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

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.

1 Cellulitis: a non-suppurative inflammation of subcutaneous tissue, extending along connective tissue planes and across intercellular spaces.

Spreading inflammation in the tissue planes is called cellulitis. There is wide spread swelling, redness and pain without definite localization.

Caused by Streptococcus pyogenes.. If general condition of the patient is undermined, as in diabetes, cellulitis spreads rapidly and leads to Septicemia (infection in the blood).Redness, itching and stiffness is present in the site of inoculation (where the bacteria enter the skin), local Gangrene (death of the tissue) may occur. The appearance of skin creases or wrinkles, indicates resolution (healing).

Treatment

1. Rest , Appropriate antibiotics.

Cellulitis of the neck: Is a complication of wounds tonsillitis or mastoiditis Ludwig’s angina is the term applied to sub-maxillary cellulitis. The two dangers of cervical cellulitis are:

1. Oedema of glottis - with possible asphyxia (respiratory obstructon )

2. Mediastinitis - In ludwig’s angina the floor of the mouth become oedematous. The tongue can be seen displaced, turned upwards by swelling and oedema. The patient is unable to close the mouth owing to oedema of the tongue and the floor of the mouth. This can also CCC when the tongue is bitten by a wasp.

Ludwig’s angina: Ludwig - characterized by a brawny (non pitting) swelling of the sub-mandibular region, corn with inflammatory oedema of the mouth. It is the combined cervical and intrabuccal signs that constitute the characteristic feature of the lesion. The cause of the condition is virulent, usually streptococcal infection of the cellular tissue surrounding the sub-mandibular salivary gland.

Clinical features

 The swollen tongue is pushed towards the palate and forwards through the open mouth, while the cellulitis extends down the neck.

The most dangerous plane, is deep to the deep fascia.

Ludwig’s angina is an infection of closed fascial space and if .untreated, the inflammatory exudate often passes via, the tunnel occupied by stylohyhoid to the submucosa of glottis, in which event the patient is in immediate danger of death from oedema of the glottis.

Treatment

1. antibiotics on Early Diagnosis

2. In cases where the swelling, both cervical and intrabuccal, does not subside rapidly with such treatment, a curved incision, beneath the jaw is made and this decompresses the closed fascial space. The incision is deepened and after displacing the superficial lobe of the sub-mandibular salivary gland, the mylohyoid muscle are divided. This decompresses the closed fascjal space referred to. The wound is lightly sutured and drained. The operation can be conducted with greatest safety under local anaesthesia.

Bacteraemia and  Septicemia

Bacteraemia and septicaemia means the organisms are present in the blood. Clinical features are those of severe infection and shock: , Pyrexia is intermittent , Rigors ,  Jaundice is due to liver damage,  Acute renal failure may occur , Peripheral circulatory failure,  lntravascular coagulation indicates a fatal outcome

 causative focus found and treated surgically .g., Appendicetomy in perforated appendix

2. Blood culture taken

3. Broad spectrum antibiotic is given

4. Blood transfusion is given.

5. Injection hydrocortisone is given.

Pyaemia

Pyaemia is due to infected emboli circulating in blood stream. Pyaemia is characterized by: -

1. Rigors

2. Intermittent fever

3. Formation of abscess in vital organs like heart or brain.

Treatment

1. Is to prevent emboli reaching the blood stream

2. Broad spectrum antibiotic is given.

3. Abscess are incised and drained

If not treated portal pyaemia with multiple abscesses in liver occur, which is a dangerous condition.

Acute Abscess :  An abscess a collection of pus.

Bacteria which cause pus formation is called pyogenic organisms. Bacteria reach the infected area by:

1. Direct route: eg. Penetrating wound

Local extension: From adjacent focus of infection

2 Lymphatics

4. Blood stream

Pyogenic membrane surrounds the abscess and is infiltration with (leukocytes and bacteria.

Pus: Pus contains dead leukocytes and bacteria. It reaches the surface of the body or is discharged into a hollow viscous.

Symptoms: patient feels ill., Throbbing pain is characteristic of suppuration. Pain becomes more severe in the dependent position. E.g. infected finger,

Classical signs

Temperature is elevated , Rigors, inflammation

Fluctuation: Present in the later stages, and reveals the presence of pus. Prevention

1. An abscess can sometimes be aborted by antibiotics in the early stage.,. Rest,  Elevation of the affected part.

Treatment

Is incision and drainage of abscess

Hilton’s method of opening an abscess:

It is used where important anatomical structures like the blood vessels and nerves are preesnt, as in the neck, axilla and groin. The skin and superficial fascia is incised. A sinus forceps is thrust into the abscess  cavity. The blades are opened and the pus is drained. A gloved finger is introduced and loculi are broken. A ribbon gauze is lightly packed and antibiotics are given. This is done under surface anaesthesia i.e., ethyl chloride spray.

Antibioma

 If antibiotic is given the pus in the abscess frequently becomes sterile and a large brawny edematous swelling remains which takes many weeks to resolve.

Treatment: explore the mass with a wide-bore aspirating needle

 Most antibiornas are due to late, inadequate, and ineffective antibiotics.

CANCRUM ORIS

Is an infective gangrene of cheek and lip.

may occur as a complication of kala azar, enteric fever and  children with poor oral hygiene.

The lesion starts as an acute inflammatory patch on oral mucosa which is seen ulcerated.

The affected part of the cheek or the lip gradually becomes gangrenous.

Focal vascular thrombosis and sepesis occur.

When slough separates, a part of the cheek or lip sloughs out to form a buccal fistula with ugly deformity. The adjacent jaw may be infected too.

Various organisms are found - specially Fusiform bacillus and_Borrellia vincenti.

The foetid odour, gangrenous patch of cheek or lip, purulent discharge from the mouth, fever and toxaemia are the characteristic features. The patient is unable to open the mouth properly.

Treatment

1. Antibiotics, multivitamins and repeated mouth washes

2 Neostibamine in kala-azar. Sequestrectomy in chronic osteomyelitis of the mandible.

4. Plastic reconstruction of the lip or cheek for unsightly deformity undertaken.

CARBUNCLE

Is an infective gangrene of the subcutaneous tissue. It is due to staphylococcal aureus infection. It is uncommon before the age of 40. Males are the usual sufferers. Diabetes may be present. It often occurs on the nape of the neck.

Clinical features

Subcutaneous tissue becomes painful and indurated. Ove skin is red. Unless treated promptly, extension will occur and late softening. The skin gives way and thick pus and slough are discharged.

Usually, there is one central large slough, surrounded by smaller areas of necrosis. Infection extends widely and fresh openings appear

Treatment

1. Many carbuncles are aborted, if penicillin is used adequately in the early stage.

2. Local treatment consists of hygroscopic dressings being given ie. magsulph-glycerin dressing Later the carbuncle is excised with a cruciate incision.

3. If the gap is large and when the granulation tissue comes to the surface, skin grafting is done.

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.

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.

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.