Patient
Twenty-eight years old, Female.
Chief complaint
At 15:40 on January 16, 2016, the patient visited emergency department and was presented with dyspnea accompanied by visual disturbance.
Present illness
She had a 3 months history of common cold like symptoms including cough, headache and fatigue. Her Symptoms did not differed depending on the times, day-and-night and working or not. On January 15, she worked as night shift from 21:00 to 9:00. She felt nausea and vomited once on duty. She visited a local hospital and received a blood test during on duty at 22:00. However she heard that she doesn’t have any clinical problems. She came back to work and continued to work. In the morning of January 16, she had dimmed vision shortly before she was dismissed from the work. However she thought that the symptom was caused by fatigue and just went to home. She went to sleep when she arrived home. When she waked up after 5 h, she had difficulty to breathe and chest tightness. Dyspnea was aggravated gradually. At the same time, the appearance of black curtain over the upper and lower side of visual field occurred.
Past medical history
No specific past medical history.
Social history
No specific hobby history, no specific drug history, the married state.
Smoking history
One pack × 9 years = 9 pack-years.
Alcohol history
Soju, 2 bottles per week.
Occupational history
According to the interview with her and her husband, she had worked in a semi-conductor factory which was located in Bucheon for 8 years. She quitted the job and rested for 6 months. She started working at a small factory which manufactured cell phone parts in Bucheon since September, 2015. She worked to find defected goods placing her own face toward the machine closely. She used air-gun to remove remaining solvent on aluminum plate without proper personal protectors like mask and gloves. She has worked as a shiftwork employee who inspects the finished products.
Family history
No specific family history.
Physical examination
In emergency room, initial vital signs were as follows: blood pressure 144/80 mmHg, pulse 78 beats/min, respiration 28 breaths/min, body temperature 36.1 °C, and saturation of O2 100%. Upon auscultation, clear breathing sound without rale and wheezing was heard in both lung fields. Regular heart beat without murmur was heard.
Diagnostic assessment
Her electrocardiogram indicated normal sinus rhythm. She received arterial blood gas analysis (ABGA) and pulmonary embolism computed tomography (CT) to evaluate the cause of dyspnea. The initial ABGA (pH 7.131, pCO2 10.3, pO2 132, Base excess -26, Bicarbonate 3.5) and serum electrolyte results (Na+ 138, K+ 4.7, Cl− 106, tCO2 6 mEq/L, anion gap 26) supported that she had increased anion-gap metabolic acidosis with respiratory compensation. In addition, pulmonary embolism CT was negative.
Interventions
She was immediately treated with sodium bicarbonate. Despite the continuous bicarbonate infusion, metabolic acidosis as well as her physical status was not improved. Rather, her mental status worsened to drowsiness with decreased respiration. Emergency intubation was performed immediately and she was put on a ventilator (Pressure regulated volume control (PRVC) mode: tidal volume 380 ml, respiration 8 breaths/min, fraction of inspired O2 40%, positive end-expiratory pressure 5cmH2O).
Brain magnetic resonance image (MRI) was taken to confirm a problem about respiratory control center. MRI results did not indicate respiratory control center problem. However it showed diffuse restriction in bilateral putamina, bilateral anterior insular cortices, and bilateral medial frontal cortices. It needed to rule out subtle diffusion restriction in bilateral precentral cortices. It also showed peripheral rim enhancement in bilateral putaminal lesions (Fig. 1a, b, c). Thereafter, she was admitted in intensive care unit (ICU) under the nephrology department.
Follow-up and outcomes
On January 17, she still had drowsy mental status and was assisted by mechanical ventilator to breath. Arterial blood gas analysis identified that she still had increased anion-gap metabolic acidosis (pH 7.220, pCO2 16.0, pO2 149, Base excess -20.2, Bicarbonate 6.3, Na+ 143, K+ 3.4, Cl− 113, tCO2 6 mEq/L, anion gap 24). On January 17–18, she received hemodialysis treatment once a day. This hemodialysis allowed her to recover from drowsy mental status as well as metabolic acidosis (pH 7.484, pCO2 32.5, pO2 93.8, Base excess 1.6, Bicarbonate 24.1).
On January 18, the nephrologist requested a consultation with a specialist of occupational and environmental medicine, because he heard from her family that the patient used to smell of liquor after work. The specialist of occupational and environmental medicine interviewed her about her occupational history including information of working process. She did not know that what kinds of materials she used in the factory. However, the specialist of occupational and environmental medicine suspected that this case was a work-related disease and recommended that her urinary and blood samples need to be collected to analyze exposure materials. Her blood and urinary samples were collected on January 19.
On January 19, 2016, she was transferred to general ward. She complained that she had blurred vision and failure to distinguish objects and person. Moreover, she showed binocular pupil dilatation. On January 20, 2016, she was transferred to ophthalmologist who performs a special ophthalmologic test following visual acuity test, visual field test, color vision test, fundus examination and optical coherence tomography (OCT). Her visual acuity was as follows: right (finger count 20 cm), left (finger count 30 cm). Both pupils were slightly dilated with light reflex. Isihara color vision test results were as follows: right (0/24), left (2/24). Moreover, OCT indicated that both optic nerves were edematous. She was diagnosed with toxic optic neuropathy by ophthalmologist and treated with steroid.
On January 21, 2016, the neurologist had an exam about her brain function and confirmed that she spoke abnormally quiet and acted too slow. Specific tests including mini mental state examination (MMSE), electroencephalography (EEG) and nerve conduction velocity (NCV) were taken to confirm neurologic problems. Her MMSE score was in the normal range (28/30). EEG showed diffuse symmetric theta to delta slow activities in the bilateral hemispheres, suggesting moderate to severe diffuse cerebral dysfunction, which is compatible with toxic or metabolic encephalopathy. NCV revealed no specific abnormality. She was diagnosed with toxic encephalopathy by neurologist and treated with choline alfoscerate. On January 25, 2016, she discharged to home with near complete nephrologic recovery. However other conditions such as ophthalmologic and neurologic dysfunction were not fully recovered until March 31, 2016.
Her urinary sample was analyzed to detect a concentration of methyl alcohol after the inspection of her factory confirmed that she had been exposed to 99.9% methyl alcohol in the workplace. Her urinary methyl alcohol concentration was detected as 7.632 mg/L (Biological Exposure Indices (BEI) is 15 mg/L of methyl alcohol in urine at end of shift) although 3 days had passed since she stopped work and she was treated hemodialysis twice.