A Review of Acute Cyanide Poisoning With a Treatment Update

2011 ◽  
Vol 31 (1) ◽  
pp. 72-82 ◽  
Author(s):  
Jillian Hamel

Cyanide causes intracellular hypoxia by reversibly binding to mitochondrial cytochrome oxidase a3. Signs and symptoms of cyanide poisoning usually occur less than 1 minute after inhalation and within a few minutes after ingestion. Early manifestations include anxiety, headache, giddiness, inability to focus the eyes, and mydriasis. As hypoxia progresses, progressively lower levels of consciousness, seizures, and coma can occur. Skin may look normal or slightly ashen, and arterial oxygen saturation may be normal. Early respiratory signs include transient rapid and deep respirations. As poisoning progresses, hemodynamic status may become unstable. The key treatment is early administration of 1 of the 2 antidotes currently available in the United States: the well-known cyanide antidote kit and hydroxocobalamin. Hydroxocobalamin detoxifies cyanide by binding with it to form the renally excreted, non-toxic cyanocobalamin. Because it binds with cyanide without forming methemoglobin, hydroxocobalamin can be used to treat patients without compromising the oxygen-carrying capacity of hemoglobin.

2013 ◽  
Vol 10 (3) ◽  
pp. 30-34 ◽  
Author(s):  
Ojashwi Nepal ◽  
BR Pokharel ◽  
K Khanal ◽  
SL Mallik ◽  
BK Kapoor ◽  
...  

Background The oxygen saturation of haemoglobin is reduced in high altitude-living organisms. Increase in the hematocrit is responsible for rise in the hemoglobin concentration so that the oxygen carrying capacity in the hypobaric hypoxic subject is elevated. Objectives To compare two different high altitude populations, in order to study the relationship between arterial oxygen saturation and hematocrit. Methods lIn the cross-sectional study of two populations residing at altitude of 2800 m and 3760 m are compared for the difference in hematocrit. The oxygen carrying capacity of arterial haemoglobin (SaO2) is determined by pulse oximetry. The sample is drawn from the natives of two small villages, Thini at Jomsom (2800 m) and Jharkot (3760 m) in Mustang district of Nepal. The natives at 2800 m are termed as lower high altitude population and local residents at 3760 m are said to be higher altitude population in this study. The sample blood was drawn by venipuncture and packed cell volume was determined by Wintrobe’s method. Results The hematocrit obtained from 3760 m altitude population and the lower high altitude population at altitude of 2800 m differ significantly with the p value < 0.0001and the SaO2 in both the population fails to show any difference with p value > 0.05. Deep breathing exercise in these populations however increased SaO2 significantly. Conclusion The higher altitude natives have greater arterial oxygen saturation than lower altitude population which is due to rise in red cell concentration. The slow deep breathing raises oxygen saturation irrespective of altitude. Kathmandu University Medical Journal | VOL.10 | NO. 3 | ISSUE 39 | JUL- SEP 2012 | Page 30-34 DOI: http://dx.doi.org/10.3126/kumj.v10i3.8014


Author(s):  
Mercedes J. Nagel ◽  
Caitlin P. Jarrard ◽  
Sophie Lalande

Intermittent hypoxia, defined as alternating bouts of breathing hypoxic and normoxic air, has the potential to improve oxygen-carrying capacity through an erythropoietin-mediated increase in hemoglobin mass. The purpose of this study was to determine the effect of a single session of intermittent hypoxia on erythropoietin levels and hemoglobin mass in young healthy individuals. Nineteen participants were randomly assigned to an intermittent hypoxia group (Hyp, n = 10) or an intermittent normoxia group (Norm, n = 9). Intermittent hypoxia consisted of five 4-min hypoxic cycles at a targeted arterial oxygen saturation of 90% interspersed with 4-min normoxic cycles. Erythropoietin levels were measured before and two hours following completion of the protocol. Hemoglobin mass was assessed the day before and seven days after exposure to intermittent hypoxia or normoxia. As expected, the intermittent hypoxia group had a lower arterial oxygen saturation than the intermittent normoxia group during the intervention (Hyp: 89 ± 1 vs. Norm: 99 ± 1%, p < 0.01). Erythropoietin levels did not significantly increase following exposure to intermittent hypoxia (Hyp: 8.2 ± 4.5 to 9.0 ± 4.8, Norm: 8.9 ± 1.7 to 11.1 ± 2.1 mU·mL−1, p = 0.15). Hemoglobin mass did not change following exposure to intermittent hypoxia. This single session of intermittent hypoxia was not sufficient to elicit a significant rise in erythropoietin levels or hemoglobin mass in young healthy individuals.


PEDIATRICS ◽  
1952 ◽  
Vol 10 (3) ◽  
pp. 293-305
Author(s):  
HARRY A. WAISMAN ◽  
JAMES A. BAIN ◽  
JULIUS B. RICHMOND ◽  
FRANKLIN A. MUNSEY

Congenital idiopathic methemoglobinemia in a 12 year old boy was corrected by the administration of either ascorbic acid or methylene blue, the latter being more efficient. The oxygen dissociation curve was normal but as would be expected the oxygen-carrying capacity of the blood was increased after methylene blue was given. Arterial oxygen saturation was determined by an oximeter to demonstrate the increased oxygen-carrying capacity after methylene blue. Para-amino propriophenone administration caused an increase in methemoglobin level but not to the maximum value for this patient. Sodium nitrite by mouth did give the maximum level. Enzyme studies revealed no difference in oxygen uptake of hexosediphosphate either with or without methylene blue in normal or methemoglobinemic cells in a medium which contained glucose. No "cytochrome-reductase like" activity was demonstrated in the methemoglobinemic cell. No definitive evidence exists to support the belief that reduced co-enzyme I reacts directly with methemoglobin in normal cells.


2006 ◽  
Vol 21 (S2) ◽  
pp. s49-s55 ◽  
Author(s):  
Marc Eckstein ◽  
Paul M. Maniscalco

AbstractThe contribution of smoke inhalation to cyanide-attributed morbidity and mortality arguably surpasses all other sources of acute cyanide poisoning. Research establishes that cyanide exposure is: (1) to be expected in those exposed to smoke in closed-space fires; (2) cyanide poisoning is an important cause of incapacitation and death in smoke-inhalation victims; and (3) that cyanide can act independently of, and perhaps synergistically with, carbon monoxide to cause morbidity and mortality. Effective prehospital management of smoke inhalation-associated cyanide poisoning is inhibited by: (1) a lack of awareness of fire smoke as an important cause of cyanide toxicity; (2) the absence of a rapidly returnable diagnostic test to facilitate its recognition; and (3) in the United States, the current unavailability of a cyanide antidote that can be used empirically with confidence outside of hospitals. Addressing the challenges of the prehospital management of smoke inhalation-associated cyanide poisoning entails: (1) enhancing the awareness of the problem among prehospital responders; (2) improving the ability to recognize cyanide poisoning on the basis of signs and symptoms; and (3) expanding the treatment options that are useful in the prehospital setting.


2018 ◽  
Vol 47 (1-3) ◽  
pp. 240-245 ◽  
Author(s):  
Laura M. Rosales ◽  
Hanjie Zhang ◽  
Marilou Mateo ◽  
Brenda Chan ◽  
Israel Campos ◽  
...  

Background: The time between the creation of an arteriovenous fistula (AVF) and its successful use is significantly longer in hemodialysis (HD) patients in the United States compared to those in other countries, and there is an urgent need to reduce the residence time of central-venous catheters (CVC). Methods: Successful AVF creation and maturation results in typical hemodynamic changes, such as an increase in cardiac output and upper body blood flow (UBBF). In patients with CVC as vascular access, we measured once per minute intradialytic central-venous oxygen saturation (ScvO2) and hemoglobin levels simultaneously using the Crit-Line Monitor. Under conditions of stable upper body oxygen consumption and arterial oxygen saturation, ScvO2 and hemoglobin concentration allows the calculation of estimated UBBF (eUBBF). In a quality improvement project, we used ScvO2 and eUBBF to track the hemodynamic changes accompanying AVF maturation. Results: Out of 11 patients (9 incident to HD, 1 female, age 61 ± 13 years), AVF maturation was successful in 9. In 1 patient, the AVF did not mature. One patient died from sudden cardiac death with a maturing AVF. In the 9 patients with successful AVF maturation, ScvO2 increased from 60.9 ± 2.7% prior to AVF creation to 73.4 ± 3.6% a week after AVF creation (19.6 ± 6.3% increase). eUBBF increased from 1.3 ± 0.3 to 2.2 ± 0.6 L/min (62.7 ± 37.5% increase); no material ScvO2 or eUBBF changes occurred in the other 2 patients. Conclusion: Our results indicate the potential utility of ScvO2 and eUBBF to track the hemodynamic response to AVF maturation. To what extent these insights translate into shortening of the time between AVF creation and successful cannulation warrants further investigations.


1999 ◽  
Vol 14 (4) ◽  
pp. 191-197 ◽  
Author(s):  
Dan Torbati ◽  
Bala R. Totapally ◽  
Maria T. Camacho ◽  
Jack Wolfsdorf

2020 ◽  
Vol 13 (3) ◽  
pp. e232875 ◽  
Author(s):  
Victoria Davies ◽  
Jake Turner ◽  
Michael Greenway

A middle-aged patient presented with toxic inhalational injury, and was resuscitated prehospitally and treated in the emergency department for smoke inhalation, carbon monoxide (CO) exposure and cyanide poisoning with the use of antidotes. Due to the CO effects on spectrophotometry, an anaemia initially identified on blood gas analysis was thought to be artefactual, but was later confirmed by laboratory testing to be accurate. In addition, cyanide can confound haemoglobin testing due to its use in the analytical process and non-cyanide analysis is required when there is suspected exposure. Although no consensus exists on a first-line cyanide antidote choice, hydroxocobalamin is the only antidote without a serious side effect profile and/or deleterious cardiovascular effects. We propose prehospital enhanced care teams consider carrying hydroxocobalamin for early administration in toxic inhalational injury.


2020 ◽  
Vol 16 (3) ◽  
Author(s):  
Jack Green

Cyanide poisoning via the oral route is a remarkably rare entity in the United States. Though acute toxicity from this poison may present with classic signs and symptoms (smell of bitter almonds on breath and cherry-red skin), these signs are frequently not clinically observed in the intoxicated patient, making it low on the routine differential diagnosis leading to both diagnostic and therapeutic challenges for the bedside clinician. This is a case of a 17-yearold male with a history of depression who presented to the Emergency Room (ER) with altered mental status, abdominal pain, and emesis. A severely elevated and worrisome lactic acidosis triggered the ER’s septic shock bundle and algorithm, but further investigation ultimately led to the unifying diagnosis of intentional cyanide poisoning.


2006 ◽  
Vol 21 (S2) ◽  
pp. s40-s48 ◽  
Author(s):  
Tee Guidotti

AbstractEffective management of cyanide poisoning from chemical terrorism, inhalation of fire smoke, and other causes constitutes a critical challenge for the pre-hospital care provider. The ability to meet the challenge of managing cyanide poisoning in the prehospital setting may be enhanced by the availability of the cyanide antidote hydroxocobalamin, currently under development for potential introduction in the United States. This paper discusses the causes, recognition, and management of acute cyanide poisoning in the prehospital setting with emphasis on the emerging profile of hydroxocobalamin, an antidote that may have a risk:benefit ratio suitable for empiric, out-of-hospital treatment of the range of causes of cyanide poisoning. If introduced in the US, hydroxocobalamin may enhance the role of the US prehospital responder in providing emergency care in a cyanide incident.


2020 ◽  
Vol 91 (10) ◽  
pp. 785-789
Author(s):  
Dongqing Wen ◽  
Lei Tu ◽  
Guiyou Wang ◽  
Zhao Gu ◽  
Weiru Shi ◽  
...  

INTRODUCTION: We compared the physiological responses, psychomotor performances, and hypoxia symptoms between 7000 m and 7500 m (23,000 and 24,600 ft) exposure to develop a safer hypoxia training protocol.METHODS: In altitude chamber, 66 male pilots were exposed to 7000 and 7500 m. Heart rate and arterial oxygen saturation were continuously monitored. Psychomotor performance was assessed using the computational task. The hypoxic symptoms were investigated by a questionnaire.RESULTS: The mean duration time of hypoxia was 323.0 56.5 s at 7000 m and 218.2 63.3 s at 7500 m. The 6-min hypoxia training was completed by 57.6% of the pilots and 6.1% of the pilots at 7000 m and at 7500 m, respectively. There were no significant differences in pilots heart rates and psychomotor performance between the two exposures. The Spo2 response at 7500 m was slightly severer than that at 7000 m. During the 7000 m exposure, pilots experienced almost the same symptoms and similar frequency order as those during the 7500 m exposure.CONCLUSIONS: There were concordant symptoms, psychomotor performance, and very similar physiological responses between 7000 m and 7500 m during hypoxia training. The results indicated that 7000-m hypoxia awareness training might be an alternative to 7500-m hypoxia training with lower DCS risk and longer experience time.Wen D, Tu L, Wang G, Gu Z, Shi W, Liu X. Psychophysiological responses of pilots in hypoxia training at 7000 and 7500 m. Aerosp Med Hum Perform. 2020; 91(10):785789.


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