2,4-Dinitrophenol (DNP) is reported to cause rapid loss of weight, but unfortunately is associated with an unacceptably high rate of significant adverse effects. DNP is sold mostly over the internet under a number of different names as a weight loss/slimming aid. It causes uncoupling of oxidative phosphorylation; the classic symptom complex associated with toxicity of phenol-based products such as DNP is a combination of hyperthermia, tachycardia, diaphoresis and tachypnoea, eventually leading to death. Fatalities related to exposure to DNP have been reported since the turn of the twentieth century. To date, there have been 62 published deaths in the medical literature attributed to DNP. In this review, we will describe the pattern and pathophysiology of DNP toxicity and summarise the previous fatalities associated with exposure to DNP.
The aim of this study is to provide a systematic review of the literature reporting agreement between arterial and venous pH, partial pressure of carbon dioxide (PCO2), bicarbonate (HCO3⁻), base excess and lactate; and to perform a meta-analysis of the differences. Medline and Embase searches using Eduserv Athens from 1950 to present were conducted using the terms 'VBG', 'ABG', 'arterial', 'venous', 'blood', 'gas', 'lactate', 'emergency' and 'department'. References of the published papers were hand searched and full-text versions of those deemed helpful to the question were obtained. Mean difference (MD) and 95% limits of agreement (LOA) were either reported or calculated from the published data. Pooled MDs with 95% confidence intervals (CIs) were calculated for differences between arterial and venous pH, PCO2, bicarbonate and lactate. Thirteen articles relevant to pH, 12 relevant to PCO2, 10 relevant to bicarbonate and three relevant to lactate were found. The pooled MD (venous-arterial) for pH was -0.033 pH units (95% CI -0.039 to 0.027) with narrow 95% LOA, the pooled MD for PCO2 was 4.41 mmHg (95% CI 2.55-6.27) with 95% LOA ranging from -20.4 to 25.8 mmHg, the pooled MD for bicarbonate was 1.03 mmol/l (95% CI 0.56-1.50) with 95% LOA ranging from -7.1 to 10.0 mmol/l and the pooled MD for lactate was 0.25 mmol/l (95% CI 0.15-0.35) with 95% LOA ranging from -2.0 to 2.3 mmol/l. Venous and arterial pH and bicarbonate agree reasonably at all values, but the agreement is highest at normal values. Arteriovenous agreement for PCO2 is poor and PvCO2 cannot be relied upon as an absolute representation of PaCO2. However, normal peripheral PvCO2 has a good negative predictive value for normal arterial PCO2, and a normal PvCO2 can be used as a screen to exclude hypercapnic respiratory disease. There may be a poor agreement between arterial and venous lactate at abnormal values; however, if the venous lactate is normal, it is likely the arterial values of this parameter will also be normal.
Analytically confirmed exposure to MDMB-CHMICA was associated with acidosis (often of respiratory origin), reduced level of consciousness, mydriasis, heart rate disturbances and convulsions.
Since the 1980s, methylenedioxymethamphetamine (MDMA) has been a popular recreational drug, used particularly among those who attend raves and nightclubs. Over the past 3 years, the popularity of this drug has once again increased and there has been an associated rise in deaths. The pathophysiology of MDMA toxicity is complex and much remains to be understood. This article aims to increase readers' knowledge of patient presentations, the pathophysiology behind life-threatening toxicity, current treatments and the use of extracorporeal membrane oxygenation as a potential future treatment.
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