Zygomatic Bone Reduction

When performing a reduction of the zygomatic bone, particularly in the context of maxillary arch fractures, several key checkpoints are used to assess the success of the procedure. Here’s a detailed overview of the important checkpoints for both zygomatic bone and zygomatic arch reduction.

Zygomatic Bone Reduction

1. Alignment at the Sphenozygomatic Suture:

   • While this is considered the best checkpoint for assessing the reduction of the zygomatic bone, it may not always be the most practical or available option in certain clinical scenarios.

2. Symmetry of the Zygomatic Arch:

   • Importance: This is the second-best checkpoint and serves multiple purposes:
     • Maintains Interzygomatic Distance: Ensures that the distance between the zygomatic bones is preserved, which is crucial for facial symmetry.
     • Maintains Facial Symmetry and Aesthetic Balance: A symmetrical zygomatic arch contributes to the overall aesthetic appearance of the face.
     • Preserves the Dome Effect: The prominence of the zygomatic arch creates a natural contour that is important for facial aesthetics.

3. Continuity of the Infraorbital Rim:

   • A critical checkpoint indicating that the reduction is complete. The infraorbital rim should show no step-off, indicating proper alignment and continuity.

4. Continuity at the Frontozygomatic Suture:

   • Ensures that the junction between the frontal bone and the zygomatic bone is intact and properly aligned.

5. Continuity at the Zygomatic Buttress Region:

   • The zygomatic buttress is an important structural component that provides support and stability to the zygomatic bone.

Zygomatic Arch Reduction

1. Click Sound:

   • The presence of a click sound during manipulation can indicate proper alignment and reduction of the zygomatic arch.

2. Symmetry of the Arches:

   • Assessing the symmetry of the zygomatic arches on both sides of the face is crucial for ensuring that the reduction has been successful and that the facial aesthetics are preserved.

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.

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,

Inflammation is the respone of the body to an irritant.

Stages of Inflammation

1. General: Temperature Raised. In severe cases bacteremia or septicemia ,rigors may occur.

2. Local: classical signs of inflammation are due to hyperemia and inflammation exudate

i) Heat:  inflammed area feels warmer than the surrounding tissues.

ii) Redness

iii) Tenderness: Due to pressure of exudate on the surrounding nerves  If the exudate is  under tension, e.g. a furuncle (boil) of the ear, pain is severe.

iv) swelling

v) Loss of function.

The termination of Inflammation

This may be by:1. Resolution 2. Suppuration 3. Ulceration 4. Ganangren s. Fibrosis

Management

i. Increase the patients resistance., Rest,  Relief of pain by analgesics,  Diet: High protein and high calorie diet with vitamins,  Antibiotics,  Prevent further contamination of wound.

Surgical measures

1. Excision: If possible as in appendicectomy.

2. Incision and drainage: If an abscess forms.

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.