Carbon monoxide is colorless, oolorless, tasteless and non-irritating gas produced by the incomplete combustion of carbonaceous rnaterial. It combines with hemoglobin and displaces oxygen because the affinity of hemoglobin for carbon monoxide is two hundred times greater than oxygen. Symptoma and signs of carbon monoxide poisoning include headache, nausea, vomiting, dizziness, collapse, unconsciousness, blindness, convulsion, coma and skin lesions. Recently we have observed seven patients with carbon monoxide poisoning who expressed cutaneous syrnptoms. In this work we investigated the pathogenesis of cutaneous manifestations of carbon monoxide poisoning through clinical, histologic and electronmicroscopic study. The results are summarized as follows: 1. Mental states of the patients were comatose in two, Semicomatcse in two, stuporous in two, and drowsy in one patient. In routine laboratory tests, we observed elevated blood sugar in six, elevated sorum creatinine phosphokinase in four and abnormal findings in urinalysis in all patients. 2. Cutaneous lesions were vesicobullae, plaque or swelling, erythema, gangrene and 'ulceration in order of frequency and located in the dependent areas in six caies. 3. Histopathologically, the sites of the bullae were subepidermal in four cases and intraepidermal in. one case and there was one case with ulceration. 4. In electronmicroscopic findings, secretory and ductal cells showed degenerative
Blindness ; Blood Glucose ; Carbon Monoxide Poisoning* ; Carbon Monoxide* ; Carbon* ; Coma ; Creatinine ; Dizziness ; Erythema ; Gangrene ; Headache ; Humans ; Nausea ; Oxygen ; Seizures ; Skin ; Stupor ; Ulcer ; Unconsciousness ; Urinalysis ; Vomiting

Background ; Carbon Monoxide is colorless, ordorless, highly toxic gas produced by fire and by motor vehicles and appliances which use carbon-based fuels. In Korea, since coals were the main domestic fuel for cooking and for heating the floor, many cases of carbon monoxide intoxication have occurred annually. Until now, systemic complications & clinical manifestations as well as neurologic complications following carbon monoxide poisoning have rarely been reported. METHODS: I have researched systemic complications and clinical manifestations including neurologic complications from 1986 to 1997. I reviewed retrospectively medical records of 188 admitted patients to the Yonsei Medical Center due to carbon monoxide intoxication, and analyzed them according to the neurological, cardiovascular, respiratory, urogenital, dermatological and other systems. RESULTS: 1)The number of the admitted patients due to CO intoxication to Yonsei Medical Center between 1986 and 1997 has decreased compared to that between 1976 and 1981. 2)In this study, the cause of CO intoxication were furnaces in 170 cases(93.9%), fire accidents in 2 cases(1.1%), gas boilers in 2 cases(1.1%), LPG gas in 1 case(0.55%) and propan gas in 1 case(0.55%) in order. 3)Systemic complications and clinical manifestations after CO intoxication were 167(88.8%) nervous , 59(31.4%) musculoskeletal, 56(29.8%) respiratory, 49(26%) dermatologic, 44(23.4%) cardiovascular, 30(16.0%) genitourinary and 9(4.8%) other complications. Other systemic complications as well as neurological complications were not rare. 4)The clinical manifestations of neurological complications were decreased mental status(drowsy in 57 cases(30.3%), stupor in 63 cases(33.5%), semicoma in 33 cases(17.6%), coma in 13 cases(6.9%), alert in 22 cases(11.7%), focal sign related to the stroke in 16 cases (7.4%), incontinence in 22 cases(11.7%), seizure in 4 cases(2.4%), psychiatric behavior in 4 cases(2.4%), peripheral neuropathy in 4 cases(2.4%), bracheal plexopathy in 4 cases(2.4%), and torticollis in 1 case(0.5%). Delayed neurologic sequelae were akinetic mutism in 13 cases(76.5%), mental deterioration in 6 cases(35.3%), incontinence in 6 cases(35.3%), psychiatric behavior in 3 cases(17.6%), speech disturbance in 2 cases(11.8%), involuntary movement in 2 cases(11.8%), and depression in 1 case(5.9%) in order. 5)Cardiovascular complications showed tachycardia in 47 cases(28.3%), ischemic heart disease in 34 cases(18.6%), right bundle branch block in 6 cases(3.6%), left axis deviation in 4 cases(2.4%), atrial fibrillation in 3 cases(1.8%), sinus arrhythmia in 2 cases(1.2%), premature atrial contraction in 1 case(0.6%), premature ventricular contraction in 1 case(0.6%), primary atrio-ventricular block in 1 case(0.6%), prolonged QT in 1 case(0.6%). 6)Pulmonary complications were pneumonia in 23 cases(13.1%), pulmonary edema in 22 cases(12.6%), pneumonia with pulmonary edema in 3 cases(1.7%), and atelectasis, pulmonary hemorrhage, empyema, pleurisy in each 1 case(0.6%). 7)Azotemias were 26 cases(14.2%), clinically confirmed acute renal failures were 4 cases(2%) 8)Rhabdomyolysis was not rare as 63 cases(33.5%) compared to the previous report. 9)Dermatologic complications were erythema with bullae in 21 cases(11.9%), erythema without bullae in 14 cases(7.9%), bullae only in 10 cases(5.6%), laceration in 3 cases(1.65%), and ulceration in 1 case(0.55%). Conclusion ; We must consider other systemic manifestations as well as neurological symptoms in patients with CO intoxication since those are not infrequent in Korea.
Acute Kidney Injury ; Akinetic Mutism ; Arrhythmia, Sinus ; Atrial Fibrillation ; Atrial Premature Complexes ; Axis, Cervical Vertebra ; Bundle-Branch Block ; Carbon Monoxide Poisoning ; Carbon Monoxide* ; Carbon* ; Coal ; Coma ; Cooking ; Depression ; Dyskinesias ; Empyema ; Erythema ; Fires ; Heating ; Hemorrhage ; Hot Temperature ; Humans ; Korea ; Lacerations ; Medical Records ; Motor Vehicles ; Myocardial Ischemia ; Penicillin G Benzathine ; Peripheral Nervous System Diseases ; Pleurisy ; Pneumonia ; Pulmonary Atelectasis ; Pulmonary Edema ; Retrospective Studies ; Seizures ; Stroke ; Stupor ; Tachycardia ; Torticollis ; Ulcer ; Ventricular Premature Complexes

The elongation and widening of intracranial vessels(fusiform aneurysm, ectasia) known to be related to various etiologies often causes neurologic focal signs because of the pressure on the adjacent structures and/or impaired circulation distal to ectatic vessel. We report two cases with pupil sparing ophthalmoplegia as a manifestation of carotid artery ectasia(the second case had signs of recurrent cerebrovascular attacks due to contralateral carotid artery occlusion).
Aneurysm* ; Carotid Arteries* ; Ophthalmoplegia* ; Pupil*

BACKGROUND: Presently, it is well known that there are neurological and systemic complications after carbon monox-ide (CO) intoxication. Until recently, delayed-onset movement disorders after CO intoxication were rarely reported. We analyzed 32 patients with delayed onset movement disorders after CO intoxication. METHODS: We reviewed the medical records of 242 patients admitted to the Yonsei University Medical Center from January 1986 to December 1996 due to CO intoxication. Patients were analyzed with respect to movement disorders, onset, latency, and radiological findings. RESULTS: Among the 242 patients of CO intoxication, 32 (13.2%) patients had delayed-onset movement disorders. Of these, 23 (71.9%) had parkinsonism, 5 (15.6%) had dystonia, 3 (9.4%) had chorea, and 1 (3.1%) had myoclonus. The mean age of the patients was 46.66 +/-16.91 years. Among the 4 patients with CO intoxication occuring at age 17 or younger (Childhood group), 2 had parkinsonism and 2 had focal dystonia. The mean age of the Childhood group was 1 7 . 7 5 +/-6.99 years. Among the 28 patients with CO intoxication occuring at age 18 or older (Adult group), 21 (75%) had parkinsonism, 3(10.7%) dystonia, 3(10.7%) chorea, and 1(3.6%) myoclonus. Among the 3 patients with dystonia in the Adult group, 1 had focal dystonia and 2 had segmental dystonia. The mean age of the adult group was 50.79 +/-1 3 . 4 6 years. The mean latency between CO intoxication and the onset of movement disorders was 27.20 +/-27.94 weeks in the Childhood group and 9.60 +/-14.97 weeks in the Adult group. The mean latency between CO intoxication and the onset of movement disorders was 6.44 +/-6.76 weeks in parkinsonism, 41.76 +/-27.99 weeks in dystonia, 4.0 weeks in chorea, and 8.0 weeks in myoclonus. The mean latency in dystonia was longer than in the others. Among the 23 patients who underwent brain computed tomography, 12 (52.2%) had abnormal findings. Low density lesions were found in the globus pallidus (13.0%), cerebral white matter (13.0%), and both globus pallidus and cerebral white matter (17.4%). One (14.3%) patient showed cortical atrophy while another patient showed both cortical atrophy and low density in cerebral white matter. CONCLUSIONS: The development of a delayed-onset movement disorder after CO intoxication is not rare. In our research, the radiological findings of patients with delayed-onset movement disorders after CO intoxication were inconsistant. The findings revealed no correlations with the various types of delayed-onset movement disorders.
Academic Medical Centers ; Adult ; Atrophy ; Brain ; Carbon Monoxide* ; Carbon* ; Chorea ; Dystonia ; Dystonic Disorders ; Globus Pallidus ; Humans ; Medical Records ; Movement Disorders* ; Myoclonus ; Parkinsonian Disorders

Conduction velocity of the saphenous nerve was studied antidromically. The value in 20 control subjects was 42.22 +/- 4.83 (SD) m/sec. In 7 patients with femoral neuropathy, the sensory nerve conduction in the symptomatic nerves was definitely abnormal : nerve potential was absent in 4 and conduction velocity was slow in 2. In 1 patient, a possible asymptomatic femoral neuropathy was suggested by this test. Conduction velocity of the saphenous nerve can be used as an objective diagnostic aid in femoral neuropathy, saphenous neuropathy and polyneuropathy.
Adult ; Female ; Femoral Nerve* ; Human ; Male ; Middle Age ; Neural Conduction* ; Peripheral Nervous System Diseases/physiopathology ; Thigh/innervation*

Twenty cases of peripheral neuropathy as sequelae of carbon monoxide intoxication have been analyzed clinically. The incidence of pheripheral neuropathy was 0.84% in a total of 2,360 cases and 3.64% in 549 admitted cases of carbon monoxide intoxication. The ratio of male to female was 1:1.2 (9:11). Their ages ranged from 17 to 52 years (mean 29.5 years), with a peak incidence in the 3rd decade (55%). The lower extremity was exclusively involved, and the left side was more involved than the right. Symptoms were a burning sensation, tingling sensation, shooting pain and weakness. Other associated sequelae were local swelling, acute renal failure, delayed neurologic sequelae, and Volkman's contracture in that order. Of 20 cases, 6 showed abnormal findings in the electromyogram only, and 14 were abnormal in both electro-myogram and nerve conduction velocity. Fifteen cases recoved within 3 to 6 months.
Adolescent ; Adult ; Carbon Monoxide Poisoning/complications* ; Extremities ; Female ; Human ; Male ; Middle Age ; Peripheral Nervous System Diseases/etiology*

This study was performed to observe the changes of blood sugar levels in 200 cases with acute Carbon monoxide (CO) poisoning. Successive tests of blood sugar on the day of onset and the lst, 2nd, 3rd & 4th day after anoxic insult were done in 12 patients with acute CO poisoning. In addition, to determine the derangement of thyroid function, blood levels of triiodothyronine(T3), tetraiodothyronine(T4), thyroid-stimulating hormone (TSH) were measured on the day of admission in 29 with C0 poisoning. The blood levels of T3, T4 and TSH were within normal ranges, but over two-thirds were distributed in lower range of normal mean values. This lower tendency within normal range was especially prominent in the blood level of T3. The blood level of sugar was increased, and 79.5% was higher than the upper limit of normal range. The blood levels of T3 and T4 were significantly decreased as CO exposure time period- prolonged. There was significant negative correlation between blood T3 levels and consciousness levels. Blood TSH levels were not significantly affected in acute CO poisoning. As consciousness levels were depressed and exposure time period were prolonged, blood sugar was increased. There found a rapid increase in blood sugar, followed by a abrupt dropping, and then progressive decrease to normal level over a period of 5 days after exposure to CO. In conclusion, acute CO poisoning obviously changes the thyroidal physiology. Even though blood TSH levels were variable, there was an obvious decrease in T3. The assumed CO-induced decrease in thyroid hormone secretion is seemingly not mediated by depressed TSH secretion but thyroid hormone metabolic dysfunction or extrathyroidal cotiverslon defect The alterations of blood sugar were also found to be acute and temporal which may be the result of physiologic compensation to hypoxic state caused by CO poisoning.
Blood Glucose ; Carbon Monoxide Poisoning* ; Carbon Monoxide* ; Carbon* ; Compensation and Redress ; Consciousness ; Humans ; Physiology ; Poisoning ; Reference Values ; Thyroid Gland* ; Thyroid Hormones* ; Thyrotropin

Idiopathic hypertrophic pachymeningitis is a rare inflammatory disease of unknown origin in which the recurrence is frequently observed despite an initial response to steroid therapy. Four patients, two men and two women aged 63 to 67 years, with severe headaches were evaluated by a brain MRI, and two patients were evaluated by follow up MRI receiving azathioprine therapy. All patients were given initial oral prednisolone 60mg or steroid pulse therapy followed by oral prednisolone and azathioprine therapy. Four patients improved with prednisolone but became steroid depen-dent. Azathioprine therapy permitted a reduction of the corticosteroid which may lead to clinical and radiological improvement. At present, high dose corticosteroid therapy is the treatment of choice, followed by immunosuppressive agents, such as azathioprine, if necessary. Further long-term follow-up studies of these patients are needed to clarify the outcome of this rare disease.
Azathioprine* ; Brain ; Female ; Follow-Up Studies ; Headache ; Humans ; Immunosuppressive Agents ; Magnetic Resonance Imaging ; Male ; Meningitis* ; Prednisolone ; Rare Diseases ; Recurrence

Idiopathic hypertrophic pachymeningitis is a rare inflammatory disease of unknown origin in which the recurrence is frequently observed despite an initial response to steroid therapy. Four patients, two men and two women aged 63 to 67 years, with severe headaches were evaluated by a brain MRI, and two patients were evaluated by follow up MRI receiving azathioprine therapy. All patients were given initial oral prednisolone 60mg or steroid pulse therapy followed by oral prednisolone and azathioprine therapy. Four patients improved with prednisolone but became steroid depen-dent. Azathioprine therapy permitted a reduction of the corticosteroid which may lead to clinical and radiological improvement. At present, high dose corticosteroid therapy is the treatment of choice, followed by immunosuppressive agents, such as azathioprine, if necessary. Further long-term follow-up studies of these patients are needed to clarify the outcome of this rare disease.
Azathioprine* ; Brain ; Female ; Follow-Up Studies ; Headache ; Humans ; Immunosuppressive Agents ; Magnetic Resonance Imaging ; Male ; Meningitis* ; Prednisolone ; Rare Diseases ; Recurrence

The meningitis occur within a closed anatomic space, so they have many similar clinical features and characteristic CSF abnormalities. But the temporal profile of many meningitis is distinctive from aseptic meningitis with spontaneous remission to bacterial or tuberculous meningitis with fatal outcome without treatment. Therefore early accurate differential diagnosis is required. The development of diagnostic tools and treatment, and increase of immunodeficient state and resistant pathogens have changed the distribution of main pathogens of meningitis from the past. Therefore we analyzed 241 medical records with final diagnosis as 'infectious meningitis' to evaluate the distribution of pathogens in Korea and any differential points of clinical, laboratory, and radiologic, profile according to etiology. 1. The etiologic distributions were followings, Aseptic meningitis in 100 patient(41.5%), tuberculous meningitis in 58 patients(24.1%), bacterial meningitis in 48 patients(19.9%), and fungal in 16 patients(6.6%). 2. The intense seasonal occurrence was noted in aseptic meningitis with summer. 3. Fever and headache were noted in almost all patients Altered mental status were noted in 39.6% of bacterial meningitis, 53.41% of tuberculous meningitis but not in fungal and aseptic meningitis. Meningeal irritation signs were noted in less patients(25%) with fungal meningitis but in more with aseptic, bacterial or tuberculous meningitis m 52-66.7%. Most of all focal neurologic signs were present in bacterial or tuberculous meningitis. 4. Many immunocompromized patients had fungal meningitis, three of which showed normal CSF leukocyte counts And it pointed up the importance of intensive etiologic evaluation in immunodeficient patients with clinically suspected symptoms of meningitis. 5. CSF findings at admission were following. CSF leukocytes were mean 206-258/yL in aseptic, tuberculous or fungal meningitis. But in bacterial meningitis leukocyte counts were greater than 1,000/mL in mom than half of patients. The differential counts of leukocytes were monocyte predominant except in bacterial meningitis. The reductions of CSF sugar were noted in bacterial, tuberculous, or fungal meningitis. Characteristically all patients with extremely low CSF sugar(less than 10mg/dL) had bacterial meningitis. 6. The most frequent pathologic findings in neuroimaging study were hydrocephalus(20patients: 9.1%) and meningeal enhancement(19patient,: 8.6%). Small enhancing mass(8patients: 3.6%.) and focal infarction(8patients: 3.6%) were noted less frequently. These abnormal radiologic findings were noted in 2 patients(2.0%) with aseptic meningitis, 15 patients(38.7%) with bacterial meningitis, 29 patients(50.0%) with tuberculous meningitis and 5 patients(35.7%) with fungal meningitis.
Adult* ; Diagnosis ; Diagnosis, Differential ; Fatal Outcome ; Fever ; Headache ; Humans ; Korea ; Leukocyte Count ; Leukocytes ; Medical Records ; Meningitis* ; Meningitis, Aseptic ; Meningitis, Bacterial ; Meningitis, Fungal ; Monocytes ; Neuroimaging ; Neurologic Manifestations ; Remission, Spontaneous ; Seasons ; Tuberculosis, Meningeal