Case Report

Acute Massive Rhabdomyolysis Due to Inhalation of

LPG
S Prasad*, Ruchi Singh**, Rajesh Manocha***, M Narang****, BD Sharma#, P Rajwanshi##,
B Gupta+

Abstract
LPG (liquefied petroleum gas) is a commonly used commercial and domestic fuel. Due to its common usage,
unintentional prolonged exposure to LPG poses a potential health hazard to the general population, ranging
from mild irritation to life threatening sequelae. Usually, LPG inhalation presents with complications like
hypoxia, cardiorespiratory arrest and neurological complications as reported in earlier studies. A very rare case
of accidental prolonged LPG inhalation involving three members of the same family with varied sequelae is being
reported. Two family members, the child and his mother made a complete recovery while the father expired.
Autopsy conducted on the latter confirmed asphyxia as the possible cause of death. Out of the three, only the
mother developed massive rhabdomyolysis. Apart from this, only three cases of massive rhabdomyolysis after
LPG exposure have been reported earlier. .No such presentation has been reported in hitherto published Indian
literature of LPG exposure.

Introduction for limitation of body movement due to pain. There was no

L PG is a mixture of aliphatic hydrocarbon gases used as a
fuel in cooking appliances and vehicles. It is widely used as
a “green fuel” for internal combustion engines as it decreases
exhaust emissions. It is extensively used both commercially as
well as a domestic and automobile fuel. LPG includes primarily
propane (20%) and butane (80%) which are inflammable gases.
Propylenes and butylenes are added in small concentrations.
Mercaptans are added to make any leakage detectable due to
their malodorous smell. LPG is sold in pressurised cylinders.
Propane gas is heavier than air and thus flows along floors and
tends to settle at floor level. This should be kept in mind during
accidental and unintentional exposure. Timely and correct
clinical diagnosis of LPG poisoning remains elusive because of
the non-specific and protean nature of its signs and symptoms.
The present case report illustrates the need for improved
education regarding accidental LPG poisoning for doctors, LPG
providers and consumers alike.
Case History
A 30 years old female, non-smoker, non-alcoholic, housewife
presented with history of generalised bodyache since getting
up from bed. There was history of exposure to LPG for the past
eight hours during sleep caused by a leaking gas tube with
the flame switched off. The pain was described by the patient
as diffuse, dull aching type, poorly localised and without any
associated swelling. It increased on moving the limbs and on
applying pressure. She did not have any focal weakness except
Consultant and Reader, **Senior Resident, ***Senior Physician and Asst
*
history of fever, altered sensorium, trauma, seizures, burns,
alcohol or drug intake. There was no history of any urinary or
fecal incontinence. There were no apparent relieving factors.
Over the next few days during hospitalisation, the patient
experienced gradual symptomatic relief in pain and was able
to move comfortably by the eighth day.
At the time of presentation to the casualty, she was conscious,
oriented, walking with support with much difficulty. Her
vitals were stable. Pulse- 80/min, BP- 118/70 mm Hg, RR-
16/min. Body temperature was 37.2 degree C. There was no
pallor, icterus or cyanosis, JVP was not raised. There were no
abnormal systemic findings. Chest, CVS, CNS and per abdomen
examination were essentially normal. Severe tenderness was
elicited on palpation of muscles all over the body. It increased on
applying pressure and on active and passive limb movements.
On investigation, blood counts were within normal limits
(Hb-10gm%, TLC-6200, DL-P52 L42 M4 E2, ESR-40, S Bil-0.8
mg/dl, SGPT-42 IU/dl, SGOT-46 IU/dl, ALP-124 IU/dl, blood
urea-30 mg/dl, s creatinine-0.8 mg/dl, s uric acid-4.2 mg/dl,
RBS-93 mg/dl, s Na-140 meq/l and s K-4.8 meq/l). Repeat serial
blood counts including daily RFT did not show any abnormality.
ABG revealed mild metabolic alkalosis (pO2 92, pCO2 36, pH
7.48, SaO2 96%). The most significant finding was a CPK value
of 11,350 IU/dl at the time of admission, the normal range being
30-170 IU/dl. Repeat serial CPK level done every other day,
showed values of 10,355, 3670, 281 and subsequently 52 IU/dl.
Urine routine and microscopy was normal. Urinary myoglobin
was found to be positive and cardiac troponins were negative.
Chest radiograph and ECG were normal. The patient was treated

Professor, ****Physician and Asst Professor, #Senior Physician and Asst

Professor, ##Senior Physician and Reader, +Consultant, Professor and
Head, Vardhman Mahavir Medical College & Safdarjung Hospital,
New Delhi 110029
Received: 18.12.2006; Revised: 12.2.2009; Accepted: 12.2.2009
symptomatically with intravenous normal saline infusion. She
did not develop any complications of rhabdomyolysis and was
discharged on the ninth day of hospitalization.
The patient’s husband and son also had history of similar and
simultaneous exposure to LPG. The family lived in a small single

472 © JAPI • JUNE 2009 • VOL. 57

room ill-ventilated hutment as elicited on history. They were all
sleeping on the floor. The husband,possibly under the influence
of alcohol, was sleeping closest to the the gas stove, which was
placed at ground level. Following exposure, the husband expired
during sleep and was brought dead to the casualty. Autopsy
was conducted on him which revealed congestion of the liver,
spleen, kidneys, brain and lungs indicating hypoxia as the
possible cause of death.
The patient’s three year old child, who was sleeping between
his parents, presented with features of respiratory distress.
Examination revealed pneumonitis. He had normal biochemical
parameters. The child improved with symptomatic treatment
over the next four days. He was subsequently discharged from
the hospital and is doing well on follow up.
Discussion
This case report presents a unique case of LPG exposure,
perhaps the first of its kind, in published literature in India.
As per the literature published elsewhere, initial inhalational
exposure to LPG causes local irritation in the nose, eyes and
pharynx.1,2 Sustained inhalation leads to headache and dizziness
progressing to difficulty in breathing, loss of consciousness
and cardiorespiratory arrest. The most commonly documented
cause of death is hypoxia secondary to inhalation of asphyxiant
substances released by incomplete combustion of LPG. These
include carbon monoxide, sulphur dioxide, nitrous oxide
and total suspended particulate matter. Autopsy findings
demonstrate severe pulmonary edema and suggest advanced
circulatory failure. Biochemical findings reveal myocardial
ischemia and hypoxia. Acute renal failure occurs in 30-40%
of patients with rhabdomyolysis, especially in dehydrated
patients. Headache, giddiness and rarely coma occur secondary
to the neurotoxic effects of these gases especially mercaptans.
Hemolysis occurs due to the oxidant effects of methyl
mercaptans, especially in G6PD deficient individuals. In most
of these cases, there was history of inadequate ventilation and
combustion of LPG leading to the production of asphyxiant
gases like carbon monooxide.2,3 In this particular case report, the
patient’s family inhaled the leaking LPG for about eight hours
during sleep in a closed room and not its combustion byproducts
as the gas flame was switched off.
The presentation can be attributed to the direct toxic and
oxidant effects of butane, propane and mercaptans.4 This effect
has been seen in certain animal studies performed on catfish5
and hen.6 The mother presented with features suggestive of
acute massive rhabdomyolysis without any respiratory, cardiac
or neurological complications. Rhabdomyolysis is a clinical
syndrome in which injury to skeletal muscles results in the
leakage of intracellular contents from myocytes in the plasma.
Out of the several causes of rhabdomyolysis in literature, the
most likely etiology is direct muscle injury and drug abuse.
The diagnosis of acute massive rhabdomyolysis was based on
generalized muscle tenderness, raised muscle enzyme in serum
and the presence of myoglobin in urine. The clinical presentation
of rhabdomyolysis is often subtle, requiring a high index of
suspicion. The cause of death in such cases includes acute renal
failure, hyperkalemia, acute cardiomyopathy, DIC and various
other complications. Failure to recognise rhabdomyolysis
on initial presentation and delay in institution of early and
aggressive volume replacement are the major contributing
factors in fatal cases. Our patient made a complete recovery
without any sequelae. This was confirmed both clinically and
biochemically. This can be attributed to prompt diagnosis
and intensive symptomatic therapy including intravenous
crystalloids and urine alkalinising agents. The close proximity of
the patient’s husband to the leaking gases along with the possible
history of alcohol exposure could have contributed to his death.
Considering the common usage of LPG by all strata of society,
there is significant possibility of exposure to small leakages over
a passage of time and such accidents are probably underreported.
Therefore, it is important that the general population, LPG
providers and healthcare professionals all should be made aware
of the toxicity and its potential as a health hazard.
References
1. Frangides CY, Tzortzatos GV. Acute massive rhabdomyolysis due
to prolonged inhalalation of liquid gas. Eur J Emerg Med 2003;10:44-
6.
2. Khatouf M, Ifkharen B. Acute rhabdomyolysis due to butane
inhalation.Report of two cases. Ann Fr Anaesth Reanim 2004;23:1080-
3.
3. Zhu BL, Ishikawa T. Five fatalities due to inhalation of “asphyxiant
gases”:pathophysiological analysis in autopsy cases. Chudoku
Kenkyu 2005;18:77-81.
4. Fukunaga T, Yamanoto H. Liquified petroleum gas (LPG)
poisoning:report of to cases. Forensic Sci Int 1996;25;82:193-200.
5. Mather - Mihaich E, Di Giulio RT. Antioxidant enzyme activities and
malondialdehyde,gluthathione and methemoglobin concentrations
in channel catfish exposed to DEF and n-butyl mercaptan. Comp
Biochem Physiol C 1986;85:427-32.
6. Abdo KM, Timmons PR. Heinz body production and haematological
changes in hen after administration of a single oral dose of n-butyl
mercaptan and n-butyl disulfide. Fundam Appl Toxicol 1983;39:69-74.

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