TMJ Ankylosis

Temporomandibular Joint (TMJ) ankylosis is a condition characterized by the abnormal fusion of the mandibular condyle to the temporal bone, leading to restricted jaw movement. This condition can significantly impact a patient's ability to open their mouth and perform normal functions such as eating and speaking.

Causes and Mechanisms of TMJ Ankylosis

1. Condylar Injuries:

   • Most cases of TMJ ankylosis result from condylar injuries sustained before the age of 10. The unique anatomy and physiology of the condyle in children contribute to the development of ankylosis.

2. Unique Pattern of Condylar Fractures in Children:

   • In children, the condylar cortical bone is thinner, and the condylar neck is broader. This anatomical configuration, combined with a rich subarticular vascular plexus, predisposes children to specific types of fractures.
   • Intracapsular Fractures: These fractures can lead to comminution (fragmentation) and hemarthrosis (bleeding into the joint) of the condylar head. A specific type of intracapsular fracture known as a "mushroom fracture" occurs, characterized by the comminution of the condylar head.

3. Formation of Fibrous Mass:

   • The presence of a highly osteogenic environment (one that promotes bone formation) following a fracture can lead to the organization of a fibrous mass. This mass can undergo ossification (the process of bone formation) and consolidation, ultimately resulting in ankylosis.

4. Trauma from Forceps Delivery:

   • TMJ ankylosis can also occur due to trauma sustained during forceps delivery, which may cause injury to the condylar region.

Etiology and Risk Factors

Laskin (1978) outlined several factors that may contribute to the etiology of TMJ ankylosis following trauma:

1. Age of Patient:

   • Younger patients have a significantly higher osteogenic potential and a more rapid healing response. The articular capsule in younger individuals is not as well developed, allowing for easier displacement of the condyle out of the fossa, which can damage the articular disk. Additionally, children may exhibit a greater tendency for prolonged self-imposed immobilization of the mandible after trauma.

2. Type of Fracture:

   • The condyle in children has a thinner cortex and a thicker neck, which predisposes them to a higher proportion of intracapsular comminuted fractures. In contrast, adults typically have a thinner condylar neck, which usually fractures at the neck, sparing the head of the condyle within the capsule.

3. Damage to the Articular Disk:

   • Direct contact between a comminuted condyle and the glenoid fossa, either due to a displaced or torn meniscus (articular disk), is a key factor in the development of ankylosis. This contact can lead to inflammation and subsequent bony fusion.

4. Period of Immobilization:

   • Prolonged mechanical immobilization or muscle splinting can promote orthogenesis (the formation of bone) and consolidation in an injured condyle. Total immobility between articular surfaces after a condylar injury can lead to a bony type of fusion, while some movement may result in a fibrous type of union.

Cardiovascular Effects of Sevoflurane, Halothane, and Isoflurane

• Sevoflurane:

  • Maintains cardiac index and heart rate effectively.

  • Exhibits less hypotensive and negative inotropic effects compared to halothane.

  • Cardiac output is greater than that observed with halothane.

  • Recovery from sevoflurane anesthesia is smooth and comparable to isoflurane, with a shorter time to standing than halothane.

• Halothane:

  • Causes significant decreases in mean arterial pressure, ejection fraction, and cardiac index.

  • Heart rate remains at baseline levels, but overall cardiovascular function is depressed.

  • Recovery from halothane is less favorable compared to sevoflurane and isoflurane.

• Isoflurane:

  • Preserves cardiac index and ejection fraction better than halothane.

  • Increases heart rate while having less suppression of mean arterial pressure compared to halothane.

  • Cardiac output during isoflurane anesthesia is similar to that of sevoflurane, indicating a favorable cardiovascular profile.

Cricothyroidotomy

Cricothyroidotomy is a surgical procedure that involves making an incision through the skin over the cricothyroid membrane, which is located between the thyroid and cricoid cartilages in the neck. This procedure is performed to establish an emergency airway in situations where intubation is not possible or has failed, such as in cases of severe airway obstruction, facial trauma, or anaphylaxis.

Indications

Cricothyroidotomy is indicated in the following situations:

• Acute Airway Obstruction: When there is a complete blockage of the upper airway due to swelling, foreign body, or trauma.
• Failed Intubation: When attempts to secure an airway via endotracheal intubation have been unsuccessful.
• Facial or Neck Trauma: In cases where traditional airway management is compromised due to injury.
• Severe Anaphylaxis: When rapid airway access is needed and other methods are not feasible.

Anatomy

• Cricothyroid Membrane: The membrane lies between the thyroid and cricoid cartilages and is a key landmark for the procedure.
• Surrounding Structures: Important structures in the vicinity include the carotid arteries, jugular veins, and the recurrent laryngeal nerve, which must be avoided during the procedure.

Procedure

Preparation

1. Positioning: The patient should be in a supine position with the neck extended to improve access to the cricothyroid membrane.
2. Sterilization: The area should be cleaned and sterilized to reduce the risk of infection.
3. Anesthesia: Local anesthesia may be administered, but in emergency situations, this step may be skipped.

Steps

1. Identify the Cricothyroid Membrane: Palpate the thyroid and cricoid cartilages to locate the membrane, which is typically located about 1-2 cm below the thyroid notch.
2. Make the Incision: Using a scalpel, make a vertical incision through the skin over the cricothyroid membrane, approximately 2-3 cm in length.
3. Incise the Membrane: Carefully incise the cricothyroid membrane horizontally to create an opening into the airway.
4. Insert the Airway Device:
   • A tracheostomy tube or a large-bore cannula (e.g., a 14-gauge catheter) is inserted into the opening to establish an airway.
   • Ensure that the device is positioned correctly to allow for ventilation.
5. Secure the Airway: If using a tracheostomy tube, secure it in place to prevent dislodgment.

Post-Procedure Care

• Ventilation: Connect the airway device to a bag-valve-mask (BVM) or ventilator to provide oxygenation and ventilation.
• Monitoring: Continuously monitor the patient for signs of respiratory distress, oxygen saturation, and overall stability.
• Consider Further Intervention: Plan for definitive airway management, such as a formal tracheostomy or endotracheal intubation, once the immediate crisis is resolved.

Complications

While cricothyroidotomy is a life-saving procedure, it can be associated with several complications, including:

• Infection: Risk of infection at the incision site.
• Hemorrhage: Potential bleeding from surrounding vessels.
• Damage to Surrounding Structures: Injury to the recurrent laryngeal nerve, carotid arteries, or jugular veins.
• Subcutaneous Emphysema: Air escaping into the subcutaneous tissue.
• Tracheal Injury: If the incision is not made correctly, there is a risk of damaging the trachea.

Types of Brain Injury

Brain injuries can be classified into two main categories: primary and secondary injuries. Understanding these types is crucial for effective diagnosis and management.

1. Primary Brain Injury

• Definition: Primary brain injury occurs at the moment of impact. It results from the initial mechanical forces applied to the brain and can lead to immediate damage.
• Examples:
  • Contusions: Bruising of brain tissue.
  • Lacerations: Tears in brain tissue.
  • Concussions: A temporary loss of function due to trauma.
  • Diffuse axonal injury: Widespread damage to the brain's white matter.

2. Secondary Brain Injury

• Definition: Secondary brain injury occurs after the initial impact and is often preventable. It results from a cascade of physiological processes that can exacerbate the initial injury.
• Principal Causes:
  • Hypoxia: Reduced oxygen supply to the brain, which can worsen brain injury.
  • Hypotension: Low blood pressure can lead to inadequate cerebral perfusion.
  • Raised Intracranial Pressure (ICP): Increased pressure within the skull can compress brain tissue and reduce blood flow.
  • Reduced Cerebral Perfusion Pressure (CPP): Insufficient blood flow to the brain can lead to ischemia.
  • Pyrexia: Elevated body temperature can increase metabolic demands and worsen brain injury.

Glasgow Coma Scale (GCS)

The Glasgow Coma Scale is a clinical tool used to assess a patient's level of consciousness and neurological function. It consists of three components: eye opening, verbal response, and motor response.

Eye Opening (E)

• Spontaneous: 4
• To verbal command: 3
• To pain stimuli: 2
• No eye opening: 1

Verbal Response (V)

• Normal, oriented: 5
• Confused: 4
• Inappropriate words: 3
• Sounds only: 2
• No sounds: 1

Motor Response (M)

• Obeys commands: 6
• Localizes to pain: 5
• Withdrawal flexion: 4
• Abnormal flexion (decorticate): 3
• Extension (decerebrate): 2
• No motor response: 1

Scoring

• Best Possible Score: 15/15 (fully alert and oriented)
• Worst Possible Score: 3/15 (deep coma or death)
• Intubated Cases: For patients who are intubated, the verbal score is recorded as "T."
• Intubation Indication: Intubation should be performed if the GCS score is less than or equal to 8.

Additional Assessments

Pupil Examination

• Pupil Reflex: Assess size and light response.
• Uncal Herniation: In cases of mass effect on the ipsilateral side, partial third nerve dysfunction may be noted, characterized by a larger pupil with sluggish reflex.
• Hutchinson Pupil: As third nerve compromise increases, the ipsilateral pupil may become fixed and dilated.

Signs of Base of Skull Fracture

• Raccoon Eyes: Bilateral periorbital hematoma, indicating possible skull base fracture.
• Battle’s Sign: Bruising over the mastoid process, suggesting a fracture of the temporal bone.
• CSF Rhinorrhea or Otorrhea: Leakage of cerebrospinal fluid from the nose or ear, indicating a breach in the skull base.
• Hemotympanum: Blood in the tympanic cavity, often seen with ear bleeding.

SHOCK

Shock  is  defined  as  a  pathological  state  causing  inadequate  oxygen  delivery  to  the peripheral tissues and resulting in lactic acidosis, cellular hypoxia and disruption of normal metabolic condition.

CLASSIFICATION

Shock is generally classified into three major categories:

1.    Hypovolemic shock

2.    Cardiogenic shock

3.    Distributive shock

Distributive shock is further subdivided into three subgroups:

a.    Septic shock

b.    Neurogenic shock

c.    Anaphylactic shock

Hypovolemic  shock  is  present  when  marked  reduction  in  oxygen  delivery results from diminished cardiac output secondary to inadequate vascular volume. In general, it results from loss of fluid from circulation, either directly or indirectly.
e.g.    ?    Hemorrhage
    •    Loss of plasma due to burns
    •    Loss of water and electrolytes in diarrhea
    •    Third space loss (Internal fluid shift into inflammatory exudates in
        the peritoneum, such as in pancreatitis.)

Cardiogenic shock is present when there is severe reduction in oxygen delivery secondary to impaired cardiac function. Usually it is due to myocardial infarction or pericardial tamponade.

Septic Shock (vasogenic shock) develops as a result of the systemic effect of infection. It is the result of a septicemia with endotoxin and exotoxin release by gram-negative and gram-positive bacteria. Despite normal or increased cardiac output and oxygen delivery, cellular oxygen consumption is less than normal due to impaired extraction as a result of impaired metabolism.

Neurogenic shock results primarily from the disruption of the sympathetic nervous system which may be due to pain or loss of sympathetic tone, as in spinal cord injuries.

PATHO PHYSIOLOGY OF SHOCK

Shock stimulates a physiologic response. This circulatory response to hypotension is to conserve perfusion to the vital organs (heart and brain) at the expense of other tissues. Progressive vasoconstriction of skin, splanchnic and renal vessels leads to renal cortical necrosis and acute renal failure. If not corrected in time, shock leads to organ failure and sets up a vicious circle with hypoxia and acidosis.

CLINICAL FEATURES

The clinical presentation varies according to the cause. But in general patients with hypotension and reduced tissue perfusion presents with:
•    Tachycardia
•    Feeble pulse
•    Narrow pulse pressure
•    Cold extremities (except septic shock)
•    Sweating, anxiety
•    Breathlessness / Hyperventilation
•    Confusion leading to unconscious state

PATHO PHYSIOLOGY OF SHOCK

Shock stimulates a physiologic response. This circulatory response to hypotension is to conserve perfusion to the vital organs (heart and brain) at the expense of other tissues. Progressive vasoconstriction of skin, splanchnic and renal vessels leads to renal cortical necrosis and acute renal failure. If not corrected in time, shock leads to organ failure and sets up a vicious circle with hypoxia and acidosis.

CLINICAL FEATURES

The clinical presentation varies according to the cause. But in general patients with hypotension and reduced tissue perfusion presents with:
•    Tachycardia
•    Feeble pulse
•    Narrow pulse pressure
•    Cold extremities (except septic shock)
•    Sweating, anxiety
•    Breathlessness / Hyperventilation
•    Confusion leading to unconscious state

Sinus

It is a tubular track lined by granulation tissue and open at one end which is at the surface,

eg. Tuberculous Sinus

Fistula

A tubular track lined by granulation tissue and open at both ends.at least one of which communicates with a hollow viscus. it can be internal or external.

Causes

1. Inadequate drainage

• Abscess bursting at the non dependent part
• Incision at the non-dependent part.
• Narrow outer opening leading to collection of exudates in the cavity.

2. Presence of foreign body like sequestrum or slough.

3. Persistence of infection.

4. When the track is lined by epithelium

5. Specific causes, TB., Syphilis, etc.

6. Marked fibrosis of the wall with obliteration of blood vessels.

7. Poor general condition causing delayed healing.

Treatment

1. control of specific infection,

2. Thorough excision of track to open up the cavity. Removal of foreign body and scraping of the epithelium

3. Through Scrapping of the wall to expose healthy tissue

4. Wound laid open and allowed to heal from the bottom leaving no pocket,