Safety of hyperbaric oxygen therapy in patients with heart failure: A retrospective cohort study.

BACKGROUND: Hyperbaric oxygen therapy (HBOT) has several hemodynamic effects including increases in afterload (due to vasoconstriction) and decreases in cardiac output. This, along with rare reports of pulmonary edema during emergency treatment, has led providers to consider HBOT relatively contraindicated in patients with reduced left ventricular ejection fraction (LVEF). However, there is limited evidence regarding the safety of elective HBOT in patients with heart failure (HF), and no existing reports of complications among patients with HF and preserved LVEF. We aimed to retrospectively review patients with preexisting diagnoses of HF who underwent elective HBOT, to analyze HBOT-related acute HF complications. METHODS: Research Ethics Board approvals were received to retrospectively review patient charts. Patients with a history of HF with either preserved ejection fraction (HFpEF), mid-range ejection fraction (HFmEF), or reduced ejection fraction (HFrEF) who underwent elective HBOT at two Hyperbaric Centers (Toronto General Hospital, Rouge Valley Hyperbaric Medical Centre) between June 2018 and December 2020 were reviewed. RESULTS: Twenty-three patients with a history of HF underwent HBOT, completing an average of 39 (range 6-62) consecutive sessions at 2.0 atmospheres absolute (ATA) (n = 11) or at 2.4 ATA (n = 12); only two patients received fewer than 10 sessions. Thirteen patients had HFpEF (mean LVEF 55 ± 7%), and seven patients had HFrEF (mean LVEF 35 ± 8%) as well as concomitantly decreased right ventricle function (n = 5), moderate/severe tricuspid regurgitation (n = 3), or pulmonary hypertension (n = 5). The remaining three patients had HFmEF (mean LVEF 44 ± 4%). All but one patient was receiving fluid balance therapy either with loop diuretics or dialysis. Twenty-one patients completed HBOT without complications. We observed symptoms consistent with HBOT-related HF exacerbation in two patients. One patient with HFrEF (LVEF 24%) developed dyspnea attributed to pulmonary edema after the fourth treatment, and later admitted to voluntarily holding his diuretics before the session. He was managed with increased oral diuretics as an outpatient, and ultimately completed a course of 33 HBOT sessions uneventfully. Another patient with HFpEF (LVEF 64%) developed dyspnea and desaturation after six sessions, requiring hospital admission. Acute coronary ischemia and pulmonary embolism were ruled out, and an elevated BNP and normal LVEF on echocardiogram confirmed a diagnosis of pulmonary edema in the context of HFpEF. Symptoms subsided after diuretic treatment and the patient was discharged home in stable condition, but elected not to resume HBOT. CONCLUSIONS: Patients with HF, including HFpEF, may develop HF symptoms during HBOT and warrant ongoing surveillance. However, these patients can receive HBOT safely after optimization of HF therapy and fluid restriction.

Initiating Continuous Renal Replacement Therapy in Patients With Transurethral Resection of Prostate Syndrome: A Case Report.

With advances and developments in hysteroscopy, cystoscopy, transurethral resection of bladder tumor, and arthroscopy, transurethral resection of prostate (TURP) syndrome has been increasingly reported. TURP syndrome is often accompanied by severe hyponatremia, fluid overload, and a plasma hypotonic state, resulting in heart failure and pulmonary and cerebral edema. Conventional treatment methods, such as intravenous infusion of hyperosmotic saline, can rapidly reverse the downward trend of serum sodium levels in efforts to prevent and treat cerebral edema. However, this may not be suitable for patients with cardiac and renal insufficiency and may induce central pontine myelinolysis due to the possibility of worsening volume load and difficulty in controlling the correction rate of serum sodium. The patient described in this report presented with severe hyponatremia (sodium<100 mmol/L) combined with intraoperative pulmonary edema; his cardiac function and oxygenation status deteriorated after an intravenous infusion of 3% hypertonic saline. He underwent continuous renal replacement therapy (CRRT) to prevent the progression of multiple-organ edema and cardiac insufficiency. CRRT has demonstrated efficacy in the treatment of chronic hyponatremia in patients with renal failure, and can slowly and continuously correct water-electrolyte imbalance, acid-base imbalance, and volume overload. TURP syndrome with severe hyponatremia and pulmonary edema was diagnosed; accordingly, the patient was treated with 3% hypertonic saline, furosemide, and CRRT, without the development of overt neurological sequelae.

Unexpected systolic anterior motion of the mitral valve-related hypoxemia during transurethral resection of the prostate under spinal anesthesia: a case report.

BACKGROUND: Dynamic obstruction of the left ventricular outflow tract resulting from systolic anterior motion of the mitral valve can be an unexpected cause of acute and severe perioperative hypotension in noncardiac surgery. We report a patient undergoing spinal anesthesia for transurethral resection of the prostate who experienced sudden hypoxemia caused by systolic anterior motion-induced mitral regurgitation but with a clinically picture simulating fluid overload. CASE PRESENTATION: An 83-year-old man with a history of hypertension was scheduled for transurethral resection of the prostate. One hour after spinal anesthesia, he developed acute restlessness and dyspnea, with pink frothy sputum and progressive hypoxemia. Slight hypertension was noted, and an electrocardiogram showed atrial fibrillation with a rapid ventricular response. Furosemide and nitroglycerin were thus administered for suspected fluid overload or transurethral resection of the prostate syndrome; however, he then became severely hypotensive. After tracheal intubation, intraoperative transesophageal echocardiography was promptly performed, which revealed an empty hypercontractile left ventricle, significant mitral regurgitation and mosaic flow signal in the left ventricular outflow tract. Following aggressive fluid therapy, his hemodynamic changes stabilized. Repeat echocardiography in intensive care unit confirmed the presence of systolic anterior motion of the anterior mitral leaflet obstructing the left ventricular outflow tract. We speculate that pulmonary edema was induced by systolic anterior motion-associated mitral regurgitation and rapid atrial fibrillation, and the initial management had worsened his hypovolemia and provoked left ventricular outflow tract obstruction and hemodynamic instability. CONCLUSIONS: Pulmonary edema caused by systolic anterior motion of the mitral valve can be difficult to clinically differentiate from that induced by fluid overload. Therefore, bedside echocardiography is paramount for timely diagnosis and prompt initiation of appropriate therapy in the perioperative care setting.

Amelioration of allergic asthma by Ziziphora clinopodioides via upregulation of aquaporins and downregulation of IL4 and IL5.

Ziziphora clinopodioides has been frequently used as an anti asthmatic plant in traditional medication. Recent work explores the anti-asthmatic activity of Z. clinopodioides in allergen-induced asthmatic mice. Intraperitoneal sensitization followed by intranasal challenge were given with ovalbumin (allergen) to develop allergic asthma. Investigational groups of animals were administered with drug methylprednisolone (MP) (15 mg/kg body weight), n-hexane fraction, ethylacetate fraction, and methanolic extract of Z. clinopodioides extract (500 mg/kg b.w.) for successive 07 days. Hematoxyline and eosin (H&E) and periodic acid-Schiff (PAS) stains were used to evaluate histopathological parameters on lung tissues. As an index of lungs tissues edema, wet/dry weight ratio of lungs was determined. Evaluation of expression levels of AQP1, AQP5, IL4, and IL5 was conducted by using RT-PCR. The data exhibited that both Z. clinopodioides and MP attenuated differential and total leukocyte counts in hematological examination i.e. in BALF and blood. Treatment with Z. clinopodioides also caused suppression of inflammatory cell infiltration and expression levels of IL4 and IL5, the later could have caused attenuation of pulmonary inflammation. The study also found decline in lung wet/dry ratio and goblet cellh hyperplasia in treated groups which indicates amelioration of lung edema. Treatment with Z. clinopodioides significantly increased the expression levels of aquaporin-1 and -5, which could have led to reduction in lung edema. The treatment with MP showed comparable results to Z. clinopodioides. Current investigation revealed that Z. clinopodioides possessed anti-asthmatic property which might be accredited to upregulagted AQP1 and AQP5 levels and downregulated IL4 and IL5 levels.

Convulsive seizure and pulmonary edema during hyperbaric oxygen therapy:A case report.

Hyperbaric oxygen therapy (HBOT) for carbon monoxide (CO) poisoning is widely performed to prevent delayed neuropsychiatric syndrome. Although HBOT can generally be performed with safety, the appropriate management of HBOT still remains unestablished. A 31-year-old man was transferred to our facility to undergo HBOT in a multiplace chamber with a diagnosis of CO poisoning. The first HBOT session ended uneventfully. During the second HBOT session, the patient suddenly experienced convulsive seizures. The accompanying doctor administered intravenous propofol to stop the convulsion and terminated the HBOT. Soon after the convulsion, the patient developed frothy secretions through the endotracheal-tube with impaired oxygenation. Head computed tomography scan showed no abnormalities, suggesting the seizure was associated with complications of HBOT. A chest X-ray revealed bilateral pulmonary edema, and echocardiography revealed normal cardiac function, indicating that the pulmonary edema resulted from HBOT or neurogenic mechanism secondary to the seizure. The patient's respiratory status improved without recurrence of the seizure and no delayed neurological sequelae was seen afterwards. Here we report unexpected rare adverse events during HBOT. Hyperbaric oxygen therapy for acute indications should be performed in multiplace chambers, with appropriate preparation and medical equipment. J. Med. Invest. 65:286-288, August, 2018.

Fatal Pulmonary Edema in a Child After Jellyfish Stings in Korea.

Jellyfish have been increasing at a global scale in recent years. These blooms not only have deleterious effects on marine ecosystems, they also increase the risk of jellyfish stings and accompanying envenomation. Here, we report a fatal case of pulmonary edema caused by jellyfish envenomation in a child in Korea. The patient died 4 h after envenomation despite cardiopulmonary resuscitation. Nemopilema nomurai was the suspected species of jellyfish encountered by the patient, although we are unable to confirm this. With this case report, we aim to inform on the serious issue of toxicity associated with jellyfish species that bloom mainly along Korean, east Chinese, and Japanese shores and to discuss appropriate first aid methods in case of jellyfish stings.

p-Coumaric acid as a prophylactic measure against normobaric hypoxia induced pulmonary edema in mice.

AIMS: Previous studies indicate that the anti-hypoxia effects of Tibetan Turnip (Brassica rapa ssp. rapa) were closely related to its characteristic components being p-coumaric acid (CA) and p-coumaric acid­ß­d­glucopyranoside (CAG). Since CAG would be converted to CA in vivo, this study aims to further examine the efficacy and mechanism of CA against pulmonary edema induced by normobaric hypoxia. MAIN METHODS: Male ICR mice were assigned to the normoxia group and several hypoxia groups, given sterile water, CA or dexamethasone orally, once daily for four consecutive days. One hour after the final gavage, mice in the above hypoxia groups were put into the normobaric hypoxia chamber (9.5% O2) for 24 h while mice in normoxia group remained outside the chamber. After hypoxia exposure, lung water content (LWC), pulmonary vascular permeability, the protein content of bronchoalveolar lavage fluid (BALF), plasma total nitrate/nitrite (NOx) and endothelin-1 (ET-1) content, histological and ultra-microstructure analyses were performed. Expression of occludin was assayed by immunohistochemistry. KEY FINDINGS: In a hypoxic environment of 9.5% O2, mice treated with 100 mg/kg body wt CA had significantly lower LWC and BALF protein content than mice in the hypoxia vehicle group. Meanwhile, mice in CA group showed intact lung blood-gas-barrier, increased levels of plasma total NO, decreased levels of plasma ET-1 and upregulation of occludin expression. SIGNIFICANCE: CA exerts preventive effects against normobaric hypoxic pulmonary edema in mice, its mechanisms involved improving the integrity of the lung barrier, inhibiting oxidative stress and inflammation.

Severe beta blocker and calcium channel blocker overdose: Role of high dose insulin.

A 54-year-old female presented after taking an overdose of an unknown amount of hydrochlorothiazide, doxazocin, atenolol and amlodipine. She was initially refractory to treatment with conventional therapy (intravenous fluids, activated charcoal, glucagon 5 mg followed with glucagon drip, calcium gluconate 10%, and atropine). Furthermore, insulin at 4 U/kg was not effective in improving her hemodynamics. Shortly after high dose insulin was achieved with 10 U/kg, there was dramatic improvement in hemodynamics resulting in three of five vasopressors being weaned off in 8 h. She was subsequently off all vasopressors after six additional hours. The role of high dose insulin has been documented in prior cases, however it is generally recommended after other conventional therapies have failed. However, there are other reports that suggest it as initial therapy. Our patient failed conventional therapies and responded well only with maximum dose of insulin. Physicians should consider high dose insulin early in severe beta blocker or calcium channel blocker overdose for improvement in hemodynamics. This leads to early discontinuation of vasopressors. It is important that emergency physicians be aware of the beneficial effects of high dose insulin when initiated early as opposed to waiting for conventional therapy to fail; as these patients often present first to the emergency department. Early initiation in the emergency department can be beneficial in these patients.

Cardiovascular Abnormalities in Carbon Monoxide Poisoning.

Acute carbon monoxide (CO) poisoning is the most common cause of poisoning and poisoning-related death in the United States. It manifests as broad spectrum of symptoms ranging from mild headache, nausea, and fatigue to dizziness, syncope, coma, seizures resulting in cardiovascular collapse, respiratory failure, and death. Cardiovascular complications of CO poisoning has been well reported and include myocardial stunning, left ventricular dysfunction, pulmonary edema, and arrhythmias. Acute myocardial ischemia has also been reported from increased thrombogenicity due to CO poisoning. Myocardial toxicity from CO exposure is associated with increased short-term and long-term mortality. Carboxyhemoglobin (COHb) levels do not correlate well with the clinical severity of CO poisoning. Supplemental oxygen remains the cornerstone of therapy for CO poisoning. Hyperbaric oxygen therapy increases CO elimination and has been used with wide variability in patients with evidence of neurological and myocardial injury from CO poisoning, but its benefit in limiting or reversing cardiac injury is unknown. We present a comprehensive review of literature on cardiovascular manifestations of CO poisoning and propose a diagnostic algorithm for managing patients with CO poisoning.

Revascularization of atherosclerotic renal artery stenosis for chronic heart failure versus acute pulmonary oedema.

AIM: The aim of the study is to determine whether the apparent benefit of revascularization of renal artery stenosis for 'flash' pulmonary oedema extends to heart failure patients without a history of prior acute pulmonary oedema. METHODS: A prospective study of patients with renal artery stenosis and heart failure at a single centre between 1 January 1995 and 31 December 2010. Patients were divided into those with and without previous acute pulmonary oedema/decompensation. Survival analysis compared revascularization versus medical therapy in each group using Cox regression adjusted for age, estimated glomerular filtration rate, blood pressure and co-morbidities. RESULTS: There were 152 patients: 59% male, 36% diabetic, age 70 ± 9 years, estimated glomerular filtration rate 29 ± 17 mL/min per 1.73 m2 ; 52 had experienced previous acute pulmonary oedema (34%), whereas 100 had no previous acute pulmonary oedema (66%). The revascularization rate was 31% in both groups. For heart failure without previous acute pulmonary oedema, the hazard ratio for death after revascularization compared with medical therapy was 0.76 (0.58-0.99, P = 0.04). In heart failure with previous acute pulmonary enema, the hazard ratio was 0.73 (0.44-1.21, P = 0.22). For those without previous acute pulmonary oedema, the hazard ratio for heart failure hospitalization after revascularization compared with medical therapy was 1.00 (0.17-6.05, P = 1.00). In those with previous acute pulmonary oedema, it was 0.51 (0.08-3.30, P = 0.48). CONCLUSION: The benefit of revascularization in heart failure may extend beyond the current indication of acute pulmonary oedema. However, findings derive from an observational study.

Severe pulmonary edema following hyperbaric oxygen therapy for acute carbon monoxide poisoning: a case report and clinical experience.

PURPOSE: Pulmonary edema following hyperbaric oxygen (HBO2) therapy is a rare clinical phenomenon. This case report describes such a patient - a 56-year-old woman who suffered from severe pulmonary edema after HBO2 therapy for carbon monoxide (CO) poisoning. CASE: Patient experienced ecphysesis and dyspnea suddenly after HBO2 therapy (100% oxygen at 0.25 MPa, for 60 minutes with a five-minute air break and decompression at 0.01 MPa/minute). Post therapy her heart rate (HR), blood pressure (BP), respiratory rate (RR) and oxygen saturation (SO2) were 140 bpm, 60/40 mmHg, 38 bpm and 84%, respectively. Diagnoses of acute pulmonary edema and shock were made. Various treatments including antishock, tracheal intubation, mechanical ventilation for respiratory support, a diuretic, dexamethasone, asthma relief, and acidosis correction were administered. Pulmonary computed tomography (CT) indicated significant pulmonary edema. Due to active treatment, the patient showed gradual improvement. Pulmonary CT re-examination showed pulmonary edema markedly improved. At the two-year follow-up, the patient reported no abnormal mental or neurological symptoms. CONCLUSION: Acute pulmonary edema is rare but can lead to serious side effects of HBO2 therapy in patients with severe acute CO poisoning. This complication must be must considered when administering HBO2 therapy to patients with severe CO poisoning.

Carbonic anhydrase inhibitor attenuates ischemia-reperfusion induced acute lung injury.

Ischemia-reperfusion (IR)-induced acute lung injury (ALI) is implicated in several clinical conditions including lung transplantation, cardiopulmonary bypass surgery, re-expansion of collapsed lung from pneumothorax or pleural effusion and etc. IR-induced ALI remains a challenge in the current treatment. Carbonic anhydrase has important physiological function and influences on transport of CO2. Some investigators suggest that CO2 influences lung injury. Therefore, carbonic anhydrase should have the role in ALI. This study was undertaken to define the effect of a carbonic anhydrase inhibitor, acetazolamide (AZA), in IR-induced ALI, that was conducted in a rat model of isolated-perfused lung with 30 minutes of ischemia and 90 minutes of reperfusion. The animals were divided into six groups (n = 6 per group): sham, sham + AZA 200 mg/kg body weight (BW), IR, IR + AZA 100 mg/kg BW, IR + AZA 200 mg/kg BW and IR+ AZA 400 mg/kg BW. IR caused significant pulmonary micro-vascular hyper-permeability, pulmonary edema, pulmonary hypertension, neutrophilic sequestration, and an increase in the expression of pro-inflammatory cytokines. Increases in carbonic anhydrase expression and perfusate pCO2 levels were noted, while decreased Na-K-ATPase expression was noted after IR. Administration of 200mg/kg BW and 400mg/kg BW AZA significantly suppressed the expression of pro-inflammatory cytokines (TNF-α, IL-1, IL-6 and IL-17) and attenuated IR-induced lung injury, represented by decreases in pulmonary hyper-permeability, pulmonary edema, pulmonary hypertension and neutrophilic sequestration. AZA attenuated IR-induced lung injury, associated with decreases in carbonic anhydrase expression and pCO2 levels, as well as restoration of Na-K-ATPase expression.

Integrated Stress Response Mediates Epithelial Injury in Mechanical Ventilation.

Ventilator-induced lung injury (VILI) is a severe complication of mechanical ventilation that can lead to acute respiratory distress syndrome. VILI is characterized by damage to the epithelial barrier with subsequent pulmonary edema and profound hypoxia. Available lung-protective ventilator strategies offer only a modest benefit in preventing VILI because they cannot impede alveolar overdistension and concomitant epithelial barrier dysfunction in the inflamed lung regions. There are currently no effective biochemical therapies to mitigate injury to the alveolar epithelium. We hypothesize that alveolar stretch activates the integrated stress response (ISR) pathway and that the chemical inhibition of this pathway mitigates alveolar barrier disruption during stretch and mechanical ventilation. Using our established rat primary type I-like alveolar epithelial cell monolayer stretch model and in vivo rat mechanical ventilation that mimics the alveolar overdistension seen in acute respiratory distress syndrome, we studied epithelial responses to mechanical stress. Our studies revealed that the ISR signaling pathway is a key modulator of epithelial permeability. We show that prolonged epithelial stretch and injurious mechanical ventilation activate the ISR, leading to increased alveolar permeability, cell death, and proinflammatory signaling. Chemical inhibition of protein kinase RNA-like endoplasmic reticulum kinase, an upstream regulator of the pathway, resulted in decreased injury signaling and improved barrier function after prolonged cyclic stretch and injurious mechanical ventilation. Our results provide new evidence that therapeutic targeting of the ISR can mitigate VILI.

Effects of Propofol on Excitatory and Inhibitory Amino Acid Neurotransmitter Balance in Rats with Neurogenic Pulmonary Edema Induced by Subarachnoid Hemorrhage.

INTRODUCTION: Propofol exhibits neuroprotective effects mediated by the inhibition of excitatory amino acid (EAA) neurotransmitter release and potentiation of inhibitory amino acid (IAA) neurotransmitters. To our knowledge, this is the first study to investigate the effects of propofol on the EAA and IAA balance in neurogenic pulmonary edema (NPE). METHODS: Sixty male Wistar rats were randomized to Sham, NPE, Low-dose propofol, and High-dose propofol groups. NPE was induced via rapid injection of autologous blood (0.5 ml) into the cisterna magna. The Low- and High-dose propofol groups were pretreated with boluses of 2 and 5 mg kg(-1), respectively, prior to blood injection, followed by continuous propofol infusion at 6 and 15 mg kg(-1) h(-1), respectively. The mean arterial pressure (MAP), heart rate, intracranial pressure (ICP), peak inspiratory pressure (PIP), and arterial blood gases were continuously recorded. After 2 h, the lung wet-to-dry weight ratio, total protein concentration in the bronchoalveolar lavage fluid (BALF), brain water content, cortical EAA and IAA levels, chest X-ray, and histological staining of lung sections were evaluated. RESULTS: Blood injections into the cisterna magna induced NPE and hemodynamic changes. Propofol alleviated the increases in the MAP, ICP, and PIP, improved oxygenation and histopathological changes, ameliorated pulmonary and cerebral edema, increased the IAA brain levels, and decreased the ratio of Glu to γ-aminobutyric acid. CONCLUSIONS: The current findings suggest that propofol improves NPE likely via IAA accumulation and the regulation of EAA and IAA balance, which may represent an effective treatment for NPE.

The T cell-selective IL-2 mutant AIC284 mediates protection in a rat model of Multiple Sclerosis.

Targeting regulatory T cells (Treg cells) with interleukin-2 (IL-2) constitutes a novel therapeutic approach for autoimmunity. As anti-cancer therapy with IL-2 has revealed substantial toxicities a mutated human IL-2 molecule, termed AIC284 (formerly BAY 50-4798), has been developed to reduce these side effects. To assess whether AIC284 is efficacious in autoimmunity, we studied its therapeutic potential in an animal model for Multiple Sclerosis. Treatment of Lewis rats with AIC284 increased Treg cell numbers and protected the rats from Experimental Autoimmune Encephalomyelitis (EAE). AIC284 might, thus, also efficiently prevent progression of autoimmune diseases in humans.

The Effects of Portulaca oleracea on Hypoxia-Induced Pulmonary Edema in Mice.

Portulaca oleracea L. (PO) is known as "a vegetable for long life" due to its antioxidant, anti-inflammatory, and other pharmacological activities. However, the protective activity of the ethanol extract of PO (EEPO) against hypoxia-induced pulmonary edema has not been fully investigated. In this study, we exposed mice to a simulated altitude of 7000 meters for 0, 3, 6, 9, and 12 h to observe changes in the water content and transvascular leakage of the mouse lung. It was found that transvascular leakage increased to the maximum in the mouse lung after 6 h exposure to hypobaric hypoxia. Prophylactic administration of EEPO before hypoxic exposure markedly reduced the transvascular leakage and oxidative stress, and inhibited the upregulation of NF-kB in the mouse lung, as compared with the control group. In addition, EEPO significantly reduced the levels of proinflammatory cytokines and cell adhesion molecules in the lungs of mice, as compared with the hypoxia group. Our results show that EEPO can reduce initial transvascular leakage and pulmonary edema under hypobaric hypoxia conditions.

Ability of vitamin D receptor activator to prevent pulmonary congestion in advanced chronic kidney disease.

BACKGROUND: Vitamin D deficiency is common among patients with chronic kidney disease (CKD). However, the benefits of vitamin D supplementation versus vitamin D receptor activator (VDRA) administration have yet to be established. Recently, an association between activated vitamin D and cardiovascular factors was reported. To evaluate the benefits of VDRA in advanced CKD, we analyzed the association between VDRA administration and the prevalence of pulmonary congestion. METHODS: This retrospective, cross-sectional analysis included patients initiated on dialysis between October 2011 and September 2013 at 17 Japanese institutions. Data from 952 participants were analyzed using a multivariate logistic regression model and a linear regression model. We also analyzed subgroup data for groups classified by selection of peritoneal dialysis or hemodialysis. RESULTS: Of the 952 participants, 303 patients received VDRA. VDRA administration was associated with a low prevalence of pulmonary congestion in the multivariate logistic regression model (odds ratio [OR], 0.64; 95 % confidence interval [CI], 0.44-0.94; P = 0.02). There was no significant association between VDRA administration and systolic blood pressure, diastolic blood pressure, or pulse pressure. Subgroup analysis revealed a tendency that VDRA administration was associated with low prevalence of pulmonary congestion in both groups. CONCLUSIONS: In this study, VDRA administration was associated with a low prevalence of pulmonary congestion in patients initiated on dialysis. Appropriate VDRA administration may prevent pulmonary congestion.

Peri-partum cardiomyopathy in a pregnant woman at term revealed by acute pulmonary edema: what to do in front this catastrophic situation?

Peripartum cardiomyopathy is insufficient congestive heart occurring in the last month of pregnancy and 5 months after delivery, in the absence of preexisting heart disease and identified etiology. This heart disease is associated with echocardiography systolic dysfunction and left ventricular dilatation. Its incidence ranges from 1/3000 to 1/15000, depending on the region, including much higher in some African countries, it particularly concern women over 30 years, multiparous and multiple pregnancies. The pathogenesis remains unclear, the prognosis is closely related to the complete recovery of cardiac function. We report through the clinical case of a woman aged 33 years admitted to the ICU for acute pulmonary edema of sudden onset of a term pregnancy and what to do before this critical situation.