High-Altitude Decompression Sickness Treated with Hyperbaric Therapy and Extracorporeal Oxygenation

2020 ◽  
Vol 91 (2) ◽  
pp. 106-109
Author(s):  
Jacek Siewiera ◽  
Przemysław Szałański ◽  
Dariusz Tomaszewski ◽  
Jacek Kot

BACKGROUND: High-altitude decompression sickness (HADCS) is a rare condition that has been associated with aircraft accidents. To the best of our knowledge, the present paper is the first case report of a patient treated for severe HADCS using recompression therapy and veno-venous extracorporeal oxygenation (VV-ECMO) with a complete recovery.CASE REPORT: After depressurization of a cabin, the 51-yr-old jet pilot was admitted to the Military Institute of Medicine with a life-threatening HADCS approximately 6 h after landing from a high-altitude flight, in a dynamically deteriorating condition, with progressing dyspnea and edema, reporting increasing limb paresthesia, fluctuating consciousness, and right-sided paresis. Hyperbaric oxygen therapy in the intensive care mode was initiated. A therapeutic recompression with U.S. Navy Treatment Table 6 was performed with neurological improvement. Due to cardiovascular collapse, sedation, mechanical ventilation, and significant doses of catecholamines were started, followed by continuous veno-venous hemodialysis. In the face of disturbances in oxygenation, during the second day of treatment the patient was commenced on veno-venous extracorporeal oxygenation. Over the next 6 d, the patient’s condition slowly improved. On day 7, VV-ECMO was discontinued. On day 19, the patient was discharged with no neurological deficits.DISCUSSION: We observed two distinct stages during the acute phase of the disease. During the first stage, signs of hypoperfusion, neurological symptoms, and marbled skin were observed. During the second stage, multiple organ dysfunction dominated, including heart failure, pulmonary edema, acute kidney injury, and fluid overload, all of which can be attributed to extensive endothelial damage.Siewiera J, Szałański P, Tomaszewski D, Kot J. High-altitude decompression sickness treated with hyperbaric therapy and extracorporeal oxygenation. Aerosp Med Hum Perform. 2020; 91(2):106–109.

2019 ◽  
pp. 673-683
Author(s):  
Richard E. Moon ◽  

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.


2019 ◽  
Vol 7 (11) ◽  
pp. 2231-2234
Author(s):  
Sami Ullah ◽  
Ahmad Zaheer Qureshi ◽  
Kholoud Kedowah ◽  
Afnan AlHargan ◽  
Asim Niaz

2017 ◽  
Vol 2017 ◽  
pp. 1-4 ◽  
Author(s):  
Re-I Chin ◽  
John J. Monda ◽  
Maulik Sheth ◽  
William Ogle ◽  
Gloria Merenda ◽  
...  

We describe a case of a young male without stroke risk factors who presented with a sudden onset of left-sided weakness, left hand numbness, and left eye blurriness. CT scan of the head without contrast and diffusion-weighted MRI of the brain with contrast revealed an ischemic stroke in the right middle cerebral artery distribution. Transesophageal echocardiography (TEE) revealed a mobile pedunculated mass on the posterior surface of the mitral valve. This mass was resected and pathology showed a cardiac papillary fibroelastoma (CPFE), which was determined to be the cause of the patient’s cardioembolic stroke. Further workup also found that patient had microcytic anemia secondary toβ-thalassemia intermedia, a rare hematologic disorder due to defective hemoglobin synthesis. Recently, another case report suggestedβ-thalassemia major may underlie the pathogenesis of CPFE.β-Thalassemia major causes a state of chronic inflammation and endothelial damage, which can mediate CPFE formation. Based on literature review, this is the first case report of a CPFE in a patient withβ-thalassemia intermedia. This hypothesis-generating case report calls attention to the need for elucidating the relationship between CPFE andβ-thalassemia in future studies to better understand the diagnosis and management of a rare cardiac tumor.


2017 ◽  
Vol 14 (3) ◽  
pp. 46-48
Author(s):  
Yam Bahadur Roka ◽  
Mohan Karki

Chronic encapsulated intracerebral hematoma (CE-ICH) is an uncommon pathology that presents with headache, seizure, focal neurological deficits, or as a tumor. Trauma as a cause for CE-ICH is even rare and we believe this is the first case report as “trauma causing chronic encapsulated intracerebral hematoma “search in PubMed did not reveal any results. Repeated micro-hemorrhages in the CM or AVM are supposed to cause this lesion which progress from an earlier encapsulated phase to a thick capsulated stage with edema and clinical symptoms. CT or MRI is the diagnostic modality and it mimics, tumor, AVM, CM, angiomableed, cerebral abscess, metastatic mass or neurocysticercosis. Burr hole, mini-craniotomy, craniotomy, CT guided stereotactic aspiration or endoscopic excision are some options with equally good results. The present case with history of trauma was managed successfully with craniotomy with no recurrence for past one year. Nepal Journal of Neuroscience, Volume 14, Number 3, 2017, page: 46-48


Author(s):  
Rahman Maraqa Sima Abdel ◽  
Robert McMahon ◽  
Anusha Pinjala ◽  
Gastelum Alheli Arce ◽  
Mohsen Zena
Keyword(s):  

Author(s):  
Mosaad Soliman ◽  
Khaled Mowafy ◽  
Reem Soliman ◽  
Rana Soliman
Keyword(s):  

Author(s):  
Alaa AlAyed ◽  
Manar Samman ◽  
Abdul Peer-Zada ◽  
Mohammed Almannai
Keyword(s):  

Background: Binasal Occlusion (BNO) is a clinical technique used by many neurorehabilitative optometrists in patients with mild traumatic brain injury (mTBI) and increased visual motion sensitivity (VMS) or visual vertigo. BNO is a technique in which partial occluders are added to the spectacle lenses to suppress the abnormal peripheral visual motion information. This technique helps in reducing VMS symptoms (i.e., nausea, dizziness, balance difficulty, visual confusion). Case Report: A 44-year-old AA female presented for a routine eye exam with a history of mTBI approximately 33 years ago. She was suffering from severe dizziness for the last two years that was adversely impacting her ADLs. The dizziness occurred in all body positions and all environments throughout the day. She was diagnosed with vestibular hypofunction and had undergone vestibular therapy but reported little improvement. Neurological exam revealed dizziness with both OKN drum and hand movement, especially in the left visual field. BNO technique resulted in immediate relief of her dizziness symptoms. Conclusion: To our knowledge, this is the first case that illustrates how the BNO technique in isolation can be beneficial for patients with mTBI and vestibular hypofunction. It demonstrates the success that BNO has in filtering abnormal peripheral visual motion in these patients.


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