Mihaela Ignatescu

Diving Diseases Research Centre, Plymouth, England, United Kingdom

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Publications (4)6.95 Total impact

  • Mihaela Ignatescu · Philip Bryson · Christoph Klingmann
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    ABSTRACT: Decompression sickness (DCS) is caused by formation and growth of bubbles from excess dissolved gas in body tissues following reduction in ambient pressure. Inner ear decompression sickness (IEDCS) is a complex disorder involving the vestibulo-cochlear apparatus whose pathophysiology remains incompletely understood. The records of 662 consecutive DCS cases treated over a 7-yr period at 2 UK hyperbaric units were examined for symptoms suggesting IEDCS (nausea, vomiting, dizziness, and hearing loss arising within 2 h of surfacing). For IEDCS cases, demographics, dive, treatment, and outcome data were extracted with particular attention to the outcome of testing for a right-to-left shunt. Included were 31 men and 2 women with a mean age of 46 yr (range 31-61 yr). Of these, 16 patients had isolated IEDCS and 17 patients had associated symptoms ranging from joint pain to tingling and numbness. The depth of the dive leading to the incident ranged from 49-256 ft (15-78 m). As primary treatment, 21 patients received a U.S. Navy Treatment Table 6 (USN TT6) and 11 patients received a Comex 30. No difference in the speed of recovery or number of treatments needed was seen between the two tables. All patients were advised to have a right to left shunt (RLS) check, but only 30 complied with that, with 24 (80%) testing RLS positive. Our retrospective study confirms the correlation between IEDCS and the presence of a significant patent foramen ovale (PFO). In our series 48% of patients had an isolated IEDCS. IEDCS responds slowly to treatment irrespective of the initial table used. Recovery is thought to be mainly a central compensation process.
    No preview · Article · Dec 2012 · Aviation Space and Environmental Medicine
  • Jean-Michel Pontier · Emmanuel Gempp · Mihaela Ignatescu
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    ABSTRACT: Bubble-induced platelet aggregation offers an index for evaluating decompression severity in humans and in a rat model of decompression sickness. Endothelial cells, blood platelets, or leukocytes shed microparticles (MP) upon activation and during cell apoptosis. The aim was to study blood platelet MP (PMP) release and bubble formation after a scuba-air dive in field conditions. Healthy, experienced divers were assigned to 1 experimental group (n = 10) with an open-sea air dive to 30 msw for 30 min and 1 control group (n = 5) during head-out water immersion for the same period. Bubble grades were monitored with a pulsed doppler according to Kissman Integrated Severity Score (KISS). Blood samples for platelet count (PC) and PMP (annexin V and CD41) were taken 1 h before and after exposure in both groups. The result showed a decrease in post-dive PC compared with pre-dive values in experimental group with no significant change in the control group. We observed a significant increase in PMP values after the dive while no change was revealed in the control group. There was a significant positive correlation between the PMP values after the dive and the KISS bubble score. The present study highlighted a relationship between the post-dive decrease in PC, platelet MP release, and bubble formation. Release of platelet MPs could reflect bubble-induced platelet aggregation and could play a key role in alteration of the coagulation. Further studies must investigate endothelial and leukocyte MP release in the same field conditions.
    No preview · Article · Jun 2012 · Applied Physiology Nutrition and Metabolism
  • Mihaela Ignatescu
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    ABSTRACT: Dear Editor, I have read with great interest the recently published series of patients treated with hyperbaric oxygen therapy (HBOT) for malignant otitis externa (MOE).¹ I agree that the treatment of this disease presents a challenge and, because of its low incidence, randomised controlled studies are impossible. I am surprised by the high percentage of serious adverse effects of HBOT encountered in this study. The authors report that five out of 17 patients had serious adverse effects with two cases of pulmonary oedema, one hyperoxic seizure (which after careful reading turns out to be more likely a hypoglycaemic episode), one tympanic membrane perforation and one case of claustrophobia which occurred during the patient's first session. Even after discounting the case of claustrophobia, the remaining incidence of 24 % is still extremely high compared to the expected incidence of side effects in this patient group. In the discussion (page 199, paragraph 2), it says "complications such as oxygen toxic seizures and acute pulmonary oedema are directly related to high intra-arterial oxygen tensions and are well documented in the literature". The quoted paper here (reference 14, Leach et al 1998) refers to pulmonary symptoms and subsequently pulmonary oxygen toxicity and not to acute pulmonary oedema.² Pulmonary oedema as a side effect purely of HBOT is extremely rare and we have not seen pulmonary oxygen toxicity in patients treated for 2 hours per day, as would be the case in MOE. Further on in the discussion (page 199, paragraph 2), the authors quote a recent review which has the wrong reference (this should be reference 21 not 18) and where they report a complication rate of 20 %, whereas in the original quoted paper by Huang et al it is 1.83 %.³ Further on, the incidence of serious complications quoted in this publication by Saxby et al is 1.7% (they include pulmonary oedema, even though the original paper by Huang only talks about central nervous system toxicity), but the incidence in the original publication by Huang et al was 0.109 %.³ At the 2010 Annual Scientific Meeting of the European Underwater and Baromedical Society, we presented a series of nine patients with MOE who received HBOT at Whipps Cross Hospital, London.4 In our series, none of the patients experienced any severe adverse events during a similarly long treatment programme of 23 to 40 sessions. This treatment was sufficient to yield a benefit in seven of the nine patients (with benefit defined as both a significant improvement of symptoms - pain, discharge and cranial nerve palsies - and normalisation of inflammatory markers post-treatment).4 We have similar positive results in the patient series in Plymouth (unpublished observations). The high incidence of serious side effects reported by the authors gives me cause to wonder how patients in this retrospective study were screened for their suitability for HBOT. I am concerned that non-hyperbaric specialists reading this paper might conclude that the risk-benefit of using hyperbaric oxygen in MOE is in favour of avoiding its use, with a high risk (29 %) of serious side effects and a very low benefit. Indeed, we had problems convincing our local health authorities to fund treatment for our patients, hence a published paper talking about five out of 17 patients having serious side effects from the treatment would just reinforce their belief that HBOT is dangerous and not beneficial. Hyperbaric physicians should be careful when publishing data that could be interpreted in the wrong way by specialists unversed in hyperbaric medicine.
    No preview · Article · Sep 2011 · Journal of the South Pacific Underwater Medicine Society
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    ABSTRACT: Decompression sickness (DCS) with alterations in coagulation system and formation of platelet thrombi occurs when a subject is subjected to a reduction in environmental pressure. Blood platelet consumption after decompression is clearly linked to bubble formation in humans and offers an index for evaluating DCS severity in animal models. Previous studies highlighted a predominant involvement of platelet activation and thrombin generation in bubble-induced platelet aggregation (BIPA). To study the mechanism of the BIPA in DCS, we examined the effect of acetylsalicylic acid (ASA), heparin (Hep), and clopidogrel (Clo), with anti-thrombotic dose pretreatment in a rat model of DCS. Male Sprague-Dawley rats (n = 208) were randomly assigned to one experimental group treated before the hyperbaric exposure and decompression protocol either with ASA (3×100 mg·kg(-1)·day(-1), n = 30), Clo (50 mg·kg(-1)·day(-1), n = 60), Hep (500 IU/kg, n = 30), or to untreated group (n = 49). Rats were first compressed to 1,000 kPa (90 msw) for 45 min and then decompressed to surface in 38 min. In a control experiment, rats were treated with ASA (n = 13), Clo (n = 13), or Hep (n = 13) and maintained at atmospheric pressure for an equivalent period of time. Onset of DCS symptoms and death were recorded during a 60-min observation period after surfacing. DCS evaluation included pulmonary and neurological signs. Blood samples for platelet count (PC) were taken 30 min before hyperbaric exposure and 30 min after surfacing. Clo reduces the DCS mortality risk (mortality rate: 3/60 with Clo, 15/30 with ASA, 21/30 with Hep, and 35/49 in the untreated group) and DCS severity (neurological DCS incidence: 9/60 with Clo, 6/30 with ASA, 5/30 with Hep, and 12/49 in the untreated group). Clo reduced fall in platelet count and BIPA (-4,5% with Clo, -19.5% with ASA, -19,9% with Hep, and -29,6% in the untreated group). ASA, which inhibits the thromboxane A2 pathway, and Hep, which inhibits thrombin generation, have no protective effect on DCS incidence. Clo, a specific ADP-receptor antagonist, reduces post-decompression platelet consumption. These results point to the predominant involvement of the ADP release in BIPA but cannot differentiate definitively between bubble-induced vessel wall injury and bubble-blood component interactions in DCS.
    Preview · Article · Mar 2011 · Journal of Applied Physiology