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Emergency Medicine Australasia (2014) 26, 208–213
LETTERS TO THE EDITOR
Limitations and consumer aspects of point-of-care in snake envenomation Dear Editor, The article by Cubitt et al. was indeed interesting.1 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.2 Most POC INR devices are designed to report INR less than 6.0 and to monitor patients receiving long-term warfarin.3 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.1 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.
Competing interests None declared.
References 1. Cubitt M, Armstrong J, McCoubrie D, White J, Williams V, Isbister GK. Point-of-care testing in snakebite: an envenomed case with false negative coagulation studies. Emerg. Med. Australas. 2013; 25: 372–3. 2. Celenza A, Skinner K. Comparison of emergency department point-of-care
international normalised ratio (INR) testing with laboratory-based testing. Emerg. Med. J. 2011; 28: 136–40. 3. Havrda DE, Hawk TL, Marvin CM. Accuracy and precision of the CoaguChek S versus laboratory INRs in a clinic. Ann. Pharmacother. 2002; 36: 769–75.
Subramanian SENTHILKUMARAN,1 Suresh S DAVID,2 Narendra Nath JENA3 and Ponniah Thirumalaikolundusubramanian4 1 Department of Emergency and Critical Care, Sri Gokulam Hospital and Research Institute, Salem, India, 2 Department of Emergency Medicine, Christian Medical College and Hospital, Vellore, India, 3 Department of Emergency Medicine, Meenakshi Mission Hospital and Research Centre, Madurai, India, and 4Department of Internal Medicine, Chennai Medical College Hospital and Research Center, Trichy, India doi: 10.1111/1742-6723.12161
Frostbite caused by liquid CO2 exposure Dear Editor, A 50-year-old man presented to the ED because of worsening right hand pain 2 h after exposure to leaking gas from a damaged fire extinguisher. Immediately after exposure, his fingers were pale, cold and numb; however, on admission, he was complaining of throb-
bing pain. Physical examination was significant for erythema and oedema on the second, third and fourth fingers (Figs 1,2). Radial pulse and the capillary refill time were normal. After an hour, clear superficial blisters developed in the affected area with no haemorrhagic blisters. The diagnosis
of superficial frostbite caused by liquid carbon dioxide was made. Frostbite is the prototype of freezing injury. The pathophysiology of frostbite consists of vasoconstriction, crystal formation and cellular dehydration.1 Crystal formation is both extracellular and intracellular that
© 2014 Australasian College for Emergency Medicine and Australasian Society for Emergency Medicine
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209
LETTERS TO THE EDITOR
Figure 1. Erythema and oedema on the second, third and fourth fingers due to liquid CO2 exposure.
the hospital. In hospital, the affected hand was rewarmed by immersion in warm water (40°C) for approximately 30 min in order to prevent vasoconstriction and ischaemia. 1 Limb elevation and splinting were used to reduce oedema.2 Clear blisters were drained in order to minimise the concentration of prostaglandins and thromboxane. However, haemorrhagic blisters (which were not present in this patient) should not be debrided because of the risk of further injury secondary to desiccation of deeper dermal layers.1 Ibuprofen (a potent inhibitor of thromboxane) and topical aloe vera (an antiprostaglandin agent) were prescribed. 4 Analgesics and tetanus prophylaxis were also administered. After undertaking the aforementioned measurements, the patient recovered without complications.
Competing interests None declared.
References Figure 2.
Erythema and oedema on second finger (magnified).
impairs membranous function and results in cell death. Vasoconstriction also induces hypoxaemia and tissue death. Moreover, thromboxane release leads to vasoconstriction and progressive dermal ischaemia. Furthermore, oedema, thrombosis and leucocyte infiltration cause necrosis.1,2 Although frostbite is caused by environmental exposure in most cases, exposure to the liquid form of CO2 could cause rapid cooling and vasoconstriction leading to severe tissue injury.3 Two methods are used to classify frostbite. According to the first method, four degrees of injury exist after rewarming. First-degree injury is a white
plaque surrounded by erythema. Second degree is defined by clear milky blisters and third degree includes haemorrhagic blisters. Tissue necrosis and damage is a fourth-degree injury. The other method divides frostbite into superficial and deep. Superficial frostbite is limited to the skin and subcutaneous tissue causing clear blisters, whereas deep involvement affecting the muscles, tendons and bones is accompanied by haemorrhagic blisters.1,2 Different steps in management were considered for this patient to minimise tissue damage. In the prehospital setting, wet clothing was removed to prevent further hypothermia and the patient was immediately transferred to
1. Reamy BV. Frostbite: review and current concepts. J. Am. Board Fam. Pract. 1998; 11: 34–40. 2. Biem J, Koehncke N, Classen D, Dosman J. Out of the cold: management of hypothermia and frostbite. CMAJ 2003; 168: 305–11. 3. Sever C, Kulahci Y, Uygur F, Sahin C. Frostbite injury of the foot from portable fire extinguisher. Dermatol. Online J. 2009; 15: 10. 4. Imray C, Grieve A, Dhillon S. Cold damage to the extremities: frostbite and non-freezing cold injuries. Postgrad. Med. J. 2009; 85: 481–8.
Mona ARBAB and Hadi MIRFAZAELIAN Department of Emergency Medicine, Tehran University of Medical Sciences, Tehran, Iran doi: 10.1111/1742-6723.12211
© 2014 Australasian College for Emergency Medicine and Australasian Society for Emergency Medicine
Emergency Medicine Australasia (2014) 26, 208–213
LETTERS TO THE EDITOR
Limitations and consumer aspects of point-of-care in snake envenomation Dear Editor, The article by Cubitt et al. was indeed interesting.1 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.2 Most POC INR devices are designed to report INR less than 6.0 and to monitor patients receiving long-term warfarin.3 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.1 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.
Competing interests None declared.
References 1. Cubitt M, Armstrong J, McCoubrie D, White J, Williams V, Isbister GK. Point-of-care testing in snakebite: an envenomed case with false negative coagulation studies. Emerg. Med. Australas. 2013; 25: 372–3. 2. Celenza A, Skinner K. Comparison of emergency department point-of-care
international normalised ratio (INR) testing with laboratory-based testing. Emerg. Med. J. 2011; 28: 136–40. 3. Havrda DE, Hawk TL, Marvin CM. Accuracy and precision of the CoaguChek S versus laboratory INRs in a clinic. Ann. Pharmacother. 2002; 36: 769–75.
Subramanian SENTHILKUMARAN,1 Suresh S DAVID,2 Narendra Nath JENA3 and Ponniah Thirumalaikolundusubramanian4 1 Department of Emergency and Critical Care, Sri Gokulam Hospital and Research Institute, Salem, India, 2 Department of Emergency Medicine, Christian Medical College and Hospital, Vellore, India, 3 Department of Emergency Medicine, Meenakshi Mission Hospital and Research Centre, Madurai, India, and 4Department of Internal Medicine, Chennai Medical College Hospital and Research Center, Trichy, India doi: 10.1111/1742-6723.12161
Frostbite caused by liquid CO2 exposure Dear Editor, A 50-year-old man presented to the ED because of worsening right hand pain 2 h after exposure to leaking gas from a damaged fire extinguisher. Immediately after exposure, his fingers were pale, cold and numb; however, on admission, he was complaining of throb-
bing pain. Physical examination was significant for erythema and oedema on the second, third and fourth fingers (Figs 1,2). Radial pulse and the capillary refill time were normal. After an hour, clear superficial blisters developed in the affected area with no haemorrhagic blisters. The diagnosis
of superficial frostbite caused by liquid carbon dioxide was made. Frostbite is the prototype of freezing injury. The pathophysiology of frostbite consists of vasoconstriction, crystal formation and cellular dehydration.1 Crystal formation is both extracellular and intracellular that
© 2014 Australasian College for Emergency Medicine and Australasian Society for Emergency Medicine
bs_bs_banner
209
LETTERS TO THE EDITOR
Figure 1. Erythema and oedema on the second, third and fourth fingers due to liquid CO2 exposure.
the hospital. In hospital, the affected hand was rewarmed by immersion in warm water (40°C) for approximately 30 min in order to prevent vasoconstriction and ischaemia. 1 Limb elevation and splinting were used to reduce oedema.2 Clear blisters were drained in order to minimise the concentration of prostaglandins and thromboxane. However, haemorrhagic blisters (which were not present in this patient) should not be debrided because of the risk of further injury secondary to desiccation of deeper dermal layers.1 Ibuprofen (a potent inhibitor of thromboxane) and topical aloe vera (an antiprostaglandin agent) were prescribed. 4 Analgesics and tetanus prophylaxis were also administered. After undertaking the aforementioned measurements, the patient recovered without complications.
Competing interests None declared.
References Figure 2.
Erythema and oedema on second finger (magnified).
impairs membranous function and results in cell death. Vasoconstriction also induces hypoxaemia and tissue death. Moreover, thromboxane release leads to vasoconstriction and progressive dermal ischaemia. Furthermore, oedema, thrombosis and leucocyte infiltration cause necrosis.1,2 Although frostbite is caused by environmental exposure in most cases, exposure to the liquid form of CO2 could cause rapid cooling and vasoconstriction leading to severe tissue injury.3 Two methods are used to classify frostbite. According to the first method, four degrees of injury exist after rewarming. First-degree injury is a white
plaque surrounded by erythema. Second degree is defined by clear milky blisters and third degree includes haemorrhagic blisters. Tissue necrosis and damage is a fourth-degree injury. The other method divides frostbite into superficial and deep. Superficial frostbite is limited to the skin and subcutaneous tissue causing clear blisters, whereas deep involvement affecting the muscles, tendons and bones is accompanied by haemorrhagic blisters.1,2 Different steps in management were considered for this patient to minimise tissue damage. In the prehospital setting, wet clothing was removed to prevent further hypothermia and the patient was immediately transferred to
1. Reamy BV. Frostbite: review and current concepts. J. Am. Board Fam. Pract. 1998; 11: 34–40. 2. Biem J, Koehncke N, Classen D, Dosman J. Out of the cold: management of hypothermia and frostbite. CMAJ 2003; 168: 305–11. 3. Sever C, Kulahci Y, Uygur F, Sahin C. Frostbite injury of the foot from portable fire extinguisher. Dermatol. Online J. 2009; 15: 10. 4. Imray C, Grieve A, Dhillon S. Cold damage to the extremities: frostbite and non-freezing cold injuries. Postgrad. Med. J. 2009; 85: 481–8.
Mona ARBAB and Hadi MIRFAZAELIAN Department of Emergency Medicine, Tehran University of Medical Sciences, Tehran, Iran doi: 10.1111/1742-6723.12211
© 2014 Australasian College for Emergency Medicine and Australasian Society for Emergency Medicine
