Block D.1.

Emergency
Laboratory Work Report
Department of Pharmacology & Therapy
Faculty Of Medicine, Public Health, and Nursing
Universitas Gadjah Mada

Name of student : Klarissa Salma Raesita Day/Date : Tuesday, 20/09/2022

Student ID Number : 19/444290/KU/21640 Time : 12.30 PM
Group :4 Instructure : Dr. dr. Rustamadji,
M.Kes

Title : Acute Poisoning and Its Antidote

Results :
 Animal’s weight = 0.750 kg
 Cyanide Dose (0.25%) = 3.75 mg = 1.5 mL
 Na-thiosulfate dose (10%) = 187.5 mg = 1.875mL

Organs are observed Before Administration of Cyanide Administration of Na-

administra thiosulfate
tion of
cyanide
5’ 10’ 15’ 20’ 25’ 30’ 5’ 10’ 15’ 20’ 25’ 30'

Ear + -
Cyanosis Mouth +++ -
Nose ++ -
Respiration Abdominal 130 140 125
frequency Thoracal 125 135 120
Heart rate 140 155 140
Salivation - ++ Minim

Tremor - + -
Convultion - + -

Reflexes Right eye - +/- +

Cornea
Left eye - +/- +

Right Bright 0.5 cm 0.51 0.5

Pupil Diameter eye Light
Dim 0.5 cm 0.51 0.5
Light
Left Bright 0.5 cm 0.6 0.5
eye Light
Dim 0.5 cm 0.61 0.5
Light
 Questions

1. What is poison and poisoning? Clarify!

Poison is a substance that can have negative effects on a person when the
circumstances are right. From the Greek word "Toxicon" which means poison
are several kinds of chemical substances which in small amounts are capable
of producing reactions that damage biological systems, are capable of
destroying life, or fatally injure functions. Most toxins include exposure to
medical drugs, chemicals, plants, foods, or cosmetics. Drugs, vitamins,
pesticides, pollutants, and proteins all fall under the category of "substance,"
which is nearly often identical with "chemical." Even radioactive material is
harmful. Most radiations are produced by radioisotopes, which are chemicals
even though they are not typically thought of as "chemicals." In the previous
sentence, the phrase "adverse effects" referred to the harm, such as tissue
structural damage. The dosage of the chemical required to produce these
unwanted effects is referred to as "appropriate conditions." The dosage theory
is crucial because it states that even a substance as harmless as water can be
harmful if consumed in excess. The dose determines whether a drug functions
as a therapy or a poison.

Poisoning in general is a condition in which a person is not acceptable either

medically or socially, due to being under the influence of exogenous
substances in doses that are too high for the person concerned; exposure to
toxins in the body that results in a health-damaging response. A person who is
poisoned by a substance can experience signs and symptoms that vary,
depending on the type of substance, dose, and duration of exposure to the
substance. Poisoning involves four elements, including: (1) the poison
substance itself, (2) the organism exposed to the poison, (3) injury to cells, (4)
signs and symptoms or even death. The cause, subject, effect, and
consequence of poisoning are represented by the four elements. When an
organism is exposed to a poisonous chemical, poisoning occurs. The cell will
be harmed if these compounds build up inside of it, disrupting both its
structure and function. Clinically significant clinical signs of impaired cell
function can possibly result in mortality.

References:
Mayo Clinic Staff (2018). Poisoning: First aid. [online] Mayo Clinic. Available at:
https://www.mayoclinic.org/first-aid/first-aid-poisoning/basics/art-20056657.
Poison | biochemistry. (2019). In: Encyclopædia Britannica. [online] Available at:
https://www.britannica.com/science/poison-biochemistry.
www.poison.org. (n.d.). What is a poison and what is Poison Control? [online]
Available at: https://www.poison.org/what-is-a-poison-and-what-is-an-overdose.
2. Clarify the differences of clasification of poisoning!

 Classification based on origin

Animal, plant, microbial, and synthetic sources can all produce poisons.
Microscopic organisms like bacteria and fungi produce microbial toxins. For
instance, the bacteria Clostridium botulinum produces the botulinus toxin, which
can cause weakness and paralysis when consumed in undercooked, nonacidic
canned foods or other foods contaminated with the spores. The belladonna alkaloid
hyoscyamine, which is present in belladonna (Atropa belladonna) and jimsonweed,
is an illustration of a plant toxin (Datura stramonium). Animal poison is typically
spread by the bites and stings of venomous terrestrial or aquatic creatures, the
former of which includes deadly snakes, scorpions, spiders, and ants, and the latter
of which includes sea snakes, stingrays, and jellyfish. The majority of poisonings
are caused by synthetic poisons. Chemicals purified from natural sources, such as
metals from ores and solvents from petroleum, as well as chemicals created by
chemists, such as pharmaceuticals and insecticides, are both referred to as
"synthetic." Pesticides, home cleansers, cosmetics, drugs, and hydrocarbons are
examples of synthetic poisons.

 Classification based on physical form

The exposure and absorbability of a chemical are influenced by its physical state,
which might be solid, liquid, gas, vapour, or aerosol.

Solids must be dissolved in the aqueous fluids lining the intestinal tract if they are
consumed or the respiratory tract if they are inhaled because solids are often not
well absorbed into the blood. However, the rate at which solids dissolve in liquids
varies. Granules of lead, for instance, are practically benign when consumed
compared to lead sulphate granules because elemental lead is essentially insoluble
in water while lead sulphate is slightly soluble and absorbable. Due to variations in
dissolution rates, even different-sized granules of the same chemical might exhibit
distinct relative toxicities. For instance, because the smaller granules dissolve more
quickly, arsenic trioxide in smaller form is more dangerous than the same mass of
bigger granules.

A poison that is liquid can be ingested, inhaled, or absorbed via the skin. Vapours,
which are the gas phase of compounds that are liquids at room temperature and
atmospheric pressure, as well as poisons that are gases at room temperature (for
example, carbon monoxide) are absorbed mostly through breathing (e.g., benzene).
Inhalation of organic vapours is more frequent because organic liquids are more
volatile than inorganic liquids. Although most vapours are absorbed in the lungs,
some vapours (like furfural), which are extremely soluble in lipids, can also be
absorbed via the skin.

Aerosols are solid or liquid particles that are tiny enough to float in the air for a
short period of time. Dust and fibers are both solid aerosols. When aerosols are
inhaled or deposited on the skin, aerosol exposures take place. The toxicity of
aerosols is typically greater in the lungs than on the skin. Asbestos is an illustration
of a hazardous fiber that can result in a rare type of lung cancer (mesothelioma).

Although very volatile liquids, like benzene, are rarely found in liquid aerosol
form, many liquid toxins can. A fairly volatile liquid poison is capable of existing
as a vapour and an aerosol. Only aerosolized liquid compounds with low volatility
are airborne.

 Classification based on chemical nature

Chemical properties such as metallic versus nonmetallic, organic versus inorganic,

and acidic versus alkaline can be used to categorize poisons. When exposed
repeatedly, metallic poisons are more likely to be poisonous since they are
frequently removed from the body slowly and accumulate more than nonmetallic
poisons. In general, organic compounds may flow through lipid-rich cell
membranes more easily than inorganic chemicals because they are more soluble in
lipids. Because of this, organic substances tend to be absorbed more thoroughly
than inorganic ones. While both acids and alkalis are corrosive to the eyes, skin,
and digestive system, classification based on acidity is important since alkalis
typically penetrate the tissue more deeply than acids do and likely to cause more
serious tissue damage.

 Classification based on chemical activity

The nucleophilic (nucleus-loving) regions of the cell's macromolecules, such as

deoxyribonucleic acid (DNA), are attacked by electrophilic (electron-loving)
substances, resulting in mutations, malignancies, and deformities. Additionally,
poisons can be categorized based on how well they can mimic the structure of
specific vital cell molecules. In chemical reactions, they replace the molecules of
the cells, disturbing crucial biological processes. For instance, methotrexate
interferes with the production of DNA and ribonucleic acid (RNA).

 Other classifications

First, it can be based on the severity of poisoning, according to the Poisoning

Severity Score divided into several groups: (1) None: no symptoms or signs related
to poisoning (2) Minor: mild symptoms, temporary, and symptoms subside
spontaneously (3) Moderate : prolonged symptoms (4) Severe: exhibits severe or
life-threatening symptoms (5) Fatal: causes death

Second, based on how it occurs: (1) Intentional self poisoning, trying to consume a
substance/poison with the aim of harming oneself. (2) accidental poisoning;
consume the substance/poison without knowing its toxic effect. (3) Heavy Metal
poisoning, poisoning that occurs due to intake of As, Pb, Hg or Fe salts causing
toxic effects (4) Poisoning due to drug dependence; An unmeasured/uncontrolled
increase in dose can result in a fatal overdose. (5) Homicidal poisoning. (6)
Cyanide poisoning: This poisoning occurs by inhalation of fumes of hydrocyanic
acid (HCN) or inorganic cyanide salts.

Third, based on the duration of the poisoning process: (1) acute poisoning; (single
exposure) symptoms of poisoning appear quickly after ingestion or contact with
toxic (but often reversible) substances, such as food poisoning, cyanide and
insecticides. (2) Chronic poisoning; there is repeated exposure to poison but
symptoms appear for a relatively long time so that the victim is often unconscious
of poisoning. Chronic poisonings that often occur include bromide, salicylate,
phenytoin and digitalis poisoning because they are not monitored. Often it is
irreversible.

References:
Cornell University. Toxicity. (2022). Available at: Cornell.edu.
https://ehs.cornell.edu/book/export/html/138
Curtis D. Klaassen. (2013). Casarett and Doull's toxicology : the basic science of poisons,
8th ed. New York :McGraw-Hill Education
Uges, D.R.A., 2001. What is the definition of a poisoning? Journal of Clinical Forensic
Medicine 8, 30–33. https://doi.org/10.1054/jcfm.2000.0465

3. Clarify the relationship of supportive therapy with the target site of toxic
substance!

Handling cases of poisoning of a substance, of course if possible anamnesis

(whether the patient if possible, family/relatives, witnesses) and physical
examination to identify the poisoned patient. Primary assessment Airway
(oropahryngeal or nasopharyngeal airway), Breathing (nasal prong or face
mask with effort or intubation and mechanical ventilation), Circulation
(inotrope) remains the first priority. However, the general management of
these cases is anticipatory and supportive; The majority of patients who
present with poisoning need supportive therapy to recover. Supportive
measures including mechanical ventilation and circulatory support will allow
the survival of most viable patients on arrival at the hospital. The overall
management plan is to provide supportive care, prevent toxin absorption, use
antidotes wherever indicated, and improve elimination techniques. In
poisoned patients, diagnostic evaluation and therapeutic intervention are often
initiated simultaneously.

Again, the importance of assessing the airway, breathing and circulation

cannot be overemphasized. If the airway can be protected, active charcoal
may be indicated to reduce absorption if the patient presents within 1 hour of
ingesting the poison. Whole bowel irrigation is rarely performed and
sometimes endoscopic removal may be indicated for body stuffers. Urgent
surgery may be required for body stuffers and/or body packers and these cases
should be discussed with the surgeon early. For every patient treated with
poisoning first, their vitals must be stabilized.

For any acute problems, such as in the case of patients with convulsions due to
endosulfan poisoning, antiepileptic drugs should be given. All patients should
be given gastric lavage (except for corrosive poisoning with sulfuric acid,
kerosene, paraffin and diesel). All patients regardless of the time of venom
intake should be given active charcoal to prevent absorption of the drug and
MgSO4 (magnesium sulfate) to increase motility and accelerate excretion.
Supportive therapy and initial management need to be carried out as soon as
possible without waiting for the results of toxicological screening. Back again,
history and physical examination of toxic syndrome to start supportive therapy
/ initial management.

Supportive therapy:

1. Airway management
Loss of protective airway reflexes and concern about aspiration or respiratory
failure determine the need to secure the airway in a poisoned patient. Rapid
sequence intubation (RSI) with preoxygenation and neuromuscular blockade
is the best approach to secure the airway, except in patients who are near
death. Delayed sequence intubation (DSI) can be used as an alternative
method to RSI, which consists of administering a sedative that does not blunt
the airway reflex, followed by a brief preoxygenation period prior to paralytic
administration.

2. Respiratory support
Some toxins can interfere with oxygenation and ventilation. Therefore,
respiratory adequacy should be assessed as soon as the airway is secured.
When determining ventilator settings, lung protection strategies should be
used to prevent the development of ARDS from barotrauma and oxygen
toxicity. However, this strategy has not been studied in poisoned patients.
 3. Circulation and Hemodynamics
In poisoned patients, the most common cardiovascular abnormalities seen are
hypertension, hypotension, cardiac arrhythmias, or conduction disturbances.
The most common cause of elevated blood pressure is benzodiazepine or
ethanol withdrawal; discontinuation of therapeutically prescribed drugs, such
as clonidine or minoxidil; leading to rebound hypertension and untreated
underlying hypertension.

Fluid resuscitation of poisoned patients should be done individually. Initial

resuscitation includes intravenous crystalloid fluids (if indicated); Vasopressor
infusion should be started as early as possible during resuscitation. In
distributive shock or cardiogenic shock, administration of vasopressors or
inotropes (noradrenaline) is more appropriate than fluid administration.
Nonadrenergic vasoactive drugs are effective therapy for shock caused by
adrenergic blocking agents and calcium channel antagonists.

A 5–10 mg glucagon dose given intravenously over 10 minutes should be

followed by a glucagon infusion (3–15 mg/hour). Antiemetics should be given
with glucagon because of the effect of decreasing lower esophageal tone,
causing emesis. In addition to glucagon, high-dose insulin euglycemia (HIE)
therapy is used to treat the toxicity of adrenergic-blocking agents and calcium
channel antagonists.

Although the majority of cases of patients experiencing poisoning can be

treated with standard supportive care. However, in some circumstances,
special therapy or antidotes may be required.

References:

Chandran, J., Krishna, B. (2019). Initial Management of Poisoned Patient. Indian

J Crit Care Med; 23(Suppl 4):S234–S240. doi: 10.5005/jp-journals-10071-
23307.
FK-KMK UGM. (2022). Student Book Blok D.1 Emergency. Yogyakarta: FK-
KMK UGM.
Klaassen, C., D., and Watkins, J., B. (2010). Casarett & Doull's essentials of
toxicology. McGraw-Hill Medical Pub. Division.
Tarlok, S., Amit, S., Shina, P., Sourabh, K. and Shalini, D., 2015. Introduction to
poisoning-A systematic review. Int J Pharm Teach Pract, 6(4), pp.2609-19.

4. In observing the cyanosis, what happened with the mucous membrane of

nose, mouth and ear of the laboratory animal in this experiment? Why?

Around the nose, mouth, and ears of the guinea pig, there is a blue color
 change in the mucosal layer. The ability to bind iron ions is what carbon
monoxide (CO) and cyanide (CN) have in common; but where CO interferes
with the ability of erythrocytes to transfer oxygen, cyanide binds to
erythrocytes but does not affect oxygen transfer. Cyanide primarily blocks the
mitochondrial respiratory chain and inhibits the formation of intracellular
adenosine triphosphate (ATP). Cyanide inhibits cytochrome oxidase, causing
electron transport in the mitochondria to not occur and a decrease in oxygen
utilization in cells (histotoxic hypoxia). The result is cytotoxic hypoxia caused
by inhibition of CCO (Cytochrome c oxidase) by the high affinity of CN to
heme a3 of the enzyme. The effect is structural changes and decreased
enzyme activity and increased lactate production resulting in metabolic
acidosis.

References:

Adeyinka, A., & Kondamudi, N,.P. (2022). Cyanosis. In: StatPearls [Internet].
Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK482247/
Carlson, M. P. & Bruce, A., (2013). Cyanide Poisoning. Available from:
https://extensionpublications.unl.edu/assets/pdf/g2184.pdf
Graham J, Traylor J. Cyanide Toxicity. [Updated 2022 Feb 17]. In: StatPearls
[Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available
from: https://www.ncbi.nlm.nih.gov/books/NBK507796/

5. What will be happened with the respiration, heart rate, pupil size and reflexes
after the administration of cyanide? Why?

The clinical manifestations of cyanide poisoning can be divided into early and
late categories. Early clinical signs and symptoms, such as: dizziness,
headache, confusion, mydriasis, nausea, vomiting, tachypnea, tachycardia,
anxiety, and feeling weak can already be caused by exposure to small
amounts of cyanide; and these symptoms may appear within minutes of
exposure. This is due to tissue hypoxia; the occurrence of direct stimulation of
chemo receptors of the carotid body and aorta by the CN. Cyanide will also
stimulate nociceptors, causing a brief sensation of dryness and burning in the
nose and throat. Then, if the body is exposed to large amounts of cyanide, the
clinical manifestations caused are more severe, such as: convulsions
(convulsions), loss of consciousness, hypotension, lung damage, bradycardia,
and respiratory failure.

Early manifestations are mainly due to disorders of the central nervous

system, including headache, confusion, and mydriasis (tissue hypoxia). If this
hypoxic condition continues to progress and does not get treatment, the
 patient will experience a decrease / loss of consciousness. Early
manifestations that occur in the cardiorespiratory system include tachypnea
and tachycardia. If not treated immediately, the patient will experience apnea,
hypotension, and arrhythmias; and even if the patient has tissue hypoxia, the
skin color may appear normal or slightly gray. In the case of cyanide
intoxication, keep in mind that the patient may not appear cyanotic, but rather
appear cherry red in color. This is due to the inability of cells to utilize O2 so
that O2 levels in the circulation become high.

In addition, after cyanide ingestion, there is an increase in respiratory rate,

pulse rate, and pupillary dilation. This process is caused by histotoxic hypoxia
associated with the effects of cyanide poisoning. This happens because
cyanide will attach to the ferric ion cytochrome oxidase and inhibit electron
transport so that oxygen in the body cannot be used by tissues and the tissues
undergo anaerobic metabolism. Furthermore, the lactic acid produced will
cause metabolic acidosis which is detected by central and peripheral
chemoreceptors. The signal is then relayed to the respiratory center in the
trunk cerebri and the body will hyperventilate which causes tachypnea.
Meanwhile, the process of tachycardia can be caused by a signaling
mechanism from cells that do not get enough oxygen. The active sympathetic
nervous response will also release various catecholamine neurotransmitters
which result in increased heart rate, increased blood pressure, mydriasis and
bronchodilation.

References:
ATSDR (2006). TOXICOLOGICAL PROFILE FOR CYANIDE. [online] Available at:
https://www.atsdr.cdc.gov/toxprofiles/tp8.pdf.
Graham, J. and Traylor, J. (2018). Cyanide Toxicity. [online] Nih.gov. Available at:
https://www.ncbi.nlm.nih.gov/books/NBK507796/.
www.cdc.gov. (2018). CDC - The Emergency Response Safety and Health Database:
Systemic Agent: POTASSIUM CYANIDE - NIOSH. [online] Available at:
https://www.cdc.gov/niosh/ershdb/emergencyresponsecard_29750037.html.

6. What is the potential source of cyanide substance?

Natural compounds found in some foods and in some plants, such cassava,
limabeans, and almonds, produce cyanide. Common fruit pits and seeds, like
those from peaches, apricots, and apples, may contain significant levels of
compounds that can be converted to cyanide. These compounds are present in
considerably lower concentrations in the edible sections of these plants.

Cigarette smoke and the byproducts of the combustion of synthetic goods, such
plastics, contain cyanide. When something burns, it releases compounds called
combustion products.

The production of paper, textiles, and plastics all involve cyanide. The
chemicals
used to develop pictures include it. In metallurgy, cyanide salts are employed
for
electroplating, metal cleaning, and the extraction of gold from its source.
Cyanide
gas is used to exterminate pests and vermin in ships and buildings.

Other sources can be found, such as Laetrile, as a chemotherapy drug that is

still used in some countries, but is prohibited from use in the US by the Food
and Drug Administration for. Laetrile is another name for amygdalin, aka the
pure form of natural cyanide compounds. Amygdalin is a cyanogenic
glucoside, a sugar compound with cyanide attached. When laetrile is
administered intravenously, it is excreted unchanged in the urine, and cyanide
toxicity is not a significant concern. However, when this product is ingested,
the b-glucosidase enzyme in the digestive tract metabolizes amygdalin to
hydrogen cyanide, resulting in toxicity.

Lastly, nitrile, is a form of cyanide found in solvents and glue removers;

Acetonitrile and propioninitrile are the most commonly encountered nitriles.
Then metabolized to cyanide in the liver, acetonitrile is the active ingredient in
 artificial nail removal and has been linked to cases of cyanide poisoning.

References:
Gracia, R. and Shepherd, G. (2004). Cyanide poisoning and its treatment.
Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy,
24(10), pp.1358-1365.
Jaszczak, E., Polkowska, Ż., Narkowicz, S. and Namieśnik, J. (2017). Cyanides in the
environment—analysis—problems and challenges. Environmental Science and
Pollution Research, [online] 24(19), pp.15929–15948. doi:10.1007/s11356-017-9081-
7.

7. What is the mechanism of cyanide toxicity?

In ships and structures, cyanide gas is used to eradicate pests and rodents.
Cyanide-ion-containing substances are poisonous right away because they
stop cells from breathing. Cytochrome oxidase, a vital enzyme in the
respiratory chain, is combined with trivalent iron to produce the fundamental
impact of cyanide activity. Combining these two causes lactic acid synthesis
to increase and the intracellular respiratory system to be blocked. It is
important to keep in mind that the CN ions also inhibit the following
enzymes: glutamate decarboxylase, xanthine oxidase, superoxide dismutase,
NO synthase, and nitrite reductase, even though blocking cytochrome oxidase
has the greatest impact. By oxidizing lipids, cyanide ions can directly harm
the neurological system. The brain and heart muscle, which have the fastest
oxygen metabolism, are the tissues most susceptible to the harmful effects of
cyanides, but hypoxia affects how all body cell’s function.

References:
Emergency.cdc.gov. (2019). CDC | Facts About Cyanide. [online] Available at:
https://emergency.cdc.gov/agent/cyanide/basics/facts.asp#:~:text=Cyanide%20is
 %20released%20from%20natural.
Jaszczak, E., Polkowska, Ż., Narkowicz, S. and Namieśnik, J. (2017). Cyanides in the
environment—analysis—problems and challenges. Environmental Science and
Pollution Research, [online] 24(19), pp.15929–15948. doi:10.1007/s11356-017-9081-
7.
www.cdc.gov. (2018). CDC - The Emergency Response Safety and Health Database:
Systemic Agent: POTASSIUM CYANIDE - NIOSH. [online] Available at:
https://www.cdc.gov/niosh/ershdb/emergencyresponsecard_29750037.html.

8. What are the antidotes of cyanide toxicity? How are their mechanism?

Severe cyanide poisoning is treated with dicobalt edetate. However, because

dicobalt edetate itself is also toxic (and is associated with anaphylactic
reactions) so alternatively, sodium nitrite or sodium thiosulfate can be given.
They all need to be stored in places where there is a risk of cyanide poisoning,
such as factories and laboratories; other than for hospital emergencies. The
differential diagnosis for acute cyanide poisoning is relatively small, and
antidotes must be administered empirically. It is important to administer an
antidote even when the patient's condition appears fatal.

 Dicobalt edetate: chelates cyanide to cobalticanide. However, this

antidote was not approved by the FDA because of its toxicity (this
antidote is still found in Pionas)

 Sodium nitrite: Sodium nitrite is given intravenously and increases

methemoglobin by about 8-20%. In children, the dose of sodium
nitrite should be adjusted based on the hemoglobin level. Cyanide
binds to methemoglobin iron more than cytochrome iron in
mitochondria. It is known that increased amounts of cyanide are
transferred to the extracellular space as well as released from the
cytochromes, allowing mitochondria to reactivate electron
transport.

Dosage: by intravenous injection for 5-20 minutes (as sodium nitrite injection
30 mg/mL), 300 mg (children 4-10 mg/kg bw) followed by sodium thiosulfate
12.5 grams (as sodium thiosulfate injection 500 mg/mL ) by intravenous
injection for 10 minutes (children 400 mg/kg bw).

Side effects: red face and headache due to vasodilation. These effects can be
problematic, especially if they are exacerbated by a cogestant or a pre-existing
medical condition. It is recommended to avoid nitrite in victims of smoke
inhalation because of the risk of exacerbating the oxygen-carrying capacity
deficit.
  Sodium thiosulfate: This antidote enhances cyanide clearance by
acting as a sulfhydryl donor. The thiosulfate combines reversibly with
cyanide in the extracellular space to form a thiocyanate which is
minimally toxic and is excreted via the kidneys. This can enhance the
mitochondrial sulfurtransferase reaction. The effectiveness of sodium
thiosulfate as an antidote is limited by its delayed onset of action, short
half-life, and small volume of distribution. However, in inhalation of
fumes suspected of containing cyanide, sodium thiosulfate may be
administered without nitrite therapy.

Dosage: same as sodium nitrite

Side effects: The only significant adverse reactions were infrequent

hypersensitivity reactions and hypotension that depended on the rate of
infusion. However, chronic exposure to thiocyanates can cause toxicity
because thiocyanate and cyanide are in balance. The visible effects of acute
treatment of cyanide exposure are almost non-existent, but must be borne in
mind. It is important to note that thiocyanate toxicity can be found in renal
insufficiency, but can be dialyzed

References:
Meillier, A. and Heller, C. (2015). Acute Cyanide Poisoning: Hydroxocobalamin and
Sodium Thiosulfate Treatments with Two Outcomes following One Exposure Event. Case
Reports in Medicine, 2015, pp.1–4. doi:10.1155/2015/217951.
‌
www.osha.gov. (n.d.). Cyanide Antidotes | Occupational Safety and Health Administration.
[online] Available at: https://www.osha.gov/laws-regs/standardinterpretations/2020-03-31.