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Oral and Maxillofacial Surgery - NEETMDS- courses
Oral and Maxillofacial Surgery

Coagulation Tests: PT and PTT

Prothrombin Time (PT) and Partial Thromboplastin Time (PTT) are laboratory tests used to evaluate the coagulation pathways involved in blood clotting. Understanding these tests is crucial for diagnosing bleeding disorders and managing patients with specific factor deficiencies.

Prothrombin Time (PT)

  • Purpose: PT is primarily used to assess the extrinsic pathway of coagulation.
  • Factors Tested: It evaluates the function of factors I (fibrinogen), II (prothrombin), V, VII, and X.
  • Clinical Use: PT is commonly used to monitor patients on anticoagulant therapy (e.g., warfarin) and to assess bleeding risk before surgical procedures.

Partial Thromboplastin Time (PTT)

  • Purpose: PTT is used to assess the intrinsic pathway of coagulation.
  • Factors Tested: It evaluates the function of factors I (fibrinogen), II (prothrombin), V, VIII, IX, X, XI, and XII.
  • Clinical Use: PTT is often used to monitor patients on heparin therapy and to evaluate bleeding disorders.

Specific Factor Deficiencies

In certain bleeding disorders, specific factor deficiencies can lead to increased bleeding risk. Preoperative management may involve the administration of the respective clotting factors or antifibrinolytic agents to minimize bleeding during surgical procedures.

  1. Hemophilia A:

    • Deficiency: Factor VIII deficiency.
    • Management: Administration of factor VIII concentrate before surgery.
  2. Hemophilia B:

    • Deficiency: Factor IX deficiency.
    • Management: Administration of factor IX concentrate before surgery.
  3. Hemophilia C:

    • Deficiency: Factor XI deficiency.
    • Management: Administration of factor XI concentrate or fresh frozen plasma (FFP) may be considered.
  4. Von Willebrand’s Disease:

    • Deficiency: Deficiency or dysfunction of von Willebrand factor (vWF), which is important for platelet adhesion.
    • Management: Desmopressin (DDAVP) may be administered to increase vWF levels, or factor replacement therapy may be used.
  5. Antifibrinolytic Agent:

    • Aminocaproic Acid: This antifibrinolytic agent can be used to help stabilize clots and reduce bleeding during surgical procedures, particularly in patients with bleeding disorders.

Augmentation of the Inferior Border of the Mandible

Mandibular augmentation refers to surgical procedures aimed at increasing the height or contour of the mandible, particularly the inferior border. This type of augmentation is often performed to improve the support for dentures, enhance facial aesthetics, or correct deformities. Below is an overview of the advantages and disadvantages of augmenting the inferior border of the mandible.

Advantages of Inferior Border Augmentation

  1. Preservation of the Vestibule:

    • The procedure does not obliterate the vestibule, allowing for the immediate placement of an interim denture. This is particularly beneficial for patients who require prosthetic support soon after surgery.
  2. No Change in Vertical Dimension:

    • Augmentation of the inferior border does not alter the vertical dimension of the occlusion, which is crucial for maintaining proper bite relationships and avoiding complications associated with changes in jaw alignment.
  3. Facilitation of Secondary Vestibuloplasty:

    • The procedure makes subsequent vestibuloplasty easier. By maintaining the vestibular space, it allows for better access and manipulation during any future surgical interventions aimed at deepening the vestibule.
  4. Protection of the Graft:

    • The graft used for augmentation is not subjected to direct masticatory forces, reducing the risk of graft failure and promoting better healing. This is particularly important in ensuring the longevity and stability of the augmentation.

Disadvantages of Inferior Border Augmentation

  1. Extraoral Scar:

    • The procedure typically involves an incision that can result in an extraoral scar. This may be a cosmetic concern for some patients, especially if the scar is prominent or does not heal well.
  2. Potential Alteration of Facial Appearance:

    • If the submental and submandibular tissues are not initially loose, there is a risk of altering the facial appearance. Tight or inelastic tissues may lead to distortion or asymmetry postoperatively.
  3. Limited Change in Superior Surface Shape:

    • The augmentation primarily affects the inferior border of the mandible and may not significantly change the shape of the superior surface of the mandible. This limitation can affect the overall contour and aesthetics of the jawline.
  4. Surgical Risks:

    • As with any surgical procedure, there are inherent risks, including infection, bleeding, and complications related to anesthesia. Additionally, there may be risks associated with the grafting material used.

  • Torque testing:
    • Successful osseointegration: 10 – 20 N/cm force without unscrewing.
    • Clinical signs: Percussion, immobility, no movement with 5 lb lateral force.
    • Failure: Horizontal mobility >1 mm or movement <500 g force.
  • Radiographic sign of implant failure: Loss of crestal bone.
  • MRI/CT with titanium implants: Safe; CT can subtract titanium to eliminate scatter.

  • NOE fracture test: Bow string test
  • Blow-out fracture types:
    • Pure: Orbital rim intact
    • Impure: Rim + facial bones involved
  • LeFort fracture hemorrhage source: Fractured septum
  • CSF rhinorrhea test: Beta-2 transferrin

Overview of Infective Endocarditis (IE):

  • Infective endocarditis is an inflammation of the inner lining of the heart, often caused by bacterial infection.
  • Certain cardiac conditions increase the risk of developing IE, particularly during dental procedures that may introduce bacteria into the bloodstream.

High-Risk Cardiac Conditions: Antibiotic prophylaxis is recommended for patients with the following high-risk cardiac conditions:

  • Prosthetic cardiac valves
  • History of infective endocarditis
  • Cyanotic congenital heart disease
  • Surgically constructed systemic-pulmonary shunts
  • Other congenital heart defects
  • Acquired valvular dysfunction
  • Hypertrophic cardiomyopathy
  • Mitral valve prolapse with regurgitation

Moderate-Risk Cardiac Conditions:

  • Mitral valve prolapse without regurgitation
  • Previous rheumatic fever with valvular dysfunction

Negligible Risk Conditions:

  • Coronary bypass grafts
  • Physiological or functional heart murmurs

Prophylaxis Recommendations

When to Administer Prophylaxis:

  • Prophylaxis is indicated for dental procedures that involve:
    • Manipulation of gingival tissue
    • Perforation of the oral mucosa
    • Procedures that may cause bleeding

Antibiotic Regimens:

  • The standard prophylactic regimen is a single dose administered 30-60 minutes before the procedure:
    • Amoxicillin:
      • Adult dose: 2 g orally
      • Pediatric dose: 50 mg/kg orally (maximum 2 g)
    • Ampicillin:
      • Adult dose: 2 g IV/IM
      • Pediatric dose: 50 mg/kg IV/IM (maximum 2 g)
    • Clindamycin (for penicillin-allergic patients):
      • Adult dose: 600 mg orally
      • Pediatric dose: 20 mg/kg orally (maximum 600 mg)
    • Cephalexin (for penicillin-allergic patients):
      • Adult dose: 2 g orally
      • Pediatric dose: 50 mg/kg orally (maximum 2 g)

Induction of Local Anesthesia

The induction of local anesthesia involves the administration of a local anesthetic agent into the soft tissues surrounding a nerve, allowing for the temporary loss of sensation in a specific area. Understanding the mechanisms of diffusion, the organization of peripheral nerves, and the barriers to anesthetic penetration is crucial for effective anesthesia management in clinical practice.

Mechanism of Action

  1. Diffusion:

    • After the local anesthetic is injected, it begins to diffuse from the site of deposition into the surrounding tissues. This process is driven by the concentration gradient, where the anesthetic moves from an area of higher concentration (the injection site) to areas of lower concentration (toward the nerve).
    • Unhindered Migration: The local anesthetic molecules migrate through the extracellular fluid, seeking to reach the nerve fibers. This movement is termed diffusion, which is the passive movement of molecules through a fluid medium.
  2. Anatomic Barriers:

    • The penetration of local anesthetics can be hindered by anatomical barriers, particularly the perineurium, which is the most significant barrier to the diffusion of local anesthetics. The perineurium surrounds each fascicle of nerve fibers and restricts the free movement of molecules.
    • Perilemma: The innermost layer of the perineurium, known as the perilemma, also contributes to the barrier effect, making it challenging for local anesthetics to penetrate effectively.

Organization of a Peripheral Nerve

Understanding the structure of peripheral nerves is essential for comprehending how local anesthetics work. Here’s a breakdown of the components:

Organization of a Peripheral  Nerve

Structure         

Description

Nerve fiber

Single nerve cell

Endoneurium

Covers each nerve fiber

Fasciculi

Bundles of  500 to 1000 nerve fibres

Perineurium

Covers fascicule

Perilemma

Innermost layer of perinuerium

Epineurium

Alveolar connective tissue supporting fasciculi andCarrying nutrient vessels

Epineural sheath

Outer layer of epinuerium

 

Composition of Nerve Fibers and Bundles

In a large peripheral nerve, which contains numerous axons, the local anesthetic must diffuse inward toward the nerve core from the extraneural site of injection. Here’s how this process works:

  1. Diffusion Toward the Nerve Core:

    • The local anesthetic solution must travel through the endoneurium and perineurium to reach the nerve fibers. As it penetrates, the anesthetic is subject to dilution due to tissue uptake and mixing with interstitial fluid.
    • This dilution can lead to a concentration gradient where the outer mantle fibers (those closest to the injection site) are blocked effectively, while the inner core fibers (those deeper within the nerve) may not be blocked immediately.
  2. Concentration Gradient:

    • The outer fibers are exposed to a higher concentration of the local anesthetic, leading to a more rapid onset of anesthesia in these areas. In contrast, the inner core fibers receive a lower concentration and are blocked later.
    • The delay in blocking the core fibers is influenced by factors such as the mass of tissue that the anesthetic must penetrate and the diffusivity of the local anesthetic agent.

Clinical Implications

Understanding the induction of local anesthesia and the barriers to diffusion is crucial for clinicians to optimize anesthesia techniques. Here are some key points:

  • Injection Technique: Proper technique and site selection for local anesthetic injection can enhance the effectiveness of the anesthetic by maximizing diffusion toward the nerve.
  • Choice of Anesthetic: The selection of local anesthetic agents with favorable diffusion properties can improve the onset and duration of anesthesia.
  • Monitoring: Clinicians should monitor the effectiveness of anesthesia, especially in procedures involving larger nerves or areas with significant anatomical barriers.

Upper Airway Components

  • Nasal cavity: First line filtration, warming, humidification
  • Oral cavity: Alternative route, larger diameter
  • Pharynx: Nasopharynx, oropharynx, hypopharynx
  • Larynx: Voice production, airway protection
  • Trachea: Conduit to lower respiratory tract

Critical Anatomical Considerations

  • Tongue: Largest soft tissue mass in oral cavity
  • Epiglottis: Primary airway protection mechanism
  • Vocal cords: Narrowest part of adult airway
  • Cricothyroid membrane: Emergency surgical access point
  • Pediatric differences: Proportionally larger tongue, higher larynx

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