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Fatal Paint Thinner Ingestion- A Case Report

Article  in  Journal of Indian Academy of Forensic Medicine · December 2016

DOI: 10.5958/0974-0848.2016.00124.X

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Pradeep Kumar Mishra Divyesh Saxena

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J Indian Acad Forensic Med. Oct. - Dec 2016, Vol. 38, No. 4 ISSN 0971-0973

Case Report

Fatal Paint Thinner Ingestion- A Case Report

1 2 3 4 4
Jitendra Singh Tomar, Pradeep Kr Mishra, Mandar Ramchandra Sane, Divyesh Saxena, Manish
Kumar

Abstract
Household poisons can cause serious damage to the health of children. Turpentine is a volatile
hydrocarbon used in polishes, solvents, paints and textile industry. It is capable of causing serious
toxicity, whether ingested or inhaled. When hydrocarbons are aspirated into the lung, they cause
chemical pneumonitis, acute respiratory distress syndrome (ARDS), and rarely pneumatoceles and
pneumothorax. We report a case of accidental ingestion of turpentine oil by a 13 year old female child
brought to SAMC and PGI, Indore, leading to aspiration pneumonitis and ultimately causing death after 6
days of hospitalization.

Key Words: Turpentine oil, Aspiration potential, Aspiration pneumonitis, Consolidations

Introduction: After 2 hours, she experienced acute

Turpentine oil is a distillate of pine gum.
Along with pine oil, it belongs to a class of
hydrocarbons called cyclic turpenes or turpene
derivatives. It is used in shoe polishes, waxes,
paints, varnishes, and insect repellents. Largely
replaced in the West with white spirit and
turpentine substitute, it is still widely used in the
developing world. Kerosene is, by far, the most
common hydrocarbon responsible for poisoning
in children in studies published from developing
countries.[1,2]
Case History
On 14/5/2014 , a 13 yr old female child
was brought to casualty with the alleged h/o
accidental paint thinner ingestion 2 days back in
the afternoon when she woke up and took few
sips of a liquid kept in the refrigerator, which
later on turned out to be turpentine oil.
Corresponding Author:
1
Assistant Professor,
FMT, Index Medical College & Research centre,
Indore, M.P
4 and she expired on 17/5/14 at 8:30pm.The
Assistant Professor,
FMT , Sukhsagar Medical College, Jabalpur
2
Professor,
3
Assisstant Professor,
5
Research Assisstant,
Department of Forensic Medicine & Toxicology, Sri
Aurobindo Medical College & P G Institute, Indore.
Email: drjitendersinghtomar @gmail.com
DOR: 14/08/2016 DOA: 31/12/2016
DOI: 0.5958/0974-0848.2016.00124.X
spasmodic abdominal pain- non radiating &
generalized. She developed difficulty in
breathing within 6 hours of ingestion. Chief
complaints at the time of admission were 2-3
episodes of vomiting, pain abdomen and fast
breathing. She was taken to a local private
hospital where she was put on ventilator & after
two days, referred to SAMC & PGI with BP-
130/90 mm of Hg, HR- 110/min, RR- 66/min,
+ +
SPO2- on ventilator- 90%, Pallor /jaundice /
-
cyanosis / edema/ lymphadenopathy. Endo-
tracheal Tube was in situ and Ryle's Tube was
also in situ. Bilateral ronchi with crepts were
heard and air entry was decreased (R>>L). She
was admitted in view of chemical pneumonitis
which she developed due to aspiration and was
treated for the same. During the course of
hospitalization patient was intubated and was
put on ventillator. Continuously she was having
fever which was not associated with chills or
rigor. She had spasmodic abdominal pain
throughout. She was treated with I/V fluids,
antibiotics, relaxants and sedatives. Despite of
all the treatment patients condition worsened
deceased was shifted to mortuary for autopsy.
Investigations-
• CBC, S. Creatinine & S. Electrolytes were
within normal limits.
• LFT - Bilirubin (T/D/I)- 5.76/1.79/3.97 mg/dL
and SGOT/SGPT- 35/99 IU/L
• Total protein/ Albumin/ Globulin – 5.37 / 2.62
/ 2.75gm/dL, INR – 1.9 IU
• Urine R/M - Alb. ++,RBC – 20-25/hpf, Pus
cells – 10-12/hpf and Epithelial Cells – 10-
12/hpf

503
J Indian Acad Forensic Med. Oct. - Dec 2016, Vol. 38, No. 4
• RT aspirate was sent for toxicological
analysis.
Test for turpentine- 2 ml. of ether
extract is evaporated to dryness on a spotting
tile. 1 drop of conc. sulphuric acid is added. A
deep reddish brown color is produced which
confirms the presence of Turpentine. (Picture 1
and 2)
Autopsy findings
Average built female child aged about
13 yrs. Greenish color fluid coming out of both
nostrils. Rigor mortis was present all over the
body. Postmortem lividity was present over back
and fixed. On internal examination, trachea
contained little amount of greenish fluid material,
similar to gastric content (picture 5). Mucosa
was congested. Right lung was collapsed with
pus present at the base (picture 3). Pus was
present on the base of left lung (picture 4).
Consolidations with signs of pneumonitis were
present in both the lungs. Stomach contained
about 50 cc of dark greenish fluid; mucosa was
congested with patchy hemorrhages at places
(picture 6). Liver was enlarged and pale. Spleen
and both the kidneys were congested. Opinion
was given as death due to cardio-respiratory
failure as a result of suspected poisoning and its
complications and viscera was preserved. Lung
and liver were sent for histopathological
examination. Histopathology of both the lungs
revealed lobar pneumonia and histopathology of
liver showed signs of necrosis (picture 7 and 8).
Discussion
Turpentine is a fluid obtained by the
distillation of resin obtained from live pine
trees.[3] There are two forms - Gum form (the
pitch obtained from living pine trees; a sticky
viscous liquid) and Oil form (a volatile liquid
obtained by steam distillation of gum turpentine).
Turpentine is composed of terpenes, mainly the
monoterpenes alpha-pinene and beta-pinene
with lesser amounts of carene, camphene,
dipentene, and terpinolene. Since turpentine is a
lipophilic substance, it accumulates in fatty
tissues.[3] It is used in perfumes, sprays,
insecticides, disinfectants, human and veterinary
medicines, preparation of shoe and furniture
polish, manufacturing of synthetic camphor and
menthol, thinner for paint and varnishes and
removing paint stains.
Mechanism of Toxicity[3]- Turpentine
is readily absorbed through the gastrointestinal
and respiratory tracts and skin. Terpenes are
oxidized by cytochrome P450, conjugated
principally with glucuronic acid in the liver, and
are excreted by the kidney.Liver microsomal
504
ISSN 0971-0973
epoxide hydrase and uridine
diphosphoglucuronosyl transferase activities
were elevated during chronic turpentine
exposures. Turpentine may be eliminated
unchanged through the lungs. Most turpentine
and its metabolites are eliminated through the
urinary tract as glucuronides. The excretory
product of turpentine has a characteristic odor of
violet. Exposure routes are throughinhalational,
ingestional, and dermal contact.
Aspiration potential of a
hydrocarbon[4]- It depends on 3 properties-
viscosity, surface tension, and volatility.
Viscosity is the tendency of a substance to resist
flow (the ability to resist stirring) which is
measured in Saybolt Seconds Universal (SSU).
The lower the viscosity (i.e. below 60 SSU), the
higher the tendency for aspiration.Surface
tension refers to the adherence of a liquid
compound along its surface (the ability to creep).
It is the result of cohesive forces generated by
the attraction between molecules (van der Waals
forces). The lower the surface tension, the
higher the tendency for aspiration. Volatility
refers to the ability of a liquid to become a gas.
The higher the volatility, the higher the tendency
for aspiration.Ingestion of turpentine products
produces a significantly lower incidence of
pneumonitis compared with petroleum
distillates.[5] Turpentine produces more GI and
CNS symptoms than a similar ingestion of a
petroleum distillate.[6]
Acute and short-term toxicity[3,7]-
Mostly ingestion of turpentine seen in children
are accidental. Exposure to a 75 ppm -irritates
the nose and throat, 175 ppm - irritates the eyes.
The lowest estimated oral dose reported to be
lethal in humans is 441 mg/ kg.
Signs and symptoms - Nausea,
vomiting, diarrhoea, abdominal pain, can also
lead to haematemesis. Aspiration lead to
coughing, choking and gasping. Bronchospasm
may develop, resulting in mismatch of
ventillation and perfusion resulting in hypoxia
and CNS depression. Hemoptysis may also
occur. Acute effects include coma and seizures.
It may produce initial euphoria, agitation,
hallucinations. Hepatic and renal damage may
be seen leading to hematuria, albuminuria,
oliguria, and dysuria and DIC can also be seen.
Myocardial injury, cardiac arrhythmias and
myoglobinuria can be seen. Parenteral injection
causes hypoxemia and non cardiogenic
pulmonary edema, cellulitis and a sterile
abscess at the injection site.[8]
Treatment[4,7,9]- Removal of
unabsorbed poison from the system,
administration of antidotes, elimination of
 J Indian Acad Forensic Med. Oct. - Dec 2016, Vol. 38, No. 4 ISSN 0971-0973

absorbed poison, symptomatic tre treatment and Conc. sulphuric acid is added to evaporated ether extract
maintenance of the patient’s general condition. If (picture 1) gives deep reddish
ish brown color (picture 2) which
turpentine is inhaled the patient should confirms turpentine
immediately be moved to fresh air. If eyes are
exposed to turpentine, the eyes should be
flushed with large amounts of water. Upon skin
exposure, the contaminated
taminated skin should be
washed with soap and water. If turpentine is
ingested victim should be given water to dilute
stomach contents. Emesis induction is C/I as it is
a risk for aspiration. After endotracheal
intubation the stomach can be emptied
emptied. No role
of prophylactic corticosteroids or prophylactic
antibiotic therapy. On the other crystalloid Right lung was collapsed (picture 3) with pus present at the
solutions must be administered judiciously. base of both the lungs (picture 3 and 4).

Prevention
Be aware of poisons in and around your
home. Take steps to protect young children from
toxic substances .Children should be taught
about the dangers of substances that contain
poison. Proper storage and labelling of all
poisonous substance used at home should be
done. Don't store household chemicals in food
containers, even if they are labelled.
Picture 5.Showing trachea with greenish fluid material,
References: similar to gastric content.
1. Lifshitz M, Sofer S, Gorodischer R.. Hydrocarbon poisoning in Picture 6.Showing
.Showing stomach containing dark greenish fluid;
children: a 5-year
year retrospective study. Wilderness Environ Med. mucosa was congested with patchy hemorrhages at places
2003;14(2):78–82.
2. Nhachi CF, Kasilo OM.. Household chemicals poisoning
admissions in Zimbabwe’s main urban centres. Hum Exp Toxi Toxicol.
1994;13(2):69-72.
3. Wexler P, Anderson B, Peyster A.. Encyclopedia of toxicology vol.
4. 2nd ed. Elsevier Inc. 2005:394-397.
4. Pillay VV.. Modern Medical Toxicology, 4th Ed. JJaypeebrothers
Medical Publishers. 2013:375.
5. Beamon RF, Siegel CJ, Landers G, Gree Green V. Hydrocarbon
ingestion in children: A six year retrospective study JACEP
1976;5:771-775.
6. Hill RM, Barer J, Hill LL, Butler CM, Harvey DJ, Horning MG MG. An
investigation of recurrent pine oil poisoning in an infant by the use of
gas chromatographic - mass spectrometric methods. J Pediatrics.
1975;87:115-118. Picture 7. Microphotograph showing lobar
7. Vij K.. Textbook of forensic medicine and toxicology, principles and pneumonia(10X).Picture 8. Microphotograph showing Liver
practice. 5th Ed. Elsevier Inc. 2012:558-559. necrosis(40X).
8. Wason S, Greiner PT.. Intravenous hydrocarbon abuse. Am J
Emerg Med. 1986;4:543-544.
9. Deoskar
oskar AS. Medicine jurisprudence, toxicology, & forensic science
for class room, investigation & court room with case laws. 3rd Ed.
New Delhi. 2014:936- 937.

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