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1.
Undersea Hyperb Med ; 46(5): 633-634, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31683361

RESUMO

A 54-year-old man suffered a leg cramp while diving in the ocean at a depth of 20 meters. He began to surface, with his ascent based on a decompression table. He lost consciousness at the surface and was rescued by a nearby boat. The boat staff judged him to be in cardiac arrest, so they performed chest compressions. When the boat reached port where an ambulance was waiting, emergency medical technicians confirmed that the patient was in cardiac arrest; his initial rhythm was asystole. Treated with basic life support, the patient was then transported to a rendezvous point, where a physician-staffed helicopter waited. The patient remained in cardiac arrest, so the staff of the helicopter performed tracheal intubation with mechanical ventilation, securing a venous route, infusion of adrenaline, and mechanical chest compression. On arrival at our hospital 100 minutes after collapse, he remained in cardiac arrest. Continued advanced cardiac life support failed to obtain spontaneous circulation. Whole-body computed tomography (CT) at 120 minutes after the collapse showed multiple gas bubbles in the heart, aorta, inferior vena cava, cerebral artery, coronary artery and portal vein with lung edema. This is the first case to show gas in the bilateral coronary arteries on CT. The present case clearly demonstrates that decompression sickness can also induce acute coronary syndrome.


Assuntos
Síndrome Coronariana Aguda/diagnóstico por imagem , Vasos Coronários/diagnóstico por imagem , Doença da Descompressão/complicações , Embolia Aérea/diagnóstico por imagem , Síndrome Coronariana Aguda/etiologia , Aorta/diagnóstico por imagem , Reanimação Cardiopulmonar/métodos , Mergulho/efeitos adversos , Embolia Aérea/etiologia , Evolução Fatal , Coração/diagnóstico por imagem , Parada Cardíaca/terapia , Humanos , Masculino , Pessoa de Meia-Idade , Tomografia Computadorizada por Raios X/métodos
2.
Undersea Hyperb Med ; 46(5): 673-683, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31683367

RESUMO

Gas can enter arteries (arterial gas embolism, AGE) due to alveolar-capillary disruption (caused by pulmonary over-pressurization, e.g. breath-hold ascent by divers) or veins (venous gas embolism, VGE) as a result of tissue bubble formation due to decompression (diving, altitude exposure) or during certain surgical procedures where capillary hydrostatic pressure at the incision site is subatmospheric. Both AGE and VGE can be caused by iatrogenic gas injection. AGE usually produces stroke-like manifestations, such as impaired consciousness, confusion, seizures and focal neurological deficits. Small amounts of VGE are often tolerated due to filtration by pulmonary capillaries; however VGE can cause pulmonary edema, cardiac "vapor lock" and AGE due to transpulmonary passage or right-to-left shunt through a patient foramen ovale. Intravascular gas can cause arterial obstruction or endothelial damage and secondary vasospasm and capillary leak. Vascular gas is frequently not visible with radiographic imaging, which should not be used to exclude the diagnosis of AGE. Isolated VGE usually requires no treatment; AGE treatment is similar to decompression sickness (DCS), with first aid oxygen then hyperbaric oxygen. Although cerebral AGE (CAGE) often causes intracranial hypertension, animal studies have failed to demonstrate a benefit of induced hypocapnia. An evidence based review of adjunctive therapies is presented.


Assuntos
Embolia Aérea/terapia , Oxigenação Hiperbárica/métodos , Algoritmos , Altitude , Artérias , Pressão Atmosférica , Descompressão/efeitos adversos , Doença da Descompressão/complicações , Mergulho/efeitos adversos , Embolia Aérea/diagnóstico , Embolia Aérea/etiologia , Forame Oval Patente/complicações , Humanos , Embolia Intracraniana/etiologia , Embolia Intracraniana/terapia , Posicionamento do Paciente/métodos , Veias
3.
Psychiatr Danub ; 31(2): 172-181, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-31291221

RESUMO

BACKGROUND: Decompression sickness (DCS) primarily manifests musculoskeletal pain, cutaneous manifestations, lymphatic symptoms, and neurological symptoms. DCS might affect the central nervous system and induce the stress in the patients, but few studies about the psychiatric morbidity after DCS have been conducted. This study aimed to investigate the association between DCS and the risk of developing psychiatric disorders. SUBJECTS AND METHODS: This study was a population-based, matched-cohort design. A total of 738 enrolled patients, with 123 study subjects who had suffered from DCS, and 615 controls matched for sex and age, from the Longitudinal Health Insurance Databank from 2000-2010 in Taiwan, and selected from the National Health Insurance Research Database. After adjusting for the confounding factors, Cox proportional hazards analysis was used to compare the risk of developing psychiatric disorders during the 10 years of follow-up period. RESULTS: Of the study subjects, 10 (8.13%) developed psychiatric disorders when compared to 35 (5.69%) in the control group. The study subjects were more likely to develop psychiatric disorders (crude hazard ratio [HR]: 2.79 (95% CI=1.37-5.69, P<0.01). After adjusting for sex, age, monthly income, urbanization level, geographic region, and comorbidities, the adjusted HR was 3.83 (95% CI=1.60-9.16, P<0.01). Sleep disorders was associated with DCS with the adjusted HR as 5.74 (95% CI=1.04-31.56, P<0.01). Hyperbaric oxygenation therapy was not associated with a lower risk of psychiatric disorders. CONCLUSIONS: Patients who suffered from DCS have a 3.8-fold risk of developing psychiatric disorders, and a 5.7-fold risk of sleep disorders. This finding is a reminder for the clinicians that a regular psychiatric follow-up might well be needed for these patients.


Assuntos
Doença da Descompressão/complicações , Doença da Descompressão/epidemiologia , Transtornos do Sono-Vigília/epidemiologia , Transtornos do Sono-Vigília/etiologia , Adulto , Idoso , Estudos de Coortes , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Fatores de Risco , Taiwan/epidemiologia , Fatores de Tempo , Adulto Jovem
4.
Undersea Hyperb Med ; 46(1): 81-85, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31154689

RESUMO

Decompression sickness is a disease caused by abrupt pressure change and presents various symptoms. To date, acute kidney injury associated with decompression sickness has been reported frequently, but there is no report of hepatic infarction associated with decompression sickness. We report a case of acute kidney injury and acute hepatic infarction treated with hyperbaric oxygen (HBO2) therapy and dialysis in a patient with severe decompression sickness after work diving.


Assuntos
Lesão Renal Aguda/terapia , Doença da Descompressão/terapia , Mergulho/efeitos adversos , Infarto/terapia , Fígado/irrigação sanguínea , Lesão Renal Aguda/complicações , Adulto , Doença da Descompressão/complicações , Doença da Descompressão/diagnóstico por imagem , Humanos , Infarto/complicações , Infarto/diagnóstico por imagem , Fígado/diagnóstico por imagem , Masculino , Diálise Renal , Tomografia Computadorizada por Raios X
5.
Echocardiography ; 36(6): 1179-1180, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-31087401

RESUMO

A 39-year-old male commercial diver developed cutis marmorata after a dive. He had a full recovery after therapy in a hyperbaric oxygen chamber. Transthoracic echocardiography revealed an atrial septal aneurysm and a large shunt during normal respirations. This form of decompression sickness may progress to type II DCS, thus is important to identify and treat. Cutis marmorata as a result of diving is highly associated with an atrial septal defect or a large patent foramen ovale. It is particularly important to assess these patients for a right-to-left shunt as part of a medical evaluation prior to returning to diving.


Assuntos
Doença da Descompressão/complicações , Mergulho , Ecocardiografia/métodos , Forame Oval Patente/complicações , Dermatopatias Vasculares/diagnóstico por imagem , Dermatopatias Vasculares/etiologia , Adulto , Humanos , Oxigenação Hiperbárica , Masculino , Dermatopatias Vasculares/terapia
6.
Undersea Hyperb Med ; 46: 217-220, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31051069

RESUMO

Diving as a method of fishing is used worldwide in small-scale fisheries. However, one of the main causes of morbidity and mortality among fishermen is decompression sickness (DCS). We report the case of a 46-year-old male fisherman diver who presented with chronic inguinal pain that radiated to the lower left limb. Living and working in a fishing port in Yucatan, he had a prior history of DCS. A diagnosis of avascular necrosis in the left femoral head secondary to DCS was made via analysis of clinical and radiological findings. The necrosis was surgically resolved by a total hip arthroplasty. Dysbaric osteonecrosis is a more probable diagnosis. In this region fishermen undergo significant decompression stress in their daily fishing efforts. Further studies regarding prevalence of dysbaric osteonecrosis among small-scale fisheries divers are needed. In a community where DCS is endemic and has become an epidemic, as of late, the perception of this health risk remains low. Furthermore, training and decompression technique are lacking among the fishing communities.


Assuntos
Doença da Descompressão/complicações , Mergulho/efeitos adversos , Necrose da Cabeça do Fêmur/etiologia , Doenças Profissionais/complicações , Artrografia , Necrose da Cabeça do Fêmur/diagnóstico por imagem , Pesqueiros , Virilha , Humanos , Masculino , México , Pessoa de Meia-Idade , Dor/etiologia
8.
Rev Med Interne ; 40(1): 38-42, 2019 Jan.
Artigo em Francês | MEDLINE | ID: mdl-30342791

RESUMO

BACKGROUND: Capillary leak syndrome is a rare type of decompression sickness (DCS) that may be responsible for hypovolemic shock with edema. CLINICAL CASE: A 21-year-old amateur diver suffered from an inner ear DCS following air diving to 96msw. He presented subsequent deterioration with hypovolemia and facial edema secondary to capillary leak syndrome. DISCUSSION: In DCS, bubbles formation alters the wall of blood vessels and activates complex biochemical mechanisms inducing extravascular protein leakage. The clinical expression of this syndrome is variable, ranging from simple hemoconcentration to hypovolemic shock. Close clinical-biological monitoring of patients with elevated hematocrit with or without hypoalbuminemia is advisable. Early vascular filling with albumin infusion may prevent the occurrence of hypovolemic shock and improve the prognosis.


Assuntos
Síndrome de Vazamento Capilar/etiologia , Doença da Descompressão/complicações , Mergulho/efeitos adversos , Adulto , Síndrome de Vazamento Capilar/terapia , Doença da Descompressão/terapia , Humanos , Masculino
9.
Undersea Hyperb Med ; 45(4): 473-479, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30241128

RESUMO

Severe decompression illness (DCI) is an uncommon medical issue affecting divers and results mainly from rapid surfacing using inadequate decompression protocols. Massive gas embolism with central nervous system involvement often leads to a poor prognosis, with permanent residual neurologic defects. Moreover, DCI complicated with multiple organ dysfunction syndrome (MODS) is tremendously rare and difficult to cure, although hyperbaric oxygen (HBO2) therapy following the U.S. Navy Treatment Tables is a consensus. We report a case of severe DCI with profound shock and MODS after an initial treatment with HBO2 therapy using U.S. Navy Treatment Table 6A. Following the Surviving Sepsis Campaign Guidelines, low-dose hydrocortisone was administered. Although this treatment went against recommendation of the U.S. Navy Diving Manual, it resulted in a dramatic clinical improvement. After a second round of HBO2 treatments, the patient was discharged from hospital two weeks after the diving accident.


Assuntos
Anti-Inflamatórios/uso terapêutico , Doença da Descompressão/terapia , Mergulho/efeitos adversos , Hidrocortisona/uso terapêutico , Insuficiência de Múltiplos Órgãos/terapia , Doença da Descompressão/complicações , Humanos , Masculino , Pessoa de Meia-Idade , Insuficiência de Múltiplos Órgãos/etiologia , Guias de Prática Clínica como Assunto , Valores de Referência , Terapia de Substituição Renal , Choque/etiologia , Resultado do Tratamento
11.
Ther Hypothermia Temp Manag ; 8(3): 176-180, 2018 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-30016198

RESUMO

Cerebral arterial gas embolism (CAGE) shows various manifestations according to the quantity of gas and the brain areas affected. The symptoms range from minor motor weakness, headache, and confusion to disorientation, convulsions, hemiparesis, unconsciousness, and coma. A 46-year-old man was transferred to our emergency department due to altered sensorium. Immediately after a controlled ascent from 33 m of seawater, he complained of shortness of breath and rigid extremities, lapsing into unconsciousness. He was intubated at another medical center, where a brain computerized axial tomography scan showed no definitive abnormal findings. Pneumothorax and obstructing lesions were apparent in the left thorax of the computed tomography scan. Following closed thoracostomy, we provided hyperbaric oxygen therapy (HBOT) using U.S. Navy Treatment Table (USN TT) 6A. A brain magnetic resonance imaging diffusion image taken after HBOT showed acute infarction in both middle and posterior cerebral arteries. We implemented targeted temperature management (TTM) to prevent worsening of cerebral function in the intensive care unit. After completing TTM, we repeated HBOT using USN TT5 and started rehabilitation therapy. He fully recovered from the neurological deficits. This is the first case of CAGE treated with TTM and consecutive HBOTs suggesting that TTM might facilitate salvage of the penumbra in severe CAGE.


Assuntos
Infarto Cerebral/terapia , Doença da Descompressão/complicações , Mergulho/efeitos adversos , Embolia Aérea/complicações , Hipotermia Induzida , Infarto Cerebral/diagnóstico por imagem , Infarto Cerebral/etiologia , Doença da Descompressão/diagnóstico por imagem , Doença da Descompressão/terapia , Embolia Aérea/diagnóstico por imagem , Embolia Aérea/terapia , Humanos , Oxigenação Hiperbárica , Imagem por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Radiografia Torácica , Tomografia Computadorizada de Emissão de Fóton Único
12.
Undersea Hyperb Med ; 45(3): 351-362, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30028921

RESUMO

Nuclear factor kappa B (NF-κB) is the critical transcriptional factor in the pathogenesis of acute lung injury (ALI). NF-κB regulates the expression changes of inflammatory factors such as tumor necrosis factor alpha (TNF-α), interleukin-1ß (IL-1ß) and interleukin 6 (IL-6). In a previous study we showed that decompression sickness (DCS) caused by simulated unsafe fast buoyancy ascent escape (FBAE) could result in ALI, which was characterized by expression changes of inflammatory factors in rat lung tissue. The purpose of the present work was to study the roles of NF-κB and TNF-α in the process of DCS-induced rat lung injury caused by simulated unsafe FBAE. The research methods aimed to detect the rat lung tissue messenger ribonucleic acid (mRNA) and protein level variations of NF-κB, inhibitory ×B (I×B), TNF-α, IL-1ß, IL-6, IL-10 and IL-13 by using pretreatment of the NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) and TNF-α antibody (Ab). Our experimental results demonstrated that PDTC could improve the survival rate of the rats with DCS caused by unsafe FBAE more effectively than TNF-α Ab. However, the inhibition of TNF-α Ab on the nuclear translocated protein expression of NF-κB was more effective than PDTC. Both PDTC and TNF-α Ab can abrogate the increment of the rat lung tissue mRNA levels of TNF-α, IL-1ß, IL-6 and protein levels of NF-κB, TNF-α, IL-1ß effectively and increase the rat lung tissue content of I×B significantly. In conclusion, TNF-α-mediated NF-κB signaling may be one of the critical signaling pathways in the pathogenesis of DCS-induced rat lung injury caused by simulated unsafe FBAE. PDTC may ameliorate this type of injury partly through inhibiting the NF-κB pathway.


Assuntos
Lesão Pulmonar Aguda/metabolismo , Antioxidantes/farmacologia , Doença da Descompressão/complicações , Interleucinas/metabolismo , NF-kappa B/metabolismo , Pirrolidinas/farmacologia , Tiocarbamatos/farmacologia , Fator de Necrose Tumoral alfa/metabolismo , Lesão Pulmonar Aguda/etiologia , Lesão Pulmonar Aguda/patologia , Animais , Interleucina-10/metabolismo , Interleucina-13/metabolismo , Interleucina-1beta/metabolismo , Interleucina-6/metabolismo , Pulmão/metabolismo , Pulmão/patologia , Masculino , NF-kappa B/antagonistas & inibidores , RNA Mensageiro/metabolismo , Distribuição Aleatória , Ratos , Ratos Sprague-Dawley , Taxa de Sobrevida , Fator de Necrose Tumoral alfa/antagonistas & inibidores
13.
Diving Hyperb Med ; 48(2): 112-113, 2018 Jun 30.
Artigo em Inglês | MEDLINE | ID: mdl-29888385

RESUMO

A diver presented with total loss of vision in the left eye and right hemiparesis following a routine no-stop scuba dive to 20 metres' depth. A diagnosis of decompression illness (DCI) with acute ophthalmic artery air embolism and left carotid artery insult causing acute anterior circulatory ischaemia was made. He underwent seven hyperbaric treatments leading to a full recovery. Magnetic resonance angiography revealed an underlying left anterior cerebral artery A1 segment hypoplasia. Making a prompt diagnosis and early hyperbaric oxygen treatment are crucial to halt further tissue damage from ischaemia in central nervous system DCI. In this case, the finding of a left A1 anterior cerebral artery segment hypoplasia variant may have increased the severity of DCI due to deficient collateral circulation.


Assuntos
Doença da Descompressão/complicações , Mergulho , Artéria Oftálmica/patologia , Adulto , Artéria Cerebral Anterior , Humanos , Masculino , Técnica de Amplificação ao Acaso de DNA Polimórfico
14.
Diving Hyperb Med ; 48(2): 114, 2018 Jun 30.
Artigo em Inglês | MEDLINE | ID: mdl-29888386

RESUMO

Cutis marmorata (CM) manifests as bluish-red spots on the skin following decompression. These are often itchy or painful to touch, and appear half to one hour after surfacing. The pathogenesis of skin lesions in decompression illness (DCI) remains unresolved. The common belief has been that bubbles that shunted to the arterial circulation reached the skin and clogged blood vessels. An alternative explanation from studies in which air was injected into the internal carotid artery of swine is that arterial bubbles at the brain stem disturb the control of skin blood flow, causing CM. Other brain syndromes have also been seen to cause CM. It was suggested that bubbles affecting the brain stem result in the release of neuropeptides in the skin which control vasodilatation and vasoconstriction. However, this does not explain the inflammation in the skin lesions, with red blood cells, haemorrhage and neutrophil infiltrates. The percentage of right-to-left circulatory shunts in divers who suffered CM was 77% compared with 28% in divers with no record of CM, a finding which supports either of these explanations. Another study in swine concluded that there was "strong evidence to support autochthonous bubbles as the etiology of skin lesions". Lesions appeared without right-to-left shunting. Skin thickness from the squamous keratin to the dermis increased by 10% in the affected areas. The lesions showed congestion, haemorrhage and neutrophil infiltrates. Superficial counter-diffusion as a cause of CM, the increased risk of CM in a dry as opposed to a wet dive and the prevalence of CM in proximity to subcutaneous fat (which acts as a nitrogen reservoir), all support an autochthonous origin. Decompression bubbles can develop and expand only from pre-existing gas micronuclei. It is known that nanobubbles form spontaneously when a smooth hydrophobic surface is submerged in water containing dissolved gas. We have shown that these nanobubbles are the gas micronuclei underlying decompression bubbles and DCI. After decompression, bubbles evolved at definite hydrophobic sites composed of the lung surfactant dipalmitoylphosphatidylcholine. Nanobubbles are formed on the surface of these lamellar layers of phospholipids, and on decompression expand into venous and arterial bubbles. Lamellar bodies of phospholipids produced in the granular layer of the skin are used for the formation of a hydrophobic barrier at the cornified layer. We suggest that the hydrophobic layers in the skin may be the site at which bubbles develop from nanobubbles and cause CM, just as occurs at the active hydrophobic spots on the luminal aspect of a blood vessel. This is the reason no bubbles were observed in the skin microcirculation. Unlike bubbles on the inner wall of venous blood vessels, which are supplied with high quantities of nitrogen from the incoming venous blood, the expansion of skin bubbles will be limited due to a low supply of nitrogen (possibly from the nearby subcutaneous fat). Therefore, skin bubbles should be small and have a short life span, which may be why they have hitherto remained undetected. The sensitivity of some divers to CM and its localization to specific skin areas may be related to individual variability in the lamellar bodies and phospholipid skin barriers. Support for the present hypothesis may be found in the observation in some cases (though not all) of the movement of gas under the skin by means of echography (Balestra C, personal communication, 2018). CM is more frequent in female divers, and more so in subtropical than in cold European waters (van Ooij P-JAM, personal communication, 2018). This may be explained by women having more subcutaneous fat than men, coupled with the higher skin perfusion (and nitrogen loading) in warm water. This suggestion of possible autochthonous bubble formation in the skin does not exclude other causes, but may open a window for further investigation.


Assuntos
Doença da Descompressão/complicações , Mergulho , Exantema/etiologia , Livedo Reticular/etiologia , Feminino , Humanos , Masculino
15.
Diving Hyperb Med ; 47(4): 257-259, 2017 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-29241237

RESUMO

Arterial gas embolism is a catastrophic event. Bubbles in the arterial circulation may lodge in the brain and cause infarction in the affected area and/or in a coronary vessel causing acute myocardial ischaemia. There is no well-defined window of time beyond which a response to hyperbaric oxygen is not expected. Major improvement may occur if the patient is treated as soon as possible, but is less likely in divers with severe decompression illness who have delayed intervention. We report on a 51-year-old, male rebreather diver who suffered loss of consciousness and cardiovascular collapse within minutes of a 30-metre deep dive at a remote Micronesian dive site. Recompression treatment did not start for six days for reasons to be presented, during which time he remained deeply comatose, cardiovascularly unstable and intubated on ventilator support. Despite this, following aggressive hyperbaric treatment over many days he made a functional recovery. At one year post injury, he is leading a functional life but has not returned to his previous occupation as a diver and suffers from moderately severe tinnitus and impaired right ear hearing and occasional mild speech problems. He is undertaking a number of on-line courses with a view to re-employment.


Assuntos
Doença da Descompressão/terapia , Oxigenação Hiperbárica , Tempo para o Tratamento , Doença da Descompressão/complicações , Humanos , Masculino , Pessoa de Meia-Idade , Recuperação de Função Fisiológica , Resultado do Tratamento
17.
Undersea Hyperb Med ; 44(1): 57-62, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28768086

RESUMO

BACKGROUND: Decompression sickness may involve the central nervous system. The most common site is spinal cord. This study was conducted to determine the relationship between magnetic resonance(MR) imaging findings of spinal damage. METHODS: We conducted a retrospective review of 12 patients (male=10, female=2) who presented with spinal cord symptoms. We investigated their clinical features, neurological findings and radiologic findings. RESULTS: The depth and bottom time of the dive were 34.5 meters (range 22-56) and 22.7 minutes (range 10-55) respectively. Most divers ascended within appropriate time frame as shown by the decompression tables. The most frequent initial symptoms were lower limb weakness (n=12), followed by sensory disturbances (n=10) and bladder dysfuction (n=5). The chief radiologic abnormalities were continuous (n=3), or non-continuous (n=5) high-signal intensity on T2-weighted images at posterior paramedian portion of the spinal cord, mainly thoracic level. There were no abnormal findings in the remaining four (4) patients, and they showed good prognosis. All patients were treated with hyperbaric oxygen therapy and some received high-dose dexamethasone. On discharge, five (5) patients had made a full recovery, seven (7) had some residual neurological sequelae, and all patients except one (1) regained normal bladder function. CONCLUSIONS: Spinal cord decompression sickness is a neurological emergency. Early recognition and treatment may minimize neurological damage. Initial normal finding in MR imaging was a good predictor for prognosis in spinal decompression sickness.


Assuntos
Doença da Descompressão/complicações , Mergulho/efeitos adversos , Traumatismos da Medula Espinal/diagnóstico , Traumatismos da Medula Espinal/etiologia , Adulto , Anti-Inflamatórios/uso terapêutico , Doença da Descompressão/terapia , Dexametasona/uso terapêutico , Feminino , Humanos , Oxigenação Hiperbárica , Imagem por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Paraparesia/diagnóstico , Paraparesia/etiologia , Recuperação de Função Fisiológica , Estudos Retrospectivos , Traumatismos da Medula Espinal/diagnóstico por imagem , Traumatismos da Medula Espinal/terapia , Vértebras Torácicas , Fatores de Tempo , Transtornos Urinários/etiologia
18.
Undersea Hyperb Med ; 44(3): 279-281, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28779584

RESUMO

INTRODUCTION: In Yucatán, Mexico, during the sea cucumber season fishermen dive intensely to obtain good catches but are often at risk of decompression sickness (DCS). We present a single case fatality. OBJECTIVE: We analyzed the clinical course, medical assessment and recompression treatment plan of an untrained fisherman. CASE REPORT: A 35-year-old male ascended rapidly using compressed-air diving. Before reaching the coast, he reported dizziness, shortness of breath, and pain in the abdomen and legs. Three hours later, when symptoms worsened, he went to the hospital. He was admitted with increased osteotendinous reflexes and cutis marmorata in the abdomen. The patient was diagnosed with carbon monoxide (CO) poisoning and Type I DCS, receiving the U.S. Navy Treatment Table 5 (USN TT5). Before completing his treatment at depth, he developed myocardial infarction and died. The death certificate indicated Type I DCS, thrombotic pulmonary embolism and cardiac arrest. DISCUSSION: Upon reviewing his medical records, we uncovered no evidence to support the diagnosis of CO poisoning and thrombotic pulmonary embolism. The clinical presentation seems to be compatible with a serious decompression insult, not a Type I hit. Based on the information gathered, it seems likely that the patient died as a result of cardiopulmonary DCS. This case report suggests a need to provide fishermen divers in this region with formal dive training. There also seems to be a need to improve medical education for physicians who work at hyperbaric programs, and to ensure that sufficient and qualified staff is present to supervise patients inside the chambers.


Assuntos
Doença da Descompressão/complicações , Mergulho/efeitos adversos , Infarto do Miocárdio/etiologia , Adulto , Intoxicação por Monóxido de Carbono/diagnóstico , Doença da Descompressão/diagnóstico , Diagnóstico Diferencial , Evolução Fatal , Parada Cardíaca/etiologia , Humanos , Masculino , México , Doenças Profissionais/diagnóstico , Embolia Pulmonar/diagnóstico
20.
Diving Hyperb Med ; 47(1): 17-23, 2017 03.
Artigo em Inglês | MEDLINE | ID: mdl-28357820

RESUMO

BACKGROUND AND AIMS: Severe decompression sickness (DCS) is a multi-organ injury. This study investigated the preventive effects of rosiglitazone on liver injury following rapid decompression in mice and examined the underlying mechanisms. METHODS: Mice were randomly divided into four groups: a control group, vehicle group, and rosiglitazone (5 and 10 mg·kg⁻¹) groups, the latter three being exposed to a pressure of 911 kPa. Haematoxylin and eosin staining, plasma levels of alanine transaminase (ALT), aspartate transaminase (AST) and lactate dehydrogenase and blood cell counts were used to evaluate liver injury at 30 min after rapid decompression. The expression of endothelial and inducible nitric oxide synthase (iNOS) and its phosphorylation were measured to uncover the underlying molecular mechanisms. RESULTS: A significant increase in plasma ALT, red blood cells and platelets, and a decrease in neutrophils were observed in the vehicle group. Furthermore, the expression of iNOS, E-selectin and the total level of NO in hepatic tissue, and soluble E-selectin in the plasma were significantly elevated in the vehicle group. Rosiglitazone pre-treatment prevented the increases in ALT (and AST), soluble E-selectin concentration, red blood cells and platelet counts. Moreover, rosiglitazone reduced over-expression of iNOS and the NO level, prevented the fall in neutrophil count and promoted the phosphorylation of iNOS in the liver. CONCLUSIONS: Pre-treatment with rosiglitazone ameliorated liver injury from severe DCS. This preventive effect may be partly mediated by stimulating endothelial NO production, improving endothelial function and limiting inflammatory processes.


Assuntos
Doença da Descompressão/complicações , Hipoglicemiantes/farmacologia , Fígado/efeitos dos fármacos , Fígado/lesões , Tiazolidinedionas/farmacologia , Alanina Transaminase/sangue , Animais , Aspartato Aminotransferases/sangue , Doença da Descompressão/sangue , Doença da Descompressão/metabolismo , Modelos Animais de Doenças , Selectina E/metabolismo , Contagem de Eritrócitos , L-Lactato Desidrogenase/sangue , Contagem de Leucócitos , Fígado/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos ICR/sangue , Camundongos Endogâmicos ICR/metabolismo , Neutrófilos/efeitos dos fármacos , Óxido Nítrico/metabolismo , Óxido Nítrico Sintase Tipo II/metabolismo , Óxido Nítrico Sintase Tipo III/metabolismo , Fosforilação/efeitos dos fármacos , Contagem de Plaquetas , Distribuição Aleatória , Rosiglitazona
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