2
February 2014
To
(i)
Chief Justice of India , Supreme
Court of India
(ii)
Chief Justice Ramana, Delhi High Court
(iii)
The Registrar General,
Delhi High
Court
(iv)
Chairman, Bar Council
of Delhi
(v)
All other members of
Bar Council of Delhi
(vi)
Delhi Police
Commissioner
(vii)
Registrar Vigilance, Delhi High Court
To the Chief Justice of India , to the Chief Justice of the Delhi High Court, to the Bar Council of Delhi ,
to the Registrar General of the Delhi High
Court, to the Police Commissioner for Delhi
Ref:
Whistle-blower corruption and right to life Writ Petition pending in the Delhi
High Court since February 2012 – Writ Petition (Civil) 1280/ 2012 – in the
matter of Seema Sapra versus General Electric Company & Others AND
complaint that I was poisoned with ethylene glycol in July 2011 because of my
corruption complaints against General Electric Company and Montek Singh
Ahluwalia which are the subject matter of
WP Civil 1280/ 2012
I was poisoned with Ethylene
Glycol in July 2011.
I reproduce below some information on the physiological
effects of ethylene glycol poisoning from the website
http://www.atsdr.cdc.gov/csem/csem.asp?csem=12&po=10 (Agency of Toxic
Substances & Disease Registry).
Ethylene Glycol and
Propylene Glycol Toxicity
What Are the Physiological Effects of Ethylene Glycol Poisoning?
Introduction Ingestion
of ethylene glycol has significant toxicologic implications if undetected or
left untreated. The preceding section described the clinical features of
ethylene glycol poisoning in three stages that are based on the time after
ingestion. This section depicts the systemic effects associated with
significant ethylene glycol exposure.
Neurologic
Effects The
initial phase of ethylene glycol poisoning is characterized by inebriation
caused by unmetabolized ethylene glycol. In acute poisoning cases, the
following symptoms are common (Parry and Wallach 1974; Buell, Sterling et al. 1998)
·
ataxia
·
slurred speech
·
drowsiness
·
irritation
·
restlessness
- disorientation
Possible
Sequelae Possible
sequelae of severe poisonings (Walder and Tyler 1994; Hantson, Vanbinst et al. 2002) include
·
myoclonic jerks
·
convulsions
·
coma
·
death
Cerebral edema and deposition of calcium oxalate crystals
in the walls of small blood vessels in the brain contribute to this CNS toxicity
(Jobard, Harryet al. 1996;
Bey, Walter et al. 2002; Tobe, Braam et al. 2002). Some studies also documented
brain dysfunction with corresponding cranial computed tomography findings after
ethylene glycol ingestion (Chung and Tuso 1989; Zeiss, Velasco et al. 1989; Morgan, Ford et al. 2000).
Cranial Nerve Damage Recovery in survivors is usually
rapid and complete. However, the following cranial nerve palsies have been
reported one or more weeks after acute exposure
·
facial palsy
·
hearing loss
·
dysphagia
·
opthalmoplegia
·
visual disturbances
Such adverse effects are not seen often, but delayed
treatment may contribute to their development (Momont and Dahlberg 1989;
Broadley, Ferguson et al. 1997; Lewis, Smith et al. 1997; Tobe, Braam et al. 2002).
·
Throat and upper
respiratory irritation were the most common complaints following prolonged
experimental exposures in humans (4 weeks at concentrations of 1-25 ppm).
·
Exposure to 60 ppm
aerosolized ethylene glycol caused very noticeable irritation.
·
Exposure to 80 ppm
aerosolized ethylene glycol was judged “intolerable” because respiratory
discomfort developed rapidly (Wills, Coulston et
al.1974).
Pulmonary effects typically occur 12 to 72 hours after
ingestion of ethylene glycol. Pulmonary edema and adult respiratory distress
syndrome (ARDS) have been reported in ethylene glycol victims (Haupt, Zull et al. 1988; Piagnerelli, Carlier et al. 1999).
The following respiratory
effects often occur 12 hours or more after exposure in victims of severe
ethylene glycol poisoning.
·
tachypnea,
·
hyperventilation,
·
Kussmaul respirations.
Such effects most often reflect physiological compensation
for severe metabolic acidosis rather than primary lung disease (Friedman,
Greenberg et al.1962;
Parry and Wallach 1974; Godolphin, Meagher et
al. 1980). Autopsies of
ethylene glycol victims revealed the following
·
pulmonary edema with
diffuse hemorrhagic exudates,
·
bronchopneumonia
(probably caused by aspiration), and
- deposits of
calcium oxalate crystals in lung parenchyma (Vale 1979).
Cardiovascular
Effects The
following severe cardiovascular effects have been reported in ingestion
victims, during stage 2 (Friedman, Greenberg et
al. 1962; Parry and Wallach
1974; Vale 1979):
·
Congestive heart
failure with cardiogenic pulmonary edema
·
Circulatory collapse
Severe metabolic and fluid electrolyte abnormalities
(Friedman, Greenberg et al. 1962; Parry and Wallach 1974) may
cause
·
cardiac dysrhythmias
·
cardiac arrest
Ingestion of antifreeze (Walder and Tyler 1994), (Jobard,
Harry et al. 1996; Rasic, Cengic et al. 1999) may affect blood pressure,
causing either
·
hypertension or
- hypotension,
which may progress to cardiogenic shock.
·
Onset occurs within 24
hours after ingestion.
·
Acidosis is caused
primarily by the accumulation of glycolic and glyoxylic acid. Oxalic and excess
lactic acid also contribute.
The metabolic acidosis of ethylene glycol poisoning is
characterized as normochloremic (Berman, Schreiner et al. 1957; Curtin, Kraner et al. 1992; Hantson, Hassoun et al. 1998; Bey, Walter et al. 2002) with
·
low serum bicarbonate
level and pH and
·
elevated acidemia and
anion gap.
Ethylene glycol is a small,
osmotically active molecule that
·
markedly increases
plasma osmolality and
·
causes a large osmolal
gap.
Osmolality reflects the
number of solute particles in a solution. Numerical measures of osmolality
express the number of particles present in a given weight of solvent.
Tetany
can sometimes occur due to hypocalcemia that results from precipitation of
calcium by the oxalate formed during ethylene glycol metabolism (Parry and
Wallach 1974).
·
Kidney damage
manifests as acute oliguric renal failure.
·
Costovertebral angle
tenderness is the most common physical finding (Friedman, Greenberg et al. 1962).
·
The most
characteristic abnormality is the presence of large numbers of “tent-shaped”
(octahedral) or needle-shaped oxalate crystals in the urine (Olivero 1993; Huhn
and Rosenberg 1995).
·
Absence of oxalate
crystals does not rule out the diagnosis of ethylene glycol poisoning (Haupt,
Zull et al. 1988; Curtin, Kraner et al. 1992; Baum, Langman et al. 2000; Boyer, Mejia et al. 2001; Hantson, Vanbinst et al. 2002).
Other typical urinalysis
abnormalities are
·
low specific gravity
·
proteinuria
·
microhematuria
·
pyuria
·
elevated serum BUN and
creatinine
Disturbed renal function may be mild and short-lived or
severe and persistent for several months. Permanent renal insufficiency is
uncommon but does occur (Berman, Schreiner et
al. 1957; Friedman,
Greenberg et al. 1962; Parry and Wallach 1974; Buell,
Sterling et al. 1998; Hantson, Hassoun et al. 1998).
The toxicity of ethylene
glycol is linked with two metabolites.
·
Glycolic acid, which
causes the acidosis.
·
Oxalic acid.
o
Oxalic acid is poorly
soluble in the presence of calcium.
o
Calcium oxalate
crystals in the urine are diagnostic.
o
The precipitation of
oxalate crystals in the tubular lumen leads to luminal blockage and
compression-induced loss of glomerular filtration (renal failure).
In transformed kidney cells, the oxalate ion induces
cytotoxic damage (McMartin and Cenac 2000). Another study, however, stated that
glycoaldehyde and glyoxylate are the principal metabolites responsible for
ethylene glycol nephrotoxicity (Poldelski, Johnson et al. 2001).
Carcinogenicity and Teratogenicity Data are
insufficient to determine whether ethylene glycol causes cancer or
developmental defects.
·
Human studies have
shown no link between ethylene glycol exposure and cancer or reproductive or
developmental hazards.
·
Animal studies have
not found an association between ethylene glycol exposure and cancer.
- Ethylene glycol exposure was teratogenic to mice and
rats, resulting in craniofacial and neural tube closure defects and
skeletal dysplasia (Lamb, Maronpot et
al. 1985; Price, Kimmel et al. 1985; Marr, Price et al. 1992; Tyl, Ballantyne et al. 1995). Ethylene glycol itself is
used to cryopreserve embryos of many mammal and is thus an unlikely cause
of these abnormalities.
Other
Effects Nausea,
vomiting (with or without blood), and abdominal pain are frequent early
findings following ethylene glycol ingestion (Meditext 2004). Ethylene glycol
is only a minor skin and mucous membrane irritant, although a few cases of
allergic contact dermatitis have been documented (Clayton GD & Clayton FE
1994). Reported effects on the blood have included leukocytosis, occasional methemoglobinemia,
and bone marrow arrest (Verrilli, Deyling et
al. 1987; Hantson, Hassoun et al. 1998; Rasic, Cengic et al. 1999). Reported musculoskeletal
effects have included muscle tenderness and elevation of creatine kinase
(Friedman, Greenberg et al. 1962; Parry and Wallach 1974;
Verrilli, Deyling et al. 1987).
·
Key Points Signs of inebriation are among the first symptoms to appear
after ethylene glycol ingestion.
·
Delays in initiating
treatment can result in more severe adverse effects.
·
The most common cause
of tachypnea is uncompensated metabolic acidosis.
·
Ethylene glycol
poisoning through ingestion can cause noncardiogenic pulmonary edema and ARDS.
·
Ethylene glycol
poisoning can cause dysrhythmias and heart failure.
·
Ethylene glycol
exposure is characterized by an osmolal gap and a metabolic acidosis with an
elevated anion gap.
·
Nephrotoxicity is the
dominant effect of significant ethylene glycol poisoning.
- Human studies
have shown no link between ethylene glycol exposure and cancer or
reproductive or developmental hazards.
My medical reports from July and
August 2011 support a diagnosis of ethylene glycol poisoning.
I had mentioned in open court
before then Chief Justice of India (Judge Kapadia) in open court in the week of
12 July 2011 that my life was in danger because of my complaints of corruption
against Montek Singh Ahluwalia and General Electric Company. I had made police
complaints at the same time (in July and August 2011) claiming that my life was
in danger and that I was being poisoned.
On 20 July 2011, I went to Max Hospital
On 22 July 2011, I underwent the
diagnostic tests for this health check up on 22 July 2011 at Max Gurgaon. I had
then been staying with Amika and Chetan Chitnis in Gurgaon since 20 July 2011.
My test reports from 22 July 2011
and thereafter establish ethylene glycol poisoning.
First, the urine analysis dated 22
July 2011 shows a large amount of calcium oxalate crystals (++) in the urine. Calcium oxalate crystals in the urine are
diagnostic of ethylene glycol poisoning.
The abdominal
ultrasound does not show any calculi in the kidneys. So I did not have kidney
stones. Therefore the presence of calcium oxalate crystals cannot be explained
on account of kidney stones. Further, subsequent urine analysis tests including
in February 2012 did not contain positive findings of calcium oxalate crystals,
thus ruling out kidney stones as the cause of calcium oxalate crystals.
The ECG dated 22 July 2011 was
abnormal, borderline and with a rightward axis that suggested fluid in the
lungs and heart rhythm abnormalities.
The chest Xray dated 22 July 2011
showed fluid in the lungs – this was covered up by the radiologist.
The lung spirometry dated 22 July
2011 was abnormal – this was covered up in the report.
I had fluid retention at that time
and in fact had severe fluid retention for several months thereafter –
photographic evidence available. This shows that my renal function was
disturbed for several months thereafter.
I had severe chest pain on 9 and
11 August 2011.
My heart rate was abnormally high
all through August and September 2011.
I had nausea, vomiting and
abdominal pain in July 2011 including in the days immediately preceding 22 July
2011.
My urine analysis dated 22 July
2011 shows low specific gravity. There were leukocytes in the urine.
The packed cell volume and ESR in
my haemogram dated 22 July 2011 were abnormal.
I had respiratory complaints in
July and August 2011 including cough, mucus discharge, and breathlessness.
Dr Sandeep Budhiraja prescribed
calcium on 14 September 2011 showing that I had low calcium levels which is
another consequence of ethylene glycol poisoning. Ethylene glycol toxicity
(hypocalcemia is a common finding in the chemistry panel of dogs and cats
poisoned with antifreeze. Precipitation of calcium by oxalate, one of the
metabolites of ethylene glycol, is thought to be the mechanism. Any signs of
hypocalcemia are overshadowed by those due to the primary problem.
I had low transferrin saturation
on 17 August 2011.
My Ferritin levels on 17 August
2011 were low.
Dr Kiran Bhushan (who it appears
had also been spoken to as I was under complete surveillance) was asked to
recommended Vitaman B complex for me, which is a therapy for ethylene glycol
poisoning.
It looks as if I may have been
poisoned with ethylene glycol on more than one occasion and even in 2012.
It appears that I was being
chronically poisoned with ethylene glycol over several weeks in July and August
2011. Chronic exposure to ethylene glycol in
diet will cause kidney toxicity and liver effects.
I also had symptoms of severe
lower back pain during this period.
Sublethal ethylene
glycol poisoning can cause fatal chronic oxalosis.
It looks as if the
doctors at Max Healthcare were covering up the ethylene glycol poisoning and
were attempting false diagnoses to cover up visible symptoms of resultant
health effects.
Ethylene glycol can
be used to contaminate water. Ethylene glycol can also be used to contaminate
food.
My water supply
tank had been separated from that of the other residents of G 4 in Jangpura
Extension during the time I was living there. The police documents filed with
the police counter affidavit in my writ petition falsely attempt to cover up
this fact. I recall that in the summer of 2011 I had noticed a green residue on
the insides of the plastic bottles that I used to store water filled from the
kitchen tap.
I had complained to
the police a few days before 22 July 2011 that my front door lock had been
tampered with and my house was being entered into in my absence.
A Dail Mail news
report dated 19 July 2013 showing an example of poisoning by causing chronic
ingestion of ethylene glycol over several weeks is attached.
All the medical
reports/ records referred to above are part of the court record in Writ
Petition Civil 1280/ 2012 as are the written complaints made to the Police and
to the Chief Justice of India in July and August 2011.
Seema
Sapra
Advocate
& whistleblower and witness in corruption complaints against General
Electric Company and Montek Singh Ahluwalia
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