Ludwig's Angina

Ludwig's angina is a serious, potentially life-threatening cellulitis or connective tissue infection of the submandibular space. It typically arises from infections of the teeth, particularly the second or third molars, and can lead to airway obstruction due to swelling. This condition is named after the German physician Wilhelm Friedrich von Ludwig, who first described it in the 19th century.

Etiology

• Common Causes:

  • Dental infections (especially from the lower molars)
  • Infections from the floor of the mouth
  • Trauma to the submandibular area
  • Occasionally, infections can arise from other sources, such as the oropharynx or skin.

• Microbial Agents:

  • Mixed flora, including both aerobic and anaerobic bacteria.
  • Common organisms include Streptococcus, Staphylococcus, and Bacteroides species.

Pathophysiology

• The infection typically begins in the submandibular space and can spread rapidly due to the loose connective tissue in this area.
• The swelling can lead to displacement of the tongue and can obstruct the airway, making it a medical emergency.

Clinical Presentation

• Symptoms:

  • Swelling of the submandibular area, which may be bilateral
  • "Brawny induration" (firm, non-fluctuant swelling)
  • Pain and tenderness in the submandibular region
  • Difficulty swallowing (dysphagia) and speaking (dysarthria)
  • Fever and malaise
  • Possible elevation of the floor of the mouth and displacement of the tongue

• Signs:

  • Swelling may extend to the neck and may cause "bull neck" appearance.
  • Trismus (limited mouth opening) may be present.
  • Respiratory distress due to airway compromise.

Diagnosis

• Clinical Evaluation: Diagnosis is primarily clinical based on history and physical examination.
• Imaging:
  • CT scan of the neck may be used to assess the extent of the infection and to rule out other conditions.
  • X-rays may show air in the soft tissues if there is a necrotizing infection.

Management

Initial Management

• Airway Management:
  • Ensure the airway is patent; this may require intubation or tracheostomy in severe cases.

Medical Treatment

• Antibiotics:
  • Broad-spectrum intravenous antibiotics are initiated to cover both aerobic and anaerobic bacteria. Common regimens may include:
    • Ampicillin-sulbactam
    • Clindamycin
    • Metronidazole combined with a penicillin derivative

Surgical Intervention

• Drainage:
  • Surgical drainage may be necessary if there is an abscess formation or significant swelling.
  • Incisions are typically made in the submandibular area to allow for drainage of pus and to relieve pressure.

Complications

• Airway Obstruction: The most critical complication, requiring immediate intervention.
• Sepsis: Can occur if the infection spreads systemically.
• Necrotizing fasciitis: Rare but serious complication that may require extensive surgical intervention.
• Thrombosis of the internal jugular vein: Can occur due to the spread of infection.

Prognosis

• With prompt diagnosis and treatment, the prognosis is generally good. However, delays in management can lead to significant morbidity and mortality due to airway compromise and systemic infection.

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.

An ulcer is a break in the continuity of the skin or the mucous membrane.

Mode of onset:  Traumatic ulcers heal when the traumatic agent is removed., If it persists it becomes chronic as in the case of dental ulcer of the tongue. Ulcers may develop spontaneously as in the case of gumma (syphilitic ulcer). It may develop with varicose veins called varicose ulcer, which develops in the lower third of the leg.

Sometimes a malignant ulcer develops in a scar called Marjolin’s ulcer. Special features are:

 No pain - as there are no nerves. It does not spread - as there is scar tissue. No metastases - as there are no lymphatics Treatment:- Wide excision.

Classification of Ulcer

A) Pathologically

I. Non-specific ulcers:

a. Due to infected wound after trauma, that is physical or chemical agents.

b. Due to local infection example dental ulcer, pressure sore

 Specific ulcers: Caused by specific infection

a. Syphilitic ulcers (Hunterian chancre)

b. Tubercular  ulcers, actinomycosis

Trophic ulcer:- Caused by two factors:

Diminished nutrition due to inadequate blood supply to the tissues

Eg. Ulcers in Buerger’s Disease, Artherosclerosis

b. Diminished or absence of sensation of the skin leading to perforating ulcer of the foot

iv. Malignant ulcer: Due to squamous cell carcinoma, rodent ulcers and melanoma.

B) Clinical classification of ulcers

1. Acute Ulcer:  The edge is inflamed oedematous and painful with slough in the floor and n o granulation tissue. Profuse purulent Discgarge seen

2. Healing ulcers: edge sloping with bluish margin The floor is covered with a red, healthy granulation tissue.

3. Chronic or callous ulcer (non- healing) There is no tendency to heal by itself, the base is jndurated  unhealthy granulation tissue is present in the floor The edge is rounded and thickened.

Chronic ulcer occur due to:

Chronic infection , Defective circulation , Foreign body, Persistent local oedema , Malignancy , Diabetes , Malnutrition (loss of proteins), Gout

Specific Ulcers

Tubeculous Ulcer

Edge Undermined, floor contains granulation tissue a watery discharge is present. Caseous material is found in the floor of the ulcer. It usually occurs in tubercular lymphadenitis in the neck, axilla or groin.

Syphilitic Ulcer

a) Huntarian Chancre or  primary sore or hard chancre: usuaIly occurs over the genitalia especially on penis. Occurs in the primary stage of syphilis Ulcer is round or oval, it is hard,indurated, elevated and painless It feels like a button, discharges serum containing spirochetes (cork screw) which is highly infective.

b) In the Secondary stage mucous patches and condylomata occurs The ulcers are shallow white patches, of sodden thickness which occur in the mouth and tongue. Condyloma are hypertrophied epithelium with serous discharge occurring in mucocutaneous junction around the anus. The regional lymphnod (inguinal transverse chain) are enlarged.

c) In tertiary stage of syphilis gummatous ulcers occur They have a punched  out edge and wash Ieather floor. They occur on the subcutaneous bones like sternum and tibia. They are painless and refuse to heal.

Soft Sore (chanchroid)

They are painful muitiple ulcers, with copious discharge. They are caused by Bacillus Ducrey  lncubation time is 3 to 4 days. located on glans penis and prepuce is due to venereal infection. They are associated with enlarged called bilateral inguinal lymphnodes

Tropical ulcer:

a) Oriental Sore - due to L. Tropica (lieshmaniasis)

b) Ulcers and sinuses are due to guinea worm abscess

c) Histoplasmosis with multiple ulcers on the tibia.

d) Chronic ulcers due to yaws

e) Amoebic ulcers occur in colon_and rectum , flask shaped ulcers , undermined edge , caused by  Entamoeba Histolytica

Varicose Ulcer:

Associated with varicose veins. Occurs on the inner aspect of the lower third of leg , chronic ulcer The surrounding area is pigmented and eczema is present. The sore is longitudinally oval It does not penetrate the deep fascia and is painless The base is adherent to the periosteum of the tibia

Rodent ulcer

Usually Occurs on the face above a line joining the lobule of the ear to the angle of the mouth. Usually occurs at the inner canthous of the eye . Edge is raised and rolled, Erodes the deeper structures and the bone, the lyrnph nodes are not involved.

Treatment: If small wide excision is done with skin grafting, If large, radiotherapy is given.

Malignant Ulcer

Occurs due to chronic irritation as in the case of malignant ulcer of the tongue. The edge is everted. The floor is covered with slough and tumor tissue The regional lymph nodes are hard.

Initially mobile later becomes hard

Treatment: Wide excision is done.

Marjolin ulcer: Malignant Ulcer occurring on scar of Burns

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.

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.

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