Venous Channels Research Articles

S2383 When Blood Meets Liver: An Interesting Case of Budd-Chiari Syndrome

INTRODUCTION: Budd-Chiari is a syndrome characterized by hepatic venous outflow obstruction. Primary Budd-Chiari is due to pro-coagulant states causing venous thrombosis. Secondary Budd-Chiari is due to compression or invasion of the hepatic veins, such as malignancy. Budd-Chiari is rare and has a high mortality if not properly identified and managed. CASE DESCRIPTION/METHODS: A 67-year-old Hispanic female with past medical history of chronic liver mass, liver cirrhosis secondary to NAFLD, type 2 diabetes mellitus, and obesity, presents with abdominal pain for several days. Physical exam was notable for right upper quadrant abdominal pain, anasarca, and abdominal wall cellulitis. Laboratory tests were remarkable for white blood cell count, 3.2; platelet count, 84; and AST 66. The remainder of laboratory data were unremarkable. CT abdomen pelvis showed enlarging right hepatic lobe lesion; expansion of the right hepatic vein into the suprahepatic IVC, concerning for tumor thrombus; and infrahepatic IVC prominent caliber suggestive of backflow pressure related to tumor thrombus. MRI abdomen showed 4.2 cm mass in the right hepatic lobe, possibly hepatocellular carcinoma. The location of the mass did not allow for safe percutaneous biopsy. Tumor marker AFP was noted to be 1,682. Hypercoagulable panel and immunologic work up were unremarkable. The patient was started on IV heparin and IV antibiotics. She was eventually transitioned to by mouth Eliquis. After a 14-day hospital stay, she was discharged home on continued Eliquis treatment and outpatient follow up appointments with Gastroenterology and Hematology. DISCUSSION: The presentation of Budd-Chiari is highly variable. When considering the diagnosis clinicians should be suspicious of patients with risk factors, such as malignancy, hypercoagulable states, and liver infections. Typical signs and symptoms of Budd-Chiari include acute liver failure patients with ascites, right upper quadrant abdominal pain, and hepatomegaly. The diagnosis is generally made with imaging. Abdominal ultrasound may show hypertrophied caudate liver lobe secondary to venous outflow channels distinct from the hepatic veins. CT or MRI abdomen can provide confirmatory imaging if ultrasound is unremarkable, but suspicion is high. Liver biopsy is not required to establish diagnosis and increases risk of bleeding. Although there are significant bleeding risks in patients, long term anticoagulation is required.

Cortical and bridging veins of the upper cerebral convexity: a magnetic resonance imaging study.

There is no study exploring the cortical veins (CVs) and connecting bridging veins (BVs) with neuroimaging modalities. The present study aimed to characterize these veins of the upper cerebral convexity. A total of 89 patients with intact cerebral hemispheres and covering meninges underwent thin-sliced, contrast magnetic resonance imaging (MRI). In addition, three injected specimens were dissected in this study. In cadaver dissection, the BVs were observed to course in the arachnoid sheaths, suspended from the dura mater. The medial parts of the BVs, located near the superior sagittal sinus (SSS)-BV junction site, were occasionally exposed subdurally. The CVs were formed by venous channels arising from the cerebral gyri and those emerging from the sulci. On MRI, the CVs and connecting BVs were identified in the medial and latera convexity areas and medial surface of the cerebrum. These veins were highly variable in number, thickness, length, course, and distribution. In the medial convexity area, the CVs arising from the gyri were identified in 58% of patients, while they were found only in 11% of patients in the lateral convexity area. In the medial convexity area, involving the parasagittal region, the CVs connect more densely with the BVs that may predispose to injury during neurosurgical procedures. Mechanical impact exerted the area, diameter of the veins in the craniocaudal direction, and number of venous afferences may affect the SSS-BV junctional region in an indirect manner and lead to the development of acute subdural hematoma.

Multiple Venous Malformations as a Cause of Pulsatile Tinnitus

Introduction Pulsatile tinnitus is a relatively common presentation in otolaryngology clinics, most cases of which have a treatable cause. This presentation warrants a thorough workup to identify treatable, and rule out life-threatening, etiologies. We present a case of a patient with pulsatile tinnitus arising from multiple dilated venous channels in the head and neck. Case Presentation. We present the case of a 65-year-old Caucasian female with a two-year history of progressive, bilateral pulsatile tinnitus, which had become debilitating. Computed-tomographic angiography (CTA) studies ruled out an intracranial vascular cause for her symptoms. However, computed tomography (CT) scanning and magnetic resonance imaging (MRI) revealed multiple dilated bilateral, low-flow, venous channels throughout the head and neck. The proximity of such dilated venous channels to the temporal bone provides a route for sound to be transmitted to the inner ear. Conclusion Arterial, venous, and systemic etiologies can cause pulsatile tinnitus. Arteriovenous malformations (AVMs) of the head and neck represent less than 1% of cases. In our patient, dilated low-flow venous malformations are the likely source of her symptoms, which is the first reported case in the literature.

Dural Venous Channels: Hidden in Plain Sight-Reassessment of an Under-Recognized Entity.

Tentorial sinus venous channels within the tentorium cerebelli connecting various cerebellar and supratentorial veins, as well as the basal vein, to adjacent venous sinuses are a well-recognized entity. Also well-known are "dural lakes" at the vertex. However, the presence of similar channels in the supratentorial dura, serving as recipients of the Labbe, superficial temporal, and lateral and medial parieto-occipital veins, among others, appears to be underappreciated. Also under-recognized is the possible role of these channels in the angioarchitecture of certain high-grade dural fistulas. A retrospective review of 100 consecutive angiographic studies was performed following identification of index cases to gather data on the angiographic and cross-sectional appearance, location, length, and other features. A review of 100 consecutive dural fistulas was also performed to identify those not directly involving a venous sinus. Supratentorial dural venous channels were found in 26% of angiograms. They have the same appearance as those in the tentorium cerebelli, a flattened, ovalized morphology owing to their course between 2 layers of the dura, in contradistinction to a rounded cross-section of cortical and bridging veins. They are best appreciated on angiography and volumetric postcontrast T1-weighted images. Ten dural fistulas not directly involving a venous sinus were identified, 6 tentorium cerebelli and 4 supratentorial. Supratentorial dural venous channels are an under-recognized entity. They may play a role in the angioarchitecture of dural arteriovenous fistulas that appear to drain directly into a cortical vein. We propose "dural venous channel" as a unifying name for these structures.

PECULIARITIES OF HUMAN PROSTATE VENOUS BLOOD FLOW

This article reviews scientific sources on the venous bed of the human prostate. In general, venous blood outflow from the prostate gland is provided by the prostate venous plexus. This plexus anastomoses with the deep dorsal vein of the penis, posterior scrotal veins, as well as with the hemorrhoidal and urinary bladder plexuses and with the Santorini’s venous plexus (collects blood from the prostate gland, the bottom of the bladder and seminal vesicles and enters the internal iliac vein). It is the Santorini’s venous plexus, which is often associated with massive blood loss during the surgical operations on the prostate. Since the structure of the venous intraorgan bloodstream in the prostate mainly corresponds to that for the arteries, three groups of veins are respectively distinguished. These are the intergland veins, which run to the venous plexus of the prostate capsule, the veins entering the venous plexus of the submucosal base of the urethra and, finally, the veins of the venous plexus, lying next to the ejaculatory duct. Blood flows from the parenchyma of the gland into the prostatic venous plexus through intraorgan veins, which has a complex structure and surrounds the prostate from almost all the sides. Some authors consider the periprostatic venous plexus to be a part of a single urogenital plexus. In the structure of the genitourinary venous plexus, numerous adduction and abduction pathways take place that deliver blood from the external and internal genital organs, the bladder, the distal parts of the ureters and partially from the walls of the rectum and pelvic bones. Analysis of the literature has shown that there are omissions in the study of the structure of the venous channel of the human prostate gland. They are the lack of data on the links of the circulatory microvasculature and the features of its spatial organization; the connection of the venous bed with the secretion and secretion processes; systematized data on anastomoses and their exact localization.

Modelling of the arteriovenous malformation embolization optimal scenario.

Cerebral arteriovenous malformation (AVM) is a congenital brain vessels pathology, in which the arterial and venous blood channels are connected by tangles of abnormal blood vessels. It is a dangerous disease that affects brain functioning causing the high risk of intracerebral haemorrhage. One of AVM treatment methods is embolization—the endovascular filling of the AVM vessel bundle with a special embolic agent. This method is widely used, but still in some cases is accompanied by intraoperative AVM vessels rupture. In this paper, the optimal scenario of AVM embolization is studied from the safety and effectiveness of the procedure point of view. The co-movement of blood and embolic agent in the AVM body is modelled on the basis of a one-dimensional two-phase filtration model. Optimal control problem with phase constraints arising from medicine is formulated and numerically solved. In numerical analysis, the monotone modification of the CABARET scheme is used. Optimal embolization model is constructed on the basis of real patients' clinical data collected during neurosurgical operations. For the special case of embolic agent, input admissible and optimal embolization scenarios were calculated.

ОЦЕНКА ХАРАКТЕРА МИКРОЦИРКУЛЯТОРНОГО ОТВЕТА НА ЭКСПЕРИМЕНТАЛЬНУЮ ТЕРМИЧЕСКУЮ ТРАВМУ

Burn disease affects the functioning of almost all functional systems, having a negative effect on them due to the development of endotoxicosis and vascular disorders. At the same time, the greatest attention is paid to the shifts that form in the systemic hemodynamics, primarily in the coronary and pulmonary blood flow, which can cause the development and progression of life-threatening conditions. At the same time, the microcirculatory system is also undergoing changes, but these changes have been studied in much less detail. The aim of this research was to study the state of skin microcirculation in healthy and burned rats. The experiment was carried out on 20 adult male Wistar rats divided into two equal groups. The first group of animals (n=10) was a control group (intact), with its representatives there were not any manipulations, except for a single study of the state of microcirculation. Rats of the second (main) group (n=10) were simulated contact thermal burn using their own patented method. The assessment of microcirculation parameters in the main group of animals was carried out by laser Doppler flowmetry on the device "LAKK-M" on the 1st day (2-3 hours after the injury), on the third and tenth days after the burn period. It was found that thermal injury has a negative impact on the microcirculation system, which is seen in a decrease in the intensity of blood flow through small-diameter vessels. This is achieved by reflex vasospasm, reducing the release of nitrogen oxide by endothelial cells and activating precapillary sphincters, and simultaneously activating the shunting ways of cardiac shunt from the arterial directly to the venous channel, bypassing the capillaries. Thus, in the post-thermal period, a compensatory "robbing phenomenon" is realized in the border zone of the burn, which requires pathogenetic correction.

Post-Glenn Shunt Systemic Desaturation—Is Venovenous Collateral the Culprit?

AbstractAfter classic Glenn shunt or bidirectional cavopulmonary anastomosis, the reappearance or deepening of cyanosis may be due to systemic venous collateral channels. There are only few case reports on this issue in the present literature. Here, we present two cases that underwent bidirectional Glenn shunt, who later presented with cyanosis and desaturation and both of them were found to have venovenous collaterals.

Downregulation of lysyl oxidase in venous malformations: Association with vascular destabilization and sclerotherapy.

Venous malformations (VM) are localized defects in vascular morphogenesis manifested by dilated venous channels with reduced perivascular cell coverage. As a vital enzyme for extracellular matrix (ECM) deposition, lysyl oxidase (LOX) plays important roles in vascular development and diseases. However, the expression and significance of LOX are unknown in VM. Herein, 22 VM specimens and eight samples of normal skin tissues were evaluated immunohistochemically for the expression of LOX, α-smooth muscle cell actin (α-SMA) and transforming growth factor-β (TGF-β). In vitro studies on human umbilical vein endothelial cells (HUVEC) were employed for determining potential mechanisms. Our results showed that LOX expression was significantly reduced in VM compared with normal skin tissues, in parallel with attenuated perivascular α-SMA+ cell coverage and TGF-β downregulation in VM. Further correlation analysis indicated that LOX expression was positively correlated with perivascular α-SMA+ cell coverage and TGF-β expression in VM. Moreover, marked elevation of LOX, TGF-β and α-SMA was observed in bleomycin-treated VM samples. Furthermore, our in vitro data demonstrated that both recombinant TGF-β and bleomycin induced obvious increase of LOX expression and activity and a concomitant increase in ECM components in HUVEC, which could be reversed by LOX inhibition. To our best knowledge, this study revealed for the first time the downregulation of LOX in VM and its correlation with vascular destabilization and TGF-β-induced endothelial ECM deposition. Moreover, our results highlighted that LOX may be implicated in the sclerotherapy of VM and holds promise as a therapeutic target.

Correction: The axillary vein and its tributaries are not in the mirror image of the axillary artery and its branches

[This corrects the article DOI: 10.1371/journal.pone.0210464.].

Intravenous leiomyomatosis with intracardiac extension managed by one-stage surgical excision: a case presentation

BackgroundIntravenous leiomyomatosis is characterized by the extension of pathologically benign smooth muscle tumor into venous channels. Its extension into the heart is a very rare occurrence, which may lead to heart failure and occasionally sudden death. Due to its rarity, the condition is poorly understood and often misdiagnosed.Case presentationWe report a case of intravenous leiomyomatosis with intracardiac extension in a 40 years old woman who underwent hysterectomy for uterine leiomyoma (one year earlier), managed successfully through one-stage surgical approach with main focus on its imaging features.ConclusionThe diagnosis of intravenous leiomyomatosis should be considered in women who present with cardiac symptoms associated with a right atrial mass and who also have a pelvic mass or have previously undergone hysterectomy because of uterine leiomyoma.

Pathways of spread in rectal cancer: a reappraisal of the true routes to distant metastatic disease

Rectal cancer can spread in a number of ways which have been previously recognised and validated as prognostic markers. These routes of spread are not adequately recognised in the stage grouping of the tumour-node-metastasis system, which focuses predominantly on the depth of invasion and nodal status, thus limiting its prognostic accuracy. Tumour spread involving veins occurs in 40% of patients. Venous channels have greater direct access to distant sites by means of a vascular ‘anatomical highway’. This rapid spread of tumour cells to distant metastatic sites by veins cannot occur by means of lymph node pathways. Thus, lymph nodes have been overestimated in their importance. Distinction between local tumour spread (lymph node metastases, perineural and lymphatic invasion) and tumour spread mediated by a direct vascular pathway to distant dissemination (extramural venous invasion and tumour deposits) must be made as the implications for prognosis and choice of treatment are not likely to be equal. Improved precision of radiological and pathological assessment is needed to scrutinise and carefully document each route of tumour spread. Only with this accurate information will it be possible to correctly weight each feature and develop a more prognostically accurate staging method that would allow separation of true high- and low-risk groups and subsequent improvements in patient care.

The emissary veins of the foramen ovale: an anatomical study using magnetic resonance imaging.

The emissary veins (EVs) passing through the foramen ovale (FO) are not well understood. The aim of this study was to characterize these veins using contrast magnetic resonance imaging (MRI). In total, 85 patients underwent thin-sliced, contrast MRI. Coronal and sagittal images were used for the analysis. The EVs of the FO were well delineated in 100% on sagittal and 97% on coronal images. On the sagittal images, these veins could be classified into the lateral, medial, and perineural types in association with the mandibular division of the trigeminal nerve (V3) segment in the FO. In 22% of the slides, the medial EV was more predominant than lateral one, while in 64% of the slides, the latter was more predominant. On the coronal images, the identified EVs of the FO coursed medially to the V3 in 68% and laterally in 72% of 165 sides. The perineural EVs most frequently coursed along both the lateral and medial surfaces of the V3. On the sagittal images, the angles formed by the midline of the V3 segment in the FO and lower margin of the FO were 81.5 ± 11.9° on the left side and 80.0 ± 12.2° on the right, while on the coronal images, they were 61.5 ± 12.1° on the left side and 64.8 ± 11.3° on the right. The EVs of the FO are structures that may be characterized by a well-developed venous channel in the lateral aspect of the V3 and nearly symmetrical orientation of both V3s lying in the FO.

Embryology of the Cavernous Sinus and Relevant Veins.

The cavernous sinus (CS) is a parasellar dural envelope containing an important venous pathway. The venous channels, which have an endothelial layer and no smooth muscle layer, are located in connective tissue. In the early embryonic stages, the neural tube is surrounded by the primitive capillary plexus and undifferentiated mesenchymal tissue, the primary meninx, and initially drains into the primary head sinus (PHS) through the anterior, middle, and posterior dural plexus (ADP, MDP, and PDP). Subsequently, following enlargement of the brain and differentiation of the mesenchyme, two major primary sinuses, the pro-otic sinus and the primitive tentorial sinus, become prominent. The pro-otic sinus is the remnant of the short segment of the PHS cranial to the MDP and the stem of the MDP. The CS originates from the plexiform channels medial to the trigeminal ganglion, namely the medial tributaries of the pro-otic sinus. The stem of the pia-arachnoidal vein draining into the ADP represents the primitive tentorial sinus. It is considerably elongated due to expansion of the cerebral hemisphere, and migrates medially toward the CS. The morphological changes in the CS and primitive tentorial sinus exhibit considerable variation in cerebral venous drainage patterns. Embryological knowledge facilitates interpretation of the anatomy of the CS, and it is useful to perform safe and beneficial endovascular treatment for the CS.

Chapter 6 - Middle fossa meningiomas

The middle cranial fossa is bounded anteriorly by the sphenoid ridge, medially by the lateral wall of the cavernous sinus and Meckel's cave, posteriorly by the sphenoid wing and petrous bone, and laterally by the greater wing of sphenoid and squamous temporal bone. In normal individuals, unnamed venous channels within the dura and arachnoid granulations can be seen on the floor of this fossa by the operating surgeon. Meningiomas arising mainly from the dura of the floor are uncommon, and middle fossa meningiomas have been arbitrarily named so based on an attachment of more than 75% to this location. They tend to present clinically at a large size and require special considerations for surgical treatment.

Prognostic significance of venous invasion in node-negative head and neck squamous cell carcinoma.

Venous invasion (VI) is not frequently evaluated on routine histologic examination of head and neck squamous cell carcinoma (HNSCC), and the prognostic significance is largely unknown. Studies have shown that extramural venous invasion is an adverse prognostic factor in colorectal carcinoma. To our knowledge, this is the first study evaluating the prognostic significance of venous invasion in node-negative (without clinical or pathologic evidence of lymph node involvement) HNSCC, utilizing the elastic stain. A total of 105 consecutive lymph node-negative (N0) HNSCC were evaluated for the presence of venous channel invasion by tumor utilizing the elastin stain. Clinical, demographic, and follow-up data were recorded. Of 37 patients with venous invasion, 19% had loco-regional recurrence, as opposed to 12% of those without. Univariate analysis revealed statistically significant decreased recurrence-free survival in the presence of venous invasion (log-rank [Mantel-Cox] test P-value .025). Identification of VI is greatly aided by elastic stain. In patients with node-negative HNSCC, presence of VI resulted in decreased recurrence-free survival on univariate analysis. The impact of VI as a prognostic marker should be further evaluated.

The Superficial Venous System of the Forelimb of the Anubis Baboon (Papio anubis): The Distribution of Perforating Veins and Venous Valves.

The superficial veins of the forelimb show high variability, both in man and in other primates, regarding the number of main venous trunks, their course, as well as the origin and location of openings. The distinction between two venous systems–the superficial and deep was made based on the relation of specific venous channels to the deep fascia; both groups of veins anastomose to each other through perforators piercing the deep fascia. In our work, we paid special attention to the organization of the venous system within the forelimb of the Anubis baboon (Papio anubis), as well as communications between the superficial and deep venous system. The main aim of the study was a detailed examination of the location of venous valves and perforating veins in forelimb of Anubis baboon. In the Anubis baboon, we observed the absence of the basilic vein. The main vessel within the forelimb, in the superficial venous system, was a well-developed cephalic vein. In all the cases, the cephalic vein opened into the external jugular vein. Also, in all of the examined specimens, there was an additional anastomosis connecting the cephalic and external jugular vein, i.e., persistent jugulocephalic vein located anterior to the clavicle. The venous vessels in the Anubis baboon were arranged in two main layers: superficial and deep, with both systems being connected by perforators located at the level of the carpus and cubital fossa. The number of venous valves within the cephalic vein was greater on the forearm the same as the mean intervalvular distance.

Venous encephalopathy

Dural arteriovenous fistulae (DAVF) accounts for 10-15% of rare acquired intracranial vascular malformations which can present with a wide range of symptoms but DAVF presenting with onset of encephalopathy and cognitive decline as non-hemorrhagic neurological deficits has rarely been reported. A 44-year-old gentleman complained of headache followed by episodes of confusional behavior presenting to the emergency with two episodes of GTC seizures. He had history of cortical superficial venous sinus thrombosis and was treated with anticoagulants for one year. On admission his vitals were stable, GCS-6, no meningeal signs but decerebrate posturing with bilateral extensor planter response. CT venography reported non-opacification of superior sagittal, straight, left transverse and bilateral sigmoid sinuses (Fig1&2). Extensive collateral venous channels were seen in brain, parenchyma, basal cisterns and along the convexities. Few types of collateral were opacified in the arterial phase though intracranial arteries were normal. DSA revealed multiple DAVF (>5) fed by various arteries (Fig3&4). Endovascular embolization and recanalization was attempted but was not successful and patient was started on subcutaneous heparin. DAVF is referred to the abnormal communication between the intracranial artery and dural venous sinuses. DAVF can present with a myriad of clinical features so it is frequently misdiagnosed. The two unique features in this patient of DAVF were the presence of multiple sinuses and rare clinical presentation as venous encephalopathy. We assume that in this case the transformation in symptomatology from encephalopathy to seizures was heralded by increased arterial blood supply due to multiple sites of the fistulae.

Posterior Fossa

The posterior fossa houses essential brainstem nuclei, cranial nerves, cerebral vasculature, and mechanisms for cerebrospinal fluid drainage. Anesthetic considerations for posterior fossa surgery include thorough preoperative evaluation, intraoperative monitoring, and anesthetic planning to allow neurophysiological monitoring. Careful positioning is imperative to optimize surgical conditions and to risk stratify patients for complications, including venous air embolus. Venous air embolus is a common complication of posterior fossa surgery given the plentitude of venous channels in the posterior fossa, and rapid recognition is key to managing this complication. Posterior fossa surgery also has a number of other known complications including postoperative apnea, prolonged ventilation, and possible brainstem stroke. This review contains 4 tables, 1 video, and 31 references. Keywords: Posterior fossa surgery, Brainstem surgery, Neuroanesthesiology, Venous air embolism/embolus, Sitting craniotomy, Prone craniotomy, Transesophageal echocardiogram, Neurophysiologic monitoring

Strategies for the diagnosis and treatment of the iliac vein compression syndrome

AimTo evaluate the diagnosis and treatment strategies for the iliac vein compression syndrome (IVCS) and the factors that affect the treatment outcome. MethodsIn total, 69 patients with IVCS were enrolled in the study. The patients underwent computed tomography (CT) venography before treatment. CT observations included assessment of the iliac venous channel sagittal diameter (IVCD) before the lower lumbar vertebra, causes of oppression, thrombus density, and embolization range. The patients with IVCS were divided into the simple IVCS (sIVCS, n = 22), lumbar degeneration-related type IVCS (dIVCS, n = 33), and IVCS of other causes (oIVCS, n = 14) including lumbar fracture, hematoma of infection, and abscess wraping around and compressing the iliac vein, groups. The treatment methods included target venous catheter-directed thrombolysis (CDT), a mechanical breaking and sucking treatment for the thrombi, followed by balloon dilatation and iliac vein stent implantation. The factors that may possibly affect the treatment outcomes included IVCS type, duration of disease, thrombus hardness, embolization length, and treatment regimen. Logistic regression was used to analyze the factors that affected the therapeutic efficacy. ResultsAt the first stage, CDT was only effective in 15 cases (5 dIVCSs and 10 oIVCSs) and was ineffective in the remaining 54 cases, which required further mechanical breaking and sucking of the thrombi and intravenous balloon dilatation. In the second stage, combination of thrombi breaking and suction and balloon dilatation was preliminarily effective in 26 cases (6 sIVCSs, 16 dIVCSs and 4 oIVCSs), but during follow-up from 1 to 6 months, treatment was considered futile for 9 recurrent cases (3 sIVCSs and 6 dIVCSs). So, 28 cases of preliminary ineffective treatment and 9 relapse in the second stage were arranged to the third stage of treatment by iliac vein stent implantation. All 37 cases were treated effectively and achieved a satisfactory iliac vein patency, and were followed-up for 24 months without recurrence. Logistic regression analysis showed that IVCS type (β = 4.14; Wald test, P < 0.01), duration of illness (β = -5.33; Wald test, P = 0.02), thrombus density (β = -6.46; Wald test, P = 0.01), embolization length (β = 2.74; Wald test, P = 0.03), and treatment regimens (β = 11.92; Wald test, P = 0.01) all had a significant effect on the treatment outcomes. ConclusionThe selection of a suitable intervention treatment regimen for different types of IVCS may aid in improving the curative effect.