Septic pulmonary embolization (SPE) is a rare but serious disorder. It is a well-recognized potential problem in the settings of tricuspid valve endocarditis, septic thrombophlebitis, infected central venous catheters, and postanginal septicemia. Less well documented is the occurrence of SPE in patients with periodontal disease without suppurative thrombophlebitis of the great vessels of the neck. We report a patient with SPE in whom periodontal disease was the only identifiable nidus of infection and review the literature regarding the four other patients reported to have suffered this complication.

O tromboembolismo pulmonar causado por obstrução de ramos arteriais pulmonares por trombos originados de outras partes do corpo apresenta elevada incidência. Em 5% dos casos ocorre a cronificação do processo e manutenção ou agravamento da hipertensão pulmonar Duas hipóteses explicam a cronificação nos casos de embolia pulmonar: 1. manutenção do fator oclusivo como fundamental para o desenvolvimento da resposta vascular pulmonar caracterizada por hipertrofia da camada média; 2. hipertensão pulmonar secundária a uma arteriopatia inicial, nos pacientes que evoluíram de maneira desfavorável. Este estudo tem por objetivo avaliar sob critérios histopatológicos qualitativos e quantitativos o comportamento do leito arterial pulmonar distal (pré e intra-acinar), comparativamente em pulmões de pacientes sem tromboembolismo prévio e de pacientes portadores de tromboembolismo agudo e crônico. Para tanto, estudou-se a resposta vascular através de estudo histológico de 31 casos de embolia (aguda e crônica), comparando-os com 24 pacientes do grupo controle (Infarto agudo do miocárdio) (análise de autópsias). As lâminas de tecido pulmonar foram preparadas e coradas em hematoxilina-eosina e Miller. A análise realizada foi dividida em qualitativa (vasoconstrição e proliferação intimal concêntrica) e quantitativa (hipertrofia da camada média). Foram observadas alterações histopatológicas do leito arterial pulmonar distal nos pacientes portadores de quadro tromboembólico agudo e crônico, em relação aos pacientes sem tromboembolismo prévio. Estas alterações, entre os grupos agudo e crônico, foram: diferentes quanto aos critérios qualitativos, caracterizadas por maior vasoconstrição nos quadros tromboembólicos agudos e maior proliferação intimal concêntrica nos crônicos; semelhantes quanto aos critérios quantitativos, caracterizadas por hipertrofia da camada média. A isquemia decorrente da obstrução parece exercer um importante papel nestas alterações, o que, entretanto, necessita de comprovação futura / The pulmonary embolism, caused by pulmonary artery branches obstruction from thrombus originated on other parts of the body, has a high incidence. However, just 5% of the cases develop the cronification and pulmonary hypertension. Two hypotheses can explain the cronification of tromboembolic pulmonary events: 1. maintenance of occlusive factor with pulmonary vascular response characterized by medial hypertrophy; 2. pulmonary hypertensive response as an initial arteriopathy in patients with bad evolution. This study aims to evaluate histologic aspects of pulmonary arterial bed (quantitative and qualitative), and to compare the results from embolic cases with non embolic cases. The study evaluated 55 patients (31 with pulmonary embolic disease and 24 in the control group myocardium infarction). From the selected cases, the blades with pulmonary tissue were colored by two techniques (haematoxilin-eosin and Miller). The analysis encompassed qualitative (vasoconstriction and intimal proliferation) and quantitative (mensuration of medial thickness) observations. It has been observed histologic changes between the two groups with pulmonary embolic disease (chronic or acute), and the control group. The changes between the embolic groups were: 1. higher vasoconstriction in the acute group, 2. more intimal proliferation in the chronic group, 3. no difference in the quantitative response (medial thickness). The ischemic response to obstruction can perform an important role in these changes, but further studies are necessary. There was a similar response in chronic and acute cases

OBJECTIVE: CLOVES syndrome (CLO: congenital lipomatous overgrowth, V: vascular anomalies E: epidermal nevi S: spinal anomalies) is a rare, non-heritable sporadic overgrowth disorder with serious morbidity. Previous anecdotal reports indicate that CLOVES patients are at risk for serious thromboembolic events in the perioperative period. The purpose of this study is to systematically determine the adverse events associated with anesthesia and diagnostic or interventional procedures for CLOVES patients, so appropriate assessment of risk can be performed and adequate precautions can be taken in the future to prevent complications. METHODS: We selected our study cohort by gathering patients in the Vascular Anomalies Center (VAC) database with the diagnosis of CLOVES syndrome. Our primary group of interest was patients that were anesthetized at Boston Children's Hospital (BCH) since 2005. All patients having the diagnosis of CLOVES were included. IRB approval was obtained prior to patient selection. Data was collected from BCH electronic medical records. Patient age, gender, ASA level, estimated amount of blood loss (EBL), surgery status, MRI status, complication(s), type of complication if any, and medical history was recorded in a Microsoft Excel document on a password-protected computer. Data analysis was carried out with no statistical analysis beyond simple incidence and prevalence of certain characteristics due to the extremely small patient population. RESULTS: We found that out of the 38 patients in our cohort, 15 (or 39%) suffered from complications during the perioperative period. A total of 23 (or 61%) did not have any complications. Results further showed that pulmonary emboli, respiratory issues, and hypo/hypertension were the most prevalent complications. In addition we found that there was no correlation between substantial EBL and complication occurrence in this cohort. CONCLUSION: In comparison to preliminary studies of Alomari, 2008 and Sapp et al., 2007, we report a lower occurrence of thromboembolic events in CLOVES patients. We hypothesize that this is because patients at BCH were treated aggressively with various prophylactic methods to help minimize the risk of such events. We recommend that early prophylactic anticoagulation methods are applied to future patients. Additionally, we recommend that CLOVES patients be followed by a hematologist and care team that are familiar with the condition throughout their stay at the hospital to reduce the risk of thromboembolic events.

O tromboembolismo pulmonar causado por obstrução de ramos arteriais pulmonares por trombos originados de outras partes do corpo apresenta elevada incidência. Em 5% dos casos ocorre a cronificação do processo e manutenção ou agravamento da hipertensão pulmonar Duas hipóteses explicam a cronificação nos casos de embolia pulmonar: 1. manutenção do fator oclusivo como fundamental para o desenvolvimento da resposta vascular pulmonar caracterizada por hipertrofia da camada média; 2. hipertensão pulmonar secundária a uma arteriopatia inicial, nos pacientes que evoluíram de maneira desfavorável. Este estudo tem por objetivo avaliar sob critérios histopatológicos qualitativos e quantitativos o comportamento do leito arterial pulmonar distal (pré e intra-acinar), comparativamente em pulmões de pacientes sem tromboembolismo prévio e de pacientes portadores de tromboembolismo agudo e crônico. Para tanto, estudou-se a resposta vascular através de estudo histológico de 31 casos de embolia (aguda e crônica), comparando-os com 24 pacientes do grupo controle (Infarto agudo do miocárdio) (análise de autópsias). As lâminas de tecido pulmonar foram preparadas e coradas em hematoxilina-eosina e Miller. A análise realizada foi dividida em qualitativa (vasoconstrição e proliferação intimal concêntrica) e quantitativa (hipertrofia da camada média). Foram observadas alterações histopatológicas do leito arterial pulmonar distal nos pacientes portadores de quadro tromboembólico agudo e crônico, em relação aos pacientes sem tromboembolismo prévio. Estas alterações, entre os grupos agudo e crônico, foram: diferentes quanto aos critérios qualitativos, caracterizadas por maior vasoconstrição nos quadros tromboembólicos agudos e maior proliferação intimal concêntrica nos crônicos; semelhantes quanto aos critérios quantitativos, caracterizadas por hipertrofia da camada média. A isquemia decorrente da obstrução parece exercer um importante papel nestas alterações, o que, entretanto, necessita de comprovação futura / The pulmonary embolism, caused by pulmonary artery branches obstruction from thrombus originated on other parts of the body, has a high incidence. However, just 5% of the cases develop the cronification and pulmonary hypertension. Two hypotheses can explain the cronification of tromboembolic pulmonary events: 1. maintenance of occlusive factor with pulmonary vascular response characterized by medial hypertrophy; 2. pulmonary hypertensive response as an initial arteriopathy in patients with bad evolution. This study aims to evaluate histologic aspects of pulmonary arterial bed (quantitative and qualitative), and to compare the results from embolic cases with non embolic cases. The study evaluated 55 patients (31 with pulmonary embolic disease and 24 in the control group myocardium infarction). From the selected cases, the blades with pulmonary tissue were colored by two techniques (haematoxilin-eosin and Miller). The analysis encompassed qualitative (vasoconstriction and intimal proliferation) and quantitative (mensuration of medial thickness) observations. It has been observed histologic changes between the two groups with pulmonary embolic disease (chronic or acute), and the control group. The changes between the embolic groups were: 1. higher vasoconstriction in the acute group, 2. more intimal proliferation in the chronic group, 3. no difference in the quantitative response (medial thickness). The ischemic response to obstruction can perform an important role in these changes, but further studies are necessary. There was a similar response in chronic and acute cases

Elizabethkingia Meningoseptica (E. Meningoseptica) an oxidase-positive gram-negative aerobic rod.1-2 Although ubiquitous in nature and widely distributed in soil and water, it is not a part of normal human flora. Cases of outbreaks of meningitis in premature neonates or infants have been reported, however, very few cases have been reported in adults.3 Infection is primarily nosocomial, or hospital acquired and has been implicated in bacteremia, meningitis, pneumonia, endocarditis especially in immunocompromised individuals.2-4 We report a 29-year-old male with past medical history significant for intravenous drug abuse, hepatitis C, oxymorphone induced hemolytic uremic syndrome, who presented to hospital with altered mental status. On admission, patient was unresponsive to vocal commands, febrile (102.3 F), tachycardic and tachypneic. He had pinpoint pupils and diffuse petechiae. In addition, he had erythematous flat macular lesions on his palms and dorsum of hands as well as injection marks in left cubital fossa. Cardiac examination was significant for a grade III systolic murmur at apical region and diastolic murmur at left second intercostal space. Laboratory studies revealed thrombocytopenia (43,000m/microL), lactic acidosis (4.9mmol/L), serum creatinine (Cr) of 6.6 mg/dL, glomerular filtration rate (GFR) of 10 ml/min. Transthoracic echocardiogram (TTE) revealed large mobile vegetation on aortic valve measuring 3.6 x 0.72 cm. Patient’s presentation was consistent with infective endocarditis with the vegetation seen on TTE and patient’s physical findings. Magnetic Resonance Imaging of the brain showed numerous small hemorrhagic infarcts, likely secondary to emboli from aortic valve vegetation. Patient required intubation for airway protection and started on hemodialysis. He was initially started on Meropenem and Vancomycin for infective endocarditis and later switched to Ciprofloxacin based on blood cultures and sensitivities which revealed methicillin sensitive staphylococcus aureus and multi-drug resistant E. Meningoseptica. Patient was transferred to long term care facility after acute care at the hospital. The increasing incidence of polymicrobial infective endocarditis and increasing resistance to antibiotic therapy pose challenges to the rapid assessment and treatment to mitigate the multi-organ involvement with septic emboli. Reports of pathogenicity associated with native valve endocarditis with this organism is scarce and exist primarily in a very few case reports and is resistant to many traditional antibiotics.5,6 E. Meningoseptica has shown antimicrobial susceptibility to the newer quinolones, rifampin, trimethoprim/sulfamethoxazole and ciprofloxacin with reasonable activity.7 Due to the unusual pattern of antibiotic resistance, early switching to appropriate antibiotics based on sensitivities is crucial for survival in patients with E. Meningoseptica. References 1..Kim KK, Kim MK, Lim JH, Park HY, Lee ST. Transfer of Chryseobacterium meningosepticum and Chryseobacterium miricola to Elizabethkingia gen. nov. as Elizabethkingia meningoseptica comb. nov. and Elizabethkingia miricola comb. nov. Int J Syst Evol Microbiol.2005 May;55(Pt 3):1287-93. 2:Shinha T, Ahuja R. Bacteremia due to Elizabethkingia meningoseptica. IDCases. 2015 Jan 17;2(1):13-5. doi: 10.1016/j.idcr.2015.01.002. eCollection 2015. 3..Jung SH, Lee B, Mirrakhimov AE, Hussain N. Septic shock caused by Elizabethkingia meningoseptica: a case report and review of literature. BMJ Case Rep. 2013 Apr 3;2013. pii: bcr2013009066. doi: 10.1136/bcr-2013-009066. 4.Ratnamani MS, Rao R. Elizabethkingia meningoseptica: Emerging nosocomial pathogen in bedside hemodialysis patients. Indian J Crit Care Med. 2013 Sep;17(5):304-7. 5.Bomb K, Arora A, Trehan N. Endocarditis due to Chryseobacterium meningosepticum. Indian J Med Microbiol. 2007 Apr;25(2):161-2. 6.Yang J, Xue W, Yu X. Elizabethkingia meningosepticum endocarditis: A rare case and special therapy. Anatol J Cardiol. 2015 May;15(5):427-8. 7. Hsu MS, Liao CH, Huang YT, Liu CY, Yang CJ, Kao KL, Hsueh PR. Clinical features, antimicrobial susceptibilities, and outcomes of Elizabethkingia meningoseptica (Chryseobacterium meningosepticum) bacteremia at a medical center in Taiwan,1999-2006. Eur J Clin Microbiol Infect Dis. 2011 Oct;30(10):1271-8.

L’exposition hyperbare induit des risques sanitaires, en particulier d’accidents de décompression (ADD), dont la probabilité dépend de multiples facteurs, tant externes qu’individuels. Parmi ceux-ci, l’altération de la barrière alvéolo-capillaire est peu ou pas étudiée. Nous avons donc cherché à identifier les effets d’une altération pulmonaire caractérisée par une diminution de la capacité de diffusion alvéolo-capillaire du monoxyde de carbone (DLCO) sur le risque d’ADD. Après un bilan d’aptitude préalable, chaque volontaire a été évalué avant et après la plongée.15 plongeurs professionnels civils répartis en 2 groupes en fonction de leur DLCO, normale (Contrôle) ou diminuée (DLCO), ont réalisé une plongée standardisée à 20 mètres pendant 40 minutes dans le bassin d’eau de mer d’IFREMER. Nous avons mesuré le score de bulles intravasculaires (VGE), la réponse microcirculatoire par débitmétrie laser doppler et les concentrations de différents paramètres biologiques en particulier l’aldostéronémie. Même en l’absence de survenue d’ADD, tous les plongeurs produisent des VGE. Le groupe DLCO est caractérisé par un pic de VGE plus tardif (60 minutes vs 30 minutes) et une tendance à des scores plus importants (Grade IV : 17% vs 11%). Par ailleurs, l’hypoaldostéronémie n’est observée que dans le groupe contrôle (-30.4±24.6%), pas dans le groupe DLCO (+14.8±34.7%). En dehors d’une diminution du risque thrombotique chez tous les plongeurs, les autres paramètres mesurés sont inchangés. Ces résultats évoquent une augmentation du risque d’ADD devant être confirmée par d’autres études. / Hyperbaric exposure leads to a risk of decompression sickness (DCS). The likelihood of DCS depends on multiple factors, external as well as individual. Among them, the alteration of the blood-air barrier has been poorly studied.Therefore, we measured the effect of pulmonary impairment characterized by a decreased diffusing lung capacity of carbon monoxide (DLCO) on the risk of DCS.15 professional divers were splited into 2 groups according to their DLCO, normal (control) or decreased (DLCO), and enrolled after an initial full “fit-to-dive” clinical check-up. They made a standardized 20 meters/40 minutes SCUBA dive in a sea water pool (IFREMER) Vascular Gas Emboli (VGE) score, micro-circulatory response, inflammatory biomarkers, thrombotic factors, and aldosteron rate were measured pre- and post-dive. Although no DCS occurred, all the divers showed VGE after diving. Compared to the control group, we observed in the DLCO group an increased latency to the VGE peak (60 vs 30 minutes) and a tendency for higher VGE scores (Grade IV: 17% vs 11%). A significant decrease (-30.4±24.6%) of aldosteron rate was observed in control and not in the DLCO group (+14.8±34.7%). Most of the biological parameters and microvascular response remained unchanged while all divers had a lowered post-dive thrombotic risk.These results imply that divers with a decreased DLCO might be exposed to an increased DCS risk.Further studies are required to confirm the implication and significance of pulmonary impairment in DCS.

Decompression sickness (DCS) is a risk associated with high-altitude aviation and diving. During these activities, decompression may lead to supersaturation of inert gas dissolved in bodily tissues and subsequently activate bubble formation in various bodily tissues, including in venous blood, known as venous gas emboli (VGE). It has been shown that the amount of VGE detected during and after decompression is linked to the risk of developing DCS. Thus, lowering the incidence of VGE would lower the risk of developing DCS. Previous studies have demonstrated that a session of whole-body vibration prior to a diving session is effective in lowering VGE formation. However, no study has investigated the effect of whole-body vibration on high-altitude-induced VGE. For the present study, 3 participants were recruited. The subjects performed on separate days (interspaced by 48 h) and in a randomised manner, three different preconditioning strategies: (A) 40-min seated rest, (B) 30-min seated rest followed by 150 knee squats performed over a 10 min period and (C) 30-min whole-body vibration (40 Hz) proceeded by a 10 min seated rest. Thereafter, subjects were exposed to an altitude of 24,000 ft continuously for 90 min, whilst laying in a supine position and breathing a normoxic gas mixture (PIO2 = 21 kPa). Heart rate (HR), cardiac output (CO) and stroke volume (SV) were monitored throughout the high-altitude exposure. Every 5 min, VGE prevalence was assessed ultrasonically and graded according to the Eftedal-Brubakk 5-point scale. In addition, every 15 min, subjects were asked to perform three fast, unloaded knee-bends while in their left-side horizontal recumbent position, with VGE prevalence being estimated both before and after the three knee-bends. The control strategy was associated with a higher VGE scores (2.7 ± 1.2) compared to vibration (1.0 ± 1.0) and squats (1.3 ± 0.6) strategies. VGE appeared earlier during the control strategy (35 ± 23 min) compared to the vibration (65 ± 31 min) and squats (50 ± 17 min) strategies. A strong negative correlation was only observed in the control strategy between VGE and CO (r = -0.63) and SV (r = -0.64). This study demonstrated that whole-body vibration is the most effective preconditioning strategy in lowering the amount of high-altitude-induced VGE compared with 40-min of seated-rest and 150 knee squats performed over a period of 10 min. / Att drabbas av dekompressionssjuka (DKS) utgör en risk vid såväl höghöjdsflygning som dykning. I samband med dessa aktiviteter, kan dekompression leda till övermättnad av inert-gas löst i kroppens vävnader, vilket i sin tur kan leda till bubbelformation i olika vävnader, inklusive i venblodet, där bubblorna benämns venösa gasembolier (VGE). Det har visats föreligga ett samband mellan mängden VGE som uppmäts under och efter dekompression och risken att utveckla DKS. Således kan det antas att en minskad incidens av VGE är förknippad med minskad risk att utveckla DKS. Tidigare undersökningar har påvisat att en period med helkroppsvibration före dykning påtagligt minskar bildningen av VGE. Hittills har man dock inte undersökt om helkroppsvibration påverkar höghöjdsinducerade VGE. I föreliggande undersökning, medverkade tre försökspersoner. De exponerades vid separata tillfällen (med 48 timmars mellanrum), och i olika ordningsföljd, för tre prekonditioneringsstrategier: (A) 40 min sittande vila, (B) 30 min sittande vila följt av 150 djupa knäböjningar som genomfördes under en 10-minutersperiod och (C) 10 min sittande vila följt av 30 min helkroppsvibration (40 Hz). Därefter exponerades försökspersonerna för en simulerad höjd motsvarande 24,000 fot ö.h. kontinuerligt under 90 min, under det att de i liggande ryggläge andades en normoxisk gasblandning (inspiratoriskt syrepartialtryck = 21 kPa). Hjärtfrekvens (HF), hjärtminutvolym (HMV) och hjärtats slagvolym (SV) mättes kontinuerligt under höghöjdsexponeringen. Var femte min bedömdes prevalensen av VGE med hjälp av ultraljudsteknik och en 5-gradig skattningsskala. Var femtonde min genomförde försökspersonerna 3 obelastade knäböjningar, liggande i vänster sidoläge, varvid VGE-prevalensen bedömdes såväl före som efter knäböjningarna. Kontrollbetingelsen (A) framkallade högre VGE-nivå (2,7 ± 1,2) än vibrationsbetingelsen (B; 1 ± 1) och knäböjbetingelsen (C; 1,3 ± 0,6). VGE uppträdde tidigare under kontrollbetingelsen (35 ± 23 min) än i vibrations- (65 ± 31 min) och knäböj-betingelserna (50 ± 17 min). Starka negativa samband påvisades mellan VGE och CO (r = -0,63) respektive SV (r = -0,64). Således visade föreliggande undersökning att helkroppsvibration.