Aydın Deniz Karataş

Is there a relationship between the blood cholinesterase and QTc interval in the patients with acute organophosphate poisoning

Organophosphates cause poisoning as a result of the excessive accumulation of acetylcholine at the cholinergic synapses due to inhibition of acetylcholinesterase (ChE). In the literature, it has been reported that there have been electrocardiographic abnormalities, including QT‐interval prolongation in most patients with acute organophosphate poisoning (OPP), and a relation between blood ChE level and clinical severity in acute OPP. The aim of this study is to assess the relationship between blood ChE level and QTc interval in the patients with acute OPP. This retrospective study consists of 20 patients admitted to the emergency intensive care unit. A total of 93 QTc interval and blood ChE measures obtained on the same day from 20 cases were compared for their correlation. There were prolonged QTc intervals in 35.4% of the ECGs. There was a negative correlation between QTc interval and blood ChE measures. In following up the patients with acute OPP, QTc interval may be useful when blood ChE levels are low and may provide complementary information concerning the severity of poisoning. However, further prospective studies, supporting the present results, are needed.

What is the meaning of “temporary” forensic reports for Emergency physicians? Self protection? Bias? Habit?...

Marmara Üniversitesi Pendik Eğitim ve Araştırma Hastanesi, Acil Tıp Kliniği, İstanbul; Toros Devlet Hastanesi, Acil Servis, Mersin; İskenderun Devlet Hastanesi, Acil Servis, Hatay Serkan Emre EROĞLU,1 Sıddıka Nihal TOPRAK,2 Aydın Deniz KARATAŞ,3 Özge ONUR,1 Çiğdem ÖZPOLAT,1 Emre SALÇIN,1 Arzu DENİZBAŞI1 Acil Hekimleri için “Geçici” Adli Raporların Anlamı Nedir? Kendini Koruma? Önyargı? Alışkanlık?...

Fatal poisoning from eating carp (Ctenopharyngodon idella)

In this family, four of seven female siblings developed headache fulfilling diagnostic criteria for migraine without aura (9). Three had new onset of migraine around the time of the menopause. Three other female family members (mother, sister and niece) also had a history compatible with migraine without aura, two with premenopausal onset. Consistent with the observation that migraine is underdiagnosed and undertreated, the family only came to neurological attention by chance, none had consulted a neurologist and only one had ever received triptans. As the British National Formulary points out, there is little information available on the use of triptans in the elderly, and one might anticipate an increasing frequency of contraindications to triptan use (ischaemic heart disease, previous myocardial infarction, coronary vasospasm, uncontrolled or severe hypertension) with increasing age. The expression of the migraine phenotype may be characterised as a consequence of the interaction between a biological disposition to migraine, such as a familial (genetically determined) brain threshold, operating at the level of the brainstem, and a variety of external precipitating factors (neural triggers) which, individually or collectively, lower the threshold to the critical point at which attacks occur (8). Changes in sex hormone levels may represent one such triggering factor, accounting for migraine onset at menarche or with oral contraceptive use, improvement in pregnancy and exacerbation with HRT use or at the menopause (1,3). The heterogeneity of age at migraine onset in this family, and its absence in some members, is of note. Considering the model of migraine aetiology suggested above (8), this might be accounted for by differences in biological threshold, and ⁄ or by different precipitating factors. Both genetic and epigenetic factors might modulate expression of the migraine phenotype. For instance, polymorphisms in genes encoding glutathione Stransferase (10) and angiotensin-converting enzyme (11) have been implicated as risk factors for migraine. Contrary to the findings in this family, epidemiological studies (12,13) suggest that smoking is more common in migraineurs, although no association with smoking status was found in a study of twin-pairs discordant for migraine with aura (14). Study of pedigrees such as the one reported might permit a teasing apart of these various possibilities. As a practical clinical point, this family indicates that de novo migraine, rather than worsening of existing migraine, may present at the time of the menopause.