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NEET MDS Synopsis - Lecture Notes
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📖 General Surgery

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Types of Head Injury
General Surgery

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.

SINUS & FISTULA

General Surgery

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,

SHOCK

General Surgery

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.    â–ª    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

TMJ Ankylosis
General Surgery

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.