Life-threatening Pulmonary Edema Research Articles

Can acute high-altitude sickness be predicted in advance?

In high-altitude environments, the oxygen andair density are decreased, and the temperature and humidity are low. When individuals enter high-altitude areas, they are prone to suffering from acute mountain sickness (AMS) because they cannot tolerate hypoxia. Headache, fatigue, dizziness, and gastrointestinal reactions are the main symptoms of AMS. When these symptoms cannot be effectively alleviated, they can progress to life-threatening high-altitude pulmonary edema or high-altitude cerebral edema. If the risk of AMS can be effectively assessed before people enter high-altitude areas, then the high-risk population can be promptly discouraged from entering the area, or drug intervention can be established in advance to prevent AMS occurrence and avoid serious outcomes. This article reviews recent studies related to the early-warning biological indicators of AMS to provide a new perspective on the prevention of AMS.

Application of primary sutureless repair for obstructed total anomalous of pulmonary venous connection at the Vietnam National Children's Hospital

Objectives: This study evaluates the results of applying primary sutureless technique in surgical repair of total anomalous pulmonary venous connection at Children Heart Center, Vietnam National Children's Hospital. Methods: A retrospective study was conducted to evaluate the short-term outcomes of primary sutureless repair for all patients diagnosed with obstructed total anomalous venous connection (TAPVC) from July 2015 to December 2016. Results: There were 25 patients undergoing primary sutureless repair during the study period. The mean age and the mean weight are 77.00 ± 23.26 days and 3.93 ± 1.16 kg, respectively. There were 19/25 (76%) cases with preoperative respiratory failure with 14 cases (56%) requiring mechanical ventilation before surgery, of which 9 patients (36%) had life-threatening acute pulmonary edema from before emergency surgical repair. There were 17 cases admitted to the hospital with cardiogenic shock. Evaluation of transthoracic echocardiography showed 15 cases of supracardiac TAPVC, 5 cases of infracardiac TAPVC, 2 cases of intracardiac, 2 cases of mixed, and 1 case of partial TAPVC. The mean aortic cross-clamp time was 65.40 ± 23.34 minutes, the average cardiopulmonary bypass time was 119.72 ± 34.85 minutes, the mean surgery time was 200.04 ± 39.42 minutes. 9 cases underwent circulatory arrest and 7 cases underwent low-flow bypass during surgery. 3 patients died in the postoperative period, of which 2 from septic shock and multi-organ failure, 1 patient from respiratory failure after extubation due to laryngomalacia. The reoperation rate was 2/25 as a consequence of recurrent pulmonary vein stenosis. Conclusions: The primary sutureless repair for obstructed anomalous pulmonary venous connection is safe and favorable. Long-term outcomes follow-up are essentially required.

Might life-threatening acute pulmonary edema occur after using recombinant tissue plasminogen activator? A case report

BackgroundRecombinant tissue plasminogen activator (rt-pa) is the first-line drug for the treatment of acute ischemic stroke, and can lead to some complications.There were rare reports of death due to acute pulmonary edema during rt-pa thrombolysis treatment.Case presentationThis study reports a 30-year-old man was diagnosed with acute ischemic stroke and underwent rt-pa thrombolytic therapy. Finally he died despite active rescue.ConclusionsThe autopsy revealed that he died of acute pulmonary edema. This case suggests that it is necessary to pay close attention to the changes of vital signs during thrombolysis and be aware of possibility of pulmonary edema during thrombolysis.

The role of cardiopulmonary exercise test in identifying pulmonary veno-occlusive disease

Pulmonary veno-occlusive disease (PVOD) is a rare form of pulmonary hypertension that shares some clinical and haemodynamic features with idiopathic pulmonary arterial hypertension (PAH). However, suspicion of PVOD is crucial, considering that PAH-specific treatment may precipitate life-threatening pulmonary oedema and lung transplant should be considered from diagnosis [1, 2]. Cardiopulmonary exercise tests provide additional data for the noninvasive diagnosis of pulmonary veno-occlusive disease <https://bit.ly/3p6Dzc5>

Pulmonary veno-occlusive disease: a rare and enigmatic cause of pulmonary hypertension\u2014a case report

BackgroundPulmonary veno-occlusive disease (PVOD) is a rare form of pulmonary hypertension characterized by remodelling of the pulmonary venules. PVOD and pulmonary arterial hypertension share similar clinical presentation. It is important to differentiate between these two conditions as PVOD carries a worse prognosis and life-threatening pulmonary oedema may occur following the initiation of conventional therapy.Case presentationWe are reporting a case of pulmonary hypertension in a middle-aged lady who presented with hemoptysis and features of right heart failure. After extensive work up, no definite aetiology of pulmonary hypertension could be found out. Standard therapy did not cause any symptomatic improvement. After right heart catheterization, we got pre capillary pulmonary hypertension and along with typical findings in HRCT scan of thorax we established PVOD. We did not try lung biopsy as the procedure often lands up with complications. As we could not arrange for lung transplant we eventually lost the patient.ConclusionsHigh suspicion and thorough systematic evaluation helped us to diagnose PVOD in this case. Thus, early diagnosis should be the primary aim in suspected cases of PVOD so that we can prepare for lung transplant at the earliest.

Transfusion-associated circulatory overload (TACO): Significance of appropriate pre-transfusion risk assessment to prevent fatal health outcomes.

Madam, Transfusion of blood products is a life rescuing medical intermediation; however, associated adverse transfusion reactions are major pitfalls. Transfusion-associated circulatory overload (TACO) is life-threatening pulmonary oedema that develops secondary to volume overload. Underlying precipitating factors include ages &gt;60 years or &lt;3 years, low body mass index (BMI), rapid transfusion rate and pre-existing volume overload conditions such as heart disease, renal failure, lung disease or low albumin levels. Sign and Symptoms include dyspnoea, tachypnoea, tachycardia, hypoxia, raised jugular venous pressure, broad pulse pressure and hypertension, that appears during or either six hours posttransfusion [1]. TACO should be discriminated from transfusion-related acute lung injury (TRALI) by high jugular venous pressure, pulmonary arterial pressure to &gt;18mmHg, hypertension, brain natriuretic peptide levels (&gt;1200pg/ml) and response to diuretics. Management of TACO includes immediate discontinuation of transfusion, diuretics, supplementary oxygen, and assisted ventilation if indicated [2]. Serious Hazards of Transfusion (SHOT) in 2018 reported TACO as the most typical reason for transfusion-related deaths. Over the period of 11 years (2007-2018), overall cases raised from six to one hundred and ten, including the increase in mortality from one to five and one significant morbidity from three to thirty-six cases [3]. Interestingly, timely and appropriate preventive actions can reduce this severe reaction to zero. A precise risk assessment before transfusion is recommended by SHOT for TACO elimination, especially if the patient has underlying risk factors. Preventive strategies in such predisposed patients include reviewing the need for transfusion, deferring the transfusion until issue can be resolved, transfuse according to body weight, measure fluid balance, consider prophylactic diuretic, slow transfusion rate and monitoring vital signs including oxygen saturation. Thus, TACO is a serious but avoidable transfusion reaction. Appropriate assessment prior to transfusion in every patient is important to ensure safe blood transfusion practice. Continuous...

Might a high hemoglobin mass be involved in non-cardiogenic pulmonary edema? The case of the chronic maladaptation to high-altitude in the Andes

Exposure to hypoxic environments when ascending at high altitudes may cause life-threatening pulmonary edema (HAPE) due to a rapid accumulation of extracellular fluid flooding in the pulmonary alveoli. In Andeans, high-altitude adaptation occurs at the expense of being more prone to chronic mountain sickness: relative hypoventilation, excess pulmonary hypertension, and secondary polycythemia. Because HAPE prevalence is high in the Andes, we posit the hypothesis that a high hemoglobine mass may increase HAPE risk. In support of it, high intrapulmonary hypertension along with hyperviscosity produced by polycytemia may enhance sear forces and intravascular hemolysis, thus leading to increased acellular hemoglobin and the subsequent damage of the alveolar and endothelial barrier. It is proposed to investigate the relationship between the vaso-endothelial homeostasis and erythropoiesis in the maladaptation to high altitude and HAPE. This research is especially important when reentry HAPE, since rheologic properties of blood changes with rapid ascent to high altitudes.

Prediction of hemodynamics after atrial septal defect closure using a framework of circulatory equilibrium in dogs.

In patients with heart failure, atrial septal defect (ASD) closure has a risk of inducing life-threatening acute pulmonary edema. The objective of this study was to develop a novel framework for quantitative prediction of hemodynamics after ASD closure. The generalized circulatory equilibrium comprises right and left cardiac output (CO) curves and pulmonary and systemic venous return surfaces. We incorporated ASD into the framework of circulatory equilibrium by representing ASD shunt flow (QASD) by the difference between pulmonary flow (QP) and systemic flow (QS). To examine the accuracy of prediction, we created ASD in six dogs. Four weeks after ASD creation, we measured left atrial pressure (PLA), right atrial pressure (PRA), QP, and Qs before and after ASD balloon occlusion. We then predicted postocclusion hemodynamics from measured preocclusion hemodynamics. Finally, we numerically simulated hemodynamics under various ASD diameters while changing left and right ventricular function. Predicted postocclusion PLA, PRA, and QS from preocclusion hemodynamics matched well with those measured [PLA: coefficient of determination (r2) = 0.96, standard error of estimate (SEE) = 0.89 mmHg, PRA: r2 = 0.98, SEE = 0.26 mmHg, QS: r2 = 0.97, SEE = 5.6 mL·min-1·kg-1]. A simulation study demonstrated that ASD closure increases the risk of pulmonary edema in patients with impaired left ventricular function and normal right ventricular function, indicating the importance of evaluation for the balance between right and left ventricular function. ASD shunt incorporated into the generalized circulatory equilibrium accurately predicted hemodynamics after ASD closure, which would facilitate safety management of ASD closure.NEW & NOTEWORTHY We developed a framework to predict the impact of atrial septal defect (ASD) closure on hemodynamics by incorporating ASD shunt flow into the framework of circulatory equilibrium. The proposed framework accurately predicted hemodynamics after ASD closure. Patient-specific prediction of hemodynamics may be useful for safety management of ASD closure.

Negative Pressure Pulmonary Edema: A Case Report

Negative pressure pulmonary edema is an uncommon complication of the extubation of the endotracheal tube. An increase in intrathoracic pressure and negative pressure of the lung caused by acute laryngeal spasm results from acute upper respiratory obstruction causing life-threatening pulmonary edema by alveolar-capillary damage is called negative pressure pulmonary edema. We here describe 28-years old female case the preoperative diagnosis of pelvic inflammatory disease undergoing exploratory laporoscopy caused negative pressure pulmonary edema while extubation. With the immediate treatment, the patient was discharged without any abnormalities.

Molecular Profiling of Vascular Remodeling in Chronic Pulmonary Disease

Pulmonary hypertension and pulmonary vascular remodeling (PVR) are common in many lung diseases leading to right ventricular dysfunction and death. Differences in PVR result in significant prognostic divergences in both the pulmonary arterial and venous compartments, as in pulmonary arterial hypertension (PAH) and pulmonary veno-occlusive disease (PVOD), respectively. Our goal was to identify compartment-specific molecular hallmarks of PVR, considering the risk of life-threatening pulmonary edema in PVOD, if treated by conventional pulmonary hypertension therapy. Formalin-fixed and paraffin-embedded tissues from fresh explanted human lungs of patients with PVOD (n = 19), PAH (n= 20), idiopathic pulmonary fibrosis (n = 13), and chronic obstructive pulmonary disease (n =15), were analyzed for inflammation and kinome-related gene regulation. The generated neuronal network differentiated PVOD from PAH samples with a sensitivity of 100% and a specificity of 92% in a randomly chosen validation set, a level far superior to established diagnostic algorithms. Further, various alterations were identified regarding the gene expression of explanted lungs withPVR, compared with controls. Specifically, the dysregulation of microtubule-associated serine/threonine kinase 2 and protein-o-mannose kinase SGK196 in all disease groups suggests a key role in pulmonary vasculopathy for the first time. Our findings promise to help develop novel target-specific interventions and innovative approaches to facilitate clinical diagnostics in an elusive group of diseases.

Endothelial mitochondria determine rapid barrier failure in chemical lung injury.

Acid aspiration, which can result from several etiologies, including postoperative complications, leads to direct contact of concentrated hydrochloric acid (HCl) with the alveolar epithelium. As a result, rapid endothelial activation induces alveolar inflammation, leading to life-threatening pulmonary edema. Because mechanisms underlying the rapid endothelial activation are not understood, here we determined responses in real time through optical imaging of alveoli of live mouse lungs. By alveolar micropuncture, we microinfused concentrated HCl in the alveolar lumen. As expected, acid contact with the epithelium caused rapid, but transient, apical injury. However, there was no concomitant membrane injury to the endothelium. Nevertheless, H2O2-mediated epithelial-endothelial paracrine signaling induced endothelial barrier failure, as detected by microvascular dextran leakage and lung water quantification. Remarkably, endothelial mitochondria regulated the barrier failure by activating uncoupling protein 2 (UCP2), thereby inducing transient mitochondrial depolarization that led to cofilin-induced actin depolymerization. Knockdown, or endothelium-targeted deletion of UCP2 expression, blocked these responses, including pulmonary edema. To our knowledge, these findings are the first to mechanistically implicate endothelial mitochondria in acid-induced barrier deterioration and pulmonary edema. We suggest endothelial UCP2 may be a therapeutic target for acid-induced acute lung injury.

Phosgene-induced lung edema: Comparison of clinical criteria for increased extravascular lung water content with postmortem lung gravimetry and lavage-protein in rats and dogs

Phosgene-induced acute lung injury (ALI) is characterized by a concentration x time (Cxt)-dependent increased pulmonary vascular permeability, phenotypically manifested as potentially life-threatening acute lung edema. In contemporary animal bioassays, the quantification of protein in bronchoalveolar lavage fluid (BAL) is taken as an unequivocal endpoint suggestive of disruption of alveolar barrier function. However, extravasated protein can only be a surrogate endpoint for assessing the extravascular fluid dynamics of the lung. This pathophysiological hallmark of ALI is diagnosed and quantified in vivo in humans by assessing the accumulation of excess extravascular lung water (EVLW). The Point of Departure (POD) of the Cxt relationship of this adverse outcome pathway should also constitute the basis for setting safe occupational and emergency response values. Unlike the EVLW approach, toxicology-based animal models utilize postmortem analyses of total protein in BAL and lung weights as the basis for human risk assessment. With either approach, it remains difficult to unequivocally evaluate pulmonary edema in terms of etiopathology and specificity, i.e., cardiogenic and hydrostatic versus increased permeability edema. The objective of this paper is to retrospectively analyze the clinical scoring of the severity grades of in vivo EVLWs from humans with the respective postmortem biomarkers BAL protein and collagen versus wet lung weights in rats and dogs exposed by inhalation to phosgene gas. Despite the different methodological approaches taken in humans and animals, the EVLW-based predicted thresholds for the onset of pulmonary edema and potentially life-threatening severe pulmonary edema were in remarkable agreement. Data from dogs appear to more aptly reflect the human etiopathology and should be given preference over data from rodents. Especially in rats, elevations in BAL protein may lead to a marked overestimation of the edematous potency of phosgene due to secreted protein into airways. In summary, increased lung weight in rats and dogs scaled favorably with the human-EVLW and was shown to be the biomarker of choice for the scaling lung edema. Caution is advised when using BAL protein in isolation as a surrogate endpoint of pulmonary edema.

Successful rescue therapy with venovenous extracorporeal membrane oxygenation for re-expansion pulmonary oedema in a patient with one lung

Re-expansion pulmonary oedema following the drainage of pleural fluid is rare. We report a patient with 1 lung who developed life-threatening re-expansion pulmonary oedema following thoracentesis and was rescued with venovenous (VV) extracorporeal membrane oxygenation (ECMO), surviving to discharge 28 days later. An aggressive early rescue therapy with VV ECMO should be pursued for all types of acute lung injury regardless of patient age, comorbidities or transplant candidacy, given the likelihood of native lung recovery following ECMO support.

Early disruption of the intercelullar junction proteins leads to alveolar-capillary barrier dysfunction and pulmonary edema in a mouse ricin intoxication model of Acute Respiratory Distress Syndrome.

Abstract Acute respiratory distress syndrome (ARDS), charactarized by an intense pulmonary inflammation involving neutrophil recruitment, is accompanied by a severe disruption of the alveolar-capillary barrier leading to life-threatening pulmonary edema. Ricin, a plant-toxin derived from the seeds of Ricinus communis, irreversibly inactivates ribosomes by site-specific depurination, thereby arresting cell protein synthesis, while its clinical manifestation following pulmonary exposure is that of rapidly developing severe ARDS. We evaluated the role of the members of tight, adherens and gap junction proteins in pulmonary edema formation in a clinically relevant mouse model of ARDS induced by ricin intoxication, since the respiratory endothelium and epithelium barrier function depends on the integrity of intercellular junctions. We found a significant reduction in Claudin5, Claudin18, VE-Cadherin and Connexin43 in mice lungs 3 hours after ricin intoxication. Neutrophil depletion markedly attenuated pulmonary edema and in combination with a matrix metalloproteinase (MMP) inhibitor restored the expression of VE-Cadherin and Connexin43, providing an evidence for MMP-dependent proteolysis of these proteins. Unlike the aforementioned proteins, disruption of Claudin18 following ricin intoxication was found to be neutrophil-independent and involved tyrosine phosphorylation. These results provide an in vivo mechanism for early impairment of the alveolar-capillary barrier by intercellular junction protein disruption, which at later time points, is enhanced by the specific loss of type II alveolar epithelial cells that no longer provide resistance to edema formation and altogether lead to respiratory failure and death.

Pulmonary veno-occlusive disease.

Pulmonary veno-occlusive disease (PVOD) is a rare form of pulmonary hypertension (PH) characterised by preferential remodelling of the pulmonary venules. In the current PH classification, PVOD and pulmonary capillary haemangiomatosis (PCH) are considered to be a common entity and represent varied expressions of the same disease. The recent discovery of biallelic mutations in the EIF2AK4 gene as the cause of heritable PVOD/PCH represents a major milestone in our understanding of the molecular pathogenesis of PVOD. Although PVOD and pulmonary arterial hypertension (PAH) share a similar clinical presentation, with features of severe precapillary PH, it is important to differentiate these two conditions as PVOD carries a worse prognosis and life-threatening pulmonary oedema may occur following the initiation of PAH therapy. An accurate diagnosis of PVOD based on noninvasive investigations is possible utilising oxygen parameters, low diffusing capacity for carbon monoxide and characteristic signs on high-resolution computed tomography of the chest. No evidence-based medical therapy exists for PVOD at present and lung transplantation remains the preferred definitive therapy for eligible patients.

What is new in the diagnostics and treatment of acute heart failure?

Acute heart failure (AHF) is the term used to describe a rapid onset or changes in the symptoms and signs of heart failure. It is a life-threatening condition that requires immediate attention and medical care and usually leads to an emergency hospital admission. In most cases, AHF is a result of deterioration of health in patients with previously diagnosed chronic heart failure (CHF) whether with reduced (HF-REF) or preserved (HF-PEF) left ventricular ejection fraction (EF). Heart failure is defined as an abnormality of cardiac structure or function, which leads to the inability of the heart to deliver oxygen at a rate which is adequate to the requirements of metabolism in tissues, despite normal cardiac filling pressure (or only at the cost of increased filling pressure). The most common causes of AHF are myocardial diseases which lead to ventricular dysfunction and a reduction in cardiac ejection fraction but also the abnormality of diastolic function or heart valve disease, pericardium, endocardium and heart rhythm disorders. In suspected AHF there are two approaches for exact diagnosis: through the use of rapid essay of BNP hormones or by echocardiographic examination with measurement of ejection fraction or diastolic anomalies and myocardial hypertrophy. Acuteness may vary, from the situation that within a few days there occurs a deterioration (dyspnea or edema) in some patients, while others develop AHF within a few minutes or hours (e.g., in acute myocardial infarction). The patient may have a range of conditions, from life-threatening pulmonary edema or cardiogenic shock, to the clinical picture that is primarily characterized by worsening of peripheral edema. Diagnosis and treatment are carried out concurrently, especially in seriously ill patients and all measures must be applied quickly. Continuous monitoring of the patient's vital functions is essential during the initial evaluation and treatment and certain patients are best treated in the intensive or coronary care unit like patients with acute coronary syndromes. Long-term goals of the treatment are the prevention of recurrent AHF and improvement of prognosis. 5 aspects are evaluated simultaneously: adequacy of ventilation, presence of threatening arrhythmias, state of tension (hypotension, shock), presence of acute coronary syndrome and acute mechanical reasons. All these evaluations should lead to a rapid response to the presence of a threatening condition, such as, for example, urgent revascularization and so on. Changes in the treatment strategy are early administration of vasodilatators and diuretics therapy for target organs protection(heart, liver and kidnies) in relation to mortality reduction. Key medications in AHF are the same as in the CHF: oxygen therapy, diuretics and vasodilators. Opiates and inotropic drugs are used more selectively and mechanical circulatory support devices only rarely. Non-invasive ventilation becomes a common practice, while invasive ventilation is required in a small number of cases. Systolic pressure, heart rate and frequency, and peripheral blood saturation and diuresis should be measured and often repeated until the patient becomes stable. All aspects are summarized in the algorithm AHF of the European Society of Cardiology (ESC).

Effect of PEEP on phosgene-induced lung edema: Pilot study on dogs using protective ventilation strategies

Various therapeutic regimes have been proposed for treatment of phosgene-induced acute lung injury (P-ALI). Most of these treatments rely on late-stage supportive measures to maintain the oxygenation of the lung. This exploratory proof-of-concept study on Beagle dogs focused on protective positive end-expiratory pressure (PEEP) ventilation, initiated early at the yet asymptomatic stage after phosgene exposure. Conscious, spontaneously breathing dogs were head-only exposed to a potentially lethal inhalation dose of phosgene (870ppm×min). Shortly after exposure, the dogs were anesthetized, intubated and then subjected to mechanical ventilation (PEEP; tidal volume (VT)=10–12mL/kg body weight, 40 breaths/min) at 0, 4, or 12cm H2O over a post-exposure period of 8h (one dog per setting). For reference, one additional dog received the same dose of phosgene without anesthesia and mechanical ventilation. Time-course changes of hematocrit, leukocytes, and thrombocytes were determined in peripheral blood. At necropsy, changes lung weights, bronchoalveolar lavage, and histology were used to assess the efficacy of treatment. The most salient outcome in the non-ventilated dog was a time-related hemoconcentration and leukocytosis and autopsy findings suggestive of pulmonary congestion and edema. The pulmonary epithelium of the major airways was generally intact; however, in their lumen inflammatory cells, cellular debris and mucus were present. Relative to the dog receiving no intervention, the lung edema was markedly alleviated by PEEP at both 4 and 12cm H2O but not at 0cm H2O PEEP. In summary, the time-dependent progression into a life-threatening pulmonary edema can effectively be suppressed by protective, low-pressure PEEP when implemented early enough after exposure to phosgene. However, due to the exploratory nature of this study, the findings may suggest an association between PEEP and protection from pulmonary edema. However, definite conclusions and recommendations cannot be made yet based upon the small sample size and the limited variables examined.

Network Analysis Reveals Distinct Clinical Syndromes Underlying Acute Mountain Sickness

Acute mountain sickness (AMS) is a common problem among visitors at high altitude, and may progress to life-threatening pulmonary and cerebral oedema in a minority of cases. International consensus defines AMS as a constellation of subjective, non-specific symptoms. Specifically, headache, sleep disturbance, fatigue and dizziness are given equal diagnostic weighting. Different pathophysiological mechanisms are now thought to underlie headache and sleep disturbance during acute exposure to high altitude. Hence, these symptoms may not belong together as a single syndrome. Using a novel visual analogue scale (VAS), we sought to undertake a systematic exploration of the symptomatology of AMS using an unbiased, data-driven approach originally designed for analysis of gene expression. Symptom scores were collected from 292 subjects during 1110 subject-days at altitudes between 3650 m and 5200 m on Apex expeditions to Bolivia and Kilimanjaro. Three distinct patterns of symptoms were consistently identified. Although fatigue is a ubiquitous finding, sleep disturbance and headache are each commonly reported without the other. The commonest pattern of symptoms was sleep disturbance and fatigue, with little or no headache. In subjects reporting severe headache, 40% did not report sleep disturbance. Sleep disturbance correlates poorly with other symptoms of AMS (Mean Spearman correlation 0.25). These results challenge the accepted paradigm that AMS is a single disease process and describe at least two distinct syndromes following acute ascent to high altitude. This approach to analysing symptom patterns has potential utility in other clinical syndromes.

Extracorporeal Membrane Oxygenation for Acute Life-Threatening Neurogenic Pulmonary Edema following Rupture of an Intracranial Aneurysm

Neurogenic pulmonary edema (NPE) leading to cardiopulmonary dysfunction is a potentially life-threatening complication in patients with central nervous system lesions. This case report describes a 28-yr woman with life-threatening fulminant NPE, which was refractory to conventional respiratory treatment, following the rupture of an aneurysm. She was treated successfully with extracorporeal membrane oxygenation (ECMO), although ECMO therapy is generally contraindicated in neurological injuries such as brain trauma and diseases that are likely to require surgical intervention. The success of this treatment suggests that ECMO therapy should not be withheld from patients with life-threatening fulminant NPE after subarachnoid hemorrhage.

Algid malaria treated with early goal-directed therapy

Severe malaria complicated by circulatory shock is known as algid malaria. Cases of severe imported malaria are seen increasingly frequently in emergency departments in the United States, Europe, and other locales. The optimal volume resuscitation strategy for patients with severe malaria is not well-defined. A 20-year-old woman, who immigrated 2 weeks ago from Niger, Africa, presented to the emergency department of an urban teaching hospital with fever, hypotension, and malaise. She was resuscitated with 5.5 L of normal saline solution and norepinephrine. Thin blood smear demonstrated Plasmodium falciparum with parasitemia of 10% to 15%. She had rapid reversal of circulatory shock, cleared her parasitemia in less than 48 hours with antimalarial therapy, and was discharged home on hospital day 6 in good condition. The optimal resuscitation strategy for algid malaria is unknown, and volume restriction has been advocated as a means to prevent life-threatening cerebral and pulmonary edema. Although not identical, the late inflammatory response in severe malaria leading to capillary permeability shares many similarities with the immunologic response in bacterial sepsis. Our case report discusses a patient with severe imported malaria complicated by shock, successfully managed with large-volume fluid resuscitation, hemodynamic optimization, early antimalarial agents, and broad-spectrum antibiotics. This report questions the strategy of cautious fluid resuscitation in algid malaria and suggests that case series comparing goal-directed resuscitation to historic controls along with prospective multicenter controlled trials should be conducted to determine the best fluid resuscitation strategy.