Aerosolized iloprost for postoperative pulmonary hypertensive crisis in children with congenital heart disease

Limsuwan, Alisa; Wanitkul, Suthep; Khosithset, Anant; Attanavanich, Sukasom; Samankatiwat, Piya

doi:10.1016/j.ijcard.2007.08.084

Cited by 70 publications

(74 citation statements)

References 25 publications

(31 reference statements)

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“…Perioperative measures may be utilised to prevent rapid haemodynamic deterioration in the setting of right ventricular failure (RVF). These include the use of pulmonary vasodilator therapies to minimise right ventricular afterload [19,23,24], the avoidance of excessive fluid administration that may overload the right ventricle, maintaining appropriate systemic perfusion pressure for adequate coronary perfusion and enhancing myocardial contractility [25].…”

mentioning

confidence: 99%

Noncardiothoracic nonobstetric surgery in mild-to-moderate pulmonary hypertension

Price¹,

Montani²,

Jaïs³

et al. 2009

European Respiratory Journal

116

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The anaesthetic management and follow-up of well-characterised patients with pulmonary arterial hypertension presenting for noncardiothoracic nonobstetric surgery has rarely been described.The details of consecutive patients and perioperative complications during the period January 2000 to December 2007 were reviewed. Repeat procedures in duplicate patients were excluded. Longer term outcomes included New York Heart Association (NYHA) functional class, 6-min walking distance and invasive haemodynamics.A total of 28 patients were identified as having undergone major (57%) or minor surgery under general (50%) and regional anaesthesia. At the time of surgery, 75% of patients were in NYHA functional class I-II. Perioperative deaths occurred in 7%. Perioperative complications, all related to pulmonary hypertension, occurred in 29% of all patients and in 17% of those with no deaths during scheduled procedures. Most (n511, 92%) of the complications occurred in the first 48 h following surgery. In emergencies (n54), perioperative complication and death rates were higher (100 and 50%, respectively; p,0.005). Risk factors for complications were greater for emergency surgery (p,0.001), major surgery (p50.008) and a long operative time (193 versus 112 min; p50.003). No significant clinical or haemodynamic deterioration was seen in survivors at 3-6 or 12 months of post-operative follow-up.Despite optimal management in this mostly nonsevere pulmonary hypertension population, perioperative complications were common, although survivors remained stable. Emergency procedures, major surgery and long operations were associated with increased risk.

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mentioning

confidence: 99%

Noncardiothoracic nonobstetric surgery in mild-to-moderate pulmonary hypertension

Price¹,

Montani²,

Jaïs³

et al. 2009

European Respiratory Journal

116

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“…Limsuwan ve ark. (13) da, pulmoner hipertansif kriz tedavisinde iloprostun etkin olduğunu saptamıştır. Biz de, hastamızın tedavisinde bu adiditif etkiden yararlanmak amacıyla iloprost ve sildenafili birlikte kullandık.…”

Section: Discussionunclassified

“…Yenidoğanlarda ve bebeklerde pulmoner vasküler yatağın manüplasyonu; PaCO 2 , pH, PaO 2 , PaO 2 ve ventilatör mekaniklerinin manüplasyonu ile mümkün olabilmektedir (13)(14)(15) .…”

Section: Discussionunclassified

Pulmonary Hypertension Crisis in Pediatric Patient Undergoing Congenital Heart Surgery: Case Report

Altun¹,

Balci²,

Özker³

et al. 2014

GKDA Derg

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“…The advantages of an inhaled agent include improved selectivity for the pulmonary vascular bed, which is superior for patients with acute pulmonary hypertensive crisis with hemodynamic compromise and low cardiac output. This approach may improve ventilation/perfusion mismatch and oxygenation, and successful use has been reported in pediatric populations, including those with persistent pulmonary hypertension of the newborn and post cardiopulmonary bypass [85][86][87][88][89][90][91][92], and those refractory to inhaled nitric oxide or sildenafil [93,94]. Acute bronchoconstriction is a potential adverse event and compliance can be poor due to the need for frequent aerosol administrations, up to 8-12 times daily [11].…”

Section: Prostanoidsmentioning

confidence: 99%

Pharmacotherapy of Pulmonary Hypertension

2013

Handbook of Experimental Pharmacology

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Pulmonary arterial hypertension is a serious disease with significant morbidity and mortality. While it can occur idiopathically, it is more commonly associated with other cardiac or lung diseases. While most of the available therapies were tested in adult populations, and most therapies in children remain off-label, new reports and randomized trials are emerging that inform the treatment of pediatric populations. This review discusses currently available therapies for pediatric pulmonary hypertension, their biologic rationales, and evidence for their clinical effectiveness. KeywordsPulmonary hypertension; Pulmonary vasculature; Vasodilator; Nitric Oxide; Phosphodiesterase; Prostacyclin; Endothelin NORMAL PULMONARY VASCULAR TRANSITIONDuring fetal life, the placenta serves as the organ of gas exchange, and the fetal circulation uses a series of adaptive mechanisms to maximize delivery of oxygen to metabolically active organs such as the brain, gut and kidney. The most highly oxygenated blood enters the fetus via the umbilical vein. To efficiently direct oxygenated blood to the systemic circulation and minimize oxygen loss, almost 90% of fetal blood flow is diverted past the lungs through anatomic shunts through the foramen ovale and the ductus arteriosus. While the lung rapidly grows its network of small pulmonary arteries during the second half of gestation [1], blood flow in the pulmonary circulation remains highly restricted by hypoxic pulmonary vasoconstriction of small pulmonary arteries, which is reversed at birth by the sudden increase in lung oxygenation when the newborn takes his or her first breath. After birth, the first few breaths induce a rapid decrease in pulmonary vascular resistance and increase in pulmonary vascular flow in response to lung expansion, increased oxygen tension, and increased pH. Pulmonary artery pressure and vascular resistance decrease more slowly, with pulmonary arterial pressure reaching its nadir ~2-3 weeks after birth. However, the responsiveness to hypoxia is retained into adulthood, and pulmonary hypertension can be easily triggered in the newborn period by hypoxic lung disease, apnea, or other causes.© 2012 Elsevier Inc. All rights reserved. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptPediatr Clin North Am. Author manuscript; available in PMC 2013 October 01. DEFINITION AND CLASSIFICATION OF PEDIATRIC PULMONARY HYPERTENSIONPulmonary hypertension is necessary to support gas exchange in the fetus, but if pulmonary arterial pressure is elevated after birth or during infancy or childhood,...

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Aerosolized iloprost for postoperative pulmonary hypertensive crisis in children with congenital heart disease

Cited by 70 publications

References 25 publications

Noncardiothoracic nonobstetric surgery in mild-to-moderate pulmonary hypertension

Noncardiothoracic nonobstetric surgery in mild-to-moderate pulmonary hypertension

Pulmonary Hypertension Crisis in Pediatric Patient Undergoing Congenital Heart Surgery: Case Report

Pharmacotherapy of Pulmonary Hypertension

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