Narendra Nath Jena

Acute myocardial infarction and cocaine toxicity: One step closer

Sir, The article by Sarkar et al.,[1] is indeed interesting and timely as practitioners and emergency physicians have started seeing cases of cocaine intoxication in India. However, a few aspects of this paper require contemplation. The authors have administered thrombolytic agent initially for cocaine associated myocardial infraction (CAMI) which is not congruent with current evidence.[2] Current literature questions the routine use of thrombolytic therapy for patients with CAMI and there are reports of severe complications associated with thrombolytics in cocaine users.[3] The frequent presence of contraindications to thrombolysis, including severe hypertension, seizures, intracerebral hemorrhage, and aortic dissection in cocaine abusers precludes the liberal use of thrombolytic agents. Moreover, the standard electrocardiographic criteria (ST elevation) for thrombolytic therapy is hampered by the high rate of abnormal or nondiagnostic electrocardiogram (ECG)s in patients presenting with cocaine associated chest pain. The guidelines issued by American College of Cardiology and American Heart Association[4] advocate the use of thrombolytic therapy in CAMI only if ST segments remain elevated despite nitroglycerin and calcium antagonists and coronary angiography is not possible. Secondly, the recent cocaine use can alter the specificity of cardiac biomarkers and making them difficult to interpret in CAMI, especially the serum creatinine kinase level is not a reliable indicator of myocardial injury and is increased in almost half of cocaine users irrespective of concurrent MI possibly because of cocaine-induced hyperthermia, increased skeletal muscle activity, and rhabdomyolysis.[5] The awareness of reliability of cardiac biomarkers in cocaine associated chest pain is warranted for effective management. The American Heart Association recommends nitroglycerin and benzodiazepines as first-line agents for cocaine associated chest pain. Benzodiazepines are administrated especially in cocaine-addicted patients with associated hypertension, tachycardia, or anxiety after the cocaine use. Intuitively, dexmedetomidine, a central sympatholytic agent is highly effective in reversing the cocaines sympathomimetic actions.[6] Substance abuse remains one of the major public health issues across the globe, despite health education on prevention; the incidence of illicit substances is escalating. Since many patients with cocaine toxicity will present with chest pain to the emergency department, it is essential that these patients be recognized early and managed appropriately to prevent complications.

Pseudothrombocytopenia in perioperative patient: A significant laboratory artifact

Pseudothrombocytopenia secondary to ethylenediaminetetra-acetic acid induced platelet aggregation observed in a healthy perioperative male patient is reported in order to create awareness among anesthesiologist and laboratory personnel. The mechanisms for such changes have been highlighted.

Nicotinic acid in erythromelalgia associated with Clitocybe acromelalga intoxication: Theories and therapy

The case report by Nakajima and his colleagues was both interesting and informative. 1 This report is a great contribution in the management of erythromelalgia and we would like to mention the probable mechanisms for the pain and role of nicotinic acid in pain relief. Though the exact pathophysiology of erythromelalgia in Clitocybe acromelalga poisoning is not clear, it is likely that the toxin might have caused small-fi ber neuropathy through dysregulation of blood fl ow to small fi bers, resulting in microvascular ischemia. Further, stimulated sensory neurons might have initiated its action via calcitonin gene-related peptide (CGRP), which in turn deregulate the vascular tone 2 and contribute to ischemic neuropathy. This neurovascular dysfunction is clearly manifested as oxidative – nitrosative stress in the peripheral nerve and vasa nervorum . Nicotinic acid mitigates pain, not only by its vasodilatory effects, but also through multiple mechanisms such as induction of PGD2 in the skin and subsequent increase of its metabolite in the plasma which might down-regulate the output of CGRP, and halt the neurogenic infl ammation and normalize the vascular tone. 3

Methylene blue for refractory anaphylaxis--is it a magic bullet?

amongpatientswithanoncardiac causeof chestpain.AmJMed2012;125:491–498.e1. [8] Olivieri F, Galeazzi R, Giavarina D, et al. Aged-related increase of high sensitive Troponin T and its implication in acute myocardial infarction diagnosis of elderly patients. Mech Ageing Dev 2012;133:300–5. [9] Korkmaz A, Ozlu T, Ozsu S, et al. Long-term outcomes in acute pulmonary thromboembolism: the incidence of chronic thromboembolic pulmonary hypertension and associated risk factors. Clin Appl Thromb Hemost 2012;18:281–8. [10] Bradham WS, Bian A, Oeser A, et al. High-sensitivity cardiac troponin-I is elevated in patients with rheumatoid arthritis, independent of cardiovascular risk factors and inflammation. PLoS One 2012;7:e38930. [11] Darki A, Schneck MJ, Agrawal A, et al. Correlation of elevated troponin and echocardiography in acute ischemic stroke. J Stroke Cerebrovasc Dis 2012 [Epub ahead of print]. [12] Alam N, Khan HI, Chowdhury AW, et al. Elevated serum homocysteine level has a positive correlation with serum cardiac troponin I in patients with acute myocardial infarction. Bangladesh Med Res Counc Bull 2012;38:9–13. [13] Koracevic GP. Troponin units should be unified. J Emerg Med 2011;40:445–6. [14] Hake U, Hilker M, Oelert H. ‘Soft’ Snaring of the coronary artery in minimallyinvasive coronary surgery. Thorac Cardiovasc Surg 1998;46:380–1.

Antabuse reaction due to occupational exposure—an another road on the map?

With reference to the case of Bourcier et al [1], we would like to share our experience of disulfiram reaction observed in a painter due to occupational exposure of alcohol containing solvents during his deaddiction period. In fact, he was referred as septic encephalopathy by the factory medical officer. A 45-year-old industrial painter had developed vomiting, intense shivering, and delirious status while he was painting in the factory. He received parenteral metoclopramide and paracetamol at the factory health center. As therewas a drop in his blood pressure, hewas shifted to our emergency department. On admission, he was delirious, dyspneic, and febrile and had diffuse erythema over his forearm and face, without mucosal swelling or pruritus. His heart rate was 120 beats per minute, and blood pressure, 60/40 mm Hg with oxygen saturation 92% at room air. His systemic examination was unremarkable. Electrocardiogram showed sinus tachycardia and ST depression in V1 to V6. His arterial blood gases revealed metabolic acidosis (pH 7.24) with bicarbonate and lactate of 14.2 and 9.3 mmol/L, respectively. Hewas started on intravenous broad-spectrumantibiotics, after sending samples for pan culture. His central venous pressure was optimizedwithfluid resuscitation, and bloodpressure got stabilizedwith norepinephrine infusion. His complete blood count, metabolic profile, liver function test, lipid profile, electrolytes, chest x-ray, and ultrasound abdomen were with in normal limits. His sensorium and hemodynamic status dramatically improved within 3 hours of admission. His cultures remained sterile, and hence, antibiotics were discontinued. The detailed personal history revealed that he was an alcoholic of 5 years andwas started on disulfiram 100mg daily for deaddiction since 9 months. His previous medical report revealed frequent medical consultation for palpitation, chest discomfort, paresthesia, and easy fatigability after initiationofdeaddiction.Hisold records showednodetectableblood alcohol levels. On further interrogation, it was noticed that he was exposed to variety of solvents such as metal paints, thinners, varnish removers, and polish containing methanol, ethanol, isopropyl alcohol, and toluene for about 8 to 12 hours a day and 6days aweek in viewof his occupation. Being a painter, he uses his hand tomix paints with alcohols or solventswithoutadoptinganysafetymeasures, andalso,heneverused any personal protective equipment during painting. He was discharged with an advice to use cartridge respirator andwear gloveswhile painting. He felt much better after adopting the exposure precautions. In this patient, we believe that inhalation or transcutaneous absorption of these alcohols and/or solvents might have caused accumulation of aldehyde and interacted with disulfiram, resulting in the development of recurrence of symptoms and frequent medical consultations. He was symptom freewhile on leave andafter adopting strict personalprotective equipment. Interestingly, disulfiram decreases the metabolism of other solvents such as toluene and xylene, which are commonly found in thinners by inhibiting the enzymes of the cytochrome P450 [2]. These additive effects might have contributed to disulfiram ethanol reaction. Ehrlich et al [3] had documented disulfiram reaction in an artist exposed to solvents and insisted on eliciting a good occupational history for exposure to industrial solvents while dealing withmalaise in patients on disulfiram. In general, literature on occupational risk to disulfiram is limited [4]. Hence, prescribers of disulfiram may be oriented to elicit occupational historyduring counseling andbefore prescribing. Theyhave also to consider incidental, intentional, occupational inhalation or transcutaneous absorption of alcohol and/or other solvents while their patients develop fever, hemodynamic instability, and delirium, as disulfiram ethanol reaction rather than interpreting them differently

Acute alopecia: Evidence to thallium poisoning

Thallium is a toxic heavy metal often involved in criminal poisonings and occasionally in accidental poisoning. Here, we report a case of acute, nonintentional thallium poisoning due to thallium-contaminated alternative medicine for its rarity and to create awareness about the combination of rapid, diffuse alopecia with neurologic and gastrointestinal symptoms among practitioners, professionals, public, and policymakers.

Hounsfield units in pseudosubarachnoid hemorrhage-an old yet fascinating tool.

[1] Lin TC, Lee HC, Lee WH, Su HM, Lin TH, Hsu PC. Fulminant dengue myocarditis complicated with profound shock and fatal outcome under intra-aortic balloon pumping support. Am J Emerg Med 2015. http://dx.doi.org/10.1016/j.ajem.2015.03.039 [pii: S0735-6757(15)00183-7, Epub ahead of print]. [2] Wiwanitkit V. Acute shock dengue myocarditis. Rev Esp Cardiol 2014;67(6):502. [3] Wiwanitkit V. Denguemyocarditis, rare but not fatal manifestation. Int J Cardiol 2006; 112(1):122.

Limitations and consumer aspects of point-of-care in snake envenomation.

Dear Editor, The article by Cubitt et al. was indeed interesting. Today, point-of-care (POC) of prothrombin time/INR is increasingly used to monitor patients, especially those on vitamin K antagonists. In this context, we would like to highlight limitations of the device in relation to snake envenomation. The POC device measuring the INR is precise for patients with stable disease and not reliable in envenomation. Most POC INR devices are designed to report INR less than 6.0 and to monitor patients receiving long-term warfarin. When the results fall outside this range, by default these devices have a tendency to report them as normal values, despite significant derangement because of snake envenomation, as observed in this report. We wish to report our observation carried out in paired samples of 18 patients, who were severely envenomated by Russell’s viper. It was observed that there was significant discrepancy between INR results measured at a reference laboratory and POC testing. All the aforementioned patients had false negative INR values from the POC system, whereas formal coagulation studies reported them as abnormal. Our patient population was also free from antiphospholipid antibodies, lupus anticoagulants or extreme haematocrit values, which are known to affect the accuracy of the POC device. Most POC INR devices use human recombinant thromboplastins (ISI 1) as a substrate to imitate normal clotting. This does not work well in patients with severe envenomation, because the strong procoagulant enzymes of the venom directly convert the substrate. It is therefore recommended to conduct a conventional coagulation profile for all obvious and suspected cases of snake envenomation.

Clinical, laboratory, and educational challenges of diuretic doping

[1] Strait RT. A novel method for removal of penile zipper entrapment. Pediatr Emerg Care 1999;15:412-3. [2] Kanegaye JT, Schonfeld N. Penile zipper entrapment: a simple and less threatening approach using mineral oil. Pediatr Emerg Care 1993;9: 90-1. [3] Flowerdew R, Fishman IJ, Churchill BM. Management of penile zipper injury. J Urol 1977;117:671. [4] McCann PA. Case report: a novel solution to penile zipper injury—the needle holder. ScientificWorldJournal 2005;5:298-9. [5] Mishra SC. Safe and painless manipulation of penile zipper entrapment. Indian Pediatr 2006;43:252-4. [6] Raveenthiran V. Releasing of zipper-entrapped foreskin: a novel nonsurgical technique. Pediatr Emerg Care 2007;23:463-4. [7] Ezell WW, Smith EI, McCarthy RP, et al. Mechanical traumatic injury to the genitalia in children. J Urol 1969;102:788-92. [8] Mydlo JH. Treatment of a delayed zipper injury. Urol Int 2000;64:45-6. [9] Mellick LB. Wire cutters and penis skin entrapped by zipper sliders. Pediatr Emerg Care 2011;27:451-2.

Post coital hemoperitoneum: The pain of love

Acute abdominal pain in women of reproductive age is common and frequent cause for visit to emergency department which warrants emergent evaluation. We present the case of a 23-year-old nulliparous women presenting with post-coital haemoperitoneum secondary to a ruptured corpus luteum cyst. This is a rare case demonstrating the need to elicit sexual history in patients presenting with an acute abdomen in emergency department.