Late presentation of secondary cycling - nitrobenzene poisoning: A rare case report

Late presentation of secondary cycling

International Archives of Integrated Medicine, Vol.

Copy right © 2014, IAIM, All Rights Reserved.

Case Report


nitrobenzene poisoning: A rare case report

142,Taruchaya Nagar,

*Corresponding author’s email:

How to cite this article: Virendra Goyal. L

poisoning: A rare case report. IAIM, 2014; 1(3):

Available online at

Received on: 14-10-2014

Abstract

We presented here a case of acute nitrobenzene poisoning

timely management in form of repeated intravenous methylene blue

a vital role to save a life. It is very

exposure form the secondary cycling of nitrobenzene from body stores.

of this uncommon, but treatable and potential serious poisoning

Methemogobinemia can leads to high mortality but effective treatment with methylene blue is

preferential.

Key words

Acute methemoglobinemia, Methylene blue, N

Introduction

Nitrobenzene is also known as nitrobenzol,

mirbane oil or essence of mirbane

introduced into the body, it is metabolized by

reduction to aniline. Nitrobenzene and aniline

are typical aromatic nitro compounds and

aromatic amino compounds that cause

methemoglobinemia.

methemoglobinemia due to acute nitrobenzene

poisoning is uncommon and rare but life

threatening emergency condition. Once

poisoning is suspected on clinical evaluation,

early and effective management of it may

ate presentation of secondary cycling - nitrobenzene poisoning

International Archives of Integrated Medicine, Vol. 1, Issue. 3, November, 2014.

Rights Reserved.



Virendra Goyal*

142,Taruchaya Nagar, Tonk Road, Jaipur, Rajasthan, India

*Corresponding author’s email: [email protected]

Virendra Goyal. Late presentation of secondary cycling

: A rare case report. IAIM, 2014; 1(3): 39-43.

Available online at www.iaimjournal.com

2014 Accepted on:

case of acute nitrobenzene poisoning in which effective clinical evaluation and

repeated intravenous methylene blue and blood transfusions

very important to take care of patient who presented late after heavy

the secondary cycling of nitrobenzene from body stores. Clinicians should be aware

but treatable and potential serious poisoning


Acute methemoglobinemia, Methylene blue, Nitrobenzene poisoning, Blood transfusion.

Nitrobenzene is also known as nitrobenzol,

mirbane oil or essence of mirbane. When

introduced into the body, it is metabolized by

Nitrobenzene and aniline

are typical aromatic nitro compounds and

aromatic amino compounds that cause

Significant

methemoglobinemia due to acute nitrobenzene

soning is uncommon and rare but life

threatening emergency condition. Once

poisoning is suspected on clinical evaluation,

early and effective management of it may

change the outcome of a patient in positive

manner.

Case report

A 30 years old, irritable, anxious male presented

to emergency department who

other centre on mechanical ventilation with

cyanosis and a greyish

examination, he had labored

26/min, blood pressure was

pulse rate was 74/min, pupils with sluggish

reaction, and SpO2 of 89% only. There was a

history of severe pain in the abdomen, nausea,

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Page 39

Late presentation of secondary cycling -


cycling - nitrobenzene

Accepted on: 20-10-2014

in which effective clinical evaluation and

lood transfusions played

patient who presented late after heavy

Clinicians should be aware

but treatable and potential serious poisoning of nitrobenzene.


, Blood transfusion.

change the outcome of a patient in positive

anxious male presented

department who referred from

on mechanical ventilation with

greyish-brown hue. On

labored respiration of

was 129/74 mm of Hg,

pupils with sluggish

of 89% only. There was a

history of severe pain in the abdomen, nausea,




vomiting, and dizziness, which was treated on

admission at primary centre. At primary

oral methylene blue was given (5 ml,

as to non-availability of intravenous therapy

urgent ultrasonography of abdomen

which ruled out any abdominal catastrophe

and showed a generalized mild to

hepatic inflammation. Blood samples

drawn for arterial blood gas (

which had a chocolate brown

not improve on exposure to 100% oxygen and

showed compensated metabolic acidosis.

of the chest and ECG were within normal limits

while WBC and liver enzymes were markedly

raised. Serum creatinine and blood urea were

within normal range. Hemoglobin at admission

was 9.4 gm%, which dropped down to 6.3

on 9th

day. Similarly serum bilirubin at admission

was 2.0 mg% which was raised to 13.0 mg%. A

clinical diagnosis of s

methemoglobinemia due to

poisoning was made.

100 mg of methylene blue (p

sterile solution) was given intravenously and

repeated after 12 hours. This im

SpO2 to 92% and then after intravenous vitamin

K; vitamin C, 10% dextrose, anxi

and intravenous antibiotic were also given

Urine output was maintained above 100

ml/hour with proper hydration, maintaining a

normal central venous pressure (CVP).

Multiple blood and blood products

frozen plasma (FFP) were transfused. Patient at

admission had severe hypokalemia

which was corrected by intravenous

potassium infusion. Methemoglobin estimation

in blood was done and it was significantly high

(11.1 units as compared to normal values of 0.00

to 2.0). He was extubated at 48 hours and

maintained on a continuous positive airway

pressure (CPAP) mask, with arterial blood gas

(ABG) analysis which showed



Rights Reserved.

vomiting, and dizziness, which was treated on

t primary centre,

(5 ml, 12 hourly),

intravenous therapy. An

abdomen was done

ruled out any abdominal catastrophe

zed mild to moderate

hepatic inflammation. Blood samples were

arterial blood gas (ABG) analysis

had a chocolate brown color, which did

not improve on exposure to 100% oxygen and

compensated metabolic acidosis. X-ray

G were within normal limits

nd liver enzymes were markedly

and blood urea were

within normal range. Hemoglobin at admission

which dropped down to 6.3 gm%

bilirubin at admission

mg% which was raised to 13.0 mg%. A

clinical diagnosis of severe acute

due to nitrobenzene

mg of methylene blue (prepared as 1%

sterile solution) was given intravenously and

. This improved patient’s

ntravenous vitamin

K; vitamin C, 10% dextrose, anxiolytics, oral iron,

were also given.

Urine output was maintained above 100

ml/hour with proper hydration, maintaining a

normal central venous pressure (CVP).

blood products like fresh

transfused. Patient at

hypokalemia (2.5 mEq/L),

which was corrected by intravenous slow

hemoglobin estimation

it was significantly high

to normal values of 0.00

He was extubated at 48 hours and

continuous positive airway

arterial blood gas

a saturation of

93% and a PaO2 of 112. He improved rapidly

after the 10th

day with SpO2

Patient had a single episode of

clonic seizure (GTCS) on 11

epsolinised, followed by oral dilantin tablets

(100 mg TDS). CT head was absolutely nor

but liver enzymes were raised. He was

discharged on the 14th

day on oral iron, folate,

ascorbic acid, and liver enzyme supplements and

breathing exercises.

Discussion

Nitrobenzene is a pale yellow, oily liquid, with

bitter almond odor and it is widely used as an

intermediate in the production of various

solvents, like paint remover. Common

occupational exposure of nitrobenzene is via

inhalation or through absorption of skin [1, 2

1886, first report of nitrobenzene poisoning was

noted [3] and then after various fatality reports

were come into noticed [

poisoning can be accidental or suicidal in

manner [5]. Accidental exposure may possible in

patients who are consuming well water with

extremely high levels of nitri

[6]. Lethal dose of it is varied from 1

different scholar authors [7, 8, 9

literature review of already published articles on

it does not provide any significant conclusive

matter regarding fatalities and

[8]. Nitrobenzene poisoning is usually presented

as chronic poisoning or as occupational hazard

with development of methemoglobinemia [10].

The clinical features of ingestion of such poison

are due to the rapid development of

methemoglobinemia [7, 11], which is a condition

of altered hemoglobin formation in which the

iron presented within the hemoglobin is

oxidized into ferric (Fe3+

) state from the ferrous

(Fe2+

) state, resulting in the inability to transport

oxygen effectively [12, 13, 14

brownish discoloration of the blood and

functional anemia [6]. After formation of

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of 112. He improved rapidly

2 of 90% on room air.

Patient had a single episode of generalized tonic

on 11th

day and was

followed by oral dilantin tablets

CT head was absolutely normal

liver enzymes were raised. He was

day on oral iron, folate,

ascorbic acid, and liver enzyme supplements and

Nitrobenzene is a pale yellow, oily liquid, with

and it is widely used as an

intermediate in the production of various

solvents, like paint remover. Common

occupational exposure of nitrobenzene is via

gh absorption of skin [1, 2]. In

1886, first report of nitrobenzene poisoning was

] and then after various fatality reports

into noticed [3, 4]. Nitrobenzene

poisoning can be accidental or suicidal in

]. Accidental exposure may possible in

patients who are consuming well water with

extremely high levels of nitrites and nitrates in it

]. Lethal dose of it is varied from 1-10 g, as per

7, 8, 9]. A systematic

literature review of already published articles on

it does not provide any significant conclusive

matter regarding fatalities and dose of ingestion

]. Nitrobenzene poisoning is usually presented

as chronic poisoning or as occupational hazard

with development of methemoglobinemia [10].

The clinical features of ingestion of such poison

are due to the rapid development of

], which is a condition

of altered hemoglobin formation in which the

iron presented within the hemoglobin is

) state from the ferrous

) state, resulting in the inability to transport

[12, 13, 14] and causes

brownish discoloration of the blood and

]. After formation of




methemoglobin, it can be reduced enzymatically

either via an adenine dinucleotide (NADH)

dependent reaction, which is catalysed by

cytochrome b5 reductase, or an

pathway utilizing the nicotine adenine

dinucleotide phosphate [15]. Certain drugs and

chemicals can accelerate production of

methemoglobin like antimalarial drugs such as

chloroquine and primaquine; nitrites or nitrates,

flutamide, inhaled nitric oxide, metoclopramide,

local anesthetic agents like benzocaine;

acetanilide, nitroprusside, sulfonamides,

phenacetin, phenazopyridine hydrochloride,

phenytoin, chlorates, probenecid etc. [1

Normal physiological level of Methemoglobin i

less than 1% of total hemoglobin [17

10-15% of methemoglobin, person is usually

asymptomatic with mild cyanotic changes.

When methemoglobin level is 20

headache, dyspnea, chest pain, tachypnea, and

tachycardia develop [18]. At 40

methemoglobin, person feels confusion,

lethargy, and metabolic acidosis which later on

leading to coma, seizures, bradycardia,

ventricular dysrythmia, and hypertension

Methemoglobin level around 70% is considered

as fatal [20]. More severe symptoms are noted

in patients with anemia or G6PD deficiency [

7]. In certain cases, leukocytosis has been

reported along with relative lymphopenia [

Altered liver function tests, hepato

splenomegaly, and Heinz body haemolytic

anaemia are other significant features [

22]. Nitrobenzene is metabolized in the body

and converted into p-nitrophenol and

aminophenol and later on excreted in urine (up

to 65%), and in stools (up to 15%) after five days

of ingestion. Liver, stomach, blood, and brain

may act as storage house and release it

gradually [21].

History of chemical ingestion, characteristic

bitter almond smell, persisting cyanosis on



Rights Reserved.

methemoglobin, it can be reduced enzymatically

either via an adenine dinucleotide (NADH)-

dependent reaction, which is catalysed by

cytochrome b5 reductase, or an alternative

pathway utilizing the nicotine adenine

Certain drugs and

chemicals can accelerate production of

methemoglobin like antimalarial drugs such as

chloroquine and primaquine; nitrites or nitrates,

, inhaled nitric oxide, metoclopramide,

local anesthetic agents like benzocaine;

acetanilide, nitroprusside, sulfonamides,

phenacetin, phenazopyridine hydrochloride,

phenytoin, chlorates, probenecid etc. [16].

Normal physiological level of Methemoglobin is

than 1% of total hemoglobin [17]. At level of

15% of methemoglobin, person is usually

asymptomatic with mild cyanotic changes.

When methemoglobin level is 20-40%,

headache, dyspnea, chest pain, tachypnea, and

]. At 40 – 50% level of

methemoglobin, person feels confusion,

lethargy, and metabolic acidosis which later on

leading to coma, seizures, bradycardia,

ventricular dysrythmia, and hypertension [19].

Methemoglobin level around 70% is considered

symptoms are noted

in patients with anemia or G6PD deficiency [4,

]. In certain cases, leukocytosis has been

reported along with relative lymphopenia [8].

Altered liver function tests, hepato-

splenomegaly, and Heinz body haemolytic

ficant features [4, 21,

]. Nitrobenzene is metabolized in the body

nitrophenol and

aminophenol and later on excreted in urine (up

to 65%), and in stools (up to 15%) after five days

of ingestion. Liver, stomach, blood, and brain

ct as storage house and release it

History of chemical ingestion, characteristic

bitter almond smell, persisting cyanosis on

oxygen therapy without severe cardiopulmonary

disease, low arterial oxygen saturation, with

normal ABG (calculated) oxygen saturation are

very important for diagnosis.

detection can be done bedside by placing few

drops of blood on white filter paper and

observing for color change in which

deoxyhemoglobin brighten and methemoglobin

holds color [23]. Dark brown blood that fails to

turn bright red on shaking, which suggests

methaemoglobinaemia and this is supported by

the chocolate red color of dried blood. Presence

of nitrobenzene compounds may be confirmed

spectrophotometrically and estimated by the

butanone test of Schrenk [1], methemoglobin

levels in the blood, and urinary presence of p

nitrophenol and p-aminophenol [

Plan of management is based upon the

principles of decontamination along with

symptomatic and supportive treatment.

Methylene blue is the drug of choice (antidote)

for the treatment of acquired (toxic)

methaemoglobinaemia [25]. It is an exogenous

cofactor, which greatly accelerates the NADPH

dependant methemoglobin reductase system

and is indicated if the methemoglobin levels,

which are more than 30% [7

intravenously at 1 – 2 mg/kg (up to 50 mg dose

in adults,) as a 1% solution over five minutes;

with a repeat in one hour, if necessary.

Methylene blue is act as an oxidant at levels of

more than 7 mg/kg, and the

methaemoglobinaemia in susceptible patients

[26]. It is contraindicated in patients with G6PD

deficiency, because it can lead to severe

haemolysis. Ascorbic acid is an antioxidant that

may also be administered in patients with

methemoglobin levels of more than 30% [

recent studies, N-acetylcysteine has been shown

to reduce methemoglobin, but it is not yet an

approved treatment for methaemoglobinaemia

[27]. Exchange transfusion is indicated in severe

cases [7, 27]. Hyperbaric oxygen

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Page 41

oxygen therapy without severe cardiopulmonary

disease, low arterial oxygen saturation, with

) oxygen saturation are

very important for diagnosis. Methemoglobin

detection can be done bedside by placing few

drops of blood on white filter paper and

observing for color change in which

deoxyhemoglobin brighten and methemoglobin

brown blood that fails to

turn bright red on shaking, which suggests

methaemoglobinaemia and this is supported by

the chocolate red color of dried blood. Presence

of nitrobenzene compounds may be confirmed

spectrophotometrically and estimated by the

ne test of Schrenk [1], methemoglobin

levels in the blood, and urinary presence of p-

aminophenol [3, 21, 24].

Plan of management is based upon the

principles of decontamination along with

symptomatic and supportive treatment.

lue is the drug of choice (antidote)

for the treatment of acquired (toxic)

]. It is an exogenous

cofactor, which greatly accelerates the NADPH-

dependant methemoglobin reductase system

and is indicated if the methemoglobin levels,

7]. It is administered

2 mg/kg (up to 50 mg dose

in adults,) as a 1% solution over five minutes;

with a repeat in one hour, if necessary.

Methylene blue is act as an oxidant at levels of

more than 7 mg/kg, and therefore, may cause

methaemoglobinaemia in susceptible patients

]. It is contraindicated in patients with G6PD

deficiency, because it can lead to severe

haemolysis. Ascorbic acid is an antioxidant that

may also be administered in patients with

in levels of more than 30% [27]. In

acetylcysteine has been shown

to reduce methemoglobin, but it is not yet an

approved treatment for methaemoglobinaemia

]. Exchange transfusion is indicated in severe

]. Hyperbaric oxygen is reserved only




for those patients who have a methemoglobin

level > 50% or those who do not respond to

standard treatment. Exchange transfusion is

more widely and rapidly available compared to

hyperbaric oxygen. Exchange transfusion

involves replacement of the patient's red cells

with donor cells and has been used in the

treatment of various hemoglobinopathies

In this case, we repeated low dose methylene

blue and blood transfusions helped in tiding

over the fluctuating symptoms due to the

release of nitrobenzene from the body stores,

without exceeding the maximum dose. Fresh

blood transfusion improved the oxygen carrying

capacity and haemoglobin content, improving

the patient symptomatically. Oral charcoal and

purgation up to five days helped to elimi

body stores of nitrobenzene and prevented

secondary deterioration in the patient

care of nutrition, adequate urine output, and

hepatoprotection prevented kidney and liver

failure, which have been cited as late effects [

21]. Regular use of charcoal and purgation by

peglag during hospital stay may be of some help

according to some centers. Forced diuresis can

lead to a rapid fall in methemoglobin levels and

improved discoloration [8]. Ascorbic acid

supplements are useful for follow

management of methaemoglobinaemia [

Conclusion

Clinicians should be aware of this uncommon,

but treatable and potential serious poisoning

nitrobenzene with secondary cycling from the

body tissues. Methemogobinemia

high mortality but effective treatment with

methylene blue is preferential.

Acknowledgement

The author is highly thankful to Jeevanrekha

CCTH, Jaipur team for their kind coop

and wholehearted support in.



Rights Reserved.

for those patients who have a methemoglobin

level > 50% or those who do not respond to

Exchange transfusion is

more widely and rapidly available compared to

hyperbaric oxygen. Exchange transfusion

f the patient's red cells

with donor cells and has been used in the

treatment of various hemoglobinopathies [15].

In this case, we repeated low dose methylene

blue and blood transfusions helped in tiding

over the fluctuating symptoms due to the

nitrobenzene from the body stores,

without exceeding the maximum dose. Fresh

blood transfusion improved the oxygen carrying

capacity and haemoglobin content, improving

Oral charcoal and

purgation up to five days helped to eliminate the

body stores of nitrobenzene and prevented

secondary deterioration in the patient .Taking

care of nutrition, adequate urine output, and

hepatoprotection prevented kidney and liver

failure, which have been cited as late effects [3,

of charcoal and purgation by

peglag during hospital stay may be of some help

according to some centers. Forced diuresis can

lead to a rapid fall in methemoglobin levels and

]. Ascorbic acid

supplements are useful for follow-up

gement of methaemoglobinaemia [28].

Clinicians should be aware of this uncommon,

but treatable and potential serious poisoning of

with secondary cycling from the

Methemogobinemia can leads to

high mortality but effective treatment with

The author is highly thankful to Jeevanrekha

Jaipur team for their kind cooperation

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Documents

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