oRIGINAL CONTRIBUTION
Carbon Monoxide Intoxication: A Review of 14 Patients M. Donald Whorton, MD, MPH Berkeley, California
In 14 c a s e s o f c a r b o n m o n o x i d e p o i s o n i n g , m e d i c a l r e c o r d s w e r e available f o r r e t r o s p e c t i v e r e v i e w in w h i c h b l o o d s a m p l e s f o r c a r b o x y h e m o g l o b i n (COHgb) w e r e o b t a i n e d . T w e l v e v i c t i m s (86%) w e r e overcome w h i l e at w o r k . C o r r e l a t i o n o f the c l i n i c a l p i c t u r e and C O H g b saturation w a s not a l w a y s p o s s i b l e a l t h o u g h h y p e r t e n s i o n w a s n o t uncommon initially. On f o l l o w - u p o n l y three p a t i e n t s w e r e m i l d l y hypertensive. S k i n or m u c o u s m e m b r a n e c o l o r c h a n g e s w e r e difficult to detect. T h r e e c a s e s are p r e s e n t e d to illustrate f a c t o r s in the d i a g n o s i s and possible s e q u e l a e .
Whorton MD: Carbon monoxide intoxication: A review of 14 patients. JACEP 5:505-509, July 1976. poisoning, carbon monoxide; hypertension, carbon monoxide poisoning, clinical correlation. INTRODUCTION Carbon monoxide, an odorless, colorless a n d t a s t e l e s s toxic gas, is a product of i n c o m p l e t e c o m b u s t i o n . Every y e a r , e s p e c i a l l y d u r i n g t h e winter, t h e r e are a c c i d e n t a l d e a t h s from acute carbon monoxide intoxication due to i n a d e q u a t e v e n t i l a t i o n at home and w o r k ) A n n u a l statistics on the incidence of n o n f a t a l episodes of carbon monoxide intoxication are incomplete. 2 One y e a r ' s e x p e r i e n c e with d i a g n o s e d c a s e s of c a r b o n monoxide i n t o x i c a t i o n in a n e m e r gency d e p a r t m e n t of an u r b a n teaching h o s p i t a l is r e v i e w e d h e r e w i t h the p a t i e n t s ' clinical evaluation.
METHODS Baltimore C i t y Hospital, a 600-bed From the Division of Emergency Medieine, Baltimore City Hospitals, Baltimore, Maryland. Address for reprints: M. Donald Whorton, MD, MPH, Director, LOHP, UC-Berkeley, 2521 Channing Way, Berkeley, California 94720.
J ~ [ : ) July 1976
acute care h o s p i t a l in a n i n d u s t r i a l ized a r e a of e a s t Baltimore, has 50,000 v i s i t s a n n u a l l y to t h e a d u l t e m e r gency d e p a r t m e n t . All of the laboratory records from October 1973 to Oct o b e r 1974 for c a r b o n m o n o x i d e a n a l y s e s were e x a m i n e d . F i f t e e n of 29 a n a l y s e s w e r e p o s i t i v e for carb o x y h e m o g l o b i n (COHgb) levels over 10%. M e d i c a l records, a v a i l a b l e for 14 of the 15, were r e v i e w e d for pertin e n t clinical a n d t h e r a p e u t i c data.
RESULTS D e m o g r a p h i c d a t a for the 14 pat i e n t s (Table 1) showed only two pat i e n t s w i t h a n y h i s t o r y of p r e existing disease. Twelve patients were exposed a t work; 11 came to t h e hospital directly from t h e workplace, having developed symptoms while working within an enclosed area w i t h o u t a d e q u a t e v e n t i l a t i o n in the presence of a gasoline engine. None of the w o r k e r s understood the potent i a l h a z a r d s of t h e w o r k s i t u a t i o n . The remaining patient exposed at work was a f i r e m a n who was b r o u g h t
to the h o s p i t a l following smoke inhalation. Twelve p a t i e n t s came to the hospital via ambulance while the other two w a l k e d in. The a m b u l a n c e pat i e n t s w e r e seen p r o m p t l y while t h e w a l k - i n p a t i e n t s p r o b a b l y w a i t e d at l e a s t one h o u r before being seen. The r a n g e of t i m e b e t w e e n last exposure a n d the o b t a i n i n g of a blood sample for the c a r b o x y h e m o g l o b i n level was from 30 to 90 m i n u t e s with an avera g e of a p p r o x i m a t e l y 45 m i n u t e s . ( P a t i e n t 14 is not included in this average. See case r e p o r t below) All, except p a t i e n t 14, h a d a diagnosis of carbon monoxide intoxication m a d e in the e m e r g e n c y d e p a r t m e n t . The clinical p r e s e n t a t i o n of each of the p a t i e n t s and p e r t i n e n t p h y s i c a l f i n d i n g s ( T a b l e 2") d e p i c t c o m m o n s y m p t o m s of carbon monoxide intoxication: dizziness, h e a d a c h e , n a u s e a a n d vomiting, i r r i t a b i l i t y a n d dyspnea. The s t a t e of consciousness var i e d a s a f u n c t i o n of t h e c a r boxyhemoglobin level. The presence of commonly r e p o r t e d physical signs 3 such as c h e r r y coloration, diaphoresis a n d fever were u n u s u a l . Ten of t h e 14 were h y p e r t e n s i v e on first evaluation while only t h r e e were noted to be even m i n i m a l l y h y p e r t e n s i v e at t h e t i m e of follow-up. T a c h y c a r d i a a n d t a c h y p n e a were c o m m o n findings. T h e r e l a t i o n of t h e p a t i e n t ' s clinical s t a t e and carboxyhemoglobin levels, a d a p t e d from G r a h a m , 1 is offered for comparison (Table 3). The h e m a t o c r i t (Hct), white blood c e l l c o u n t (WBC), a r t e r i a l b l o o d
volume 5 Number 7 Page 505
Table 1 DEMOGRAPHIC CHARACTERISTICS Patient No* Sex
Age
Race
Job
Cause of Exposure
Location
Previous Diseases
Ambulance Transportation
COHgb "~ Satura- .! tion (%)
1
M
27
White
Unemployed Automobile
Suicide Attempt
Depression
Yes
38
2
M
26
Black
Stevedore
Gasoline motor
None
Yes
37
3
M
24
White
Mechanic
Garage
Gasoline motor
None
Yes
35
4
M
51
Black
Stevedore
Ship hold
Gasoline motor
None
Yes
33.8
5
M
36
Black
Stevedore
Ship hold
Gasoline motor
None
Yes
33
6
M
31
White
Stevedore
Ship hold
Gasoline motor
None
Yes
28.6
7
M
38
Black
Stevedore
Ship hold
Gasoline motor
None
Yes
27
8
M
50
White
Stevedore
Ship hold
Gasoline motor
None
Yes
26.3
9
M
52
Black
Machine operator
Industrial plant
Gasoline motor
None
No
24
10
M
39
White
Mechanic
Garage
Gasoline motor
None
No
23
11
M
29
White
Stevedore
Ship hold
Gasoline motor
None
Yes
20.5
12
M
28
White
Stevedore
Ship hold
Gasoline motor
None
Yes
20
13
M
22
White
Fireman
House fire
Smoke
None
Yes
19
1-14
F
65
Black
Disabled
Home
Gas heater
Yes
19
Ship hold
Pickwickian syndrome
*Numbered according to decreasing carboxyhemoglobin levels. lBiood taken 13 hours after exposure.
gases and electrocardiographic (EKG) i n t e r p r e t a t i o n were c o r r e l a t e d w i t h the C O H g b level (Table 4). A lower a r t e r i a l pO2 was recorded t h a n expected at sea level for all p a t i e n t s except p a t i e n t 5 who was receiving s u p p l e m e n t a r y oxygen. The specimen from p a t i e n t 2 was p r o b a b l y venous blood. The low pCO2 levels indicate h y p e r v e n t i l a t i o n . S e v e n of t h e t e n p a t i e n t s h a d n o r m a l E K G s . In t h e three abnormal recordings, there w e r e t r a n s i e n t ST s e g m e n t e l e v a t i o n s , p e r s i s t e n t n o n s p e c i f i c ST-T wave changes a n d p e r s i s t e n t inferior wall changes. P a t i e n t 7 h a d definite m y o c a r d i a l injury. All except p a t i e n t s 9 a n d 14 were t r e a t e d w i t h o x y g e n in t h e e m e r gency department. Three patients were a d m i t t e d to the i n p a t i e n t services: p a t i e n t 7 to t h e coronary care unit for t r e a t m e n t of a m y o c a r d i a l infarction; p a t i e n t 14 to the acute medical service because he had a fever of u n k n o w n etiology, and p a t i e n t 1 to the p s y c h i a t r i c service for t r e a t m e n t :of depression. P a t i e n t s 5 and 7 were : o b s e r v e d for 18 hours while receiving o x y g e n in t h e e m e r g e n c y d e p a r t !:ment. :The r e m a i n d e r w e r e t r e a t e d and o b s e r v e d for less t h a n six hours. ~Page506 V o l u m e 5 Number 7
T h r e e case p r e s e n t a t i o n s demons t r a t e the v a r i a b i l i t y of clinical presentation a n d consequences of acute carbon monoxide intoxication.
CASE REPORTS Patient Seven. A 38-year-old, previously healthy, male stevedore collapsed i n . t h e hold of a ship while l o a d i n g a u t o m o b i l e s w i t h gasolinepowered h e a v y e q u i p m e n t . P r i o r to collapsing, he h a d a headache, shortness of b r e a t h and a dry, nonproduct i v e cough, as w e l l as n a u s e a a n d vomiting. He lost consciousness and was found by o t h e r workers. W i t h i n 15 m i n u t e s he was b r o u g h t to t h e e m e r g e n c y d e p a r t m e n t where he was l e t h a r g i c a n d h y p e r v e n t i l a t i n g . On admission his t e m p e r a t u r e was 99.6 (37.5 C); b l o o d p r e s s u r e , 180/98; pulse rate, 80 b e a t s / m i n u t e and respirations, 28/minute. A r t e r i a l blood gases were pO2 = 73 m m Hg; pCOu = 20 m m Hg. A r t e r i a l pH was 7.66, and COHgb was 27% s a t u r a t i o n (Table 2 and Table 4). The p a t i e n t spent ten days in the coronary care unit. Serial EKGs showed persistent ST-T changes in leads II, III a n d AVF. Serial cardiac r e l a t e d enzymes were consistent w i t h m y o c a r d i a l injury.
The p a t i e n t developed mild hyper. t e n s i o n d u r i n g h o s p i t a l i z a t i o n that continued following discharge. Four m o n t h s a f t e r t h e i n i t i a l cardiac in-~ jury, a s u b - m a x i m a l stress test indicated the p a t i e n t h a d good functiona reserve a n d no need for l i m i t a t i o n of physical performance. C o m m e n t : C a r d i a c d a m a g e fron~ carbon monoxide intoxication in the form of p a t c h y necrosis of the heart in m a n a n d l a b o r a t o r y a n i m a l s has r e s u l t e d w h e n t h e carboxyhemogl0' bin level goes above 50%. 4-6 Schar~ r e p o r t e d a c a s e of t r a n s m u r a l m y o c a r d i a l i n f a r c t i o n in a 38-year. old c o n s t r u c t i o n w o r k e r whose car. b o x y h e m o g l o b i n level was not over 25%. O r i n i u s 8 h a s shown t h a t EKG changes were the only cardiac man. i f e s t a t i o n s i n f i v e p a t i e n t s hospitalized for carbon monoxide intoxi' cation. O u r p a t i e n t ' s subendocardial m y o c a r d i a l i n f a r c t i o n a n d subse" q u e n t n o r m a l stress t e s t would make a diagnosis of u n d e r l y i n g coronary" a r t e r y d i s e a s e u n l i k e l y . Therefore, the d a m a g e m a y h a v e been a direct effect of the carbon monoxide intoxi" cation.
P a t i e n t F o u r t e e n . This was one of July 1976 J ~ P
f
Table 2 SIGNS AND SYMPTOMS COHgb Stateof patient Satura- Conscious- DizziNo. tion (%) ness ness
Head- Nausea& IrritaSkin or Mucous ache Vomiting bility Dyspnea Membrane Color Sweating Temp
Blood Pressure
ResplraPulse tions
1
38
Lethargic
NR
NR
-
NR
NA
Norm
-
99
112/64
108
2
37
Coma
NA
NA
NA
NA
NA
Norm
-
98.6
140/110
108
NR
98.4
120/70
100
NR
NR
3
35
Alert
+
+
-
-
-
Norm
-
4
33.8
NR
+
NR
+
NR
+
Norm
-
NR
200/114
88
24
5
33
Coma
NA
NA
NA
NA
NA
NR
-
98.8
190/106
112
22
6
28.6
Alert
+
-
-
NR
+
Red
-
NR
140/90
108
20
7
27
Lethargic
+
+
+
+
+
Red
-
99.6
180/98
80
28
8
26.3
Alert
+
+
-
-
-
Norm
-
NR
180/110
112
20
9
24
Lethargic
+
+
+
-
NR
Norm
-
NR
124/74
72
18
Norm
-
98.6
170/100
92
NR
Norm
-
98.6
114/76
100
16
Norm
-
182/110
114
NR
NR
-
98
158/96
116
24
Norm
+
101.6
260/130
56
20
10
23
Alert
+
+
11
20.5
Alert
+
.
12
20
Alert
+
-
-
+
+
13
19
Alert
NR
NR
+
NR
NR
14
19
Confused
+
+
-
+
+
+ NR NA
= = = =
+ .
NR .
NR
.
NR
Present Absent Not recorded Not applicable due to conditions
Table 31 R E L A T I O N B E T W E E N THE P E R C E N T A G E OF C A R B O N M O N O X I D E IN I N S P I R E D AIR, THE P E R C E N T A G E OF H E M O G L O B I N S A T U R A T E D AIR A N D THE C L I N I C A L S T A T E COHgb Saturation (%)
CO in Air (%)
Effect
Effect
None
0-01
A l l o w a b l e 3"-4 hours
10-20
Headache?
0-04
Allowable 1 hour
20-30
T h r o b b i n g head. Giddy on e x e r t i o n
0-06
Causes effect in 1 hour
Weak, dizzy, dim vision. Nausea
0-10
U n p l e a s a n t . Not dangerous
Collapse. Pulse and r e s p i r a t i o n increase
0-15
S t u p o r . May c o n v u l s e , death known
0-4 +
0-10
30-40 40-50 50-60 60-70
Coma. D e p r e s s e d card i o v a s c u l a r system and r e s p i r a t i o n
70-80
Death likely
80 +
Death a l m o s t certain
~any a d m i s s i o n s for this 65-year-old lisabled w o m a n w i t h a h i s t o r y of Pickwickian s y n d r o m e . H e r s o n ~rought h e r to t h e e m e r g e n c y de-
•PJuly
1976
Dangerous 1 hour Fatal 1 h o u r or less
S h e c o m p l a i n e d of d i z z i n e s s , headache, i n a b i l i t y to see and shortness of b r e a t h . She was m a r k e d l y irritable. There were no new a b n o r m a l physical findings. On admission, her t e m p e r a t u r e w a s 101.6 F (38.6 C); blood pressure, 260/130; pulse rate, 56 b e a t s / m i n u t e and respirations, 20/ m i n u t e . A r t e r i a l blood g a s e s were p ( h , 47 m m H g a n d p C ( h , 37 m m Hg; a r t e r i a l p H was 7.59. WBC was 13,600 cu mm; Hct, 51%. She was a d m i t t e d to t h e acute medical service due t o h e r fever. T h i r t e e n hours after a d m i s s i o n the C O H g b was ordered and found to be 19%. After she w a s t r e a t e d w i t h o x y g e n for 24 hours, h e r C O H g b level d i m i n i s h e d to zero. By t h a t time, she h a d become afebrile a n d m e n t a l l y alert. W h e n t h e h e a l t h d e p a r t m e n t inv e s t i g a t e d h e r house t h e y discovered an inadequately vented heater, which was l a t e r repaired.
p a r t m e n t because of the acute onset of a g i t a t i o n a n d confusion. She was r e p o r t e d as h a v i n g done well u n t i l the d a y of admission.
Comment: The fact that carbon monoxide intoxication can produce a fever and leukocytosis is not widely k n o w n even t h o u g h Finck, s in a review of t h e l i t e r a t u r e , p o i n t e d out t h i s r e l a t i o n s h i p . This r e l a t i o n s h i p was r e c e n t l y e m p h a s i z e d in a r e p o r t V o l u m e 5 N u m b e r 7 Page 507
COHgb Saturation(%)
Hct
WBC
38
47
9,500
37
48
6,600
33
31
7.40 ST elevated VI-V4
35
47
9,800
77
36
7.44 Norm
33.8
53
6,100
60
28
7.40 No specific ST-T changes
5
33
49
10,400
305
37
7,46 Norm
6
28.6
NS
NS
72
23
7,57 Norm
Comment: This case represe~ t possible neurological sequelae to thl anoxia of .carbon monoxide intoxicoi tion. C e r e b r a l h e m i s p h e r e demyel][ n a t i o n w i t h o u t significant n e u r o ~ damage, u w i d e s p r e a d foci of cell d~ g e n e r a t i o n in the c e r e b r u m , cerebel) "~ lum and such s t r u c t u r e s as the bas:il ganglia, as well as focal hemorrhage~i,~/ have been r e p o r t e d as delayed effect~ ] of carbon monoxide intoxication. I~ s t u d i e s of dogs e x p o s e d to carb0~ monoxide, Lewey and Drabkin found c e r e b r a l cortical d a m a g e thai t e n d e d to follow t h e course of th~ blood vessels. B e h a v i o r impalrme~q h a s also been reported.3,13
7
27
44
6,600
73
20
7.66 Inf Wall MI, V5-6
DISCUSSION
8
26.3
46
6,400
72
32
7.44 Norm
9
24
52
10,800
NS
NS
NS
NS
10
23
NS
NS
NS
NS
NS
NS
11
20.5
45
9,900
71
29
7.45 Norm
12
20
48
7,300
101
20
7.62 Norm
13
19
NS
NS
NS
NS
14
19
51
13,600
47
37
Table 4 PERTINENT LABORATORY RESULTS Patient No.
Arterial Blood Gas Results* pO2 pCO2 pH NS NS NS
NS
EKG NS
NS
7.59 No change from previous
*All blood gas results were arterial, done on room air except patient three and patient five (see text). NS = Not Done or Stated
of a family of seven who had fever and leukocytosis in association with carbon monoxide i n t o x i c a t i o n 2 Our p a t i e n t had a fever of u n k n o w n etiology a n d a n a l t e r e d m e n t a l s t a t u s . Only the next day, when other sources for t h e fever were e l i m i n a t e d , was carbon monoxide intoxication considered. Had she had normal p u l m o n a r y v e n t i l a t o r y a n d perfusion function, she would not have had an e x c e s s i v e c a r b o x y h e m o g l o b i n level 13 hours after exposure because the h a l f t i m e for carbon monoxide excretion, b r e a t h i n g room air, is 240 to 320 minutes.3, ~° Patient F o u r . A 51-year-old, previously h e a l t h y , stevedore developed dizziness, weakness, nausea and vomiting while driving a gasoline powered forklift. The forklift was located in a r e f r i g e r a t e d space in the hold of a ship. He and four other m e n h a d been w o r k i n g for less t h a n one hour when all five developed s i m i l a r s y m p t o m s a n d were b r o u g h t to the hospital via ambulanoe.
Page 508 Volume 5 Number 7
In the e m e r g e n c y d e p a r t m e n t he c o m p l a i n e d of w e a k n e s s , dizziness, n u m b n e s s in his legs and nausea. He denied a n y h i s t o r y of h e a r t di~sease or h y p e r t e n s i o n . O n a d m i s s i o n , his blood p r e s s u r e was 200/114; pulse, 88 b e a t s / m i n u t e a n d r e s p i r a t i o n s , 24/ m i n u t e . T e m p e r a t u r e w a s n o t recorded. A r t e r i a l pO2 was 60 m m H g ; pCO2, 28 m m Hg. A r t e r i a l p H was 7.40. C O H g b s a t u r a t i o n was 33.8%. After b e i n g t r e a t e d w i t h oxygen for less t h a n one h o u r , he d e c i d e d to leave w i t h his coworkers. Two d a y s later, he r e t u r n e d comp l a i n i n g of f e e l i n g ill b u t w i t h o u t specific c o m p l a i n t s . He was m i l d l y h y p e r t e n s i v e and a p p r o p r i a t e t r e a t m e n t w a s i n i t i a t e d . W i t h i n five weeks after the exposure to carbon monoxide he developed mild congesrive h e a r t f a f l u r e , a n g i n a p e c t o r i s a n d his blood p r e s s u r e became harder to r e g u l a t e . T h r e e ~months after the i n i t i a l exposure, he had a cereb r a l v a s c u l a r accident t h a t left h i m w i t h a spastic left hemiplegia.
T
T.hree of the m o r e common sourc~ o f c a r b o n monoxide are the intera combustion engine - - especially thi automobile - - the home h e a t i n g uni] a n d the ~w a t e r h e a t e r . I n each, thl d a n g e r arises from i n a d e q u a t e venti l a t i o n of t h e e n v i r o n m e n t . Carb01 m o n o x i d e is a l s o a s s o c i a t e d wit steel production, explosives, sm0~ i n h a l a t i o n , d i s t i l l a t i o n of coal wood a n d c e r t a i n m a r s h g a s e s ) The 14 p a t i e n t s here d i s p l a y a var] ied clinical s p e c t r u m in both presenl t a t i o n a n d course in r e l a t i o n to ca: boxyhemoglobin levels. The comm~ s y m p t o m s of carbon monoxide int0x c a t i o n a r e h e a d a c h e , dizzines= n a u s e a a n d v o m i t i n g , d y s p n e a an i r r i t a b i l i t y . D i n m a n 14 s a i d th~ b a n d l i k e h e a d a c h e occurs with mir i m a l i n t o x i c a t i o n , 10% to 301 COHgb. He f u r t h e r s t a t e d t h a t th1 o t h e r s y m p t o m s w o u l d occur a1 C O H g b l e v e l s of 30% to 40%, b!l t h e r e would be no d y s p n e a at rest.I] our series dizziness and headad I were t h e m a j o r s y m p t o m s in th01 who w e r e conscious w h e n they a~ rived at t h e e m e r g e n c y departmel~J t The presence of dizziness would n1 h a v e b e e n p r e d i c t a b l e in those p~ t i e n t s w i t h COHgb less t h a n 30% u~ less w o r k exertion p l a y e d an imp0~ t a n t role. The o t h e r s y m p t o m s dli not a p p e a r to c o r r e l a t e significantl. w i t h the degree of COHgb. The syncope a n d l e t h a r g y of f0u p a t i e n t s would n o t h a v e been pre dicted from t h e i r C O H g b levels. 130tl G r a h a m ~ a n d D i n m a n ~4 suggest tb~ loss of c o n s c i o u s n e s s occurs in t~' r e s t i n g s t a t e only w i t h carboxyhe~° globin levels above 30%. Five of 0u July 1976 J ~ l
patients with disturbed states of consciousness h a d c a r b o x y h e m o g l o b i n levels r a n g i n g from 24% to 38%. A cherry p i n k color to the skin or $ucot~s m e m b r a n e s is a classic find-
ing of carbon monoxide poisoning. 3 ~Vhile Dinman14 stated t h a t a person ~vith t r a i n e d eyes c a n n o t e color changes w i t h c a r b o x y h e m o g l o b i n levels of 25% to 30%, our housestaff ~ad considerable difficulty i n identifying carbon monoxide intoxication ~y changes in color of the mucous sembranes or skin. In a n y case, the diagnosis of carbon monoxide intoxication was considered early for most patients a n d the lack of perceptable color changes did not cause the phyiician to exclude this diagnosis. One of the responses to acute stress from carbon m o n o x i d e i n t o x i c a t i o n was h y p e r v e n t i t a t i o n . The a r t e r i a l blood gas s t u d i e s d e m o n s t r a t e d a respiratory alkalosis with a relative ~ypoxia i n most cases. This would appear p r e d i c t a b l e as Aipes et a115 has shown a s m a l l decrease i n arterial pO2 as well as venous pO2 when humans were exposed to low levels of carbon monoxide (COHgb < 9%). Treatment of carbon monoxide in~0xication is predicated on i n c r e a s i n g the rate of the dissociative reaction of the c a r b o n m o n o x i d e - h e m o g l o b i n (COHgb) complex. Carbon monoxide binds to h e m o g l o b i n a p p r o x i m a t e l y 220 to 250:1 compared with oxygen. Thus, in essence, it replaces t h e oxyten. The carbon monoxide decreases ~he r e l e a s e of o x y g e n i n o x y g e n hemoglobin d i s s o c i a t i o n a n d therefore, increases the tissue hypoxia. ~4 The h a l f time of COHgb clearance ~ith n o r m a l a m b i e n t air at sea level laries from 240 to 320 m i n u t e s . 3,~° If lhe oxygen pressure is increased to I60 mm Hg, the half-time decreases to80 m i n u t e s , while at 2280 m m Hg /3atmospheres) it is only 25 minutes. Carbon m o n o x i d e
1976 •PJuly
intoxication
s h o u l d be m a n a g e d w i t h o x y g e n t h e r a p y at the highest FiO2 possible. Although hyperbaric oxygen is more rapid, most i n s t i t u t i o n s do not have the necessary facilities. Thus, a high concentration of oxygen via mask is more practical. Loeper is discussed the problems of altered physiology in chronic carbon monoxide intoxication. He contends t h a t a n excessive a m o u n t of carbon monoxide m a y persist in the blood for several weeks after exposure has ceased. The m e c h a n i s m of r e t a i n i n g carbon monoxide is not k n o w n b u t m a y be related to b i n d i n g of carbon monoxide by tissues chronically exposed to the gas. Follow-up of all p e r s o n s a c u t e l y exposed to carbon monoxide is import a n t b e c a u s e of the p o t e n t i a l late sequelae. Some of.the p a t i e n t s in this report felt weak, tired or nonspecifically ill for up to one week after exposure. Laboratory assistance i n diagnosis is important. Since 14 cases in this r e p o r t v a r y from r e p o r t e d c l i n i c a l diagnostic signs a n d symptoms, the blood c a r b o x y h e m o g l o b i n level was a n i n e x p e n s i v e a n d i m p o r t a n t adj u n c t to diagnosis. The fact t h a t 12 of the 14 cases were work-related c a n n o t b e overemphasized. Anyone working in an enclosed area with a n i n t e r n a l comb u s t i o n e n g i n e is m a r k e d for trouble unless there is adequate ventilation. Also, lack of, u n d e r s t a n d i n g about the hazards of carbon monoxide a m o n g the workers, e m p l o y e r s , i n s u r a n c e a g e n t s a n d g o v e r n m e n t safety a n d h e a l t h o f f i c i a l s as e x e m p l i f i e d i n these cases is a l a r m i n g . All of the w o r k - r e l a t e d i n c i d e n c e s were completely preventable.
REFERENCES. 1. Graham JP: The Diagnosis and Treatment of Acute Poisoning. London, Oxford
University Press, 1962, pp 191-212. 2. Harrison TR, Wintrobe MM, Beeson PB, et at: H a r r i s o n ' s Principles o f Internal Medicine, ed 7. New York, McGraw-Hill Book Co, 1974, pp 656-657. 3. Hamilton A, Hardy HL: I n d u s t r i a l Toxicology, ed 3. Massachusetts, Publishing Sciences Group Inc, 1974, pp 239-258. 4. Shafer N, Smiloy MG, MacMillian F: Primary myocardial disease in man resulting from acute carbon monoxide poisoning. A m J Med 38:316-320, 1965. 5. Anderson RF, Allensworth DC, Degroot WJ: Myocardial toxicity from carbon monoxide poisoning. A n n I n t e r n Med 67:1172-1182, 1967. 6. Orinius E: The late cardiac prognosis after acute carbon monoxide intoxication. Acta Med Scand,183:239-241, 1968. 7. Scharf SM, Thames MD, Sargent RK: Transmural myocardial infarction after exposure to carbon monoxide in coronaryartery disease. N Engl J Med 291:85-86, 1974. 8. Finck PA: Exposure to carbon monoxide: review of the literature and 567 autopsies. Milit Med 131:1513-1539, 1966. 9. Mortality and Morbidity, CDC Weekly Report: Epidemiological notes and reports. Carbon Monoxide Poisoning - - Mississippi 23:January 11, 1974. 10. Cobur RF, Forster RE, Kane PB: Consideration of the physiological variables that determine the blood carboxyhemoglobin concentration in man. J Clin I n v e s t 44:1899-1910, 1965. 11. Plum F, Posner JB, Hain RF: Delayed neurological deterioration aider anoxia. Arch Intern Med 110:56-63, 1962. 12. Lewey FH, Drabkin DL: Experimental chronic carbon monoxide poisoning in dogs. A m J Med Sci 208:502-511, 1944. 13. Gilbert GJ, Glaser GH: Neurologic manifestations of chronic carbo_nmonoxide poisoning. N E n g l J Med 261:1217-1220, 1959. 14. Dinman BD: Tb~emanagement of acute carbon monoxide intoxication.J Occup Med 16:662-664, 1974. 15. Aipes M, Mueller HS, Gregory JJ, et al: Systemic and myocardial hemodynanics response to relatively small concentration of carboxyhemoglobin. A r c h E n v i r Health 18:699-709, 1969. 16. Loeper M: Sun roxycarbonism professionell chronique. Progress Med 86:163-164. 1958.
Volume 5 Number 7 Page 509
Carbon Monoxide Intoxication: A Review of 14 Patients M. Donald Whorton, MD, MPH Berkeley, California
In 14 c a s e s o f c a r b o n m o n o x i d e p o i s o n i n g , m e d i c a l r e c o r d s w e r e available f o r r e t r o s p e c t i v e r e v i e w in w h i c h b l o o d s a m p l e s f o r c a r b o x y h e m o g l o b i n (COHgb) w e r e o b t a i n e d . T w e l v e v i c t i m s (86%) w e r e overcome w h i l e at w o r k . C o r r e l a t i o n o f the c l i n i c a l p i c t u r e and C O H g b saturation w a s not a l w a y s p o s s i b l e a l t h o u g h h y p e r t e n s i o n w a s n o t uncommon initially. On f o l l o w - u p o n l y three p a t i e n t s w e r e m i l d l y hypertensive. S k i n or m u c o u s m e m b r a n e c o l o r c h a n g e s w e r e difficult to detect. T h r e e c a s e s are p r e s e n t e d to illustrate f a c t o r s in the d i a g n o s i s and possible s e q u e l a e .
Whorton MD: Carbon monoxide intoxication: A review of 14 patients. JACEP 5:505-509, July 1976. poisoning, carbon monoxide; hypertension, carbon monoxide poisoning, clinical correlation. INTRODUCTION Carbon monoxide, an odorless, colorless a n d t a s t e l e s s toxic gas, is a product of i n c o m p l e t e c o m b u s t i o n . Every y e a r , e s p e c i a l l y d u r i n g t h e winter, t h e r e are a c c i d e n t a l d e a t h s from acute carbon monoxide intoxication due to i n a d e q u a t e v e n t i l a t i o n at home and w o r k ) A n n u a l statistics on the incidence of n o n f a t a l episodes of carbon monoxide intoxication are incomplete. 2 One y e a r ' s e x p e r i e n c e with d i a g n o s e d c a s e s of c a r b o n monoxide i n t o x i c a t i o n in a n e m e r gency d e p a r t m e n t of an u r b a n teaching h o s p i t a l is r e v i e w e d h e r e w i t h the p a t i e n t s ' clinical evaluation.
METHODS Baltimore C i t y Hospital, a 600-bed From the Division of Emergency Medieine, Baltimore City Hospitals, Baltimore, Maryland. Address for reprints: M. Donald Whorton, MD, MPH, Director, LOHP, UC-Berkeley, 2521 Channing Way, Berkeley, California 94720.
J ~ [ : ) July 1976
acute care h o s p i t a l in a n i n d u s t r i a l ized a r e a of e a s t Baltimore, has 50,000 v i s i t s a n n u a l l y to t h e a d u l t e m e r gency d e p a r t m e n t . All of the laboratory records from October 1973 to Oct o b e r 1974 for c a r b o n m o n o x i d e a n a l y s e s were e x a m i n e d . F i f t e e n of 29 a n a l y s e s w e r e p o s i t i v e for carb o x y h e m o g l o b i n (COHgb) levels over 10%. M e d i c a l records, a v a i l a b l e for 14 of the 15, were r e v i e w e d for pertin e n t clinical a n d t h e r a p e u t i c data.
RESULTS D e m o g r a p h i c d a t a for the 14 pat i e n t s (Table 1) showed only two pat i e n t s w i t h a n y h i s t o r y of p r e existing disease. Twelve patients were exposed a t work; 11 came to t h e hospital directly from t h e workplace, having developed symptoms while working within an enclosed area w i t h o u t a d e q u a t e v e n t i l a t i o n in the presence of a gasoline engine. None of the w o r k e r s understood the potent i a l h a z a r d s of t h e w o r k s i t u a t i o n . The remaining patient exposed at work was a f i r e m a n who was b r o u g h t
to the h o s p i t a l following smoke inhalation. Twelve p a t i e n t s came to the hospital via ambulance while the other two w a l k e d in. The a m b u l a n c e pat i e n t s w e r e seen p r o m p t l y while t h e w a l k - i n p a t i e n t s p r o b a b l y w a i t e d at l e a s t one h o u r before being seen. The r a n g e of t i m e b e t w e e n last exposure a n d the o b t a i n i n g of a blood sample for the c a r b o x y h e m o g l o b i n level was from 30 to 90 m i n u t e s with an avera g e of a p p r o x i m a t e l y 45 m i n u t e s . ( P a t i e n t 14 is not included in this average. See case r e p o r t below) All, except p a t i e n t 14, h a d a diagnosis of carbon monoxide intoxication m a d e in the e m e r g e n c y d e p a r t m e n t . The clinical p r e s e n t a t i o n of each of the p a t i e n t s and p e r t i n e n t p h y s i c a l f i n d i n g s ( T a b l e 2") d e p i c t c o m m o n s y m p t o m s of carbon monoxide intoxication: dizziness, h e a d a c h e , n a u s e a a n d vomiting, i r r i t a b i l i t y a n d dyspnea. The s t a t e of consciousness var i e d a s a f u n c t i o n of t h e c a r boxyhemoglobin level. The presence of commonly r e p o r t e d physical signs 3 such as c h e r r y coloration, diaphoresis a n d fever were u n u s u a l . Ten of t h e 14 were h y p e r t e n s i v e on first evaluation while only t h r e e were noted to be even m i n i m a l l y h y p e r t e n s i v e at t h e t i m e of follow-up. T a c h y c a r d i a a n d t a c h y p n e a were c o m m o n findings. T h e r e l a t i o n of t h e p a t i e n t ' s clinical s t a t e and carboxyhemoglobin levels, a d a p t e d from G r a h a m , 1 is offered for comparison (Table 3). The h e m a t o c r i t (Hct), white blood c e l l c o u n t (WBC), a r t e r i a l b l o o d
volume 5 Number 7 Page 505
Table 1 DEMOGRAPHIC CHARACTERISTICS Patient No* Sex
Age
Race
Job
Cause of Exposure
Location
Previous Diseases
Ambulance Transportation
COHgb "~ Satura- .! tion (%)
1
M
27
White
Unemployed Automobile
Suicide Attempt
Depression
Yes
38
2
M
26
Black
Stevedore
Gasoline motor
None
Yes
37
3
M
24
White
Mechanic
Garage
Gasoline motor
None
Yes
35
4
M
51
Black
Stevedore
Ship hold
Gasoline motor
None
Yes
33.8
5
M
36
Black
Stevedore
Ship hold
Gasoline motor
None
Yes
33
6
M
31
White
Stevedore
Ship hold
Gasoline motor
None
Yes
28.6
7
M
38
Black
Stevedore
Ship hold
Gasoline motor
None
Yes
27
8
M
50
White
Stevedore
Ship hold
Gasoline motor
None
Yes
26.3
9
M
52
Black
Machine operator
Industrial plant
Gasoline motor
None
No
24
10
M
39
White
Mechanic
Garage
Gasoline motor
None
No
23
11
M
29
White
Stevedore
Ship hold
Gasoline motor
None
Yes
20.5
12
M
28
White
Stevedore
Ship hold
Gasoline motor
None
Yes
20
13
M
22
White
Fireman
House fire
Smoke
None
Yes
19
1-14
F
65
Black
Disabled
Home
Gas heater
Yes
19
Ship hold
Pickwickian syndrome
*Numbered according to decreasing carboxyhemoglobin levels. lBiood taken 13 hours after exposure.
gases and electrocardiographic (EKG) i n t e r p r e t a t i o n were c o r r e l a t e d w i t h the C O H g b level (Table 4). A lower a r t e r i a l pO2 was recorded t h a n expected at sea level for all p a t i e n t s except p a t i e n t 5 who was receiving s u p p l e m e n t a r y oxygen. The specimen from p a t i e n t 2 was p r o b a b l y venous blood. The low pCO2 levels indicate h y p e r v e n t i l a t i o n . S e v e n of t h e t e n p a t i e n t s h a d n o r m a l E K G s . In t h e three abnormal recordings, there w e r e t r a n s i e n t ST s e g m e n t e l e v a t i o n s , p e r s i s t e n t n o n s p e c i f i c ST-T wave changes a n d p e r s i s t e n t inferior wall changes. P a t i e n t 7 h a d definite m y o c a r d i a l injury. All except p a t i e n t s 9 a n d 14 were t r e a t e d w i t h o x y g e n in t h e e m e r gency department. Three patients were a d m i t t e d to the i n p a t i e n t services: p a t i e n t 7 to t h e coronary care unit for t r e a t m e n t of a m y o c a r d i a l infarction; p a t i e n t 14 to the acute medical service because he had a fever of u n k n o w n etiology, and p a t i e n t 1 to the p s y c h i a t r i c service for t r e a t m e n t :of depression. P a t i e n t s 5 and 7 were : o b s e r v e d for 18 hours while receiving o x y g e n in t h e e m e r g e n c y d e p a r t !:ment. :The r e m a i n d e r w e r e t r e a t e d and o b s e r v e d for less t h a n six hours. ~Page506 V o l u m e 5 Number 7
T h r e e case p r e s e n t a t i o n s demons t r a t e the v a r i a b i l i t y of clinical presentation a n d consequences of acute carbon monoxide intoxication.
CASE REPORTS Patient Seven. A 38-year-old, previously healthy, male stevedore collapsed i n . t h e hold of a ship while l o a d i n g a u t o m o b i l e s w i t h gasolinepowered h e a v y e q u i p m e n t . P r i o r to collapsing, he h a d a headache, shortness of b r e a t h and a dry, nonproduct i v e cough, as w e l l as n a u s e a a n d vomiting. He lost consciousness and was found by o t h e r workers. W i t h i n 15 m i n u t e s he was b r o u g h t to t h e e m e r g e n c y d e p a r t m e n t where he was l e t h a r g i c a n d h y p e r v e n t i l a t i n g . On admission his t e m p e r a t u r e was 99.6 (37.5 C); b l o o d p r e s s u r e , 180/98; pulse rate, 80 b e a t s / m i n u t e and respirations, 28/minute. A r t e r i a l blood gases were pO2 = 73 m m Hg; pCOu = 20 m m Hg. A r t e r i a l pH was 7.66, and COHgb was 27% s a t u r a t i o n (Table 2 and Table 4). The p a t i e n t spent ten days in the coronary care unit. Serial EKGs showed persistent ST-T changes in leads II, III a n d AVF. Serial cardiac r e l a t e d enzymes were consistent w i t h m y o c a r d i a l injury.
The p a t i e n t developed mild hyper. t e n s i o n d u r i n g h o s p i t a l i z a t i o n that continued following discharge. Four m o n t h s a f t e r t h e i n i t i a l cardiac in-~ jury, a s u b - m a x i m a l stress test indicated the p a t i e n t h a d good functiona reserve a n d no need for l i m i t a t i o n of physical performance. C o m m e n t : C a r d i a c d a m a g e fron~ carbon monoxide intoxication in the form of p a t c h y necrosis of the heart in m a n a n d l a b o r a t o r y a n i m a l s has r e s u l t e d w h e n t h e carboxyhemogl0' bin level goes above 50%. 4-6 Schar~ r e p o r t e d a c a s e of t r a n s m u r a l m y o c a r d i a l i n f a r c t i o n in a 38-year. old c o n s t r u c t i o n w o r k e r whose car. b o x y h e m o g l o b i n level was not over 25%. O r i n i u s 8 h a s shown t h a t EKG changes were the only cardiac man. i f e s t a t i o n s i n f i v e p a t i e n t s hospitalized for carbon monoxide intoxi' cation. O u r p a t i e n t ' s subendocardial m y o c a r d i a l i n f a r c t i o n a n d subse" q u e n t n o r m a l stress t e s t would make a diagnosis of u n d e r l y i n g coronary" a r t e r y d i s e a s e u n l i k e l y . Therefore, the d a m a g e m a y h a v e been a direct effect of the carbon monoxide intoxi" cation.
P a t i e n t F o u r t e e n . This was one of July 1976 J ~ P
f
Table 2 SIGNS AND SYMPTOMS COHgb Stateof patient Satura- Conscious- DizziNo. tion (%) ness ness
Head- Nausea& IrritaSkin or Mucous ache Vomiting bility Dyspnea Membrane Color Sweating Temp
Blood Pressure
ResplraPulse tions
1
38
Lethargic
NR
NR
-
NR
NA
Norm
-
99
112/64
108
2
37
Coma
NA
NA
NA
NA
NA
Norm
-
98.6
140/110
108
NR
98.4
120/70
100
NR
NR
3
35
Alert
+
+
-
-
-
Norm
-
4
33.8
NR
+
NR
+
NR
+
Norm
-
NR
200/114
88
24
5
33
Coma
NA
NA
NA
NA
NA
NR
-
98.8
190/106
112
22
6
28.6
Alert
+
-
-
NR
+
Red
-
NR
140/90
108
20
7
27
Lethargic
+
+
+
+
+
Red
-
99.6
180/98
80
28
8
26.3
Alert
+
+
-
-
-
Norm
-
NR
180/110
112
20
9
24
Lethargic
+
+
+
-
NR
Norm
-
NR
124/74
72
18
Norm
-
98.6
170/100
92
NR
Norm
-
98.6
114/76
100
16
Norm
-
182/110
114
NR
NR
-
98
158/96
116
24
Norm
+
101.6
260/130
56
20
10
23
Alert
+
+
11
20.5
Alert
+
.
12
20
Alert
+
-
-
+
+
13
19
Alert
NR
NR
+
NR
NR
14
19
Confused
+
+
-
+
+
+ NR NA
= = = =
+ .
NR .
NR
.
NR
Present Absent Not recorded Not applicable due to conditions
Table 31 R E L A T I O N B E T W E E N THE P E R C E N T A G E OF C A R B O N M O N O X I D E IN I N S P I R E D AIR, THE P E R C E N T A G E OF H E M O G L O B I N S A T U R A T E D AIR A N D THE C L I N I C A L S T A T E COHgb Saturation (%)
CO in Air (%)
Effect
Effect
None
0-01
A l l o w a b l e 3"-4 hours
10-20
Headache?
0-04
Allowable 1 hour
20-30
T h r o b b i n g head. Giddy on e x e r t i o n
0-06
Causes effect in 1 hour
Weak, dizzy, dim vision. Nausea
0-10
U n p l e a s a n t . Not dangerous
Collapse. Pulse and r e s p i r a t i o n increase
0-15
S t u p o r . May c o n v u l s e , death known
0-4 +
0-10
30-40 40-50 50-60 60-70
Coma. D e p r e s s e d card i o v a s c u l a r system and r e s p i r a t i o n
70-80
Death likely
80 +
Death a l m o s t certain
~any a d m i s s i o n s for this 65-year-old lisabled w o m a n w i t h a h i s t o r y of Pickwickian s y n d r o m e . H e r s o n ~rought h e r to t h e e m e r g e n c y de-
•PJuly
1976
Dangerous 1 hour Fatal 1 h o u r or less
S h e c o m p l a i n e d of d i z z i n e s s , headache, i n a b i l i t y to see and shortness of b r e a t h . She was m a r k e d l y irritable. There were no new a b n o r m a l physical findings. On admission, her t e m p e r a t u r e w a s 101.6 F (38.6 C); blood pressure, 260/130; pulse rate, 56 b e a t s / m i n u t e and respirations, 20/ m i n u t e . A r t e r i a l blood g a s e s were p ( h , 47 m m H g a n d p C ( h , 37 m m Hg; a r t e r i a l p H was 7.59. WBC was 13,600 cu mm; Hct, 51%. She was a d m i t t e d to t h e acute medical service due t o h e r fever. T h i r t e e n hours after a d m i s s i o n the C O H g b was ordered and found to be 19%. After she w a s t r e a t e d w i t h o x y g e n for 24 hours, h e r C O H g b level d i m i n i s h e d to zero. By t h a t time, she h a d become afebrile a n d m e n t a l l y alert. W h e n t h e h e a l t h d e p a r t m e n t inv e s t i g a t e d h e r house t h e y discovered an inadequately vented heater, which was l a t e r repaired.
p a r t m e n t because of the acute onset of a g i t a t i o n a n d confusion. She was r e p o r t e d as h a v i n g done well u n t i l the d a y of admission.
Comment: The fact that carbon monoxide intoxication can produce a fever and leukocytosis is not widely k n o w n even t h o u g h Finck, s in a review of t h e l i t e r a t u r e , p o i n t e d out t h i s r e l a t i o n s h i p . This r e l a t i o n s h i p was r e c e n t l y e m p h a s i z e d in a r e p o r t V o l u m e 5 N u m b e r 7 Page 507
COHgb Saturation(%)
Hct
WBC
38
47
9,500
37
48
6,600
33
31
7.40 ST elevated VI-V4
35
47
9,800
77
36
7.44 Norm
33.8
53
6,100
60
28
7.40 No specific ST-T changes
5
33
49
10,400
305
37
7,46 Norm
6
28.6
NS
NS
72
23
7,57 Norm
Comment: This case represe~ t possible neurological sequelae to thl anoxia of .carbon monoxide intoxicoi tion. C e r e b r a l h e m i s p h e r e demyel][ n a t i o n w i t h o u t significant n e u r o ~ damage, u w i d e s p r e a d foci of cell d~ g e n e r a t i o n in the c e r e b r u m , cerebel) "~ lum and such s t r u c t u r e s as the bas:il ganglia, as well as focal hemorrhage~i,~/ have been r e p o r t e d as delayed effect~ ] of carbon monoxide intoxication. I~ s t u d i e s of dogs e x p o s e d to carb0~ monoxide, Lewey and Drabkin found c e r e b r a l cortical d a m a g e thai t e n d e d to follow t h e course of th~ blood vessels. B e h a v i o r impalrme~q h a s also been reported.3,13
7
27
44
6,600
73
20
7.66 Inf Wall MI, V5-6
DISCUSSION
8
26.3
46
6,400
72
32
7.44 Norm
9
24
52
10,800
NS
NS
NS
NS
10
23
NS
NS
NS
NS
NS
NS
11
20.5
45
9,900
71
29
7.45 Norm
12
20
48
7,300
101
20
7.62 Norm
13
19
NS
NS
NS
NS
14
19
51
13,600
47
37
Table 4 PERTINENT LABORATORY RESULTS Patient No.
Arterial Blood Gas Results* pO2 pCO2 pH NS NS NS
NS
EKG NS
NS
7.59 No change from previous
*All blood gas results were arterial, done on room air except patient three and patient five (see text). NS = Not Done or Stated
of a family of seven who had fever and leukocytosis in association with carbon monoxide i n t o x i c a t i o n 2 Our p a t i e n t had a fever of u n k n o w n etiology a n d a n a l t e r e d m e n t a l s t a t u s . Only the next day, when other sources for t h e fever were e l i m i n a t e d , was carbon monoxide intoxication considered. Had she had normal p u l m o n a r y v e n t i l a t o r y a n d perfusion function, she would not have had an e x c e s s i v e c a r b o x y h e m o g l o b i n level 13 hours after exposure because the h a l f t i m e for carbon monoxide excretion, b r e a t h i n g room air, is 240 to 320 minutes.3, ~° Patient F o u r . A 51-year-old, previously h e a l t h y , stevedore developed dizziness, weakness, nausea and vomiting while driving a gasoline powered forklift. The forklift was located in a r e f r i g e r a t e d space in the hold of a ship. He and four other m e n h a d been w o r k i n g for less t h a n one hour when all five developed s i m i l a r s y m p t o m s a n d were b r o u g h t to the hospital via ambulanoe.
Page 508 Volume 5 Number 7
In the e m e r g e n c y d e p a r t m e n t he c o m p l a i n e d of w e a k n e s s , dizziness, n u m b n e s s in his legs and nausea. He denied a n y h i s t o r y of h e a r t di~sease or h y p e r t e n s i o n . O n a d m i s s i o n , his blood p r e s s u r e was 200/114; pulse, 88 b e a t s / m i n u t e a n d r e s p i r a t i o n s , 24/ m i n u t e . T e m p e r a t u r e w a s n o t recorded. A r t e r i a l pO2 was 60 m m H g ; pCO2, 28 m m Hg. A r t e r i a l p H was 7.40. C O H g b s a t u r a t i o n was 33.8%. After b e i n g t r e a t e d w i t h oxygen for less t h a n one h o u r , he d e c i d e d to leave w i t h his coworkers. Two d a y s later, he r e t u r n e d comp l a i n i n g of f e e l i n g ill b u t w i t h o u t specific c o m p l a i n t s . He was m i l d l y h y p e r t e n s i v e and a p p r o p r i a t e t r e a t m e n t w a s i n i t i a t e d . W i t h i n five weeks after the exposure to carbon monoxide he developed mild congesrive h e a r t f a f l u r e , a n g i n a p e c t o r i s a n d his blood p r e s s u r e became harder to r e g u l a t e . T h r e e ~months after the i n i t i a l exposure, he had a cereb r a l v a s c u l a r accident t h a t left h i m w i t h a spastic left hemiplegia.
T
T.hree of the m o r e common sourc~ o f c a r b o n monoxide are the intera combustion engine - - especially thi automobile - - the home h e a t i n g uni] a n d the ~w a t e r h e a t e r . I n each, thl d a n g e r arises from i n a d e q u a t e venti l a t i o n of t h e e n v i r o n m e n t . Carb01 m o n o x i d e is a l s o a s s o c i a t e d wit steel production, explosives, sm0~ i n h a l a t i o n , d i s t i l l a t i o n of coal wood a n d c e r t a i n m a r s h g a s e s ) The 14 p a t i e n t s here d i s p l a y a var] ied clinical s p e c t r u m in both presenl t a t i o n a n d course in r e l a t i o n to ca: boxyhemoglobin levels. The comm~ s y m p t o m s of carbon monoxide int0x c a t i o n a r e h e a d a c h e , dizzines= n a u s e a a n d v o m i t i n g , d y s p n e a an i r r i t a b i l i t y . D i n m a n 14 s a i d th~ b a n d l i k e h e a d a c h e occurs with mir i m a l i n t o x i c a t i o n , 10% to 301 COHgb. He f u r t h e r s t a t e d t h a t th1 o t h e r s y m p t o m s w o u l d occur a1 C O H g b l e v e l s of 30% to 40%, b!l t h e r e would be no d y s p n e a at rest.I] our series dizziness and headad I were t h e m a j o r s y m p t o m s in th01 who w e r e conscious w h e n they a~ rived at t h e e m e r g e n c y departmel~J t The presence of dizziness would n1 h a v e b e e n p r e d i c t a b l e in those p~ t i e n t s w i t h COHgb less t h a n 30% u~ less w o r k exertion p l a y e d an imp0~ t a n t role. The o t h e r s y m p t o m s dli not a p p e a r to c o r r e l a t e significantl. w i t h the degree of COHgb. The syncope a n d l e t h a r g y of f0u p a t i e n t s would n o t h a v e been pre dicted from t h e i r C O H g b levels. 130tl G r a h a m ~ a n d D i n m a n ~4 suggest tb~ loss of c o n s c i o u s n e s s occurs in t~' r e s t i n g s t a t e only w i t h carboxyhe~° globin levels above 30%. Five of 0u July 1976 J ~ l
patients with disturbed states of consciousness h a d c a r b o x y h e m o g l o b i n levels r a n g i n g from 24% to 38%. A cherry p i n k color to the skin or $ucot~s m e m b r a n e s is a classic find-
ing of carbon monoxide poisoning. 3 ~Vhile Dinman14 stated t h a t a person ~vith t r a i n e d eyes c a n n o t e color changes w i t h c a r b o x y h e m o g l o b i n levels of 25% to 30%, our housestaff ~ad considerable difficulty i n identifying carbon monoxide intoxication ~y changes in color of the mucous sembranes or skin. In a n y case, the diagnosis of carbon monoxide intoxication was considered early for most patients a n d the lack of perceptable color changes did not cause the phyiician to exclude this diagnosis. One of the responses to acute stress from carbon m o n o x i d e i n t o x i c a t i o n was h y p e r v e n t i t a t i o n . The a r t e r i a l blood gas s t u d i e s d e m o n s t r a t e d a respiratory alkalosis with a relative ~ypoxia i n most cases. This would appear p r e d i c t a b l e as Aipes et a115 has shown a s m a l l decrease i n arterial pO2 as well as venous pO2 when humans were exposed to low levels of carbon monoxide (COHgb < 9%). Treatment of carbon monoxide in~0xication is predicated on i n c r e a s i n g the rate of the dissociative reaction of the c a r b o n m o n o x i d e - h e m o g l o b i n (COHgb) complex. Carbon monoxide binds to h e m o g l o b i n a p p r o x i m a t e l y 220 to 250:1 compared with oxygen. Thus, in essence, it replaces t h e oxyten. The carbon monoxide decreases ~he r e l e a s e of o x y g e n i n o x y g e n hemoglobin d i s s o c i a t i o n a n d therefore, increases the tissue hypoxia. ~4 The h a l f time of COHgb clearance ~ith n o r m a l a m b i e n t air at sea level laries from 240 to 320 m i n u t e s . 3,~° If lhe oxygen pressure is increased to I60 mm Hg, the half-time decreases to80 m i n u t e s , while at 2280 m m Hg /3atmospheres) it is only 25 minutes. Carbon m o n o x i d e
1976 •PJuly
intoxication
s h o u l d be m a n a g e d w i t h o x y g e n t h e r a p y at the highest FiO2 possible. Although hyperbaric oxygen is more rapid, most i n s t i t u t i o n s do not have the necessary facilities. Thus, a high concentration of oxygen via mask is more practical. Loeper is discussed the problems of altered physiology in chronic carbon monoxide intoxication. He contends t h a t a n excessive a m o u n t of carbon monoxide m a y persist in the blood for several weeks after exposure has ceased. The m e c h a n i s m of r e t a i n i n g carbon monoxide is not k n o w n b u t m a y be related to b i n d i n g of carbon monoxide by tissues chronically exposed to the gas. Follow-up of all p e r s o n s a c u t e l y exposed to carbon monoxide is import a n t b e c a u s e of the p o t e n t i a l late sequelae. Some of.the p a t i e n t s in this report felt weak, tired or nonspecifically ill for up to one week after exposure. Laboratory assistance i n diagnosis is important. Since 14 cases in this r e p o r t v a r y from r e p o r t e d c l i n i c a l diagnostic signs a n d symptoms, the blood c a r b o x y h e m o g l o b i n level was a n i n e x p e n s i v e a n d i m p o r t a n t adj u n c t to diagnosis. The fact t h a t 12 of the 14 cases were work-related c a n n o t b e overemphasized. Anyone working in an enclosed area with a n i n t e r n a l comb u s t i o n e n g i n e is m a r k e d for trouble unless there is adequate ventilation. Also, lack of, u n d e r s t a n d i n g about the hazards of carbon monoxide a m o n g the workers, e m p l o y e r s , i n s u r a n c e a g e n t s a n d g o v e r n m e n t safety a n d h e a l t h o f f i c i a l s as e x e m p l i f i e d i n these cases is a l a r m i n g . All of the w o r k - r e l a t e d i n c i d e n c e s were completely preventable.
REFERENCES. 1. Graham JP: The Diagnosis and Treatment of Acute Poisoning. London, Oxford
University Press, 1962, pp 191-212. 2. Harrison TR, Wintrobe MM, Beeson PB, et at: H a r r i s o n ' s Principles o f Internal Medicine, ed 7. New York, McGraw-Hill Book Co, 1974, pp 656-657. 3. Hamilton A, Hardy HL: I n d u s t r i a l Toxicology, ed 3. Massachusetts, Publishing Sciences Group Inc, 1974, pp 239-258. 4. Shafer N, Smiloy MG, MacMillian F: Primary myocardial disease in man resulting from acute carbon monoxide poisoning. A m J Med 38:316-320, 1965. 5. Anderson RF, Allensworth DC, Degroot WJ: Myocardial toxicity from carbon monoxide poisoning. A n n I n t e r n Med 67:1172-1182, 1967. 6. Orinius E: The late cardiac prognosis after acute carbon monoxide intoxication. Acta Med Scand,183:239-241, 1968. 7. Scharf SM, Thames MD, Sargent RK: Transmural myocardial infarction after exposure to carbon monoxide in coronaryartery disease. N Engl J Med 291:85-86, 1974. 8. Finck PA: Exposure to carbon monoxide: review of the literature and 567 autopsies. Milit Med 131:1513-1539, 1966. 9. Mortality and Morbidity, CDC Weekly Report: Epidemiological notes and reports. Carbon Monoxide Poisoning - - Mississippi 23:January 11, 1974. 10. Cobur RF, Forster RE, Kane PB: Consideration of the physiological variables that determine the blood carboxyhemoglobin concentration in man. J Clin I n v e s t 44:1899-1910, 1965. 11. Plum F, Posner JB, Hain RF: Delayed neurological deterioration aider anoxia. Arch Intern Med 110:56-63, 1962. 12. Lewey FH, Drabkin DL: Experimental chronic carbon monoxide poisoning in dogs. A m J Med Sci 208:502-511, 1944. 13. Gilbert GJ, Glaser GH: Neurologic manifestations of chronic carbo_nmonoxide poisoning. N E n g l J Med 261:1217-1220, 1959. 14. Dinman BD: Tb~emanagement of acute carbon monoxide intoxication.J Occup Med 16:662-664, 1974. 15. Aipes M, Mueller HS, Gregory JJ, et al: Systemic and myocardial hemodynanics response to relatively small concentration of carboxyhemoglobin. A r c h E n v i r Health 18:699-709, 1969. 16. Loeper M: Sun roxycarbonism professionell chronique. Progress Med 86:163-164. 1958.
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