This meta-analysis suggests a modest association between neuromuscular blocking agents and neuromuscular dysfunction acquired in critical illness; limitations include studies with a high risk of bias and a disproportionate contribution from studies examining patients for critical illness polyneuropathy/critical illness myopathy and those with severe sepsis/septic shock.

Neuromuscular blocking agents (NMBAs), or “paralytics,” often are deployed in the sickest patients in the intensive care unit (ICU) when usual care fails. Despite the publication of guidelines on the use of NMBAs in the ICU in 2002, clinicians have needed more direction to determine which patients would benefit from NMBAs and which patients would be harmed. Recently, new evidence has shown that paralytics hold more promise when used in carefully selected lung injury patients for brief periods of time. When used in early acute respiratory distress syndrome (ARDS), NMBAs assist to establish a lung protective strategy, which leads to improved oxygenation, decreased pulmonary and systemic inflammation, and potentially improved mortality. It also is increasingly recognized that NMBAs can cause harm, particularly critical illness polyneuromyopathy (CIPM), when used for prolonged periods or in septic shock. In this review, we address several practical considerations for clinicians who use NMBAs in their practice. Ultimately, we conclude that NMBAs should be considered a lung protective adjuvant in early ARDS and that clinicians should consider using an alternative NMBA to the aminosteroids in septic shock with less severe lung injury pending further studies.

Hypocalcaemia is a rare complication of calcium channel blocker overdose, having been reported only once previously (J Toxicol Clin Toxicol, 1992, 30, 309). In this article, we report a case of a 37-year-old woman who developed hypocalcaemia after a verapamil overdose, review the literature and propose a mechanism for this rare finding.Calcium channel blockers (CCBs) are responsible for a large number of drug-related fatalities. The 2011 Annual report of the American Association of Poison Control Centers' National Poison Data System showed that CCBs accounted for 61% (78 cases) of all the deaths from cardiovascular medications [1]. Significant toxicity is reported more often with non-dihydropyridines (e.g. diltiazem and verapamil) than with dihydropyridines (e.g. amlodipine) [2]. Classically, patients with CCB overdose present with hypotension and bradycardia. Other findings can include altered mental status, hyperglycaemia, metabolic acidosis, pulmonary oedema and ischaemia to any organ system [3]. While dihydropyridines such as amlodipine mainly affect peripheral vasculature, in overdose, all selectivity is lost. Significant dihydropyridine overdose can lead to significant hypotension and death [4]. Hypocalcaemia is thought to be a rare complication of CCB overdose. Here, we report a case of CCB overdose followed by a precipitous drop in serum calcium from 9.3 mg/dl to 5.5 mg/dl. Case ReportA 37-year-old woman presented to the Emergency Department with a chief complaint of chest pain 12 hr after ingesting five tablets of unknown dose of verapamil. The patient had a history of migraine headaches treated with verapamil and a suicide attempt with nortriptyline 6 months earlier. The patient withheld her ingestion of verapamil from the treatment team as she was afraid that her husband would think this was a second suicide attempt and leave her.One hour after ingestion, the patient felt dizzy and nauseous. She then developed chest pain described as being 'punched in her chest'. The pain radiated to her neck and her arm and prompted her presentation to the emergency department.On presentation, her temperature was 37.2°C, blood pressure was 90/54 mmHg, heart rate was 100 beats/min. and oxygen saturation was 96% on room air. When vital signs were rechecked 150 min. later, the blood pressure was 69/52 and her heart rate was 51 beats/min. Physical examination revealed a somnolent obese female with dry oral mucosa, reactive pupils and warm extremities. Her ECG revealed junctional bradycardia ( fig. 1) with heart rate of 58 but no evidence of acute ischaemia. Her initial serum electrolytes were notable for a creatinine of 1.24 mg/dl (previously 1.0 mg/dl) and a calcium of 9.3 mg/dl (8.6-10.5 mg/dL). Her complete blood count was remarkable for a white blood cell count of 21.1 with 82.3% neutrophils. Arterial blood gas examination revealed a mild metabolic acidosis (pH: 7.30, PaCO 2 : 37 mmHg, PaO 2 : 60 mmHg, serum HCO 3 À: 21). Troponin was <0.01 ng/ml, and lactic acid was mildly elevated at 2.3 mEq/L (0.3-2.2 mE...

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