Non-cardiogenic pulmonary edema and life-threatening shock due to calcium channel blocker overdose and its management: a case report and a clinical review.

May 2013

Siddiqi TA, Hill J, Huckleberry Y, Parthasarathy S.

Source

Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, University of Arizona Medical Center, Tucson, Arizona.

Abstract

Calcium channel blockers (CCB) overdose can be life-threatening when manifest as catastrophic shock and non-cardiogenic pulmonary edema. We describe a case of massive overdose of multiple medications, including sustained-release verapamil that was resistant to conventional support. Initial treatment for CCB overdose is primarily supportive and includes fluid resuscitation. The mechanism of non-cardiogenic pulmonary edema is not well known and reported cases in the literature were successfully treated with mechanical ventilation. Circulatory shock may fail to respond to atropine, glucagon and calcium in severely poisoned patients, and vasopressors are usually required. Attempts to overcome calcium-channel antagonism with the use of supratherapeutic doses of calcium salts are clinically indicated to reverse hypotension and bradycardia. There is evidence that hyperinsulinemia-euglycemia (HIE) therapy is superior to other therapies for CCB poisoning, and the potential mechanism is thought to be the insulin-mediated active transport of glucose into the cells that counters the CCBinduced intra-cellular carbohydrate-deficient state. Conventional decontamination measures are ineffective in accelerating clearance of CCB. Experience with intravenous lipid emulsion for lipophilic drug overdose, such as verapamil, is limited but has been proposed as a rescue therapy with improvements in cardiac inotropy through intravascular sequestration of the lipophilic CCB.

Keywords

ARDS, Calcium Channel Blockers, Hyperinsulinemia-euglycemiatherapy, Intravenous lipid emulsion, Overdose, Pulmonary edema, Shock, Toxicology, Verapamil

PubMed

http://www.ncbi.nlm.nih.gov/pubmed/23674813

(or)   Respiratory Care

http://rc.rcjournal.com/content/early/2013/05/14/respcare.02244.short

Cardiogenic Acute Pulmonary Edema

Image from the article:

Cardiogenic Acute Pulmonary Edema – Causes, Symptoms, Diagnosis And Treatment





From:  Heart Failure and Your Lungs



Medical Exhibits

Severe hypertension and pulmonary edema associated with systemic absorption of topical phenylephrine in a child during retinal surgery.

2012

Abdelhalim AA, Mostafa M, Abdulmomen A, Othman EA.

Source

Department of Anesthesia, King Abdul Aziz University Hospital, King Saud University, Riyadh, Saudi Arabia.

Abstract

Topical phenylephrine solutions are widely used in eye procedures to promote pupil dilation without cycloplegia. We report a case of intraoperative severe hypertension and acute pulmonary edema occurring in a child during retinal surgery after possible systemic absorption of topical phenylephrine eyedrops. Our objective is to discuss the proper treatment and preventive strategies for such a complication. A 4-year-old, male patient, 18.4 kg in weight, physical status ASA I was admitted for right retinal detachment surgery. Anesthesia was induced with sevoflurane in oxygen, followed by glycopyrrolate (5.0 μg/kg), propofol 25 mg, fentanyl 50 μg and cisatracurium 0.15 mg/kg given intravenously. Anesthesia was maintained with sevoflurane 2-2.5% in a mixture of nitrous oxide and oxygen (60%:40%). After incision, two drops of 10% aqueous phenylephrine were administered topically by the surgeon to the right eye for further pupil dilation. Few minutes later, the noninvasive blood pressure rose to 220/120 mmHg and the heart rate increased to 140 beats/min. Oxygen saturation (SpO(2)) dropped from 99% (with an inspired oxygen concentration (FiO(2)) of 0.4) to 82%. Auscultation revealed crepitations throughout the chest and a blood-stained frothy fluid was aspirated from the trachea with possible development of acute pulmonary edema. Hydralazine (5 mg) and furosemide (10 mg) were administered intravenously. Seven minutes later, the blood pressure returned to normal and the SpO(2) increased to 92% on FiO(2) of 1.0, with decreased intratracheal secretions. After approximately 20 minutes, the SpO(2) had improved to 99%, with a FiO(2) of 1.0 and the blood pressure was 109/63 mmHg and heart rate was 121 beats/min. The FiO(2) gradually reduced back to 0.4 over 30 min with no further desaturation. The patient was discharged from the post anesthesia care unit 5 h after surgery with adequate spontaneous breathing, SpO(2) 99% on room air, normal blood pressure and pulmonary auscultation. Anesthesiologists and ophthalmologists should be aware of the possible cardiovascular side-effects of topical phenylephrine, and it should be used cautiously with appropriate intraoperative monitoring of hemodynamic variables. Moreover, preventive strategies to minimize systemic absorption of the drug should be taken.

PubMed

A Human Disease Model of Drug Toxicity-Induced Pulmonary Edema in a Lung-on-a-Chip Microdevice.

Nov 2012

Huh D, Leslie DC, Matthews BD, Fraser JP, Jurek S, Hamilton GA, Thorneloe KS, McAlexander MA, Ingber DE.

Source

Wyss Institute for Biologically Inspired Engineering at Harvard University, Boston, MA 02115, USA.

Abstract

Preclinical drug development studies currently rely on costly and time-consuming animal testing because existing cell culture models fail to recapitulate complex, organ-level disease processes in humans. We provide the proof of principle for using a biomimetic microdevice that reconstitutes organ-level lung functions to create a human disease model-on-a-chip that mimics pulmonary edema. The microfluidic device, which reconstitutes the alveolar-capillary interface of the human lung, consists of channels lined by closely apposed layers of human pulmonary epithelial and endothelial cells that experience air and fluid flow, as well as cyclic mechanical strain to mimic normal breathing motions. This device was used to reproduce drug toxicity-induced pulmonary edema observed in human cancer patients treated with interleukin-2 (IL-2) at similar doses and over the same time frame. Studies using this on-chip disease model revealed that mechanical forces associated with physiological breathing motions play a crucial role in the development of increased vascular leakage that leads to pulmonary edema, and that circulating immune cells are not required for the development of this disease. These studies also led to identification of potential new therapeutics, including angiopoietin-1 (Ang-1) and a new transient receptor potential vanilloid 4 (TRPV4) ion channel inhibitor (GSK2193874), which might prevent this life-threatening toxicity of IL-2 in the future.

Science Translocational Medicine

An Orally Active TRPV4 Channel Blocker Prevents and Resolves Pulmonary Edema Induced by Heart Failure.

Nov 2012

Thorneloe KS, Cheung M, Bao W, Alsaid H, Lenhard S, Jian MY, Costell M, Maniscalco-Hauk K, Krawiec JA, Olzinski A,Gordon E, Lozinskaya I, Elefante L, Qin P, Matasic DS, James C, Tunstead J, Donovan B, Kallal L, Waszkiewicz A, Vaidya K, Davenport EA, Larkin J, Burgert M, Casillas LN, Marquis RW, Ye G, Eidam HS, Goodman KB, Toomey JR, Roethke TJ,Jucker BM, Schnackenberg CG, Townsley MI, Lepore JJ, Willette RN.

Source

Heart Failure Discovery Performance Unit, Metabolic Pathways and Cardiovascular Therapy Area Unit, GlaxoSmithKline, 709 Swedeland Road, King of Prussia, PA 19406, USA.

Abstract

Pulmonary edema resulting from high pulmonary venous pressure (PVP) is a major cause of morbidity and mortality in heart failure (HF) patients, but current treatment options demonstrate substantial limitations. Recent evidence from rodent lungs suggests that PVP-induced edema is driven by activation of pulmonary capillary endothelial transient receptor potential vanilloid 4 (TRPV4) channels. To examine the therapeutic potential of this mechanism, we evaluated TRPV4 expression in human congestive HF lungs and developed small-molecule TRPV4 channel blockers for testing in animal models of HF. TRPV4 immunolabeling of human lung sections demonstrated expression of TRPV4 in the pulmonary vasculature that was enhanced in sections from HF patients compared to controls. GSK2193874 was identified as a selective, orally active TRPV4 blocker that inhibits Ca(2+) influx through recombinant TRPV4 channels and native endothelial TRPV4 currents. In isolated rodent and canine lungs, TRPV4 blockade prevented the increased vascular permeability and resultant pulmonary edemaassociated with elevated PVP. 

Furthermore, in both acute and chronic HF models, GSK2193874 pretreatment inhibited the formation of pulmonary edema and enhanced arterial oxygenation. Finally, GSK2193874 treatment resolved pulmonary edemaalready established by myocardial infarction in mice. These findings identify a crucial role for TRPV4 in the formation of HF-induced pulmonary edema and suggest that TRPV4 blockade is a potential therapeutic strategy for HF patients.

PubMed-Science Translocational Medicine

Negative pressure pulmonary edema with laryngeal mask airway use: Recognition, pathophysiology and treatment modalities

Negative pressure pulmonary edema with laryngeal mask airway use: Recognition, pathophysiology and treatment modalities

2012
Rashmi Vandse¹, Deven S Kothari¹, Ravi S Tripathi¹, Luis Lopez¹, Stanislaw P A Stawicki², Thomas J Papadimos^1
1 Department of Anesthesiology, The Ohio State University Medical Center, Columbus, Ohio, USA
² Department of Surgery, The Ohio State University Medical Center, Columbus, Ohio, USA

Correspondence Address:
Thomas J Papadimos
Department of Anesthesiology, Room N431, 410 West Tenth Avenue, Columbus, Ohio 43210
USA

Negative pressure pulmonary edema (NPPE) following the use of the laryngeal mask airway (LMA) is an uncommon and under-reported event. We present a case of a 58-year-old male, who developed NPPE following LMA use. After biting vigorously on his LMA, the patient developed stridor upon emergence, with concurrent appearance of blood-tinged, frothy sputum and pulmonary edema. He subsequently required three days of mechanical ventilation. After discontinuation of mechanical ventilation the patient continued to require additional pulmonary support using continuous positive airway pressure, with a full facemask, to correct the persistent hypoxemia. His roentgenographic findings demonstrated an accelerated improvement with judicious administration of intravenous furosemide.

International Jounral of Critical Illness & Injury Science

Neurogenic pulmonary edema following intracranial coil embolization for subarachnoid hemorrhage -A case report.

Oct 2012

Kim JE, Park JH, Lee SH, Lee Y.

Source

Department of Anesthesiology and Pain Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea.

Abstract

Neurogenic pulmonary edema (NPE) is a well-known complication of acute central neurologic injury, particularly aneurysmal subarachnoid hemorrhage. Both increased intracranial pressure and severe over-activation of the sympathetic nervous system seem to be pathogenetic for the onset of NPE. Although intracranial endovascular therapy is minimally invasive, it may affect brain stem regions and result in sympathetic activation. We now report the case of a 70-year-old woman who suddenly developed pulmonary edema during coil embolization of a ruptured aneurysm. During the intervention, oxygen saturation declined suddenly and a chest radiograph revealed pulmonary edema. The delayed appearance of NPE in this patient implies a risk for sympathetically mediated NPE during endovascular therapy.

PubMed

Effective Treatment of Edema and Endothelial Barrier Dysfunction With Imatinib.

Oct 2012

Aman J, van Bezu J, Damanafshan A, Huveneers S, Eringa EC, Vogel SM, Groeneveld AB, Vonk Noordegraaf A, van Hinsbergh VW, van Nieuw Amerongen GP.

Source

1 Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, the Netherlands;

Abstract

BACKGROUND:

Tissue edema and endothelial barrier dysfunction as observed in sepsis and acute lung injury carry high morbidity and mortality, but currently lack specific therapy. In a recent case-report, we described fast resolution of pulmonary edema upon treatment with the tyrosine kinase inhibitor imatinib through an unknown mechanism. Here, we explored the effect of imatinib on endothelial barrier dysfunction and edema formation.

METHODS AND RESULTS:

We evaluated the effect of imatinib on endothelial barrier function in vitro and in vivo. In human macro- and microvascular endothelial monolayers, imatinib attenuated endothelial barrier dysfunction induced by thrombin and histamine. siRNA knock-downs of the imatinib-sensitive kinases revealed that imatinib attenuates endothelial barrier dysfunction via inhibition of Abl-Related Gene kinase (Arg/Abl2), a previously unknown mediator of endothelial barrier dysfunction. Indeed, Arg was activated by endothelial stimulation with thrombin, histamine and VEGF. Imatinib limited Arg-mediated endothelial barrier dysfunction by enhancing Rac1 activity and enforcing adhesion of endothelial cells to the extra-cellular matrix. Using mouse models of vascular leakage as proof-of-concept, we found that pretreatment with imatinib protected against VEGF-induced vascular leakage in the skin, and effectively prevented edema formation in the lungs. In a murine model of sepsis imatinib treatment (6h and 18h after induction of sepsis) attenuated vascular leakage in the kidneys and the lungs (24h after induction of sepsis).

CONCLUSIONS:

Thus, imatinib prevents endothelial barrier dysfunction and edema formation via inhibition of Arg. These findings identify imatinib as a promising approach to permeability edema, and indicate Arg as novel target for edema treatment.

AHA Journals CIRCULATION

Nitric Oxide-Associated Pulmonary Edema in Children With Pulmonary Venous Hypertension.

Oct 2012

Baird JS, Havalad V, Aponte-Patel L, Ravindranath TM, October TW, Starc TJ, Smerling AJ.

Source

College of Physicians and Surgeons, Children's Hospital of New York-Presbyterian, Columbia University, 3959 Broadway, CHN 10-24, New York, NY, 10032, USA, jsb106@columbia.edu.

Abstract

Nitric oxide (NO)-associated pulmonary edema is rarely reported in children; in adults, it is often associated with left-sided heart failure. We report a case series of children with NO-associated pulmonary edema, which was defined as new multilobar alveolar infiltrates and worsening hypoxemia within 24 h of initiation or escalation of NO and radiologic or clinical improvement after NO discontinuation. We identified six patients (0.4-4 years old) with ten episodes of NO-associated pulmonary edema. Diagnoses included atrioventricular canal defect with mitral valve disease (n = 2), pulmonary atresia and major aorta-pulmonary collateral arteries (n = 2), total anomalous pulmonary venous return (n = 1), and pulmonary veno-occlusive disease (n = 1). All patients had evidence of pulmonary venous hypertension, and two had mitral valve disease resulting in clinical evidence of left-sided heart failure. Pulmonary edema improved or resolved within 24 h of discontinuing NO. At cardiac catheterization, mean left atrial pressure was <15 artery="artery" disease="disease" in="in" mitral="mitral" mmhg="mmhg" nbsp="nbsp" none="none" occlusion="occlusion" of="of" patients="patients" pressure="pressure" pulmonary="pulmonary" three="three" valve="valve" was="was" whereas="whereas" with="with">15 mmHg in two of five patients. In conclusion, we describe six young children with NO-associated pulmonary edema and pulmonary venous hypertension. Only two of these children had left-sided heart failure: Left atrial pressure as well as pulmonary artery occlusion pressure may not be helpful in identifying children at risk for NO-associated pulmonary edema.

Springerlink

Can Running a Marathon Cause Pulmonary Edema?

A study presented at the European Respiratory Society's Annual Congress revealed that running a marathon has been linked to pulmonary edema. The researchers studied 26 people before and after a race. They found that 50 percent of the runners exhibited signs of pulmonary edema. Further research is planned to explain this connection.

Pulmonary Edema

Pulmonary edema "is an abnormal buildup of fluid" in the lungs and can lead to complete respiratory failure. Although it is often linked to congestive heart failure, this is not the only cause of the edema. Pulmonary edema can also occur because of trauma, infections, kidney failure and high altitudes. Some of the symptoms include coughing, problems breathing, paleness and sweating. If untreated, it can lead to cardiac arrest or death.

The Connection between Marathons and Pulmonary Edema

Researchers have debated the connection between marathons and pulmonary edema in the past and often disagreed about the link. However, the study presented at the European Respiratory Society's Annual Congress clearly showed a link between them. The 26 runners included in the research exhibited pulmonary edema on chest radiographs taken after the race. The study found 50 percent had the edema, and women were affected more than men. Additionally, they discovered that there was "no relation between marathon time" and the edema, so runners who were quicker were not more or less likely to be affected.

A Contradiction with Other Research

Recent research has recommended that older marathon runners can safely continue participating in the sport without increased risk. This study from the University of Manitoba in Canada seems to contrast with the findings at the European Respiratory Society's Annual Congress. Pulmonary edema is actually more common in older individuals, yet the Canadian study found that runners over the age of 50 can safely continue with marathons.

The connection between marathons and pulmonary edema must continue to be studied. The limited scope of previous research and small number of participants makes conclusions difficult. It has been an accepted fact that marathons place strain on the hearts of even the most experienced and young runners. However, pulmonary edema has been neglected in many studies.

More from this contributor:

Why Athletes Need to Be Aware of the Concussion Threshold

Erythropoietin Abuse Among Athletes Can Lead to Vascular Problems

5 Simple Exercise Tips to Do at Your Computer

Lana has a B.S. degree in Biology and Chemistry. She is an avid athlete, youth coach and follows several sports. Follow @Lana_Bandoim on Twitter.

Sport Yahoo

Flash Pulmonary Edema in Multiple Sclerosis.

Sept 2012

Plummer C, Campagnaro R.

Source

Centre for Neuroscience and Neurological Research, St Vincent's Hospital, Fitzroy, Melbourne, Victoria, Australia.

Abstract

BACKGROUND:

Neurogenic pulmonary edema (NPE) occurs in the setting of an acute neurological insult and in the absence of a primary cardiopulmonary cause. No unifying theory on NPE pathogenesis exists. NPE triggered by a discrete neurological lesion is rare, but such cases offer valuable insight into NPE pathogenesis.

OBJECTIVE:

To describe an unusual and instructive case of NPE in multiple sclerosis.

CASE REPORT:

A young woman with multiple sclerosis presented to the Emergency Department in acute respiratory failure. She was cyanotic centrally, hypertensive, and tachycardic. The chest X-ray study suggested pulmonary edema. She required non-invasive mechanical ventilation for 12 h. Echocardiography revealed left ventricular hypokinesis. The asymmetrical pulmonary infiltrate raised the suspicion of pneumonia; she was given intravenous antibiotics. By 36 h, she had persistent dyspnea, paroxysmal tachycardia, nausea, and facial flushing; carcinoid syndrome was excluded. By 48 h, she had facial numbness and ataxia. Magnetic resonance imaging (MRI) revealed a demyelinating lesion at the rostromedial medulla. Her symptoms promptly resolved with intravenous steroids, as did the perilesional edema on follow-up MRI.

CONCLUSION:

Life-threatening pulmonary edema can complicate medullary demyelination. Lack of awareness of this diagnostic possibility and an asymmetrical pulmonary infiltrate culminated in diagnostic delay in this case. The case provides clinico-radiological evidence of the pathogenic link between medullary lesions and NPE. The pathogenesis is likely to rely on lesion involvement of the nucleus tractus solitarius or its immediate pathways. Non-uniform vasoconstriction of the pulmonary arterial bed might account for the other peculiarity of this case: the asymmetrical pulmonary infiltrate. Timely diagnosis of NPE is essential because the condition is best managed by nullifying the "neurogenic" trigger.

PubMed

High Altitude Pulmonary Edema and Augmented Vasoreactivity in Highlanders.

Interactions among Vascular-Tone Modulators Contribute to High Altitude Pulmonary Edema and Augmented Vasoreactivity in Highlanders.

2012

Ali Z, Mishra A, Kumar R, Alam P, Pandey P, Ram R, Thinlas T, Mohammad G, Pasha MA.

Source

Institute of Genomics and Integrative Biology, Delhi, India ; Department of Biotechnology, University of Pune, Pune, India.

Abstract

BACKGROUND: The interactions among various biomarkers remained unexplored under the stressful environment of high-altitude. Present study evaluated interactions among biomarkers to study susceptibility for high altitude pulmonary edema(HAPE) in HAPE-patients (HAPE-p) and adaptation in highland natives (HLs); both in comparison to HAPE-free sojourners (HAPE-f).

METHODOLOGY/PRINCIPAL FINDINGS:

All the subjects were recruited at 3500 m. We measured clinical parameters, biochemical levels in plasma and gene expression using RNA from blood; analyzed various correlations between and among the clinical parameters, especially arterial oxygen saturation (SaO(2)) and mean arterial pressure (MAP) and biochemical parameters like, asymmetric dimethylarginine (ADMA), serotonin (5-HT), 8-iso-prostaglandin F2α (8-isoPGF2α), endothelin-1 (ET-1), plasma renin activity (PRA), plasma aldosterone concentration (PAC), superoxide dismutase (SOD) and nitric oxide (NO) in HAPE-p, HAPE-f and HLs. ADMA, 5-HT, 8-isoPGF2α, ET-1 levels, and PAC were significantly higher and SOD activity non-significantly lower in HLs than HAPE-f. The expression of respective genes differed in the three groups. In the correlations, SaO(2) inversely correlated with ADMA, 5-HT and 8-isoPGF2α and positively with SOD in HAPE-MAP correlated positively with 5-HT and 8-isoPGF2α in HAPE-p and HLs (p≤0.004). A strong positive correlation was observed between ADMA and 5-HT, 5-HT and 8-isoPGF2α (p≤0.001), whereas inverse correlation of SOD with ET-1 in HAPE-p and HLs (p≤0.004), with 5-HT and 8-isoPGF2α in HAPE-p (p = 0.01) and with 5-HT in HLs (p = 0.05).

The expression of respective genes differed in the three groups. In the correlations, SaO(2) inversely correlated with ADMA, 5-HT and 8-isoPGF2α and positively with SOD in HAPE-p (p≤0.009). MAP correlated positively with 5-HT and 8-isoPGF2α in HAPE-p and HLs (p≤0.004). A strong positive correlation was observed between ADMA and 5-HT, 5-HT and 8-isoPGF2α (p≤0.001), whereas inverse correlation of SOD with ET-1 in HAPE-p and HLs (p≤0.004), with 5-HT and 8-isoPGF2α in HAPE-p (p = 0.01) and with 5-HT in HLs (p = 0.05).

CONCLUSIONS/SIGNIFICANCE:

The interactions among these markers confer enhanced vascular activity in HLs and HAPE in sojourners.

PLOSone

An unusual transudative pleural effusion succeeded by pulmonary and brain edema and death.

2012

Mortazavimoghaddam SG, Riasi HR.

Source

Pulmonary Ward, Vali-e-Asr Hospital, Birjand University of Medical Sciences, Birjand 9718766995, Iran.

Abstract

Here we report a 22-year old woman with massive and bilateral transudative effusion succeeded by pulmonary edema and brain edema and death. Investigations for systemic disorders were negative. Exacerbation of dyspnea after intravenous fluid infusion was a main problem. As effusion was refractory to medical treatment, the patient was referred for surgical pleurodesis and bilateral surgical pleurodesis were done separately. Postsurgically, dyspnea exacerbation occurred after each common cold infection. Vertigo and high intracranial pressure were also a problem postsurgically. CSF pressure was 225 mm/H(2)O. Therapeutic lumbar puncture was done in two sequential weeks, and the patient was on acetazolamide 250 mg/trivise a day. Despite the medical treatment, progressive dyspnea, headache, and high intracranial pressure followed by death nine months after pleurodesis. As there is a gradient of pressure between pleura and CSF, after pleurodesis brain edema must be a consequence of inversing this gradient. In conclusion, when there are any abnormalities about fluid volume or pressure in any of these cavities, we have to study other cavities.

PubMed

Naloxone-induced pulmonary edema : Case report with review of the literature and critical evaluation

Feb 2012

.

[Article in German]

Lassen CL, Zink W, Wiese CH, Graf BM, Wiesenack C.

Source

Klinik für Anästhesiologie, Universitätsklinikum Regensburg, Regensburg, Deutschland, christoph.lassen@klinik.uni-regensburg.de.

Abstract

A case of pulmonary edema after the administration of naloxone for laparoscopic splenectomy is reported. Previous reports of naloxone-induced pulmonary edema are listed and reviewed. The clinical course is compared to other forms of non-cardiogenic pulmonary edema. Uncertainty remains about the underlying pathophysiological process and the true impact of naloxone on the development of pulmonary edema.

PubMed