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

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.

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.

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.

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,