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SAGE Open Medical Case Reports 2024Pulmonary embolism is one of the rarest complications of high-altitude sickness that can coexist with high altitude pulmonary edema. The risk of developing this...
Pulmonary embolism is one of the rarest complications of high-altitude sickness that can coexist with high altitude pulmonary edema. The risk of developing this phenomenon increases significantly with prolonged stay in high altitudes especially above 5000 m. Given the fatality of the condition, early screening and management is crucial; however, there is no gold standard approach in diagnosis. A 44-year-old male, a Tanzanian tourist first time hiking Mt. Kilimanjaro developed difficulty in breathing on the 4th day of ascending on a route that takes 6 days to summit whereby he was saturating at 38% on room air at the height of 4775 m. He was admitted with the clinical diagnosis of high altitude pulmonary edema. However, in the course of treatment for 72 h with no improvement, further investigations including computed tomography scan were suggestive of pulmonary embolism whereby he was treated with full recovery. Pulmonary embolism case reports are increasingly rising with the difficult to notice among high altitude pulmonary edema patients given their presentation similarities. A high index of suspicion based on clinical examination and investigations should prompt a clinician to include or exclude it.
PubMed: 38764918
DOI: 10.1177/2050313X241254739 -
American Journal of Cardiovascular... 2024The current traditional pathophysiologic concept of pulmonary edema of cardiogenic origin explains its development by a hydrostatic effect due to increased pulmonary... (Review)
Review
The current traditional pathophysiologic concept of pulmonary edema of cardiogenic origin explains its development by a hydrostatic effect due to increased pulmonary capillary pressure resulting in fluid flux to alveolar and interstitial areas from capillaries. However, several experimental studies and clinical data of poor response to hemodynamic and diuretic treatment in many scenarios provide further evidence of the involvement of several other contributing factors to the development of cardiogenic pulmonary edema. Several experimental and clinical studies have found that sympathetic overactivity with elevated plasma catecholamine concentrations may play an important role in the development of cardiovascular-associated pulmonary edema. Catecholamine-induced pulmonary injury may be one of the key mechanisms in acute cardiogenic pulmonary edema triggering proinflammatory cytokine overactivation, oxidative stress and myocardial injury. In the everyday treatment of acute heart failure, physicians should consider the possibility of other noncardiogenic mechanisms involved in the progression of acute pulmonary edema, particularly catecholamine overactivity, lymphatic drainage, inflammatory and oxidative stress, high surfactant protein. The classic, hemodynamic treatment approach in pulmonary edema with the coexistence of other contributing factors may not provide adequate clinical benefit during treatment.
PubMed: 38764545
DOI: 10.62347/YGQQ8696 -
Clinical Medicine Insights. Case Reports 2024Excessive water consumption is an extremely rare and potential asthma risk factor with very few cases reported in the literature. Common triggers of asthma include...
Excessive water consumption is an extremely rare and potential asthma risk factor with very few cases reported in the literature. Common triggers of asthma include genetic factors, smoking, allergens, and viral respiratory infections. The adult patient with asthma reportedly drank too much water and was unable to get relief from his asthma while hospitalized. The patient's asthma was better controlled with the use of diuretics and control of the patient's fluid intake and output. This case explores asthma induced by excessive drinking of water.
PubMed: 38746687
DOI: 10.1177/11795476241253107 -
Journal of Veterinary Cardiology : the... Jun 2024A nine-year-old spayed female domestic shorthair cat with a previous diagnosis of hypertrophic cardiomyopathy and treated for one month with atenolol (6.25 mg q 12 h)...
A nine-year-old spayed female domestic shorthair cat with a previous diagnosis of hypertrophic cardiomyopathy and treated for one month with atenolol (6.25 mg q 12 h) was referred for respiratory distress and anorexia. The cat was diagnosed with pulmonary oedema secondary to obstructive hypertrophic cardiomyopathy. After stabilisation, she was discharged with furosemide (1 mg/kg q 12 h), clopidogrel (18.75 mg q 24 h), atenolol (6.25 mg q 12 h), and mirtazapine (2 mg/cat q 24 h) to increase appetite. At recheck, the cat was lethargic and presented with severe bradycardia with a junctional escape rhythm and ventriculoatrial conduction. The mirtazapine was discontinued due to its possible side-effects on cardiac rhythm. After three days, the atenolol was halved because the bradyarrhythmia was still present. After 10 days, the rhythm returned to sinus; atenolol was reintroduced twice daily with no further side-effects. The absence of a sinus rhythm with a junctional escape rhythm and P' retroconduction is compatible with a third-degree sinus block or a sinus standstill; the differentiation of these rhythm disturbances is impossible, based on the surface electrocardiogram (ECG). The sinus rhythm was restored after mirtazapine was withdrawn. However, it is not possible to rule out the role of the atenolol or the combined effect of the two drugs. The cat was affected by hypertrophic cardiomyopathy, and the role of myocardial remodelling cannot be excluded. This is the first time that a bradyarrhythmia consequent to the treatment with atenolol and mirtazapine was described in a cat.
Topics: Female; Mirtazapine; Animals; Atenolol; Cats; Cat Diseases; Cardiomyopathy, Hypertrophic; Bradycardia; Mianserin; Adrenergic beta-1 Receptor Antagonists
PubMed: 38735230
DOI: 10.1016/j.jvc.2024.03.003 -
Sensors (Basel, Switzerland) May 2024Heart failure (HF) is a complex clinical syndrome associated with significant morbidity, mortality, and healthcare costs. It is characterized by various structural... (Review)
Review
Heart failure (HF) is a complex clinical syndrome associated with significant morbidity, mortality, and healthcare costs. It is characterized by various structural and/or functional abnormalities of the heart, resulting in elevated intracardiac pressure and/or inadequate cardiac output at rest and/or during exercise. These dysfunctions can originate from a variety of conditions, including coronary artery disease, hypertension, cardiomyopathies, heart valve disorders, arrhythmias, and other lifestyle or systemic factors. Identifying the underlying cause is crucial for detecting reversible or treatable forms of HF. Recent epidemiological studies indicate that there has not been an increase in the incidence of the disease. Instead, patients seem to experience a chronic trajectory marked by frequent hospitalizations and stagnant mortality rates. Managing these patients requires a multidisciplinary approach that focuses on preventing disease progression, controlling symptoms, and preventing acute decompensations. In the outpatient setting, patient self-care plays a vital role in achieving these goals. This involves implementing necessary lifestyle changes and promptly recognizing symptoms/signs such as dyspnea, lower limb edema, or unexpected weight gain over a few days, to alert the healthcare team for evaluation of medication adjustments. Traditional methods of HF monitoring, such as symptom assessment and periodic clinic visits, may not capture subtle changes in hemodynamics. Sensor-based technologies offer a promising solution for remote monitoring of HF patients, enabling early detection of fluid overload and optimization of medical therapy. In this review, we provide an overview of the CardioMEMS device, a novel sensor-based system for pulmonary artery pressure monitoring in HF patients. We discuss the technical aspects, clinical evidence, and future directions of CardioMEMS in HF management.
Topics: Humans; Heart Failure; Cardiology; Monitoring, Physiologic; Disease Management; Hemodynamics
PubMed: 38733027
DOI: 10.3390/s24092922 -
Journal of Clinical Medicine May 2024Re-expansion pulmonary edema is a rare and potentially life-threatening complication that can occur after the rapid re-expansion of a collapsed lung due to pneumothorax... (Review)
Review
Re-expansion pulmonary edema is a rare and potentially life-threatening complication that can occur after the rapid re-expansion of a collapsed lung due to pneumothorax or pleural effusion. It has a multifactorial pathogenesis, and risk factors for re-expansion pulmonary edema, such as chronic lung collapse, rapid re-expansion, and changes in pulmonary vascular permeability, have been identified. Clinical manifestations vary, ranging from almost asymptomatic to a rapidly fatal condition, and its incidence may be more common and less fatal than previously believed. The literature emphasizes the importance of early recognition and management to ensure favorable outcomes. However, there is ongoing debate regarding the indications for ventilatory support and the timing of non-invasive or invasive ventilation. Herein, we report a case series of three paradigmatic examples of massive re-expansion pulmonary edema occurring over a period of 10 years in our institution among a population of 815 patients with spontaneous pneumothorax. We also conducted a literature review on re-expansion pulmonary edema, with a particular focus on diagnosis and management. In each case, despite initially normal clinical parameters, severe respiratory distress developed following the insertion of a thoracic drainage tube for a massive spontaneous pneumothorax. Two patients required High-Flow Nasal Oxygen, and one was addressed to intensive management, including CPAP. In all cases, the patient's outcome was optimal.
PubMed: 38731196
DOI: 10.3390/jcm13092667 -
Clinical Kidney Journal May 2024Acute kidney injury (AKI) in patients with cirrhosis is a diagnostic challenge due to multiple and sometimes overlapping possible etiologies. Many times, diagnosis... (Review)
Review
Acute kidney injury (AKI) in patients with cirrhosis is a diagnostic challenge due to multiple and sometimes overlapping possible etiologies. Many times, diagnosis cannot be made based on case history, physical examination or laboratory data, especially when the nephrologist is faced with AKI with a hemodynamic basis, such as hepatorenal syndrome. In addition, the guidelines still include generalized recommendations regarding withdrawal of diuretics and plasma volume expansion with albumin for 48 h, which may be ineffective and counterproductive and may have iatrogenic effects, such as fluid overload and acute cardiogenic pulmonary edema. For this reason, the use of new tools, such as hemodynamic point-of-care ultrasound (PoCUS), allows us to phenotype volume status more accurately and ultimately guide medical treatment in a noninvasive, rapid and individualized manner.
PubMed: 38726210
DOI: 10.1093/ckj/sfae112 -
Anesthesia and Pain Medicine Apr 2024Diffuse alveolar hemorrhage (DAH) is a potentially life-threatening condition that can occur due to a variety of disorders. Hence, rapid diagnosis and prompt initiation...
BACKGROUND
Diffuse alveolar hemorrhage (DAH) is a potentially life-threatening condition that can occur due to a variety of disorders. Hence, rapid diagnosis and prompt initiation of appropriate treatment are imperative.
CASES
A 55-year-old woman with a deep neck infection underwent emergent tonsillectomy. General anesthesia and surgery proceeded uneventfully. Upon transfer to the post-anesthesia care unit, ongoing respiratory distress and occasional expectoration of blood-tinged sputum were noted. Lung ultrasonography (LUS) revealed multiple B-profiles and irregular pleural lines with subpleural consolidations. Emergent bronchoscopy with bronchoalveolar lavage was diagnostic of DAH. She underwent a comprehensive evaluation for rheumatologic and infectious etiologies of DAH, all of which yielded negative results. The patient was managed with steroids and conservative treatment.
CONCLUSIONS
The integration of LUS with clinical information allows for more rapid differentiation of acute respiratory failure causes. Therefore, anesthesiologists' awareness and utilization of LUS findings of DAH can significantly contribute to appropriate management.
PubMed: 38725169
DOI: 10.17085/apm.23101 -
Microvascular Research Jul 2024Critical illness is associated with organ failure, in which endothelial hyperpermeability and tissue edema play a major role. The endothelial angiopoietin/Tie2 system, a...
INTRODUCTION
Critical illness is associated with organ failure, in which endothelial hyperpermeability and tissue edema play a major role. The endothelial angiopoietin/Tie2 system, a regulator of endothelial permeability, is dysbalanced during critical illness. Elevated circulating angiopoietin-2 and decreased Tie2 receptor levels are reported, but it remains unclear whether they cause edema independent of other critical illness-associated alterations. Therefore, we have studied the effect of angiopoietin-2 administration and/or reduced Tie2 expression on microvascular leakage and edema under normal conditions.
METHODS
Transgenic male mice with partial deletion of Tie2 (heterozygous exon 9 deletion, Tie2) and wild-type controls (Tie2) received 24 or 72 pg/g angiopoietin-2 or PBS as control (n = 12 per group) intravenously. Microvascular leakage and edema were determined by Evans blue dye (EBD) extravasation and wet-to-dry weight ratio, respectively, in lungs and kidneys. Expression of molecules related to endothelial angiopoietin/Tie2 signaling were determined by ELISA and RT-qPCR.
RESULTS
In Tie2 mice, angiopoietin-2 administration increased EBD extravasation (154 %, p < 0.05) and wet-to-dry weight ratio (133 %, p < 0.01) in lungs, but not in the kidney compared to PBS. Tie2 mice had higher pulmonary (143 %, p < 0.001), but not renal EBD extravasation, compared to wild-type control mice, whereas a more pronounced wet-to-dry weight ratio was observed in lungs (155 %, p < 0.0001), in contrast to a minor higher wet-to-dry weight ratio in kidneys (106 %, p < 0.05). Angiopoietin-2 administration to Tie2 mice did not further increase pulmonary EBD extravasation, pulmonary wet-to-dry weight ratio, or renal wet-to-dry weight ratio. Interestingly, angiopoietin-2 administration resulted in an increased renal EBD extravasation in Tie2 mice compared to Tie2 mice receiving PBS. Both angiopoietin-2 administration and partial deletion of Tie2 did not affect circulating angiopoietin-1, soluble Tie2, VEGF and NGAL as well as gene expression of angiopoietin-1, -2, Tie1, VE-PTP, ELF-1, Ets-1, KLF2, GATA3, MMP14, Runx1, VE-cadherin, VEGFα and NGAL, except for gene and protein expression of Tie2, which was decreased in Tie2 mice compared to Tie2 mice.
CONCLUSIONS
In mice, the microvasculature of the lungs is more vulnerable to angiopoietin-2 and partial deletion of Tie2 compared to those in the kidneys with respect to microvascular leakage and edema.
Topics: Animals; Receptor, TIE-2; Angiopoietin-2; Male; Capillary Permeability; Lung; Kidney; Signal Transduction; Mice, Knockout; Mice; Mice, Inbred C57BL; Pulmonary Edema; Disease Models, Animal; Edema; Mice, Transgenic; Ribonuclease, Pancreatic
PubMed: 38723844
DOI: 10.1016/j.mvr.2024.104694 -
Cureus Apr 2024Preeclampsia is a rare complication of pregnancy and can cause maternal death. This case report serves to increase awareness of the range and severity of symptoms in...
Preeclampsia is a rare complication of pregnancy and can cause maternal death. This case report serves to increase awareness of the range and severity of symptoms in postpartum preeclampsia and highlights a stepwise approach to provide prompt management. The cause of preeclampsia is not fully understood but is correlated with many placental and maternal factors. Preeclampsia typically resolves with delivery, and it is uncommon to have symptoms in the postpartum period. Due to the rarity of the disease, it is not typically at the top of a differential list for postpartum women. A 35-year-old first-time mother presents with shortness of breath, tightness in her chest, and mild pulmonary edema. A series of chest X-rays, computed tomographic angiogram of the chest, and serial labs reveal she has postpartum preeclampsia. Many pre-eclamptic symptoms are common to a variety of conditions leading to an extensive list of differential diagnoses. Used in a stepwise fashion, clinical analysis allows physicians to accurately diagnose postpartum preeclampsia and provide lifesaving treatment for these mothers. This study highlights the need for vigilance in symptom analysis and diagnostic testing.
PubMed: 38721196
DOI: 10.7759/cureus.57834