Extracorporeal support in an adult with severe carbon monoxide poisoning and shock following smoke inhalation: a case report

Perfusion ◽  
2000 ◽  
Vol 15 (2) ◽  
pp. 169-173 ◽  
Author(s):  
Maureen McCunn ◽  
H Neal Reynolds ◽  
Christine A Cottingham ◽  
Thomas M Scalea ◽  
Nader M Habashi
Keyword(s):  
Carbon Monoxide ◽  
Transitional Care ◽  
Carbon Monoxide Poisoning ◽  
Care Facility ◽  
Blood Gases ◽  
Smoke Inhalation ◽  
Cardiovascular Collapse ◽  
Prone Positioning ◽  
Life Threatening ◽  
Extracorporeal Support

The objective of this study was to discuss the case of a patient with severe smoke inhalation-related respiratory failure treated with extracorporeal support. The study was set in a 12-bed multi-trauma intensive care unit at a level one trauma center and hyperbaric medicine center. The patient under investigation had carbon monoxide poisoning, and developed acute respiratory distress syndrome and cardiovascular collapse following smoke inhalation. Rapid initiation of extracorporeal support, extreme inverse-ratio ventilation and intermittent prone positioning therapy were carried out. Admission and serial carboxyhemoglobin levels, blood gases, and computerized tomography of the chest were obtained. The patient developed severe hypoxia and progressed to cardiovascular collapse resistant to resuscitation and vasoactive infusions. Veno-venous extracorporeal support was initiated. Cardiovascular parameters of blood pressure, cardiac output, and oxygen delivery were maximized; oxygenation and ventilation were supported via the extracorporeal circuit. Airway pressure release ventilation and intermittent prone positioning therapy were instituted. Following 7 days of extracorporeal support, the patient was decannulated and subsequently discharged to a transitional care facility, neurologically intact. Smoke inhalation and carbon monoxide poisoning may lead to life-threatening hypoxemia associated with resultant cardiovascular instability. When oxygenation and ventilation cannot be achieved via maximal ventilatory management, extracorporeal support may prevent death if initiated rapidly.

scholarly journals Carbon Monoxide Poisoning

2018 ◽  
Vol 67 (1) ◽  
pp. 47-48 ◽  
Author(s):  
Stephanie Hammond ◽  
Jennan A. Phillips
Keyword(s):  
Carbon Monoxide ◽  
Occupational Health ◽  
Carbon Monoxide Poisoning ◽  
Life Threatening ◽  
Life Threatening Event

Carbon monoxide poisoning is a serious and life-threatening event. Educating workers and communities on exposure sources, symptoms, and prevention is an important role for occupational health nurses.

Carbon monoxide poisoning can act as a stress test to reveal underlying coronary artery disease: case report

2020 ◽  
pp. 151-169
Author(s):  
Lindell K. Weaver ◽  
◽  
Keyword(s):  
Carbon Monoxide ◽  
Hyperbaric Oxygen ◽  
Carbon Monoxide Poisoning ◽  
Stress Test ◽  
The United States ◽  
Brain Inflammation ◽  
Smoke Inhalation ◽  
Co Poisoning ◽  
Exposure Limits ◽  
Disease Case

Despite established exposure limits and safety standards as well as the availability of carbon monoxide (CO) alarms, each year 50,000 people in the United States visit emergency departments for CO poisoning. Carbon monoxide poisoning can occur from brief exposures to high levels of CO or from longer exposures to lower levels. Common symptoms can include headaches, nausea and vomiting, dizziness, general malaise, and altered mental status. Some patients may have chest pain, shortness of breath, and myocardial ischemia, and may require mechanical ventilation and treatment of shock. Individuals poisoned by CO often develop brain injury manifested by neurological problems, including cognitive sequelae, anxiety and depression, persistent headaches, dizziness, sleep problems, motor weakness, vestibular and balance problems, gaze abnormalities, peripheral neuropathies, hearing loss, tinnitus, Parkinsonian-like syndrome, and other problems. In addition, some will have cardiac issues or other ailments. While breathing oxygen hastens the removal of carboxyhemoglobin (COHb), hyperbaric oxygen (HBO2) hastens COHb elimination and favorably modulates inflammatory processes instigated by CO poisoning, an effect not observed with breathing normobaric oxygen. Hyperbaric oxygen improves mitochondrial function, inhibits lipid peroxidation transiently, impairs leukocyte adhesion to injured microvasculature, and reduces brain inflammation caused by the CO-induced adduct formation of myelin basic protein. Based upon three supportive randomized clinical trials in humans and considerable evidence from animal studies, HBO2 should be considered for all cases of acute symptomatic CO poisoning. Hyperbaric oxygen is indicated for CO poisoning complicated by cyanide poisoning, often concomitantly with smoke inhalation.

scholarly journals A case of cyanide poisoning complicated with carbon monoxide poisoning caused by smoke inhalation

2014 ◽  
Vol 25 (10) ◽  
pp. 797-803
Author(s):  
Yasumasa Iwasaki ◽  
Akira Narame ◽  
Kazunobu Une ◽  
Kohei Ota ◽  
Yoshiko Kida ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Carbon Monoxide Poisoning ◽  
Smoke Inhalation ◽  
Cyanide Poisoning

Recurrent Acute Life-threatening Events and Lactic Acidosis Caused by Chronic Carbon Monoxide Poisoning in an Infant

PEDIATRICS ◽  
1999 ◽  
Vol 104 (3) ◽  
pp. e34-e34 ◽  
Author(s):  
Marta Foster ◽  
Salvatore R. Goodwin ◽  
Charles Williams ◽  
Janice Loeffler
Keyword(s):  
Carbon Monoxide ◽  
Lactic Acidosis ◽  
Carbon Monoxide Poisoning ◽  
Life Threatening

Abstract 324: An Engineered Protein as an Antidote for Carbon Monoxide Poisoning That Can Reverse Cardiovascular Collapse Through Scavenging of Carbon Monoxide and Rescue of Mitochondrial Respiration

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Jason J Rose ◽  
Qinzi Xu ◽  
Kaitlin A Bocian ◽  
Timothy N Bachman ◽  
Jian Hu ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Carbon Monoxide Poisoning ◽  
T Test ◽  
Activity Level ◽  
Tissue Respiration ◽  
Cardiovascular Collapse ◽  
Co Poisoning ◽  
Cardiovascular Dysfunction

Background: Carbon monoxide (CO) is the most common human poisoning. There is no antidote. One-third of hospitalized patients will have cardiac dysfunction and increased mortality. Little is known about the nature of cardiovascular dysfunction during acute CO poisoning. CO toxicity results from: (1) global hypoxia and decreased oxygen delivery through CO binding to hemoglobin, (2) inhibition of oxidative phosphorylation from CO binding to cytochrome c oxidase, and (3) ensuing superoxide injury. We have developed a recombinant neuroglobin molecule (rNgb) with a high affinity for CO, that can chelate CO from intrinsic heme proteins. Hypothesis: The addition of rNgb will scavenge CO from hemoglobin and cytochrome c oxidase, reversing CO-induced cardiovascular dysfunction. Methods: We inserted micromanometer-tip catheters into the left ventricle of ventilated, severely CO poisoned mice to study the mechanisms of CO-induced cardiovascular collapse. In a similar model, we measured blood pressure and heart rate of severely CO poisoned, ventilated mice through a carotid arterial catheter and treated with phosphate buffered saline (PBS) or rNgb. Hearts were isolated from these mice and we measured tissue respiration using a Clark-type oxygen electrode. We compared the respiration rates of these animals and compared with non-poisoned, sedated control mice. We also compared the enzymatic activity of electron transport chain complexes. Results and Conclusions: When compared to control mice (exposed to 21% oxygen/no CO), CO poisoned mice develop a decreased contractility index (-32.3% baseline vs. -10.8% in control, t-test, p=0.002), hypotension and death, indicating primary cardiac toxicity. CO-poisoned mice treated with PBS had heart tissue respiration that was 62.3% (+/- 7.5%) of sedated control mice (t-test, P=0.015). Treatment of mice with rNgb restored tissue respiration (P=0.037 versus PBS treated mice) similar to control values. CO poisoning reduced the activity level of complex IV in PBS treated mice (P=0.011), but levels were similar to control in rNgb treated mice. These molecular changes were associated with reversal of cardiovascular collapse in rNgb treated mice versus PBS, demonstrating the potential of rNgb as a CO poisoning antidote.

Diabetes Insipidus after Carbon Monoxide Poisoning and Smoke Inhalation

1985 ◽  
Vol 25 (7) ◽  
pp. 662-663 ◽  
Author(s):  
PAUL HALEBIAN ◽  
ROGER YURT ◽  
CAROL PETITO ◽  
G. TOM SHIRES
Keyword(s):  
Carbon Monoxide ◽  
Diabetes Insipidus ◽  
Carbon Monoxide Poisoning ◽  
Smoke Inhalation
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