Gastric Lavage Procedure: Indications and Steps | OHSU Toxicology Demo

Endotracheal intubation is a critical medical procedure that establishes a protected airway by inserting an endotracheal tube through the vocal cords into the trachea, utilizing anatomical landmarks including the epiglottis, thyroid cartilage, and cricoid cartilage; the procedure involves using a laryngoscope to visualize and open the airway, inserting the tube with an inflatable cuff that seals against the tracheal wall to prevent aspiration of oral secretions and gastric contents into the lungs.

Endotracheal intubation secures the airway during anesthesia by inserting a tube through the mouth into the trachea. The procedure requires: (1) Muscle relaxation via succinylcholine to paralyze oropharyngeal muscles, (2) Laryngoscope insertion to visualize vocal cords, (3) Tube passage through vocal cords, and (4) Cuff inflation to seal the airway. The cuff prevents aspiration of gastric contents into lungs. Without muscle relaxation, the patient cannot open their mouth, risking injury during forced insertion. The tube's cuff creates a seal that allows positive pressure ventilation and protects against aspiration during transport and sedation.

Successful endotracheal intubation requires thorough preparation of both provider and patient. Key principles include: proper patient positioning with head lifted so ear aligns with sternal notch, face parallel to the bed surface, and semi-recumbent position if tolerated. The laryngoscope blade is inserted into the right side of the mouth, with the tip placed in the vallecula before lifting the epiglottis to visualize vocal cords. Two approaches exist—gradual insertion with incremental lifting versus deep insertion followed by slow upward lifting. The bougie is essential for every intubation attempt, passed through the vocal cords and used to railroad the endotracheal tube. Tube depth should be approximately 21-23 cm (three times the internal diameter). Suction should be readily accessible under the right shoulder for immediate use during the procedure.

This comprehensive segment covers the entire endotracheal intubation procedure and fundamental airway management principles. The video demonstrates the complete workflow from pre-oxygenation through post-intubation maintenance. Key phases include: (1) Pre-oxygenation with 100% oxygen to create an oxygen reservoir in body tissues; (2) Patient positioning with occipital support for optimal airway alignment; (3) Assessment of nasal passages by palpation to identify the more patent nostril; (4) Administration of the classical intubation sequence: opioid, hypnotic, and neuromuscular blocking agent (3-5 minute onset); (5) Laryngoscopy using Macintosh blade and tube advancement through the nasal passage; (6) Cuff inflation and ventilator connection; (7) Anesthetic maintenance using propofol infusion and inhalational agents; (8) Manual ventilation technique using bag-mask device when respiratory drive is compromised. Critical principles include strategic hyperoxia, aspiration risk in non-fasted patients, and the distinction between pre-oxygenation (spontaneous breathing) and ventilation (positive pressure).

This comprehensive section covers advanced airway management principles and endotracheal intubation procedures. Establishing and maintaining the airway is the single most important manipulative EMT skill, as the airway must be secured immediately or the patient will die. The respiratory system anatomy includes the upper airway (nose, mouth, throat, pharynx, larynx) and lower airway (trachea, bronchi, lungs), with gas exchange occurring at alveolar-capillary and capillary-cellular levels. The first step in airway management is opening the airway using head tilt chin lift (no spinal injury) or jaw thrust (possible spinal injury). Endotracheal intubation involves inserting a tube into the trachea, with orotracheal (mouth) or nasotracheal (nose) approaches. Essential equipment includes laryngoscope with Miller or Macintosh blades, properly sized ET tube (7.0-8.5 mm for adults), stylet, 10ml syringe, suction unit, and secondary confirmation device. The stylet should never be inserted past the Murphy's Eye to avoid puncturing delicate tissue. An intubation attempt should not exceed 30 seconds. Team dynamics are critical: first EMT uses AED, second and third perform CPR at 30:2 ratio, fourth intubates. Secondary confirmation uses EGDs, syringes, or capnography monitors. Primary confirmation includes visualization of tube passing through vocal cords, bilateral breath sounds, and chest rise with ventilation. Complications include right mainstem bronchus intubation, esophageal intubation, laryngospasm, trauma, and mechanical failure.

Toxicology is a clinical discipline where students will apply their knowledge to save patients' lives in emergency situations. The instructor emphasizes that students should not treat toxicology as merely a subject to pass exams, but rather as a practical skill for real medical emergencies. Toxicology follows similar principles to pharmacology, studying substances in terms of their pharmacokinetics, mechanism of action, and effects. Toxidromes are groups of symptoms that, when found together, typically indicate exposure to a specific type of toxin. Poisoning should be suspected in patients presenting with deterioration in consciousness level when they were previously normal, especially with no obvious cause. Four key factors affect toxin absorption: amount, route of administration (inhalation fastest, then IV, oral, IM, SC), physical form (gases fastest, then liquids, powders, tablets), and cumulative toxicity from repeated doses faster than metabolism.

Toxicology is the science studying the life cycle of poisons from origin to management. Clinical toxicology focuses on clinical manifestations. Poisons enter through various sources: household items (pesticides), industrial settings (mercury, lead), drugs (overdose), and animals (venom, hydrogen sulfide). Classification by action: local (affects exposure site), remote (affects distant organs after absorption), and multiple action (affects multiple systems). Neurotoxic poisons affect nervous system (brain, spinal cord, peripheral nerves). Cardiovascular poisons affect heart (cyanide, cardiac glycosides). Respiratory poisons affect breathing (carbon monoxide, hydrogen sulfide). Pharmacokinetics involves absorption, distribution, metabolism, and excretion. Route of entry affects absorption speed. Food can affect absorption (tannins bind some poisons, alcohol reduces cyanide toxicity). Age affects susceptibility (children more vulnerable due to smaller body weight and immature systems). Toxicity depends on dose-response relationship, concentration, and chemical form. Individual susceptibility varies by age, health status, and genetics. The ABC approach prioritizes life-saving interventions: Airway, Breathing, and Circulation. The coma cocktail (dextrose, naloxone, thiamine) is used empirically for unknown coma. Temperature monitoring is critical. Physical examination includes vital signs and specific tests. Recognizing toxic syndromes (anticholinergic, sympathomimetic, cholinergic) guides empiric treatment.

Toxicology studies toxicants—substances harmful to biological organisms. A fundamental principle states that all substances can be toxic depending on dose; even water can be fatal in excess. Toxicants enter through four routes: ingestion (mouth to stomach), inhalation (mouth/nose to lungs), injection (through skin cuts), and dermal absorption (through skin membrane). Severity varies: injection has greatest effect (direct bloodstream entry), followed by inhalation, then ingestion, and dermal absorption has least effect. The GI tract plays the most significant role in absorption through ingestion, with rate and selectivity depending on chemical properties, molecular size, and shape. The respiratory system (bronchi and alveoli) facilitates inhalation absorption. Dust particle size determines penetration: >5 micrometers filtered in upper respiratory system, 2-5 micrometers reach bronchial system (danger zone), <1 micrometer reach alveoli causing serious damage.

Toxicology is a branch of medical science studying toxic substances, their mechanisms of action, clinical features, management, postmortem appearances, chemical analysis, and medico-legal aspects. Poisons exist in solid, liquid, or gas forms and enter the body through local (topical) or systemic (oral, inhalation, injection, rectal) administration. Poison action is classified into local (affects application site), remote (affects distant areas), and combined (affects both). Exposure patterns include acute (within 24 hours), sub-acute (1-3 months), and chronic (months to years from repeated exposure). Cumulative action occurs when poisons taken repeatedly over extended periods suddenly cause toxicity when accumulated to a threshold. Absorption and distribution depend on route and site of exposure, with intravenous administration leading to faster distribution.

This segment presents the crucial toxicology test results that transformed the investigation. Jennifer's test was positive for cocaine and high alcohol doses, while Carlos Alberto's test showed no illegal substances or alcohol, proving he was sober and acting consciously. The reconstructed timeline indicates he approached Jennifer the day before her disappearance, offered drugs and alcohol to maintain sexual relations, and she became unconscious on the way to the motel. He exited the car to avoid staff seeing her condition, then sexually assaulted her when she woke up. A struggle ensued where he hit her head, killing her. The motel housekeeper claimed to see Jennifer without injuries, suggesting she may not have been awake when she entered.

Corrosive substances are classified into acids and alkalis. Organic acids cause local tissue damage through direct chemical action, while organic alkalis cause both local and systemic effects. Alkalis cause liquefactive necrosis, breaking down tissue proteins, collagen, and fats, allowing deep penetration into tissues. Acids cause coagulative necrosis, drawing water from tissues and creating a protective eschar layer that limits further damage. This fundamental difference in mechanism explains why alkalis are generally more dangerous than acids.

Acids and alkalis cause tissue damage through fundamentally different mechanisms. Acids donate protons that denature proteins, causing cells to die without dissolving. This creates a protective eschar (coagulative necrosis) that limits deeper penetration, making acid burns generally more superficial. Alkalis accept protons, causing liquefaction necrosis where cells dissolve and liquefy, creating pockets allowing deeper penetration. Alkalis also break down fats through saponification. Unlike acids, alkalis do not form protective barriers and cause more severe burns. The stomach is primarily affected by acid ingestion while the esophagus is less affected since liquid acids slide quickly to the stomach. Hydrofluoric acid uniquely combines both local tissue destruction and systemic toxicity through fluoride ion effects on calcium and magnesium metabolism.

Corrosives are substances that destroy tissue by changing heme into hematin. The two main types are acids and alkalis, with acids being most commonly encountered in household settings. Acids cause coagulative necrosis (C) leading to eschar formation that limits penetration, while alkalis cause liquefactive necrosis (L) causing extensive tissue damage. Columnar epithelium of the stomach resists alkali, while squamous epithelium of the esophagus resists acid. This explains why acid ingestion primarily damages the stomach, while alkali ingestion primarily damages the esophagus.

Corrosive substances are classified into acids and alkalis, with acids causing superficial tissue damage through coagulation necrosis (forming a protective layer) and alkalis causing deeper tissue destruction through liquefactive necrosis (penetrating progressively), making alkalis more dangerous; common organic acids include carboxylic, oxalic, acetic, and tartaric acids, while common inorganic acids include sulfuric, hydrochloric, and nitric acids, and common alkalis include sodium hydroxide, potassium hydroxide, sodium carbonate, and calcium carbonate.

Body-dependent conditions affecting poisoning include gender (women more susceptible to alcohol), age (children and elderly more vulnerable), body weight, individual predispositions, hypersensitivity, and habituation. Hypersensitivity can be congenital or acquired; idiosyncrasy is sudden rapid reaction without prior sensitization (unlike allergy). Habituation through repeated consumption increases enzyme production for toxin metabolism, but enzyme depletion can make small amounts fatal. Corrosive substances have local effects causing tissue burns and necrosis, including acids, alkalis, phenol, hydrogen peroxide, and potassium permanganate. Acids dissociate in aqueous solution, producing hydrogen ions that absorb water from tissues, coagulate proteins, and denature proteins. Different acids produce distinct effects: nitric acid causes yellowish mucosa, sulfuric acid causes blackish burns, hydrochloric acid causes green discoloration. Morphological changes include chemical burns, stomatitis, esophagitis, gastritis, mediastinitis, and peritonitis. Necrosis is hard and dried with rough crust formation. Alkalis contain hydroxyl groups that attract water, produce edema, and penetrate deeper tissues, causing colliquated soft necrosis (jelly-like, whitish-gray) with multiple ulceration and perforation complications.