A diver with immersion pulmonary oedema and prolonged respiratory symptoms.

Immersion pulmonary oedema (IPE) is particularly associated with an excessive reaction to exercise and/or cold stress. IPE usually resolves without recompression therapy within a day or two. Herein we report a diver diagnosed with IPE, in whom symptoms persisted for five days. A 58-year-old man presented with sudden onset of dyspnoea, cough and haemoptysis after surfacing. He was an experienced diving instructor with a history of moderate mitral valve regurgitation. While IPE was diagnosed and oxygen administered, respiratory symptoms deteriorated, and serum C-reactive protein elevated. No evidence of infection was seen. Three hyperbaric oxygen treatments were given on the basis of suspected decompression sickness, and symptoms subsequently resolved. The recently diagnosed mitral valve regurgitation and inflammatory response were considered to have contributed to the prolongation of symptoms.

Revascularization of atherosclerotic renal artery stenosis for chronic heart failure versus acute pulmonary oedema.

AIM: The aim of the study is to determine whether the apparent benefit of revascularization of renal artery stenosis for 'flash' pulmonary oedema extends to heart failure patients without a history of prior acute pulmonary oedema. METHODS: A prospective study of patients with renal artery stenosis and heart failure at a single centre between 1 January 1995 and 31 December 2010. Patients were divided into those with and without previous acute pulmonary oedema/decompensation. Survival analysis compared revascularization versus medical therapy in each group using Cox regression adjusted for age, estimated glomerular filtration rate, blood pressure and co-morbidities. RESULTS: There were 152 patients: 59% male, 36% diabetic, age 70 ± 9 years, estimated glomerular filtration rate 29 ± 17 mL/min per 1.73 m2 ; 52 had experienced previous acute pulmonary oedema (34%), whereas 100 had no previous acute pulmonary oedema (66%). The revascularization rate was 31% in both groups. For heart failure without previous acute pulmonary oedema, the hazard ratio for death after revascularization compared with medical therapy was 0.76 (0.58-0.99, P = 0.04). In heart failure with previous acute pulmonary enema, the hazard ratio was 0.73 (0.44-1.21, P = 0.22). For those without previous acute pulmonary oedema, the hazard ratio for heart failure hospitalization after revascularization compared with medical therapy was 1.00 (0.17-6.05, P = 1.00). In those with previous acute pulmonary oedema, it was 0.51 (0.08-3.30, P = 0.48). CONCLUSION: The benefit of revascularization in heart failure may extend beyond the current indication of acute pulmonary oedema. However, findings derive from an observational study.

Cardiovascular Abnormalities in Carbon Monoxide Poisoning.

Acute carbon monoxide (CO) poisoning is the most common cause of poisoning and poisoning-related death in the United States. It manifests as broad spectrum of symptoms ranging from mild headache, nausea, and fatigue to dizziness, syncope, coma, seizures resulting in cardiovascular collapse, respiratory failure, and death. Cardiovascular complications of CO poisoning has been well reported and include myocardial stunning, left ventricular dysfunction, pulmonary edema, and arrhythmias. Acute myocardial ischemia has also been reported from increased thrombogenicity due to CO poisoning. Myocardial toxicity from CO exposure is associated with increased short-term and long-term mortality. Carboxyhemoglobin (COHb) levels do not correlate well with the clinical severity of CO poisoning. Supplemental oxygen remains the cornerstone of therapy for CO poisoning. Hyperbaric oxygen therapy increases CO elimination and has been used with wide variability in patients with evidence of neurological and myocardial injury from CO poisoning, but its benefit in limiting or reversing cardiac injury is unknown. We present a comprehensive review of literature on cardiovascular manifestations of CO poisoning and propose a diagnostic algorithm for managing patients with CO poisoning.

Severe pulmonary edema following hyperbaric oxygen therapy for acute carbon monoxide poisoning: a case report and clinical experience.

PURPOSE: Pulmonary edema following hyperbaric oxygen (HBO2) therapy is a rare clinical phenomenon. This case report describes such a patient - a 56-year-old woman who suffered from severe pulmonary edema after HBO2 therapy for carbon monoxide (CO) poisoning. CASE: Patient experienced ecphysesis and dyspnea suddenly after HBO2 therapy (100% oxygen at 0.25 MPa, for 60 minutes with a five-minute air break and decompression at 0.01 MPa/minute). Post therapy her heart rate (HR), blood pressure (BP), respiratory rate (RR) and oxygen saturation (SO2) were 140 bpm, 60/40 mmHg, 38 bpm and 84%, respectively. Diagnoses of acute pulmonary edema and shock were made. Various treatments including antishock, tracheal intubation, mechanical ventilation for respiratory support, a diuretic, dexamethasone, asthma relief, and acidosis correction were administered. Pulmonary computed tomography (CT) indicated significant pulmonary edema. Due to active treatment, the patient showed gradual improvement. Pulmonary CT re-examination showed pulmonary edema markedly improved. At the two-year follow-up, the patient reported no abnormal mental or neurological symptoms. CONCLUSION: Acute pulmonary edema is rare but can lead to serious side effects of HBO2 therapy in patients with severe acute CO poisoning. This complication must be must considered when administering HBO2 therapy to patients with severe CO poisoning.

Endometriosis de pared abdominal. Caso clínico y revisión / Abdominal wall endometriosis. Clinical case and review

Se presenta un caso de endometriosis de pared abdominal, en una mujer de 33 años, G1C1, con cesárea 13 años antes. Apareció nódulo subcutáneo cerca de la cicatriz de Pfannenstiel de la cesárea 6 años antes, y presentó dolor cíclico en la zona, desde hacía 6 meses. En la ecografía abdominal tenía nódulo irregular de 12x25 mm, que ya se había visto en una tomografía computadorizada. El diagnóstico clínico de edema pulmonar agudo, se confirmó con la anatomía patológica de biopsia con anestesia local, viendo tejido adiposo y fragmentos de endometriosis, y posteriormente en la resección del nódulo (AU)

We present a rare case of abdominal wall endometriosis in a 33 year-old woman, G1C1, with cesarean section 13 years before. She had a subcutaneous mass near to Pfannenstiel surgical scar 6 years before, and she presented cyclic pain in the area from 6 months back. In the transabdominal sonography there was a hypoechoic mass of 12x25 mm, déjà vu in the computed tomography. The clinical diagnostic of abdominal wall endometriosis was confirmed in the Pathology of local anesthesic biopsy, showing adipose tissue and endometriosis fragments, and was confirmed after resection of the mass (AU)

Reexpansion pulmonary edema following local anesthetic thoracoscopy: correlation and evolution of radiographic and ultrasonographic findings.

Local anesthetic (medical) thoracoscopy is used with increasing frequency by pulmonologists worldwide for both diagnostic and therapeutic purposes, notably in comorbid patients who may not be physiologically robust enough for general anesthesia. Understanding the complications that can arise and how to manage them is crucial for any physician performing this procedure. Reexpansion pulmonary edema is a rare but recognized complication of draining pleural effusions and pneumothoraces that has not been described previously in association with physician-led thoracoscopy. This case provides an opportunity for an overview of what is known about this unusual but potentially fatal condition. Data correlating ultrasonographic, radiographic, and clinical progression are also presented to highlight the potential usefulness of ultrasonography in identifying lung parenchymal abnormalities such as extravascular lung water.

Wilderness Medical Society practice guidelines for treatment of exercise-associated hyponatremia.

Exercise-associated hyponatremia (EAH) typically occurs during or up to 24 hours after prolonged physical activity, and is defined by a serum or plasma sodium concentration below the normal reference range of 135 mEq/L. It is also reported to occur in individual physical activities or during organized endurance events conducted in austere environments in which medical care is limited or often not available, and patient evacuation to definitive care is often greatly delayed. Rapid recognition and appropriate treatment are essential in the severe form to ensure a positive outcome. Failure in this regard is a recognized cause of event-related fatality. In an effort to produce best practice guidelines for EAH in the austere environment, the Wilderness Medical Society convened an expert panel. The panel was charged with the development of evidence-based guidelines for management of EAH. Recommendations are made regarding the situations when sodium concentration can be assessed in the field and when these values are not known. These recommendations are graded based on the quality of supporting evidence and balance between the benefits and risks/burdens for each parameter according to the methodology stipulated by the American College of Chest Physicians.

Device monitoring strategies in acute heart failure syndromes.

Acute heart failure syndromes (AHFS) represent the most common discharge diagnoses in adults over age 65 and translate into dramatically increased heart failure-associated morbidity and mortality. Conventional approaches to the early detection of pulmonary and systemic congestion have been shown to be of limited sensitivity. Despite their proven efficacy, disease management and structured telephone support programs have failed to achieve widespread use in part due to their resource intensiveness and reliance upon motivated patients. While once thought to hold great promise, results from recent prospective studies on telemonitoring strategies have proven disappointing. Implantable devices with their capacity to monitor electrophysiologic and hemodynamic parameters over long periods of time and with minimal reliance on patient participation may provide solutions to some of these problems. Conventional electrophysiologic parameters and intrathoracic impedance data are currently available in the growing population of heart failure patients with equipped devices. A variety of implantable hemodynamic monitors are currently under investigation. How best to integrate these devices into a systematic approach to the management of patients before, during, and after AHFS is yet to be established.

[Acute pulmonary edema in adult caused by tonsillar hypertrophy following removal of laryngeal mask airway].

Negative pressure pulmonary edema (NPPE) has been described after acute airway obstruction. In the following case, we observed a rare occurrence of pulmonary edema caused by chronic tonsillar hypertrophy in a woman following removal of laryngeal mask airway (LMA). A 38-year-old woman with breast cancer underwent mastectomy under general anesthesia using the LMA. With the patient fully awake, the LMA was removed. Abruptly 7 minutes afterward, she showed signs of intense dyspnea, generalized rhonchus and progressive desaturation, and obstructive tonsillar hypertrophy was noticed. Acute lung edema was suspected and treatment started with oxygen therapy, bronchodilators, intravenous corticoids and loop diuretics. She was then intubated to secure airway and provide adequate ventilation with PEEP. Fortunately, the symptoms progressively remitted satisfactorily, and she was subsequently extubated 18 hours later with no complications. NPPE is an infrequent medical emergency and its early diagnosis and recognition are likely to lead to successful management of this potentially serious complication.

Negative pressure pulmonary edema complicating an electrophysiological study.

We report on a case of acute non-cardiogenic negative-pressure pulmonary edema developed during an ablation procedure of an accessory pathway in a patient with no structural heart disease. That potentially serious complication has not been previously reported during an interventional cardiology procedure.

Recompression treatment for decompression illness: 5-year report (2003-2007) from National Centre for Hyperbaric Medicine in Poland.

A serious diving accident can occur in recreational diving even in countries where diving is not very popular due to the fact that diving conditions there are not as great as in some tropical diving locations. The estimated number of injured divers who need recompression treatment in European hyperbaric facilities varies between 10 and 100 per year depending on the number of divers in the population, number of dives performed annually, and number of hyperbaric centres in the country. In 5 years of retrospective observation in Poland (2003-2007) there were 51 cases of injured recreational divers recorded. They either dived locally or after returning home by air from a tropical diving resort. All of them were treated with recompression treatment in the National Centre for Hyperbaric Medicine in Gdynia which has capability to treat any patient with decompression illness using all currently available recompression schedules with any breathing mixtures including oxygen, nitrox, heliox or trimix. The time interval between surfacing and first occurrence of symptoms was significantly lower in the group of patients with neurological decompression sickness or arterial gas embolism (median 0.2 hours) than in the group of patients with other types of decompression sickness (median 2.0 hours). In both groups, there were different types of recompression tables used for initial treatment and different number of additional sessions of hyperbaric oxygenation (HBO) prescribed, but the final outcome was similar. Complete resolution of symptoms after initial recompression treatment was observed in 24 cases, and this number was increased to 37 cases after additional HBO sessions (from 1 to 20). In the final outcome, some residual symptoms were observed in 12 cases. In 2 cases initial diagnosis of decompression sickness type I was rejected after initial recompression treatment and careful re-evaluation of diving profiles, risk factors and reported symptoms.

[Serious and sometimes fatal consequences of high-altitude pulmonary oedema]. / Ernstige en soms fatale gevolgen van hoogtelongoedeem.

Three women aged 25, 34 and 22 years respectively, experienced high-altitude pulmonary oedema during a climbing holiday. The first patient presented with complaints arising from a fast ascent to high altitude and was treated with acetazolamide and rapid descent. She recovered without any complications. The second patient developed symptoms during the night, which were not recognised as high-altitude pulmonary oedema. The next morning she died while being transported down on a stretcher without having received any medication or oxygen. The third case was not a specific presentation of high-altitude pulmonary oedema but autopsy revealed pulmonary oedema. This woman had already been higher up on the mountain before she developed complications. The cases illustrate the seriousness of this avoidable form of high altitude illness. The current Dutch national guidelines advise against the use of medication by lay people. A revision is warranted: travellers to high altitude should be encouraged to carry acetazolamide, nifedipine and corticosteroids on the trip. Travel guides ought to be trained to use these drugs. In addition climbing travellers should be encouraged to adopt appropriate preventive behaviour and to start descending as soon as signs of high-altitude pulmonary oedema develop.

Carbon monoxide toxicity with neurological and cardiac complications

A family suffered carbon monoxide toxicity, with cerebral and / or cardiac complications, while sleeping in the cabin on a recreational boat. This article describes a couple exposed to a malfunctioning air-conditioning system on the boat, which subsequently developed the unique combination of cerebral symptoms and a non Q/non-ST elevation myocardial infarction, with enzyme elevations and electrocardiographic abnormalities. This interesting complication of a myocardial infarction secondary to carbon monoxide toxicity, associated with neurological manifestations, is reviewed.

Adenosine A2A receptor activation reduces inflammation and preserves pulmonary function in an in vivo model of lung transplantation.

BACKGROUND: Reperfusion injury continues to significantly affect patients undergoing lung transplantation. Isolated lung models have demonstrated that adenosine A 2A receptor activation preserves function while decreasing inflammation. We hypothesized that adenosine A 2A receptor activation by ATL-146e during the initial reperfusion period preserves pulmonary function and attenuates inflammation in a porcine model of lung transplantation. METHODS: Mature pig lungs preserved with Viaspan (Barr Laboratories, Pomona, NY) underwent 6 hours of cold ischemia before transplantation and 4 hours of reperfusion. Animals were treated with (ATL group, n = 7) and without (IR group, n = 7) ATL-146e (0.05 microg kg -1 . min -1 ATL-146e administered intravenously for 3 hours). With occlusion of the opposite pulmonary artery, the animal was maintained for the final 30 minutes on the allograft alone. Recipient lung physiology was monitored before tissue evaluation of pulmonary edema (wet-to-dry weight ratio), myeloperoxidase assay, and tissue tumor necrosis factor alpha by means of enzyme-linked immunosorbent assay. RESULTS: When the ATL group was compared with the IR group, the ATL group had better partial pressure of carbon dioxide (43.8 +/- 4.1 vs 68.9 +/- 6.3 mm Hg, P < .01) and partial pressure of oxygen (272.3 +/- 132.7 vs 100.1 +/- 21.4 mm Hg, P < .01). ATL-146e-treated animals exhibited lower pulmonary artery pressures (33.6 +/- 2.1 vs 47.9 +/- 3.5 mm Hg, P < .01) and mean airway pressures (16.25 +/- 0.08 vs 16.64 +/- 0.15 mm Hg, P = .04). ATL-146e-treated lungs had lower wet-to-dry ratios (5.9 +/- 0.39 vs 7.3 +/- 0.38, P < .02), lower myeloperoxidase levels (2.9 x 10 -5 +/- 1.2 x 10 -5 vs 1.3 x 10 -4 +/- 4.0 x 10 -5 DeltaOD mg -1 . min -1 , P = .03), and a trend toward decreased lung tumor necrosis factor alpha levels (57 +/- 12 vs 96 +/- 15 pg/mL, P = .06). The ATL group demonstrated significantly less inflammation on histology. CONCLUSION: Adenosine A 2A activation during early reperfusion attenuated lung inflammation and preserved pulmonary function in this model of lung transplantation. ATL-146e and similar compounds could play a significant role in improving outcomes of pulmonary transplantation.

Carbon monoxide toxicity with neurological and cardiac complications.

A family suffered carbon monoxide toxicity, with cerebral and / or cardiac complications, while sleeping in the cabin on a recreational boat. This article describes a couple exposed to a malfunctioning air-conditioning system on the boat, which subsequently developed the unique combination of cerebral symptoms and a non Q/non-ST elevation myocardial infarction, with enzyme elevations and electrocardiographic abnormalities. This interesting complication of a myocardial infarction secondary to carbon monoxide toxicity, associated with neurological manifestations, is reviewed.

Use of the Gamow Bag by EMT-basic park rangers for treatment of high-altitude pulmonary edema and high-altitude cerebral edema.

As part of an emergency medical system protocol, national park service rangers certified at the level of an emergency medical technician-basic (EMT-B) are taught to recognize and treat high-altitude pulmonary edema and high-altitude cerebral edema. In Sequoia and Kings Canyon National Parks, this is done with the assistance of physician on-line medical control as a backup. High-altitude pulmonary edema and high-altitude cerebral edema are both potentially fatal altitude illnesses that can be particularly problematic in the backcountry, where evacuation may be delayed. We report a case of high-altitude pulmonary edema and high-altitude cerebral edema occurring at moderate altitude that was successfully treated by park rangers with the Gamow Bag.