Neurologic Decompression Sickness Research Articles

Detection of Patent foramen Ovale with Contrast Enhanced Transcranial Doppler at Divers

Abstract Patent foramen ovale (PFO) is a condition present in 25% of the adult population. It is a remnant of fetal foramen ovale which allows blood to pass from the right to the left atrium, bypassing the fetal lungs. In majority adults it does not have any clinical significance, but in some people it may allow shunting of venous blood into the left atrium (right – left – shunt or RLS), circumventing the lung filter, especially during sneezing, cough, lifting heavy equipment. Is such case, PFO may be a route for venous emboli or gas bubbles from veins to the arterial system. It is known as a paradoxical embolism and may be cause of ischaemic stroke or neurologic decompression sickness (DCI), inner-ear DCI and cutis marmorata. Transesophageal echocardiography is considered as a reference standard in detection of intracardial shunts. Its sensitivity and specificity ranges between 94%-100%. However, TEE is an invasive examination with potentially serious side effects. An alternative examination in RLS detection is contrast enhanced Transcranial Doppler (the bubble study or c-TCD). In comparison to TEE, Transcranial Doppler is not invasive, relatively not expensive and save technique. With its high sensitivity and specificity in detection of PFO, 97% and 93% respectively, it may improve detection of RLS and allow to conduct screening examination for PFO in divers.

Nanobubbles Form at Active Hydrophobic Spots on the Luminal Aspect of Blood Vessels: Consequences for Decompression Illness in Diving and Possible Implications for Autoimmune Disease-An Overview.

Decompression illness (DCI) occurs following a reduction in ambient pressure. Decompression bubbles can expand and develop only from pre-existing gas micronuclei. The different hypotheses hitherto proposed regarding the nucleation and stabilization of gas micronuclei have never been validated. It is known that nanobubbles form spontaneously when a smooth hydrophobic surface is submerged in water containing dissolved gas. These nanobubbles may be the long sought-after gas micronuclei underlying decompression bubbles and DCI. We exposed hydrophobic and hydrophilic silicon wafers under water to hyperbaric pressure. After decompression, bubbles appeared on the hydrophobic but not the hydrophilic wafers. In a further series of experiments, we placed large ovine blood vessels in a cooled high pressure chamber at 1,000 kPa for about 20 h. Bubbles evolved at definite spots in all the types of blood vessels. These bubble-producing spots stained positive for lipids, and were henceforth termed “active hydrophobic spots” (AHS). The lung surfactant dipalmitoylphosphatidylcholine (DPPC), was found both in the plasma of the sheep and at the AHS. Bubbles detached from the blood vessel in pulsatile flow after reaching a mean diameter of ~1.0 mm. Bubble expansion was bi-phasic—a slow initiation phase which peaked 45 min after decompression, followed by fast diffusion-controlled growth. Many features of decompression from diving correlate with this finding of AHS on the blood vessels. (1) Variability between bubblers and non-bubblers. (2) An age-related effect and adaptation. (3) The increased risk of DCI on a second dive. (4) Symptoms of neurologic decompression sickness. (5) Preconditioning before a dive. (6) A bi-phasic mechanism of bubble expansion. (7) Increased bubble formation with depth. (8) Endothelial injury. (9) The presence of endothelial microparticles. Finally, constant contact between nanobubbles and plasma may result in distortion of proteins and their transformation into autoantigens.

Xenon Blocks Neuronal Injury Associated with Decompression.

Despite state-of-the-art hyperbaric oxygen (HBO) treatment, about 30% of patients suffering neurologic decompression sickness (DCS) exhibit incomplete recovery. Since the mechanisms of neurologic DCS involve ischemic processes which result in excitotoxicity, it is likely that HBO in combination with an anti-excitotoxic treatment would improve the outcome in patients being treated for DCS. Therefore, in the present study, we investigated the effect of the noble gas xenon in an ex vivo model of neurologic DCS. Xenon has been shown to provide neuroprotection in multiple models of acute ischemic insults. Fast decompression compared to slow decompression induced an increase in lactate dehydrogenase (LDH), a well-known marker of sub-lethal cell injury. Post-decompression administration of xenon blocked the increase in LDH release induced by fast decompression. These data suggest that xenon could be an efficient additional treatment to HBO for the treatment of neurologic DCS.

White matter hyperintensities on MRI in high-altitude U-2 pilots

To demonstrate that U-2 pilot occupational exposure to hypobaria leads to increased incidence of white matter hyperintensities (WMH) with a more uniform distribution throughout the brain irrespective of clinical neurologic decompression sickness history. We evaluated imaging findings in 102 U-2 pilots and 91 controls matched for age, health, and education levels. Three-dimensional, T2-weighted, high-resolution (1-mm isotropic) imaging data were collected using fluid-attenuated inversion recovery sequence on a 3-tesla MRI scanner. Whole-brain and regional WMH volume and number were compared between groups using a 2-tailed Wilcoxon rank sum test. U-2 pilots demonstrated an increase in volume (394%; p = 0.004) and number (295%; p < 0.001) of WMH. Analysis of regional distribution demonstrated WMH more uniformly distributed throughout the brain in U-2 pilots compared with mainly frontal distribution in controls. Pilots with occupational exposure to hypobaria showed a significant increase in WMH lesion volume and number. Unlike the healthy controls with predominantly WMH in the frontal white matter, WMH in pilots were more uniformly distributed throughout the brain. This is consistent with our hypothesized pattern of damage produced by interaction between microemboli and cerebral tissue, leading to thrombosis, coagulation, inflammation, and/or activation of innate immune response, although further studies will be necessary to clarify the pathologic mechanisms responsible.

Hyperintense White Matter Lesions in 50 High-Altitude Pilots With Neurologic Decompression Sickness

Neurologic decompression sickness (NDCS) can affect high-altitude pilots, causing variable central nervous system symptoms. Five recent severe episodes prompted further investigation. We report the hyperintense white matter (HWM) lesion imaging findings in 50 U-2 pilot volunteers, and compare 12 U-2 pilots who experienced clinical NDCS to 38 U-2 pilots who did not. The imaging data were collected using a 3T magnetic resonance imaging scanner and high-resolution (1-mm isotropic) three-dimensional fluid-attenuated inversion recovery sequence. Whole-brain and regional lesion volume and number were compared between groups. The NDCS group had significantly increased whole brain and insular volumes of HWM lesions. The intergroup difference in lesion numbers was not significant. A clinical episode of NDCS was associated with a significant increase in HWM lesion volume, especially in the insula. We postulate this to be due to hypobaric exposure rather than hypoxia since all pilots were maintained on 100% oxygen throughout the flight. Further studies will be necessary to better understand the pathophysiology underlying these lesions.

Prevalence of Neurologic Decompression Sickness and Necrotic Brain Lesions in High-Altitude Pilots (S08.005)

Objective: To determine the prevalence of NDCS and necrotic brain lesions in a cohort of high-altitude pilots and to discover predictive factors. Background The U.S. Air Force U-2 community has experienced an increase in neurologic decompression sickness (NDCS). This is the first nonanonymous aircrew study combining clinical and neuroimaging findings. Design/Methods: Fifty pilots underwent flight and NDCS history questionnaires as well as 3T brain magnetic resonance imaging at the Research Imaging Center. To date, 29 images have been analyzed for the presence of necrotic lesions. Results: Eleven pilots (22%) were treated for NDCS. Data were compared between pilots with and without NDCS, respectively: total U-2 hours – 500±330 to 745±417; number of missions – 65±51 to 107±71; operational tempo (OT) between high-flights (in days) – 3.1±0.7 to 2.9±0.9. Six pilots developed NDCS within their first three flights, while five developed it near the end of their deployment. Analyzed images of 4 of 7 pilots with NDCS displayed necrotic lesions compared to 10 of 22 pilots without NDCS. Comparative data for pilots with necrotic lesions versus pilots without necrotic lesions were not significantly different (total U-2 hours – 648±371 to 684±399; missions – 69±48 to 105±66; and OT – 2.8±0.5 to 3.0±0.6). Conclusions: The prevalence of NDCS in this sample was 11/50. There is no statistical difference in total hours, missions, and operational tempo between those with and without NDCS. An early and late group among NDCS was identified. Fifty-five percent of NDCS cases occurred earlier in pilots with fewer flight hours and missions, suggesting susceptibility to NDCS in pilot subpopulations. Necrotic lesions were found in 57% of NDCS pilots analyzed and, surprisingly, 45% of non-NDCS pilots analyzed. Research is ongoing to study the clinical and operational significance of these findings. Supported by: USAF AFMSA/SG9 study grant I-11-10 and AFMSA/SG9 study grant I-11-44. Disclosure: Dr. Robinson has nothing to disclose. Dr. Sherman has nothing to disclose. Dr. Kochumov has nothing to disclose. Dr. Grogan has received personal compensation for activities with Pfizer Inc. and US Worldmeds as a speaker. Dr. McGuire has nothing to disclose.

White Matter Hyperintensities and Necrosis in High Altitude Pilots with Neurologic Decompression Sickness (P03.154)

White Matter Hyperintensities and Necrosis in High Altitude Pilots with Neurologic Decompression Sickness (P03.154)

Neurologic Decompression Sickness Following Cabin Pressure Fluctuations at High Altitude

Decompression sickness (DCS) occurs in diving, altitude chamber exposures, and unpressurized or depressurized high-altitude flights. Because DCS takes many forms, in-flight cases may be misinterpreted as hypoxia, hyperventilation, or viral illness, with resulting failure to respond appropriately. In this case, a 28-yr-old male pilot of a single-seat, tactical aircraft experienced 12 rapid pressure fluctuations while flying at 43,000 ft above sea level. He had no symptoms and decided to complete the flight, which required an additional 2 h in the air. Approximately 1 h later he began to experience fatigue, lightheadedness, and confusion, which he interpreted as onset of a viral illness. However, symptoms progressed to visual, cognitive, motor, and sensory degradations and it was with some difficulty that he landed safely at his destination. Neurologic DCS was suspected on initial evaluation by flight line medical personnel because of the delayed onset and symptom progression. He was transferred to a local Emergency Department and noted to have altered mental status, asymmetric motor deficits, and non-dermatomal paresthesias of the upper and lower extremities. Approximately 3.5 h after the incident and 2.5 h after the onset of symptoms he began hyperbaric oxygen therapy. He received partial relief at 30 min of the Navy DiveTable 6 and full resolution at 90 min; there were no recurrent symptoms at a 1-yr follow-up. This case highlights the importance of early recognition of in-flight DCS symptoms and landing as soon as possible rather than as soon as practical in all likely scenarios.

Patent foramen ovale: an underrated risk for divers?

The foramen ovale which is the fetal connection between the right and left atrium persists in about 30 % of the adult population. In the presence of a persistent foramen ovale (PFO) shunting of blood may occur from the right to the left atrium, and bubbles can reach the systemic circulation during or after the decompression phase of a dive with compressed air. Therefore, divers with PFO may have an increased risk to develop ischemic cerebral lesions and neurologic decompression sickness (DCS). Significant right-to-left shunting may be diagnosed using transcranial doppler ultrasound of the medial cerebral artery and echocardiography with echo contrast media and Valsalva provocation. However, there are no official guidelines concerning PFO screening in medical fitness exams for professional or recreational divers in Germany. Therefore, it remains in the diver's choice to be screened for PFO. Divers with a history of DCS should be monitored for PFO, especially when diving strictly adhered to decompression tables. Divers with PFO who refuse to stop diving after DCS should be advised to adhere to very save dive profiles.

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Dysbaric cerebral air embolism in Hawaii

Cerebral air embolism is a major cause of death and disability among sport scuba divers. To better define the epidemiologic and clinical manifestations of this infrequently encountered disorder, the records of all recompression treatments in Hawaii from 1976 through 1979 were reviewed. Forty-two cases of dysbaric air embolism (DAE) were identified on the basis of clinical criteria, accounting for 18% of the patients undergoing recompression treatment for diving-related disorders during this four-year period. In 22 patients (52%), DAE was part of a dysbarism syndrome that involved one or more forms of decompression sickness and/or in which DAE could not be differentiated from neurologic decompression sickness. The presenting signs and symptoms varied, with asymmetric multiplegia being the most common finding. Two patients died, giving a case fatality rate of 5% for those who survived until reaching the recompression chamber. Overall, 78% of the cases manifested either complete (61%) or substantial (17%) recovery with recompression and adjunctive medical measures. Traditional concepts of dysbaric cerebral air embolism are not adequate to explain the spectrum of clinical manifestations encountered in this condition.

Neurologic presentation of decompression sickness and air embolism in sport divers.

In a retrospective study of scuba divers with neurologic injuries, we found that mild symptoms were common. Seventy divers had decompression sickness, most often with paresthesias or numbness, rarely with paresis. Thirty-nine divers had air embolism that often caused unconsciousness or mild symptoms of cerebral injury. Many divers with neurologic decompression sickness gave histories of dives that were within conventional limits, and many with air embolism gave no history of breath-holding during ascent. Mild symptoms sometimes regressed spontaneously. Recompression delays were responsible for poor responses to therapy.