A review of ocular perfusion pressure and retinal thickness: A case for the role of systemic hypotension in glaucoma

Background: Ocular perfusion pressure (OPP) is defined as blood pressure (BP) minus intraocular pressure (IOP). Low OPP may result in decreased ocular blood flow (OBF) and oxygen to the optic nerve head (ONH) and retina.Aim: To review the role of systemic hypotension and similar conditions in OPP and its influence on retinal nerve fibre layer (RNFL) thickness and the ganglion cell complex (GCC).Method: A literature search was conducted using the following search terms: ‘systemic hypotension’; ‘glaucoma’; ‘retinal nerve fibre layer’; ‘optic nerve’; ‘ocular blood flow’ and ‘ocular perfusion pressure’.Results: The Los Angeles Eye Study and Barbados Eye Study found that decreased OPP and BP increased the risk of glaucoma development by up to six times. Reduced retinal perfusion with resultant thinning of the RNFL in conditions with a similar mechanism, such as obstructive sleep apnoea syndrome, has indicated the importance of reduced OPP in retinal thickness. In the absence of any study directly showing the effect of systemic hypotension on OPP and retinal thickness, a working hypothesis proposes that reduced BP with or without normal-to-raised IOP will reduce OPP. The reduced OPP and OBF in those with systemic hypotension may result in oxidative stress and hypoxia which may then cause retinal ganglion cell death and the resultant retinal thinning.Conclusion: The increased risk of glaucoma development and progression relating to decreased BP and OPP has been proven to be of importance. Monitoring patients with systemic hypotension and evaluating the macula, ONH RNFL and GCC thickness may alert clinicians to possible glaucomatous changes.

Maternal and neonatal risk factors for neonatal respiratory distress syndrome in term neonates in Cyprus: a prospective case–control study

Background Neonatal respiratory distress syndrome (NRDS) is strongly associated with premature birth, but it can also affect term neonates. Unlike the extent of research in preterm neonates, risk factors associated with incidence and severity of NRDS in term neonates are not well studied. In this study, we examined the association of maternal and neonatal risk factors with the incidence and severity of NRDS in term neonates admitted to Neonatal Intensive Care Unit (NICU) in Cyprus. Methods In a prospective, case-control design we recruited term neonates with NRDS and non-NRDS admitted to the NICU of Archbishop Makarios III hospital, the only neonatal tertiary centre in Cyprus, between April 2017–October 2018. Clinical data were obtained from patients’ files. We used univariate and multivariate logistic and linear regression models to analyse binary and continuous outcomes respectively. Results During the 18-month study period, 134 term neonates admitted to NICU were recruited, 55 (41%) with NRDS diagnosis and 79 with non-NRDS as controls. In multivariate adjusted analysis, male gender (OR: 4.35, 95% CI: 1.03–18.39, p = 0.045) and elective caesarean section (OR: 11.92, 95% CI: 1.80–78.95, p = 0.01) were identified as independent predictors of NRDS. Among neonates with NRDS, early-onset infection tended to be associated with increased administration of surfactant (β:0.75, 95% CI: − 0.02-1.52, p = 0.055). Incidence of pulmonary hypertension or systemic hypotension were associated with longer duration of parenteral nutrition (pulmonary hypertension: 11Vs 5 days, p < 0.001, systemic hypotension: 7 Vs 4 days, p = 0.01) and higher rate of blood transfusion (pulmonary hypertension: 100% Vs 67%, p = 0.045, systemic hypotension: 85% Vs 55%, p = 0.013). Conclusions This study highlights the role of elective caesarean section and male gender as independent risk factors for NRDS in term neonates. Certain therapeutic interventions are associated with complications during the course of disease. These findings can inform the development of evidence-based recommendations for improved perinatal care.

Partial Right Atrial Inflow Occlusion for Transient Systemic Hypotension During Deployment of Thoracic Stentgrafts

Purpose Temporary balloon occlusion of the inferior vena cava to lower cardiac output is a relatively infrequently used technique to induce controlled systemic hypotension. In this technical note, we describe the feasibility, reliability, and safety of partial occlusion of right atrial inflow and the effect on systemic blood pressure during the deployment of a thoracic stentgraft. Materials and Methods Twenty consecutive patients undergoing thoracic endovascular aortic repair, with proximal landing in zone 0–3 of the thoracic aorta, were prospectively included. Right atrial inflow occlusion was performed with a compliant occlusion balloon. Results Median time to reach a mean arterial pressure of 50 mmHg was 43 s. Median recovery time of blood pressure was 42 s. Conclusion Partial right atrial inflow occlusion with an occlusion balloon is feasible with reliable results and without procedure-related complications.

Management of systemic hypotension in term infants with persistent pulmonary hypertension of the newborn: an illustrated review

In persistent pulmonary hypertension of the newborn (PPHN), the ratio of pulmonary vascular resistance to systemic vascular resistance is increased. Extrapulmonary shunts (patent ductus arteriosus and patent foramen value) allow for right-to-left shunting and hypoxaemia. Systemic hypotension can occur in newborns with PPHN due to variety of reasons, such as enhanced peripheral vasodilation, impaired left ventricular function and decreased preload. Systemic hypotension can lead to end organ injury from poor perfusion and hypoxaemia in the newborn with PPHN. Thus, it must be managed swiftly. However, not all newborns with PPHN and systemic hypotension can be managed the same way. Individualised approach based on physiology and echocardiographic findings are necessary to improve perfusion to essential organs. Here we present a review of the physiology and mechanisms of systemic hypotension in PPHN, which can then guide treatment.

Sphingosine-1-Phosphate Attenuates Lipopolysaccharide-Induced Pericyte Loss via Activation of Rho-A and MRTF-A

The high mortality seen in sepsis is caused by a systemic hypotension in part owing to a drastic increase in vascular permeability accompanied by a loss of pericytes. As has been shown previously, pericyte retention in the perivascular niche during sepsis can enhance the integrity of the vasculature and promote survival via recruitment of adhesion proteins such as VE-cadherin and N-cadherin. Sphingosine-1-phosphate (S1P) represents a lipid mediator regulating the deposition of the crucial adhesion molecule VE-cadherin at sites of interendothelial adherens junctions and of N-cadherin at endothelial–pericyte adherens junctions. Furthermore, in septic patients, S1P plasma levels are decreased and correlate with mortality in an indirectly proportional way. In the present study, we investigated the potential of S1P to ameliorate a lipopolysaccharide-induced septic hypercirculation in mice. Here we establish S1P as an antagonist of pericyte loss, vascular hyperpermeability, and systemic hypotension, resulting in an increased survival in mice. During sepsis S1P preserved VE-cadherin and N-cadherin deposition, mediated by a reduction of Src and cadherin phosphorylation. At least in part, this effect is mediated by a reduction of globular actin and a subsequent increase in nuclear translocation of MRTF-A (myocardin-related transcription factor A). These findings indicate that S1P may counteract pericyte loss and microvessel disassembly during sepsis and additionally emphasize the importance of pericyte–endothelial interactions to stabilize the vasculature.

Adenosine-Induced Cardiac Arrest for Transvenous Embolization of Midbrain Arteriovenous Malformation

BACKGROUND AND IMPORTANCE Few studies describe the use of adenosine-induced cardiac systole for treatment of cerebrovascular pathologies. We describe a midbrain arteriovenous malformation (AVM) treated with transvenous embolization using adenosine-induced asystole to achieve transient systemic hypotension with the purpose of furthering discussion on the technique and operative considerations for adenosine use in endovascular AVM treatments. CLINICAL PRESENTATION A 29-yr-old man presented with sudden onset of severe bilateral headache, blurred vision, and numbness on the right side of his face and tongue. Noncontrast head computed tomography revealed fourth ventricle hemorrhage. Diagnostic cerebral angiography revealed a high-flow midbrain AVM with a posterior wall perforator from the basilar artery terminus and a draining vein into the straight sinus. Transarterial AVM embolization was successful. The patient was discharged with no residual neurological deficits but returned 1 wk later with slurred speech and left-sided dysmetria. Repeat angiography revealed partial AVM filling. Attempts at transarterial embolization were unsuccessful. Thus, transvenous AVM embolization with adenosine-induced cardiac asystole and systemic hypotension was performed. A total of 60 mg of adenosine was administered, followed by 2 additional doses of 60 and 40 mg; and complete cardiac asystole with a mean arterial pressure of 40 mmHg was maintained, resulting in successful embolization of the AVM. No residual filling was visualized on postembolization arterial angiography runs. The patient was neurologically stable and discharged on postoperative day 2. CONCLUSION With appropriate and safe dosing, adenosine-induced asystole and systemic hypotension may be a feasible, safe option to reduce flow and assist endovascular transvenous embolization of high-flow AVMs.