Structure of Orbital Walls

The orbit is a complex bony structure that houses the eye and its associated structures. It is composed of several walls, each with distinct anatomical features and clinical significance. Here’s a detailed overview of the structure of the orbital walls:

1. Lateral Wall

• Composition: The lateral wall of the orbit is primarily formed by two bones:
  • Zygomatic Bone: This bone contributes significantly to the lateral aspect of the orbit.
  • Greater Wing of the Sphenoid: This bone provides strength and stability to the lateral wall.
• Orientation: The lateral wall is inclined at approximately 45 degrees to the long axis of the skull, which is important for the positioning of the eye and the alignment of the visual axis.

2. Medial Wall

• Composition: The medial wall is markedly different from the lateral wall and is primarily formed by:
  • Orbital Plate of the Ethmoid Bone: This plate is very thin and fragile, making the medial wall susceptible to injury.
• Height and Orientation: The medial wall is about half the height of the lateral wall. It is aligned parallel to the antero-posterior axis (median plane) of the skull and meets the floor of the orbit at an angle of about 45 degrees.
• Fragility: The medial wall is extremely fragile due to its proximity to:
  • Ethmoid Air Cells: These air-filled spaces can compromise the integrity of the medial wall.
  • Nasal Cavity: The close relationship with the nasal cavity further increases the risk of injury.

3. Roof of the Orbit

• Composition: The roof is formed by the frontal bone and is reinforced laterally by the greater wing of the sphenoid.
• Thickness: While the roof is thin, it is structurally reinforced, which helps protect the contents of the orbit.
• Fracture Patterns: Fractures of the roof often involve the frontal bone and tend to extend medially. Such fractures can lead to complications, including orbital hemorrhage or involvement of the frontal sinus.

4. Floor of the Orbit

• Composition: The floor is primarily formed by the maxilla, with contributions from the zygomatic and palatine bones.
• Thickness: The floor is very thin, typically measuring about 0.5 mm in thickness, making it particularly vulnerable to fractures.
• Clinical Significance:
  • Blow-Out Fractures: The floor is commonly involved in "blow-out" fractures, which occur when a blunt force impacts the eye, causing the floor to fracture and displace. These fractures can be classified as:
    • Pure Blow-Out Fractures: Isolated fractures of the orbital floor.
    • Impure Blow-Out Fractures: Associated with fractures in the zygomatic area.
  • Infraorbital Groove and Canal: The presence of the infraorbital groove and canal further weakens the floor. The infraorbital nerve and vessels run through this canal, making them susceptible to injury during fractures. Compression, contusion, or direct penetration from bone spicules can lead to sensory deficits in the distribution of the infraorbital nerve.

Odontogenic Keratocyst (OKC)

The odontogenic keratocyst (OKC) is a unique and aggressive cystic lesion of the jaw with distinct histological features and a high recurrence rate. Below is a comprehensive overview of its characteristics, treatment options, and prognosis.

Characteristics of Odontogenic Keratocyst

1. Definition and Origin:

   • The term "odontogenic keratocyst" was first introduced by Philipsen in 1956. It is believed to originate from remnants of the dental lamina or basal cells of the oral epithelium.

2. Biological Behavior:

   • OKCs exhibit aggressive behavior and have a recurrence rate of 13% to 60%. They are considered to have a neoplastic nature rather than a purely developmental origin.

3. Histological Features:

   • The cyst lining is typically 6 to 10 cells thick, with a palisaded basal cell layer and a surface of corrugated parakeratin.
   • The epithelium may produce orthokeratin (10%), parakeratin (83%), or both (7%).
   • No rete ridges are present, and mitotic activity is frequent, contributing to the cyst's growth pattern.

4. Types:

   • Orthokeratinized OKC: Less aggressive, lower recurrence rate, often associated with dentigerous cysts.
   • Parakeratinized OKC: More aggressive with a higher recurrence rate.

5. Clinical Features:

   • Age: Peak incidence occurs in individuals aged 20 to 30 years.
   • Gender: Predilection for males (approximately 1:5 male to female ratio).
   • Location: More commonly found in the mandible, particularly in the ramus and third molar area. In the maxilla, the third molar area is also a common site.
   • Symptoms: Patients may be asymptomatic, but symptoms can include pain, soft-tissue swelling, drainage, and paresthesia of the lip or teeth.

6. Radiographic Features:

   • Typically appears as a unilocular lesion with a well-defined peripheral rim, although multilocular varieties (20%) can occur.
   • Scalloping of the borders is often present, and it may be associated with the crown of a retained tooth (40%).

Treatment Options for Odontogenic Keratocyst

1. Surgical Excision:

   • Enucleation: Complete removal of the cyst along with the surrounding tissue.
   • Curettage: Scraping of the cyst lining after enucleation to remove any residual cystic tissue.

2. Chemical Cauterization:

   • Carnoy’s Solution: Application of Carnoy’s solution (6 ml absolute alcohol, 3 ml chloroform, and 1 ml acetic acid) after enucleation and curettage can help reduce recurrence rates. It penetrates the bone and can assist in freeing the cyst from the bone wall.

3. Marsupialization:

   • This technique involves creating a window in the cyst to allow for drainage and reduction in size, which can be beneficial in larger cysts or in cases where complete excision is not feasible.

4. Primary Closure:

   • After enucleation and curettage, the site may be closed primarily or packed open to allow for healing.

5. Follow-Up:

   • Regular follow-up is essential due to the high recurrence rate. Patients should be monitored for signs of recurrence, especially in the first few years post-treatment.

Prognosis

• The prognosis for OKC is variable, with a significant recurrence rate attributed to the aggressive nature of the lesion and the potential for residual cystic tissue.
• Recurrence is not necessarily related to the size of the cyst or the presence of satellite cysts but is influenced by the nature of the lesion itself and the presence of dental lamina remnants.
• Multilocular lesions tend to have a higher recurrence rate compared to unilocular ones.
• Surgical technique does not significantly influence the likelihood of relapse.

Associated Conditions

• Multiple OKCs can be seen in syndromes such as:
  • Nevoid Basal Cell Carcinoma Syndrome (Gorlin-Goltz Syndrome)
  • Marfan Syndrome
  • Ehlers-Danlos Syndrome
  • Noonan Syndrome

Velopharyngeal Insufficiency (VPI)

Velopharyngeal insufficiency (VPI) is characterized by inadequate closure of the nasopharyngeal airway during speech production, leading to speech disorders such as hypernasality and nasal regurgitation. This condition is particularly relevant in patients who have undergone cleft palate repair, as the surgical success does not always guarantee proper function of the velopharyngeal mechanism.

Etiology of VPI

The etiology of VPI following cleft palate repair is multifactorial and can include:

1. Inadequate Surgical Repair: Insufficient repair of the musculature involved in velopharyngeal closure can lead to persistent VPI. This may occur if the muscles are not properly repositioned or if there is inadequate tension in the repaired tissue.

2. Anatomical Variations: Variations in the anatomy of the soft palate, pharynx, and surrounding structures can contribute to VPI. These variations may not be fully addressed during initial surgical repair.

3. Neuromuscular Factors: Impaired neuromuscular function of the muscles involved in velopharyngeal closure can also lead to VPI, which may not be correctable through surgical means alone.

Surgical Management of VPI

Pharyngoplasty: One of the surgical options for managing VPI is pharyngoplasty, which aims to improve the closure of the nasopharyngeal port during speech.

• Historical Background: The procedure was first described by Hynes in 1951 and has since been modified by various authors to enhance its effectiveness and reduce complications.

Operative Procedure

1. Flap Creation: The procedure involves the creation of two superiorly based myomucosal flaps from each posterior tonsillar pillar. Care is taken to include as much of the palatopharyngeal muscle as possible in the flaps.

2. Flap Elevation: The flaps are elevated carefully to preserve their vascular supply and muscular integrity.

3. Flap Insetting: The flaps are then attached and inset within a horizontal incision made high on the posterior pharyngeal wall. This technique aims to create a single nasopharyngeal port rather than the two ports typically created with a superiorly based pharyngeal flap.

4. Contractile Ridge Formation: The goal of the procedure is to establish a contractile ridge posteriorly, which enhances the function of the velopharyngeal valve, thereby improving closure during speech.

Advantages of Sphincter Pharyngoplasty

• Lower Complication Rate: One of the main advantages of sphincter pharyngoplasty over the traditional superiorly based flap technique is the lower incidence of complications related to nasal airway obstruction. This is particularly important for patient comfort and quality of life post-surgery.

• Improved Speech Outcomes: By creating a more effective velopharyngeal mechanism, patients often experience improved speech outcomes, including reduced hypernasality and better articulation.

1. Radical Neck Dissection

• Complete removal of all ipsilateral cervical lymph node groups (levels I-V) and three key non-lymphatic structures:
  • Internal jugular vein
  • Sternocleidomastoid muscle
  • Spinal accessory nerve
• Indication: Typically performed for extensive lymphatic involvement.

2. Modified Radical Neck Dissection

• Similar to radical neck dissection in terms of lymph node removal (levels I-V) but with preservation of one or more of the following structures:
  • Type I: Preserves the spinal accessory nerve.
  • Type II: Preserves the spinal accessory nerve and the sternocleidomastoid muscle.
  • Type III: Preserves the spinal accessory nerve, sternocleidomastoid muscle, and internal jugular vein.
• Indication: Used when there is a need to reduce morbidity while still addressing lymphatic involvement.

3. Selective Neck Dissection

• Preservation of one or more lymph node groups that are typically removed in a radical neck dissection.
• Classification:
  • Originally had named dissections (e.g., supraomohyoid neck dissection for levels I-III).
  • The 2001 modification proposed naming dissections based on the cancer type and the specific node groups removed. For example, a selective neck dissection for oral cavity cancer might be referred to as a selective neck dissection (levels I-III).
• Indication: Used when there is a lower risk of lymphatic spread or when targeting specific areas.

4. Extended Neck Dissection

•  Involves the removal of additional lymph node groups or non-lymphatic structures beyond those included in a radical neck dissection. This may include:
  • Mediastinal nodes
  • Non-lymphatic structures such as the carotid artery or hypoglossal nerve.
• Indication: Typically performed in cases of extensive disease or when there is a need to address additional areas of concern.

Hemostatic Agents

Hemostatic agents are critical in surgical procedures to control bleeding and promote wound healing. Various materials are used, each with unique properties and mechanisms of action. Below is a detailed overview of some commonly used hemostatic agents, including Gelfoam, Oxycel, Surgical (Oxycellulose), and Fibrin Glue.

1. Gelfoam

• Composition: Gelfoam is made from gelatin and has a sponge-like structure.

• Mechanism of Action:

  • Gelfoam does not have intrinsic hemostatic properties; its hemostatic effect is primarily due to its large surface area, which comes into contact with blood.
  • When Gelfoam absorbs blood, it swells and exerts pressure on the bleeding site, providing a scaffold for the formation of a fibrin network.

• Application:

  • Gelfoam should be moistened in saline or thrombin solution before application to ensure optimal performance. It is essential to remove all air from the interstices to maximize its effectiveness.

• Absorption: Gelfoam is absorbed by the body through phagocytosis, typically within a few weeks.

2. Oxycel

• Composition: Oxycel is made from oxidized cellulose.

• Mechanism of Action:

  • Upon application, Oxycel releases cellulosic acid, which has a strong affinity for hemoglobin, leading to the formation of an artificial clot.
  • The acid produced during the wetting process can inactivate thrombin and other hemostatic agents, which is why Oxycel should be applied dry.

• Limitations:

  • The acid produced can inhibit epithelialization, making Oxycel unsuitable for use over epithelial surfaces.

3. Surgical (Oxycellulose)

• Composition: Surgical is a glucose polymer-based sterile knitted fabric created through the controlled oxidation of regenerated cellulose.

• Mechanism of Action:

  • The local hemostatic mechanism relies on the binding of hemoglobin to oxycellulose, allowing the dressing to expand into a gelatinous mass. This mass acts as a scaffold for clot formation and stabilization.

• Application:

  • Surgical can be applied dry or soaked in thrombin solution, providing flexibility in its use.

• Absorption: It is removed by liquefaction and phagocytosis over a period of one week to one month. Unlike Oxycel, Surgical does not inhibit epithelialization and can be used over epithelial surfaces.

4. Fibrin Glue

• Composition: Fibrin glue is a biological adhesive that contains thrombin, fibrinogen, factor XIII, and aprotinin.

• Mechanism of Action:

  • Thrombin converts fibrinogen into an unstable fibrin clot, while factor XIII stabilizes the clot. Aprotinin prevents the degradation of the clot.
  • During wound healing, fibroblasts migrate through the fibrin meshwork, forming a more permanent framework composed of collagen fibers.

• Applications:

  • Fibrin glue is used in various surgical procedures to promote hemostasis and facilitate tissue adhesion. It is particularly useful in areas where traditional sutures may be challenging to apply.

Dental/Oral/Upper Respiratory Tract Procedures: Antibiotic Prophylaxis Guidelines

Antibiotic prophylaxis is crucial for patients at risk of infective endocarditis or other infections during dental, oral, or upper respiratory tract procedures. The following guidelines outline the standard and alternate regimens for antibiotic prophylaxis based on the patient's allergy status and ability to take oral medications.

I. Standard Regimen in Patients at Risk

1. For Patients Allergic to Penicillin/Ampicillin/Amoxicillin:

   • Erythromycin:
     • Dosage: Erythromycin ethyl-succinate 800 mg or erythromycin stearate 1.0 gm orally.
     • Timing: Administer 2 hours before the procedure.
     • Follow-up Dose: One-half of the original dose (400 mg or 500 mg) 6 hours after the initial administration.
   • Clindamycin:
     • Dosage: Clindamycin 300 mg orally.
     • Timing: Administer 1 hour before the procedure.
     • Follow-up Dose: 150 mg 6 hours after the initial dose.

2. For Non-Allergic Patients:

   • Amoxicillin:
     • Dosage: Amoxicillin 3.0 gm orally.
     • Timing: Administer 1 hour before the procedure.
     • Follow-up Dose: 1.5 gm 6 hours after the initial dose.

II. Alternate Prophylactic Regimens in Patients at Risk

1. For Patients Who Cannot Take Oral Medications:

   • For Penicillin/Amoxicillin Allergic Patients:
     • Clindamycin:
       • Dosage: Clindamycin 300 mg IV.
       • Timing: Administer 30 minutes before the procedure.
       • Follow-up Dose: 150 mg IV (or orally) 6 hours after the initial dose.
   • For Non-Allergic Patients:
     • Ampicillin:
       • Dosage: Ampicillin 2.0 gm IV or IM.
       • Timing: Administer 30 minutes before the procedure.
       • Follow-up Dose: Ampicillin 1.0 gm IV (or IM) or amoxicillin 1.5 gm orally 6 hours after the initial dose.

2. For High-Risk Patients Who Are Not Candidates for the Standard Regimen:

   • For Penicillin/Amoxicillin Allergic Patients:
     • Vancomycin:
       • Dosage: Vancomycin 1.0 gm IV.
       • Timing: Administer over 1 hour, starting 1 hour before the procedure.
       • Follow-up Dose: No repeat dose is necessary.
   • For Non-Allergic Patients:
     • Ampicillin and Gentamicin:
       • Dosage: Ampicillin 2.0 gm IV (or IM) plus gentamicin 1.5 mg/kg IV (or IM) (not to exceed 80 mg).
       • Timing: Administer 30 minutes before the procedure.
       • Follow-up Dose: Amoxicillin 1.5 gm orally 6 hours after the initial dose. Alternatively, the parenteral regimen may be repeated 8 hours after the initial dose.