Download Intravenous injection of elemental mercury in a 27-year

Intravenous injection of elemental mercury in a 27-year-old
male for excision of multiple subcutaneous foreign body
granuloma under general anesthesia
Chris Bryan V. Sembrana, M.D.
University of the Philippines – Philippine General Hospital
Abstract
A 27-year-old male self-injected elemental mercury through the intravenous route. The patient
allegedly self-injected at least twenty thermometers’ worth of elemental mercury in a span of one
year. He presented with generalized body fatigue, difficulty in position sense, distal hand
weakness, tremors, labile mood, insomnia, emotional instability and multiple subcutaneous
granulomas at the injection sites. Radiographic studies in the lungs, abdomen and extremities
showed multiple dense spherules and pinpoint opacities indicative of metallic mercury embolism.
Serum mercury levels were elevated. The patient underwent multiple hemodialysis sessions for
acute renal failure and tubular nephropathy secondary to mercury poisoning. The patient was
referred to anesthesia for excision of the granulomas. We describe and discuss the perioperative
management of this patient.
Key words: mercury embolism, mercury injection, foreign body granuloma
Introduction
Self-administration of elemental mercury is rare
but well-described in case reports. It is usually done by
those who are suicidal, those in search of well-being and
improved performance in certain activities, or those who
believe it produces protection from evil, witchcraft and
unknown diseases.1,2,3,4 Between 1923 and 2000, 78
cases of intravenous injection of elemental mercury have
been reported.1
Although various systemic
manifestations of poisoning can result from mercury
exposure, the neurologic, gastrointestinal, and renal
systems are the most commonly affected.5
Case Summary
The patient is a 27-year-old male cellphone and
computer technician who sought consultation for body
weakness. One year and 6 months prior to consultation,
the patient felt generalized fatigue and loss of appetite.
He was advised by a friend to try an underground local
community practice of injecting mercury into the blood
stream. It was alleged that this would make one stronger
and eventually have a sense of well-being. The patient
started injecting the whole amount of mercury taken
from a thermometer in both his upper and lower
extremities. This was done once or twice a month,
whenever he felt generalized fatigue. The patient
claimed that this self-injection of mercury made him
more productive at work. He continued this practice for
a year. At least twenty thermometers’ worth of mercury
was self-injected during this time.
Six months prior to consult, the patient started
taking Prednisone 40 milligrams daily as he was told
that steroids would add bulk to his body. He noted an
increase in appetite with steroid use. The patient
eventually noted facial swelling and pustular lesions all
over the trunk, chest and abdomen.
Two months prior to consult, the patient felt
burning epigastric pain with persistence of facial
swelling and pustular lesions. He also noted lethargy and
generalized body weakness.
One month prior to consult, the patient stopped
the intake of Prednisone because of high-grade fever,
headache, dizziness and inability to concentrate. He was
admitted at a local medical center but the diagnosis was
not divulged. Blood pressure spikes of 200/120 mm Hg
were noted. He was also noted to have episodes of
uncontrolled behavior. His medications during this
admission included amlodipine+telmisartan, cloxacillin,
hydrocortisone and risperidone. The family was then
advised transfer to this hospital for toxicology
management.
The patient was received at the emergency
room awake, in a depressed mood, and not in
cardiorespiratory distress. Vital signs during admission
were as follows: blood pressure of 140/90 mm Hg, heart
rate at 85 beats/min, respiratory rate at 20 breaths/min
and temperature at 37.2 degrees Celsius. Pertinent
physical examination findings included moon facies,
discolored teeth with caries, thin skin with muscle
wasting, pustular and vesicular lesions on the chest and
upper abdomen, and multiple subcutaneous granulomas
on the site of injection of mercury on the upper and
lower extremities. Neurological examination at this time
was unremarkable.
1
The admitting impression was:
mercury toxicity by intravenous injection, to
consider central nervous system, peripheral
nervous system, renal and pulmonary toxicity
 Cushing's syndrome from chronic steroid injection
 hypertension stage I
 steroid-induced gastritis
To lessen the mercury load, he was scheduled
for debridement and excision of multiple subcutaneous
granulomas secondary to mercury emboli. This was to
be followed by chelation by the toxicology service. The
patient’s condition, however, had to be optimized as he
had corresponding medical problems which needed to be
managed prior to the surgery.
On the first hospital day, he was drowsy,
uncooperative and with slow mentation. He was given
omeprazole to address his steroid-induced gastritis. He
was also given Vitamin B complex and gabapentin after
he complained of current-like pain over the torso and
numbness of the extremities. This was attributed to the
peripheral nervous system effects of mercury toxicity.
Chest X-ray showed multiple pinpoint opacities which
were distributed along the vascular supply of both lung
fields. The pulmonology service diagnosed the patient to
have pulmonary implants secondary to elemental
mercury toxicity. Extremity radiographs showed
multiple pinpoint opacities. Serum mercury level on
admission was at 67.14 µg/dL (normal < 1 µg/dL).
On the second hospital day, repeat
neurologic examination revealed difficulty in position
sense, hand weakness and inability to do tandem gait.
Weakness of the intrinsic muscles of the hand or distal
motor weakness was attributed to polyneuropathy from
mercury poisoning. Inability to do tandem gait was
attributed to possible cerebellar effects of elemental
mercury poisoning. The neurology service noted that the
treatment of the cerebellar effects and the
polyneuropathy attributed to mercury poisoning may or
may not resolve by decreasing the mercury load through
chelation and excision of the subcutaneous granulomas.
Nevertheless, it was imperative to remove the toxin to
prevent worsening of the neuropathy. Computed
tomography scan and arterial blood gas results were
unremarkable. On the same hospital day, the patient had
watery, foul-smelling, greenish stools (more than five
episodes per day), tenesmus, abdominal pain, increase in
abdominal girth and fever (39°C). Amoebic diarrhea was
entertained. Intravenous fluid replacement was started.
Paracetamol,
metronidazole,
ciprofloxacin
and
potassium correction were added to the treatment
regimen. Pertinent laboratory results showed the
following: sodium 134.7 mmol/L (normal 135-145
mmol/L), potassium 2.06 mmol/L (normal 3.0-5.0
mmol/L), creatinine 595 µmol/L (normal 53-115
µmol/L), and urine cortisol of 403.63 ng/ml (normal
103-1003 ng/ml).

Based on the clinical picture and laboratory
results, the endocrinology service made a diagnosis of
secondary adrenal insufficiency with corresponding
mineralocorticoid
deficiency
due
to
sudden
discontinuation of steroid intake. The patient was started
on prednisone. The elevated creatinine was attributed to
tubular nephropathy secondary to mercury poisoning
and dehydration from gastrointestinal losses.
On the fourth hospital day, the patient’s
random serum cortisol level was elevated at 660 ng/ml
(normal 60-230 ng/ml). Adrenal insufficiency was ruled
out and prednisone was discontinued. The creatinine
level at this time was at 820 µmol/L. Abdominal
deposits of mercury were noted on the abdominal x-ray.
The patient was also noted to have occasional tremors.
On the sixth hospital day, there was decreased
abdominal tenderness and abdominal girth. However,
the patient still had loose watery stools, non-bloody,
about five episodes per day with persistent fever
(38.9°C). Bilateral grade II ankle edema was noted. He
also had erythema and warmth at the sites of injection of
mercury. At this time, he developed non-productive
cough with crackles on the right lung base. Hospitalacquired pneumonia was entertained. Chest x-ray
showed
new
pneumonic
infiltrates.
2Dechocardiography showed probable vegetation near the
mitral valve. This was attributed to either infective
endocarditis or intracardiac granuloma secondary to
mercury emboli. Blood cultures were sent and infective
endocarditis prophylaxis was contemplated.
On the seventh hospital day, creatinine levels
(894 µmol/L) continued to increase despite adequate
hydration. Hemodialysis was done on the eighth hospital
day with post-hemodialysis creatinine at 658 µmol/L.
On the ninth hospital day, there was still
persistence of fever, loose bowel movement, crackles on
the right lung base, intermittent tremors and
hypokalemia (3.3 mmol/L). Erythema, warmth and
tenderness were still noted on the sites of mercury
injection.
Antibiotics
(metronidazole,
oxacillin,
ceftriaxone), correction of potassium and strict hydration
were continued.
On the eleventh hospital day, serum potassium
was 2.8 mmol/L and a swollen and tender abscess on the
right ankle was noted. Vancomycin was started. The
patient was anemic with a hemoglobin of 91 g/L and
hematocrit of 0.256. Repeat 2D Echocardiography did
not show the vegetation previously seen near the mitral
valve. Correction of hypokalemia continued.
The patient underwent hemodialysis on his
12th, 16th, and 19th hospital day. His condition was
optimized by correction of electrolytes, resolution of
pneumonia and diarrhea, and correction of pre-renal and
renal component of acute renal failure.
The patient was scheduled for excision of
subcutaneous foreign body granulomas on the 20th
2
hospital day. Serum mercury levels one day before
surgery was at 425 µg/dL.
The pre-operative diagnosis was:
 multiple foreign body granuloma secondary to
elemental mercury self-injection
 chronic mercury toxicity with central and
peripheral nervous system, renal and
pulmonary toxicity
 acute renal failure due to (1) acute tubular necrosis
secondary to mercury toxicity and (2) pre-renal
secondary to dehydration from gastrointestinal
losses
 Cushing’s syndrome secondary to chronic steroid
intake with secondary hypertension
The patient was classified as American Society
of Anesthesiologists (ASA) Physical Status 3,
Mallampati 1. Vital signs during the pre-operative visit
were: blood pressure of 120-140/80-90 mm Hg, heart
rate of 84-98 beats/min, respiratory rate of 22-26
breaths/min, and temperature of 36.9-37.4°C. Pertinent
physical
examination
findings
showed
pale
conjunctivae, dental caries with discoloration, moon
facies, erythematous vesicles and papules over the chest
and upper abdomen, subcutaneous granulomas on
bilateral upper and lower extremities, and an
erythematous, warm and tender right ankle.
Pertinent laboratory exams showed creatinine
473 µmol/L, sodium 141 mmol/L, potassium 4.1
mmol/L, hemoglobin 83 g/L, and hematocrit 0.241.
The anesthetic plan was to do general
endotracheal anesthesia with sevofurane, pre-medication
with midazolam, induction with fentanyl, propofol and
atracurium, and post-operative pain control with
tramadol. One unit of properly-typed and cross-matched
packed red blood cells was transfused prior to the
operation.
The patient came to the operating theater
sedated but arousable, following intravenous midazolam
premedication of 1.5 mg (0.025 mg/kg) given 30
minutes before. Vital signs were: blood pressure of
169/107 mm Hg, heart rate at 105 beats/minute,
respiratory rate at 14 breaths/minute, and temperature at
36.9°C.
Following preoxygenation with 100% oxygen,
induction was carried out with fentanyl 75 µg (1.25
µg/kg), propofol 70mg + 30 mg (1.67 mg/kg),
atracurium 30mg (0.5 mg/kg), and sevoflurane 4%. He
was intubated with an endotracheal tube size 8.0 using a
Macintosh 3 laryngoscope blade.
Surgery started 15 minutes after intubation. The
patient was maintained with Sevoflurane at 3-5 volume
percent. Oxygen saturation was maintained at 99-100%.
End-tidal carbon dioxide was maintained at 28-32 mm
Hg. Cold infusion with plain saline was done.
Temperature varied from 34-36.9°C.
The patient underwent incision and drainage of
subcutaneous foreign body granulomas. Evacuation of
all visible elemental mercury was performed. Mercury
appeared as metallic beads or pellets embedded within
or near the edges of the granulomas. Copious irrigation
with saline was done on all incision sites. Total blood
loss was 200 cc. The surgery lasted 1 hour and 25
minutes.
At the PACU, the patient was sedated but
arousable, with vital signs as follows: blood pressure of
140/96 mm Hg, heart rate at 98 beats/min, and
respiratory rate at 22 breaths/min. Post-operative pain
was controlled with tramadol. Febrile episodes were still
present with maximum temperature of 38.5°C, and lysed
by round-the-clock paracetamol. Persistence of fever
was attributed to the circulating levels of inflammatory
mediators still present in the patient.
After a stable immediate post-operative course,
he was transferred to the main wards where chelation
with DMSA (2,3-dimercaptosuccinic acid) was done.
Resolution of behavioral changes and generalized
fatigue was eventually noted. Two more sessions of
post-operative hemodialysis due to azotemia from acute
renal failure were done. Urine output was 0.5-1 cc/kg/hr
at the wards.
One week after surgery, serum mercury levels
went down to 237 µg/dL while creatinine levels were at
505 to 610 µmol/L. Two weeks after surgery and with
ongoing chelation therapy, serum mercury levels went
down to 28.5 µg/dL while creatinine levels decreased to
112-367 µmol/L.
Three days prior to discharge, mercury was no
longer detected in the serum. The patient was eventually
sent home well, stable, and in good functional capacity
after 43 days in the hospital. The discharge diagnosis
was:
 chronic mercury toxicity, non-accidental
 acute renal failure secondary to acute tubular
necrosis secondary to mercury poisoning
 Cushing’s syndrome secondary to chronic steroid
intake
Discussion
Mercury is a naturally occurring shiny and
silvery-white substance with many unique and
interesting properties. Its elemental symbol in the
periodic table is “Hg”, derived from the Greek word
“hydrargyrias,” which means "water silver." It is also
popularly known as “quicksilver” because of its color
and its ability to move quickly. Mercury is actually a
heavy metal but it is the only one on the periodic table
which exists as a liquid at room temperature. It contracts
or expands evenly and remains as a liquid over a range
of temperatures. It is very recognizable as an element of
thermometers and sphygmomanometers. Mercury is also
3
found in many industries, such as in the manufacture of
vaccines, fluorescent and mercury lamps, silver and gold
production, fungicides, batteries, electrical devices, and
barometers.5,6
Elemental mercury (e.g. in thermometers),
inorganic mercury (e.g. in antiseptics) and
organomercury (e.g. in contaminated seafood) are the
three chemical forms of mercury which can all produce
poisoning.1
Mercury enters the body through vapor
inhalation, injection, ingestion, or absorption through the
skin.5,7,8 Mercury vapors can be dangerous to breathe as
its lipid-soluble property allows for easy passage
through the alveoli into the bloodstream. Intravenous
elemental mercury injection can be considered less
harmful as compared to inhalation of mercury vapors.5
Surgery and medicine-related accidental
elemental mercury poisoning has been reported.
Ingestion of mercury from a leak in the esophageal
bougy used in Nissen fundoplication and after rupture of
the mercury-filled balloon in the Miller-Abbott tube has
been described.9 Elemental mercury embolism to the
hand was described as coming from a manometer used
in the arterial line during atrial septal defect repair.10
Signs and symptoms of mercury toxicity
involve different organ systems with the most common
involving the neurologic, gastrointestinal and renal
systems. The classic triad found in chronic toxicity are
tremors, gingivitis, and erethism. Erethism represents
neuropsychiatric symptoms which include insomnia,
memory loss, emotional instability and depression.
Acrodynia, also known as Pink disease, is also seen in
acute and chronic mercury toxicity. It presents as
erythema of the palms and soles, edema of the
extremities,
pruritus,
diaphoresis,
tachycardia,
hypertension, photophobia, irritability, anorexia and
insomnia.5 Renal manifestations include acute or chronic
renal failure from acute tubular necrosis which can be
seen as edema and elevated creatinine levels.2,11
Gastrointestinal
involvement
may
present
as
constipation and diarrhea.7 Cardiovascular symptoms
may be seen as electrocardiogram abnormalities and
chest pain while pulmonary complaints may manifest as
difficulty of breathing, pleuritic chest pain, tachypnea,
cough and hemoptysis.3,8
In the patient, noteworthy symptoms of mercury
toxicity were mainly neurologic and renal. Difficulty in
position sense, distal hand weakness, tremors, labile
mood, insomnia, and emotional instability were present.
These are consequences of central and peripheral
nervous system involvement. The patient’s tubular
nephropathy, elevated creatinine levels and edema
indicated renal involvement. The triad of tremors,
gingivitis, and erethism were all seen in the patient. He
also exhibited acrodynia to some extent as he manifested
with
bilateral
extremity
edema,
tachycardia,
hypertension, irritability and insomnia.
The rationale for the surgery was the excision
of subcutaneous foreign body granulomas in the
patient’s extremities. The development of the patient’s
granulomas may have been brought by vascular
embolism or by subcutaneous injection of elemental
mercury during attempts at intravenous injection. Other
than the subcutaneous granulomas, the patient also
developed inflammation and abscess formation of the
right ankle. Signs of inflammation – erythema (rubor),
tenderness (dolor), swelling (tumor), and warmth (calor)
– were noted around the areas of subcutaneous foreign
body granulomas as well as the right ankle.
Inflammatory responses occur when subcutaneous
deposits of elemental mercury are present. Sterile
abscess formation, swelling at the site of injection and
the extrusion of mercury globules may occur as a
consequence. Histopathologic findings of fibrosis,
granuloma formation, and presence of histiocytes
suggest a local foreign-body reaction to metallic
mercury.4
Metallic mercury in the body is easily
demonstrated by radiography either at the site of
introduction or in areas where mercury emboli are
found.2,3,4,7,8,10,12,13,14,15 Multiple dense spherules and
pinpoint opacities were seen in the patient’s lungs,
gastrointestinal tract, and extremities.
Elevated mercury levels confirms the toxicity
in the body. Normal mercury levels are considered to be
less than 1 µg/dL in the blood and less than 2 µg/dL in
the urine.5 Initial serum mercury levels during the
patient’s admission were at 67.14 µg/dL with the highest
being at 425 µg/dL.
Baseline determinations of renal function (e.g.
blood urea nitrogen, creatinine) and electrolyte levels
were initiated. The patient exhibited azotemia from
acute renal failure due to mercury toxicity during the
whole duration of admission. Azotemia was temporarily
treated with hemodialysis. Removal of the offending
agent which caused the acute renal failure through
chelation therapy and surgery was also done.
Hypokalemia especially during the first two weeks of
admission was addressed via parenteral correction.
Hemodialysis is used in severe cases of
mercury toxicity when the function of the renal system
has been compromised. The patient underwent dialysis
pre-operatively and post-operatively to treat the
azotemia. It is important to take note that hemodialysis
is not indicated to filter out mercury as this element is
distributed among erythrocytes.5 Removal or a decrease
in the load of the nephrotoxin (mercury) will slow the
worsening of renal function or even resolve the renal
failure.
DMSA (2,3-dimercaptosuccinic acid) was the
chelator of choice for mercury toxicity. Excretion of
mercury through the urinary route is enhanced during
4
chelation therapy but deposits in organs may remain.16 In
a recent case report, pulmonary dysfunction and
temporary organ abnormalities significantly improved
after initiation of chelation therapy.13 At the other end of
the spectrum, chelation may not be effective in
alleviating symptoms caused by mercury toxicity after
intravenous injection.12 To this day, the impact of
chelation therapy on the outcome of intravenous
elemental mercury injection remains equivocal but
potential benefits of this therapy on the patient still
outweigh the risks involved.
In terms of surgical treatment, local excision of
mercury is suggested especially if the lesions are
accessible as was seen in the patient who had multiple
subcutaneous foreign body granulomas. Local excision
results in a rapid fall in blood and urine mercury
levels.3,16 Early excision of mercury deposits in affected
tissues is suggested as the important treatment modality
in cases of subcutaneous mercury injection.14
Fortunately for this patient, serum mercury
levels decreased after the excision of foreign body
granulomas and chelation therapy with DMSA. More
importantly, signs and symptoms associated with
mercury toxicity subsided in the patient after both
surgical and medical treatment.
It is important to note that long-term effects of
mercury toxicity may occur. Pleuritic chest pain and
symptoms of angina can still occur eleven to fifteen
years after intravenous injecton of metallic mercury.
This has been confirmed by chest radiography and
elevated serum mercury.3,18 Long-term neurologic
effects from chronic mercury exposure from fish
consumption especially in children and pregnant women,
and vaccines has been lingering issues in the United
States.5,11 Regular follow-up and prompt consultation
upon recurrence of signs and symptoms are advised to
patients who have a history of intravenous injection of
metallic mercury.
There is scarcity of literature on anesthetic
considerations during surgery involving excision of
elemental mercury. Case reports usually deal with the
surgery done to excise subcutaneous granulomas and not
the anesthetic technique involved.4,10,14,16 A case report
in Greece reported the use of regional anesthesia for the
debridement and repeated excision of residual mercury
and granulations in the dorsum of the hand following an
accidental subcutaneous injection of mercury.15 The
wide extent of the operative sites in our patient prompted
the anesthesiologist to choose general inhalational
anesthesia.
Another potential anesthetic consideration was
the contamination of the operating theater as it poses a
risk to all operating room personnel. Inhalation of
mercury vapors or contact during surgery may
accidentally occur. This poses a risk to all operating
room personnel. Pregnant women should not be part of
the surgical team and should be kept away from rooms
where liquid mercury has been used. Harmful effects of
elemental mercury may be passed from mother to child
and may manifest as fetal brain damage or mental
retardation, incoordination, blindness, seizures, and
inability to speak.19 In this case, operating room access
was limited to male nurses, surgeons and
anesthesiologists.
Until shortly before admission, the patient had
been taking prednisone 40 mg for 6 months. He showed
the signs and symptoms of Cushing’s syndrome: moon
facies, thin and fragile skin, pustular and vesicular
lesions on the chest and upper abdomen, hypokalemia,
secondary hypertension, peptic ulcer disease, gastric
irritation, leukocytosis, steroid-induced myopathy and
weakness, and neuropsychiatric disorders (sleep
disturbances, depression). The immunosuppressive
effects of Cushing’s syndrome may have contributed to
the patient’s susceptibility to infection which was
manifested as pneumonia and infectious diarrhea.
Confirmation of Cushing’s syndrome was confirmed by
the elevated serum cortisol levels (660 ng/ml) on the 4th
hospital day. Serum and urinary cortisol are the usual
parameters to determine body levels of cortisol.
Treatment
of
glucocorticoid-induced
Cushing’s
syndrome should focus on removal of the cause and
optimization or reduction of glucocorticoid doses.20,21
Anesthetic considerations in Cushing’s
syndrome applied to the patient included management of
hypertension and optimization of intravascular fluid
volume and electrolytes. There has been no consensus as
to the anesthetic technique for surgeries involving
patients with Cushing’s syndrome. Indications for
general or regional anesthesia should be tailored to the
patient’s condition or limitations, and the requirements
of surgery.
Acute renal failure is described as a rapid
decline in glomerular filtration rate and accumulation of
the body’s nitrogen waste products. Acute renal failure
may present as azotemia (retention and elevation of
serum urea nitrogen and creatinine levels) or uremia
(clinically
manifested
multi-organ
system
derangements). Acute renal failure can be classified as
pre-renal, intrinsic renal and post-renal; depending on
the cause. In the patient, acute renal failure was brought
about by pre-renal causes (dehydration from diarrhea)
and intrinsic renal causes (mercury-induced acute
tubular nephropathy).22 This patient had to undergo
multiple dialysis sessions.
Management of anesthesia in patients with
acute renal failure entails maintenance of adequate blood
pressure and cardiac output intra-operatively.
Hypotension, hypovolemia, hypoxia and nephrotoxic
drugs should be avoided.23
Renal failure affects the pharmacokinetics of
anesthetic drugs through changes in elimination half-life
5
and protein binding. It prolongs elimination half-life by
increasing the volume of distribution or by decreasing
excretion of particular drugs. Since protein binding is
reduced during uremic stages of renal failure,
exaggerated clinical effects are manifested by highly
protein-bound free fraction of anesthetic drugs.20
Sevoflurane was used in the patient during
induction and maintenance of anesthesia. Since
inhalational agents enter and exit the body through the
pulmonary system, this class of drugs is not usually
affected by renal impairment. Although sevoflurane
produces a nephrotoxic metabolite known as
“Compound A” in animal trials, its effects on the human
kidney are not that well-studied. Clinically significant
renal damage does not accompany administration of
sevoflurane to patients with pre-existing kidney
disease.22.
Midazolam was given to the patient as premedication to induce anxiolysis. Slow plasma clearance
of midazolam in renal failure leads to prolonged effects
of midazolam; hence the reduced dose. In terms of
opioids, fentanyl was used in this patient with renal
failure because of its lack of active metabolites and short
duration of action. Propofol was the induction agent of
choice. The pharmacokinetics of propofol are unchanged
in patients with renal failure due to its extensive and
rapid hepatic metabolism into inactive metabolites.
Atracurium is strongly recommended in patients with
renal disease as it undergoes Hoffman degradation
(spontaneous non-enzymatic degradation). In this case,
the duration of action and clearance are not affected.22
Potassium is the body’s principal intracellular
ion. It influences the electrical activities of excitable
membranes such as nerves, skeletal muscles and cardiac
muscles, through maintenance of resting membrane
potentials and generation or inhibition of action
potentials. The normal range for serum potassium is 3.0
to 5.0 mEq/L.22
Hypokalemia in the patient may have been
caused by glucocorticoid excess (Cushing’s syndrome),
diarrhea, and renal tubular damage. Cushing’s syndrome
may include hypokalemia if the capacity of the body's
enzymes to inactivate cortisol is overwhelmed by
persistently elevated glucocorticoid levels. In
hypokalemic patients, the heart's electrical activity may
alter and may become susceptible to arrhythmias.
Classic electrocardiogram findings may show STsegment depression, flattened T-waves, U-waves,
tachycardia and/or ectopic beats. Cardiac dysfunction in
patients with hypokalemia is usually associated with
previous congestive cardiac failure or those in digoxin
therapy. Of primary concern to anesthesiologists
intraoperatively is the potential risk of cardiac
dysrhythmias and cardiovascular instability associated
with hypokalemia and anesthesia. Skeletal muscle
weakness may also occur with hypokalemia.22,24
The patient’s hypokalemia was primarily
managed by parenteral and oral potassium repletion. His
potassium level was optimized to the normal range prior
to surgery. Fortunately, the patient was stable intraoperatively with no incidence of cardiac dysrhythmias
and post-operatively without muscle weakness.
Conclusions
Management of mercury toxicity with coexisting Cushing’s syndrome poses a challenge because
of its multi-systemic involvement. Mercury toxicity
caused by intravenous injection can be treated by
medical chelation therapy and surgical excision of
accessible foreign body granulomas. Prompt treatment
of concomitant clinical and laboratory conditions such as
acute renal failure, infectious diarrhea, communityacquired pneumonia and hypokalemia must be
undertaken. Pre-operative optimization of the patient’s
condition is vital to reduce risks and morbidity during
the surgery proper. Inter-specialty referral and
communication are also central to the management of
these complicated cases.
In the excision of multiple foreign body
granulomas caused by metallic mercury embolism,
general anesthesia proved to be a satisfactory choice.
The use of fentanyl, propofol, atracurium and
sevoflurane in patients with acute renal failure has been
shown to be safe in patients with mercury toxicity and
Cushing's syndrome.
Recommendations
The underground practice of intravenous
injection of metallic mercury should be reported to the
Department of Health and to local health units.
Awareness campaigns about the devastating effects of
mercury poisoning and Cushing syndrome through
public health lectures, information dissemination,
community consultations, etc. is recommended
especially in communities where the practice of mercury
injection is prevalent.
Compilation of case reports by the National
Toxicology Center about mercury injection, including
details in the medical, surgical and anesthetic
management, is also recommended. It is also
recommended that the Philippine Society of
Anesthesiologists should have an accessible compilation
of case reports of interesting and rare cases of patients
undergoing surgery.
Mercury vapor inhalation or direct contact with
elemental mercury mandates the availability of
protective equipment for operating room personnel. Use
of cautery is discouraged because it accelerates
vaporization of mercury. Ideal temperature conditions
are also suggested to decrease the risk of vaporization of
mercury.
6
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3
Davey P, Benson M (1999). A young man with a heavy
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4
Prasad VL (2004). Subcutaneous Injection of Mercury:
“Warding Off Evil.” Environment and Health
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5
Diner BM, Brenner BE. Mercury Toxicity.
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