CO Poisoning References ======================= Here are a few abstracts re. CO poisoning. The August 1994 Annals of Emergency Medicine has several good articles with numerous references, and the JEM article was a reasonable survey of current practices (I'm *not* suggesting that there is necessarily good hard science supporting the latter practices). AN 95294389 AU Hampson NB. Dunford RG. Kramer CC. Norkool DM. IN Hyperbaric Medicine Department, Virginia Mason Medical Center, Seattle, Washington 98111, USA. TI Selection criteria utilized for hyperbaric oxygen treatment of carbon monoxide poisoning. SO Journal of Emergency Medicine. 13(2):227-31, 1995 Mar-Apr. JC ibo CP United States AB Medical directors of North American hyperbaric oxygen (HBO) facilities were surveyed to assess selection criteria applied for treatment of acute carbon monoxide (CO) poisoning within the hyperbaric medicine community. Responses were received from 85% of the 208 facilities in the United States and Canada. Among responders, 89 monoplace and 58 multiplace chamber facilities treat acute CO poisoning, managing a total of 2,636 patients in 1992. A significant majority of facilities treat CO-exposed patients with coma (98%), transient loss of consciousness (LOC) (77%), ischemic changes on electrocardiogram (91%), focal neurologic deficits (94%), or abnormal psychometric testing (91%), regardless of carboxyhemoglobin (COHb) level. Although 92% would use HBO for a patient presenting with headache, nausea, and COHb 40%, only 62% of facilities utilize a specified minimum COHb level as the sole criterion for HBO therapy of an asymptomatic patient. When COHb is used as an independent criterion to determine HBO treatment, the level utilized varies widely between institutions. Half of responding facilities place limits on the delay to treatment for patients with only transient LOC. Time limits are applied less often in cases with persistent neurologic deficits. While variability exists, majority opinions can be derived for many patient selection criteria regarding the use of HBO in acute CO poisoning. AN 95055957 AU Hardy KR. Thom SR. IN University of Pennsylvania, Institute for Environmental Medicine, Philadelphia 19104-6068. TI Pathophysiology and treatment of carbon monoxide poisoning. [Review] SO Journal of Toxicology - Clinical Toxicology. 32(6):613-29, 1994. JC kan SB A CP United States AB Carbon monoxide poisoning is the leading cause of poisoning deaths in the US, and published reports of carbon monoxide related morbidity and mortality can vary widely. Common morbidity involves myocardial and/or neurologic injury including delayed neurologic sequelae. The pathophysiology of this entity is complex, involving hypoxic stress on the basis of interference with oxygen transport to the cells and possibly impairing electron transport. Carbon monoxide can also affect leukocytes, platelets and the endothelium, inducing a cascade of effects resulting in oxidative injury. Carboxyhemoglobin levels are valuable for confirming carbon monoxide exposure but cannot be used to stratify severity of poisoning, predict prognosis, or indicate a specific treatment plan. Oxygen therapy is the key treatment of carbon monoxide intoxication, and hyperbaric oxygen has been shown to interdict and improve clinical outcome in some patients. Immediate treatment with a high fraction of inspired oxygen and careful clinical evaluation are mandatory. Timely referral for hyperbaric oxygen is indicated for patients with any history of unconsciousness, cardiovascular instability or ischemia, and persistent mental and/or neurologic deficits. Hyperbaric oxygen should also be considered in certain other patient subsets. [References: 115] AN 94311520 AU Van Meter KW. Weiss L. Harch PG. Andrews LC Jr. Simanonok JP. Staab PK. Gottlieb SF. TI Should the pressure be off or on in the use of oxygen in the treatment of carbon monoxide-poisoned patients? [editorial; comment]. CM Comment on: Ann Emerg Med 1994 Aug;24(2):242-8, Comment on: Ann Emerg Med 1994 Aug;24(2):252-5, Comment on: Ann Emerg Med 1994 Aug;24(2):269-76 SO Annals of Emergency Medicine. 24(2):283-8, 1994 Aug. JC 4z7 SB A CP United States AN 94235097 AU Seger D. TI The science (or lack thereof) in the treatment of carbon monoxide poisoning [letter; comment]. CM Comment on: Am J Emerg Med 1993 Nov;11(6):616-8 SO American Journal of Emergency Medicine. 12(3):389-90, 1994 May. JC aa2 CP United States AN 94056098 AU Kales SN. IN Cambridge Hospital, Massachusetts. TI Carbon monoxide intoxication. [Review] SO American Family Physician. 48(6):1100-4, 1993 Nov 1. JC 3bt SB A CP United States AB Carbon monoxide poisoning usually results from inhalation of exhaust fumes from motor vehicles, smoke from fires or fumes from faulty heating systems. Carbon monoxide has a high affinity for hemoglobin, with which it forms carboxyhemoglobin. The resulting decrease in both oxygen-carrying capacity and oxygen release can lead to end-organ hypoxia. The clinical presentation is nonspecific. Headache, dizziness, fatigue and nausea are common in mild to moderate carbon monoxide poisoning. In more severe cases, tachycardia, tachypnea and central nervous system depression occur. When carbon monoxide intoxication is suspected, empiric treatment with 100 percent oxygen should be initiated immediately. The diagnosis is confirmed by documenting an elevated carboxyhemoglobin level. Hyperbaric oxygen therapy is recommended in patients with neurologic dysfunction, cardiac dysfunction or a history of unconsciousness. [References: 26] DE Automobile Exhaust/ae [Adverse Effects]. Blood Gas Analysis. Carbon Monoxide Poisoning/bl [Blood]. *Carbon Monoxide Poisoning/di [Diagnosis]. Carbon Monoxide Poisoning/et [Etiology]. Carbon Monoxide Poisoning/pp [Physiopathology]. *Carbon Monoxide Poisoning/th [Therapy]. Carboxyhemoglobin/an [Analysis]. Cell Hypoxia. Fires. Heating/ae [Adverse Effects]. Hotlines. Human. Hyperbaric Oxygenation. Medical History Taking. Oxygen Inhalation Therapy. Severity of Illness Index. Support, U.S. Gov't, P.H.S.. Treatment of Carbon Monoxyde Poisoning : a critical review of human outcome studies comparing normobaric oxygen with hyperbaric oxygen. PM Tibbles, PL Perrotta Annals of Emergency Medicine, 1994, 24, 269-276. French article, by Raphaele, in the Lancet: no difference in Those presenting with coma: either one or two courses of HBO, evaluated at one month; no severe sequelae in those not presenting in coma; moderate sequelae in those presenting with coma were comparable in those with and without HBO. Those with hx of LOC but not in coma did not benefit from HBO, only those in coma; and those improve with one session but a second one doesn't help. Ducasse JL, Celsis P, Marc-Vergnes P. : patients treated early, most had history of LOC but awake on presentation. HBO helped somewhat at 2 and 12 hours after treatment. But, in critique: no clinical abnormalities on discharge or on followup. Slight EEG and cerebral bloodflow improvement in the HBO treated patients. No correlation between sx and CO level. Earlier improvement with HBO but not much if any longterm differences. Conclusion: in noncomatose patients, treat with HBO if symptoms persist after 2 hours of normobaric oxygen regardless of CO level.