HCMC_P_049062 - Hennepin County Medical Center

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Case Reports elevated and the skin may look pink. Screening should begin with co-oximetry, when available. Measured COHb should be performed in all cases where there is significant exposure or clinical symptoms. Cardiac monitoring and a 12 lead electrocardiogram (ECG) are mandatory in patients with chest pain, shortness of breath, comorbidities, or significant COHb levels. In addition to resuscitation and airway management, the mainstay of treatment for CO poisoning is oxygen. Also, 100% oxygen should be delivered via a tight fitting, non-rebreather mask or endotracheal tube as soon as possible, reducing the half-life of COHb from 300 minutes on room air to approximately 60 minutes. Myocardial depression and vasodilation may cause hypotension, needing treatment with fluids, vasopressors, and/or inotropes. should be placed on clinical findings suggesting severe toxicity rather than simple CO levels. The following indications for HBO are generally used by the Minnesota Poison Control Center and the Center for Hyperbaric Medicine at Hennepin County Medical Center which is open for emergencies 24/7. Indications for Hyperbaric Oxygen: 1. History of loss of consciousness 2. Serious toxicity including lethargy, confusion, seizures, focal neurologic deficit, ischemic chest pain, new dysrhythmia, ECG changes, hypotension 3. COHb levels > 25% plus cardiovascular disease, cerebrovascular disease, age > 60years, < 2 years, hemoglobin < 10, or exposure > 24hours 4. COHb > 40% 5. Pregnancy with COHb > 20% or signs of fetal distress 6. Symptoms refractory to normobaric oxygen Figure One. The patient was transferred to the hyperbaric oxygen (HBO) chamber where she was treated with a 90 minute 2.4 atmosphere dive by a hyperbaracist. Hyperbaric oxygen (HBO) therapy remains the optimum treatment for the elimination of CO from the human body and should be performed whenever available in cases of significant poisoning. The halflife of CO is reduced to a mere 20 minutes at 2.5 atmospheres of 100% oxygen. The best published data suggests that HBO reduces cognitive sequelae of CO poisoning from 46% in the untreated group to 24% in the group treated with HBO. Though practice will vary by institution, immediate consultation with a HBO facility is indicated when significant carbon monoxide poisoning occurs (Figure One). Importance Hydrogen Cyanide Gas Poisoning Hydrogen cyanide gas (HCN) is produced during the combustion of a variety of natural and synthetic fibers. HCN toxicity is often overlooked in fires as patients’ symptoms may be attributed to CO. HCN was detected in 59% of decedents of structure fires, and 50% of survivors in a recent Polish study. Once inhaled, HCN distributes to tissues affecting metabolic enzymes; most importantly, it binds cytochrome oxidase and halts cellular respiration. Effects vary, depending on concentration, duration of exposure, and patient factors; nonetheless, HCN is considered among the fastest poisons and may rapidly produce syncope, seizures, and cardiovascular collapse. While confusion, lethargy, hypertension, and tachycardia may occur, coma, bradycardia, and hypotension consistently precede death. It is eliminated with a variable half-life of 1 hour to > 2 days. Diagnosis relies on a timely clinical assessment rather than analytics. Like CO toxicity, HCN toxicity may result in normal pulse oximetry, and pink skin despite severe toxicity; moreover, venous oxygen saturations may be elevated. COHb levels poorly predict HCN toxicity, but serum lactate > 8mmol/L in fire victims predicts cyanide levels > 1.0μg/ml with 94% sensitivity and 70% specificity. Hydroxocobalamin has emerged as the antidote of choice. It has been safely administered pre-hospital in France since the 10 | Approaches in Critical Care | January 2013
Case Reports Figure Two: Photographs showing bright red discoloration of the patient's skin (A) and urine (B) after treatment with hydroxocobalamin for cyanide poisoning. Cescon D W , Juurlink D N. CMAJ 2009; 180:251-251. Used with permission. invaginated scolex is clearly seen inside of the cystic cavity. 1980s and was FDA approved in the US in 2006. Hydroxocobalamin is given 5g IV and may be repeated. It rapidly binds and detoxifies circulating cyanide anions to form cyanocobalamin (vitamin B12). Adverse reactions are limited to transient reddening of the skin and bodily fluids (Figure Two), minor allergy, transient hypertension, and temporary interference with colorimetric laboratory tests. Since routine serum HCN levels are lacking, administration is empiric. Suspect and treat HCN toxicity in patients with: 1. Suspected smoke inhalation (carbonaceous sputum, enclosed fire, etc.) 2. Altered mental status 3. Cardiovascular instability (especially systolic blood pressure < 90mmHg in adults) 4. Initial serum lactate > 8.0mmol/L Given the rapid mechanism of action of both HCN and the antidote, there should be no delay in antidotal treatment of unstable patients without laboratory values. After administration of hydroxocobalamin, clinicians may consider treatment with sodium thiosulfate (STS) through a separate line. STS in conjunction with endogenous rhodanase detoxifies HCN to thiocyanate. STS is a constituent of the older cyanide antidote kit, which also included amyl, butyl, and sodium nitrite. The nitrites induce methemoglobinemia and should be avoided in patients suffering from concomitant CO toxicity. should now readily identify that her profound alteration of mental status, inhalational injury, and high lactate as nearly diagnostic of cyanide toxicity. Both conditions warrant immediate treatment. Our patient was fortunate to have received timely therapies, including emergency department resuscitation, airway management, hydroxocobalamin, sodium thiosulfate, and hyperbaric oxygen. Her ultimate full recovery would not have been possible without the continued thorough inpatient treatment from a multidisciplinary care team in the burn unit. References Baud, F. J., S. W. Borron, B. Megarbane, H. Trout, F. Lapostolle, E. Vicaut, M. Debray, and C. Bismuth. Value of Lactic Acidosis in the Assessment of the Severity of Acute Cyanide Poisoning. Crit Care Med 30, No. 9. Sep 2002: 2044-50. Cone, D. C., D. MacMillan, V. Parwani, and C. Van Gelder. Threats to Life in Residential Structure Fires. Prehosp Emerg Care 12, No. 3. Jul-Sep 2008: 297-301. Grabowska, T., R. Skowronek, J. Nowicka, and H. Sybirska. Prevalence of Hydrogen Cyanide and Carboxyhaemoglobin in Victims of Smoke Inhalation During Enclosed-Space Fires: A Combined Toxicological Risk. Clin Toxicol (Phila) 50, No. 8. Sep 2012: 759-63. Nelson, Lewis, and Lewis R. Goldfrank. Goldfrank's Toxicologic Emergencies. 9th ed. New York: McGraw-Hill Medical, 2011. O'Brien, D. J., D. W. Walsh, C. M. Terriff, and A. H. Hall. Empiric Management of Cyanide Toxicity Associated with Smoke Inhalation. [In Eng]. Prehosp Disaster Med 26, No. 5. Oct 2011: 374-82. Weaver, L. K., R. O. Hopkins, K. J. Chan, S. Churchill, C. G. Elliott, T. P. Clemmer, J. F. Orme, Jr., F. O. Thomas, and A. H. Morris. Hyperbaric Oxygen for Acute Carbon Monoxide Poisoning. N Engl J Med 347, No. 14. Oct 3 2002: 1057-67. Conclusion In our patient, the COHb of 41% is consistent with severe carbon monoxide toxicity; however, clinicians Approaches in Critical Care | January 2013 | 11
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HCMC_P_049062 - Hennepin County Medical Center

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