jurnal toxin co

8/11/2019 Jurnal Toxin Co

1/19


2/19


3/19

;pidemiology

7re%uency fire-related.89

'eporting of nonfatal unintentional non > fire-related exposures from 1-

reveals an average of 16, yearly cases treated in emergency departments "ith 253

occurring in homes. !he most common source being furnaces (1=.63) follo"ed by motor

vehicles, stoves, gas lines, "ater heaters, and generators.

859

*ncreasing evidence implicates ambient urban CO levels in rates of angina,

arrhythmias, and cardiac arrest. +resuming that the evidence is %uantifiable and depending on

the true extent, this implies a significant underreporting of CO-associated deaths.

International

?uantifying the global incidence of CO poisoning is impossible because of the

transient duration of symptoms in mild intoxication, the ubi%uitous and occult nature of

exposure, and the tendency of misdiagnosis. *n contrast to findings in the


4/19

ustralian study of suicidal poisonings indicated no decrease follo"ing significantly lo"ered

CO emissions from 1:/-1::2 and revealed no difference bet"een the 0bCO levels of

occupants in cars "ith and "ithout catalytic converters.869

'ace

ll ages, ethnic populations, and social groups are affected, yet particular groups may be

at higher risk.

1!br0ken!! ;arlier data stated that, for unintentional fatalities, race-specific death rates

"ere 3 higher for blacks. @ore recent data reveal non-0ispanic "hites and non-

0ispanic blacks to have e%ually high death rates, significantly above that of 0ispanic

and those classified as Other.89

2!br0ken!! Conversely, intentional fatalities demonstrate that race-specific rates for blacks

and other minority racial groups are =/3 lo"er than for "hites, revealing a cultural

partiality to this form of suicide.

!"o #orth merican studies examined the incidence of CO toxicity from indoor heating

devices used during severe "inter storms. Both studies identified a strong association

bet"een CO toxicity and


5/19


6/19

16!br0ken!! 7ecal and urinary incontinence

17!br0ken!! @emory and gait disturbances

18!br0ken!! Biarre neurologic symptoms, coma

; Chronic exposures also present "ith the above symptoms4 ho"ever, they may present

"ith loss of dentition, gradual-onset neuropsychiatric symptoms, or, simply, recent

impairment of cognitive ability.

+hysical

+hysical examination is of limited value. *nhalation inAury or burns should al"ays alert the

clinician to the possibility of CO exposure.

; Dital signs

1!br0ken!! !achycardia

2!br0ken!! 0ypertension or hypotension

3!br0ken!! 0yperthermia

4!br0ken!! @arked tachypnea (rare4 severe intoxication often associated "ith mild

or no tachypnea)

; $kinE Classic cherry red skin is rare (ie, Fhen youGre cherry red, youGre deadF)4 pallor

is present more often.

; Ophthalmologic

1!br0ken!! 7lame-shaped retinal hemorrhages

2!br0ken!! Bright red retinal veins (a sensitive early sign)

3!br0ken!! +apilledema

4!br0ken!! 0omonymous hemianopsia

; #oncardiogenic pulmonary edema

; #eurologic andHor neuropsychiatric

1!br0ken!! +atients display memory disturbance (most common), including

retrograde and anterograde amnesia "ith amnestic confabulatory states.

2!br0ken!! +atients may experience emotional lability, impaired Audgment, and

decreased cognitive ability.


7/19

3!br0ken!! Other signs include stupor, coma, gait disturbance, movement

disorders, and rigidity.

4!br0ken!! +atients display brisk reflexes, apraxia, agnosia, tic disorders, hearing

and vestibular dysfunction, blindness, and psychosis.

5!br0ken!! ong-term exposures or severe acute exposures fre%uently result in

long-term neuropsychiatric se%uelae. dditionally, some individuals develop

delayed neuropsychiatric symptoms, often after severe intoxications associated

"ith coma.

6!br0ken!! fter recovery from the initial incident, patients present several days to

"eeks later "ith neuropsychiatric symptoms such as those Aust described. !"o

thirds of patients eventually recover completely.

7!br0ken!! @'* changes may remain long after clinical recovery. +redicting and

preventing long-term complications and delayed encephalopathy have been

the obAect of recent studies, many of "hich focus on the role of hyperbaric

oxygen therapy.

Causes

; @ost unintentional fatalities occur in stationary vehicles from preventable causes suchas malfunctioning exhaust systems, inade%uately ventilated passenger compartments,

operation in an enclosed space, and utiliation of auxiliary fuel-burning heaters inside

a car or camper.

; @ost unintentional automobile-related CO deaths in garages have occurred despite

open garage doors or "indo"s, demonstrating the inade%uacy of passive ventilation in

such situations.

; Colorado state data revealed that sources of 115: poisonings "ere residential furnaces

(53), automobile exhaust (53), and fires (13).

; 7urnaces "ere determined to be the source in 523 of nonfatal CO poisonings but in

only 13 of fatal poisonings. !his suggests that the role of home heating appliances

is prominent in the large group of underreported nonfatal exposures.

; *n the setting of structure fires, CO presents greater risk to firefighters and victims

than thermal inAury or oxygen deprivation.8=9


8/19


9/19

is not a component of routine pulse oximetry. 1 study sho"s that non-invasive

pulse CO-oximetry correlates "ith more rapid diagnosis and initiation of hyperbaric

oxygen therapy than laboratory CO-oximetry. 0o"ever, the impact on clinical

outcome is still not proven.819

1!br0ken!! ;levated levels are significant4 ho"ever, lo" levels do not rule out

exposure, especially if the patient already has received 13 oxygen or if

significant time has elapsed since exposure.

2!br0ken!! *ndividuals "ho chronically smoke may have mildly elevated CO

levels as high as 13. +resence of fetal hemoglobin, as high as 3 at

months, may be read as an elevation of 0bCO level to /3.

; rterial blood gas

1!br0ken!! +aOlevels should remain normal. Oxygen saturation is accurate only

if directly measured but not if calculated from +aO, "hich is common in

many blood gas analyers.

2!br0ken!! s "ith pulse oximetry, estimate +CO levels by subtracting the

carboxyhemoglobin (0bCO) level from the calculated saturation. +CO level

may be normal or slightly decreased. @etabolic acidosis occurs secondary to

lactic acidosis from ischemia.

; !roponin, creatinine kinase-@B fraction, myoglobin

1!br0ken!! @yocardial ischemia is fre%uently associated "ith patients hospitalied

for moderate-to-severe CO exposure and is a predictor of mortality.8119

2!br0ken!! +atients "ith preexisting disease can experience increased exertional

angina "ith 0bCO levels of Aust 6-13. t high 0bCO levels, even young

healthy patients develop myocardial depression.

; Creatinine kinase, urine myoglobinE #ontraumatic rhabdomyolysis can result from

severe CO toxicity and can lead to acute renal failure.

; Complete blood count

1!br0ken!! ook for mild leukocytosis.

2!br0ken!! &isseminated intravascular coagulation (&*C) and thrombotic

thrombocytopenic purpura(!!+) re%uire further hematologic studies.
http://emedicine.medscape.com/article/779097-overviewhttp://emedicine.medscape.com/article/206598-overviewhttp://emedicine.medscape.com/article/206598-overviewhttp://emedicine.medscape.com/article/779097-overviewhttp://emedicine.medscape.com/article/206598-overviewhttp://emedicine.medscape.com/article/206598-overview


10/19

; ;lectrolytes and glucose level - actic acidosis, hypokalemia, and hyperglycemia "ith

severe intoxication

; B


11/19

Of those patients "ith negative scan results, only 113 had neurologic

se%uelae.819

5!br0ken!! @'* is more accurate than C! scans for focal lesions and "hite matter

demyelination and is often used for follo"-up care.

6!br0ken!! $erial C! scans may be necessary, especially "ith mental status

deterioration.

7!br0ken!! recent report describes the evolution of acute hydrocephalus in a

child poisoned "ith CO, documented by serial C! scans.

Other !ests

;

;lectrocardiogram

1!br0ken!! $inus tachycardia is the most common abnormality.

2!br0ken!! rrhythmias may be secondary to hypoxia, ischemia, or infarction.

3!br0ken!! ;ven lo" 0bCO levels can have severe impact on patients "ith

cardiovascular disease.

; #europsychologic testing

1!br0ken!! 7ormal neuropsychologic testing of concentration, fine motor function,

and problem solving consistently reveal subtle deficits in even mildly

poisoned patients.

2!br0ken!! bridged versions of these tests, more applicable to the emergency

department (;&) setting, have been developed as possible means to assess the

risk of delayed neurologic se%uelae, to assess the need for hyperbaric oxygen

therapy, and to determine the success of hyperbaric therapy in preventing

delayed se%uelae.

3!br0ken!! !hese tests are used in some institutions, but studies prospectively

confirming the conclusions are lacking.

4!br0ken!! bridged tests can be performed in about minutes by a "ell-trained

examiner.

5!br0ken!! 'ecent research indicates a specific link to deficits in context-aided

memory4 such specific testing has been proposed as a tool for measuring the

severity of neurologic involvement in the ;&.


12/19

+rehospital Care

; +romptly remove from continued exposure and immediately institute oxygen therapy

"ith a nonrebreather mask.

; +erform intubation for the comatose patient or, if necessary, for air"ay protection, and

provide 13 oxygen therapy.

; *nstitute cardiac monitoring. +ulse oximetry, although not useful in detecting 0bCO,

is still important because a lo" saturation causes an even greater apprehension in this

setting.

; Iive notification for comatose or unstable patients because rapid or direct transfer to

a hyperbaric center may be indicated.

; *f possible, obtain ambient CO measurements from fire department or utility company

personnel, "hen present.

; ;arly blood samples may provide much more accurate correlation bet"een 0bCO and

clinical status4 ho"ever, do not delay oxygen administration to ac%uire them.

; Obtain an estimate of exposure time, if possible.

; void exertion to limit tissue oxygen demand.

;mergency &epartment Care

; Cardiac monitorE $udden death has occurred in patients "ith severe arteriosclerotic

disease at 0bCO levels of only 3.

; +ulse oximetryE 0bCO absorbs light almost identically to that of oxyhemoglobin.

lthough a linear drop in oxyhemoglobin occurs as 0bCO level rises, pulse oximetry

"ill not reflect it. +ulse oximetry gap, the difference bet"een the saturation asmeasured by pulse oximetry and one measured directly, is e%ual to the 0bCO level.

0o"ever, ne" pulse CO-oximetry units are available "hich can screen for CO

toxicity at the bedside.819

; Continue 13 oxygen therapy until the patient is asymptomatic and 0bCO levels are

belo" 13. *n patients "ith cardiovascular or pulmonary compromise, lo"er

thresholds of 3 have been suggested.


13/19

; Calculate a gross estimate of the necessary duration of therapy using the initial level

and half-life of -: minutes at 13 oxygen. Complicated issues of treatment of

fetomaternal poisoning are discussed in $pecial Concerns.

1!br0ken!! *n uncomplicated intoxications, venous 0bCO levels and oxygen

therapy are likely sufficient. ;valuate patients "ith significant cardiovascular

disease and initial 0bCO levels above 163 for myocardial ischemia and

infarction.

2!br0ken!! Consider immediate transfer of patients "ith levels above 53 or

cardiovascular or neurologic impairment to a hyperbaric facility, if feasible.

+ersistent impairment after 5 hours of normobaric oxygen therapy necessitates

transfer to a hyperbaric center. +regnant patients "ith lo"er

carboxyhemoglobin levels (above 163) should be considered for hyperbaric

treatment.

; $erial neurologic examinations, including funduscopy, C! scans, and, possibly, @'*,

are important in detecting the development of cerebral edema. Cerebral edema

re%uires intracranial pressure (*C+) and invasive blood pressure monitoring to further

guide therapy. 0ead elevation, mannitol, and moderate hyperventilation to =- mm

0g +COare indicated in the initial absence of *C+ monitoring. Ilucocorticoids have

not been proven efficacious, yet the negative aspects of their use in severe cases are

limited.

1!br0ken!! &o not aggressively treat acidosis "ith a p0 above /.16 because it

results in a right"ard shift in the oxyhemoglobin dissociation curve,

increasing tissue oxygen availability. cidosis generally improves "ith

oxygen therapy.

2!br0ken!! *n patients "ho fail to improve clinically, consider other toxic inhalants

or thermal inhalation inAury. Be a"are that the nitrites used in cyanide kits

cause methemoglobinemia, shifting the dissociation curve left"ard and further

inhibiting oxygen delivery at the tissue level. Combined intoxications of

cyanide and CO may be treated "ith sodium thiosulfate 1.6 g intravenously

to prevent the left"ard shift.

3!br0ken!! dmit patients to a monitored setting and evaluate acid-base status if

0bCO levels are -53 or above 63 "ith associated symptoms.
http://emedicine.medscape.com/article/815613-overviewhttp://emedicine.medscape.com/article/815613-overview


14/19


15/19

monoplace chamber is sho"n belo".

@onoplace hyperbaric chamber. Courtesy JI Benite, @&, @+0.

5!br0ken!! !reatment regimens usually involve 13 oxygen at .5- atm for :-

1 minutes. 'e-treatment, although controversial, may be performed for

acutely and chronically persistent symptoms. One study suggests that degree

of acidosis can predict the need for re-treatment.

6!br0ken!! Complications of therapy include decompression sickness, sinus and

middle ear barotrauma, seiure, progression of pneumothorax to tension

pneumothorax, gas embolism, reversible visual refractive changes, and

complications related to transport of unstable patients.

7!br0ken!! 7or treatment of complications from therapy, decongestants are useful,

prophylactic myringotomy is common and a re%uirement for intubated

patients, and chest tube placement is mandatory "ith pneumothorax. ;xercise

caution in patients "ho have experienced chest compressions, central venous

catheteriation, intubation, and positive pressure ventilation. $eiures are most

often secondary to oxygen toxicity and do not mandate anticonvulsant therapy

or discontinuation of 0BO therapy.

8!br0ken!! *n multiplace chambers, seiure therapy consists of removing the

oxygen mask. *n monoplace chambers, decompression lo"ers oxygen

concentration. *t is crucial not to do this during the tonic phase of the seiure

because it may cause pulmonary barotrauma secondary to gas expansion in the

lungs.

9!br0ken!! 1-year retrospective study found that transfer to an 0BO facility

did not need to be delayed for concern of cardiac arrest, respiratory arrest,

myocardial infarction, or "orsening mental status if they had not occurred

during initial resuscitation4 ho"ever, hypotension, dysrhythmia, seiure,


16/19


17/19

1!br0ken!! &iscuss the possibility of delayed neurologic complications, although they are

much more common in admitted patients.

2!br0ken!! $uggest minimiing physical activity for -5 "eeks.

3!br0ken!! dvise patient to stop smoking.

4!br0ken!! 7or excellent patient education resources, visit e@edicine0ealthGs 7irst id

and *nAuries Center. lso, see e@edicine0ealthGs patient education article Carbon

@onoxide +oisoning.

5!br0ken!! Contributor *nformation and &isclosures

uthor

Iuy # $hochat, @& ssociate Clinical +rofessor of ;mergency @edicine,


18/19

1!br0ken!! +eter @C &eBlieux, @& +rofessor of Clinical @edicine and +ediatrics,

$ection of +ulmonary and Critical Care @edicine, +rogram &irector, &epartment of

;mergency @edicine, ouisiana $tate


19/19

jurnal toxin co

Documents