David H. Jang

Successful outcome utilizing hypothermia after cardiac arrest in pregnancy: a case report.

Background:To date, pregnancy has been considered a contraindication to the use of therapeutic hypothermia after cardiac arrest. Case:We present the case of a 35-yr-old woman, 13 wks pregnant, who had a witnessed out-of-hospital ventricular fibrillation cardiac arrest. She was resuscitated by prehospital personnel yet remained comatose at arrival to the hospital. Therapeutic cooling (33°C) was initiated for 24 hrs, and she was discharged home with mild neurologic deficit (Cerebral Performance Category 2) on hospital day 6. The infant was delivered via cesarean section at 39 wks’ gestation. Apgar scores were 8 and 9, and neurodevelopmental testing was appropriate for age at birth and at 2 months. Conclusion:This is the first case of therapeutic hypothermia applied to postarrest care of a pregnant woman followed by a successful delivery. This therapy should be considered in pregnant patients with cardiac arrest.

Methylene blue for distributive shock: a potential new use of an old antidote.

Methylene blue is used primarily in the treatment of patients with methemoglobinemia. Most recently, methylene blue has been used as a treatment for refractory distributive shock from a variety of causes such as sepsis and anaphylaxis. Many studies suggest that the nitric oxide–cyclic guanosine monophosphate (NO–cGMP) pathway plays a significant role in the pathophysiology of distributive shock. There are some experimental and clinical experiences with the use of methylene blue as a selective inhibitor of the NO–cGMP pathway. Methylene blue may play a role in the treatment of distributive shock when standard treatment fails.

Methylene Blue in the Treatment of Refractory Shock From an Amlodipine Overdose

Amlodipine is a potent vasodilator with a long half-life and delayed onset of action that is particularly concerning after an overdose. Vasodilation occurs through stimulation of nitric oxide release with increased cyclic guanosine monophosphate (cGMP) production. Methylene blue inhibits guanylate cyclase. This enzyme is responsible for the production of cGMP. Methylene blue also has the ability to scavenge nitric oxide, as well as inhibit nitric oxide synthase. We report the use of methylene blue for refractory shock in a patient with amlodipine toxicity.

Status epilepticus and wide-complex tachycardia secondary to diphenhydramine overdose

Objective. Diphenhydramine is an H1 histamine antagonist that is commonly used for allergic reactions, colds and cough, and as a sleep aid. In addition to anticholinergic and antihistaminergic effects, sodium channel blockade becomes evident following diphenhydramine overdose. While seizures may occur following overdose of a diphenhydramine, status epilepticus is distinctly uncommon. We report a case with both status epilepticus and wide-complex dysrhythmias following an intentional diphenhydramine overdose. Case report. A 36-year-old woman with a medical history of hypothyroidism on levothyroxine was brought to the emergency department with active seizures by emergency medical services after what was later determined to be a diphenhydramine overdose. One hour after an argument with her husband he found her lethargic in a locked room. Initial vital signs were: blood pressure, 90/55 mmHg; heart rate, 160 beats/min; respiratory rate 18 breaths/min; room air oxygen saturation, 99%; temperature, 99.8°F; rapid point-of-care glucose, 130 mg/dL. The generalized seizures continued for duration of 30 min, despite the intravenous administration of 8 mg of lorazepam. The patient underwent endotracheal intubation and a propofol infusion terminated her seizures. An electrocardiogram after the status was terminated which revealed a wide-complex tachycardia with QRS duration of 127 ms. The QRS narrowed after 200 mEq of intravenous sodium bicarbonate was administrated. The patient was neurologically intact upon extubation on hospital day 2. The serum diphenhydramine concentration drawn on arrival to the ED was 1200 ng/mL (9–120 ng/mL); a tricyclic screen was negative. Discussion. While seizures and sodium channel blockade are recognized complications of diphenhydramine toxicity, reported cases of status epilepticus from diphenhydramine overdose are rare. Elements of the patients presentation were similar to a tricyclic overdose and management required aggressive control of her seizures, sodium bicarbonate therapy, and recognizing that physostigmine was contraindicated due to wide complex tachycardia. Conclusions. Diphenhydramine overdose may cause status epilepticus and wide-complex tachycardia. Management should focus on antidotal therapy with sodium bicarbonate and supportive neurological management with appropriate anticonvulsants and airway protection if clinically indicated.

Severe Opioid Withdrawal Due to Misuse of New Combined Morphine and Naltrexone Product (Embeda)

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Heavy Metal Chelation in Neurotoxic Exposures

Metals such as iron and copper are critical to living organisms, whereas other metals such as lead and arsenic have no known biologic role. Any metals in large amounts may cause toxicity. Many metals cause pervasive systemic effects involving the nervous system, which can be subtle in some cases. Although challenging, the diagnosis and treatment of metal poisoning can be made based on history, physical examination, and the proper use of metal testing. This article focuses on the use, and misuse, of chelation in the diagnosis and management of metal intoxication.

Toxin-Induced Cardiovascular Failure

Adverse cardiovascular events comprise a large portion of the morbidity and mortality in drug overdose emergencies. Adverse cardiovascular events encountered by emergency physicians treating poisoned patients include myocardial injury, hemodynamic compromise with shock, tachydysrhythmias, and cardiac arrest. Early signs of toxin-induced cardiovascular failure include bradycardia, tachycardia, and specific ECG findings. Treatment of toxicologic tachycardia relies on rapid supportive care along with proper use of benzodiazepines for sedation. Treatment of toxicologic bradycardia consists of the use of isotonic fluids, atropine, calcium salts, and glucagon. High-dose insulin euglycemia should be used early in the course of suspected severe poisoning and intravenous lipid emulsion given to patients who suffer cardiac arrest.

The In Vitro Effect of N‐Acetylcysteine on Prothrombin Time in Plasma Samples From Healthy Subjects

OBJECTIVES In the treatment of acetaminophen toxicity, clinicians believe that N-acetylcysteine (NAC) artificially elevates prothrombin time (PT), potentially obscuring signs of liver damage. However, the effect of NAC on human blood coagulation remains unverified. The purpose of this study was to evaluate the effect of NAC on PT prolongation in human plasma. METHODS The authors obtained blood samples from 33 volunteer subjects. The blood plasma samples were divided into four 1-mL aliquots. The first aliquot was used as a control. To three additional aliquots, varying amounts of NAC were added, maintaining constant volume with a maximum dilution of 0.5%. The four concentrations of NAC (control, 250, 500, or 1,000 mg/L) were incubated at 37°C for 1 hour, and PT was measured. PT values were compared using fixed effects regression. RESULTS Mean (± standard deviation [SD]) PT values for the control, 100, 500, and 1,000 mg/L NAC values were 13.9 (±1.01), 14.2 (±1.08), 15.5 (±1.21), and 17.4 (±1.72) seconds, respectively. At the 1,000 mg/L concentration, two PTs exceeded 22 seconds, and half exceeded 17 seconds. PT increased with NAC concentrations (fixed effects regression p < 0.001) in a dose-dependent manner. CONCLUSIONS In this in vitro human model, NAC had a dose-dependent effect on PT.

Measurement of Mitochondrial Respiration and Motility in Acute Care Sepsis, Trauma, and Poisoning

Metabolic biomarkers have potentially wider use in disease diagnosis and prognosis as well as in monitoring disease response to treatment. While biomarkers such as interleukins, microRNA, and lactate have been proposed for disease surveillance, there are still conflicting results regarding their clinical utility. Treatment of commonly encountered disease of acute care such as sepsis, trauma, and poisoning often relies on clinical diagnosis and therapy guided by use of surrogate markers of illness severity. The measurement of mitochondrial function, including respiration and motility, may offer superior alternatives to such markers. Assessing mitochondrial function in a clinical context has the potential to impact the area of acute care in terms of diagnosis, prognosis, and treatment. The study of mitochondrial bioenergetics has become critical in understanding the pathophysiology and treatment of complex diseases such as diabetes and cardiovascular disorders.

A preliminary study in the alterations of mitochondrial respiration in patients with carbon monoxide poisoning measured in blood cells

Abstract Objectives: Carbon monoxide (CO) is a colorless and odorless gas responsible for poisoning mortality and morbidity in the United States. At this time, there is no reliable method to predict the severity of poisoning or clinical prognosis following CO exposure. Whole blood cells, such as peripheral blood mononuclear cells (PBMCs) and platelets, have been explored for their potential use to act as sensitive biomarkers for mitochondrial dysfunction which may have a role in CO poisoning. Design: The objective of this study was to measure mitochondrial respiration using intact cells obtained from patients exposed to CO as a potential biomarker for mitochondrial inhibition with results that can be obtained in a time frame useful for guiding clinical care. This was a prospective, observational pilot study performed from July 2015 to July 2016 at a single academic tertiary care center that is the location of the region’s only multi chamber hyperbaric. Measurements: Clinical characteristics, patient demographics, mitochondrial respiration and outcomes were recorded. Main results: There were 7 patients enrolled with a mean COHb level 26.8 ± 10 and with a mean lactate of 1.1 ± 0.4 mmol/L. All 7 CO exposures were related to heat generators used during winter months with two deaths. There was a positive correlation between maximal respiration and COHb levels with both high maximal respiration and high spare respiratory capacity correlating with a high COHb level. There was a subset of PBMCs (n = 4) that were analyzed for Complex IV (cytochrome c oxidase) activity. Conclusions: In this pilot study, measurements can be performed in an appropriate timeline for clinical care with potential to serve as a prognostic marker. Further work is necessary to develop high-resolution respirometry as a clinical tool for assessing the severity of illness and guiding therapy.