Hemodynamic Imbalance Research Articles

Ischemia and reperfusion injury of the spinal cord: experimental strategies to examine postischemic paraplegia

Thoracoabdominal aortic replacement, necessary in case of injuries, aneurysms and dissections, shows a high complication rate as a consequence of the perioperative ischemia / reperfusion-sequence (I/R). Clamping above and below the lesion leads to the spinal cord suffering from ischemia. Clamping times of less than 30 minutes show only a small risk of neurological deficit, while longer periods increase paraplegia rates disproportionately. The subsequent reperfusion as a second hit causes additional damage to the spinal cord. Up to 30 % of all patients who require being treated in the thoracoabdominal part of the aorta suffer from paraplegia within the first 24 postoperative hours (Kahn et al., 2012).

Serelaxin for the treatment of acute heart failure: a review with a focus on end-organ protection.

Acute heart failure (AHF) is a complex clinical syndrome characterized by fluid overload and haemodynamic abnormalities (short-term clinical consequences) and the development of end-organ damage (long-term consequences). Current therapies for the treatment of AHF, such as loop diuretics and vasodilators, help to relieve haemodynamic imbalance and congestion, but have not been shown to prevent (and may even contribute to) end-organ damage, or to provide long-term clinical benefit. Serelaxin is the recombinant form of human relaxin-2, a naturally occurring hormone involved in mediating haemodynamic changes during pregnancy. Preclinical and clinical studies have investigated the effects mediated by serelaxin and the suitability of this agent for the treatment of patients with AHF. Data suggest that serelaxin acts via multiple pathways to improve haemodynamics at the vascular, cardiac, and renal level and provide effective congestion relief. In addition, this novel agent may protect the heart, kidneys, and liver from damage by inhibiting inflammation, oxidative stress, cell death, and tissue fibrosis, and stimulating angiogenesis. Serelaxin may therefore improve both short- and long-term outcomes in patients with AHF. In this review, we examine the unique mechanisms underlying the potential benefits of serelaxin for the treatment of AHF, in particular, those involved in mediating end-organ protection.

Cerebral Abscess in a 8 years old with uncorrected tetralogy of Fallot: Anaesthetic challenge

Patients with cyanotic heart disease are prone to develop frequent brain abscesses. Tetralogy of Fallot is a leading cause of cyanotic congenital heart disease and is responsible for as many as 10 % of all causes of congenital heart diseases. Surgery for drainage of abscess under general anaesthesia in these children is considered a challenge. Hemodynamic instability, cyanotic spells, coagulation defects, electrolyte and acid base imbalance, and sudden cardiac arrest are among the major anaesthetic concerns during perioperative period. We are here by reporting anaesthetic management of such a case with good outcome.

The clinical significance of monitoring parameters for oxygen kinetics and metabolism in the diagnosis and treatment of shock

The importance of hemodynamic monitoring is reflected in the correct interpretation of the monitoring results and taking simultaneously the appropriate treatment strategy according to the correct interpretation of the results.The essence of the shock is body tissue hypoperfusion,whtich result in tissue hypoxia and organ dysfunction.The essence of the hemodynamic imbalance is the imbalance of oxygen supply and oxygen consumption.Therefore,the end point of the fluid resuscitation for shock is now increasing emphasis on monitoring mixed/central venous oxygen saturation and the concentration of blood lactate,the rate of lactate clearance. Key words: Oxygen dynamics; Shock; Monitoring; Children

Rutin and quercetin show greater efficacy than nifedipin in ameliorating hemodynamic, redox, and metabolite imbalances in sodium chloride-induced hypertensive rats

Rutin and quercetin were investigated for their effects on blood pressure and antioxidant defense system of rats fed with 8% sodium chloride-supplemented diet (high salt diet) for 6weeks. Animals fed with high salt diet demonstrated an increase in systolic, diastolic, pulse, and mean arterial blood pressures (p<0.05) as well as lipid peroxidation but decreases in the activities of antioxidant enzymes compared with control group. Groups post-treated with rutin and quercetin for 2weeks showed significant reversals in the values of these indices compared with the group fed with only the high salt diet but not post-treated. The high salt diet also led to significant increase in serum glucose, urea, creatinine, triglycerides, low-density-lipoprotein, and total cholesterol concentrations. Treatment with rutin and quercetin ameliorated the effects of high salt diet on these biochemical indices. The reference standard, nifedipin was less effective than rutin and quercetin. The results of this study highlight the risk of high salt consumption on cardiovascular health and the potent antioxidant and antihypertensive property of rutin and quercetin.

Recurrent orthostatic syncope due to left atrial and left ventricular collapse after a continuous-flow left ventricular assist device implantation

Left ventricular assist devices (LVADs) have become an established treatment for patients with advanced heart failure as a bridge to transplantation or for permanent support as an alternative to heart transplantation. Continuous-flow LVADs have been shown to improve outcomes, including survival, and reduce device failure compared with pulsatile devices. Although LVADs have been shown to be a good option for patients with end-stage heart failure, unanticipated complications may occur. We describe dynamic left atrial and left ventricular chamber collapse related to postural changes in a patient with a recent continuous-flow LVAD implantation.

Is it possible to consider non-conventional proposals for treating Ménière's disease?

According to our model, the primum movens for the onset of Meniere's disease should be represented by a haemodynamic imbalance. From this starting point, the principal therapeutic approach should concern the necessity of achieving and maintaining a stable blood perfusion to the inner ear; this involves a number of different factors ranging from cardiac pump activity to vasomotor regulation that in turn exert an influence on membrane and cell integrity. A simple, alternative or coadjuvant and almost risk-free treatment can thus be represented by antioxidants such as melatonin, especially through its modulating activity on the autonomic nervous system, and mostly by omega-3 polyunsaturated fatty acids (omega-3 PUFAs); the latter, owing to their capability of improving myocardial function and arterial compliance, modulating blood pressure, and stabilizing cell and organelle membrane structure and function could theoretically fulfil all the requirements. When considering a resort to more strictly pharmacologi...

The evolving landscape of RAAS inhibition: from ACE inhibitors to ARBs, to DRIs and beyond

Chronic renin–angiotensin–aldosterone system (RAAS) activation has far-reaching effects on cardiometabolic risk and is a substantial contributor to cardiovascular (CV) disease and renal dysfunction. The vascular effects of sustained RAAS activation are associated with hemodynamic imbalances, as well as inflammatory stimulation and prothrombotic processes that lead to fibrosis, endothelial dysfunction and cellular remodeling. RAAS inhibition therapies, which include the use of angiotensin-converting enzyme inhibitors, angiotensin receptor blockers and more recently, direct renin inhibitors, have been used in clinical practice for more than 30 years. Our understanding of how these drugs work, alone and in combination, has contributed to an expanding landscape of treatment options and established RAAS inhibition as essential for reducing the risk of CV and renal disease. This perspective provides a historical overview of how RAAS inhibitors have evolved to their present-day status and will discuss recently discovered functions for components of this complicated and powerful regulatory system.

Plasma copeptin in the assessment of febrile neutropenia

Copeptin, the surrogate marker of arginine vasopressin (AVP), has been suggested to be a useful biomarker in monitoring sepsis reflecting hemodynamic imbalance and stress state. This prospective study conducted at a hematology ward in a Finnish University Hospital aimed to investigate whether plasma copeptin predicts the development of complicated course of neutropenic fever (bacteremia or need for treatment at intensive care unit) in 100 hematological patients experiencing their first neutropenic fever episode after intensive chemotherapy for hematological malignancy. Contrary to study presumptions, not elevated copeptin but the lack of a proper initial increase of plasma copeptin (<0.02ng/mL from day 0 to day 1) predicted blood culture positive sepsis (p=0.023) and gram-negative bacteremia (p=0.045). No correlation was observed with plasma sodium, blood pressure or evaluated osmolality. Plasma copeptin correlated inversely with the same day pentraxin 3 on day 0–day 2 (all p-values <0.001) and with C-reactive protein on day 1 (p=0.015). In conclusion, copeptin did not correlate with disease severity, but the lack of a proper initial increase was associated with bacteremic complications of febrile neutropenia in hematological patients. The findings suggest the possibility of central dysregulation of AVP release and do not support the use of copeptin as a biomarker of septic complications in this patient group.

Symmetrical Peripheral Gangrene in Four Pediatric Cardiac Surgery Patients Receiving Extracorporeal Membrane Oxygenation

Symmetrical peripheral gangrene (multilimb ischemia without large artery occlusion) is a rare condition usually associated with disseminated intravascular coagulation, hemodynamic compromise, and/or sepsis. However, it has not been described in patients on extracorporal membrane oxygenation (ECMO). Over a 5 year period, four pediatric patients developed symmetrical peripheral gangrene on ECMO after cardiac surgery. They subsequently died and came to autopsy. History, physical examination, and laboratory studies were examined. Gross and microscopic autopsy material was reviewed. Patients were 11 days to 13 years old. Extracorporal membrane oxygenation duration was 11-22 days, and limb ischemia began 2-4 days before death. Three patients had rapid onset, with ischemia developing in <48 hours. In the fourth, ischemic changes began as focal lesions and gradually spread. Two patients were septic. Three had evidence of other end-organ damage. Pressors were used in 3 patients before the limb ischemia. Autopsies disclosed ischemic changes involving all limbs, with confluent ecchymoses. In a detailed examination in 1 case, large arteries of the extremities were patent. Involved skin and soft tissue showed bland fibrin thrombi in the microcirculation, with tissue necrosis and hemorrhage. This report describes the first 4 cases of symmetrical peripheral gangrene complicating ECMO. The 4 pediatric patients all had recent surgery for congenital cardiac disease, and all had significant exposure to ECMO prior to developing limb ischemia. Symmetrical peripheral gangrene is an unusual complication of ECMO that may arise in the setting of disseminated intravascular coagulation, sepsis, or other hemostatic and/or hemodynamic imbalance.

Superior vena cava resection and reconstruction

Stage III thymic tumours often represent a major challenge; however, if complete resection is accomplished, long-term survival can be comparable with that of patients with stage I and II disease [1]. Induction and adjuvant regimens may help us to achieve these results [2]. The left brachiocephalic vein, superior vena cava (SVC), right atrium, pericardium, lung and diaphragm can be safely resected with or without reconstruction. Also, resection of one phrenic nerve or reconstruction of the ascending aorta and main pulmonary artery may be required to achieve complete resection; on the other hand, invasion through the pericardium into the myocardium usually precludes resection. Vascular reconstructions certainly pose more serious technical problems. The SVC, the brachiocephalic vein(s) and also the right atrium can be resected and reconstructed, but only if it helps to achieve complete resection. If the SVC is infiltrated for <30% of the circumference, partial resection of the wall of the vessel is usually feasible, and repair can be accomplished either by direct suture or patch reconstruction; autologous (pericardial or venous) or heterologous material (bovine pericardium) is usually employed. If a larger circumferential involvement is present, complete resection of the vessel with prosthetic reconstruction is required. This is usually accomplished by synthetic grafts [rigid polytetrafluoroethylene (PTFE)] or a tube of bovine pericardium [3, 4]; the latter allows excellent long-term patency without anticoagulation. These operations represent a major technical challenge for the potential detrimental effect of clamping a patent vessel [5] and the risk of complications. Partial or complete SVC clamping of a chronically obstructed vessel is usually well tolerated. On the other hand, if complete clamping of a patent SVC is required, a marked haemodynamic imbalance may occur, with consequent increase of the mean venous pressure in the cephalic district and a reduced arterial—venous gradient within the brain. This may result in cerebral oedema, haemorrhage and damage, and potentially intra-operative lethal reduction in cardiac output. The haemodynamic derangement may be limited by a dedicated pharmacologic support, adequate intra-operative strategy and intra—or extraluminal shunt placement. Difficult situations with direct invasion of the right atrium or intracaval—intra-atrial involvement (with or without a neoplastic thrombus) usually require the institution of cardio-pulmonary bypass (CPBP) [6–8]. In fact, transient shunts bypassing the SVC and redirecting blood flow directly into the right atrium might not be technically feasible or may not be appropriate in these situations, since the atrium must be kept empty to allow removal of both the tumour and the endovascular neoplastic thrombus with safe reconstruction. In this issue, Toker et al. describe an interesting technique [9] allowing transient cava-pulmonary shunt with complete by pass of the circulation draining in the inferior vena cava (IVC) directly into the pulmonary artery. Systemic heparinization was not required. The Trendelemburg position and the IVC pressure itself allow flow without haemodynamic instability. This shunt is easy to set and does not pose major technical problems. In the present case, it also took advantage of the complete obstruction of the SVC and left brachiocephalic vein clearly evident preoperatively; in fact, chronic obstruction of the upper caval system has probably already favoured the onset of collaterals contributing to drain blood from one venous system to the other. However, CPBP should not be regarded any more as a detrimental option in these patients. Clamping time is usually short; the use of pre-heparinized circuits dramatically reduces the need for systemic heparinization and reduces the risk of intraand post-operative complications, particularly bleeding. This is nowadays clear and it has been extensively described during lung transplantation, where CPBP is instituted much more liberally [10]. CPBP should be part of the armamentarium of thoracic surgeons and we should be ready to institute it, also with the cooperation of cardiac surgeons, if required. If less invasive options are technically feasible they should be taken into consideration without adding major risks.

Doping and Thrombosis in Sports

Historically, humans have long sought to enhance their "athletic" performance to increase body weight, aggressiveness, mental concentration and physical strength, contextually reducing fatigue, pain, and improving recovery. Although regular training is the mainstay for achieving these targets, the ancillary use of ergogenic aids has become commonplace in all sports. The demarcation between ergogenic aids and doping substances or practices is continuously challenging and mostly based on perceptions regarding the corruption of the fairness of competition and the potential side effects or adverse events arising from the use of otherwise unnecessary ergogenic substances. A kaleidoscope of side effects has been associated with the use of doping agents, including behavioral, skeletal, endocrinologic, metabolic, hemodynamic, and cardiovascular imbalances. Among the various doping substances, the most striking association with thrombotic complications has been reported for androgenic anabolic steroids (i.e., cardiomyopathy, fatal and nonfatal arrhythmias, myocardial infarction [MI], intracardiac thrombosis, stroke, venous thromboembolism [VTE], limb arterial thrombosis, branch retinal vein occlusion, cerebral venous sinus thrombosis) and blood boosting (i.e., VTE and MI, especially for epoetin and analogs). The potential thrombotic complication arising from misuse of other doping agents such as the administration of cortisol, growth hormone, prolactin, cocaine, and platelet-derived preparations is instead speculative or anecdotal at best. The present article provides an overview on the epidemiological association as well as the underlying biochemical and biological mechanisms linking the practice of doping in sports with the development of thrombosis.

Kidney disease and inner ear impairment: a simpler and closer pathogenic analogy?

The association of chronic kidney disease (CKD) and hearing disorders is well known, and was first reported more than 80 years ago by Alport, who described a case of familial kidney disease associated with hearing loss. Subsequently, a number of rare conditions or syndromes were described as occurring with a close link between hearing impairment and CKD (see Table 1). Moreover, some observational, cross-sectional, population-based studies concerning patients with CKD, or on dialysis therapy, confirmed this association suggesting the possibility that the linkage between the ear and the kidney is more than casual. In particular, Vilayur et al. report several physiological, ultrastructural and antigenic similarities between the kidney and the cochlea that strongly support the link between the hearing impairment and CKD [1]. The inner ear and the kidney share a series of basic processes for water and ion regulation as well as some specific cellular water channels known as aquaporins, which are known to have a crucial role in the functional activity of both organs. Moreover, the presence of a kidney-specific ion transport system has recently been demonstrated in the rat and human endolymphatic sac that, to date, represents the only known localization outside the kidney [2]. Once again this underlines a strict correspondence between the kidney and the inner ear, with both organs involved in highly energy-requiring processes linked to the strict necessity of maintaining the balance of ions and a stable pH. In particular, a derangement in the mechanisms regulating fluid and electrolyte homeostasis has been hypothesized both in the cochlear striavascularis, and in the kidney, to explain the possible association of inner ear and kidney diseases. A further contribution in order to clarify the importance of the analogies between kidney and inner ear comes from the progress in genetic research, revealing a possible common ground of dysfunction [3]. Finally, some cardiovascular risk factors such as age, diabetes, hypertension, electrolyte disorders and hemodialysis can affect both the ear and the kidney, and separately contribute to the development and the progression of organ-specific diseases [1]. Nevertheless, these reported connections and analogies between the ear and the kidney deserve to be considered according to a more comprehensive hypothesis. In particular, we speculate that a baseline condition of hemodynamic imbalance leading to a different extent of transient ischemia and hypoxia may elicit similar mechanisms of disease in both organs. Over the last decade, we have provided several observations supporting the hypothesis that some inner ear disorders of undetermined origin may depend on a large decrease in blood pressure values associated with an abnormal peripheral vasoconstriction [4]. This mechanism can be activated either in subjects without major cardiovascular risk factors (other than a generic sympathetic hyperreactivity), or in patients treated for hypertension or chronic congestive heart failure. In ‘‘healthy’’ subjects, the proposed model can provide a theoretical explanation for the cases of inner ear diseases usually labeled as ‘‘idiopathic’’, as well as for the different inner ear disturbances including the largely unexplained Meniere’s disease [5]. In patients with cardiovascular diseases, the symptoms of A. Pirodda Department of Specialist Surgical and Anesthesiological Sciences, S. Orsola-Malpighi University Hospital, Via Massarenti 9, 40138 Bologna, Italy

Diuretics in Meniere disease: A therapy or a potential cause of harm?

Despite the lack of clear evidence for their effectiveness in treating vertigo, tinnitus, hearing loss and aural fullness, diuretics, represent a common treatment for Meniere disease (MD), as they are supposed to decrease volume and pressure in the endolymphatic partition of the labyrinth. Our group have outlined the possibility of an adverse effect on inner ear function derived from an abrupt lowering of blood pressure: a subsequent exaggerated vasomotor response inducing local ischemia could be responsible for more or less permanent damage. The inner ear, owing both to its terminal vascular supply and to the necessity of a steady metabolism, seems a reliable target for any hemodynamic imbalance that acutely affect its perfusion. In our opinion, the complexity of the inner ear anatomy and function argues against the usefulness of diuretics to reduce endolymphatic volume, in analogy to their effect on the volemia: too many active mechanisms and “buffer” systems are involved in the labyrinth. Even considering that the finding of mean low pressure values is relatively common in subjects with MD, an attempt should be to maintain a stable blood perfusion to the labyrinth; in fact, an abrupt decrease in systemic blood pressure can trigger an adverse sympathetic reaction and transmit misleading information to the cochlear vasopressin receptors.

Leech Therapy in Reconstructive Maxillofacial Surgery

Corrective plastic surgery is indicated after accidents, burns, cancer surgery, or postoperative wound healing disorders with large tissue defects. The range of reconstructive techniques includes local skin flaps, pedicle grafts, and microvascular anastomosed flaps in the case of large defects. Main complications such as arterial and venous insufficiency caused by a vessel collapse or a vascular spasm are reported regularly in the area of anastomosed vessels and are the concern of any surgeon. Today, leeches are used if wound healing is at risk because of hemodynamic imbalance or a venous insufficiency. A retrospective evaluation of 148 patients who underwent medical leech therapy in the case of local or pedicaled flaps and some patients who had undergone reconstruction with microvascular flaps from 2005 and 2010 was conducted. Our sample had the typical symptoms of venous congestions of their flaps, despite suture removal, relief of pressure on the flap, and the elimination of a hematoma beyond the flap after surgery. Medical leech therapy was used in these cases. Our series has confirmed the excellent and predictable healing after medical leech therapy for local and microsurgical anastomosed flaps in the case of venous congestion. Leech therapy should be considered as a reliable additional procedure and an advantage in maxillofacial and plastic reconstructive surgery to remedy complications resulting from a hemodynamic imbalance or venous insufficiency in the immediate postoperative period.

Cavernous Hemangioma of the Orbital Apex: Pathogenetic Considerations in Surgical Management

To consider the pathogenesis and growth of cavernous hemangioma, particularly within the crowded orbital apex, in decisions regarding surgical indications, timing, and technique. A perspective based on analysis of the microanatomic relationships and growth potential of apical cavernous hemangiomas, with representative case studies illustrating management recommendations. Analysis of microscopic findings in typical and vision-loss cases; review of tumor growth patterns as reported in observational and interventional studies; consideration of surgical approaches and reported functional outcomes. An ongoing, local hemodynamic imbalance may drive the proliferation of a cavernous hemangioma. Extension into neighboring tissue induces a fibrous capsule, which is continually reconstituted as the lesion expands, and which may incorporate visually critical structures in the confines of the apex. The extent of this microanatomic intimacy is not detectable preoperatively. The tumor's remaining growth potential at the time of diagnosis or following incomplete resection is not predictable. Patients without significant vision deficits should be observed for progression. Those with significant deficits or signs of progression should be offered timely surgery, with recognition of the risks. The surgical approach should be individualized based on macroanatomic relationships. The decision to intervene should not be a commitment to complete resection at any cost; intraoperative recognition of "inoperable" attachments may dictate modifications in order to preserve vision.

The fragility of the hemodynamic balance in the elderly: possible influences on the inner ear

The possible occurrence of labyrinthine disorders linked to hemodynamic imbalances has been widely outlined [1-4] and well demonstrated by clinical observations concerning both young and healthy people [4] and subjects suffering from cardiovascular affections as hypertension the prevalence of tinnitus was studied in patients under antihypertensive [5] or heart failure of variable severity [6]. In all cases, a possible influence of a sharp decrease in the values of blood pressure followed by an abnormal vasomotor reaction was postulated to have some role in the genesis of the disorder, mostly when considering that blood supply of the inner ear is of terminal type. In the elderly, the problem is even more complicated by the frequent presence of isolated systolic hypertension, which is characterized by the lowered compliance of the vascular tree, presenting with an increase of the arterial stiffness and reported to be due both to age-related loss of distensibilty in the major central arteries and to endothelial dysfunction [7]: this increases, in general terms, the risk of transient hypoperfusion to an organ with a terminal circulation as the labyrinth and represents a crucial factor to deal with when treating hypertension in elderly. Moreover, the possibility of the so-called “hypertension-hypotension syndrome” [8], i.e. the coexistence of supine hypertension and orthostatic hypotension as a result of dysautonomia [7] represents a further complication in this sense. Hence the necessity of choosing, when possible, an antihypertensive therapy able to protect the endothelial wall and to avoid brusque falls of peripheral oxygenation which could damage the inner ear. Author details Department of Specialist Surgical and Anesthesiological Sciences, University of Bologna, Italy. Posgraduate School of Audiology and Phoniatrics, University of Bologna, Italy.

MENIERE’S DISEASE: UPDATE OF ETIOPATHOGENETIC THEORIES AND PROPOSAL OF A POSSIBLE MODEL OF EXPLANATION

Meniere’s Disease (MD) is an affection consisting of an association of sensorineural hearing loss, tinnitus and vertigo initially presenting by crises. A review of the most considered possible causative factors and pathophysiologic interpretations allows us to underline the uncertainties which still exist about the genesis of this illness. We propose a mechanistic model based on the effect of a haemodynamic imbalance leading to transient ischaemia which could have an effect on the pH of the inner ear as well as on the work of the inner ear proton pumps. It is hypothesized that under ischaemic conditions and consequent metabolic acidity a preserved proton pump activity can generate an overload of anions in the endolymphatic partition, which is a closed system, thus resulting in an enhancement of osmolarity and consequently in the formation of a hydrops resulting in the development of fluctuating hearing loss, tinnitus and vertigo which characterize Meniere’s Disease.

Acute peritoneal dialysis in very low birth weight neonates using a vascular catheter

We report on our experience with acute peritoneal dialysis (APD) in 16 very low birth weight neonates ranging from 24.6 to 30.2 weeks' gestation with a birth weight ranging from 630 g to 1,430 g using a 14-gauge Arrow vascular catheter for APD access. The underlying causes of acute renal failure were: sepsis (7), necrotizing enterocolitis (4), patent ductus arteriosus (3), hydrops fetalis (1), intracranial hemorrhage (3), pulmonary hemorrhage (2), pneumonia (1), and perinatal asphyxia (1). Among 12 patients, the APD was successful for the control of hyperkalemia, fluid overload, and metabolic acidosis. The peritoneal permeability and transport were at their maximum at a short dwell time with rapid exchanges. Complications associated with the APD were: peritonitis (2), leakage (2), hemoperitoneum (1), and hernia (1). During the dialysis, four patients died; there were three episodes of catheter-related complications in these patients. At 60 days after the withdrawal of the APD, 10 patients were alive, and had full recovery of their renal function. Therefore, APD in premature neonates with a 14-gauge Arrow vascular catheter was safe and effective. This procedure helped manage the hemodynamic and metabolic imbalance of acute renal failure and was associated with few complications.

Screening for twin–twin transfusion syndrome at 11–14 weeks of pregnancy: the key role of ductus venosus blood flow assessment

A discrepancy in crown-rump length (CRL) and/or nuchal translucency thickness (NT) between monochorionic twins has been found to be associated with an increased risk of twin-twin transfusion syndrome (TTTS). As one of the most plausible mechanisms for increased NT is hemodynamic imbalance and cardiac dysfunction, indirectly manifested by abnormal blood flow in the ductus venosus (DV), we aimed to clarify the role of DV blood flow assessment in identifying those monochorionic twins more prone to develop TTTS. We present 99 cases of monochorionic diamniotic twin pregnancies in which CRL, NT and DV blood flow were evaluated at 11-14 weeks' gestation. Discrepant values of CRL were not predictive of TTTS development. Intertwin NT discrepancy >or= 0.6 mm had a sensitivity of 50.0% and a specificity of 92.0%. The presence of at least one abnormal blood flow waveform in the DV was associated with a relative risk for developing TTTS of 11.86 (95% CI, 3.05-57.45), with a sensitivity of 75.0% and a specificity of 92.0%. The combination of abnormal DV blood flow with NT discrepancy >or= 0.6 mm yielded a relative risk for the development of TTTS of 21 (95% CI, 5.47-98.33). Both intertwin discrepancy in NT and abnormal flow in the DV in monochorionic twins may represent early manifestations of hemodynamic imbalance between donor and recipient. In these pregnancies, in addition to NT measurement at 11-14 weeks, the Doppler assessment of DV blood flow significantly increases the performance of screening for those at risk of developing TTTS.