Reexpansion pulmonary edema after treatment of primary spontaneous pneumothorax.

A 24-year-old male patient, without further symptoms or comorbidities presented to the emergency room with acute dyspnea after heavy lifting two days before. On auscultation an attenuated vesicular breath was noticed on the right lung. In the initial chest radiograph a right-sided primary spontaneous pneumothorax with minor mediastinal shift was diagnosed. After insertion of a 12-French chest tube the patient's clinical condition deteriorated. The following chest radiograph and computed tomography of the thorax showed a reexpansion pulmonary edema in the right lung. The patient was admitted to the ICU and supportive treatment was initiated. Pulmonary reexpansion edema after drainage of a pneumothorax is a very rare complication with mortality rates reaching up to 20%. The exact pathophysiology remains unknown. Typical Symptoms include dyspnea, hypotension, and tachycardia. To minimize the risk of a pulmonary reexpansion edema, not more than 1200-1800 ml of air should be drained at once and the drainage should be stopped when the patient starts coughing.

Diabetic Ketoacidosis Associated with Thyroxine (T4) Toxicosis and Thyrotoxic Cardiomyopathy.

Thyrotoxicosis and diabetic ketoacidosis (DKA) both may present as endocrine emergencies and may have devastating consequences if not diagnosed and managed promptly and effectively. The combination of diabetes mellitus (DM) with thyrotoxicosis is well known, and one condition usually precedes the other. Furthermore, thyrotoxicosis is complicated by some degree of cardiomyopathy in at least 5% de patients; but the coexistence of DKA, thyroxin (T4) toxicosis, and acute cardiomyopathy is extremely rare. We describe a case of a man, previously diagnosed with DM but with no past history of thyroid disease, who presented with shock and severe DKA that did not improve despite optimal therapy. The patient evolved with acute pulmonary edema, elevated troponin levels, severe left ventricular systolic dysfunction, and clinical and laboratory evidence of thyroxin (T4) toxicosis and thyrotoxic cardiomyopathy. Subsequently, the patient evolved favorably with general support and appropriate therapy for DKA and thyrotoxicosis (hydrocortisone, methimazole, Lugol's solution) and was discharged a few days later.

[Case report of re-expansion pulmonary edema in a patient with anorexia nervosa after removal of a huge ovarian tumor].

We described a case of 19-year-old female who developed re-expansion pulmonary edema (RPE) after removal of a huge ovarian tumor. Altered lung volume after the surgery was observed by chest X-ray. Preoperatively, the lung was highly compressed by the tumor. Patient was intubated under general anesthesia and was ventilated by pressure controlled mode with only 5 cmH2O of positive end-expiratory pressure (PEEP). P/F ratio was changed from 163 to 444 after removal of the tumor. At the end of the surgery, P/F ratio decreased to 263 with yellow frothy sputum in the endotracheal tube and we diagnosed re-expansion pulmonary edema based on appearing yellow frothy sputum and chest X-ray. No recruitment procedure was carried out through the course except positive pressure ventilation with 5 cmH2O of PEEP in the intensive care unit after surgery. Twelve hours after the surgery, we could not confirm the recovery of lung volume on chest X-ray; however the patient was extubated because of P/F ratio increasing to 507. After 8 days of the surgery, the chest X-ray showed recovery of the lung volume to almost normal size. In this case, the compressed lung needed almost 1 week to recover the lung volume. This change in chest X-ray might indicate inadequate recovery of lung volume by recruitment maneuver and this should be avoided in order not to allow development of unfavorable clinical course of RPE.

Application of Point-of-care Ultrasound for Screening Climbers at High Altitude for Pulmonary B-lines.

INTRODUCTION: High-altitude pulmonary edema (HAPE) occurs as a result of rapid ascent to altitude faster than the acclimatization processes of the body. Symptoms can begin at an elevation of 2,500 meters above sea level. Our objective in this study was to determine the prevalence and trend of developing B-lines at 2,745 meters above sea level among healthy visitors over four consecutive days. METHODS: We performed a prospective case series on healthy volunteers at Mammoth Mountain, CA, USA. Subjects underwent pulmonary ultrasound for B-lines over four consecutive days. RESULTS: We enrolled 21 male and 21 female participants. There was an increase in the sum of B-lines at both lung bases from day 1 to day 3, with a subsequent decrease from day 3 to day 4(P<0.001). By the third day at altitude, B-lines were detectable at base of lungs of all participants. Similarly, B-lines increased at apex of lungs from day 1 to day 3 and decreased on day 4 (P=0.004). CONCLUSION: By the third day at 2,745 meters altitude, B-lines were detectable in the bases of both lungs of all healthy participants in our study. We assume that increasing the number of B-lines could be considered an early sign of HAPE. Point-of-care ultrasound could be used to detect and monitor B-lines at altitude to facilitate early detection of HAPE, regardless of pre-existing risk factors.

Percutaneous mitral valve repair in a ventilator-dependant patient.

I report the case of a 57-year-old patient admitted to the intensive care unit with severe community-acquired pneumonia, complicated by prolonged mechanical ventilation of the lungs and intractable cardiac failure. He underwent percutaneous coronary angioplasty of the right coronary artery, but this did not improve his clinical condition. He was subsequently found to be suffering from mitral valve prolapse, that was felt to be the cause of recurrent episodes of severe pulmonary oedema. As open surgery was felt to be not feasible, the patient underwent percutaneous repair of his mitral valve using the MitraClip® device, and, after months of ventilatory support, was then weaned from the ventilator in a matter of days. While the procedure itself and the technology employed are still under evaluation, I conclude that the technique of percutaneous mitral valve repair may be considered for similar patients for whom open repair is contraindicated.

Fatal pulmonary oedema associated with severe pre-eclampsia: challenges and lessons.

Pre-eclampsia complicated by pulmonary oedema, severe hypertension, tachycardia and desaturation is a devastating condition. A comprehensive understanding of the aetiopathogenesis during such an emergency is challenging in the absence of functional and responsive point-of-care imaging, and laboratory and other critical-care services. An unbooked 26-year-old gravida 3 para 1+1 presented to a primary healthcare clinic with features of pre-eclampsia, severe hypertension and pulmonary oedema. The only available antihypertensive drug, methyldopa, was administered. The patient was transferred to a district hospital and subsequently referred to a tertiary hospital. On arrival, she was booked for caesarean delivery and in the maternity ward a central venous pressure (CVP) line was inserted. The patient developed pneumothorax and died in the intensive care unit undelivered. This case highlights many lessons, which are discussed. If CVP monitoring is indicated before caesarean delivery, consideration must be given to line insertion in the operating room to facilitate rapid delivery should the patient's condition deteriorate.

Risk of Acute Lung Injury after Esophagectomy.

To develop a new approach for identifying acute lung injury (ALI) in surgical ward setting and to assess incidence rate, clinical outcomes, and risk factors for ALI cases after esophagectomy. We also compare the degree of lung injury between operative and non-operative sides. Consecutive esophageal cancer patients (n=1022) who underwent esophagectomy from Dec 2012 to Nov 2018 in our hospital were studied. An approach for identifying ALI was proposed that integrated radiographic assessment of lung edema (RALE) score to quantify degree of lung edema. Stepwise logistic regression identified risk factors for postoperative ALI incidence. The degree of bilateral lung injury was compared using the RALE score. The approach for identifying ALI in surgical ward setting was defined as acute onset, PaO2/FiO2≤300 mmHg, bilateral opacities on bedside chest radiograph with a RALE score≥16, and exclusion of cardiogenic pulmonary edema. Incidence rate of ALI was estimated to be 9.7%. ALI diagnosis was associated with multiple clinical complications, prolonged hospital stay, higher medical bills, and higher perioperative mortality. Nine risk factors including BMI, ASA class, DLCO%, duration of surgery, neutrophil percentage, high-density lipoprotein, and electrolyte disorders were identified. The RALE score of the lung lobes of the operative side was higher than the non-operative side. A new approach for identifying ALI in esophageal cancer patients receiving esophagectomy was proposed and several risk factors were identified. ALI is common and has severe outcomes. The lung lobes on the operative side are more likely to be affected than the non-operative side.

Effects of Lung Ultrasonography-Guided Management on Cumulative Fluid Balance and Other Clinical Outcomes: A Systematic Review.

Lung ultrasonography is accurate in detecting pulmonary edema and overcomes most limitations of traditional diagnostic modalities. Whether use of lung ultrasonography-guided management has an effect on cumulative fluid balances and other clinical outcomes remains unclear. In this systematic review, we included 12 studies using ultrasonography guided-management with a total of 2290 patients. Four in-patient studies found a reduced cumulative fluid balance (ranging from -0.3 L to -2.4 L), whereas three out-patient studies found reduction in dialysis dry weight (ranging from -2.6 kg to -0.2 kg) compared with conventionally managed patients. None of the studies found adverse effects related to hypoperfusion. The use of lung ultrasonography-guided management was not associated with other clinical outcomes. This systematic review shows that lung ultrasonography-guided management, exclusively or in concert with other diagnostic modalities, is associated with a reduced cumulative fluid balance. Studies thus far have not shown a consistent effect on clinical outcomes.

[A case of neurogenic pulmonary edema due to left internal carotid artery occlusion].

A 79-year-old woman developed consciousness disturbance, left eye deviation, right hemiplegia and aphasia with hypoxemia. Chest X-ray showed bilateral pulmonary edema. MRI revealed the left internal carotid artery occlusion and entire left middle cerebral artery infarct including insular cortex. We performed mechanical thrombectomy therapy and TICI3 recanalization was obtained. During operation, the respiratory condition deteriorated and the ventilator was started after mechanical thrombectomy therapy. Chest X-ray showed butterfly shadow, which indicated pulmonary edema. Pulmonary edema improved on the 2nd day of onset, and disappeared on the 3rd day. There was no heart diseases such as Takotsubo myocardiopathy, acute cardiac failure and cardiomyopathy on echocardiography and electrocardiography. Therefore, we diagnosed her as having neurogenic pulmonary edema due to cerebral infarction including insular cortex. We consider that left insular cortex infarction was a trigger of neurogenic pulmonary edema. If hypoxemia associated with infarction including the insular cortex, neurogenic pulmonary edema should be considered for medical treatment.

Fulminant unilateral pulmonary edema on the wrong side.

A 55-year-old patient had undergone replacement of the proximal descending aorta at the age of 17 for aortic coarctation. The patient required surgical intervention at the age of 55 for development of a false aneurysm at the distal anastomosis. Surgery was complicated by bleeding from the ruptured false aneurysm into the left upper lung lobe, which had to be resected. Recovery from surgery was uneventful. The patient could be extubated and his cardiopulmonary function was stable. On the 3rd postoperative day, acute decompensation occurred and the patient had to be reintubated for severe hypoxia. Chest X-ray showed massive opacification of the right lung indicating fulminant pulmonary edema. Interestingly, no marked changes of the remaining left lung were observed. The patient was treated with antibiotics intravenously for suspected pneumonia. In addition, diuretics and catecholamines were administered for markedly elevated cardiac preload and acute loss of peripheral vascular resistance. Within only 12 hours, the patient recovered dramatically. Follow-up chest X-ray showed no remaining opacification of the right lung. The patient was extubated and cardiopulmonary function has remained stable. The subsequent postoperative course was uneventful and the patient could be discharged from hospital 4 days later.

Very late bioprosthetic aortic valve thrombosis.

A 79-year-old man with a history of bioprosthetic aortic valve (AV) replacement in 2008 and atrial fibrillation was admitted with acute pulmonary oedema. Transthoracic and transoesophageal echocardiograms revealed significantly elevated AV gradients and thickened AV leaflets. These findings were suggestive of bioprosthetic valve thrombosis (BVT). The patient was treated with intravenous heparin and commenced on vitamin K antagonist. BVT remains an under recognised cause of late prosthetic valve dysfunction. A lack of awareness of BVT occurring beyond 3 months post-implantation is likely to account for this. Furthermore, structural valve degeneration is the most common mechanism of late prosthetic valve dysfunction. Recognising the difference between the two aetiologies is crucial as the management plan differs significantly. Here, we report a case of very late bioprosthetic AV thrombosis diagnosed 8 years after implantation. This was successfully treated with systemic anticoagulation, thereby avoiding the need for redo cardiac surgery.

Role of prazosin on cardiovascular manifestations and pulmonary edema following severe scorpion stings in Saudi Arabia.

We report the ameliorating effects of prazosin on the cardiovascular CV manifestations and pulmonary edema PE after treatment with antivenom AV failed to improve the conditions of scorpion stung patients. Three cases of scorpion envenoming, 2 children and one adult, were received at the Accident and Emergency Department of Al-Birk Hospital, Asir Region, Saudi Arabia. They presented to the hospital late with features of severe perspiration, tachypnea, restlessness, drooling of saliva, priapism, sinus tachycardia, PE, and shock like syndrome. When polyvalent scorpion PVS AV and intensive supportive treatment failed to show any improvement, prazosin was administered to the patients, which resulted in dramatic improvement in the conditions of the patients. We conclude that PVS AV may not be beneficial in all cases of scorpion envenomation, and prazosin may be an effective alternative for treating scorpion sting cases with CV manifestations and PE.

Liver Transplant and Reexpansion Pulmonary Edema: A Case Report.

Hydrothorax occurs frequently in patients with endstage liver disease and usually requires drainage of pulmonary effusion during the hepatectomy phase of liver transplant. Reexpansion pulmonary edema is a rare but potentially fatal complication seen after rapid reexpansion of the collapsed lung following thoracentesis of pleural fluid or tube drainage of pneumothorax. This condition, which manifests with various degrees of clinical severity, is rarely reported following liver transplantation. Herein, we present a 62-year-old male patient who developed reexpansion pulmonary edema after drainage of massive pleural effusion, which caused a total collapse in the right hemithorax during liver transplant. Six hours after pleural fluid drainage, the patient developed a nonproductive cough, mild tachypnea, shortness of breath, and low oxygen saturation (88%). His chest radiograph showed diffuse heterogeneous opacities in the right hemithorax. Computed tomography of the thorax revealed consolidations containing air bronchograms and ground glass opacities in the parenchyma of the right lung; these findings did not extend to the periphery and were observed less frequently in the inferoposterior left lung. These symptoms and radiologic findings were diagnosed as reexpansion pulmonary edema. Complete clinical and radiologic improvements were achieved within 72 hours of mechanical ventilatory support.

Integrative Assessment of Congestion in Heart Failure Throughout the Patient Journey.

Congestion is one of the main predictors of poor patient outcome in patients with heart failure. However, congestion is difficult to assess, especially when symptoms are mild. Although numerous clinical scores, imaging tools, and biological tests are available to assist physicians in ascertaining and quantifying congestion, not all are appropriate for use in all stages of patient management. In recent years, multidisciplinary management in the community has become increasingly important to prevent heart failure hospitalizations. Electronic alert systems and communication platforms are emerging that could be used to facilitate patient home monitoring that identifies congestion from heart failure decompensation at an earlier stage. This paper describes the role of congestion detection methods at key stages of patient care: pre-admission, admission to the emergency department, in-hospital management, and lastly, discharge and continued monitoring in the community. The multidisciplinary working group, which consisted of cardiologists, emergency physicians, and a nephrologist with both clinical and research backgrounds, reviewed the current literature regarding the various scores, tools, and tests to detect and quantify congestion. This paper describes the role of each tool at key stages of patient care and discusses the advantages of telemedicine as a means of providing true integrated patient care.

[Pulmonary oedema after a knee arthroscopy]. / Oedème pulmonaire après une arthroscopie du genou.

Negative pressure pulmonary oedema is one form of non cardiogenic pulmonary oedema that can occur following any general anaesthesia in which the patient was intubated. This complication can be severe, resulting in death/life-threatening if not diagnosed and treated promptly. We report a case of negative pressure pulmonary oedema, in a 26-year-old man, secondary to inspiratory effort with laryngeal spasm. Patient was transferred to intensive care unit for monitoring and non invasive ventilation. Prevention, early diagnosis, and prompt treatment allowed a rapid and uncomplicated resolution.

Neurogenic pulmonary edema induced by subarachnoid hemorrhage:; case report on diagnostic and therapeutic implications.

An exemplary rare case of neurogenic pulmonary edema induced by intracranial hemorrhage was reported including diagnostic and therapeutic implications as well as management recommendations. A 35-year old man who was treated first by a neurosurgical approach because of a subarachnoid hemorrhage (bore hole trepanation) and subsequently on a surgical intensive care unit because of severe postoperative hemodynamic, cardiocirculatory, and pulmonary disruptions. To monitor cardiopulmonary condition and treatment effects, a Swan-Ganz catheter was placed in the pulmonary artery, since after trepanation, a critical cardiopulmonary status developed during postoperative mechanical ventilation and catecholamine administration. This condition was indicated by neurogenic pulmonary edema detected by control chest X-ray film and high oxygen load in the inspiratory air required for sufficient arterial oxygenation. After use of high positive end-exspiratory pressure (PEEP) (initially directed against neurogenic lesion), adaptation of initial dobutamine doses, initiation of norepinephrine administration, and substitution of fluids, the patient's blood pressure finally rose sufficiently to sustain regular cerebral blood perfusion and achieve better arterial oxygenation. Thus, the patient's cardiopulmonary condition stabilized and temporary cardiac insufficiency could be overcome. Subsequently, it became possible to decrease PEEP according to requirements to prevent or limit cerebral edema and to diminish catecholamine doses.