Alphos poisoning powerpoint for gian sagar medical college students.

1. Alphos Poisoning

2. What is Poisoning ?
 By definition, anything which when used
internally or on the body surface in a dose
or in repeated doses, if acts chemically
and physiologically, causing disturbances
of body functions and leads to disease or
death is a poison.

3. Aluminum phosphide
- a solid fumigant
- an inorganic pesticide (has got
insecticidal, rodenticidal and fungicidal effects)
- has been used extensively since 1940
- used all over the world but freely and easily
available in developing countries.

4. Why is it used ?
Because of its properties which are considered
near ideal:
 1) toxic to all stages of insects.
 2) highly potent
 3) does not affect seed viability
 4) free from toxic residues
 5) leaves little residues on food grains.

5. In what all forms is it available?
 commonly available as:
◦ 3 gm tablets or 0.6 gm pellets
 tablets are dark brown or
grayish in color.
 also available in porous blister
packs, sachets or as dusts

6. Usage
Crop Storage
Crop Transport (Rail)
Indoor
Crop Processing Units
AlP As fumigant in field for
burrowing rodents
Outdoor
As bait for rodents

7. Study* conducted over a year from 2004-2005 at
JNMCH, Aligarh highlighted the following demographic
profile, socio-economic conditions and intent of poisoning.
Gender distribution (80 cases)
18.80%
Male
Female
81.20%
* Gupta et al, A STUDY OF ALPHOS POISONING IN WESTERN UP

8. 4% Mode of death
Suicidal
Accidental
96%
Out of 96 % suicide cases (adults)
16%
Domestic conflict
Marital discord
39%
88%
economic
hardships
* Causes were in overlapping patterns

9. AlP suicides amongst
teenage population
10%
Exam results and
relationship failures
Others
90%

10. Comparison
 In UK, AlP is available in the form of tablets or
pellets (Phostoxin, Talunex, and Degesch) used
as rodenticides, and supply is restricted under
the Pesticides Act 1998 to qualified users.
 In US also, its supply is restricted and given
only to certified users.
 Whereas In India, it is freely and easily
available.

11. Chemical composition of the tablet
 Tablets contain 2 ◦ AlP= active
compounds: component
◦ 1) AlP
◦ 2)Al carbonate ◦ AlCO3= added to
prevent self ignition
of phosphine gas
◦ Ratio = AlP: AlCO3= 56:44 which is liberated
when AlP reacts with
moisture.

12. Rx
 In Air:
◦ AlP + 3 H2O  Al(OH)3 + PH3
Al(OH)3 = non toxic grayish colored residue which is left behind
 In Stomach:
◦ AlP + 3HCl  AlCl3 + PH3
◦ AlP + 3 H2O  Al(OH)3 + PH3
 Each 3 gm tab  1 gm PH3
 And 0.6 gm pellet  0.2 gm PH3

13. Properties of Phosphine
 Phosphine gas is colourless and odourless.
 However on exposure to air it gives a foul
odour(garlicky or decaying fish)
◦ due to the presence: substituted phosphines
and diphosphines

14. Route:
AlP
ingested
Majority of AlP reacts with
Small amount of AlP is
H20 and HCL, releasing
directly absorbed
PH3
Released PH3 gets And subsequently
absorbed into circulation metabolized in liver
Resulting in Early Signs & Resulting in Delayed
Symptoms onset of toxicity

15. Mechanism of Injury/ Action
Absorbed
PH3 causes
N.C.I. of ↑ Superoxide
Cytochrome ↓ Catalase
Oxidase dismutase
levels
(mitochondria) activity
Resulting in
Cellular
hypoxia
↑ Formation of free radicals
Cellular
damage ↑

16. Increased formation of free radicals
Acclerated lipid peroxidation
Disruption of ionic Damage to nucelic
Damage to cell mb.
barriers acid
Alterations in Na, K, Mg permeabiltiy
Altered membrane
potential and focal
myocardial necrosis
ECG abnormalities and cardiac arrhythmias.

17.  The presenting symptoms depend on the
route of administration.
 Routes are: inhalation, ingestion, dermally
 Most cases are due to ingestion of AlP

18. Poisoning – Clinical Picture
Irritation of
mucosa, dizziness, easy fatigability
, N, V , H and diarrhea
Mild
Ataxia, Numbness,
Moderate Paresthesia, Ms wk, Ms
Inhalation ply, diplopia
Severe
ARDS, convulsions,
CCF, coma

19. Ingestion leads to a worse clinical picture:
 Earliest symptoms: N, V and Abd Pain
 Failure of each and every system of body sets in but at
different pace.
 GI symptoms:
 Excessive thirst
 Abd pain
 Epigastric tenderness
 CVS:
 Profound hypotension
 Dry pericarditis
 Myocarditis
 Acute CHF
 Arrythmias

20.  Resp symptoms:
 Dyspnoea may progress to resp failure
 Nervous System:
 Headache, Dizziness, Altered mental status
 Convulsion
 Acute hypoxic enchelopathy
 Coma
 Renal and Hepatic failure
 Ms wasting, limb tenderness
 Bleeding diathesis

21. Microscopic changes (Kapoor et al, IIJFMT, 2006)
ML autopsies of 83 established AlP cases showed various microscopic changes
in all the vital organs
LIVER
100 92
100
90 74
80 57
70 55 49
60 43
50 29
40 20
30
20
10
0

22. Lungs:
100 98
100 92
90 81
80 66
70 58
60
50
40
30
20
10
0

23. Kidneys
100
100
90
74
80
70 62
60
50 38
40
30
20
10
0
Congestion Tubular Infiltration Tubular
degeration & dilatation
necrosis

24. Congestion
120
100
80
60
Congestion
40
20
0
Liver Lungs Kidneys Stomach Brain
A striking feature about microscopic changes due to AlP
poisoning is that all vital organs showed congestion in all
the cases.

25. Diagnosis
 1) Positive h/o ingestion/ inhalation
 2) Typical clinical features (including profound hypotension
and shock)
 3) Garlicky odor
 4) Highly variable arrhythmias in a young patient with shock
 5) No prior h/o cardiac disease
Confirmatory Test (Nitrate test):
a) On gastric aspirate: 5ml Asp + 15 ml H20, flask & AgNO3
b) On exhaled air: AgNO3 impregnated filter paper
• *Sensitivity a:b= 100:50
• * Most sensitive & specific method: gas chromatography

26. Lab Investigation
 Lab evaluation mainly done to assess the prognosis.
 HMG: anemia (hemolytic anemia)
 PBF: may show fragemented RBCs
 ↑SGOT, SGPT and metabolic acidosis: moderate to
severe ingestional poisoning.
 Electrolyte: Mg ↑ , K ↑ or ↓
 Urine volume: decreased (oliguria / anuria)
 Urine R/E: Inc in proteins, RBCs
 Measurement of Plasma renin: significant
◦ Level in plasma α dose of pesticide, ↑ renin= ↑ mortality

27.  Serum cortisol: usually low in severe poisoning
 CXR: hilar or perihilar congestion/ ARDS skiagram
 ECG: shows various manifestations of cardiac injury
ST depression or elevation,
 bundle branch block,
 ventricular tachycardia,
 ventricular fibrillation
 Echo:
 Wall motion abnormalities,
 generalised hypokinesia of the left ventricle,
 decreased ejection fraction and
 pericardial effusion

28. ECG findings:(Paper: Mathai et al, Indian J Anaesthesia, 2010)

29. APACHE II Vs Mortality
 In the same study, the mean
APACHE II score at
admission to the hospital
was 12.14 6.608
 Study found that, in patients
with APACHE II scores
of more than 8, the rates of
mortality were 73% .

30. APACHE II
 The APACHE II score at admission correlated well with
mortality and survivors had significantly lower score
than non-survivors (score 8.64 5.27 vs 14.56
6.66, respectively, P = 0.019).

31. Fatal dose
 The specified fatal dose is 0.15-0.5 gm.
 However, most of the patients present with ingestion of
three or more tablets which invariably results in death.

32. Management
 First Aid- On the spot
 Immediate resuscitation of shock + supportive
measures ASAP
 A, B, C
◦ Establish i.v. access
◦ Administer 2-3 lit of NS within first 8-12 hrs guided by
CVP and PCWP
◦ Aim: keep CVP at around 12-14 cm
◦ Few studies* have recommended rapid infusion of saline
(3-6 litres) in the initial 3 hrs
*Siwach et al, J API 1995

33. i.v. access – wide bore cannula
NS infusion- 3 lit (first 8 hr or rapid
within first 3 hrs)
If hypotension still persists( sys<90)
 low dose dopamine,4-6
ug/kg/min
Hydrocortisone 200- 400 mg i.v. q4-6 h

34. Oxygen: for hypoxia
If ARDS has set in  I.C.U +
Mechanical ventilation
If ECG  arrhythmias
antiarrhyhmic
If bicarb < 15 meq/l  give
NaHCO3 (50-100 meq i.v. 8hrly) till
level reaches 18-20 meq/l

35. Meanwhile,
To eliminate PH3 from
body: 2 ways
1) ↓ Absorption 2) ↑ Excretion
gastric lavage with
potassium permanganate
(1:10,000) is done
KMNO4 oxidizes PH3 non toxic
phosphate

36. 2) Excretion
Catharsis: liquid
paraffin via NG tube Maintain hydration
& Renal perfusion
By giving i.v. Give diuretics
fluids & low (furosemide) if
dose dopamine BP>90: to enhance
(4-6 ug/kg/min) excretion

37. Dialysis
Dialysis may be required for severe acidosis and acute renal failure
MgSO4
 Magnesium sulphate use (both high and low dose) did not improve
survival in controlled clinical trials *. Hence its use is not
recommended but on the contrary few past studies (Chugh et al)
emphasize on the role of MgSO4 as anti-peroxidant agent, they
carried out a study on 50 pts divided them into 2 gps mortality
was shown higher in gp which did not receive MgSO4( 44 % Vs
20%)
Coconut oil: lavage beneficial

38. Other management modalities
 Novel therapies such as N‐acetylcysteine, replenishing
cellular glutathione which has been reported to have
antioxidant properties, have been suggested (Chugh et al).
 A characteristic feature of AlP poisoning is myocardial
suppression and resistant hypotension.
 In rats exposed to AlP, N‐acetylcysteine increased
survival time and reduced myocardial oxidative injury
(Azad et al).
 Other agents include trimetazidine, which switches
myocyte metabolism to glucose from fatty acids, thus
reducing oxygen consumption, and may have a potential
role (Duenas et al).

39. Poor Prognosis
Development of:
 refractory shock,
 ARDS, aspiration pneumonitis,
 anaemia,
 metabolic acidosis, Electrolyte imbalance,
 coma,
 severe hypoxia,
 gastrointestinal bleeding, and
 pericarditis.
All these leads to poor outcome

40.  The average time interval between intake of poison and
death is 3 hours with a range of 1-48 hours.
 95% of the patients die within 24 hours and the
commonest cause of death in this group of pts. is
arrhythmia.
 Death after 24 hours is due to shock, acidosis, ARDS
and arrhythmia.
 The mortality rate is highly variable, ranging from 37-
100% and can reach more than 60% even in experienced
and well equipped centers.

41. Thank you

42. References
 Chugh S N, Kolley T, Kakkar R. et al A critical evaluation of
anti‐peroxidant effect of intravenous magnesium in acute
aluminium phosphide poisoning. Magnes Res 1997. 10225–230.
[PubMed]
 10. Azad A, Lall S B, Mittra S. Effect of N‐acetylcysteine and
L‐NAME on aluminium phosphide induced cardiovascular toxicity
in rats. Acta Pharmacol Sin 2001. 22298–304. [PubMed]
 11. Duenas A, Perez‐Castrillon J L, Cobos M A. et al Treatment of
the cardiovascular manifestations of phosphine poisoning with
trimetazidine, a new anti‐ischemic drug. Am J Emerg Med 1999.
17219–220. [PubMed]

43. Routes of exposure First Aid
Inhalation Management position. Artificial respiration if
Fresh air, rest. Half-upright
indicated.
Skin Remove contaminated clothes. Rinse and then wash skin
with water and soap.
Eyes First rinse with plenty of water for several minutes.
Ingestion Induce vomiting (ONLY IN CONSCIOUS PERSONS!).
Refer for medical attention.
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44. Hydrocortisone 200-400 mg every 4-6 h i.v.
to:
a)to combat shock
b) reduce the dose of dopamine
c)check capillary leakage (as seen in ARDS)
d)to potentiate the responsiveness of the body to
endogenous and exogenous catecholamine's
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45. Hemolytic anemia and MAHA
 Aluminum phosphide is a redox substance; so theoretically, it
can cause hemolytic anemia.
 Aluminum phosphide could be associated with disseminated
intravascular coagulation, disseminated intravascular
coagulation (DIC) is a well-recognized cause of MAHA.
 Case review by Khurrana et al published in J GID 2009
emphasizes on the possibility of AlP causing MAHA.
Mechanism of MAHA is the formation of a fibrin mesh due
to increased activation of the coagulation system. The red
blood cells are physically cut by these protein networks, and
the fragments are identical to the schistocytes seen on light
microscopy.
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