Healthcare
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alone! And certainly not to Finance: the cheapest way to com- ply with HIPANs transaction, code and identifier requirements is a sure fire way to end up losing your shirt in the long run. HIPAA Privacy requirements are causing problems from one end of the country to the other - especially for patient's fami- lies!
9. Assuring Staff Competence - Look to see 'competence'
moving beyond measuring knowledge and skills, credentials and experience, into measuring the effects of fatigue on per- formance. This move, initiated first, by nursing unions, is one that safety advocates have long targeted. And it will not be con- fined only to the nursing ranks. Moreover, with a growing workforce of part-timers, contingency workers and new grad- uates, this issue is looming large! 10. Patient Safety - It really has seeped into the public's
consciousness: hospitals are hazardous to their health! Politi- cians of all stripes and regulators from agencies public and pri- vate are extremely upset about the dangers besetting today's hospitalized patients. Moreover, with analyses of errors ex- panded to include a 'blunt end' analysis (decisions made in board rooms and the impact they have on the errors made at the bedside), a new level of accountability is added to execu- tive decision making! Nonetheless, and despite 5 years of fix- ation of safety, things have not improved one iota!
Carbon Monoxide
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dation-reduction reactions at the cellular level. Therefore, CO poisoning interferes with cellular respiration, i.e., the body’s ability to produce energy. CO also interferes with cytochrome P450 in the liver. Cy-
tochrome P450 is a group of enzymes involved in the body’s detoxification process. The ability of CO to inhibit the cy- tochrome system accounts for the profound neurological de- pression that often continues beyond the time COHb levels have been reduced to below toxic concentrations. Brain lipid peroxidation and leukocyte-mediated inflam-
matory alterations also occur during CO poisoning. A chain of biochemical reactions is triggered by the presence of CO in the brain leading to the formation of the oxygen metabolite, super- oxide anion. This oxygen radical causes lipid peroxidation and ultimately brain damage. This mechanism is similar to is- chemia-reperfusion injury associated with hypoperfusion.
Clinical Manifestations The clinical manifestations of CO poisoning are neurolog-
ical and cardiovascular because the brain and heart are most vulnerable to the lethal properties of CO. Common symptoms include: headache, fatigue, muscle pain and cramps, nausea, vomiting, diarrhea, confusion, memory loss, dizziness, chest pain, rapid heartbeat, shortness of breath, and hearing and vi- sual impairment. Although the signs and symptoms of acute CO poisoning are variable, textbooks often cite a positive cor- relation between COHb levels and clinical manifestations. For example,
COHb% Clinical Manifestations 10%
20% 30% 40% 50% 60%
asymptommatic or headaches dizziness, nausea, syncope visual disturbances confusion & syncope seizures & coma
cardiopulmonary dysfunction/death Difficulty only occurs when attempting to correlate
COHb% and clinical manifestations, and when trying to predict sequelae.
Diagnosis The PaO2 will remain normal because CO inhalation af-
fects O2 attached to hemoglobin, and not O2 dissolved in the plasma. An SaO2 value obtained from the analysis of an arterial blood sample is meaningless because the SaO2 is calculated rather than measured. A pulse oximeter will render a falsely high SpO2 in the presence of COHb. Therefore, for accuracy, the level of COHb in the blood must be measured by a cooximeter. Physicians must remain vigilant for CO poisoning signs
and symptoms especially during the winter months when risk from CO exposure is high. Because flu symptoms mimic those of CO poisoning, whenever two or more persons enter the emergency department exhibiting flu-like symptoms, CO ex- posure should be suspected. A CO analyzer can be used to measure a victim’s exhaled CO concentration.
Treatment Anyone suspected of experiencing CO poisoning should
receive 100% O2. The purpose is to improve the competition of O2 for hemoglobin binding sites. The half-life of CO in a vic- tim’s blood is about 5 hours when room air is breathed, com- pared to one hour when the FIO2 is 1.0. The half-life is further reduced to about 20 minutes when hyperbaric O2 therapy (HBOT) is administered at 100% O2 at 3 atmospheres. Most CO victims can be treated under normobaric conditions. HBOT should be reserved for patients who initially fail to meet the cri- teria for HBOT, but experience unrelenting neurological symp- toms despite hours of 100 % O2 therapy. HBOT supersaturates the plasma with O2. Research has demonstrated that HBOT inhibits the adhe-
sion of polymorphonuclear leukocytes to the vasculature in the brain and revives inactivated cytochromes.
Prognosis Neurological deficits occur in many patients who survive
acute CO poisoning. These deficits include impaired memory, personality alterations, psychiatric impairment, visual impair- ment, and persistent vegetative state.
Prevention The public should be educated concerning the sources of
CO, and the operation and maintenance of certain equipment, e.g., generators and self-cleaning ovens, to prevent CO from entering the air. More home and businesses need to be equipped with CO detectors. The public should also be taught the signs and symptoms of CO exposure to recognize this con- dition in themselves and others.
Focus Journal Winter 2012 33
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