INDUSTRIAL CHIMICALS:
CORROSIVES
Youan Bi Beniet Marius, Master student clin. Pharm. I
1
1/18/2014
OUTLINES
1/18/2014
2
INTRODUCTION
EPIDEMIOLOGY
SIGNS & SYMPTOMS
MANAGEMENT
TOXICOSIS
 Corrosives are a group of chemicals that have
the capacity to cause immediate tissue injury
on contact by a chemical rea...
INTRODUCTION(2/3)
Factors determining the corrosion potential
P H : Highly corrosive if PH is < 2 or > 11
Concentration
US...
INTRODUCTION(3/3)
Most commonly affect
the GIT, respiratory system, the eyes and the skin.
Corrosives=caustics something t...
EPIDEMIOLOGY (1/3)
International poisoning statistics
estimated prevalence : 2.5-5%
morbidity : > 50%
80% occurs in childr...
EPIDEMIOLOGY(2/3)
Small series available from several countries
In Kenya : Corrosives poisoning 10.8% of the
household and...
EPIDEMIOLOGY (3/3)
From these epidemiological data we can deduce:
children : Alkaline ingestions continue to occur
Adult :...
TOXICOSIS : ROUTES OF POISONING
Major routes of exposure are:
the skin & eyes (topic)
the lung (inhalation)
the gastrointe...
TOXICOSIS : MECHANISM OF POISONING
Tissue injury by:
altering the ionized state and structure
disrupting covalent bonds
io...
MECHANISM OF POISONING: PART I
TISSUE DAMAGE (1/4)
Structure of a protein Sturcture of a Phospholipid
OH & H
OH & H
_ +
_ ...
MECHANISM OF POISONING: PART I
TISSUE DAMAGE (2/4)
SOAP
FATS of the
cell
membrane
Proteins Proteinates
1-Proteins disrupti...
MECHANISM OF POISONING: PART I
TISSUE DAMAGE (3/4)
Acids: Acute injury, Phase I
No action on fats because of reverse react...
: tissue collagen swells
and shortens.
Responsible of edema
Inflammation
Thrombosis of the :
alkaline
ingestion :
severely...
MECHANISM OF POISONING: PART II
TISSUE REPAIR (1/2)
Ulceration
within 24-72 h
after acute
necrosis
Granulation
tissue repl...
MECHANISM OF POISONING: PART II
TISSUE REPAIR (2/2)
Phase III: Fibrosis and Stricture
Fibrosis stomach Esophagus stricture...
SIGNS & SYMPTOMS (1/6)
 The clinical presentation depends upon:
.
the condition of exposure:
the routes of entry :
the ch...
SIGNS AND SYMPTOMS (2/6)
Acute toxicity : By sudden or short term exposures
GIT
acute injury
General symptoms ( pain, vo...
SIGNS AND SYMPTOMS (3/6)
Late complications
GIT
Strictures and Stenosis of the esophagus
3 weeks after ingestion , in th...
SIGNS AND SYMPTOMS (4/6)
RT
Irritation of the RT, dryness in the throat
Dyspnea
Bronchoconstriction
Pulmonary edema
Cough...
SIGNS AND SYMPTOMS (5/6)
 EYES & SKIN
Pain at the site of exposure
Burns at the site of exposure
Erythema and vesicle for...
SIGNS AND SYMPTOMS (6/6)
Chronic toxicity : by repeated exposures over a long period of time
Inhalation of certain acid
va...
MANAGEMENT
The objectif of the management of corrosives
poisoning is twofold :
Decontaminate
Prevent late complications in...
MANAGEMENT: DECONTAMINATION (1/4)
Occular decontamination
DO DON’T
remove the patient/victim
from the source of exposure...
MANAGEMENT: DECONTAMINATION (2/4)
Care provider should wear
gloves, water-resistant gowns,
splash resistant goggles, and ...
MANAGEMENT: DECONTAMINATION(3/4)
 GI decontamination
Ensure unobstructed airway
 Neutralization
Milk and water have bee...
MANAGEMENT: DECONTAMINATION(4/4)
 Immediately remove the
patient/victim from the source
of exposure
 Ensure that the pat...
MANAGEMENT: PREVENTION OF LATE COMPLICATIONS
To prevent
Strictures
formations.
Dexamethasone 1 mg/kg/day
Prednisolone 2 mg...
LABORATORY AND DIAGNOSTIC TESTS (1/2)
 in the acute phase of
caustic injury
 may reveal presence
of mediastinal air or
f...
LABORATORY AND DIAGNOSTIC TESTS (2/2)
3- Esophagogastroduedonoscopy
 For diagnostic evaluation of acute corrosive intoxic...
LABORATORY AND DIAGNOSTIC TESTS
– I GRADE: edema and
erythema of the mucosa,
– II A GRADE:
hemorrhage, erosions,
blisters,...
CONCLUSION
1/18/2014
32
Corrosives Contact- immediate - injury=
Children continue to be affected year after year
Corrosive...
1/18/2014
33
REFERENCES
 Anderson KD, Rouse TM and
al. A controlled trial of
corticosteroids in children with
corrosive injury of the
...
35
1/18/2014
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TOXICOLOGY : CORROSIVE POISONING

Introduction- epidemiology-mechanismof poisoning-management.

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INDUSTRIAL CHEMICALS : CORROSIVES

  1. 1. INDUSTRIAL CHIMICALS: CORROSIVES Youan Bi Beniet Marius, Master student clin. Pharm. I 1 1/18/2014
  2. 2. OUTLINES 1/18/2014 2 INTRODUCTION EPIDEMIOLOGY SIGNS & SYMPTOMS MANAGEMENT TOXICOSIS
  3. 3.  Corrosives are a group of chemicals that have the capacity to cause immediate tissue injury on contact by a chemical reaction.They can also damage or destroy metal.  Tree types: Acids Alkalis Oxidants INTRODUCTION (1/3) 3 1/18/2014
  4. 4. INTRODUCTION(2/3) Factors determining the corrosion potential P H : Highly corrosive if PH is < 2 or > 11 Concentration USE: Intended for machinery or for Hand use. Formulation: Solid - Deep but localized injury. Amount Ingested: > 100 -150ml – Massive poisoning Liquid - Extensive injury 4 1/18/2014
  5. 5. INTRODUCTION(3/3) Most commonly affect the GIT, respiratory system, the eyes and the skin. Corrosives=caustics something that eats away Most common caustic agents include : TYPE EXEMPLES ALKALIS sodium hydroxide and potassium hydroxide…. ACIDS hydrochloric acid, sulfuric acid,….. OXIDANTS Hypochlorous acids, peroxide….. 5 1/18/2014
  6. 6. EPIDEMIOLOGY (1/3) International poisoning statistics estimated prevalence : 2.5-5% morbidity : > 50% 80% occurs in children below 5 years National poisoning statistics Only USA are available AAPCC 2008 : mortality : 13% number of exposures : 191 397 poisoning attributed to caustic substances:8.6% 62.9% in children and 95.5% of all were accidental 6 1/18/2014
  7. 7. EPIDEMIOLOGY(2/3) Small series available from several countries In Kenya : Corrosives poisoning 10.8% of the household and industrial agents (24% of all poisoning cases) . Some of this series gave us data on: common corrosives used circumstances of injury age distribution . 7 1/18/2014
  8. 8. EPIDEMIOLOGY (3/3) From these epidemiological data we can deduce: children : Alkaline ingestions continue to occur Adult : more suicidal attempts more common in All exposure were mostly due to alkaline. 80% are accidental women 8 1/18/2014
  9. 9. TOXICOSIS : ROUTES OF POISONING Major routes of exposure are: the skin & eyes (topic) the lung (inhalation) the gastrointestinal tract (ingestion) In general Inhalation > Ingestion> Skin exposure 9 1/18/2014
  10. 10. TOXICOSIS : MECHANISM OF POISONING Tissue injury by: altering the ionized state and structure disrupting covalent bonds ion (H+) : produce toxic effects for acids ion (OH-) : for alkaline Pathological changes divided into 2 part : Tissue Damage Tissue Repair II 10 1/18/2014
  11. 11. MECHANISM OF POISONING: PART I TISSUE DAMAGE (1/4) Structure of a protein Sturcture of a Phospholipid OH & H OH & H _ + _ + 11 1/18/2014
  12. 12. MECHANISM OF POISONING: PART I TISSUE DAMAGE (2/4) SOAP FATS of the cell membrane Proteins Proteinates 1-Proteins disruption 2-Solubilisation 3-Liquefactive necrosis 4-Further penetration ALKALI: Acute injury, Phase I Cell death occurs from emulsification and disruption of cellular membranes 12 1/18/2014
  13. 13. MECHANISM OF POISONING: PART I TISSUE DAMAGE (3/4) Acids: Acute injury, Phase I No action on fats because of reverse reaction coagulative necrosis resulting in the formation of an eschar or coagulum. 13 1/18/2014
  14. 14. : tissue collagen swells and shortens. Responsible of edema Inflammation Thrombosis of the : alkaline ingestion : severely injured tissues are oropharynx, hypopharynx, and esophagus acid ingestion : commonly involved organ is stomach small vessels MECHANISM OF POISONING: PART I TISSUE DAMAGE (4/4) & create airway obstruction 14 1/18/2014 What complication need to be consider ?
  15. 15. MECHANISM OF POISONING: PART II TISSUE REPAIR (1/2) Ulceration within 24-72 h after acute necrosis Granulation tissue replace necrotic tissue 3-4 days of exposure later. Collagen deposition continues for weeks to months Remodels resulting in stricture formation Over the next 2-4 Weeks Phase III: Fibrosis and Stricture Phase II: Granulation 1 2 3 4 15 1/18/2014
  16. 16. MECHANISM OF POISONING: PART II TISSUE REPAIR (2/2) Phase III: Fibrosis and Stricture Fibrosis stomach Esophagus stricture 16 1/18/2014
  17. 17. SIGNS & SYMPTOMS (1/6)  The clinical presentation depends upon: . the condition of exposure: the routes of entry : the characteristics of the caustic agents : Acute toxicity or chronic toxicity , GIT , RT, Skin, Eyes amount type of the substance Acid or alkali physical form of the substances Liquid, solid,gaz 17 1/18/2014
  18. 18. SIGNS AND SYMPTOMS (2/6) Acute toxicity : By sudden or short term exposures GIT acute injury General symptoms ( pain, vomiting...) Specifics symptoms  Alkali Solid form : Hoarseness & stridor Liquid form : dysphagia & odynophagia Acid Epigastric pain & hematemesis. A characteristic stain inside the mouth & lips 18 1/18/2014
  19. 19. SIGNS AND SYMPTOMS (3/6) Late complications GIT Strictures and Stenosis of the esophagus 3 weeks after ingestion , in the first three months or even after one year Stenosis of antrum and pylorus often 5 to 6 weeks after the ingestion. Feeling of full stomach……GOO Esophageal and stomach cancer The latent period may range between 40 to 50 years. 19 1/18/2014
  20. 20. SIGNS AND SYMPTOMS (4/6) RT Irritation of the RT, dryness in the throat Dyspnea Bronchoconstriction Pulmonary edema Coughing 20 1/18/2014 signs & symptoms of CHEMICAL PNEUMONITIS
  21. 21. SIGNS AND SYMPTOMS (5/6)  EYES & SKIN Pain at the site of exposure Burns at the site of exposure Erythema and vesicle formation  SYSTEMIC EXPOSURE Ca & Mg K Hypotension Dysrhythmias Metabolic acidosis or alkalosis 2+2+ + 21 1/18/2014
  22. 22. SIGNS AND SYMPTOMS (6/6) Chronic toxicity : by repeated exposures over a long period of time Inhalation of certain acid vapours cause loss of tooth enamel, eventually leading to extensive tooth decay exposure to quartz- containing dusts in the construction industry can cause scar tissue in the lungs. lung suffering from silicosis 22 1/18/2014
  23. 23. MANAGEMENT The objectif of the management of corrosives poisoning is twofold : Decontaminate Prevent late complications in case of ingestion 23 1/18/2014 The appropriate decontamination depend upon the routes of entry
  24. 24. MANAGEMENT: DECONTAMINATION (1/4) Occular decontamination DO DON’T remove the patient/victim from the source of exposure. Immediately flush the eyes with large amounts of tepid water for at least 20 minutes. Wash eyes with saline during transport. Monitor the pH of the conjunctival sac before starting other therapeutic or diagnostic interventions PH=7.4 Use oils, salves, or ointments for injured eyes. Use the gel form of calcium gluconate in eyes 24 1/18/2014
  25. 25. MANAGEMENT: DECONTAMINATION (2/4) Care provider should wear gloves, water-resistant gowns, splash resistant goggles, and masks Remove the patient/victim from the contaminated area. Remove all clothing ( at least down to their undergarments). Thoroughly wash and rinse the contaminated skin. using a soap and water solution Using hot water, strong detergents, or harsh abrasives Skin decontamination DO DON’T 25 1/18/2014
  26. 26. MANAGEMENT: DECONTAMINATION(3/4)  GI decontamination Ensure unobstructed airway  Neutralization Milk and water have been used but their effectiveness has not been proven. It is contraindicated. In order to be effective, it must be done within the first hour after ingestion of a caustic agent. Alkalis : mild vinegar, lemon or orange juice. Acids: milk, eggs or antacids; sodium bicarbonate is not recommended DO DON’T Induce vomiting (emesis) Perform Gastric lavage Give Activated charcoal ? 26 1/18/2014
  27. 27. MANAGEMENT: DECONTAMINATION(4/4)  Immediately remove the patient/victim from the source of exposure  Ensure that the patient/victim has an unobstructed airway.  Evaluate respiratory function and pulse  If shortness of breath occurs or breathing is difficult (Dyspnea), administer oxygen.  Assist ventilation as required. Always use a barrier or bag- valve-mask device.  If breathing has ceased (apnea), provide artificial respiration.  Monitor the patient/victim for signs of systemic effects and administer symptomatic treatment as necessary.  Inhalational decontamination 27 1/18/2014
  28. 28. MANAGEMENT: PREVENTION OF LATE COMPLICATIONS To prevent Strictures formations. Dexamethasone 1 mg/kg/day Prednisolone 2 mg/kg/day Steroids 3 times a day intravenously, given for at least 3 weeks. or Antibiotics consensus : patients treated with steroids should be treated with antibiotics as well. prophylactic antibiotic without steroid therapy : NO . Pos: Ampicilline 500 mg intravenously, 6 hourly 28 1/18/2014
  29. 29. LABORATORY AND DIAGNOSTIC TESTS (1/2)  in the acute phase of caustic injury  may reveal presence of mediastinal air or free air under the diaphragm that may be the evidence of esophageal or gastric perforation  Perform 25–30 days after corrosive ingestion  may give us useful information on changes in the dimensions of esophageal and gastric lumen 1- Abdominal roentgenograms 2-Esophagogastrodudodenography with gastrographin 29 1/18/2014
  30. 30. LABORATORY AND DIAGNOSTIC TESTS (2/2) 3- Esophagogastroduedonoscopy  For diagnostic evaluation of acute corrosive intoxications and lesions of the upper gastrointestinal tract  Optimal timing : the first 12–24 hours after corrosive ingestion  Emergency esogastroduodenoscopy depends on: type of the corrosive substance, its quantity the intention of ingestion the corrosive substance onset of symptoms following the ingestion 30 1/18/2014
  31. 31. LABORATORY AND DIAGNOSTIC TESTS – I GRADE: edema and erythema of the mucosa, – II A GRADE: hemorrhage, erosions, blisters, superficial ulcers, – III B GRADE: circumferential lesions, – III GRADE: deep grey or brownish-black ulcers, – IV GRADE: perforation. – Grade 0: normal mucosa, – Grade I: edema and erythema of the mucosa, – Grade II A: hemorrhage, erosions, blisters, superficial ulcers, – Grade II B: circumferential lesions, – Grade III A: focal deep gray or brownish-black ulcers, – Grade III B: extensive deep gray or brownish-black ulcers, – Grade IV: perforation. Kikendall classification Zagar classification These classifications have enormous importance in diagnosis and treatment of acute corrosive intoxications . 31 1/18/2014
  32. 32. CONCLUSION 1/18/2014 32 Corrosives Contact- immediate - injury= Children continue to be affected year after year Corrosive is a chemical hazard in the home Alkaline is likely to cause more damage than acid = decontaminate and prevent lateManagement: Prevention of corrosive poisoning is better than complications cure
  33. 33. 1/18/2014 33
  34. 34. REFERENCES  Anderson KD, Rouse TM and al. A controlled trial of corticosteroids in children with corrosive injury of the esophagus. N Engl J Med 1990; 323(10):637-40.  Chibishev A.,Simonovska N., al. Post-Corrosive Injuries Of Uppergastrointestinal Tract Contributions, Sec. Biol. Med. Sci., MASA, XXXI (2010); (1): 297–316  C.P. Lakshmi, Ranjit Vijayahari et al. A hospital- based epidemiological study of corrosive alimentary injuries with particular reference to the Indian experience .The National Medical Journal of India 2013; 26 (1): 31.  D.G. Nyamu, C.K. Maitai et al. Trends of Acute Poisoning Cases Occurring at the Kenyatta National Hospital, Nairobi, Kenya. East and Central African Journal of Pharmaceutical Sciences 2012; 15: 29-34  D. Mignonsin, S. Yassibana Et Al Intoxication par Les Produits Caustiques : Etude Epidémiologique et Approche Thérapeutique. Médecine d'Afrique Noire 1992 ; 39 (4) : 306-311.  Goldman LP, Weigert JM. Corrosive substance ingestion: a review. Am J Gastroenterol 1984;79:85–90.  J B Dilawari, Surjit Singh et al. Corrosive acid ingestion in man a clinical and endoscopic study. Gut, 1984; 25: 183-187  Kikendall J. Caustic ingestion injuries. Gastroenterol Clin North Am 1991; 220:847–57.  Kovil Ramasamy, MD, and al. Corrosive Ingestion in Adults J Clin Gastroenterol 2003; 37(2):119–124.  Lahoti D. Corrosive injury to upper gastrointestinal tract. In: Manual of medical emergencies, 3rd edition  Marten Duncan, DO, Roy K.H. Wong. Esophageal emergencies: things that will wake you from a sound sleep Gastroenterol Clin N Am 2003; 32: 1035–1052  Michael R. Macdonald et al. Caustic esophageal burn in children Canadian Family Physician March 1994; 40: 559  Moscicki ek: Gender defferences in completed and attempted suicides. Ann Epidemiol 1994; 4: 152 – 158  Paul Marchand . Caustic Strictures of the Oesophagus. Thorax ,1955; 10: 171.  R Raghu Ramulu Naik , M Vadivelan. Corrosive Poisoning Indian Journal of Clinical Practice August 2012; 23( 3): p31  Scher la. Maull k.j. Emergency management and sequelae of acid ingestion. JACEP 1978:7:206-208.  Zargar S.A. Kochher R, et al. Ingestion of Corrosive Acids. Spectrum to injury to upper gastrointestinal tract and natural History. Gastroenterology 1989; 97: 702 - 707 34 1/18/2014
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