundice,ascites, coagulopathy and hypoalbuminemia. He subsequently developed severe graft dysfunction and septicemia and expired. Conclusion: SFS can manifest despite adequate GRWR(>0.8), if outflow issues/ hyperperfusion are present. SAE works well in salvaging SFS post operatively, but older livers may not have enough reserve to recover. When accepting older livers, intra op flow and pressure recording may be used to perform Splenic artery ligation or Splenectomy to prevent SFS.

Editors' note: Early hemodynamic predictors of good outcome and reperfusion injury after endovascular treatment

To better characterize (1) the success of endovascular recanalization and (2) the functional outcomes observed following thrombectomy for acute large vessel occlusion (LVO), Dr. Baracchini and colleagues prospectively followed 185 patients with acute anterior circulation LVO using serial transcranial color-coded ultrasonography postoperatively. All patients were treated within 6 hours of the time they were last known well, had moderate-to-severe deficits (NIHSS >6), and had favorable baseline CT findings (ASPECTS 6–10). After excluding patients who died within 1 week of treatment (8%), the investigators found that successful recanalization (TICI 2b or 3) was associated with a higher probability of normal peak systolic velocities on transcranial ultrasound than partial recanalization (TICI 2a), 96% vs 32%. However, early normalization of the blood flow velocity—irrespective of post-thrombectomy recanalization success—was strongly linked to better long-term outcomes using the modified Rankin Scale. Among those with normal blood flow velocities by 48 hours, 66% of patients with TICI 2b/3 recanalization and 57% of patients with TICI 2a recanalization achieved functional independence by 90 days. Higher velocities also correlated with an increased risk of intracranial hemorrhage, as suggested in previous literature. In response, Drs. Gattringer et al. found the elevated post-thrombectomy peak systolic velocity of the previously occluded artery alarming (279 cm/s in patients with TICI 2b/3). They also commented that other serologic and neuroimaging biomarkers of hyperperfusion injury might prove useful for prognostication after thrombectomy. Dr. Baracchini and colleagues recognize that their observed peak systolic velocities exceed what had been previously published, but they acknowledge that previous studies documented velocities 72 hours after thrombectomy as opposed to immediately following the procedure, as in this investigation. To better characterize (1) the success of endovascular recanalization and (2) the functional outcomes observed following thrombectomy for acute large vessel occlusion (LVO), Dr. Baracchini and colleagues prospectively followed 185 patients with acute anterior circulation LVO using serial transcranial color-coded ultrasonography postoperatively. All patients were treated within 6 hours of the time they were last known well, had moderate-to-severe deficits (NIHSS >6), and had favorable baseline CT findings (ASPECTS 6–10). After excluding patients who died within 1 week of treatment (8%), the investigators found that successful recanalization (TICI 2b or 3) was associated with a higher probability of normal peak systolic velocities on transcranial ultrasound than partial recanalization (TICI 2a), 96% vs 32%. However, early normalization of the blood flow velocity—irrespective of post-thrombectomy recanalization success—was strongly linked to better long-term outcomes using the modified Rankin Scale. Among those with normal blood flow velocities by 48 hours, 66% of patients with TICI 2b/3 recanalization and 57% of patients with TICI 2a recanalization achieved functional independence by 90 days. Higher velocities also correlated with an increased risk of intracranial hemorrhage, as suggested in previous literature. In response, Drs. Gattringer et al. found the elevated post-thrombectomy peak systolic velocity of the previously occluded artery alarming (279 cm/s in patients with TICI 2b/3). They also commented that other serologic and neuroimaging biomarkers of hyperperfusion injury might prove useful for prognostication after thrombectomy. Dr. Baracchini and colleagues recognize that their observed peak systolic velocities exceed what had been previously published, but they acknowledge that previous studies documented velocities 72 hours after thrombectomy as opposed to immediately following the procedure, as in this investigation.

Predictors of Impaired Cerebral Perfusion After Flow Diversion Therapy

Flow-diverting stents (FDS) are relatively safe and highly efficacious in treating cerebral aneurysms; however, a small subset of patients experience devastating hemorrhagic complications owing to presumed alterations in local aneurysm and distal cerebral blood flow. The downstream effects of FDS on distal cerebral blood flow is not well understood, but isolated reports of hyperperfusion injury have been described in the literature. We investigate the incidence and clinical factors contributing to abnormal cerebral blood flow after FDS placement. A retrospective analysis of patients undergoing FDS for elective aneurysm treatment between 2014-2017 was performed. Patients who underwent perfusion imaging within 24-hours posttreatment were included for further analysis. Univariate and multivariate analyses were performed to assess the impact of multiple variables on the postoperative perfusion changes. A total of 69 patients underwent FDS therapy to treat unruptured intracranial aneurysms. Thirteen patients (18.8%) developed abnormal perfusion changes. A significant difference of the median was found in aneurysm projection width, depth, neck width, calculated approximate volume, and size ratio between the hypoperfused, normal, and hyperperfusion cases. On multivariate analysis, history of smoking (P= 0.0117), and approximate calculated volume (P= 0.0145) were significant predictors of hyperperfusion identified on posttreatment imaging. This study yielded several novel findings. We demonstrate that cerebral blood flow alterations will occur in a significant subset of patients undergoing FDS treatment. We also provide new evidence that aneurysm volume and history of smoking may predict the developing of postoperative perfusion anomalies. Future studies are needed to evaluate the clinical ramifications of cerebral blood flow disruption in large prospective studies.

New insights on glomerular hyperfiltration: a Japanese autopsy study.

It has been suggested that low nephron number contributes to glomerular hypertension and hyperperfusion injury in progressive chronic kidney disease (CKD). The incidence of CKD in Japan is among the highest in the world, but the reasons remain unclear. We estimated total nephron (glomerular) number (NglomTOTAL) as well as numbers of nonsclerosed (NglomNSG) and globally sclerosed glomeruli (NglomGSG), and the mean volume of nonsclerosed glomeruli (VglomNSG) in Japanese normotensive, hypertensive, and CKD subjects and investigated associations between these parameters and estimated glomerular filtration rate (eGFR). Autopsy kidneys from age-matched Japanese men (9 normotensives, 9 hypertensives, 9 CKD) had nephron number and VglomNSG estimated using disector/fractionator stereology. Subject eGFR, single-nephron eGFR (SNeGFR), and the ratio SNeGFR/VglomNSG were calculated. NglomNSG in Japanese with hypertension (392,108 ± 87,605; P < 0.001) and CKD (268,043 ± 106,968; P < 0.001) was less than in normotensives (640,399 ± 160,016). eGFR was directly correlated with NglomNSG (r = 0.70, P < 0.001) and inversely correlated with VglomNSG (r = -0.53, P < 0.01). SNeGFR was higher in hypertensives than normotensives (P = 0.03), but was similar in normotensives and CKD, while the ratio SNeGFR/VglomNSG was similar in normotensives and hypertensives but markedly reduced in CKD. Nephron number in Japanese with hypertension or CKD was low. This results in a higher SNeGFR in hypertensives compared with normotensive and CKD subjects, but lowered SNeGFR/VglomNSG in CKD subjects, suggesting that changes in GFR are accommodated by glomerular hypertrophy rather than glomerular hypertension. These findings suggest glomerular hypertrophy is a dominant factor in maintenance of GFR under conditions of low nephron number.

Should Low Central Venous Pressure Be Maintained during Liver Transplantation?

Low central venous pressure, which indirectly reflects free hepatic venous pressure, is maintained during hepatic resection surgery to reduce intraoperative blood loss by facilitating hepatic venous outflow. However, whether the low central venous pressure protocol established for non-transplant hepatobiliary surgery should be generalized to liver transplantation is controversial because patients with cirrhosis have decreased portal and hepatic venous blood flow and vulnerability to renal failure. However, consistent with observations from hepatic resection surgeries, lowering central venous pressure during the preanhepatic phase significantly reduces blood loss and transfusion volume. Conversely, inherent study limitations and different study designs have yielded different results in terms of renal dysfunction. Although hepatic venous outflow promoted by lowering blood volume seems to facilitate a liver graft to accommodate portal blood flow increased by portal hypertension-induced splanchnic vasodilatation, the association between low central venous pressure and reduced incidence of portal hyperperfusion injury has not been demonstrated. Stroke volume variation predicts fluid responsiveness better than central venous pressure, but it has not been associated with a greater clinical benefit than central venous pressure to date. Therefore, the safety of maintaining low central venous pressure during liver transplantation has not been verified, and further randomized controlled studies are warranted to establish a fluid management protocol for each phase of liver transplantation to reduce intraoperative blood loss and transfusion rate, thereby maintaining liver graft viability. In conclusion, low central venous pressure reduces intraoperative blood loss but does not guarantee renoprotection or graft protection.

Staged carotid artery angioplasty and stenting for patients with high-grade carotid stenosis with high risk of developing hyperperfusion injury: a retrospective analysis of 44 cases

BackgroundHyperperfusion syndrome (HPS) is a rare but potentially a life-threatening complication after carotid artery angioplasty and stenting (CAS). Staged CAS has been an alternative to prevent HPS.Materials and methods44 of...

Hemorrhagic transformation and cerebral edema in acute ischemic stroke: Link to cerebral autoregulation

BackgroundHemorrhagic transformation and cerebral edema are feared complications of acute ischemic stroke but mechanisms are poorly understood and reliable early markers are lacking. Early assessment of cerebrovascular hemodynamics may advance our knowledge in both areas. We examined the relationship between dynamic cerebral autoregulation (CA) in the early hours post ischemia, and the risk of developing hemorrhagic transformation and cerebral edema at 24h post stroke MethodsWe prospectively enrolled 46 patients from our center with acute ischemic stroke in the middle cerebral artery territory. Cerebrovascular resistance index was calculated. Dynamic CA was assessed by transfer function analysis (coherence, phase and gain) of the spontaneous blood flow velocity and blood pressure oscillations. Infarct volume, hemorrhagic transformation, cerebral edema, and white matter changes were collected from computed tomography performed at presentation and 24h. ResultsAt admission, phase was lower (worse CA) in patients with hemorrhagic transformation [6.6±30 versus 45±38°; adjusted odds ratio 0.95 (95% confidence internal 0.94–0.98), p=0.023] and with cerebral edema [6.6±30 versus 45±38°, adjusted odds ratio 0.96 (0.92–0.999), p=0.044]. Progression to edema was associated with lower cerebrovascular resistance (1.4±0.2 versus 2.3±1.5mmHg/cm/s, p=0.033) and increased cerebral blood flow velocity (51±25 versus 42±17cm/s, p=0.033) at presentation. All hemodynamic differences resolved at 3months ConclusionsLess effective CA in the early hour post ischemic stroke is associated with increased risk of hemorrhagic transformation and cerebral edema, possibly reflecting breakthrough hyperperfusion and microvascular injury. Early assessment of dynamic CA could be useful in identifying individuals at risk for these complications.

Outcomes of deep hypothermic circulatory arrest in pediatric cardiac surgery: A single center experience

BackgroundDeep hypothermic circulatory arrest (DHCA) is a technique used in the repair of complex congenital cardiac lesions that require aortic arch or pulmonary vein repair. DHCA has been linked to adverse outcomes and neurologic complications. Selective cerebral perfusion (SCP) may be added to DHCA to prevent neurological complication. Air embolism and hyperperfusion injury may be encountered. The aim of this study was to evaluate the safety and efficacy of simple DHCA and to outline the early outcomes especially the neurological ones. MethodsTwenty nine patients underwent surgical repair of congenital cardiac lesion with DHCA at a single institution from January 2010 to November 2015. DHCA was conducted with a target esophageal temperature of 18° and placement of an ice pack on the head. No selective perfusion was done. Demographic, operative and postoperative data were reviewed. Mortality, any neurological complications including seizers, coma, and stroke were recorded. ResultsThe mean age was 20.6 ± 8.2 months (range: 9 days to 154 months). The majority were males (20, 69%). The mean weight was 5.57 ± 4.2 kg (range: 2.3–17.5 kg). DHCA time was 20.03 min (range 3–52 min). There were three (10.3%) deaths. Two deaths occurred after Norwood operation, and one after interrupted aortic arch repair. None of the deaths were related to neurological injury. None of the patients developed seizers, coma, abnormal movement or neurological deficits. ConclusionsSimple DHCA without SCP is a safe, expeditious and reliable method for brain protection during repair of complex cardiac lesions, with acceptable outcomes.

Effects of portal hyperperfusion on partial liver grafts in the presence of hyperdynamic splanchnic circulation: hepatic regeneration versus portal hyperperfusion injury

Effects of portal hyperperfusion on partial liver grafts in the presence of hyperdynamic splanchnic circulation: hepatic regeneration versus portal hyperperfusion injury

How Much Portal Vein Flow Is Too Much for Liver Remnant in a Stable Porcine Model?

BackgroundThere is increasing evidence that the occurrence of small-for-size syndrome (SFSS) depends on portal hemodynamics rather than graft size. The portal hyperperfusion has been regarded as the most important contributing factor to SFSS. However, it is unknown how much portal vein flow (PVF) or what limit of PVF the liver remnant can sustain in extreme hepatectomy. This study aimed to evaluate the limit of portal hyperperfusion in a stable porcine model. MethodsTwenty pigs were subjected to different liver resection volumes of 77%–82% (80% group; n = 6), 83%–87% (85% group; n = 7), and 88%–92% (90% group; n = 7). The survival rate, hemodynamic change, energy metabolism, lipopolysaccharide (LPS)/bacterial translocation, and injury and regeneration of the residual liver were observed after surgery. ResultsAll of the 80% group could sustain ∼4 times baseline PVF per unit volume, energy metabolism, and detoxifying functions, and survived to postoperative day (POD) 14. Only 3 animals in the 85% group, with ∼5.6 times baseline of PVF, were alive on POD 14, and in the 90% group, with >6 times baseline of PVF, undergoing severe hyperperfusion injury and LPS/bacterial translocation, none survived to POD 14. ConclusionsThe deaths of animals in the 85% group supports the hypothesis that the remnant vascular bed with 15% of liver volume represents a critical residual liver parenchyma in pigs, the safe minimum residual liver volume should be >15% of liver volume, indicating that the liver remnant can regenerate successfully in ∼5.6 times baseline of PVF, whereas it fails to regenerate in >5.6 times baseline of PVF.

Extracorporeal continuous portal diversion plus temporal plasmapheresis for “small-for-size” syndrome

To investigate the effect of plasmapheresis via the portal vein for "small-for-size" syndrome (SFSS) aided by extracorporeal continuous portal diversion (ECPD). Extensive or total hepatectomy in the pig is usually adopted as a postoperative liver failure (PLF) or SFSS model. In this study, animals which underwent 85%-90% hepatectomy were randomized into either the Systemic group (n = 7) or the Portal group (n = 7). In the Systemic group, all pigs received temporal plasmapheresis (PP) via the extracorporeal catheter circuit (systemic to systemic circulation) from 24 to 30 h post-hepatectomy (PH); in the Portal group, all pigs received ECPD to divert partial portal vein flow (PVF) to the systemic circulation after hepatectomy, then converted to temporal PP from 24 to 30 h PH, and subsequently converted to ECPD again until 48 h PH. In the Portal group, the PVF was preserved at 3.0-3.3 times that of the baseline value, similar to that following 70% hepatectomy, which was regarded as the optimal PVF to the hypertrophic liver remnant. At 48 h PH, all pigs were re-opened and the portal vein pressure (PVP), PVF, and HAF (hepatic artery flow) were measured, and then diversion of the portal venous flow was terminated. After 1 h the PVP, PVF, and HAF were re-measured. The portal hemodynamic changes, liver injury, liver regeneration and bacterial/lipopolysaccharide (LPS) translocation were evaluated in the two groups. The PVP in the Portal group was significantly lower than that in the Systemic group during the time period from 2 to 49 h PH (P < 0.05). Serum alanine aminotransferase (ALT), total bilirubin (TB) and ammonia were significantly reduced in the Portal group compared with the Systemic group from 24 to 48 h PH (P < 0.05). The Portal group may have attenuated sinusoidal endothelial injury and decreased the level of HA compared with the Systemic group. In the Systemic group, there was significant sinusoidal dilation, hydropic changes in hepatocytes and hemorrhage into the hepatic parenchyma, and the sinusoidal endothelial lining was partially destroyed and detached into the sinusoidal space. CD₃₁ immunostaining revealed significant destruction of the endothelial lining. In the Portal group, there was no intraparenchymal hemorrhage and the sinusoidal endothelial cells and hepatocytes were well preserved. CD₃₁ immunostaining was mild which indicated less destruction of the endothelial lining. HA was significantly decreased in the Portal group compared with the Systemic group from 2 to 48 h PH. The rate of liver remnant regeneration was elevated, while apoptosis was attenuated in the Portal group compared with the Systemic group. Thymidine kinase activity was much higher in the Portal group than in the Systemic group at 48 h PH. The PCNA index was significantly increased and the apoptotic index was significantly decreased in the Portal group compared with the Systemic group. Bacterial translocation and endotoxin, as well as the inflammatory response, were significantly attenuated in the Portal group compared with the Systemic group. LPS, tumor necrosis factor-α and interleukin-6 levels were all significantly decreased in the Portal group compared with the Systemic group from 24 to 48 h PH, while bacterial DNA level was significantly decreased from 2 to 48 h PH. PP plus ECPD via the portal vein can attenuate toxic load and hyperperfusion injury, and should be undertaken instead of PP via the systemic circulation in SFSS or PLF.

Inhalation of hydrogen gas reduces liver injury during major hepatotectomy in swine.

To study the effect of H2 gas on liver injury in massive hepatectomy using the intermittent Pringle maneuver in swine. Male Bama pigs (n = 14) treated with ketamine hydrochloride and Sumianxin II as induction drugs followed by inhalation anesthesia with 2% isoflurane, underwent 70% hepatotectomy with loss of bleeding less than 50 mL, and with hepatic pedicle occlusion for 20 min, were divided into two groups: Hydrogen-group (n = 7), the pigs with inhalation of 2% hydrogen by the tracheal intubation during major hepatotectomy; contrast-group (n = 7), underwent 70% hepatotectomy without inhalation of hydrogen. Hemodynamic changes and plasma concentrations of alanine aminotransferase (ALT), aspartate aminotransferase (AST), hyaluronic acid (HA), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and malondialdehyde (MDA) in liver tissue were measured at pre-operation, post-hepatotectomy (PH) 1 h and 3 h. The apoptosis and proliferating cell nuclear antigen (PCNA) expression in liver remnant were evaluated at PH 3 h. Then we compared the two groups by these marks to evaluate the effect of the hydrogen in the liver injury during major hepatotectomy with the Pringle Maneuver in the swine. There were no significant differences in body weight, blood loss and removal liver weight between the two groups. There was no significant difference in changes of portal vein pressure between two groups at pre-operation, PH 30 min, but in hydrogen gas treated-group it slightly decrease and lower than its in contrast-group at PH 3 h, although there were no significant difference (P = 0.655). ALT and AST in Hydrogen-group was significantly lower comparing to contrast-group (P = 0.036, P = 0.011, vs. P = 0.032, P = 0.013) at PH 1 h and 3 h, although the two groups all increased. The MDA level increased between the two group at PH 1 h and 3 h. In the hydrogen gas treated-group, the MDA level was not significantly significant at pre-operation and significantly low at PH 1 h and 3 h comparing to Contrast-group (P = 0.0005, P = 0.0004). In Hydrogen-group, the HA level was also significantly low to contrast-group (P = 0.0005, P = 0.0005) although the two groups all increased at PH 1 h and 3 h. The expression of cluster of differentiation molecule 31 molecules Hydrogen-group was low to Contrast-group. However, PCNA index (%) was not statistically significant between the two groups (P = 0.802). Microphotometric evaluation of apoptotic index (AI) in terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling-stained tissue after hepatotectomy for 3h, the AI% level in the hydrogen was significantly low to contrast-group (P = 0.012). There were no significant difference between Hydrogen-group and contrast-group at pre-operation (P = 0.653, P = 0.423), but after massive hepatotectomy, the TNF-α and IL-6 levels increase, and its in Hydrogen-group was significantly low compared with contrast-group (P = 0.022, P = 0.013, vs. P = 0.016, P = 0.012), respectively. Hydrogen-gas inhalation reduce levels of these markers and relieved morphological liver injury and apoptosis. H2 gas attenuates markedly ischemia and portal hyperperfusion injury in pigs with massive hepatotectomy, possibly by the reduction of inflammation and oxidative stress, maybe a potential agent for treatment in clinic.

Periprocedural management of acute ischemic stroke patients undergoing endovascular therapy

The physiologic derangements in acute stroke victims are dynamic. As noted extensively in the literature, there is mounting evidence to support that patients with large strokes, measured clinically through NIH Stroke Scale (NIHSS)1 or by radiologic methods,2 have increased mortality and are severely ill. Endovascular treatment of ischemic strokes inherently imposes a host of physiologic changes. Changes in cerebral perfusion and cerebral autoregulation need adequate hemodynamic support. Unintentionally induced changes during general anesthesia and potential hyperperfusion injury after revascularization may cause adverse outcomes. The loss of blood–brain barrier integrity poses additional challenges to antiplatelet and anticoagulant regimen. The primary goal of critical care management is to cater to the constantly changing cerebral perfusion in the background of loss of cerebral autoregulation. The practice remains varied in the community, administered by intensivists, anesthesiologists, and sometimes neurointerventional physicians. The individual and collective merits and demerits of current practice are unknown and have to be evaluated systematically. Admittedly, there exists no Class Ia evidence, and it is difficult …

Prediction of flow augmentation and complications of extracranial–intracranial bypass in symptomatic cerebrovascular diseases

Augmentation of the cerebral blood supply to correct cerebral hemodynamic insufficiency by extracranial–intracranial bypass may be an appropriate method to reduce the risk of ischemic stroke. Eighty-five patients with ischemic symptoms, decreased regional cerebral blood flow, and decreased regional cerebrovascular reactivity were recruited for surgery. The post-bypass mean regional blood flow increased by 35.8% compared to the pre-bypass value (p<0.001). Only minor re-establishment of vasculature after anastomosis was detected in three of four patients with middle cerebral artery stenosis, which suggests that there are fewer benefits of bypass surgery in this situation. Cerebral infarction occurred immediately post-operation in one patient who was predisposed to stroke due to a bilateral carotid occlusion. Hyperperfusion injury was infrequent in this series; only one patient developed intracerebral hemorrhage three weeks after the bypass. One ischemic and one hemorrhagic stroke occurred during the 90months following surgery.

Renal hyperperfusion injury resulting in transient proteinuria post renal artery angioplasty for fibromuscular dysplasia

Renovascular hypertension (RVH) can be treated utilizing medical, surgical or endovascular techniques. We present a case in which severe exacerbation of pre-existing proteinuria followed percutaneous transluminal angioplasty of a highly stenotic renal artery to relieve RVH caused by fibromuscular dysplasia. We propose that the worsening proteinuria post-angioplasty was caused by a transient renal hyperperfusion injury that overcame the glomerular autoregulatory mechanisms, thereby leading to raised intraglomerular pressures and loss of proteins through the glomerular filtration barrier until the vascular autoregulatory ability of the glomeruli was successfully re-established.

HMGB1 translocation and expression is caused by warm ischemia reperfusion injury, but not by partial hepatectomy in rats

Mechanical injury or ischemia/reperfusion (I/R) injury induces high mobility of group box 1 (HMGB1) translocation and release. However, the surgical procedure itself can initiate pathophysiologic processes causing damage to the respective organ. A liver resection, as an example, leads to portal hyperperfusion injury of the remnant liver. Therefore, we aimed to elucidate the impact of different hepatic surgical injury models on cellular localization and expression of HMGB1. Focal warm I/R injury was induced by clamping the vascular blood supply to the median and left lateral liver lobes for 90 min followed by 0.5 h, 6 h and 24 h reperfusion, as reported previously. Liver injury by PH was induced by subjecting rats to 30%, 70% or 90% partial hepatectomy (PH) followed by a 24 h observation period. Additional 12 rats were subjected to 90% PH and sacrificed at 1 h and 6 h to investigate the expression and release pattern of HMGB1. Elevation of serum liver enzymes indicating hepatic injury peaked at 6 h and recovered thereafter in models, warm I/R injury and PH. Liver injury was confirmed by liver histology. HMGB1 was translocated from the nucleus to the cytoplasm in livers subjected to warm I/R; but not in livers subjected to PH. Both protein and mRNA expression of HMGB1 were significantly up-regulated in livers subjected to warm I/R. In contrast, neither 30% PH, 70% PH nor 90% PH caused an elevation of hepatic HMGB1 mRNA and protein expression. High serum levels of HMGB1 (30 ng/ml) were measured at 0.5 h reperfusion period after warm I/R, much lower levels thereafter (< 5 ng/ml). Similar low serum levels were measured at all time points after 90% PH. Subsequently expression levels of TNF-a should be changed to tumor necrosis factor-alpha (TNF-α) reached a peak (26-fold elevation) at 6 h and decreased down to 5-fold at 24 h after warm I/R. TNF-α expression levels after PH never exceeded a 5-fold elevation. In conclusion, HMGB1 translocation and expression depends on the type of liver injury as it is induced by ischemia, but not by liver resection/hyperperfusion. These results suggest that HMGB1 may be used as molecular marker to visualize ischemic damage. Mechanic injury in hepatic surgery is associated with focal warm ischemia, and thereby HMGB1 translocation reflects surgical quality in experimental PH. Expression of hepatic TNF-α follows the kinetic pattern of HMGB1, pointing to a muss less pronounced inflammatory response after successful PH compared to warm I/R injury.