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Published in Ken Addley, MCQs, MEQs and OSPEs in Occupational Medicine, 2023
Best fit. While carbon monoxide exerts its toxic effect by binding to haemoglobin to produce carboxyhaemoglobin it also produces changes to the remaining haemoglobin which causes more avid binding of oxygen with a left shift in the oxygen dissociation curve. Chronic exposure is thought to accelerate atherogenesis and it may explain some of the vascular pathology seen in smokers. The medical significance of its binding to other haem containing proteins is unclear.
Smoking
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
Jorge E. Tolosa, Niyazi Kilic, David M. Stamilio
Exposure causes formation of carboxyhemoglobin. Carboxyhemoglobin is cleared slowly from the fetal circulation and diminishes tissue oxygenation via competitive inhibition with oxyhemoglobin. There is a left shift of the oxyhemoglobin dissociation curve, causing decreased availability of oxygen to the fetus [17].
Burns
Published in Stephen M. Cohn, Alan Lisbon, Stephen Heard, 50 Landmark Papers, 2021
Brian Brisebois, Joyce McIntyre
Smoke inhalation injury should be considered in any patient with possible extended exposure to smoke. Bronchoscopic or laryngoscopic evidence of soot or injury below the vocal cords is diagnostic (Greenhalgh). Although highly specific, a negative inspection does not rule out the presence of smoke inhalation injury (Lundy). Individuals exposed to flash explosions (i.e., cigarette igniting supplemental oxygen) do not usually suffer smoke inhalation injury (Lundy, Greenhalgh). CO poisoning can be confirmed by elevated levels of carboxyhemoglobin (ABG and pulse oximeter won't be helpful). Suspected CO poisoning should be treated with 100% oxygen while carboxyhemoglobin levels are obtained (Greenhalgh).
The effects of maternal smoking on fetal cranial development. Findings from routine midtrimester sonographic anomaly screening
Published in Journal of Obstetrics and Gynaecology, 2023
Çağlar Çetin, Rabia Zehra Bakar, Taha Takmaz, Özge Pasin, Mehmet Serdar Kütük
Smoking during pregnancy is one of the most common environmental factors affecting fetal and neonatal growth and well-being. Smoking is thought to cause fetal growth restriction through its toxic ingredients. Cotinine is a long-acting metabolite of tobacco smoke and easily passes through the placenta and concentrates in the developing fetus (Luck et al.1985, Jauniaux et al.1999). This ingredient of tobacco has a myriad of untoward effects on cellular growth, uterine perfusion, the epigenetic process and ultimately, fetal growth. On the other hand, carbon monoxide is an avid substrate for hemoglobin, creates a carboxyhemoglobin (COHb) complex, and leads to tissue hypoxia (Longo and Hill 1977, Law et al.2003, Godding et al.2004). Despite the well-known effects of smoking on somatic growth, current studies have shown that it selectively affects some parts of the fetal brain, even in appropriately growing fetuses. Animal and human studies have demonstrated that smoking reduced overall fetal brain volume and this effect was prominent in the frontal lobe (Ekblad et al.2010, Abraham et al.2017). Other researchers have shown that the amygdala and pallidum regions bear the brunt of abnormal growth and the development process (Liu et al.2011, Haghighi et al.2013).
Dexamethasone therapy prevents delayed neuropsychiatric sequelae after carbon monoxide poisoning: a prospective registry-based study
Published in Clinical Toxicology, 2023
Sechan Kim, Sungwoo Choi, Yujin Ko, Choung Ah Lee, Gi Woon Kim, Ji Eun Moon, Sangun Nah, Sangsoo Han
This prospective-registry-based study was conducted in an ED of an urban tertiary care hospital (in Bucheon, Korea) that receives over 70,000 patient visits per year. We prospectively collected a registry of information on patients with CO poisoning commencing in March 2020. The diagnostic criteria of CO poisoning include the appropriate symptoms and history suggesting for exposure and an elevated the carboxyhemoglobin concentration. Symptoms that may include nausea, vomiting, dizziness, confusion, chest pain, fatigue, shortness of breath, and loss of consciousness [14]. And carboxyhemoglobin concentrations exceeding 5% in non-smokers (10% in smokers) at the time of ED arrival were used as threshold values for diagnosing CO poisoning. This study was approved by the hospital Institutional Review Board (IRB file no. 2020-03-019). Our study was based on retrospective analysis of a data registry, so informed consent was waived.
A case of Hb Rothschild (HBB: c.112T>A) with low pulse oximetry: a first familial presentation in China
Published in Hematology, 2022
Diandian Li, Qunfang Wan, Chunyu Li, Hongbing Ma, Gang Wang
Arterial blood gas (ABG) was performed when dyspnea occurred, and the results were: pH 7.39 (normal 7.35–7.45), PaO2 94.2 mmHg (normal 80–100 mmHg), SpO2 87.1% (normal 95–98%), PaCO2 43.6 mmHg (normal 35–45 mmHg) and bicarbonate 25 mmol/L (normal 22–26 mmol/L). Notably, there was a mismatch between the patient’s SpO2 and PaO2. Thus, ABG was repeated, with similar results to the previous. However, his carboxyhemoglobin and deoxyhemoglobin were increased to 2.2% (normal 0.5–1.5%) and 12.5% (normal1.4–4.9%), respectively. Methemoglobin (0.6%, normal 0.2–0.8%) was undetectable. Toxicological screening test including methylamphetamine, methylenedioxymethamphetamine, ketamine, morphine and heroin were negative. Therefore, an altered oxygen affinity variant hemoglobin (Hb) was suspected.