Toxicity of corrosives
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This is a lecture for medical students discussing the toxicity of corrosives and chemical burns. It starts by describing the differences between organic and inorganic acids followed by discussing the mechanisms of toxicity for strong acids and alkalies. It also outlines the clinical manifestations of chemical burns and the main lines of treatment including first aid measures. The lecture also describes the toxicity caused by carbolic acid and Oxalic acid. This lecture for undergraduate medical students.
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Toxicity of corrosives
- 1. THE TOXICITY OF CORROSIVES Dr. Maha Farid, MBBCh, MS, PhD. Dept. Of Forensic Medicine and Clinical Toxicology Faculty of Medicine Helwan University 4/5/2020 The Toxicity of Corrosives_MF, PhD. 1
- 2. Learning Objectives ■ Recognize the potential hazards associated with occupational and household exposure to corrosives and caustic chemicals. ■ Identify the different modes of toxicity associated with occupational and household chemicals and corrosives. ■ Differentiate between toxicity by organic and inorganic corrosives. ■ Understand the outlines of management and medical care of injured patients following the exposure to caustic substances. 4/5/2020 The Toxicity of Corrosives_MF, PhD. 2
- 3. Mode of Toxicity ■ Accidental: – Household: most common, especially in children. – Occupational: laboratory workers and industrial exposure. ■ Suicide. ■ Homicide: Acid attack. 4/5/2020 The Toxicity of Corrosives_MF, PhD. 3
- 4. The Toxicity of Corrosives_MF, PhD. 4/5/2020 4
- 5. Classification of corrosives. 4/5/2020 The Toxicity of Corrosives_MF, PhD. 5 Class Inorganic Organic Effect Strong Mild Action Local only Local and remote Examples Acids: Sulphuric Acid (H2SO4) Hydrofluoric Acid (HF) Nitric Acid (HNO3) Alkalis: Sodium Hydroxide (NaOH) Potassium Hydroxide (KOH Potash) Ammonium Hydroxide (NH4OH) Acids: Carbolic Acid (Phenol, C6H5OH) Oxalic Acid (C2H2O4)
- 6. Strong Acids And Alkalis 4/5/2020 The Toxicity of Corrosives_MF, PhD. 6
- 7. 4/5/2020 The Toxicity of Corrosives_MF, PhD. 7 https://www.epa.gov/acidrain/what-acid-rain
- 8. Sulphuric Acid Uses: 4/5/2020 The Toxicity of Corrosives_MF, PhD. 8
- 9. Nitric Acid 4/5/2020 The Toxicity of Corrosives_MF, PhD. 9
- 10. Sodium Hydroxide Uses (Lye or Caustic soda) ■ Soap ■ Rayon ■ Paper ■ Petroleum refining ■ Drain cleaners ■ Oven cleaners 4/5/2020 The Toxicity of Corrosives_MF, PhD. 10
- 11. Potassium Hydroxide (Potash) Uses ■ Soap ■ Biodiesel ■ Fuel cells ■ Fertilizers 4/5/2020 The Toxicity of Corrosives_MF, PhD. 11
- 12. Ammonium Hydroxide Uses ■ Cleaning products ■ Auto care products ■ Cosmetics ■ Explosives ■ Fertilizers ■ Hair care: hair colorants, hair glazes, and hair touch-up kits ■ Personal care products: shaving cream, lotions, creams, and acne treatments 4/5/2020 The Toxicity of Corrosives_MF, PhD. 12
- 13. Bleach (Sodium Hypochlorite) ■ Used at homes and laboratories. ■ Cleaning and sanitization purposes. ■ Alkali pH 11-12 ■ Commercial concentration → skin irritation. ■ Mixed with other chemicals: – with acid → Chlorine gas. – With Ammonia→ Chloramine gas. – Causes sever ocular and respiratory irritation. 4/5/2020 The Toxicity of Corrosives_MF, PhD. 13
- 14. Pathophysiology: Acids ■ Acids: donate a proton or H+. ■ Highly reactive compounds. ■ The lower the pH, the stronger the acid. ■ Coagulation necrosis→→ coagulum or eschar. ■ Ingestion →→ stomach is mainly affected. 4/5/2020 The Toxicity of Corrosives_MF, PhD. 14 https://emedicine.medscape.com/article/769336-overview#a5
- 15. Pathophysiology: Alkalis ■ Alkali (base): receives a proton or H+ ■ The higher the pH, the stronger the base. ■ Liquefaction necrosis and saponification of tissues. ■ Ingestion →→ esophagus is mainly affected. 4/5/2020 The Toxicity of Corrosives_MF, PhD. 15 Saponification Reaction https://casereports.bmj.com/content/2012/bcr-2012-007103
- 16. Hydrofluoric Acid ■ Uses: – Glass etching. – Metal cleaning – Electronics manufacturing. – Rust removing ■ Mechanism of toxicity: – Local: sever burn (flesh eating acid). – Remote: forms insoluble salts with Ca2+ and Mg2+ ■ Cause of death: – Hypocalcemia and hypomagnesaemia leading to cardiac arrythmias and arrest. 4/5/2020 The Toxicity of Corrosives_MF, PhD. 16
- 17. Factors affecting the severity of the injury: ■ The pH ■ The concentration ■ The time of exposure/contact ■ The amount (volume) of agent ■ The physical form of the agent ■ The stomach content (in case of ingestion) 4/5/2020 The Toxicity of Corrosives_MF, PhD. 17
- 18. Clinical manifestations ■ Eye Exposure (splash injury): – Conjunctivitis – Corneal ulcerations – Corneal opacities – injuries to the lids and the sclera. ■ Skin contact – Burns. – Eschars. – Scar formation. – Deformity. – Disfigurement. 4/5/2020 The Toxicity of Corrosives_MF, PhD. 18
- 19. 4/5/2020 The Toxicity of Corrosives_MF, PhD. 19 Severe chemical injury with early corneal neovascularization ↑ Corneal opacities → https://emedicine.medscape.com/article/798696-overview
- 20. 4/5/2020 The Toxicity of Corrosives_MF, PhD. 20 Mild skin burn following Caustic Soda exposure. http://www.danderm.dk/atlas/3-209.htmlhttps://www.sciencedirect.com/topics/medicine-and- dentistry/caustic-agent Irregular pitted appearance of caustic burn.
- 21. 4/5/2020 The Toxicity of Corrosives_MF, PhD. 21 Hydrochloric acid burn to the hand before blister removal. Hydrochloric acid burn to the hand after blister removal. https://www.sciencedirect.com/topics/pharmacology-toxicology-and- pharmaceutical-science/hydrochloric-acid
- 22. Clinical manifestations ■ Respiratory manifestations – Cough. – Dyspnea. – Hoarseness of voice. – Stridor. – Respiratory distress. – Bronchoconstriction and wheezes. – Pulmonary edema. – Chemical pneumonia. 4/5/2020 The Toxicity of Corrosives_MF, PhD. 22 Park, Kyung Sik. “Evaluation and Management of Caustic Injuries from Ingestion of Acid or Alkaline Substances.” Clinical endoscopy (2014). Injury to the larynx and epiglottis after the ingestion of alkaline material.
- 23. Clinical manifestations ■ GIT manifestations • Pain. • Excessive salivation. • Dysphagia. • Vomiting. • Hematemesis with perforation injuries. 4/5/2020 The Toxicity of Corrosives_MF, PhD. 23 Caustic injury after the ingestion of acid material. Mild esophageal injury (right) is noted compared with widespread severe injury (left) in the stomach. Park, Kyung Sik (2014).
- 24. 4/5/2020 The Toxicity of Corrosives_MF, PhD. 24 Endoscopic grading of the caustic gastrointestinal injury. (A) Grade 1 :slight swelling and redness of the mucosa. (B) Grade 2A indicates the presence of superficial ulcers, bleeding, and exudates. (C) Grade 2B indicates local or encircling deep ulceration. (D) Grade 3A indicates focal necrosis. White arrows indicate focal necrosis. (E) Grade 3B indicates extensive necrosis. Park, Kyung Sik (2014).
- 25. 4/5/2020 The Toxicity of Corrosives_MF, PhD. 25 Diffuse liquefaction necrosis of the entire esophagus is noted after the ingestion of alkaline substances. Park, Kyung Sik (2014). Barium swallow four month after caustic ingestion injury. Note the long stricture of distal esophagus and gastric cardia Kluger et. al, (2015)
- 26. 4/5/2020 The Toxicity of Corrosives_MF, PhD. 26 (a) Resected stomach due to perforation (arrow) after caustic material ingestion. Note diffuse thrombosis of gastro-epiploic veins. (b) Stomach opened longitudinally. Note necrosis of gastric mucosa. Kluger et. al, (2015)
- 27. Complications ■ Acute: – Airway obstruction – Shock • Hypovolemic shock (dehydration and bleeding) • Neurogenic shock (severe pain) • Septic shock (infection) – GIT Perforation ■ Late: – Scarring and disfigurement – Stricture and cachexia – Loss of vision – Carcinoma of the esophagus 4/5/2020 The Toxicity of Corrosives_MF, PhD. 27
- 28. First Aid Measures (Prehospital care) ■ Prompt wound irrigation with lukewarm water ■ Avoid injuring the other unaffected areas with irrigated contaminated solution ■ Remove contaminated clothes ■ Ocular exposure→ Eye irrigation 4/5/2020 The Toxicity of Corrosives_MF, PhD. 28
- 29. First Aid Measures ■ Decontamination: – Do not induce vomiting. – Do not administer oral fluids. – Do not administer activated charcoal. – Do not attempt pH neutralization. – Do not insert a nasogastric tube. ■ Enhanced Elimination – Not clinically useful. ■ Antidote – None available. 4/5/2020 The Toxicity of Corrosives_MF, PhD. 29
- 30. Management (1) ■ Detailed history ■ Physical examination ■ Lab tests: – ABG – CBC – Blood chemistry including blood sugar level – Renal function tests and urine analysis – Coagulation profile 4/5/2020 The Toxicity of Corrosives_MF, PhD. 30
- 31. Management (2) ■ Radiology: – X-rays – CT ■ Endoscopy: – Within 12-24hrs – Grading the GIT lesions and diagnosis of strictures. – Contraindicated: in suspected perforation and airway damage 4/5/2020 The Toxicity of Corrosives_MF, PhD. 31
- 32. Management (3) ■ ICU admission ■ Surgical procedures ■ Long term monitoring: – Outpatient: ■ dermal burns every 2-3 days. ■ Ocular burns every 2-3 days. – Endoscopic examination: ■ Transmucosal or Transmural esophageal burns every 2-3 weeks 4/5/2020 The Toxicity of Corrosives_MF, PhD. 32
- 33. ORGANIC ACIDS 4/5/2020 The Toxicity of Corrosives_MF, PhD. 33
- 34. Carbolic Acid (Phenol) ■ Coal Tar derivative and highly inflammable ■ Commercial names: Dettol, Lysol ■ Cheap disinfecting agent ■ Very characteristic smell ■ Also used in some drugs: sore throat medications 1.4% ■ Mode of toxicity: – Suicidal → painless death – Accidental→ children & workers, skin contamination 4/5/2020 The Toxicity of Corrosives_MF, PhD. 34
- 35. Mechanism of Toxicity ■ Local • Local corrosive effect • Local anesthetic action • Coagulative necrosis ■ Systematic • General Protoplasmic poison: (disruption of cellular membranes) • CNS: stimulation followed by depression • Myocardial toxicity→ Cardiac depression • Acid- base imbalance → Respiratory alkalosis → Metabolic Acidosis • Methemoglobinemia • Renal toxicity → Acute Glomerulonephritis 4/5/2020 The Toxicity of Corrosives_MF, PhD. 35
- 36. Clinical Presentation of Acute Poisoning (Carbolism) Local ■ Skin ulcers: – White eschars with the smell of phenol→ turns brown with oxidation – Burning, tingling sensation and numbness of the affected area ■ GIT: – Vomiting with phenolic smell – Eschars around the mouth following the ingestion – Difficulty in speech and swallowing 4/5/2020 The Toxicity of Corrosives_MF, PhD. 36
- 37. Cont: Clinical Presentation of Acute Poisoning (Carbolism) Systematic ■ CNS: – Constricted pupils – Convulsions followed by depression and coma ■ CVS: – Hypotension, arrythmias and cardiac arrest. ■ Kidney: – Oliguria, albuminuria, hemoglobinuria and may reach anuria – Frothy green urine due to phenol byproducts excreted in urine (hydroquinone) 4/5/2020 The Toxicity of Corrosives_MF, PhD. 37
- 38. Cont: Clinical Presentation of Acute Poisoning (Carbolism) Differential Diagnosis Opium poisoning: • Constricted pupils • Convulsions followed by depression and coma Causes of Death Early: Respiratory failure Late: Renal failure. 4/5/2020 The Toxicity of Corrosives_MF, PhD. 38
- 39. Management ■ History ■ Clinical examination ■ Laboratory work – Arterial blood gases – Kidney function tests – Urine analysis – Detection of met-hemoglobin level ■ ECG to detect cardiac abnormalities 4/5/2020 The Toxicity of Corrosives_MF, PhD. 39
- 40. Treatment ■ Supportive measures: ABCs ■ GIT decontamination: ■ Emesis: contraindicated ■ Gastric lavage: indicated and essential ■ Eye decontamination: irrigation with water or saline ■ Elimination of the absorbed poison: – Dialysis – Charcoal hemoperfusion – Exchange transfusion ■ No specific antidotes ■ Symptomatic treatment 4/5/2020 The Toxicity of Corrosives_MF, PhD. 40
- 41. Oxalic Acid ■ Products: disinfectants, bleaches, metal cleaning products, rust removing products and furniture polishing agents. ■ Mechanism of toxicity: – Soluble solution: ■ Local irritation ■ Systematic hypocalcemia → Ca oxalate crystals – Insoluble Ca oxalate: ■ Household plants such as Dieffenbachia ■ Local irritation with contact 4/5/2020 The Toxicity of Corrosives_MF, PhD. 41
- 42. Clinical Manifestations ■ Local – Eye or skin contact →→ corrosive injury and superficial ulcers. – Formation of eschar with high concentrations. ■ Inhalation of the fumes: – Irritation of the respiratory passages →→ sore throat, wheezing. – Large doses →→ chemical pneumonitis and pulmonary edema. ■ Systematic: – Manifestations of hypocalcemia (tetany): facial muscles twitches’, carpopedal spasm, convulsions and contraction of the respiratory muscles →→ respiratory failure. – Cardiac arrythmias →→ asystole. – Renal failure: oliguria and anuria ending by uremia. 4/5/2020 The Toxicity of Corrosives_MF, PhD. 42
- 43. Management ■ History ■ Clinical examination ■ Laboratory work – Kidney function tests – Urine analysis – Serum electrolytes: detect the Ca2+ level ■ ECG to detect cardiac abnormalities 4/5/2020 The Toxicity of Corrosives_MF, PhD. 43
- 44. Treatment: Ca by every possible route■ Supportive measures: ABCs ■ GIT decontamination: – Gastric lavage: indicated and essential – Local antidote: CaCO3 or milk ■ Elimination of the absorbed poison →→ Dialysis. ■ Antidote: Ca gluconate 10% IV slowly or orally. ■ Symptomatic treatment: – Diazepam to treat convulsions – IV fluids to prevent Ca oxalate crystals precipitation in the kidneys 4/5/2020 The Toxicity of Corrosives_MF, PhD. 44
- 45. Conclusions ■ Household chemicals have many caustic chemicals that are very dangerous if not handled with the necessary precautions. ■ Strong acids and strong alkalis have different pathophysiological mechanisms. ■ Organic acids have local and systematic effects as well as Hydrofluoric acid. ■ In management of chemical burns by strong inorganic acids and alkalis , it is contraindicated to induce emesis nor perform gastric lavage. ■ Supportive care of the patient is the main line of treatment in cases of corrosive injuries. 4/5/2020 The Toxicity of Corrosives_MF, PhD. 45
- 46. Self-learning materials ■ https://my.clevelandclinic.org/health/articles/11397- household-chemical-products-and-their-health-risk ■ https://www.concordia.ca/content/dam/concordia/ser vices/safety/docs/EHS-DOC-008_HFguidelines.pdf 4/5/2020 The Toxicity of Corrosives_MF, PhD. 46
- 47. 4/5/2020 The Toxicity of Corrosives_MF, PhD. 47
Editor's Notes
- Common household items such as cleaners, detergent, auto supplies and paint may contain dangerous chemicals. Additionally, occupational exposure to hazardous chemicals and caustic substances is very common all over the world. In this lecture, we are going to discuss cases of toxicity or injuries following the exposure to corrosives and chemical burns.
- Here is a list of the expected learning outcomes following this lecture.
- Potentially dangerous chemicals can be found in every room in your home and used in many industries and occupations. If you don't make sure that the necessary precautions for storing and handling these dangerous substances are fulfilled, then accidental toxicity is very likely to happen especially if children are around. Accidents with corrosives can range from minor injuries to serious and life-threatening and fatal conditions for all age groups. Accidental toxicity is the most common mode of toxicity. Suicidal and homicidal accidents can also happen, Especially in rural areas, suicides by ingesting carbolic acid as it is commonly available and known to cause rapid painless death. Also, it is been reported that homicidal crimes happen after throwing a corrosive material on a victim to cause disfigurement or mutilation. This kind of crimes is known as acid attacks and happens all over the world.
- If you can recall, two years ago, there was an internet challenge that got very popular among teenagers in the USA where they were ingesting laundry tabs and caused severe injuries to many teenagers and children. Even in the supermarket they had to close the containers with locks to make sure kids and teenager have no access to them in the stores without supervision. Keep in mind that most household cleaning products and pesticides are reasonably safe when used as directed, and that the level of toxicity of a product is dependent on the dose of the product used (never use more than the amount listed on the label) and the length of exposure to the product.
- If we can simply classify these hazardous chemicals, it will follow under two main categories, organic corrosive or inorganic corrosive. Organic corrosives have mild local toxic effects however they perform sever remote toxicity. Examples are Carbolic acid AKA phenol And Oxalic acid and we will take about them in details later on. Inorganic corrosives are known to have a severe local effect on tissues they contact with. Except for Hydrofluoric Acid, strong inorganic corrosives have no remote action. Examples of strong corrosives would be either strong acids such as Sulphuric Acid, Hydrofluoric acid, and Nitric acid Strong alkalis such as Sodium hydroxide, Potassium hydroxide and Ammonium Hydroxide.
- The strength of an acid is defined by how easily it gives up the proton; the strength of a base is determined by how avidly it binds a proton. Acidity and alkalinity are measured using a pH scale for which 7.0 is neutral. The lower a substance's pH (less than 7), the more acidic it is; the higher a substance's pH (greater than 7), the more alkaline it is. As you can see in this picture the, among the strongest acids is the battery liquid and among the strongest known alkalis is the drain cleaner and both are considered as household items.
- Sulfuric Acid is used in many ways, and by many different people. It can be used in our everyday lives and to manufacture different common products. In Arabic this acid is known as مية النار This slide shows some of the many applications where sulphric acid is used in. This include the manufacture of fertilizers, rubber, other acids, detergents, dyes, some medicines and in oil refining.
- Speaking about nitric oxide, It is a strong oxidizing agent and it enhances the combustion of other substances., therefore it is used in the manufacture of explosives. It is also known to make plants grow faster and thus extensively used in fertilizers. Another use of NO would be in the labs to identify different metals. In very diluted forms, it is used to assess the purity of gold, especially in low-grade alloys as it dissolves all metals except gold and platinum.
- Also known as lye or caustic soda, is an extremely caustic in Arabic is الصودا الكاوية Sodium hydroxide is used in the manufacture of soaps, rayon(s kind of fabrics), and paper, also in petroleum refining, At homes it is used in drain cleaners and oven cleaners. Solutions of sodium hydroxide in water are at the upper limit (most basic) of the pH scale.
- Potassium hydroxide, also called caustic potash. In Arabic it is called بوتاس The purified material is a white solid that is commercially available in the form of pellets and flakes. Like sodium hydroxide , it is a strong alkali, very soluble in water, and highly corrosive. It is useful for a variety of applications, including the manufacture of soaps, biodiesel, batteries, fuel cells and fertilizers. When it is dissolved in water, it gives a liquid very similar to milk. Therefore, it is commonly mistaken by young children for milk leading to many accidents with sever injuries.
- Ammonium hydroxide can be found in the bathroom, floor, glass, carpet, metal, upholstery, and all-purpose cleaners as well as starches, disinfectants, and stain treaters. Most household ammonia contains 5 to 10 % ammonium hydroxide. Other products include Auto care: such as puncture seal products, tire inflators, fiberglass cleaners, metal cleaners, and polishes. Cosmetics: mascara and lash colorants Explosives Fertilizers Hair care: hair colorants, hair glazes, and hair touch-up kits Personal care products: shaving cream, lotions, creams, and acne treatments Ammonium hydroxide is highly toxic whether it is inhaled, ingested, or absorbed through the skin. Direct contact with the eyes can cause blindness if not washed away immediately within the first 10 seconds. When skin contact occurs, it can cause burns and blisters. Ammonia is also toxic when ingested and extremely corrosive to tissue. Inhalation can cause a cough, bronchial spasms, and even lung damage. Extreme caution and care must be exercised when using it.
- Chlorites are the primary chemicals used as bleaches. One of the commonest household products that is used for cleaning and sanitization purposes. The reason for that is. It’s a very cheap product and yet effective. Household bleach is alkaline with a pH of 11-12, but it is dilute enough that it is minimally irritating to the skin. More concentrated, industrial strength chlorites may be more damaging to the skin and irritating to the respiratory passages. The problem with Bleach is that sometimes mixed with other acids and alkalis leading to the elaboration of toxic gases that may be fatal causing chemical asphyxia. When mixed with acids bleach forms chlorine gas and when mixed with alkalis it produces chloramine gas.
- Corrosive substances have local, rapid, & destructive action when they come into contact with tissues. However, alkalis and acids cause damage by two different mechanisms. They don’t cause the classic hyper thermic burns; however heat generation contributes to tissue damage. Again, remember Strong inorganic corrosives have no remote action unlike organic acids except for hydrofluoric acid. Let's first look at the pathophysiological mechanisms of acids. All the cells and tissues in our body are composed of protein molecules. As you may recall from biochemistry, Proteins form the architecture for our body, particularly in tissues like skin. Our skin is made of cells rich in proteins like keratin, which gives our skin structure and protection, and elastin and collagen which maintain skin flexibility. Acids donate protons which change the chemical structure of proteins in a process called denaturations. When a protein denatures, it loses its shape and thus its function. During the denaturing process when skin is exposed to an acid, the cells die but don't disintegrate. The result is a clear or white patch of skin that is no longer alive, but acts like a placeholder for once living tissue. This process is called coagulative necrosis. The benefit for this non-living tissues is that it makes the burn less severe compared to burns with alkali chemicals. The dead tissue, called a coagulum or eschar, prevents the acid from reaching deeper tissues, making the burn more superficial. With Acid ingestion, the stomach is the organ affected the most while the Esophagus is less affected because common strong acids are usually available as liquids, so they slide quickly to affect the stomach rather than injuring the esophagus.
- As we previously mentioned, Alkalis are chemicals that accept protons, also known as bases. And Alkalis that accept protons easily are stronger alkalis. Just the opposite of acids, stronger alkalis have a higher pH, with the strongest having a pH of 14. Alkalis, however, don't create coagulum but rather cause liquefaction necrosis, which means that cells liquefy and dissolve, creating pockets of gooey tissue that allow for the alkalis to leach into deeper structures in the body. Alkalis denature proteins, but they also break down fats in a process called saponification. Burns from alkalis tend to be much worse than burns from acids. Further injury is caused by thrombosis of the blood vessels. Alkalis most severely affect the squamous epithelium of the esophagus but the stomach only in 20% of cases.
- Hydrogen fluoride is a chemical compound that contains fluorine. It can exist as a colorless gas or as a fuming liquid, or it can be dissolved in water. When hydrogen fluoride is dissolved in water, it may be called hydrofluoric acid. Hydrogen fluoride can be released when other fluoride-containing compounds such as ammonium fluoride are combined with water. Despite it is inorganic acid, it has both severe local action, HF acid is also known as the flesh-eating acid, as the burn may reach the underlying bones, In addition, fluoride ions are released into the cells. Fluoride ions inhibit glycolytic enzymes and combine with calcium and magnesium to form insoluble complexes. The extreme local pain is believed to result from calcium immobilization, which leads to nerve stimulation by shifting potassium ions. Acute fluorosis can occur as the fluoride ions enter the systemic circulation, resulting in cardiac, respiratory, gastrointestinal, and neurologic symptoms. Severe hypocalcemia, which is resistant to large doses of calcium, can occur. The cause of death is cardiac arrythmias due to electrolyte imbalance.
- The severity of the burn is related to several factors, including the pH of the agent, pH less than 2 and more than 11 cause sever damage. The concentration of the agent: concentrated forms of some acids and bases generate significant heat when diluted or neutralized, resulting in thermal and caustic injury. The length of the contact time The volume of the offending agent, The physical form of the agent. The ingestion of solid pellets of alkaline substances results in prolonged contact time in the stomach, thus, more severe burns. In cases of ingestion the presence of food in the stomach may alter the effect of the caustic agent on the gastrointestinal tissues.
- Ocular burns consist of burns to the sclera, conjunctiva, cornea, and eyelids. Chemical burns, particularly those involving the cornea, are considered a true ophthalmologic emergency and require prompt assessment and intervention to minimize morbidity. The severity of an ocular burn is directly correlated with the duration of exposure and the causative agent. Skin manifestation result from the direct contact of the acid with the dermal tissues. Late manifestations if the patient survives include scarring, deformity and disfigurement that is sometimes difficult to be corrected by surgical intervention.
- Alkali substances can pass into the anterior chamber rapidly due to the inability to buffer alkali (within approximately 5-15 min), exposing the iris, ciliary body, lens, and trabecular network to further damage. Irreversible damage occurs at a pH value above 11.5. Acid burns cause protein coagulation in the corneal epithelium, which limits further penetration. As a rule, these burns are nonprogressive and superficial.
- Chemical burn. The irregular, pitted appearance of this injury as a result of caustic lye exposure is characteristic of chemical burns.
- These are some of clinical manifestations that appear when the respiratory system is exposed to caustic substances by inhalation of fumes or ingestion. Findings of shortness of breath, hoarseness and stridor suggest laryngeal trauma and demand laryngoscopic evaluation. As you can see in this photo, the white patches in the mucosa of the larynx and epiglottis after the ingestion of alkaline material.
- Patients with minimal ingestion may be asymptomatic but others may experience oropharyngeal, retrosternal or epigastric pain. Dysphagia, odynophagia and excessive salivation are suggestive of esophageal damage, Abdominal pain; vomiting and hematemesis may suggest gastric damage. Continued pain, peritonitis, tachycardia, persistent leukocytosis, acidosis and pleural effusion should raise the suspicion of perforation
- . (A) Grade 1 indicates only slight swelling and redness of the mucosa. (B) Grade 2A indicates the presence of superficial ulcers, bleeding, and exudates. (C) Grade 2B indicates local or encircling deep ulceration. (D) Grade 3A indicates focal necrosis. White arrows indicate focal necrosis. (E) Grade 3B indicates extensive necrosis.
- The gross picture of a resected stomach following a perforation due to caustic substance ingestion. The picture on the right shows the inside of the stomach with marked necrosis of the gastric mucosa
- The long-term effect of caustic dermal burns is scarring, and, depending on the site of the burn, scarring can be significant. Scarring, infection, and poor healing may occur with dermal burns. Skin grafting may be required. Ocular burns, especially from alkali substances and hydrofluoric acid, can result in cataract formation and/or complete vision loss. Perforation and/or bleeding and respiratory compromise from upper airway edema are the short-term complications of caustic ingestions. Stricture formation is the main long-term complication associated with caustic burns to the esophagus.
- Prompt wound irrigation with lukewarm water is the most critical aspect in limiting the extent of dermal burns from exposure to caustic substances. In many experimental studies showed that irrigation following the exposure to strong acids and alkali within several minutes neutralize the pH change of the dermal tissues and decrease the damage of the affected areas. Additionally, Clinical studies have shown that patients who received irrigation within 10 minutes following injury had a 5-fold decrease in full-thickness injury. Prevent contaminated irrigation solution from running onto unaffected skin. Remove contaminated clothes. In case of ocular exposures ,eye irrigation should be started immediately.
- These are some of the contraindications that medical professionals need to avoid when dealing with chemical burns. Never induce vomiting as it may cause further damage of the GIT and lead to aspiration. Oral fluids will also induce further damage by running the caustic substance further through the distal GIT. Activated charcoal is contraindicated because it may infiltrate burned tissue and interfere with endoscopic evaluation Attempts to neutralize a caustic acid by correcting pH with an alkaline substance [and vice versa] are contraindicated because severe exothermic reactions may result. insertion of an NGT is contraindicated because it can damage already compromised mucosal surfaces Dilution with milk or water is only useful in the first few minutes after ingesting a liquid caustic, but delayed dilution may be useful after ingesting a solid caustic. Dilution should be avoided if patients have nausea, drooling, stridor, or abdominal distention.
- Laboratory studies depend on the burn type and extent of exposure. For severe burns, consider the following: Electrolytes Creatinine, BUN, Glucose, Urinalysis, CBC count, Creatine phosphokinase Coagulation profile For localized burns, usually no laboratory tests are required. For ingestions of caustics, consider the following: Hemoglobin/hematocrit Pulse-oximetry or ABG if respiratory symptoms Imaging Studies For ingestions, consider the following: Chest radiography if any respiratory symptoms Abdominal radiography (flat and upright) if signs of peritonitis are present Endoscopy for ingestions is as follows: Perform esophagoscopy and gastroscopy on all patients with symptomatic ingestions and on patients who are asymptomatic but have a history of a significant ingestion of a substance with the potential to cause major injury. [11, 12] Esophagoscopy findings are used to guide further treatment. The presence of full-thickness or circumferential burns is associated with future stricture formation. The issue of whether to extend the endoscopic examination past the first site of injury is controversial.
- Imaging Studies For ingestions, consider Chest radiography if any respiratory symptoms Or Abdominal radiography (flat and upright) if signs of peritonitis are present All patients with persistent vomiting, oral burns, drooling or abdominal pain require further investigation to define the extent of the injury and risk for future complications. which traditionally is performing an endoscopy within 24 hours but there is a growing evidence that CT can be used as an alternative within 24 hours. Patients who are asymptomatic at 4 hours and tolerating oral fluids can be medically cleared. Symptomatic patients need to remain nil by mouth and are admitted for observation and further investigation within 24 hours. Management is then directed dependent on these findings. Patients with an airway compromise will require urgent intubation and ventilation with ongoing care on ICU. Patients with haemodynamic instability or evidence of perforation will require urgent surgical intervention and ICU admission.
- Patients who are asymptomatic at 4 hours and tolerating oral fluids can be medically cleared. Symptomatic patients need to remain nil by mouth and are admitted for observation and further investigation within 24 hours. Management is then directed dependent on the condition of the patient. Patients with an airway compromise will require urgent intubation and ventilation with ongoing care on ICU. Patients with haemodynamic instability or evidence of perforation will require urgent surgical intervention and ICU admission. Long-Term Monitoring Dermal burns treated on an outpatient basis should be rechecked every 2-3 days. Any ocular burns treated as on an outpatient basis should be rechecked in 24 hours. Endoscopic examination of all transmucosal or transmural esophageal burns should be repeated in 2-3 weeks.
- Now we will move to organic acids.
- CARBOLIC ACID Phenol (carbolic acid) is a flammable compound that is a derivative from benzene, it is also called benzenol, and It is a highly corrosive chemical which is well absorbed by all routes of exposure, inhalation, cutaneous, or oral. It has a characteristic carbolic odor & a sweetish pungent taste. Several commercial compounds are synthesized from a precursor containing phenol Commercial products that contain phenol derivatives have different famous names such as Lysol, and Dettol. It is also among the active ingredients in local antiseptic medications to treat sore throat. It is important to mention that phenol derivatives are present in many household and personal products such as laundry detergents, air fresheners, all-purpose cleaners, deodorants and hand lotions In concentrated forms of carbolic acids (the ones shown in the lower picture), the common forms of toxicity are either Suicidal due to the easy access to the product, it is cheap and causes painless death. Or Accidental especially with children and workers as it is easily absorbed through intact skin.
- Phenols denature and precipitate cellular proteins and results in tissue injury in the form of superficial ulcers. It is characterized by painless injury due to the anesthetic effect on the sensory nerve endings. Systematically, It is considered as one of the general protoplasmic poisons, (Recall from the lecture for heavy metal toxicity). It causes central nervous system stimulation followed by depression. Also it has a direct effect on the heart causing myocardial depression and cardiac arrest. It disrupt the acid-base balance in the body leading to either respiratory alkalosis as a result from respiratory center depression or metabolic acidosis resulting from renal failure. The toxic effect on the kidney is in the form of acute glomerulonephritis. CLINICAL FEATURES: poisoning by carbolic acid _ carbolism. 1.Mode of action: In concentrated form- corrosive, when applied to skin, it causes a burning sensation- tingling sensation & numbness. 2. Routes of excretion: urine, saliva, skin and stomach. 3. Symptoms: intense thirst and burning sensation in mouth, throat and stomach. Vomiting of frothy mucus. 4. Causes of death: failure of respiratory center. Shock and circulatory collapse. Renal failure. 5. Fatal dose: 2gm 6.Fatal period: 3-4 hours. POST-MORTEM APPERANCE: 1. Dark brown abrasion on the angles of the mouth and the chin. 2. The mucus membrane of lips, mouth and throat is congested, swollen. 3. The mucous membrane of esophagus is tough, grey and arranged in longitudinal folds. 4. STOMACH: brown, leathery with hemorrhagic spots and folds. contains reddish fluid mixed with mucus and pieces of epithelium with the odour of carbolic acid. 1. KIDNEYS – shows haemorrhagic nepritis. 2. LUNGS – congested and edematous. 3. BRAIN – Congested 4. BLOOD – dark, semi LUNGS – congested and edematous. 3. BRAIN – Congested 4. BLOOD – dark, semi fluid / partially coagulated. MEDICO-LE
- The picture of carbolism may be misdiagnosed with toxicity by opium as both have constricted pupils and a picture of respiratory stimulation followed by depression. However, carbolism is characterized by with the strong smell of phenol and the colored eschars of the injured tissues. The causes of death usually is respiratory failure in early cases of death or following renal failure in late cases.
- Emesis is contraindicated in this condition because of the high chances of seizures and coma. Gastric lavage is indicated and highly recommended as vomiting temporary and usually stops shortly as the anesthetic effect of carbolic acid progresses. It is also relatively safe as the coagulative necrosis causes thickening of the gastric mucosa and perforation is not likely to happen. Additionally, gastric lavage reduce the systemic effects of phenols as it helps eliminates the amount ingested. Gastric lavage may be performed by ethanol 10% as it dissolves the phenol in the stomach and it easily washed out. In case of eye contact irrigation using water or saline is indicated for at least 15 minutes. Elimination of the absorbed poison can be done by dialysis in cases of renal failure, charcoal hemoperfusion or exchange transfusion. No specific antidote for carbolic acid. Other symptomatic treatment measures are indicated according to the clinical presentation such s diazepam for convulsion, Acid base correction, and treatment of methemoglobinemia with methylene blue.
- Oxalic acid is an organic corrosive acid. Oxalic acid is a constituent of many household products. It is found in many disinfectants, household bleach, metal cleaning liquids, antirust products and furniture polishes. White cloth printing, manufacture straw hats, cleaning brass and copper articles & wooden surfaces. Bleaching powder for erasing writing and signatures from paper and printed Oxalic acid is found in several green leafy vegetables such as spinach, broccoli, carrots, cabbage lettuce etc. It also occur in fruits such as berries, concord grapes, figs, and plums along with in some seeds, nuts and grains. Oxalic acid is a Colorless, transparent, prismatic crystals, sour taste, strongly acidic. When it is soluble, oxalic acid solution has irritating corrosive effect on the skin and the mucous membranes. If ingested, it causes hypocalcemia due to binding with free Ca ions in the body and the precipitation of the insoluble ca oxalate crystals in parenchymatous organs such as the brain, the heart and the kidneys. insoluble calcium oxalate salt found in Dieffenbachia and similar plants is not absorbed, but it causes local mucous membrane irritation.
- Clinical presentation. Toxicity may occur as a result of skin or eye contact, inhalation, or ingestion. Acute skin or eye contact causes irritation and burning, which may lead to serious corrosive injury if the exposure and concentration are high. Inhalation may cause sore throat, cough, and wheezing. Large exposures may lead to chemical pneumonitis or pulmonary edema. Ingestion of soluble oxalates may result in weakness, tetany, convulsions, and cardiac arrest due to profound hypocalcemia. The QT interval may be prolonged, and variable conduction defects may occur. Oxalate crystals may be found on urine analysis Kidney failure may happen due to obstruction of the collecting tubules of the kidneys by the Ca oxalate crystals precipitation.
- Occupational history is of significance in these cases. Clinical manifestation detecting the local and the systematic symptoms and signs. Laboratory work will include:
- Treatment starts as usual by protecting the airway which may become acutely swollen and obstructed after a significant ingestion or inhalation. Administer supplemental oxygen and assist ventilation if necessary. Then the key to therapy in case of Ca oxalate poisoning is giving calcium by every possible route. GIT decontamination is performed through gastric lavage with Ca containing solution and avoid water as it dissolve more of the acid and increases absorption. Elimination of the absorbed poison sometimes requires dialysis. Oral or slow IV 10% calcium gluconate is essential to treat hypocalcemia and it is considered as the specific antidote for that poison. Other measures include treatment of the symptoms such as diazepam for convulsion and IV fluid to protect the kidneys from damage by ca oxalate crystal participation in the renal tubules.
- My take home message to you is to take care of yourself and your family and follow strict precautions when storing and handling household products containing caustic chemicals. Make sure they are stored in locked cabinets outreach of children. Also, wear protective clothes and gloves whenever you need to use these chemicals to make sure that you are safe.