695472
case-report2017
SCO0010.1177/2050313X17695472SAGE Open Medical Case ReportsSmiechowicz et al.
SAGE Open Medical Case Reports
Case Report
Occupational mercury vapour
poisoning with a respiratory failure,
pneumomediastinum and severe
quadriparesis
SAGE Open Medical Case Reports
Volume 5: 1­–4
© The Author(s) 2017
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https://doi.org/10.1177/2050313X17695472
DOI: 10.1177/2050313X17695472
journals.sagepub.com/home/sco
Jakub Smiechowicz1, Anna Skoczynska2, Agata Nieckula-Szwarc1,
Katarzyna Kulpa1 and Andrzej Kübler1
Abstract
Objectives: Despite restrictions, mercury continues to pose a health concern. Mercury has the ability to deposit in most
parts of the body and can cause a wide range of unspecific symptoms leading to diagnostic mistakes.
Methods and results: We report the case of severe mercury vapour poisoning after occupational exposure in a chloralkali
plant worker that resulted in life-threatening respiratory failure, pneumomediastinum and quadriparesis.
Conclusions: Prolonged mechanical ventilation and treatment with penicillamine and spironolactone was used with
successful outcome.
Keywords
Mercury poisoning, occupational exposure, mediastinal emphysema, respiratory insufficiency, polyneuropathies,
hyperhidrosis
Date received: 8 September 2016; accepted: 30 January 2017
Introduction
Metallic mercury is liquid at room temperature and easily
transforms to vapour. When inhaled, mercury vapour is well
absorbed through the lungs and distributes to all tissues. In
the bloodstream, most of elemental mercury is oxidized to an
ionic form, which binds to sulphur-containing amino acids
and interferes with the function of sulfhydryl enzymes leading to disruption of metabolic cellular functions.1–3
According to the Minamata Convention on Mercury
established in 2013 and European Community regulations,
occupational exposure to mercury should be restricted.4 This
applies particularly to chloralkali plants where metallic mercury was employed in electrodes in the electrolytic production of chlorine and sodium hydroxide.5 Unfortunately,
during the period of transition to mercury-free technology,
chemical plant workers could still be exposed to mercury
vapour.
Case report
A 31-year-old man, who had been working for 2 months in
chloralkali mercury electrolysis plant, developed signs and
symptoms of fatigue, dizziness, profuse sweating, tremor of
hands and calves, burning and freezing sensations in the feet
followed by maculopapular rash on the extremities and body.
He was diagnosed and treated by a family doctor, an occupational medicine physician, and hospitalized for 4 days in a
regional hospital, where elevated liver transaminases, an
enlarged liver and nonsignificant hyponatremia were found
(Table 1). The consulting toxicology specialist excluded
acute mercury vapour poisoning.
After 2 months of the onset of symptoms, he was admitted
to the university hospital with dizziness, tremor, ataxia, dysarthria, dysphagia, urinary and stool retention, diminished
1Department
of Anaesthesiology and Intensive Therapy, Wroclaw Medical
University, Wroclaw, Poland
2Department and Clinic of Internal and Occupational Diseases and
Hypertension, Wroclaw Medical University, Wroclaw, Poland
Corresponding Author:
Jakub Smiechowicz, Department of Anaesthesiology and Intensive
Therapy, Wroclaw Medical University, Borowska 213, 50-556 Wroclaw,
Poland.
Email: [email protected]
Creative Commons Non Commercial CC-BY-NC: This article is distributed under the terms of the Creative Commons AttributionNonCommercial 3.0 License (http://www.creativecommons.org/licenses/by-nc/3.0/) which permits non-commercial use, reproduction
and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages
(https://us.sagepub.com/en-us/nam/open-access-at-sage).
2
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Table 1. Laboratory data obtained on admittance to the general
hospital and the university hospital.
Aspartate transaminase (U/L)
Alanine transaminase (U/L)
Bilirubin (µmol/L)
Creatinine (µmol/L)
Hgb (g/L)
Hct (%)
WBC (109/L)
PLT (109/L)
C-reactive protein (mg/L)
Sodium (mmol/L)
General
hospital
University
hospital
151
120
14.7
69
158
46.4
14.5
367
1.3
134.6
62
96
15
64.5
151
43.3
14.9
361
0.92
126
Table 2. Neuro-diagnostic tests performed during the hospital
stay.
Test
The result
Brain CT
Brain MRI
Normal
Areas of increased signal intensity in the
pyramidal tract from the precentral gyri
to midbrain, otherwise normal
Low-voltage activity, groups of theta
waves bilaterally
Polyradiculoneuropathy, predominantly
motor and demyelinating
Severe mixed sensory motor
polyneuropathy, largely axonal, segmental
demyelination
Almost complete recovery of nerve
conduction in the upper limbs, persistent
severe mixed polyneuropathy in the
lower limbs
Protein 209 mg/dL; pleocytosis 0.33/µL
EEG
EMG I (day 5)
EMG II (day 81)
EMG III (day 168)
Hgb: haemoglobin; Hct: haematocrit; WBC: white blood cell; PLT: platelet.
deep tendon reflexes and hyponatremia (126 mmol/L). His
previous medical history was unremarkable, and he denied
tobacco, alcohol or illicit drug use. Encephalopathy and polyradiculoneuropathy of unknown aetiology were diagnosed; a
urine sample for mercury test was sent to a certified laboratory and extensive neuro-diagnostic tests were performed
(Table 2).
Due to the progression of symptoms: increased extremity
paresthesias with burning sensation of the soles, peripheral
facial nerve neuropathy and progressive lower extremity
weakness, antiviral, antibiotic and intravenous immunoglobulin treatment was used. On the 28th day of hospitalization, acute respiratory failure developed; the patient was
intubated and mechanical ventilation was started. At this
time, the result of the urine mercury level test (317.2 µg/L,
normal values < 5 µg/L) was received from the laboratory
(Table 3) and chelation therapy with penicillamine 250 mg
every 6 h was started. The patient was transferred to the
intensive care unit (ICU) and treatments with continuous
venovenous hemodiafiltration for 9 days and 2,3-dimercaptopropane-1-sulfonate (DMPS) 250 mg intravenously every
12 h for 4 days were added in hope of increasing the rate of
mercury elimination.
On admission to the ICU, crackles of subcutaneous
emphysema were palpable on the neck, and pneumomediastinum was detected on the chest X-ray (Figure 1). The
finding was confirmed by a computed tomography (CT)
scan which showed an 8-mm wide pneumomediastinum,
subcutaneous emphysema of the neck together with atelectasis and consolidation in the lower segments of the left lung
(Figure 2).
A subsequent endoscopic examination revealed thick,
purulent secretions in the bronchi with no signs of damage to
the bronchi or oesophagus. Mechanical ventilation was used
for almost 5 months before he was successfully weaned off
the ventilator. A control CT scan performed 2 weeks later
showed complete resolution of the air from the mediastinum
and neck and progression of pneumonia in the left lung.
Septic shock developed and multiresistant Acinetobacter
CSF (day 7)
CT: computed tomography; MRI: magnetic resonance imaging; EEG: electroencephalogram; EMG: electromyography; CSF: cerebrospinal fluid.
Table 3. Urine mercury concentration in the course of
treatment (the atomic absorption spectrometry method,
reference values <5 µg/L).
Day in hospital
Urine Hg (µg/L)
8
317.2
32
145.1
57
35.8
65
27.8
136
5.1
Figure 1. Plain chest X-ray showing linear air lucency on the left
border of mediastinum (arrows) and subcutaneous emphysema in
the supraclavicular area and the neck.
baumannii was cultured from tracheal secretions. Limb
weakness progressed to almost complete tetraplegia, and
flaccid paralysis remained unchanged for the next 3.5
months. Only moderate movements of the head and the
shoulder girdle and slight flexion of the fingers of the right
hand were preserved. He suffered from persistent diarrhoea,
3
Smiechowicz et al.
Figure 2. (a) Axial and (b) coronal CT scans demonstrating pneumomediastinum and subcutaneous emphysema in the neck (arrows).
recurrent Pseudomonas urinary tract infections and the formation of multiple urinary calculi. Drenching sweats resulted
in profound hypovolemia with an incident of transient loss of
consciousness.
After 3 months in the ICU, intravenous spironolactone
was added to the penicillamine treatment. After 3 weeks, the
tetraplegia began to subside, and soon he was able to move
all his extremities and stand by the bedside with the assistance. He was also weaned off the ventilator, and the tracheostomy tube was removed. The electromyography (EMG)
showed significant improvement in the function of the
peripheral nerves of the arms with persistent severe polyneuropathy in lower extremities. The mercury urine concentration decreased to normal level. Upon return to normal
gastrointestinal and urinary functioning, he was discharged
home after 196 days of hospitalization.
Discussion
Our patient developed clinical manifestations of sub-acute
mercury poisoning after being exposed to liquid mercury
when cleaning workplace facilities and an electrolysis bath
in the chloralkali plant. The possibility of dangerous exposure is easy to overlook as elemental mercury vapour is
odourless, heavier than air and has a tendency to accumulate
in poorly ventilated or low-lying areas.6
Mercury can cause a wide range of unspecific symptoms.
Initial symptoms of mercury poisoning may mimic a viral
illness7 and can lead to diagnostic mistakes.3 Due to the nonspecific signs and symptoms presented by our patient, the
diagnosis of mercury poisoning was delayed until a high
mercury concentration in the urine became apparent. The
mercury concentration in the urine (317.2 µg/L) significantly
exceeded the maximum accepted level for occupational
exposure (<30 µg/L), and values >300 µg/L are usually associated with overt symptoms of poisoning.2
Initial complaints of our patient were mainly attributed to
central and peripheral nervous system toxicity. Our patient
had electromyographic signs of mixed sensorimotor polyneuropathy that progressed to severe quadriparesis. A similar
case of quadriparesis was described by Chu et al.8 in a man,
after prolonged ingestion of herb drugs containing mercuric
sulphate. Their patient remained quadriparetic with only
minor improvement after a 2-year follow-up. However, signs
of polyneuropathy in our patient subsided after 5 months of
treatment, and he returned later to normal activity.
Acute massive exposure to vaporized elemental mercury
results in the rapid appearance of pulmonary symptoms, with
dyspnoea, cough, chest pain, fever, chills and a metallic taste
in the mouth.1,2,9 Diffuse pulmonary infiltrates, acute respiratory distress syndrome (ARDS), pneumonia, fibrosis, chemical pneumonitis, bronchiolitis and pneumothorax often
resulting in death has been described.10–13 Prolonged exposure results in signs and symptoms in other organs, notably
from the central nervous system and kidneys and also the
peripheral nerves, immune system, endocrine system, muscles and skin.3
The respiratory manifestations in the form of pneumomediastinum, pneumonia and respiratory failure developed in
our patient after only several weeks from exposure and were
not typical for mercury intoxication. Most cases of pneumothorax and pneumomediastinum in the course of mercury
vapour poisoning have been reported in children12,14,15 and
very few in adults.16
Signs of autonomic dysfunction in our patient were manifested by tachycardia, profuse sweating, diarrhoea and
abdominal pain. Some of those signs are presumed to be the
effect of the inhibition of catecholamine degradation by
mercury.7,17
The mainstay of treatment of mercury poisoning is chelation therapy. Penicillamine was used in our patient for almost
6 months. Based on sparse reports suggesting the ability to
restore impaired metabolism,18 spironolactone was added
to the penicillamine therapy. Spironolactone administration
coincided with the sudden improvement of neurological
function that ensued 3 weeks later.
4
To conclude, we hereby presented a case of mercury
vapour poisoning after occupational exposure resulting in
prolonged respiratory failure, pneumomediastinum and
quadriparesis with excellent outcome. Insidious onset and
non-specific clinical manifestations of mercury poisoning
can lead to diagnostic mistakes. Physicians should be aware
of mercury vapour poisoning especially after occupational
exposure.
Acknowledgements
The authors are pleased to acknowledge the Department of Radiology
for provision and interpretation of diagnostic imaging results.
Declaration of conflicting interests
The author(s) declared no potential conflicts of interest with respect
to the research, authorship and/or publication of this article.
Funding
The author(s) received no financial support for the research, authorship and/or publication of this article.
Informed consent
Written informed consent was obtained from the patient for the
publication of this case report.
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