Diving-related disorders in commercial breath-hold divers (Ama) of Japan

2021 ◽  
Vol 51 (2) ◽  
pp. 199-206
Author(s):  
Kiyotaka Kohshi ◽  
◽  
Hideki Tamaki ◽  
Frédéric Lemaître ◽  
Yoshitaka Morimatsu ◽  
...  
Keyword(s):  
Clinical Manifestations ◽  
Field Studies ◽  
Underlying Mechanism ◽  
Neurological Involvement ◽  
Cerebral White Matter ◽  
Breath Hold ◽  
Decompression Illness ◽  
Oxygen Breathing ◽  
Arterial Insufficiency ◽  
Nitrogen Bubbles

Decompression illness (DCI) is well known in compressed-air diving but has been considered anecdotal in breath-hold divers. Nonetheless, reported cases and field studies of the Japanese Ama, commercial or professional breath-hold divers, support DCI as a clinical entity. Clinical characteristics of DCI in Ama divers mainly suggest neurological involvement, especially stroke-like cerebral events with sparing of the spinal cord. Female Ama divers achieving deep depths have rarely experienced a panic-like neurosis from anxiety disorders. Neuroradiological studies of Ama divers have shown symptomatic and/or asymptomatic ischaemic lesions situated in the basal ganglia, brainstem, and deep and superficial cerebral white matter, suggesting arterial insufficiency. The underlying mechanism(s) of brain damage in breath-hold diving remain to be elucidated; one of the plausible mechanisms is arterialization of venous nitrogen bubbles passing through right to left shunts in the heart or lungs. Although the treatment for DCI in Ama divers has not been specifically established, oxygen breathing should be given as soon as possible for injured divers. The strategy for prevention of diving-related disorders includes reducing extreme diving schedules, prolonging surface intervals and avoiding long periods of repetitive diving. This review discusses the clinical manifestations of diving-related disorders in Ama divers and the controversial mechanisms.

scholarly journals Decompression Illness in Repetitive Breath-Hold Diving: Why Ischemic Lesions Involve the Brain?

2021 ◽  
Vol 12 ◽  
Author(s):  
Kiyotaka Kohshi ◽  
Petar J. Denoble ◽  
Hideki Tamaki ◽  
Yoshitaka Morimatsu ◽  
Tatsuya Ishitake ◽  
...  
Keyword(s):  
Cerebral Arteries ◽  
Clinical Manifestations ◽  
First Aid ◽  
Breath Hold ◽  
Decompression Illness ◽  
Gas Embolism ◽  
Normobaric Oxygen ◽  
Underlying Mechanisms ◽  
The 1960S ◽  
The Brain

Nitrogen (N2) accumulation in the blood and tissues can occur due to breath-hold (BH) diving. Post-dive venous gas emboli have been documented in commercial BH divers (Ama) after repetitive dives with short surface intervals. Hence, BH diving can theoretically cause decompression illness (DCI). “Taravana,” the diving syndrome described in Polynesian pearl divers by Cross in the 1960s, is likely DCI. It manifests mainly with cerebral involvements, especially stroke-like brain attacks with the spinal cord spared. Neuroradiological studies on Ama divers showed symptomatic and asymptomatic ischemic lesions in the cerebral cortex, subcortex, basal ganglia, brainstem, and cerebellum. These lesions localized in the external watershed areas and deep perforating arteries are compatible with cerebral arterial gas embolism. The underlying mechanisms remain to be elucidated. We consider that the most plausible mechanisms are arterialized venous gas bubbles passing through the lungs, bubbles mixed with thrombi occlude cerebral arteries and then expand from N2 influx from the occluded arteries and the brain. The first aid normobaric oxygen appears beneficial. DCI prevention strategy includes avoiding long-lasting repetitive dives for more than several hours, prolonging the surface intervals. This article provides an overview of clinical manifestations of DCI following repetitive BH dives and discusses possible mechanisms based on clinical and neuroimaging studies.

Abdominal decompression illness following repetitive diving: a case report and review of the literature

2019 ◽  
pp. 211-215
Author(s):  
Peter Beale ◽  
Levi Kitchen ◽  
W.R. Graf ◽  
M.E. Fenton ◽  
Keyword(s):  
Case Report ◽  
The Body ◽  
Decompression Illness ◽  
Review Of The Literature ◽  
Hyperbaric Chamber ◽  
Foreign National ◽  
Biochemical Effects ◽  
Elapsed Time ◽  
Nitrogen Bubbles ◽  
Abdominal Decompression

The complete pathophysiology of decompression illness is not yet fully understood. What is known is that the longer a diver breathes pressurized air at depth, the more likely nitrogen bubbles are to form once the diver returns to surface [1]. These bubbles have varying mechanical, embolic and biochemical effects on the body. The symptoms produced can be as mild as joint pain or as significant as severe neurologic dysfunction, cardiopulmonary collapse or death. Once clinically diagnosed, decompression illness must be treated rapidly with recompression therapy in a hyperbaric chamber. This case report involves a middle-aged male foreign national who completed three dives, all of which incurred significant bottom time (defined as: “the total elapsed time from the time the diver leaves the surface to the time he/she leaves the bottom)” [2]. The patient began to develop severe abdominal and back pain within 15 minutes of surfacing from his final dive. This case is unique, as his presentation was very concerning for other medical catastrophes that had to be quickly ruled out, prior to establishing the diagnosis of severe decompression illness. After emergency department resuscitation, labs and imaging were obtained; abdominal decompression illness was confirmed by CT, revealing a significant abdominal venous gas burden.

scholarly journals Central and peripheral nervous system involvement by COVID-19: A systematic review of the pathophysiology, clinical manifestations, neuropathology, neuroimaging, electrophysiology, and cerebrospinal fluid findings

2020 ◽  
Author(s):  
Juan I. Guerrero ◽  
Luis A. Barragán ◽  
Juan D. Martínez ◽  
Juan P. Montoya ◽  
Alejandra Peña ◽  
...  
Keyword(s):  
Systematic Review ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Peripheral Nervous System ◽  
Evidence Synthesis ◽  
Clinical Manifestations ◽  
Neurological Impairment ◽  
Neurological Involvement ◽  
Categorical Analysis ◽  
System Involvement

Abstract Background: SARS-CoV-2 can affect the human brain and other neurological structures. An increasing number of publications report neurological manifestations in patients with COVID-19. However, no studies have comprehensively reviewed the clinical and paraclinical characteristics of the central and peripheral nervous system's involvement in these patients. This study aimed to describe the features of the central and peripheral nervous system involvement by COVID-19 in terms of pathophysiology, clinical manifestations, neuropathology, neuroimaging, electrophysiology, and cerebrospinal fluid findings.Methods: We conducted a comprehensive systematic review of all the original studies reporting patients with neurological involvement by COVID-19, from December 2019 to June 2020, without language restriction. We excluded studies with animal subjects, studies not related to the nervous system, and opinion articles. Data analysis combined descriptive measures, frequency measures, central tendency measures, and dispersion measures for all studies reporting neurological conditions and abnormal ancillary tests in patients with confirmed COVID-19.Results: A total of 143 observational and descriptive studies reported central and peripheral nervous system involvement by COVID-19 in 10723 patients. Fifty-one studies described pathophysiologic mechanisms of neurological involvement by COVID-19, 119 focused on clinical manifestations, 4 described neuropathology findings, 62 described neuroimaging findings, 28 electrophysiology findings, and 60 studies reported cerebrospinal fluid results. The reviewed studies reflect a significant prevalence of the nervous system's involvement in patients with COVID-19, ranging from 22.5% to 36.4% among different studies, without mortality rates explicitly associated with neurological involvement by SARS-COV-2. We thoroughly describe the clinical and paraclinical characteristics of neurological involvement in these patients. Conclusions: Our evidence synthesis led to a categorical analysis of the central and peripheral involvement by COVID-19 and provided a comprehensive explanation of the reported pathophysiological mechanisms by which SARS-CoV-2 infection may cause neurological impairment. International collaborative efforts and exhaustive neurological registries will enhance the translational knowledge of COVID-19's CNS and PNS involvement and generate strategies for therapeutic decision-making.Registration: This review is registered in PROSPERO (CRD42020193140), July 24, 2020.

Possible Cefotaxime-Induced Stevens–Johnson Syndrome

2003 ◽  
Vol 37 (6) ◽  
pp. 812-814 ◽  
Author(s):  
Evagelos N Liberopoulos ◽  
George L Liamis ◽  
Moses S Elisaf
Keyword(s):  
Case Control Study ◽  
Causality Assessment ◽  
Clinical Manifestations ◽  
Underlying Mechanism ◽  
Upper Urinary Tract ◽  
Stevens Johnson Syndrome ◽  
Case Summary ◽  
Johnson Syndrome ◽  
Increased Risk ◽  
Control Study

OBJECTIVE: To report a case of possible cefotaxime-induced Stevens–Johnson syndrome (SJS). CASE SUMMARY: A 72-year-old woman with an upper urinary tract infection developed erosions and blisters on the skin and the mucous membranes, as well as fever and prostration, soon after the administration of cefotaxime. This presentation is consistent with the features of SJS. Resolution of the clinical manifestations was observed after discontinuation of the drug; all other drugs, infections, or immunologic disorders that could have caused this syndrome were carefully excluded. An objective causality assessment revealed that SJS was possibly associated with the use of cefotaxime. DISCUSSION: Although cephalosporins have been associated with an increased risk for SJS and cefotaxime has been suspected of being associated with SJS in a previous case–control study, this is the first full report for cefotaxime-related SJS in the literature. An immunologically mediated reaction may be the underlying mechanism. CONCLUSIONS: Although cefotaxime administration seems to be the underlying cause of the SJS observed in our patient, establishment of a definite causal relationship requires additional cases and supportive data.

scholarly journals General Anesthesia for a Patient With Pelizaeus-Merzbacher Disease

2016 ◽  
Vol 63 (2) ◽  
pp. 91-94 ◽  
Author(s):  
Nobuhito Kamekura ◽  
Yukie Nitta ◽  
Shigeru Takuma ◽  
Toshiaki Fujisawa
Keyword(s):  
General Anesthesia ◽  
Clinical Symptoms ◽  
Muscle Tone ◽  
Clinical Manifestations ◽  
Psychomotor Retardation ◽  
Cerebral White Matter ◽  
Airway Complications ◽  
Wisdom Teeth ◽  
History Of Epilepsy ◽  
Pelizaeus Merzbacher Disease

We report the successful management of general anesthesia for a patient with Pelizaeus-Merzbacher disease (PMD). PMD is one of a group of progressive, degenerative disorders of the cerebral white matter. The typical clinical manifestations of PMD include psychomotor retardation, nystagmus, abnormal muscle tone, seizures, and cognitive impairment. General anesthesia for a patient with PMD may be difficult mainly because of seizures and airway complications related to poor pharyngeal muscle control. In addition, the possibility of exacerbation of spasticity should be considered. A 20-year-old man with PMD required removal of impacted wisdom teeth under general anesthesia. General anesthesia was induced with thiamylal, fentanyl, and desflurane. Anesthesia was maintained with desflurane and continuous intravenous remifentanil under bispectral index and train-of-4 monitoring. Anesthesia lasted 1 hour 20 minutes and was completed uneventfully. Airway complications, seizures, and exacerbation of spasticity did not occur postoperatively. Preoperatively, our patient had no history of epilepsy attacks or aspiration pneumonia, and no clinical symptoms of gastroesophageal reflux disease. Therefore, exacerbation of spasticity was one of the most likely potential complications. Identification of these associated conditions and evaluation of risk factors during preoperative examination is important for performing safe anesthesia in these patients.

scholarly journals Transient Severe Respiratory Motion Artifacts After Application of Gadoxetate Disodium: What We Currently Know

2017 ◽  
Vol 190 (01) ◽  
pp. 20-30 ◽  
Author(s):  
Lennart Well ◽  
Julius Weinrich ◽  
Gerhard Adam ◽  
Peter Bannas
Keyword(s):  
Risk Factors ◽  
Contrast Agent ◽  
Potential Risk ◽  
Free Breathing ◽  
Underlying Mechanism ◽  
Motion Artifacts ◽  
Arterial Phase ◽  
Breath Hold ◽  
Gadoxetate Disodium ◽  
Potential Risk Factors

Background Gadoxetate disodium is an intracellular contrast agent for magnetic resonance imaging (MRI) of the liver. Recent publications revealed that injection of gadoxetate disodium can lead to imaging artifacts due to transient severe motion (TSM) in the arterial phase of contrast-enhanced liver MRI. In this review we present and discuss published frequencies of TSM, contrast injection and image acquisition protocols, potential risk factors, and proposed strategies to avoid or minimize the effects of TSM. Method Two reviewers independently searched the PubMed search engine for “transient severe motion artifact” and related terms. Reference lists of retrieved articles were also searched. The two reviewers selected in consensus nine studies that reported both frequencies of TSM and potential risk factors. Study data were extracted by both reviewers, and disagreement was resolved by consensus. Results and Conclusion TSM is caused by impaired breath-hold ability after gadoxetate disodium injection and occurs in 5 – 22 % of patients. The dose of applied contrast agent, repeated exposure to gadoxetate disodium, high BMI and pulmonary disease have been described as potential risk factors for TSM. However, there are only few concordant results on this topic and the pathophysiology of TSM has not been identified. Proposed strategies for the prevention of TSM are slow injection rates and low doses of diluted gadoxetate disodium. Accelerated and free-breathing MRI sequence protocols and breath-hold training may minimize the effects of TSM. Further prospective studies are needed to confirm these strategies and to identify the underlying mechanism of TSM. Key Points  Citation Format

scholarly journals Leprosy with Atypical Skin Lesions Masquerading as Relapsing Polychondritis

2016 ◽  
Vol 2016 ◽  
pp. 1-3 ◽  
Author(s):  
Punit Pruthi ◽  
Hariharan Munganda ◽  
Amit Bangia ◽  
Uma Rani ◽  
Rajesh Budhiraja ◽  
...  
Keyword(s):  
Immune Status ◽  
Clinical Manifestations ◽  
Relapsing Polychondritis ◽  
Skin Lesions ◽  
Neurological Involvement ◽  
Inappropriate Therapy ◽  
External Ear ◽  
Unique Case ◽  
The Individual ◽  
Common Manifestation

Leprosy can present with a variety of clinical manifestations depending on the immune status of the individual. After dermatological and neurological involvement, rheumatic features specially various forms of arthritis are the third most common manifestation of the disease. We describe a unique case of a 22-year-old patient presenting with external ear involvement mimicking relapsing polychondritis along with inflammatory joint symptoms and skin lesions. Ear involvement in relapsing polychondritis characteristically is painful and spares the noncartilaginous ear lobules, in contrast to painless ear involvement in leprosy affecting the lobules as well. Histopathology confirmed the diagnosis, although the ear and skin lesions were not classical of leprosy. Such a presentation of leprosy closely mimicking relapsing polychondritis has not been described previously. Tissue diagnosis should always be attempted whenever possible in patients presenting with autoimmune features, so that inappropriate therapy with immunosuppressants is avoided.

scholarly journals Neurological decompression illness in a Japanese breath-hold diver: a case report

2012 ◽  
Vol 52 (10) ◽  
pp. 757-761
Author(s):  
Ryu Matsuo ◽  
Shuji Arakawa ◽  
Yoshihiko Furuta ◽  
Yuka Kanazawa ◽  
Masahiro Kamouchi ◽  
...  
Keyword(s):  
Case Report ◽  
Breath Hold ◽  
Decompression Illness

scholarly journals Intraspinal Neurenteric Cysts in Children

2008 ◽  
Vol 35 (5) ◽  
pp. 609-615 ◽  
Author(s):  
Chunquan Cai ◽  
Changhong Shen ◽  
Weidong Yang ◽  
Qingjiang Zhang ◽  
Xiaoli Hu
Keyword(s):  
Spinal Cord ◽  
Imaging Modality ◽  
Spinal Dysraphism ◽  
Clinical Manifestations ◽  
The Other ◽  
Cervical Region ◽  
Neurological Involvement ◽  
Neurenteric Cyst ◽  
Lumbar Region ◽  
Magnetic Resonance Imaging Mri

Background:Neurenteric cysts are rare congenital epithelium-lined cysts of the central nervous system. They are found predominantly in the spinal cord, with lower incidence in the intracranial compartment, and may be associated with various other congenital spinal anomalies. Seven patients with symptomatic intraspinal neurenteric cysts are presented.Materials and Methods:Seven patients with intraspinal neurenteric cysts aged from nine months to ten years treated at this hospital from May 2000 to July 2006 were reviewed. The clinical manifestations, imaging and surgical findings of patients were analyzed retrospectively. All patients underwent operation. One patient's cervical neurenteric cyst was resected using the lateral cervical approach, and the other six resections were performed with posterior approach.Results:All seven patients presented with neurological involvement. One patient had an intramedullary cyst, while the other six cysts were situated ventrally. Three patients' cysts occurred in the cervical region, two in the cervicothoracic region, one in the thoracic region and one in the lumbar region. One patient had bony anomalies, and one had a lumbar posterior occult spinal dysraphism. Five patients' symptoms improved rapidly after surgery.Conclusions:Intraspinal neurenteric cysts in children are rare and most occur ventral to the spinal cord. Magnetic resonance imaging (MRI) is the most effective imaging modality. Earlier diagnosis and surgical resection of spinal neurenteric cysts improves prognosis.

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