Arsenic Poisoning

 

Arsenic

Environmental arsenic exists as sulphide complexes realgar (As2S2), Orpiment (As2S3) and iron pyrites. On heating of these ores, arsenic sublimes and oxidizes to form arsenic trioxide (As2O3), fine granular white powder also known as white arsenic. Arsine gas (AsH3) is another arsenic compound, formed by the hydrolysis of metal arsenides and by the reduction of metals of arsenic compounds in acidic solutions.

In the metallic form Arsenic is not poisonous as it is insoluble in water and cannot be absorbed from alimentary tract, but when it is oxidized by exposure to air it becomes poisonous. But some workers believe that the metallic form may undergo oxidation in the GIT producing symptoms.

Arsenic can be inhaled and absorbed through the skin or through GI tract after ingestion. Once in the tissues, arsenic exerts its toxic effect through several mechanisms, the most significant of which is the reversible combination with sulfhydryl groups. Arsenic blocks the Krebs cycle and inter­rupts oxidative phosphorylation thus resulting in a marked depletion of cellular ATP and eventually death of the metabolizing cell. 2-4 weeks after ingestion, arsenic is incorporated into hair, nails, and skin as it binds to the sulfhydryl groups of keratins. Four weeks after ingestion, arse­nic begins to localize in the bone where it subs­titutes for phosphate.

Mechanisms of action:

(i) Reversible combination with sulfhydryl groups

(ii) Reacts with SH group in tissue proteins

(iii) Interferes with number of enzyme system essential for cellular metabolism

(iv) It is a capillary poi­son, dilates capillary

 

The acute arsenic poisoning results from the: (i) Oral ingestion (ii) Inhalation of arsenic gas (iii) Rubbing into the skin (iv) Introduction into rectum or vagina.

Fatal Dose: 100-200 mg of Arsenic Trioxide

Fatal Period: 1-2 days

 

The Marsh tests

In this test zinc and sulphuric acid is used to make the nascent oxygen. The solution is boiled in marsh tube with pyrogallol, and water saturated with SO₂ (1 ml of sample + 2-3 drops of 0.5% pyrogallol + 1 ml of water saturated with SO₂ in porcelain basin for 30 min.). After which sample is poured and same process is followed for 30 min, if as is present then a black mirror like luster is seen on the cooler side of marsh tube. For confirmation of As has formed hat luster, can be tested by sealing the ends of the tube and air is allowed to flow instead of hydrogen through it and tube is heated gently, results in the formation of octahedral crystals of as trioxide formed at the cooler and narrow part of the tube, observed by high power microscope. The quantitative analysis can also be done by using this test.

The Reinsch test

It is an initial indicator to detect the presence of heavy metals in a biological sample. This method is sensitive to antimony, arsenic, bismuth, selenium, thallium, and mercury. Suspect body fluid or tissue is dissolved in a hydrochloric acid solution followed by insertion of a copper strip into the solution. The appearance of a silvery coating on the copper may indicate mercury. A dark coating indicates the presence of one of the other metals. Confirmation can be done using absorption or emission spectroscopy, X-ray diffraction, or other analytical technique suitable for inorganic analysis.

Signs and symptoms

They start within half an hour but may be delayed for several hours when it is given in rectum, vagina, or skin. The dilatation of capillaries is responsible for most of the symp­tom:

(i) Initially the patient experiences a metallic taste in the mouth and slight garlicky odour in the breath along with xerostomia and dysphagia

(ii) Stomach pain which may increase on pressure

(iii) Increased salivation and intense thirst

(iv) Purg­ing, tenesmus, pain and irri­tation around anus

(v) Generalised vasodilation caused by capillary damage

 results in transudation of plasma and severe hypovolemia

(vi) If the ingested dose is smaller, the patient will have severe

 headache, vertigo, peri­orbital oedema, skeletal muscle cram­

ping and evidence of renal damage manifested as oliguria,

 proteinuria, and If death does not occur in the first few hours

 from shock, patient may die a few days later from acute

 hepatic or renal failure.

Autopsy Findings

(i) Rigor mortis lasts longer (The most prominent postmortem

 characteristic, as the body is stiff, also shrinks like shrunken

 buccal cavity, eyeballs, etc., because of excessive loss of water

 and blood from body i.e., bloody rice water stool and

 vomiting.

(ii) General shrunken appearance due to dehydration

(iii) Eyeballs are shrunken

(iv) Cyanosis of hands and feet is there

(v) Jaundice is also present

(vi) Mucous membrane of mouth and pharynx is inflamed and

 ulcerated

(vii) Stomach is the main organ to be inflamed; food particles

 are mixed with arsenic embe­dded in the mucous. The inner

 wall of the stomach is swol­len, congested and tinged with

 streaks of blood and arsenic. On scrap­ing the mucous mem­

brane is congested inflamed and is brownish red or scarlet in

 colour. There are petechial haemorrhages. The inflammation

 is more marked in the greater curvature and the cardiac end.

 Ulce­ra­tion, gangrene and perforation have been rarely

 reported.

(viii) Small intestine is flabby and contains large flakes of

 mucous with little faecal matter, sub mucosal haemorrhages

 are present and the epi­thelium is flabby and oedematous

(ix) Large intes­tine contains seromucous and the intestinal

 glands are swollen and enlar­ged

(x) Lungs are con­ges­ted, oedematous and show sub pleural

 ecchy­mosis.

(xi) Caecum and rectum are inflamed and the mucous

 membrane is flabby.

When the dose is not large enough to kill the patient, several

 secondary effects can be seen 2-4 weeks after ingestion of the

 poi­son. Patients who recover from the acute form of poi­soning

 develop

(i) Skin and mucosal changes

(ii) Peripheral neuropathy

(iii)Linear pigmentation in the fingers

(iv)Cutaneous manifestations appear within 1-4 weeks and

 consist of dry, diffuse, and scaly desquamation with

 hyperpigmentation over the trunk and extremities and

 hyperkeratosis of palm and soles

(v) Mucosal surfaces also show signs of irritation like

 conjunctivitis, photophobia, and pharyngitis

(vi) After 5 weeks, transverse white streaks 1-2 mm width

 appears above base of each fingernail called Aldrich-Mee’s

 line.

 

  
      

Aldrich-Mee’s line and rain drop type of pigmentation

 

(vii) Genera­lized or localized, rain drop type of pigmen­

tation of the skin involving the covered parts of the body such

 as flexors, nipples, lower abdomen, temples, and eyelids.

(viii) Blackfoot disease is a vascular disease associated with

 long-term exposure to inorganic arsenic. The patients suffer

 severe systemic arteriosclerosis with black, mummified dry

 foot gangrene in severe cases.

 

Medico legal aspects

(i) It is an ideal homicidal poisoning that is used frequently in India.

(ii) It delays putre­faction (c) can be detected in decomposed bodies (d) can be found in bones, hair even years after the poisoning

(iii) It is used on abortion sticks as paste or ointment

(iv) Arsenophagists use the drug as a habit as aphrodisiac and can acquire tole­rance up to 0.3 gm or more in one dose

 

Postmortem imbibitions of arsenic: When there is a criminal charge of arsenic poisoning, the defense may take the plea that Arsenic was intro­duced after death and postmortem imbibition has occurred in the tissues.

 

Differences between Acute Arsenic poisoning and  Cholera
Findings	Acute Arsenic  Poisoning	Cholera
Vomitus	Consists of mucous, bile and blood	Watery
Stools	High coloured  discharge with  straining,  tenesmus	Involuntary, rice  water stool
Pain in throat	Present before   vomitus	Present after   vomitus
Voice	Not affected	Peculiar and rough
Conjunctiva	Inflamed	Not inflamed