Decompression Syndrome Research Articles

Immediate Postoperative Results in the Surgical Treatment of Neoplastic Pericarditis - 76 Consecutive Cases.

Introduction: Pericardial effusion, accumulation of fluid in the pericardial sac, may develop in any type of cancer. It was revealed in up to 20% of oncological patients. Method: We made a retrospective study of patients with pericardial efusion presented in our clinic between 2010 and 2015. We included 76 consecutive patients with indication for peri cardial drainage - we performed on them 80 surgical procedures: pericardocentesis, subxiphoid pericardial window, left paraxifoidian pericardial window, intercostal video-assisted thoracic surgery (VATS) pericardial fenestration, and classical thoracic surgery (fenestration or partial pericardiectomy). We had patients with ages between 28 and 83 years. 23 patients were admitted with cardiac tamponade. The immediate postoperatory survival is 97.3 % and the 30-days-postoperatory survival is 81.5 %. Results: The immediate postoperatory mortality is 2.7% and the 30-days-postoperatory mortality is 8.5%. Conclusions: The immediate prognosis of the patient with malignant pericardial effusion is influenced by the risk of postoperative Low-Cardiac-Output-Syndrome (LCOS), or pericardial decompression syndrome (PDS), which remains the main cause of mortality. The long-term prognosis is related to the type of malignant tumor. The most effective tehnique with the lowest rate of recurrence is pericardo-pleural window done thoracoscopically/ by VATS; pericardocentesis has the highest rate of recurrence - 90% and is associated with high rates of cardiac complications and mortality.

Pericardial decompression syndrome: A comprehensive review.

Pericardial decompression syndrome (PDS) is an infrequent, life-threatening complication following pericardial drainage for cardiac tamponade physiology. PDS usually develops after initial clinical improvement following pericardiocentesis and is significantly underreported and may be overlooked in the clinical practice. Although the precise mechanisms resulting in PDS are not well understood, this seems to be highly associated with patients who have some underlying ventricular dysfunction. Physicians performing pericardial drainage should be mindful of the risk factors associated with the procedure including the rare potential for the development of PDS.

Abstract 17022: Pericardial Decompression Syndrome: Incidence in a Large Consecutive Series of Echocardiographic-Guided Pericardiocentesis Procedures

Introduction: Pericardial decompression syndrome (PDS) has been reported as a spectrum of cardiac decompensation following pericardiocentesis including ventricular failure, cardiogenic shock and pulmonary edema. PDS has been reported in patients undergoing drainage ≥450 mL of pericardial fluid. Hence judicious drainage of large volume effusions to avoid complication has been recommended Hypothesis: PDS complicating undergoing transthoracic echocardiography (TTE) guided pericardiocentesis is uncommen Methods: Consecutive patients undergoing TTE guided pericardiocentesis at our center from 1/2007 to 12/2016 were reviewed. Procedures were performed in a standard fashion under moderate conscious sedation with TTE determining the location of aspiration and determining adequate resolution of pericardial fluid post procedure. All fluid was removed at time of centesis regardless of the size of effusion, except for patients with severe pulmonary hypertension (n=9), who had staged removal of 100cc every 10 minutes. Post procedure, a pigtail catheter was left in the pericardial space for ongoing intermittent drainage and removed after the total net output was <50 mL/24 hours. Patients were monitored in an intermediate level care unit. All patients underwent repeat TTE at the time of catheter removal. Large volume was defined as ≥450 mL of fluid. Patients in whom pericardiocentesis was technically unsuccessful were excluded Results: Over a 10-year period a total of 1067 patients (57% male, mean age 62±16 years) underwent 1164 technically successful pericardiocentesis procedures. Of these, 561 patients had large volume (≥450 mL) aspirated (mean 750±345 mL aspirated, range 450 - 4300 mL). Patients had a pericardial catheter in place for a mean 2.9±2 days. One patient with pre-existing severe biventricular dysfunction after aspiration of 400cc developed hypotension that improved with reversal of sedation, but proceeded to have PEA arrest and die. No other patient developed clinical events of acute left or right heart failure, ventricular dysfunction, unexplained hypotension, cardiogenic shock or other clinical events that could relate to PDS Conclusions: At most one episode of PDS was observed after technically successful percutaneous pericardiocentesis in 1164 cases (561 were large volume), although whether this case was PDS is unclear. PDS appears to be very rare, and staging pericardial decompression over time may be unnecessary, other than, perhaps, in patients with severe ventricular dysfunction or severe pulmonary hypertension

Systolic dysfunction after pericardiocentesis: A case report of Pericardial Decompression Syndrome

Rationale: Pericardial decompression syndrome is under appreciated but potentially fatal complication post pericardiocentesis. It should be part of differential diagnosis if patient presents with severe shortness of breath or hemodynamic compromise post-intervention. Prompt management is central to successful outcomes Patient concerns: An interesting 69 year old gentleman who was initially treated for myelodysplastic syndrome and thereafter converted to acute myelogenous leukemia presented with neutropenic fever. Diagnosis: On routine investigations it was identified that patient had large pericardial effusion. Soon after the identification of large pericardial effusion, patient’s condition deteriorated and had hemodynamic collapse. Intervention: An emergent pericardiocentesis was performed successfully via sub-xiphoid approach Outcome: Clinically the patient deteriorated the next day and we performed echocardiogram which showed a dramatic decrease in ejection fraction (from 60-65% to 35%). Over the course of next two days, the patient showed remarkable recovery with ejection fraction of 50% without any intervention Lessons: Pericardial decompression syndrome is not a well-recognized fatal complication of pericardiocentesis. It should be part of differential diagnosis if patient develops hemodynamic compromise post procedure. Prompt management including supportive therapies, and/or administration of heart failure is crucial to the hemodynamic recovery. The major risk factor, based on a small case series, denotes surgical drainage as potential contributor. Large case control series needs to be pooled before bona fide risk factor can be ascertained.

Acute Right Ventricular Failure After Surgical Drainage of Pericardial Tamponade: A Case Report of Pericardial Decompression Syndrome and Review of the Literature

Acute Right Ventricular Failure After Surgical Drainage of Pericardial Tamponade: A Case Report of Pericardial Decompression Syndrome and Review of the Literature

Başarılı Perikardiyosentez Sonrası Nadir ve Tehlikeli Bir Komplikasyon: Perikardiyal Dekompresyon Sendromu

Pericardial decompression syndrome (PDS) is an infrequent but mostly fatal complication after successful pericardiocentesis. We present a case of a 27-year-old female patient with suspected malignancy and cardiac tamponade treated with pericardiocentesis, followed by acute pulmonary edema and cardiac arrest 2 hours later. We also reviewed possible mechanisms involved in PDS pathophysiology in the context of literature data.

Pericardial Decompression Syndrome in a Patient With Low Volume Pericardial Fluid Removal

SESSION TITLE: Critical Care 3 SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 31, 2017 at 01:30 PM - 02:30 PM INTRODUCTION: Pericardial decompression syndrome (PDS), typically presents with hemodynamic and/or pulmonary edema, immediately or up to 1-2 days following surgical pericardiostomy or pericardiocentesis. Many of reported cases noted new onset LV dysfunction, with 70% of those studies demonstrating normalization of LV systolic function. CASE PRESENTATION: A 54-year-old male without prior cardiac or pulmonary history, presented with dyspnea for 1 week and worsening pleuritic chest pain. On presentation suddenly became hypotensive 75/36, tachypneic and diaphoretic. Cardiac enzymes were negative and electrocardiogram showed no acute ST abnormalities. Computed tomography angiography chest was negative for pulmonary embolism. 2-D echocardiogram showed moderate-to-large pericardial effusion with mitral inflow abnormalities suggestive of tamponade. A left anterior thoracotomy with pericardial window & biopsy was performed and approximately 200cc of cloudy watery fluid was removed, with 594 cc removed via chest tubes over the next three days Subsequently, 36 hours later he developed increased dyspnea, requiring Bilevel Positive Airway Pressure (BiPAP) to maintain oxygenation. X-ray (Fig 1) demonstrated diffuse bilateral interstitial and alveolar disease. Treated with lasix and remained on BiPAP for 4 days, and weaned to high flow nasal cannula. Repeat X-ray (Fig 2), decreased bilateral interstitial and alveolar parenchymal. Three weeks later, the echocardiogram revealed ejection fraction, 50-55% with left ventricular diastolic dysfunction. DISCUSSION: Several mechanisms have been proposed for PDS, the hemodynamic hypothesis theorizes that with removal of the pericardial fluid, the rapid restoration of the right ventricular function would result in increased venous return and bowing of the right ventricle into the left, resulting in pulmonary edema and left-sided heart failure. In the case of the ischemic hypothesis the increased pericardial pressure would compress the epicardial arteries, which has shown to reduce coronary blood flow and may incite myocardial stunning and hibernation. Finally, elevated pericardial pressure would also promote activation of sympathetic nervous system, a high catecholamine state, and relief of pressure could unmask a pre-existing compensated LV and/or RV dysfunction. Current understanding has proposed that gradual pericardial fluid removal until the tamponade physiology resolves may reduce the risk of PDS. Interestingly, only 200cc of pericardial fluid was removed initially, with 590cc over 3 days, slowing the hemodynamic change, but still resulting in PDS, but without adverse outcome. CONCLUSIONS: Our case suggests low volume pericardial fluid removal does not negate the occurrence of PDS, but may decrease the severity. Reference #1: Rajesh, Pradhan, et al. Patient characteristics and predictors of mortality associated with pericardial decompression syndrome: a comprehensive analysis of published cases. EHJ-ACVC 2015, Vol. 4(2) 113-120 DISCLOSURE: The following authors have nothing to disclose: Tamer Said Ahmed, Jonathan BarreraCalix, Larry Woods, Daniel Woredekal No Product/Research Disclosure Information

Two types of bone necrosis in the Middle Triassic Pistosaurus longaevus bones: the results of integrated studies.

Avascular necrosis, diagnosed on the basis of either a specific pathological modification of the articular surfaces of bone or its radiologic appearance in vertebral centra, has been recognized in many Mesozoic marine reptiles as well as in present-day marine mammals. Its presence in the zoological and paleontologic record is usually associated with decompression syndrome, a disease that affects secondarily aquatic vertebrates that could dive. Bone necrosis can also be caused by infectious processes, but it differs in appearance from decompression syndrome-associated aseptic necrosis. Herein, we report evidence of septic necrosis in the proximal articular surface of the femur of a marine reptile, Pistosaurus longaevus, from the Middle Triassic of Poland and Germany. This is the oldest recognition of septic necrosis associated with septic arthritis in the fossil record so far, and the mineralogical composition of pathologically altered bone is described herein in detail. The occurrence of septic necrosis is contrasted with decompression syndrome-associated avascular necrosis, also described in Pistosaurus longaevus bone from Middle Triassic of Germany.

Unusual intraosseous fossilized soft tissues from the Middle Triassic Nothosaurus bone.

Fossilized soft tissues, occasionally found together with skeletal remains, provide insights to the physiology and functional morphology of extinct organisms. Herein, we present unusual fossilized structures from the cortical region of bone identified in isolated skeletal remains of Middle Triassic nothosaurs from Upper Silesia, Poland. The ribbed or annuli-shaped structures have been found in a sample of partially demineralized coracoid and are interpreted as either giant red blood cells or as blood vessel walls. The most probable function is reinforcing the blood vessels from changes of nitrogen pressure in air-breathing diving reptiles. These structures seem to have been built of extensible muscle layers which prevent the vessel damage during rapid ascent. Such suspected function presented here is parsimonious with results of previous studies, which indicate rarity of the pathological modification of bones associated with decompression syndrome in Middle Triassic nothosaurs.

“Trap within a Trap”–A Case of Takotsubo Cardiomyopathy Following Drainage of a Large Pericardial Effusion

A 52-year-old female presented for evaluation of dyspnoea. Background history was significant for ischaemic heart disease with previous PCI to the LAD and Crohn's disease managed with balsalazide and budesonide. On examination, she appeared distressed and unwell. She had a narrow pulse pressure (blood pressure, 120/100 mmHg), sinus tachycardia (heart rate, 110 beats/min), tachypnoea (respiratory rate 24 breaths/min) and hypoxia (O2 sats 91% on RA). The JVP was elevated 5 cm. Heart sounds were soft and the chest was clear to auscultation. Bedside echo demonstrated a large pericardial effusion with signs of cardiac tamponade including diastolic collapse of the RA/RV. Pericardiocentesis drained 1.2L of blood stained fluid. Post-pericardiocentesis echo showed normal right heart filling and normal left ventricular systolic function. A few hours post the procedure the patient complained of chest discomfort. ECG showed new T wave inversion antero-laterally. Serial troponins were 20 and 472 ng/L. Coronary angiography was performed which revealed a patent stent in the LAD with non-obstructive disease elsewhere. Left ventriculogram confirmed classical Takotsubo cardiomyopathy. She was managed with bisoprolol and ramipril. Echo ten days later showed normal LV size and function. Cytology from the pericardial aspirate was consistent with adenocarcinoma. A PET scan suggested a primary lung malignancy with widespread metastatic disease. Unfortunately the patient had a rapid decline and passed away with her family by her side. In conclusion Takotsubo cardiomyopathy is rare occurrence post pericardiocentesis. Pericardial decompression syndrome, myocardial perforation and coronary artery laceration should be also be considered in the unstable patient post pericardiocentesis.

Relationship between reconstruction of the clivo -axial angle and curative effect in posterior approach surgery for the treatment of upper cervical spine anomaly instability

Objective The aim of this study was to describe the clinical outcomes and improvement of clivo-axial angle (CAA) during the posterior approach surgery of upper cervical anomaly instability patients. Methods All of 32 patients with symptomatic upper cervical anomaly instability were followed up from 2004 Apr. to 2014 Aug. in which 1 patient was excluded because of reoperation. There were 10 patients with OS odontiodeum,5 with odontoid deformity, 4 with Klipple-Feil syndrome, 4 with atlantoaxial dislocation, 4 with atlantoaxial instability, 1 with rheumatoid arthritis, 1 with old odontoid fracture, 1 with OS odontoideum and foramen magnum stenosis, 1 with basilarinvagination and Klipple-Feil syndrome. They were all performed posterior reduction internal fixation and fusion, and then released spinal cord compression with the promotion of CAA. The patients were divided into two groups on the basis of decompression or not: nondecompression group 17 cases (male 8 cases, female 9 cases; age 13-65 years old, average 50.1 years old) and decompression group 14 cases (male 7 cases, female 7 cases; age 19-68 years old, average 49.6 years old). The CAA numbers were measured and compared. The clinic date was compared between preoperatively and postoperatively, which included Neck Disability Index and Nurick Classification System for Myelopathy. Results All patients were followed up, the follow-up time of non-decompression group was 0.7-10.7 years, average 2.9 years; the follow-up time of compression group was 0.3-5.5 years, average 2.9 years. Analysis of CAA, NDI and Nurick score were performed with t-test. The postoperative CAA, NDI and Nurick score improved significantly compared to preoperative ones. There was no difference between non-decompression group and decompression group. One patient felt nausea and vomited, one got soleal vein thrombosis, one had a swelling face and blurring vision and one had decompression syndrome after operation, all of these were improved using respectively therapy. No such serious complications as injury to vertebral artery, infection or internal fixation loosening occurred. Conclusion Neck ability and spinal cord function was significantly improved through increasing CAA for the upper cervical anomaly instability patients underwent posterior reduction internal fixation andfusion. Key words: Atlanto-axial joint; Atlanto-occipital joint; Joint instability; Spinal cord compression; Cranial fossa, posterior

Use of hyperbaric oxygenation for wound management

Hyperbaric oxygenation consists in exposing patients to increased gas pressures while inhaling pure oxygen. It involves the use of hyperbaric chambers that can double or triple gas pressure inside them. Hyperbaric oxygenation may be useful in different clinical situations, but mostly for the treatment of decompression syndrome. In the last decades, it has been used for the management of different kinds of wounds. Hyperbaric oxygenation not only increases the delivery of oxygen to damaged tissues, but also stimulates angiogenesis, collagen synthesis, stem cell migration and local immune response. Clinical trials that have addressed the use of hyperbaric oxygenation are difficult to compare due to their heterogeneity in terms of experimental design, kind of injuries involved and assessment of outcome. Even though, most studies support the concept that hyperbaric oxygenation accelerates the healing process.

Pericardial decompression syndrome: A rare and potentially dramatic complication of pericardiocentesis

Pericardial decompression syndrome: A rare and potentially dramatic complication of pericardiocentesis

Decompression syndrome and diving behavior in Odontochelys, the first turtle

Odontochelys semitestacea, the oldest known turtle, from the Late Triassic of China, shows a pathology. Sharply defined, focal depressions were noted on the articular surfaces of both humeri, documenting avascular necrosis. Diving habits of Mesozoic marine reptiles have been characterized on the basis of this localized form of bone death attributed to decompression syndrome. Pursuit by a predator was likely the cause of dangerously rapid depth changes by swimming turtles. The prevalence of avascular necrosis decreased geometrically from the Cretaceous to the Pleistocene. This study suggests that the habit of repetitive diving in turtles was already present in the Late Triassic, but that protective physiological and behavioral adaptations had not yet evolved.

PATIENT CHARACTERISTICS AND PREDICTORS OF MORTALITY ASSOCIATED WITH PERICARDIAL DECOMPRESSION SYNDROME

Pericardial decompression syndrome (PDS) is a rare and potentially fatal complication of apparently successful pericardiocentesis, characterized by paradoxical hemodynamic deterioration, ventricular dysfunction and pulmonary edema. We sought to elucidate epidemiology and clinical factors associated

Perspectives on decompression syndrome and the methodology of science

Perspectives on decompression syndrome and the methodology of science

Adaptations for marine habitat and the effect of Triassic and Jurassic predator pressure on development of decompression syndrome in ichthyosaurs

Decompression syndrome (caisson disease or the "the bends") resulting in avascular necrosis has been documented in mosasaurs, sauropterygians, ichthyosaurs, and turtles from the Middle Jurassic to Late Cretaceous, but it was unclear that this disease occurred as far back as the Triassic. We have examined a large Triassic sample of ichthyosaurs and compared it with an equally large post-Triassic sample. Avascular necrosis was observed in over 15% of Late Middle Jurassic to Cretaceous ichthyosaurs with the highest occurrence (18%) in the Early Cretaceous, but was rare or absent in geologically older specimens. Triassic reptiles that dive were either physiologically protected, or rapid changes of their position in the water column rare and insignificant enough to prevent being recorded in the skeleton. Emergency surfacing due to a threat from an underwater predator may be the most important cause of avascular necrosis for air-breathing divers, with relative frequency of such events documented in the skeleton. Diving in the Triassic appears to have been a "leisurely" behavior until the evolution of large predators in the Late Jurassic that forced sudden depth alterations contributed to a higher occurrence of bends.

Decompression syndrome, ear-plug and barotrauma

Sir, We read with great interest the paper by Phatak et al. which was published in Jul-Sep issue of your journal.[1] They described a severe case of decompression sickness in a breath-hold diver in India. After stating that no formal education was given to divers regarding diving diseases and preventive measures in India, they imply that diving injuries can be prevented with proper education and training. We hope that this case will ignite a discussion of the problems of divers in India. The authors also recommend that “divers should use ear-plugs for protection from barotrauma”. We think that a general recommendation of the use of ear-plugs for divers may be harmful and a clear explanation of how and when to use ear-plugs during diving is required. Since regular (solid) ear-plugs will totally obstruct external ear cannel, a closed space will be created between the ear-plug and tympanic membrane. As other air-filled spaces in the body, this “new” closed space will be subjected to pressure alterations during diving. The air between the ear-plug and tympanic membrane will shrink during decent according to Boyle's law and either the ear-plug will move toward the tympanic membrane or the tympanic membrane will burst to equalize the pressure inside this space and environment. Ear-plugs may be used during swimming to protect the ear canal from water but it is not recommended during diving because of the increased risk of barotrauma as explained above. There are commercially available ear-plugs that allow the air to vent, so called “vented” ear-plugs. It is suggested that since vented ear-plugs allow pressure equalization, they may be used in divers to prevent ear squeeze. However, if the hole in the vented ear-plug is closed by ear wax, there is a risk of barotrauma. Furthermore, the data on the effectiveness and safety of vented ear-plugs is anecdotal and no clinical trial has been reported yet. In conclusion, considering that there is no formal education for divers in India, recommendations to the diving community should be made by being cautious. Solid (non-vented) ear-plugs are not recommended for diving.

Decompression syndrome (Caisson disease) in an Indian diver

Acute decompression syndrome (Caisson’s disease) is an acute neurological emergency in divers. It is caused due to release of nitrogen gas bubbles that impinge the blood vessels of the spinal cord and brain and result in severe neurodeficit. There are very few case reports in Indian literature. There are multiple factors in the pathogenesis of Acute decompression syndrome (Caisson’s disease) such as health problems in divers (respiratory problems or congenital heart diseases like atrial septal defect, patent ductus arteriosus etc), speed of ascent from the depth and habits like smoking that render divers susceptible for such neurological emergency. Usually, immediate diagnosis of such a condition with MRI is not possible in hospitals in the Coastal border. Even though, MRI is performed, it has very low specificity and sensitivity. Facilities like hyperbaric oxygen treatment are virtually non-existent in these hospitals. Therefore, proper education of the divers and appropriate preventive measures in professional or recreational divers is recommended.

Acute management of vascular air embolism

Vascular air embolism (VAE) is known since early nineteenth century. It is the entrainment of air or gas from operative field or other communications into the venous or arterial vasculature. Exact incidence of VAE is difficult to estimate. High risk surgeries for VAE are sitting position and posterior fossa neurosurgeries, cesarean section, laparoscopic, orthopedic, surgeries invasive procedures, pulmonary overpressure syndrome, and decompression syndrome. Risk factors for VAE are operative site 5 cm above the heart, creation of pressure gradient which will facilitate entry of air into the circulation, orogenital sex during pregnancy, rapid ascent in scuba (self contained underwater breathing apparatus) divers and barotrauma or chest trauma. Large bolus of air can lead to right ventricular air lock and immediate fatality. In up to 35% patient, the foramen ovale is patent which can cause paradoxical arterial air embolism. VAE affects cardiovascular, pulmonary and central nervous system. High index of clinical suspicion is must to diagnose VAE. The transesophgeal echocardiography is the most sensitive device which will detect smallest amount of air in the circulation. Treatment of VAE is to prevent further entrainment of air, reduce the volume of air entrained and haemodynamic support. Mortality of VAE ranges from 48 to 80%. VAE can be prevented significantly by proper positioning during surgery, optimal hydration, avoiding use of nitrous oxide, meticulous care during insertion, removal of central venous catheter, proper guidance, and training of scuba divers.