Caustics ingestion powerpoint presentation

it includes poisnous ingestion of acids alkalis and other agents

1. Caustic ingestions

2. Introduction Caustics/corrosives are substances that damage and erode the surface with which it comes in contact. They destroyes the body tissues with which they come in contact. They are - Acids Alkalis Others

3. Introduction The upper digestive tract is the primary site of tissue damage due to caustic ingestion. This part of the gut runs from the head, neck, mediastinum, and epigastric area. The oral region, pharynx, esophagus, stomach, and duodenum comprise the upper gastrointestinal tract

4. Introduction Caustic ingestions can injure any part of the upper digestive tract. The esophagus is most vulnerable to alkaline damage, while the stomach is most prone to acidic injury. Severe cases can cause overspills or gut perforation that can spread the damage to neighboring structures. Caustic ingestions are severe causes of morbidity and mortality and can affect all age groups

5. Etiology Caustic exposure can be accidental or intentional. Accidental exposures are most common in young children, often termed "exploratory ingestions." Accidental caustic ingestion often occurs in small amounts and typically involves household cleaners with low concentrations of chemicals like bleach and ammonia. Meanwhile, intentional exposures often result from self-harm attempts and involve large amounts of highly concentrated caustic chemicals. Most caustic exposures involve oral ingestion (76%) and occur at home (93%). More than 80% of cases are unintentional. Substances ingested are either highly acidic or highly alkaline, requiring different treatment approaches

6. Pathophysiology Generally, the pathophysiology underscoring tissue damage depends on the ingested agent's pH. Substances with pH over 7.0 are alkaline, and below 7.0 are acidic. Extremes of pH—specifically below 3.0 and above 11.0—are of greatest concern in human exposures. Strong alkalis and acids can damage tissues by different mechanisms.

7. Pathophysiology Alkalis are classically associated with liquefactive necrosis. The process involves saponification and subsequent disruption of the lipid-rich cell membranes. Cell lysis releases digestive enzymes, dissolving the surrounding tissues. Strong alkalis can penetrate tissues more deeply than acids and cause more extensive tissue damage

8. Pathophysiology In contrast, acids are classically associated with coagulative necrosis. Acid-related tissue injury is more superficial due to eschar formation, which limits acid penetration into the underlying tissues. Acid ingestions are associated with "skip lesions," where the esophagus sustains discontinuous areas of damage Strong alkalis and acids are equally capable of severe, full-thickness injury to the gastrointestinal tract

9. Pathophysiology Other factors that will influence the extent and severity of damage include the physical state of the caustic substance (solid, liquid, or gel), tissue contact time, and quantity and concentration of the offending agent

10. History and Physical Individuals with caustic injuries may be unresponsive, breathless, and pulseless. After a quick primary survey, resuscitation must be administered promptly for patients with signs of cardiorespiratory arrest, regardless of the cause. Airway, breathing, and circulation must be stabilized.  Patients should be monitored continuously on telemetry, with frequent assessments of vital signs. Once stabilized, the secondary survey may be initiated.

11. History and Physical Patients with caustic ingestion may be asymptomatic in one extreme or develop severe manifestations in another.  Vomiting, drooling, chest pain, abdominal pain, and breathing and swallowing difficulty may be reported.  Hematemesis may be caused by blood vessel erosion

12. History and Physical Physical examination may reveal oral and tongue edema and drooling. Upper airway edema may lead to vocal changes, stridor, and respiratory distress. Esophageal perforation can cause mediastinitis and peritonitis. Mediastinitis typically presents with nonspecific signs like tachycardia and fever.

13. History and Physical Occasionally, it may produce the Hamman sign—a systolic precordial crunching sound heard on auscultation. Peritonitis presents with abdominal tenderness and rigidity. A complete exam should be performed to assess for other injuries, particularly oral and orbital burns.

14. Evaluation Initial lab studies may include a complete blood count (CBC), coagulation studies, complete metabolic profile (CMP), and arterial or venous blood gas. The CBC may show inflammation-associated neutrophilia. Hematemesis may reduce hemoglobin to abnormal levels if severe

15. Evaluation The CMP can help detect electrolyte imbalances in patients with repeated vomiting. This test can also provide baseline renal and liver function information, which is crucial if surgery is contemplated. Blood gases help examine the severity of respiratory damage.

16. Evaluation Plain chest and abdominal radiography may identify free air in the mediastinum (pneumomediastinum) or peritoneum (pneumoperitoneum). Caustic substance aspiration may produce infiltrates on chest x-ray

17. Esophageal Radiography With Contrast EGD is currently the gold standard in evaluating injuries from caustic ingestion. EGD should be strongly considered in symptomatic patients, especially if they have posterior pharyngeal burns, stridor, respiratory distress, chest or abdominal pain, or inability to tolerate oral liquids

18. Others Alternative or adjunctive modalities for evaluating caustic ingestion-related injuries include endoscopic ultrasound (EUS) and contrast-enhanced computed tomography (CECT)

19. Treatment  The airway should be secured in patients with signs of impending respiratory failure, including drooling, hypoxia, and vocal changes. Vasopressors should be initiated for patients who remain hypotensive despite adequate fluid challenge . Early interventions that have been described for caustic ingestion include pH neutralization and dilution with water or milk. The pH may be neutralized by giving a weak acid or base Dilution with milk or water was once proposed to help reduce alkali injury

20. Treatment  However, this intervention may only be beneficial within the first few minutes. This treatment may even cause distention-related injury. Dilution with milk or water is currently not recommended in clinical practice. Activated charcoal administration should be considered if the caustic agent is zinc or mercuric chloride. Heavy metals can damage mucosal surfaces and be absorbed systemically, causing severe multi-organ toxicity. Activated charcoal can absorb metals in the gut, prevent their enterohepatic recirculation, and hasten their clearance.

21. Treatment Emesis induction should not be used in managing caustic ingestion. Nasogastric (NG) tube insertion is controversial. NG tube placement in the emergency department risks bacterial infection and esophageal perforation. Besides acute injury management, the long-term sequelae of caustic ingestion must also be addressed. The most concerning complication is stricture formation. Corticosteroid treatment can theoretically attenuate inflammation and reduce granulation and fibrous tissue formation.

22. Treatment H igh-dose methylprednisolone may prevent stenosis in patients with grade 2b injury. Procedural interventions in the treatment of strictures include bougienage, esophageal stent placement and endoscopic dilatation.  Individuals with suspected mediastinitis, peritonitis, or hemodynamic instability require emergent surgical consultation. Patients with large ingestions and are in shock, acidotic, or coagulopathic may have more severe findings on surgical exploration.  Surgical consultation may also be required for patients with high-grade injuries on EGD, CECT, or both.

23. Treatment The goal of emergency surgery is to remove all necrotic tissue. Exploratory laparotomy is the standard approach. The size of the resected area depends on the extent of damage. Small fragments may be removed in some cases. A pancreaticoduodenectomy may be necessary if pancreatic and duodenal injuries are extensive