Types of Head Injury

1. Extradural Hematoma (EDH)

Overview

• Demographics: Most common in young male patients.
• Association: Always associated with skull fractures.
• Injured Vessel: Middle meningeal artery.
• Common Site of Injury: Temporal bone at the pterion (the thinnest part of the skull), which overlies the middle meningeal artery.
• Location of Hematoma: Between the bone and the dura mater.

Other Common Sites

1. Frontal fossa
2. Posterior fossa
3. May occur following disruption of major dural venous sinus.

Classical Presentation

• Initial Injury: Followed by a lucid interval where the patient may only complain of a headache.
• Deterioration: After minutes to hours, rapid deterioration occurs, leading to:
  • Contralateral hemiparesis
  • Reduced consciousness level
  • Ipsilateral pupillary dilatation (due to herniation)

Imaging

• CT Scan: Shows a lentiform (lens-shaped or biconvex) hyperdense lesion between the brain and skull.

Treatment

• Surgical Intervention: Immediate surgical evacuation via craniotomy.
• Mortality Rate: Overall mortality is 18% for all cases of EDH, but only 2% for isolated EDH.

2. Acute Subdural Hematoma (ASDH)

Overview

• Location: Accumulates in the space between the dura and arachnoid.
• Injury Mechanism: Associated with cortical vessel disruption and brain laceration.
• Primary Brain Injury: Often associated with primary brain injury.

Presentation

• Consciousness: Impaired consciousness from the time of impact.

Imaging

• CT Scan: Appears hyperdense, with hematoma spreading diffusely and having a concavo-convex appearance.

Treatment

• Surgical Intervention: Evacuation via craniotomy.
• Mortality Rate: Approximately 40%.

3. Chronic Subdural Hematoma (CSDH)

Overview

• Demographics: Most common in patients on anticoagulants and antiplatelet agents.
• History: Often follows a minor head injury weeks to months prior.
• Pathology: Due to the tear of bridging veins leading to ASDH, which is clinically silent. As the hematoma breaks down, it increases in volume, causing mass effect on the underlying brain.

Clinical Features

• Symptoms may include:
  • Headache
  • Cognitive decline
  • Focal neurological deficits (FND)
  • Seizures
• Important to exclude endocrine, hypoxic, and metabolic causes in this group.

Imaging

• CT Scan Appearance:
  • Acute blood (0–10 days): Hyperdense
  • Subacute blood (10 days to 2 weeks): Isodense
  • Chronic (> 2 weeks): Hypodense

Treatment

• Surgical Intervention: Bur hole evacuation rather than craniotomy.
• Anesthesia: Elderly patients can often undergo surgery under local anesthesia, despite comorbidities.

4. Subarachnoid Hemorrhage (SAH)

Overview

• Causes: Most commonly due to aneurysms for spontaneous SAH, but trauma is the most common cause overall.
• Management: Conservative treatment is often employed for trauma cases.

5. Cerebral Contusions

Overview

• Definition: Bruising of the brain tissue due to trauma.
• Mechanism: Often occurs at the site of impact (coup) and the opposite side (contrecoup).
• Symptoms: Can range from mild confusion to severe neurological deficits depending on the extent of the injury.

Imaging

• CT Scan: May show areas of low attenuation (hypodense) or high attenuation (hyperdense) depending on the age of the contusion.

Treatment

• Management: Depends on the severity and associated injuries; may require surgical intervention if there is significant mass effect.

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

Intubation

Intubation is a critical procedure in airway management, and the choice of technique—oral intubation, nasal intubation, or tracheostomy—depends on the clinical situation, patient anatomy, and specific indications or contraindications. 

Indications for Each Intubation Technique

1. Oral Intubation

Oral intubation is often the preferred method in emergency situations and when nasal intubation is contraindicated. Indications include:

• Emergent Intubation: Situations such as cardiopulmonary resuscitation (CPR), unconsciousness, or apnea.
• Oral or Mandibular Trauma: When there is significant trauma to the oral cavity or mandible that may complicate nasal access.
• Cervical Spine Conditions: Conditions such as ankylosis, arthritis, or trauma that may limit neck movement.
• Gagging and Vomiting: In patients who are unable to protect their airway due to these conditions.
• Agitation: In cases where the patient is agitated and requires sedation and airway protection.

2. Nasal Intubation

Nasal intubation is indicated in specific situations where oral intubation may be difficult or impossible. Indications include:

• Nasal Obstruction: When there is a blockage in the oral route.
• Paranasal Disease: Conditions affecting the nasal passages that may necessitate nasal access.
• Awake Intubation: In cases where the patient is cooperative and can tolerate the procedure.
• Short (Bull) Neck: In patients with anatomical challenges that make oral intubation difficult.

3. Tracheostomy

Tracheostomy is indicated for long-term airway management or when other methods are not feasible. Indications include:

• Inability to Insert Translational Tube: When oral or nasal intubation fails or is not possible.
• Need for Long-Term Definitive Airway: In patients requiring prolonged mechanical ventilation or airway support.
• Obstruction Above Cricoid Cartilage: Conditions that obstruct the airway at or above the cricoid level.
• Complications of Translational Intubation: Such as glottic incompetence or inability to clear tracheobronchial secretions.
• Sleep Apnea Unresponsive to CPAP: In patients with severe obstructive sleep apnea who do not respond to continuous positive airway pressure (CPAP) therapy.
• Facial or Laryngeal Trauma: Structural contraindications to translaryngeal intubation.

Contraindications for Nasal Intubation

• Severe Fractures of the Midface: Nasal intubation is contraindicated due to the risk of further injury and complications.
• Nasal Fractures: Similar to midface fractures, nasal fractures can complicate nasal intubation and increase the risk of injury.
• Basilar Skull Fractures: The risk of entering the cranial cavity or causing cerebrospinal fluid (CSF) leaks makes nasal intubation unsafe in these cases.

• Contraindications for Oral Intubation

  1. Severe Facial or Oral Trauma:

     • Significant injuries to the face, jaw, or oral cavity may make oral intubation difficult or impossible and increase the risk of further injury.

  2. Obstruction of the Oral Cavity:

     • Conditions such as large tumors, severe swelling, or foreign bodies that obstruct the oral cavity can prevent successful intubation.

  3. Cervical Spine Instability:

     • Patients with unstable cervical spine injuries may be at risk of further injury if neck extension is required for intubation.

  4. Severe Maxillofacial Deformities:

     • Anatomical abnormalities that prevent proper visualization of the airway or access to the trachea.

  5. Inability to Open the Mouth:

     • Conditions such as trismus (lockjaw) or severe oral infections that limit mouth opening can hinder intubation.

  6. Severe Coagulopathy:

     • Patients with bleeding disorders may be at increased risk of bleeding during the procedure.

  7. Anticipated Difficult Airway:

     • In cases where the airway is expected to be difficult to manage, alternative methods may be preferred.

Contraindications for Tracheostomy

1. Severe Coagulopathy:

   • Patients with significant bleeding disorders may be at risk for excessive bleeding during the procedure.

2. Infection at the Site of Incision:

   • Active infections in the neck or tracheostomy site can increase the risk of complications and should be addressed before proceeding.

3. Anatomical Abnormalities:

   • Significant anatomical variations or deformities in the neck that may complicate the procedure or increase the risk of injury to surrounding structures.

4. Severe Respiratory Distress:

   • In some cases, if a patient is in severe respiratory distress, immediate intubation may be prioritized over tracheostomy.

5. Patient Refusal:

   • If the patient is conscious and refuses the procedure, it should not be performed unless there is an immediate life-threatening situation.

6. Inability to Maintain Ventilation:

   • If the patient cannot be adequately ventilated through other means, tracheostomy may be necessary, but it should be performed with caution.

7. Unstable Hemodynamics:

   • Patients with severe hemodynamic instability may not tolerate the procedure well, and alternative airway management strategies may be required.

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.

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.

Neuromuscular Blockers in Cardiac Anesthesia

In  patient on β-blockers, the choice of neuromuscular blockers (NMBs) is critical due to their potential cardiovascular effects. Here’s a detailed analysis of the implications of using fentanyl and various NMBs, particularly focusing on vecuronium and its effects.

Key Points on Fentanyl and β-Blockers

• Fentanyl:

  • Fentanyl is an opioid analgesic that can cause bradycardia due to its vagolytic activity. While it has minimal hemodynamic effects, the bradycardia it induces can be problematic, especially in patients already on β-blockers, which reduce heart rate and blood pressure.

• β-Blockers:

  • These medications reduce heart rate and blood pressure, which can compound the bradycardic effects of fentanyl. Therefore, careful consideration must be given to the choice of additional medications that may further depress cardiac function.

Vecuronium

• Effects:

  • Vecuronium is a non-depolarizing neuromuscular blocker that has minimal cardiovascular side effects when used alone. However, it can potentiate decreases in heart rate and cardiac index when administered after fentanyl.
  • The absence of positive chronotropic effects (unlike pancuronium) means that vecuronium does not counteract the bradycardia induced by fentanyl, leading to a higher risk of significant bradycardia and hypotension.

• Vagal Tone:

  • Vecuronium may enhance vagal tone, further predisposing patients to bradycardia. This is particularly concerning in patients on β-blockers, as the combination can lead to compounded cardiac depression.

Comparison with Other Neuromuscular Blockers

1. Pancuronium:

   • Vagolytic Action: Pancuronium has vagolytic properties that can help attenuate bradycardia and support blood pressure. It is often preferred in cardiac anesthesia for its more favorable hemodynamic profile compared to vecuronium.
   • Tachycardia: While it can induce tachycardia, this effect may be mitigated in patients on β-blockers, which can blunt the tachycardic response.

2. Atracurium:

   • Histamine Release: Atracurium can release histamine, leading to hemodynamic changes such as increased heart rate and decreased blood pressure. These effects can be minimized by slow administration of small doses.

3. Rocuronium:

   • Minimal Hemodynamic Effects: Rocuronium is generally associated with a lack of significant cardiovascular side effects, although occasional increases in heart rate have been noted.

4. Cis-Atracurium:

   • Cardiovascular Stability: Cis-atracurium does not have cardiovascular effects and does not release histamine, making it a safer option in terms of hemodynamic stability.