A case of toxin induced cyanosis

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Text of A case of toxin induced cyanosis

A CASE OF CELL OIL POISONING

IMCU & TOXICOLOGY UNIT IIMDR.B.MIDHUN KUMARI ST YEAR POST GRADUATE

A CASE OF TOXIN INDUCED CYANOSIS

INTRODUCTION

We present a case of a patient who developed methemoglobinemia after consuming cell oil (anti termite oil) for suicidal intention.

Methemoglobinemia is an uncommon , but potentially fatal hemoglobinopathy.

It leads to rapid oxygen desaturation, and therefore requires prompt recognition and treatment.

HISTORY A 45 year old male pt was brought on 19/07/2012 at 3 PM to our toxicology ward in an unconscious state,

With Alleged history of consumption of around 1 bottle (100 ml) of anti termite oil(CORAL) in his house at Perambur at 1 p.m.

Pt did not have any seizures or vomiting or frothing from the mouth after he was seen by his relative at 1.30 PM who brought him here

No h/o any tremors/ fasciculations/ other abnormal movements noted by the attenders No h/o increased urination or defecation

No h/o any injuries

No h/o other co-morbidities

No previous h/o poisoning/ suicidal attempts

Known alcoholic for the past 20 years frequent binge drinking for last 1 week EXAMINATIONPt was unconscious, Not responding to deep pain

GCS-E1V1M1

He was Afebrile,Dyspnoeic,Tachypneic ( RR-30/min)

He was pale, peripheries cold

CYANOSIS +,FINGERS,TOES,LIPS AND TONGUE

Not Icteric,No Clubbing,No pedal edema

His spontaneous respiratory effort was poor

Smell of cell oil (Anti-Termite oil) was present

VITAL SIGNS:

PR: 96/min,Small volume, Felt in all peripheral vesselsBP: 90/60 mm HgRR: 30 / min , irregular, accessory muscles actingTemp: 98.8 F SpO2: 70 % in room air,75 % with O2 6l/minCBG- 148 mg/dl SYSTEMIC EXAMINATIONCVS: S1S2+, No murmurs or added soundsRS : B/L NVBS+, No added soundsP/A: Soft ,No Organomegaly, BS + CNS: Pupils : B/L 4 mm RTL sluggishly No neck rigidity No fasciculations Plantar reflex: B/L No response An intravenous (IV) line was inserted

Blood taken from the patient was dark brown in colour and sent for complete blood count,serum electrolytes, blood urea nitrogen (BUN), glucose, ABG and serum methemoglobin levels

Initial investigationsCBC TC-16,400 DC-P95/L2/ E3 ESR-20 HB-11.9G/dl PCV-34 PLT-2 LAKHS RFT UREA-75 CREATININE-1.7 SODIUM-142 POTASSIUM-2.8 CALCIUM- 9.3 mg/dl.

LFT TB- 1 DB- 0.4 SAP-84 TP-6.9 ALB-3.7ABG- SEVERE METABOLIC ACIDOSISURINE R/E- 1+ ALBUMINURIASERUM LDH-196 U/LSERUM METHEMOGLOBIN> 3%URINE Hb , MYOGLOBIN - NEGATIVE TREATMENTPt was Intubated and started on Assisted ventilation

Stomach wash and Activated charcoal was given

Pt started on IV fluids at the rate of 200ml/hr

Inj. Methylene blue 100mg(2mg/kg/dose) in 100ml of 5% Dextrose IV Infusion given over 10 mins, 2nd dose repeated after 1 hr(2mg/kg/dose). Cyanosis improved.

Pt started on Inotropic support as BP did not improve with IV fluids

Inj.Vitamin C started at a dose of 500 mg IV TDS IV antibioticsCOURSECyanosis showed little improvement and hence pt was started on exchange transfusion and 7 cycles were done

Pts SpO2 continued to be around 75% even with ventilatory support

Pts respiratory effort and sensorium improved and hence he was connected to T piece ventilation with O2 after weaning gradually on Day 2Pt was Extubated on Day 3 and put on O2 mask as he became totally conscious

His saturation was 80% with O2 6l/min

.

His RFT values started rising and his creatinine became 3.7mg/dl on Day 5 .He also developed Myoglobinuria and Albuminuria

His LFT also started showing increasing Bilirubin levelsForced alkaline diuresis was started

Patient improved and on 7 th day of admission he was completely normal.

His cyanosis disappeared and his saturation went up to 95% on room air, sr. methemoglobin levels came below 3%.

THE COMPOUNDThe compound which the patient consumed was cell oil (CORAL ,HYPOL-SLM) which is an anti termite oil used for varnishing the furniture,Its ingredients are pine tarNitro toluene compoundsChlorobenzene compounds

Of these ,nitro toluene and chlorobenzene are powerful oxidizing agents which are implicated in causing methemoglobinemia, METHEMOGLOBINOxidized form of normal hemoglobin, in which the iron atom in hemoglobin loses 1 electron to an oxidant, and the ferrous (Fe2+) state of iron is transformed into the ferric (Fe3+) state .

Methemoglobin not only decreases the available oxygen-carrying capacity, but also increases the affinity of the unaltered hemoglobin for oxygen.

This shifts the oxygen hemoglobin dissociation curve to the left, which further impairs oxygen delivery , leading to tissue hypoxia.

FELIX HOPPE SEYLER

Methemoglobin was first described by Felix Hoppe-Seyler in 1842.

German physiologist and chemist.

He also discovered the functions of hemoglobin.

Methemoglobinemia may produce symptoms of cellular hypoxia and should be considered in the differential diagnosis of the cyanotic patient who has no apparent cardiovascular cause.

In the cases of methemoglobinemia and sulfhemoglobinemia, cyanosis is not caused by deoxyhemoglobin but rather by the color imparted to the skin as a result of oxidized hemoglobin

Because of the spontaneous and toxins induced oxidation of hemoglobin, the erythrocyte has developed multiple mechanisms to maintain the normal level of methemoglobin at