What is FARRE

FARRE (Frequently Asked Regularly Repeated Exam Questions) is an innovative exam-

prep tool from PW MedEd. It is your ultimate companion for acing the MBBS Professional
University Exams with confidence and ease.

WHY CHOOSE FARRE?

FARRE brings you a meticulously curated collection of 100 key questions per subject—
sourced from professional exam papers of leading universities across different states.
Aligned with the Competency-Based Medical Education (CBME) curriculum outlined
by the National Medical Commission (NMC), FARRE offers a structured, student-
friendly approach to mastering essential concepts in just one week.

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1. Comprehensive Content for Success
™ 100 critical questions in each subject, focusing on high-yield topics most likely to
appear in exams.

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™ Easy-to-understand answers enhanced with diagrams and flowcharts, helping
you replicate information during exams effectively.

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™ Integrated with the latest AETCOM module, providing a well-rounded preparation
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™ Master essential material in just seven days, helping you manage time efficiently
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™ Answers are provided in clear and concise language, making complex topics
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Equip yourself with MedEd FARRE and unlock the key to passing your MBBS exams with
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With FARRE, “Passing Proffs just got easier!”
 General Surgery
1. Briefly describe wound healing, its types, stages, and differentiate between
clean, clean-contaminated, contaminated and dirty wounds. (5 Marks)

Answer:

WOUND HEALING

€ Wound healing is a complex process aimed at restoring the anatomical and

functional integrity of disrupted tissue through various components such as
neutrophils, macrophages, lymphocytes, fibroblasts, and collagen, In an organized
staged pathway:-

Ha�mo�ta�is

Inflam��ti�n

Pr�li�er�ti�n

Ma�ri� Sy�th�si�
(c�ll�ge� & pr�te�gl�ca� su��ta�ce�

ma�ur�ti�n

Re�od�ll�ng

Ep�th�li��is�ti�n

Wo�nd co�tr�ct�on
(b� my�fibr��la�t)

Types Of Wound Healing

1. Primary healing (First intention):

™ It occurs in a clean incised wound or surgical wound.

™ Wound edges are approximated with sutures.

™ There is more epithelial regeneration than fibrosis.

™ The wound heals rapidly with complete closure.

™ The scar will be linear and smooth.

MedEd FARRE: Surgery

2. Secondary healing (Second intention):

™ It occurs in wounds with extensive soft tissue loss, such as those caused by major
trauma, burns, or wounds with sepsis.
™ It heals slowly with fibrosis.
™ It results in a wide scar, which is often hypertrophied and contracted.
™ It may also lead to disability

3. Tertiary wound healing/delayed primary closure (Third intention):

™ after wound debridement and control of local infection, the wound is closed with
sutures or covered using skin grafts.
™ A primarily contaminated or mixed-tissue wound heals by tertiary intention.

Stages/phases Of Wound Healing

1. Inflammatory phase (Lag/substrate/exudative phase):
™ it begins immediately after wound formation and lasts for 72 hours.
™ There is initial arteriolar vasoconstriction, thrombus formation, and platelet
aggregation due to endothelial damage and the release of Adenosine Diphosphate
(ADP).
™ Later, vasodilation and increased vascular permeability develop.
™ During this phase, hemostasis, coagulation, and chemotaxis occur.
™ These processes lead to the features of acute inflammation: rubor, calor, dolor,
tumor, and loss of function.
2. Proliferative phase (Collagen/fibroblastic phase):
™ it begins on the 3rd day and lasts for 3-6 weeks.
™ There is formation of granulation tissue and repair of the wound.
™ Granulation tissue contains fibroblasts, neocapillaries, collagen, fibronectin,
and hyaluronic acid.
3. Remodelling phase (Maturation phase):
™ it begins at 6 weeks and lasts for 6 months to 1 or 2 years.
™ There is maturation of collagen through cross-linking and realignment of collagen
fibers along the line of tension, which is responsible for the tensile strength of the
scar.
™ Vascularity in the wound is reduced.
™ Fibroblast and myofibroblast activity causes wound contraction.
™ Type II collagen is replaced by Type I collagen, leading to the maturation of the
collagen. The ratio of Type I collagen to Type III collagen becomes 4:1.
™ In the early extracellular matrix, fibronectin and Type II collagen are present;
eventually, it contains glycosaminoglycans and proteoglycans. The final matrix
contains Type I collagen.
™ Scar strength is 39% at 1 week, 20% at 3 weeks, and 80% at 12 weeks. The
final matured scar is acellular and avascular.

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 General Surgery

DIFFERENCES BETWEEN CLEAN, CLEAN-CONTAMINATED, CONTAMINATED AND

DIRTY WOUNDS

Wound Class Definition Examples of Infection Common

Procedures Rate (%) Organism
Clean € Non-traumatic € Mastectomy 2 Staphylo-
surgical wounds € Vascular coccus
created under sterile surgery aureus
conditions
€ Thyroidectomy
€ No entry into the
gastrointestinal,
respiratory, or
genitourinary tracts
Clean- € Controlled surgical € Gastrectomy <10 Related to
Contaminated entry into the € Hysterectomy the organ
respiratory, entered
€ Cholecystec-
gastrointestinal, or
tomy
genitourinary tracts
€ Minimal
contamination, no
infection present
Contaminated € Fresh, open € Surgery for 20 Depends on
traumatic wounds or a ruptured underlying
surgeries involving appendix cause
uncontrolled or bowel
spillage from the resection with
gastrointestinal tract contamination
€ Includes procedures
with a breach in
sterile technique
Dirty € Wounds with € Gangrene 30–70 Depends on
devitalized tissue, surgery, underlying
active infection, € operations cause
or pre-existing on perforated
perforation viscera
€ Presence of pus or
severe contamination
in the surgical field
Reference: Manipal Manual Of Surgery, 4th Edition, Page no. 4-10.

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 MedEd FARRE: Surgery

2. Classify the different types of ulcers. Write briefly about Marjolin ulcer.
 (5 Marks)

Answer:

ULCER

€ An ulcer is a break in the continuity of the covering epithelium, either skin or

mucous membrane, caused by tissue necrosis.

Classification of Ulcers
Type of Ulcer Features

Spreading Ulcers € Edge: Inflamed, irregular, edematous

€ Acute, painful ulcer without healthy granulation tissue

€ Profuse purulent discharge

€ Surrounding area: Red and edematous

€ Regional lymph nodes: Enlarged and tender due to

inflammation

Healing Ulcers € Edge: Sloping with healthy pink/red granulation tissue

€ Scanty/minimal serous discharge in the floor

€ Regional lymph nodes: May or may not be enlarged

(Non-tender if enlarged)
€ Surrounding area: No signs of inflammation or induration.

€ Three zones:

1. Innermost red zone of healthy granulation

2. Middle bluish zone of growing epithelium
3. Outer whitish zone of fibrosis and scar formation

Non-Healing Ulcers € May be a chronic ulcer depending on the cause

€ Regional draining lymph nodes: Enlarged but non-tender

€ Floor: Contains unhealthy granulation tissue and slough

Callous Ulcers € Chronic, non-healing ulcer

(Stationary Ulcers)
€ Floor: Pale, unhealthy, whitish-yellow granulation tissue
with thin serous discharge
€ No tendency to heal

€ Lasts for many months to years

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 General Surgery

MARJOLIN ULCER

€ A Marjolin ulcer refers to a malignant transformation, typically into well-

differentiated squamous cell carcinoma, arising in chronic scars or ulcers. It most
commonly develops in burn scars but can also occur in scars from venous ulcers or
other long-standing wounds.

Characteristics
€ Onset: Occurs in unstable scars of prolonged duration
€ Growth: Slow-growing but locally aggressive
€ Behavior: Considered a curable malignancy; however, if left untreated, it can spread
to lymph nodes.

Pathophysiology
€ Develops due to chronic irritation in scar tissue.
€ Scar tissue lacks lymphatic drainage, reducing the spread of malignancy initially.
€ As scars are avascular, the tumor grows painlessly in the beginning.
€ If the lesion spreads to normal skin, it behaves like typical squamous cell carcinoma
and can invade lymph nodes.

Clinical Features
€ Indurated, non-tender ulcer with raised and everted edges.
€ Surrounding scar tissue shows marked fibrosis.
€ Painless in early stages but may cause discomfort in advanced stages.

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MedEd FARRE: Surgery

Diagnosis
€ Histopathological examination via biopsy

Treatment
€ Small lesions: Wide local excision
€ Large lesions: Amputation may be required in severe cases.
€ Lymph node dissection may be considered if lymphatic spread is suspected.

Reference: Manipal Manual of Surgery, 4th Edition, Page no. 142-145.

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6
 General Surgery

3. (a) Write a short note on sinus and fistula.

(b) Differentiate between sinus and fistula. (5 Marks)

Answer:

SINUS AND FISTULA

Definitions
€ Sinus: A blind tract lined with granulation tissue, leading from the surface of the
skin into deeper tissues.

€ Fistula: An abnormal communication between two hollow organs (Internal fistula)

or between a hollow organ and the body surface (External fistula).

Causes
€ Sinus:
™ Congenital:
 Preauricular sinus
™ Acquired:
 Median mental sinus (Tooth abscess)

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MedEd FARRE: Surgery

 Pilonidal sinus (Midline in the anal region)

 Osteomyelitis (Pus discharge with bony spicules)

 Tubercular lymphadenitis (Discharging cheesy material)

€ Fistula:

™ Internal: Tracheo-esophageal, colovesical fistulas

™ External: Orocutaneous, branchial, and thyroglossal fistulas

Pathophysiology

1. Sinus forms due to a persistent foreign body or infection leading to granulation tissue
formation.

2. Fistulas develop secondary to trauma, infection, malignancy, or specific diseases like

tuberculosis or actinomycosis.

Clinical Features
€ Sinus:
™ Discharge based on the underlying cause:

 Cheesy (Tuberculosis)

 Yellow purulent (Staphylococcal)

 Faecal (Fistula)

€ Surrounding skin: Bluish discoloration (Tuberculosis) or redness (Inflammatory)

€ Fistula:

™ Communication may result in abnormal discharge from both ends.

Investigations
1. Blood tests:
™ Complete Blood Picture (CBP): Signs of infection

™ ESR: Increase in tuberculosis

2. Urine analysis:
™ Fasting/postprandial sugars to rule out diabetes.

3. Imaging:
™ X-ray (Rule out osteomyelitis)

™ X-ray Kidney, Ureter, Bladder (KUB) for urinary fistulas.

4. Fistulography/Sinography:
™ To delineate the track using contrast (e.g., Lipiodal oil).

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 General Surgery

Management
€ Antibiotics for infections
€ Adequate rest and drainage
€ Surgical excision of the entire epithelialized track if formed.
€ Removal of foreign bodies
€ Specific treatment for tuberculosis and osteomyelitis.

Complications
1. Persistence due to improper drainage or fibrosis.
2. Spread of infection to deeper tissues or systemic involvement.

DIFFERENCES BETWEEN SINUS AND FISTULA

Feature Sinus Fistula

Definition A blind-ended tract A tract connecting two
opening onto the skin epithelial-lined surfaces
Communication No communication with Connects two organs or an
other organs organ and the skin
Number of Openings One external opening Two openings (Internal and
external)
Common Causes Chronic infections, foreign Infections, trauma, surgery,
bodies congenital conditions
Examples Pilonidal sinus, tubercular Anal fistula, vesicovaginal
sinus fistula

Reference: Manipal Manual of Surgery, 4th Edition, Page no. 28-31.

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MedEd FARRE: Surgery

4. (a) Write a short note on tubercular lymphadenitis. (5 Marks)

(b) Write in brief about cold abscess.

Answer:

TUBERCULOUS LYMPHADENITIS

€ Tuberculous lymphadenitis is the most common form of extrapulmonary tuberculosis

caused by Mycobacterium tuberculosis.

Common Sites
€ Neck lymph nodes – 80%
€ Upper/deep cervical lymph nodes – 54%
€ Posterior triangle lymph nodes – 22%

Features
€ Modes of infection:
™ Through tonsils or blood from lungs.
™ Spreads to jugulodigastric nodes and further to other nodes.

Stages of Tuberculous Lymphadenitis

1. Stage I: Lymphadenitis
™ Discrete, non-tender, hard mobile nodes.

2. Stage II: Matting

™ Firm, non-tender nodes moving together.

3. Stage III: Cold Abscess

™ Spreads to deep fascia

4. Stage IV: Collar-stud Abscess

™ Ruptures through deep fascia, adheres to skin.

5. Stage V: Sinus Formation

™ Formation of a draining sinus.

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 General Surgery

Treatment
€ Antitubercular therapy:
™ Rifampicin 450 mg OD
™ INH 300 mg OD
™ Ethambutol 800 mg OD
™ Pyrazinamide 1500 mg OD

(Duration: 6–9 months)

€ Aspiration:
™ Wide-bore needle introduced at a non-dependent site in a zig-zag pathway to
prevent sinus formation.
€ Incision & drainage:
™ If reoccurs, abscess is drained.
€ Surgical removal:
™ Reserved for persistent sinuses.

COLD ABSCESS

Definition
€ A cold abscess is a localized collection of pus, commonly associated with tuberculosis,
characterized by the absence of acute inflammatory signs typically seen in other
abscesses

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 MedEd FARRE: Surgery

Features
1. Location:
™ Commonly occurs in the neck.
™ Other possible sites: groin, intercostal spaces, and any area where tuberculosis-
caused caseating material can accumulate and localize.
2. Origin:
™ May arise from tuberculosis involving the spine (e.g., Thoracic or cervical spine),
lymph nodes, internal organs, bones, etc.
3. Demographics:
™ Often seen in young individuals but can occur at any age.
™ Affects both sexes equally.

Clinical Signs
€ Swelling in the neck: Smooth, non-tender, soft with restricted movement of the
cervical spine.
€ Additional symptoms:
™ Neck pain and neck rigidity
™ Evening fever
™ Weight loss and anorexia
™ Anemia

Treatment
1. Pharmacological therapy:
™ Anti-tuberculous drugs (e.g., Rifampicin, INH, Ethambutol, Pyrazinamide) for 6–9
months
2. Surgical management:
™ Aspiration or drainage of the abscess at a non-dependent site.
™ Excision of affected lymph nodes if necessary.

3. Additional measures:
™ Immobilization of the cervical spine with a plaster cast for approximately 4 months
in cases involving spinal tuberculosis.
Reference: Manipal Manual of Surgery, 4th Edition, Page no. 18.

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 General Surgery

5. Write a short note on Lipoma. (5 Marks)

Answer:

LIPOMA

€ Lipoma is a benign neoplasm arising from yellow fat, often due to hyperplasia, a
combination of neoplasm, or hypertrophy.

Key Features
€ Composition: Made of mature adipocytes with uniform nuclei similar to normal
adult fat.
€ Metabolism: Fat in lipomas is unavailable for general metabolism.
€ Prevalence: Most common benign tumor with a prevalence of 2-1 per 100 people;
associated with karyotype 12q change.
€ Distribution: Called the universal tumor as it can develop anywhere in the body
except the brain.

Types
€ Localized (Encapsulated): Yellowish-orange in color.
€ Diffuse (Non-encapsulated): Common in palm, sole, head, and neck; recurrence is
high.
€ Superficial or Deep: Superficial is more common, while deep ones are often
intramuscular.
€ Single or Multiple: Single is more common than multiple.

Clinical Features
€ Characteristics:
™ Localized, lobular, non-tender swelling.
™ Mobile with edges slipping under palpation (Slip sign).
€ Age: Rare in children.
€ Symptoms:
™ Can compress nerves causing pain.
™ Trunk is the most common site.
™ May appear as single, multiple, or diffuse lesions.

Investigations
€ Imaging: Ultrasound, CT, or MRI for deep, large, or intra-cavitary lipomas.
€ Biopsy: FNAC or incision biopsy confirms benign nature.

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 MedEd FARRE: Surgery

Complications
€ Myxomatous changes in retroperitoneal lipomas.
€ Saponification or calcification (11% cases).

Treatment
€ Excision (Enucleation):
™ Small lipomas: Excised under local anesthesia.
™ Larger lipomas: Require general anesthesia.
€ Recurrence Rate: 11%.

Reference: Manipal Manual of Surgery, 4th Edition, Page no. 214.

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 General Surgery

6. a) Enumerate the causes of hyponatremia.  (5 Marks)

b) E
 xplain the clinical features and management of a patient with
hyponatremia. Additionally, provide a brief overview of hypernatremia.

Answer:

HYPONATREMIA
€ Normal Serum Sodium Level: 135–145 mmol/L.
€ Definition: Serum sodium concentration <135 mmol/L.

Causes of Hyponatremia
1. Sodium and water loss
™ Renal Causes:
 Diuretics
 Mineralocorticoid deficiency.
 Osmotic diuresis (e.g., Glucose, mannitol, urea).
 Renal tubular acidosis.
™ Extrarenal Causes:
 Vomiting
 Diarrhea
 Burns
 Pancreatitis
 Rhabdomyolysis

2. Euvolemic Hyponatremia
™ Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH).
™ Hypothyroidism
™ Psychogenic polydipsia
™ Glucocorticoid deficiency

3. Water and Sodium Excess (Water >> Sodium)

™ Nephrotic syndrome.
™ Congestive cardiac failure.
™ Cirrhosis
™ Acute and chronic renal failure.

Clinical Features of Hyponatremia

€ Neurological Symptoms:
™ Headache, confusion.
™ Anorexia, nausea, vomiting.

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MedEd FARRE: Surgery

™ Watery diarrhea, lacrimation, salivation.

€ Other Symptoms:
™ Weakness, fatigue, muscle cramps.
™ Hypertension, bradycardia, oliguria.

Management of Hyponatremia
1. Hypovolemic Hyponatremia:
™ Isotonic saline administration.

2. Euvolemic Hyponatremia:
™ Water restriction.

3. Hypervolemic Hyponatremia:
™ Sodium and water restriction.
™ Free water excess should be corrected first, followed by sodium correction.

4. Severe Cases:
™ Neurological symptoms: Treat with 3% saline.
™ Treat with 0.9% saline; ensure the rate of correction does not exceed 12 mEq /L/day
to prevent central pontine myelinolysis (Osmotic demyelination syndrome).

Formula for Sodium Deficit Calculation

€ Sodium deficit = Total body water × (130 − measured sodium).
€ Volume = Sodium deficit/154 (Saline in liters).

HYPERNATREMIA

€ Definition: Serum sodium concentration >145 mmol/L.

€ Pathophysiology: Hyperosmolar condition due to total body water loss or sodium
gain.

Causes of Hypernatremia
1. Sodium and Water Loss
™ Renal Causes:
 Loop diuretics.
 Osmotic diuresis (e.g., Glucose, mannitol, urea).
™ Extrarenal Causes:
 Diarrhea, burns.
 Nasogastric aspirations.

2. Euvolemic Hypernatremia
™ Diabetes insipidus.
™ Insensible losses from skin and respiratory tract.

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 General Surgery

™ Psychogenic hypodipsia.

3. Water and Sodium Excess (Sodium >> Water)

™ Primary aldosteronism.
™ Cushing syndrome.
™ Hypertonic dialysis.
™ Bicarbonate infusion.

Clinical Features of Hypernatremia

€ Neurological Symptoms:
™ Restlessness, irritability.
™ Lethargy, delirium, seizures, coma.
€ Other Symptoms:
™ Weakness, oliguria.
™ Dry mucous membranes, red swollen tongue.
™ Decreased saliva and tears.
™ Tachycardia, hypotension.

Management of Hypernatremia
1. Initial Management:
™ Identify and correct water deficit.
™ Correction should be slow to prevent cerebral edema.

2. Treatment Strategies:
™ Hypovolemic hypernatremia: Restore fluid with isotonic saline initially.
™ Euvolemic hypernatremia: Free water administration.
™ Hypervolemic hypernatremia: Loop diuretics along with hypotonic fluids.

Note: Acute hypernatremia should be corrected within 24 hours, whereas chronic

hypernatremia should be corrected slowly.
Reference: Manipal Manual of Surgery, 4th Edition, Page no. 204.

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MedEd FARRE: Surgery

7. a) Define the following terms: (5 Marks)

Š Primary hemorrhage

Š Reactionary hemorrhage

Š Secondary hemorrhage

b) L
 ist the complications of blood transfusion and provide a brief explanation
of their management.

Answer:

HEMORRHAGE

Definitions
1. Primary hemorrhage:
™ Bleeding that occurs immediately after injury or at the time of surgery.
™ Example: A cut finger or bleeding from a surgical incision.

2. Reactionary hemorrhage:
™ Bleeding that occurs within 24 hours after surgery or injury, typically 4-6 hours
later.
™ Commonly associated with procedures on the kidney, thyroid, or breast, as well as
surgeries like total hysterectomy.

3. Secondary hemorrhage:
™ Bleeding that arises due to infection causing erosion of blood vessel walls.
™ This type of bleeding occurs after the initial event, often at a delayed interval.

BLOOD TRANSFUSION

Complications of Blood Transfusion and Their Management

1. General Overview
™ Incidence: 10%
™ Rate of Infection Transfer:
 HBV: 30%.
 HCV: 3%.
 HIV: 0.3%.
™ Most Common Cause: Human error.

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 General Surgery

Complication Description Management

Acute Hemolytic Reaction € Due to ABO € Stop transfusion

incompatibility, immediately, provide
presenting with pain supportive therapy, and
at the IV site, flushing, monitor vital signs.
chest/back pain, and
hemoglobinuria.

Delayed Hemolytic € Occurs days later with € Monitor hemoglobin,

Reaction anemia, elevated provide supportive care.
bilirubin, and a positive
Coombs test.

Febrile Non-Hemolytic € Most common reaction € Administer

Transfusion Reaction caused by cytokine antipyretics (e.g.,
(FNHTR) release, presenting as Paracetamol).
fever and chills.

Allergic Reaction/ € Mild cases present € Use antihistamines

Anaphylaxis with rash and for mild reactions;
itching; severe cases epinephrine for severe
may involve airway reactions.
compromise.

TACO (Transfusion- € Rapid transfusion € Administer diuretics,

Associated Circulatory causing pulmonary provide oxygen therapy,
Overload) edema due to volume and slow transfusion
overload. rate.

TRALI (Transfusion- € Immune reaction € Oxygen therapy and

Related Acute Lung causing non-cardiogenic supportive care.
Injury) pulmonary edema,
occurring within 6 hours
post-transfusion.

Infections € Caused by bacteria € Ensure proper

(Gram-positive/negative), screening of blood
viruses (e.g., HBV, HCV, products and use aseptic
HIV), or parasites (e.g., techniques.
Plasmodium).

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MedEd FARRE: Surgery

Complications Associated with Massive Transfusion

Complication Description Management

Hypocalcemia € Citrate in stored blood binds € Administer calcium

calcium, causing low calcium supplements.
levels

Hyperkalemia € Potassium levels rise due to € Monitor and correct

breakdown of stored red blood potassium levels as needed.
cells.

Hypothermia € Transfusion of cold blood € Warm blood products prior

products lowers body to transfusion.
temperature.

Coagulopathy € Deficiency of platelets and € Replace platelets and

clotting factors due to large clotting factors as required.
volume transfusion.

Iron Overload € Excessive iron deposition € Monitor iron levels and

occurs after repeated consider chelation therapy.
transfusions.

Infections € Contamination of blood € Use aseptic techniques and

products or transmission of screen blood products.
infections.

Key Points for Management of Blood Transfusion Complications

€ Preventive Measures: Proper blood typing and cross-matching, aseptic techniques,
and regular monitoring during transfusion.
€ Early Recognition: Monitor for symptoms such as fever, rash, dyspnea, or signs of
hemolysis.
€ Supportive Care: Tailored interventions for each complication, such as stopping
transfusion, oxygen therapy, or medication (e.g., Antihistamines, diuretics).

Reference: Manipal Manual of Surgery, 4th Edition, Page no. 177.

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20
 General Surgery

8. Write a note on the indications, techniques and complications of Total

Parenteral Nutrition (TPN) administration. (5 Marks)

Answer:

TOTAL PARENTERAL NUTRITION (TPN)

€ Total Parenteral Nutrition (TPN) is the intravenous delivery of essential nutrients,

bypassing the digestive system.

Fundamental Goals of Nutritional Support

€ Meeting energy requirements for metabolic purposes.
€ Promoting tissue repair.

€ Maintaining core body temperature.

€ Minimizing protein breakdown and preserving lean body mass.

Indications for Total Parenteral Nutrition

Category Examples

Severe malnutrition/sepsis € Critically ill patients unable to tolerate enteral

feeding.

Neonatal conditions € Tracheoesophageal fistula, omphalocele,

gastroschisis.

Pediatric issues € Meconium ileus, short bowel syndrome.

Gastrointestinal (GI) € High-output enterocutaneous fistula,

postoperative ileus, ulcerative colitis, or enteritis.

Oncology € Radiation enteritis, acute chemotherapy toxicity,

or cachexia.

Pre-surgery € Weight loss in preparation for major surgery.

Critical conditions € Pancreatitis with prolonged ileus, hypoproteinemia,

pancreatic insufficiency.

Contraindications for TPN

€ Hemodynamic instability.

€ Severe electrolyte imbalances.

€ Prognosis that does not support parenteral nutrition.

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 MedEd FARRE: Surgery

Techniques of Administration

Type Details

Peripheral Parenteral € Used for ≤2 weeks when osmolality < 900

Nutrition mOsm/L via a peripheral line.

Central Parenteral Nutrition € Delivered through a central venous catheter for

long-term use.

Constituents of TPN

Constituent Function Details

Carbohydrates € Provide 50–70% of calorie € 15–25% dextrose solution.

needs.

Proteins € Prevent protein breakdown. € 3–5% crystalline amino

acid solution.

Lipids € Provide essential fatty € Soybean/safflower oil for

acids. 15% calorie needs.

Vitamins & Minerals € Correct deficiencies. € Vitamin K supplementation

required.

Complications of TPN:

Category Examples

Access Site Complications Cardiac dysrhythmias, pneumothorax, catheter

infections, or air embolism.

Metabolic Complications Hyperglycemia (Most common), hypoglycemia,

refeeding syndrome, trace element deficiencies.

Liver & GI Complications Liver dysfunction, fatty infiltration, gallstones.

Refeeding Syndrome
€ Refeeding syndrome is a potentially life-threatening condition that occurs when
nutritional support is initiated in severely malnourished patients. It results from
the rapid reintroduction of carbohydrates, leading to significant metabolic and
electrolyte imbalances.
€ Characterized by hypokalemia, hypomagnesemia, and hypophosphatemia.
€ Sodium retention leading to fluid overload, edema, and congestive heart failure.

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 General Surgery

Management of Complications
€ Gradual initiation of feeding.
€ Monitoring for electrolyte imbalances.
€ Adjusting fluid volumes and glucose rates.

Prevention
1. Identify at-risk patients: Screen for malnutrition and risk factors.
2. Initiate feeding gradually: Start with 10–20 kcal/kg/day and increase slowly over
4–7 days.
3. Electrolyte monitoring: Regularly monitor and correct serum phosphate, potassium,
magnesium, and glucose levels.
4. Supplementation: Provide vitamins and minerals, including thiamine (To prevent
Wernicke’s encephalopathy).
5. Fluid balance: Avoid excessive fluid administration to prevent overload.
Reference: Manipal Manual of Surgery, 4th Edition, Page no. 209.

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 MedEd FARRE: Surgery

9. Write a note on Shock under the following headings: (10 Marks)

1. Definition
2. Causes
3. Pathophysiology
4. Course
5. Stages
6. Types
7. Management

Additionally, provide a note on septic shock and anaphylactic shock.

Answer:

SHOCK

Definition
€ Shock is defined as a state of cellular and tissue hypoxia caused by:
™ Reduced oxygen delivery
™ Poor oxygen utilization

This occurs due to circulatory failure (Collapse) and poor perfusion. It disrupts normal
aerobic metabolism, leading to a shift to anaerobic metabolism and resulting in lactic
acidosis. Shock is initially reversible but, if untreated, can progress to multiorgan
failure and death.

Causes of Shock
1. Hypovolemic Shock (Reduction in total blood volume):
™ Hemorrhage
™ Severe burns (Loss of plasma)
™ Vomiting and diarrhea of any cause

2. Cardiac shock:
™ Acute myocardial infarction
™ Acute pulmonary embolism
™ Drug-induced

3. Septic shock:
™ Due to bacterial infection releasing toxins

4. Neurogenic shock:
™ Sudden painful stimuli or spinal cord injury
™ Can result from anesthesia

24
 General Surgery

5. Anaphylactic shock:
™ Type I hypersensitivity reaction

6. Respiratory causes:
™ Atelectasis (lung collapse)
™ Thoracic injuries
™ Tension pneumothorax

7. Other causes:
™ Addison’s disease
™ Myxedema

Pathophysiology of Shock
€ Shock disrupts normal circulation and metabolism as shown below:

ETIOPATHOGENESIS / PATHOPHYSIOLOGY OF SHOCK

Any cause of shock

Low cardiac output

Vasoconstriction occurs as a compensation to

perfuse vital organs like Brain, Heart, kidneys, Liver

Because of vasoconstriction & tachycardia

Dynamic circulation increases

Tachypnea occur, to increase the oxygen

Saturation

Peripheral veins constrict diverting blood from

splanchnic system towards essential
vital organs

Decreased renal blood flow, reduces the GFR &

there by urine output

Renin-angiotensin mechanism gets activated

causing further Vasoconstriction & aldosterone release

Causes salt & water retention

ADH is released

Further concentration of urine occurs

When shock persists, Cardiac output falls further

25

Hypotension & tachycardia occurs leading to

 Causes salt & water retention

ADH is released
MedEd FARRE: Surgery
Further concentration of urine occurs

When shock persists, Cardiac output falls further

Hypotension & tachycardia occurs leading to

poor perfusion of coronaries

Hypoxia- metabolic acidosis

Release of cardiac depressants

Cardiac (pump) failure

Course of Shock
Hypoxia

Anaerobic metabolism

Lactic Acidosis

Cell wall damage

Na+ & Ca 2+
enters cell

K+ leaks out of cell

Causes Hyponatremia
and Hypocalcemia

Intracellular Lysozymes breakdown releasing powerful

enzymes which destroy their own cells

Sickle Cell Syndrome

Platelets are activated forming small

clots in many places

Disseminated Intravascular Coagulation

(DIC)

Further bleeding

26
 General Surgery

Stages of Shock

Stage Description
1. Reversible Shock Systemic Inflammatory Response Syndrome (SIRS): Causes
vasodilation, leukocyte activation, and thrombosis.
2. Established Shock Microvascular occlusion, cellular dysfunction, and DIC.
Progresses to cardiac pump failure.
3. Irreversible Shock Multiorgan Dysfunction (MODS): Failure of lungs, kidneys,
liver, and brain.

Types of Shock

Type Description
1. Vasovagal Shock Sudden peripheral vasodilation → Decreased cardiac
output.
2. Neurogenic Shock Spinal cord injury → Splanchnic vessel dilation.
Treated with vasoconstrictor drugs.
3. Hypovolemic Shock Causes: Hemorrhage, burns, vomiting, diarrhea. Leads to
sodium and water loss.
4. Cardiogenic Shock Acute myocardial infarction or tamponade → Circulatory
failure
5. Septic Shock Caused by toxins from organisms like E. coli and
Klebsiella.

Management of Shock
€ Its management involves a systematic approach focused on stabilizing the patient,
identifying the underlying cause, and preventing further complications.
Initial acute critical care management:
€ ABCDE approach:
™ A (Airway): Ensure a patent airway
™ B (Breathing): Provide adequate ventilation and oxygenation.
™ C (Circulation): Restore adequate circulation to vital organs.
™ D (Disability): Assess neurological status
™ E (Exposure): Identify external signs of trauma or infection.
€ Primary assessment and resuscitation are vital.

Fluid replacement:
€ Types of fluids:
™ Crystalloids: Normal saline, Ringer’s lactate
™ Colloids: Used when required
™ Blood transfusion for significant blood loss.

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MedEd FARRE: Surgery

€ Method:
™ Fluid therapy starts with crystalloids, avoiding overloading.
™ Dynamic fluid response is evaluated using 500 mL of warm saline over 10 minutes
via two wide-bore IV cannulas. Improvement indicates effective resuscitation.

Use of drugs:
€ Inotropic Agents:
™ Dopamine and adrenaline infusions are used, particularly in distributive shocks
like septic shock.
€ Correction of acid-base imbalance:
™ Administer sodium bicarbonate to address acidosis.
€ Steroids:
™ Hydrocortisone (500-1000 mg) is used to improve perfusion and reduce
inflammation.
€ Antibiotics:
™ For septic shock, control infections and manage blood sugar levels in diabetic
patients.
€ Catheterization:
™ Monitor urine output (30-50 mL/hr).
€ Gastroprotection:
™ Administer ranitidine IV, omeprazole IV, or pantoprazole IV.

SEPTIC SHOCK

Cause
€ Arises from infections by Gram-positive/Gram-negative bacteria, fungi, viruses, or
protozoa.

Pathophysiology
™ Endotoxins/toxins from organisms (e.g., E. coli, Klebsiella, Pseudomonas) trigger:
 Inflammation, activation of macrophages and neutrophils.
 Cytokine release and free radical production.
 Chemotaxis of cells, endothelial injury, and coagulation cascade (SIRS).
™ Pathophysiology of Septic Shock:

1. Toxins/Endotoxins → 2. Inflammation and Cellular Activation → 3. Cytokine

Release & Chemotaxis → 4. SIRS → 5. Hyperdynamic Warm Stage → 6. MODS →
7. Cold Irreversible Stage

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 General Surgery

Stages
€ Hyperdynamic (Warm): Reversible, associated with fever and tachycardia.
€ Hypodynamic (Cold): Irreversible, severe circulatory failure with MODS (Multi-Organ
Dysfunction Syndrome).

ANAPHYLACTIC SHOCK

Cause
€ Hypersensitivity reaction to allergens (e.g., Penicillin, anesthetics, insect stings,
venom).

Pathophysiology
™ Antigen combines with IgE on mast cells/basophils, releasing histamine and Slow-
Reacting Substances of Anaphylaxis (SRS-A).
™ Results in:
 Bronchospasm
 Laryngeal edema
 Cardiovascular collapse.

Reference: Manipal Manual of Surgery, 4th Edition, Page no. 170.

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 MedEd FARRE: Surgery

10 (a) Define the terms Sepsis, Bacteraemia and SIRS.

(b) What is MODS? Describe the pathogenesis, features and management of
MODS.

Answer:

SEPSIS
€ Sepsis is a life-threatening complication of an infection.
€ It occurs when chemicals released in the bloodstream to fight an infection trigger
widespread inflammation.
€ This results in a cascade of changes that can damage multiple organ systems,
leading to failure and, in severe cases, death.

BACTEREMIA
€ Bacteremia refers to the presence of viable bacteria in the bloodstream.
€ It is commonly caused by infections that spread from wounds or other parts of the
body.

SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS)

€ SIRS is the systemic manifestation of inflammation due to various causes, such as
infection, pancreatitis, burns, or malignancy.
€ Diagnosis is based on two or more of the following conditions:
™ Temperature: >38°C (Hyperthermia) or <36°C (Hypothermia)
™ Heart rate: >90 beats per minute (Tachycardia)
™ Respiratory rate: >20 breaths per minute or PaCO₂ <32 mm Hg
™ White Blood Cell Count: >12,000/cu mm or <4,000/cu mm, or >10% immature band
forms
€ SIRS often progresses to severe conditions like shock if inflammatory cascades fail
to localize.

MULTIPLE ORGAN DYSFUNCTION SYNDROME (MODS)

Definition
€ MODS refers to the progressive dysfunction of two or more organ systems,
where the body cannot maintain homeostasis without external interventions like
ventilators or dialysis.

Stages of MODS
1. Primary MODS:
™ Direct organ damage due to an initial injury or event (e.g., Trauma or sepsis).
™ Example: Severe burns causing immediate tissue damage or blood loss from trauma
reducing oxygen supply to organs.

30
 General Surgery

2. Secondary MODS:
™ Occurs days or weeks later due to an uncontrolled inflammatory response initiated
by the primary insult.
™ Example: An infection in a burn wound causing systemic sepsis.

Pathophysiology - How MODS Develops

1. Initial trigger (Infectious or non-infectious insult):
™ Infectious causes:
 Pneumonia, Urinary Tract Infections (UTIs), peritonitis, necrotizing fasciitis, etc.
™ Non-infectious causes:
 Trauma, burns, pancreatitis, ischemia-reperfusion injury (e.g., post-surgery), or
massive blood loss
2. Immune system activation:
™ The body releases chemicals like cytokines (e.g., TNF-a, IL-1, IL-6) to combat the
insult.
™ These pro-inflammatory cytokines attract immune cells (Like neutrophils) to the
site of injury and infection.
™ Simultaneously, the Compensatory Anti-inflammatory Response Syndrome
(CARS) develops, which suppresses parts of the immune system to prevent excessive
inflammation.
™ When the pro-inflammatory and anti-inflammatory systems lose balance, this
causes:
 Unchecked inflammation (SIRS)
 Suppressed immune function (CARS), leading to secondary infections

3. Microvascular injury:
™ Cytokines and free radicals damage the endothelial lining of blood vessels.
™ This causes:
 Capillary leak: Fluid leaks out of blood vessels into surrounding tissues.
 Impaired oxygen delivery: Reduced blood flow to organs leads to hypoxia
(Low oxygen levels).

4. Coagulation abnormalities:
™ The endothelium activates coagulation pathways, leading to micro-clots in
capillaries (Microthrombi).
™ Result: Blood flow is further obstructed, worsening oxygen delivery to tissues.

5. Energy failure and cellular death:

™ Reduced oxygen means cells shift to anaerobic metabolism, producing lactic acid
(A marker of organ failure).
™ Without enough ATP (Energy), cells begin to die, leading to organ dysfunction.

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MedEd FARRE: Surgery

Organ-Specific Manifestations in MODS

1. Lungs (First organ to fail):
™ Develop Acute Respiratory Distress Syndrome (ARDS):
 Fluid leaks into the lungs, reducing oxygen exchange.
 Symptoms: Severe shortness of breath, low oxygen levels despite mechanical
ventilation.
2. Kidneys:
™ Develop Acute Kidney Injury (AKI):
 Reduced blood flow and oxygen cause kidney cells to die.
 Symptoms: Decreased urine output, accumulation of toxins in the blood.

3. Liver:
™ Develop Hepatic Dysfunction:
 The liver fails to detoxify the blood or produce clotting factors.
 Symptoms: Jaundice, increased bleeding risk, elevated liver enzymes (ALT, AST)

4. Heart:
™ Myocardial Depression: The heart struggles to pump efficiently due to inflammation
and reduced oxygen supply.
 Symptoms: Low blood pressure, arrhythmias

5. Gastrointestinal tract:
™ Loss of the gut mucosal barrier allows bacteria to enter the bloodstream
(Translocation).
 Symptoms: Severe infection, sepsis

Factors Influencing MODS Development

€ Severity of the Initial Injury: Greater initial damage increases risk
€ Patient’s Age: Elderly patients have reduced organ reserves, making recovery harder.
€ Chronic Illnesses: Conditions like diabetes, COPD, or heart disease worsen outcomes.

Management of MODS
1. Treat the underlying cause:
 For infection: Immediate antibiotics or antifungal treatment
 For trauma: Surgery to control bleeding and repair damage

2. Support oxygen delivery to organs:

™ Mechanical ventilation for ARDS
™ Vasopressors (e.g., Norepinephrine): To improve blood pressure and perfusion

32
 General Surgery

3. Minimize inflammation:
™ Early identification and control of SIRS through anti-inflammatory drugs or immune
modulators.
4. Support organ function:
™ Dialysis for kidney failure
™ Nutritional support (Enteral or parenteral feeding) to meet metabolic needs.
™ Blood transfusions for anemia or clotting factor deficiencies.

5. Monitor for secondary infections:

™ Secondary infections are common in patients with immune suppression from CARS.

Reference: Manipal Manual of Surgery, 4th Edition, Page no. 170.

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 MedEd FARRE: Surgery

11. What is minimally invasive surgery? List its different techniques. (5 Marks)

Answer:

MINIMALLY INVASIVE SURGERY

Definition
€ Minimally Invasive Surgery (MIS) refers to surgical procedures performed through
the smallest possible incisions, aiming to minimize physical, physiological, and
psychological trauma to the patient. It is characterized by the use of advanced
technologies and instruments to reduce tissue damage, blood loss, and recovery
time, making it an efficient alternative to traditional open surgeries.

Key Features of MIS

1. Smaller incisions compared to conventional surgery.
2. Reduced risk of infection and postoperative complications.
3. Faster recovery and shorter hospital stays.
4. Reduced pain and scarring post-surgery.

Advancements Leading to MIS

€ The evolution of technologies such as high-definition imaging, specialized
surgical instruments, and robotics has made minimally invasive surgery widely
accessible and efficient.

TECHNIQUES IN MINIMALLY INVASIVE SURGERY (MIS)

€ The various techniques under MIS are categorized based on their approach and
application:

1. Laparoscopy
€ A technique involving small abdominal incisions for diagnostic or therapeutic
procedures.
€ Commonly used for surgeries involving the gallbladder, appendix, or reproductive
organs.

2. Thoracoscopy
€ Performed to visualize or operate on thoracic (Chest) organs such as the lungs and
pleura.
€ Primarily used in treating conditions like pleural effusions or lung biopsies.

3. Retroperitoneoscopy
€ Utilized for surgeries in the retroperitoneal space, such as kidney surgeries.
€ Minimizes the need to enter the abdominal cavity directly.

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 General Surgery

4. Mediastinoscopy
€ Focuses on the mediastinum (Central chest area) for biopsy or diagnostic purposes.
€ Commonly used in staging lung cancer or diagnosing infections.

5. Endoscopy
€ Involves the use of endoscopes equipped with cameras and light to access internal
structures.
€ Types include:
™ ERCP (Endoscopic Retrograde Cholangiopancreatography): For bile and
pancreatic duct visualization.
™ Colonoscopy: For large intestine examination.
™ Upper Gastrointestinal (UGI) Endoscopy: For visualizing the esophagus, stomach,
and duodenum.
™ Bronchoscopy: To visualize the airways.
™ Cystoscopy: For bladder or urethral examination.
™ Sigmoidoscopy: For examining the sigmoid colon.
™ Endovascular Surgery: For vascular procedures, including aneurysm repairs.
™ Arthroscopy: For joint conditions.

6. NOTES (Natural Orifice Transluminal Endoscopic Surgery)

€ A revolutionary technique where surgical access is gained through natural body
orifices, such as the mouth or vagina, eliminating external incisions.

7. SILS (Single Incision Laparoscopic Surgery)

€ Also referred to as single-port surgery.
€ Involves a single incision, typically at the umbilicus, offering an advanced cosmetic
outcome and reduced postoperative pain.

8. Robotic Surgery
€ Integrates robotic systems to enhance precision, control, and visualization during
surgery.
€ Common in procedures such as prostatectomy or cardiac surgery.

Reference: Manipal Manual of Surgery, 4th Edition, Page no. 1174.

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35
 MedEd FARRE: Surgery

12. a) Write a short note on: (5 Marks)

1. Pleomorphic adenoma.

2. Parotid abscess.

b) E
 numerate the differences between: Clinical features of Benign and
malignant tumors of the parotid gland.

Answer:

PLEOMORPHIC ADENOMA

Introduction
€ Pleomorphic adenoma is the most common benign tumor of the salivary glands.
€ It is also known as a mixed salivary tumor due to its epithelial and mesenchymal
origin.
€ Accounts for 80% of salivary gland tumors, with 80% occurring in the parotid
gland, 10% in the submandibular gland, and 0.5% in the sublingual gland.

Pathology
€ It arises from myoepithelial and duct reserve cells.
€ Histologically, it contains a mix of epithelial, myoepithelial, and mesenchymal
components (Cartilage, cystic spaces, solid tissue).
€ Even though encapsulated, it can exhibit pseudopods, leading to extensions beyond
the capsule.

Clinical Features
€ Occurs in both sexes and can occur at any age, though commonly seen in the 4th
and 5th decades.
€ Presents as a painless, slow-growing, mobile, smooth swelling in the parotid
region, anterior to the ear.
€ It exhibits a positive curtain sign, as the deep fascia of the parotid gland attached
to the zygomatic bone limits upward movement of the swelling.

Treatment
1. Surgery is the treatment of choice:
™ Superficial parotidectomy if the tumor involves only the superficial lobe.
™ Total conservative parotidectomy (Preserving the facial nerve) if the tumor
involves both superficial and deep lobes.

2. The facial nerve is preserved unless malignancy is suspected.

36
 General Surgery

PAROTID ABSCESS

Definition
€ Parotid abscess, or suppurative parotitis, is a result of acute bacterial inflammation
of the parotid gland, leading to formation of pus within the gland.

Etiology

Commonly occurs due to:

€ Ascending bacterial parotitis secondary to reduced salivary flow.

€ Predisposing factors: Dehydration, poor oral hygiene, starvation, sepsis, post-

surgery, or radiotherapy.
€ Most common causative organism: Staphylococcus aureus, followed by Streptococcus
viridans and anaerobic bacteria.

Pathophysiology
€ Parotid fascia being thick and dense delays fluctuation, leading to late-stage abscess
formation.

Clinical Features
€ Pyrexia, malaise, pain, and trismus.

€ Red, tender, firm swelling localized to the parotid region.

€ Tender cervical lymphadenopathy.

€ Severe cases may show bacteremia features.

€ Pus or turbid saliva may exude from the Stensen’s duct opening.

Treatment

1. Antibiotics based on culture and sensitivity.

2. For localized abscess, incision and drainage are done under general anesthesia.

3. Supportive measures:
™ Proper hydration.

™ Antiseptic mouthwashes (e.g., Povidone-iodine or potassium permanganate).

4. Surgical drainage via Blair’s incision if necessary.

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MedEd FARRE: Surgery

DIFFERENCES BETWEEN CLINICAL FEATURES OF BENIGN AND MALIGNANT

TUMORS OF THE PAROTID GLAND

Feature Benign Tumors Malignant Tumors

Growth Rate € Slow-growing € Sometimes fast-growing

Consistency € Soft or rubbery € Hard

Incidence € 85% of parotid tumors are € 45% of minor salivary gland

benign tumors are malignant

Ulceration € No ulceration € May ulcerate and invade

bone

Nerve Involvement € No associated nerve € May cause cranial nerve

involvement palsies

Reference : Manipal Manual of Surgery, 4th Edition, Page no. 302.



38
 General Surgery

13. Define a burn. List the types of burns and classify burn injuries.(10 Marks)
13(1). Explain the management of a patient with burns involving 40% of the Total
Body Surface Area (TBSA).

Answer:
BURN

Definition
€ A burn is defined as an injury to the skin and underlying tissues caused by
exposure to heat, chemicals, electricity, radiation, or friction.
€ Burns cause tissue damage by denaturing cellular proteins, leading to cell death,
and triggering an inflammatory response.
€ The severity depends on:
™ Temperature/intensity of the causative agent.
™ Duration of exposure.
™ Depth and extent of the injury.

Types of Burns
€ Burns are classified based on the depth of tissue damage, which determines their
clinical appearance, healing process, and management approach.

Tissue
Type of Clinical Healing
Involve- Causes Pain Management
Burn Appearance Process
ment

First- Epidermis - Sunburn -R

 ed, dry, -H
 eals in 5–7 Painful -C
 ool with
Degree only. and non- days. (intact water or
-B
 rief
Burn blistered nerve saline.
scalds -N
 o scarring
skin. endings).
(Superficial as the dermis -A
 pply aloe
-M
 ild
Burn) -M
 ay is unaffected. vera or
thermal
have mild moisturizer.
exposure -R
 egenera-tion
swelling.
occurs from -P
 ain relief
-P
 eels as it basal cells of with oral
heals. the epidermis. analgesics
(e.g.,
ibuprofen).

Second- Epidermis -P
 rolonged -R
 ed and -S
 uperficial Very painful -C
 lean with
Degree + partial exposure moist. burns: Heal (nerve saline.
Burn dermis. to hot within 10–14 endings
-B
 listers -U
 se non-
liquids or days, minimal exposed).
(Partial may form. adherent
objects. scarring.
Thickness) dressing.
-S
 uperficial
-F
 lash -D
 eep burns:
burns: -A
 pply topical
flames. Take 2–3
bright red. antimicrobial
weeks,
(e.g., silver
- Deep burns: higher risk of
sulfadiazine).
pale and scarring and
mottled. contractures. - Deep burns
may require
grafting.

39
 MedEd FARRE: Surgery

Third- Entire - Prolonged -D

 ry, -N
 o Painless -E
 scharotomy
Degree epidermis exposure leathery, spontaneous (nerve or
Burn and to flames, and stiff. healing. endings fasciotomy
dermis scalds, or destroyed). if circulation
(Full -W
 hite, - Requires skin
destroyed. chemicals. compromised.
Thickness black, or grafting or
Burn) -H
 igh- charred reconstructive - Surgical inter-
voltage appearance. surgery. vention (e.g.,
electrical debridement
-N
 o -L
 eads to
burns. and grafting).
blanching. permanent
scarring. - IV fluids
for systemic
support.

Fourth- Skin, subcu- - Severe - Charred - Requires Painless - Surgical

Degree taneous electrical and extensive (nerves debridement
Burn tissue, burns. blackened recons- completely and reconst-
muscle, tissue. tructive destroyed). ruction.
- Extended
or bone surgery.
flame - Deep -A
 mputation if
involved.
exposure. structures - Often results necessary.
(e.g., bone, in loss of
- Chemical -A
 ggressive
tendons) may affected limb.
burns. systemic
be visible.
- Risk of support for
infection and infection
sepsis is very control and
high. metabolic
demands.

Key Differences by Type

€ First-degree burns are superficial and affect only the epidermis, allowing quick
healing without scarring.
€ Second-degree burns extend into the dermis, forming blisters due to fluid accumulation.
€ Third-degree burns destroy regenerative layers of the skin, necessitating surgical
intervention for recovery.
€ Fourth-degree burns involve deeper tissues, often resulting in severe functional and
structural loss.

Reasons for Pain Variations

€ Superficial burns are painful because nerve endings are exposed and intact.
€ Deeper burns (Third and fourth degree) destroy nerve endings, leading to loss of
sensation.

Importance of Timely Management

€ Delayed intervention in second- and third-degree burns can lead to infections,
contractures, and poor outcomes.
€ Fourth-degree burns demand aggressive systemic support due to risks of sepsis and
multi-organ failure.

40
 General Surgery

Classification of Burn Injuries

€ Burns can also be classified based on the extent of body surface area (TBSA)
involved, as this guides fluid resuscitation and prognosis.

Classification Extent of Injury Examples Management

Minor Burns -P
 artial thickness: <15% Localized Outpatient care.
in adults. burns with no Wound dressing
complications and supportive
-F
 ull thickness: <2%
or inhalational therapy.
TBSA.
injury.

Moderate Burns - P
 artial thickness: 15– Burns sparing Hospitalization. IV
25% TBSA. face, hands, feet, fluids and wound
or perineum. care.
-N
 o critical areas
involved.

Major Burns - Partial thickness >25%. Extensive burns Intensive

with systemic care. Requires
- Full thickness >10%
complications. resuscitation
TBSA.
and surgical
-I
 nvolves critical areas interventions.
or inhalational injury.

MANAGEMENT OF BURNS INVOLVING 40% TBSA

€ Managing a burn injury involving 40% TBSA requires addressing systemic complications
like hypovolemic shock, infection, and impaired healing.

Initial (Pre-Hospital) Management

€ Stop the burning process:
™ Remove the patient from the source.
™ Remove clothing to prevent heat retention.
€ Cool the burn area:
™ Use cool water to limit thermal injury but avoid hypothermia.
€ Cover the burn:
™ Use clean sheets to protect from infection.

Hospital Management
1. Airway and breathing:
™ Rationale: Burns to the face or inhalation of smoke can cause airway obstruction
due to edema.
™ Steps:
 Assess for signs of airway compromise (e.g., Hoarseness, stridor).

41
MedEd FARRE: Surgery

 Administer humidified oxygen.

 Intubate early if there are signs of impending obstruction.

2. Fluid resuscitation:
™ Burns >20% TBSA cause significant fluid loss due to increased vascular permeability.
™ Parkland Formula:
 4 mL × TBSA (%) × Body Weight (kg) of Ringer’s lactate.
 Distribute over 24 hours:
Š 50% in the first 8 hours.

Š 50% in the next 16 hours.

3. Goal:
™ Maintain urine output at 30–50 mL/hour to prevent hypovolemia.

4. Wound care:
™ Clean with saline or antiseptic solutions.
™ Cover with non-adherent dressing.
™ Apply topical antimicrobials (e.g., silver sulfadiazine) to prevent infection.
™ Escharotomy may be needed for circumferential burns to relieve pressure and
improve circulation.
5. Nutritional support:
™ Burns induce a hypermetabolic state, increasing energy demands.
™ Nutritional requirements:
 High-protein, high-calorie diet to support wound healing.
 Start enteral feeding early to reduce catabolism.

6. Pain and psychological management:

™ Pain relief:
 Use opioids (e.g., Morphine) for effective pain control.
™ Psychological care:
 Burn injuries are traumatic; counseling or therapy may be needed.
Reference: Manipal Manual of Surgery, 4th Edition, Page no. 185.



42
 General Surgery

14. (a) E
 xplain the concept of field management during disasters. Write a note
on triage, primary, secondary and tertiary survey.
(b) Write a short note on Abdominal Trauma. (10 Marks)

Answer:

DISASTER
€ A disaster is a sudden event causing widespread human, material, and environmental
losses beyond the community’s ability to cope. It may result from natural or human
causes.
€ Disasters occur when hazards impact vulnerable populations lacking the resources to
respond effectively.

Challenges During a Disaster

Field management in disasters aims to address several challenges that arise, such as:
1. Communication Breakdown: Disruption of networks delays coordination.
2. Access Issues: Damaged infrastructure hampers rescue efforts.
3. Time Sensitivity: The first 72 hours are crucial for survival.
4. Underdeveloped Infrastructure: Limited resources and emergency systems hinder
response.

Key Components of Field Management in Disasters

€ To mitigate the disaster’s impact, a systematic approach is essential. This involves:

1.  eadership and Organization: Appointing a disaster leader ensures efficient

L
task allocation and decision-making.
2.  esource Mobilization: Rapid deployment of response teams and supplies is
R
critical.
3.  ommunication: Temporary networks ensure smooth coordination and prevent
C
panic.
4.  escue Operations: Teams use specialized equipment to locate and save
R
survivors.

Triage in Disaster Management

€ Triage is a method used to prioritize patients based on the severity of their
injuries and the likelihood of survival. This ensures the efficient use of limited medical
resources.
€ Triage categories:

1. Red (Immediate):
Š Life-threatening injuries that require urgent care, e.g., uncontrolled bleeding,
head injuries.
Š Goal: Stabilize the patient to increase survival chances.

43
MedEd FARRE: Surgery

2. Yellow (Urgent):
Š Serious but not life-threatening injuries, e.g., Fractures.

Š Goal: Provide treatment once red category patients are stabilized.

3. Green (Non-Urgent):
Š Minor injuries like bruises or small wounds.

Š Goal: Treat later, allowing medical teams to focus on critical patients.

4. Black (Unsalvageable):
Š Patients with little or no chance of survival, e.g., severe burns or trauma.

Š Goal: Prioritize resources for those with better chances of recovery.

Importance of Triage
€ Reduces the burden on medical teams by optimizing resource allocation.
€ Increases the survival rate by addressing critical cases first.

Field Hospitals in Disaster Management

€ Field hospitals are temporary medical facilities set up in disaster zones to treat
patients quickly and efficiently.

Types of Field Hospitals

1. Tent-based field hospitals:
™ Easy to set up in remote areas.
™ Suitable for providing basic first aid and initial stabilization.

2. Modular field hospitals:

™ More advanced facilities equipped with surgical units and ICU setups.
™ Used for complex cases requiring extended care.

Functions of Field Hospitals

1. First aid:
™ Treating minor injuries and stabilizing critical patients for transfer to permanent
healthcare centers.

2. Damage control surgery:

™ Performing life-saving procedures to stabilize patients.
™ Example: Stopping internal bleeding or managing fractures.

3. Non-life-threatening injury management:

™ Addressing injuries that do not require immediate intervention, ensuring efficient
use of resources.

44
 General Surgery

Flowchart Representation
Disaster Strikes
↓
Assess Damage and Needs
↓
Appoint Leaders and Mobilize Teams
↓
Set Up Communication Channels
↓
Triage Patients
↓
Provide Shelter, Food, and Medical Aid
↓
Establish Field Hospitals and Conduct Rescues
↓
Monitor Recovery and Long-Term Rehabilitation

Primary Survey
€ The primary survey focuses on identifying and treating life-threatening conditions
as a priority. It uses the ABCDE protocol (ATLS guidelines):

1. Airway: Ensure a patent airway. Look for obstructions or compromise.

2.  reathing: Assess ventilation and oxygenation; address tension pneumothorax
B
or flail chest.
3.  irculation: Control active bleeding and restore hemodynamic stability with IV
C
fluids or blood.
4. Disability: Neurological assessment using Glasgow Coma Scale (GCS).
5.  xposure: Fully expose the patient for a complete examination while preventing
E
hypothermia.
€ Additionally, AMPLE history is taken:
™ A: Allergy
™ M: Medications
™ P: Past medical history
™ L: Last meal
™ E: Events leading to injury

45
 MedEd FARRE: Surgery

Secondary Survey
€ This involves a detailed physical examination after stabilization in the primary survey.

1.  nitial Clinical Assessment: Evaluate pain, tenderness, gastrointestinal

I
hemorrhage, and signs of hypovolemia.
2. Abdominal examination:
Š Abrasions, contusions, or ecchymosis may indicate underlying trauma.

Š Specific Signs:

- London’s Sign: Bruising in the abdomen suggests hollow viscus perforation.

- S
 eat Belt Sign: Contusion over the lower abdomen, associated with bowel
injuries.
- S
 aree Sign: Across the upper abdomen, indicating pancreatic or bowel
injury.
- Cullen’s Sign: Periumbilical ecchymosis, hinting at intra-abdominal bleeding.
- Grey Turner’s Sign: Flank ecchymosis, suggesting retroperitoneal bleeding.
€ Rib Fractures: Look for associated liver or spleen injuries (Right side for liver; left
side for spleen).
€ Auscultation: Detects bowel sounds in the thorax, indicating diaphragmatic injury.
€ Rectal Examination: Check for high-riding prostate (Urethral injury) or pelvic fracture.
™ Vermooten’s Sign: Indicates urethral rupture due to a displaced prostate.

Tertiary Survey
€ The tertiary survey is a thorough re-evaluation to detect injuries missed during the
primary or secondary surveys.
€ Reassess all clinical findings
€ Repeat imaging studies (CT, ultrasound, or X-rays) to confirm or rule out injuries.
€ Monitor for delayed complications like sepsis, hematomas, or perforations.

ABDOMINAL TRAUMA

€ Abdominal trauma refers to injuries to the abdomen caused by blunt or penetrating

forces that may damage internal organs, blood vessels, or abdominal wall structures.

Types
1. Blunt Abdominal Trauma (BAT):
™ Occurs due to blows, falls, or motor vehicle accidents.
™ Commonly affects organs like the spleen, liver, and intestines.
™ Symptoms may be subtle, requiring imaging for diagnosis.

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 General Surgery

2. Penetrating Abdominal Trauma:

™ Caused by stab wounds, gunshots, or sharp objects.
™ Frequently results in direct organ damage or hemorrhage.

Clinical Features
€ Pain or tenderness in the abdomen
€ Distension of the abdomen
€ Signs of internal bleeding (Hypotension, tachycardia)
€ Rebound tenderness or rigidity, indicating peritonitis
€ In severe cases, shock or organ failure

Diagnostic Approaches
€ Focused Assessment with Sonography for Trauma (FAST): Detects free fluid or
blood in the abdomen.
€ CT Scan: Provides a detailed evaluation of organ injury.
€ X-ray: Identifies fractures or foreign objects.
€ Laboratory Tests: Assess hemoglobin levels, liver enzymes, and arterial blood gases.

Management
€ Initial resuscitation:
™ Airway stabilization, breathing, and circulation support (ABC approach).
™ Intravenous fluids or blood transfusions
€ Surgical Intervention:
™ Exploratory laparotomy for unstable patients or significant internal injury.
™ Damage control surgery for life-threatening bleeding.
€ Non-operative Management (NOM):
™ Suitable for stable patients with injuries like minor liver or splenic lacerations

Complications
€ Infections: Peritonitis, abscess formation
€ Hemorrhagic shock
€ Organ failure due to delayed diagnosis.

Prevention
€ Use of seat belts and adherence to road safety measures.
€ Education on handling sharp objects and avoiding high-risk activities.

Reference: Manipal Manual of Surgery, 4th Edition, Page no. 885.

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 Anesthesia
66. Explain in detail about Local Anaesthesia. (5 Marks)

Answer:

LOCAL ANAESTHESIA

Introduction
Local anaesthesia involves using drugs to block nerve impulses in a localized area,
providing temporary analgesia and anaesthesia without affecting consciousness.

Definition and Key Characteristics

€ Local anaesthetics are drugs injected around nerves to block impulse conduction,
causing loss of sensation in the specific area.
€ These drugs act on sodium channels to prevent nerve signal transmission.

Classification of Local Anaesthetics

Local anaesthetics are categorized based on their chemical structure:
1. Aminoesters:
™ Examples: Procaine, chloroprocaine, tetracaine
™ Metabolized by plasma esterases
™ Shorter duration of action

2. Aminoamides:
™ Examples: Lignocaine, bupivacaine, ropivacaine
™ Metabolized in the liver.
™ Longer duration and more stable.

Mechanism of Action
1. Primary action:
™ Local anaesthetics block sodium channels, inhibiting sodium influx, which prevents
depolarization and conduction of nerve impulses.
™ This is termed sodium channel blockade.

2. Ionized vs. non-ionized forms:

™ Non-ionized form: Lipophilic, crosses cell membranes easily.
™ Ionized form: Blocks the sodium channel from the intracellular side.
 MedEd FARRE: Surgery

Factors Influencing Activity

1. Lipid Solubility: Higher lipid solubility increases potency by enhancing penetration

into the lipoprotein membrane.

2. pKa: Lower pKa values result in a higher proportion of non-ionized drug, leading to
a faster onset of action
™ E.g., Lignocaine (pKa 7.9) acts faster than bupivacaine (pKa 8.1).

3. pH: Acidosis decreases non-ionized drug proportion, reducing efficacy (Important

in infected tissues).

4. Protein Binding: Higher protein binding prolongs drug duration.

Choice of Local Anaesthetic Agents

Agent Concentration Uses

Lignocaine 0.5–5% Skin infiltration, minor nerve blocks, epidural, spinal
anaesthesia.
Bupivacaine 0.25–0.5% Epidural and spinal anaesthesia
Ropivacaine 0.2–0.75% Postoperative analgesia, spinal anaesthesia, peripheral
nerve blocks
Clinical Effects
Local effects:
€ Blocks sodium channels in neuronal membranes, stopping impulse propagation.

Systemic effects:
€ CNS Effects: Tingling, convulsions, coma (dose-dependent toxicity).

€ Cardiovascular Effects: Myocardial depression, arrhythmias, or ventricular arrest

at high plasma levels.

Toxicity of Local Anaesthetics

1. Systemic toxicity:
™ CNS toxicity occurs first, followed by cardiovascular toxicity.
™ CNS toxicity:

 Low plasma levels: Tingling, light-headedness, slurred speech.

 High plasma levels: Convulsions, coma, respiratory arrest.

™ Cardiovascular toxicity

 Myocardial depression, arrhythmias, and ventricular arrest.

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 Anesthesia

2. Plasma concentration and effects:

Concentration (µg/ml) CNS Effects CVS Effects

5 Tingling, numbness Myocardial depression
10 Convulsions Cardiac arrhythmias
25 Respiratory arrest Ventricular arrest

3. Factors increasing toxicity:

™ Rapid injection, vascular sites, large doses, or poor cardiac/renal function.

Prevention and Treatment of Toxicity

Prevention:
€ Avoid exceeding recommended doses.

€ Always aspirate before injecting to avoid accidental intravascular administration.

€ Use adrenaline (Except in end-arterial sites like fingers, toes, penis).

Treatment:
€ Maintain airway and ventilation

€ Oxygen therapy

€ Intravenous diazepam or thiopentone for convulsions.

€ Ephedrine, inotropes, and vasoconstrictors for cardiovascular collapse.

Special Considerations
1. Adrenaline caution:
™ Avoid using adrenaline in extremities (Fingers, toes, penis) due to risk of ischemia.

2. Bupivacaine & lignocaine caution:

™ Bupivacaine and preservative-containing lignocaine are not suitable for intravenous
use.

Clinical Applications
€ Skin Infiltration: For minor surgical procedures

€ Spinal Anaesthesia: High-concentration lignocaine or bupivacaine for lower

abdominal and pelvic surgeries.
€ Epidural Anaesthesia: Provides analgesia for surgeries and labor.

€ Nerve Blocks: For postoperative pain relief and minor procedures.

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MedEd FARRE: Surgery

Summary Table

Aspect Details
Classification Aminoesters, aminoamides
Mechanism of Action Sodium channel blockade
Factors Affecting Activity Lipid solubility, pKa, pH, protein binding
Toxicity CNS (First), CVS (Later)
Prevention & Treatment Dose control, airway maintenance, CPR

Note
€ Central nervous system toxicity always precedes cardiovascular toxicity.

€ Never use adrenaline preparations for end-arterial nerve blocks.

€ Dose-dependent toxicity is common, so always adhere to recommended guidelines.

Reference: Manipal Manual of Surgery, 4th Edition, Page no. 1089.

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 Anesthesia

67. Write a short note on types, indications and complications of Regional

Anaesthesia.  (5 Marks)

Answer:

REGIONAL ANAESTHESIA

Definition
€ Regional anaesthesia refers to a technique that blocks sensation and/or motor
function in a specific region of the body while the patient remains conscious or
lightly sedated.

Types of Regional Anaesthesia

1. Spinal anaesthesia:
™ Injection of a local anaesthetic into the Cerebrospinal Fluid (CSF) in the subarachnoid
space.
™ Commonly used for lower abdominal, pelvic, or lower limb surgeries.

2. Epidural anaesthesia:
™ Administration of local anaesthetic into the epidural space.

™ Provides analgesia for surgeries, labour pain, or chronic pain management.

3. Nerve blocks:
™ Injection of a local anaesthetic near a specific nerve or nerve plexus.

™ Examples: Brachial plexus block, femoral nerve block.

4. Intravenous Regional Anaesthesia (IVRA):

™ Local anaesthetic is injected into a vein of a limb after applying a tourniquet.

™ Commonly used for minor limb surgeries.

Indications
€ Surgeries involving the extremities, abdomen, or pelvis.

€ Pain management during labour or in chronic pain conditions.

€ Situations where general anaesthesia is contraindicated.

Contraindications
€ Patient refusal

€ Coagulopathy or bleeding disorders.

€ Infection at the injection site.

€ Severe hypovolemia or shock.

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 MedEd FARRE: Surgery

Advantages
€ Provides effective pain control.
€ Minimizes systemic side effects compared to general anaesthesia.
€ Reduces the need for postoperative opioids.
€ Allows faster recovery and early ambulation.

Complications
€ Local: Nerve injury, haematoma, infection at the injection site.
€ Systemic: Hypotension, bradycardia, local anaesthetic toxicity (e.g., CNS and cardiac
toxicity).
€ Specific: Post-dural puncture headache (In spinal anaesthesia).

Reference: Manipal Manual of Surgery, 4th Edition, Page no. 1091.

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 Anesthesia

68. Write a short note on day care anaesthesia. (5 Marks)

Answer:

DAY CARE ANAESTHESIA

Definition
€ Day care anaesthesia is the administration of anaesthesia for procedures that allow
the patient to be admitted, treated, and discharged on the same day without
requiring overnight hospital stay.

Features of Day Care Anaesthesia

1. Patient selection:
™ Ideal for ASA (American Society of Anesthesiologists) Grade I and II patients.
™ Conditions requiring minor or intermediate procedures (e.g., Laparoscopic
cholecystectomy, hernia repair, diagnostic endoscopy).

2. Anaesthetic techniques:
™ Use of short-acting agents:
 Intravenous agents: Propofol, Etomidate.
 Inhalational agents: Sevoflurane, Desflurane.
™ Regional anaesthesia:
 Spinal, epidural, or peripheral nerve blocks for surgeries on limbs or lower
abdomen.

3. Advantages:
™ Reduced healthcare costs and hospital stays.
™ Decreased risk of hospital-acquired infections.
™ Faster recovery and quicker return to daily life.

4. Preoperative preparation:
™ Comprehensive pre-anaesthetic evaluation (PAC) to assess fitness.
™ Clear fasting instructions: 6 hours for solids, 2 hours for clear fluids.
™ Patient counselling about the anaesthetic plan, recovery, and discharge criteria.

5. Intraoperative care:
™ Monitoring of vital parameters (ECG, SpO2, BP).
™ Minimal use of long-acting opioids to avoid delayed recovery.
™ Effective pain management using oral analgesics (e.g., Paracetamol, ibuprofen).
™ Prevention of Postoperative Nausea and Vomiting (PONV) using antiemetics like
ondansetron.

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 MedEd FARRE: Surgery

6. Discharge criteria (Common ALDRETE SCORE):

™ Stable vital signs (Heart rate, blood pressure, respiratory rate).
™ Ability to walk, drink fluids, and urinate without difficulty.
™ Absence of excessive pain, nausea, or dizziness.
™ Availability of a responsible adult to escort the patient home.

Applications of Day Care Anaesthesia

€ Surgical procedures: Hernia repair, circumcision, cataract surgery, laparoscopic
sterilization.
€ Diagnostic procedures: Colonoscopy, cystoscopy, bronchoscopy.
€ Therapeutic interventions: Radiofrequency ablation, lithotripsy.

Limitations
€ Not suitable for high-risk patients (e.g., ASA Grade III or above).
€ Requires a well-equipped setup and skilled anaesthesiologists.
€ Risk of readmission due to unforeseen complications (e.g., Excessive pain, PONV).

Remember with Mnemonics

1. Advantages of day care anaesthesia (FAST):
™ F – Faster recovery.
™ A – Avoids hospital infections.
™ S – Saves time and cost.
™ T – Time-efficient for the healthcare system.

2. Discharge criteria (SURE):

™ S – Stable vitals.
™ U – Urination completed.
™ R – Responsible adult escort.
™ E – Eating or drinking tolerated.
Reference: Manipal Manual of Surgery, 4th Edition, Page no. 1071.

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 Orthopedics
73. Classify bone fractures. (5 Marks)

Answer:

BONE FRACTURES

Classification of Bone Fractures

€ Bone fractures are classified to assist in diagnosis, management, and prognosis.

1. Classification Based on Etiology

Type Description Examples

Traumatic € Caused by significant trauma € Road traffic accidents
Fracture to healthy bone, which can € Falls
withstand considerable force
€ Fights
until a threshold is exceeded.
Pathological € Occurs in bones weakened € Osteoporotic fractures,
Fracture by underlying disease (e.g., € Fractures due to bone cysts or
Osteoporosis, bone tumors). tumors.
€ These may occur with minimal
or no force (e.g., Metastasis-
related fracture).
Stress € Results from repetitive stress € Tibial fractures in athletes,
Fracture causing microtrauma to the € Metatarsal fractures in soldiers.
bone over time.
€ Initially, these may not be
visible on X-rays and often
present as pain.
MedEd FARRE: Surgery

2. Classification Based on Mechanism of Injury

Type Description Examples

High-Velocity Injury € Caused by severe trauma, such as € Pelvic fractures in
in traffic accidents. car crashes.
€ Associated with significant soft
tissue damage and complex
fractures.
Low-Velocity Injury € Result of mild trauma, often in € Wrist fractures from
elderly or osteoporotic patients. falls.
€ Fractures are simple and heal
predictably.

3. Classification Based on Displacement

Type Description
Undisplaced Fracture € Bone fragments remain aligned, usually stable and
easy to treat conservatively.
Displaced Fracture € Bone fragments lose alignment due to external forces,
muscle pull, or gravity, requiring reduction.
Forms of Displacement:
1. Shift: Lateral displacement of fragments.
2. Angulation: Angular deformity at the fracture site.
3. Rotation: Twisting of fragments around the long axis.

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4. Classification Based on Relationship with External Environment

Type Description Examples

Closed € Fracture with intact skin, meaning € Femur fracture from
Fracture no communication with the external a fall.
environment.
Open € Skin and soft tissue are breached, € Open tibial fracture
Fracture exposing the fracture site to the external from trauma.
environment.

Subtypes of Open Fractures:

€ Internally Open: Bone fragments pierce
the skin from within.
€ Externally Open: External objects penetrate
the skin, causing the fracture.

5. Classification Based on Fracture Pattern

Pattern Description
Transverse € The fracture line is perpendicular € Transverse humerus fracture
to the bone’s long axis; caused by
bending forces.
Oblique € The fracture line is diagonal € Oblique fracture of the tibia
to the long axis; results from
combined bending and axial forces.
Spiral € Fracture line spirals along the € Spiral fracture of the femur
bone; caused by twisting forces.
Comminuted € Bone breaks into multiple € Comminuted tibial fracture
fragments; associated with severe
trauma.
Segmental € Two distinct fractures within the € Segmental fracture of the
same bone, creating a segment of femur
free-floating bone.

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MedEd FARRE: Surgery

6. Classification based on complexity of treatment:

Type Description Examples

Simple Fracture € Bone breaks into two pieces, € Transverse fracture
making it easier to treat of the radius
conservatively or operatively.
Complex Fracture € Bone breaks into multiple € Comminuted tibial
fragments, requiring advanced fracture
surgical techniques.
7. Fractures with Eponyms:
€ Eponymous fractures are named after their discoverers or unique characteristics.

Eponym Description
Colles’ Fracture € Fracture of the distal radius with dorsal tilt.

Smith’s Fracture € Reverse of Colles, with ventral tilt.

Monteggia € Fracture of the ulna with dislocation of the radial head.

Fracture
Galeazzi Fracture € Fracture of the radius with dislocation of the distal radio-
ulnar joint.
Jefferson’s € Fracture of the first cervical vertebra (atlas).
Fracture

CLASSIFICATION OF BONE FRACTURES

1. Etiology:
™ Traumatic
™ Pathological
™ Stress

2. Environment:
™ Closed
™ Open (Internal/External)

3. Displacement:
™ Undisplaced
™ Displaced (Shift, Angulation, Rotation)

4. Pattern:
™ Transverse, Oblique, Spiral, Comminuted, Segmental

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5. Complexity:
™ Simple
™ Complex

6. Force:
™ High-Velocity
™ Low-Velocity

Reference: Essential Orthopaedics, J. Maheshwari, 5th Edition, Page no. 1-2.

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MedEd FARRE: Surgery

74. (a) D
 escribe the stages of fracture healing, factors affecting the fracture
healing and discuss complications such as delayed union, non-union, and
malunion.

(b) Differentiate primary and secondary bone healing. (5 Marks)

Answer:

FRACTURE HEALING

€ The process of fracture healing shares similarities with the healing of soft tissue
wounds, but unlike soft tissue, which heals with fibrous tissue, bone healing results
in mineralized mesenchymal tissue, i.e., bone.

€ Once a fracture occurs, the healing process initiates immediately and progresses
through a series of distinct stages outlined below.

Stages of Healing

Stage Time Frame Key Features

Haematoma Formation Up to 7 Blood vessels rupture at the fracture
days site, forming a haematoma
Ischaemic necrosis occurs in fracture
ends due to disrupted blood supply
Osteocytes die in the necrotic zone,
while precursor cells are sensitized to
differentiate into daughter cells
Granulation Tissue 2–3 weeks Precursor cells differentiate into
fibroblasts, osteoblasts, and
vascular endothelial cells
A soft granulation tissue forms,
which anchors the fracture fragments
Blood clot is replaced with a fibrous
mesh, allowing capillary ingrowth
Callus Formation 4–12 weeks Fibroblasts create a collagen matrix,
which mineralizes with calcium salts
to form a woven bone (Callus)
Callus bridges fracture ends and
provides stability; visible radiologically
in ~3 weeks

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 Orthopedics

Remodelling 1–2 years Woven bone is replaced by lamellar

bone through a multicellular unit-
based process
Callus resorption and structural
reorganization occur

Modelling Many years Cortical and periosteal surfaces are

reshaped, restoring bone’s original
structure
Influenced by weight-bearing and
muscle stresses during functional
recovery

FACTORS AFFECTING FRACTURE HEALING

€ Several intrinsic and extrinsic factors influence the rate and quality of fracture
healing:

Intrinsic Factors
1. Age:

™ Children heal faster due to a higher metabolic rate and vascularity. Callus forms
as early as 2 weeks.
™ Healing time doubles in adults compared to children.

2. Type of bone:
™ Cancellous bones heal faster than cortical bones due to their greater vascular
supply.
™ Flat bones (e.g., Skull) heal faster than tubular bones (e.g., Long bones).

3. Fracture pattern:
™ Spiral fractures heal faster than transverse fractures due to a greater surface
area of contact.
™ Comminuted fractures heal slower because of severe trauma and poor vascularity.

4. Vascular supply:
™ Bones with poor blood supply (e.g., Scaphoid) take longer to heal or may not heal
at all.

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MedEd FARRE: Surgery

Extrinsic Factors
1. Reduction quality:
™ Proper alignment ensures contact between fracture fragments, promoting faster
healing.

2. Immobilization:
™ Rigid fixation prevents mobility at the fracture site, critical for healing.

3. Compression:
™ Increases rigidity and enhances healing in cancellous bones.

4. Open fractures:
™ Soft tissue disruption and infection risks can lead to delayed or impaired healing.

Pathoanatomical Changes
1. Soft tissue interposition:
™ Surrounding tissue blocks callus formation, hindering healing.

2. Ischaemic necrosis:
™ Occurs due to interrupted blood supply at fracture ends.

Complications in Fracture Healing

1. Delayed union:
™ Healing takes longer than expected due to:
 Poor blood supply
 Infection at the fracture site
 Inadequate stabilization

2. Non-union:
™ Permanent failure of healing due to:
 Soft tissue interposition
 Severe vascular disruption
 Infection or improper fixation
™ Types:
 Hypertrophic Non-Union: Excessive callus formation but failure to unite.
 Atrophic Non-Union: No callus formation due to poor vascularity.

3. Malunion:
™ Fracture heals in an incorrect position, leading to:
 Deformity
 Reduced functionality

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 Orthopedics

PRIMARY VS SECONDARY BONE HEALING

Parameter Primary Healing Secondary Healing

Mechanism Requires direct cortical Occurs naturally via multiple

contact stages

Callus Formation No visible callus Visible callus on X-rays

Process Bone heals directly without Involves haematoma, callus, and

intermediate stages remodelling

Indication Operative fixation with rigid Non-operative treatment or

stabilization minimal fixation
Note:
€ Mnemonic for Stages: H-G-C-R-M
™ (Haematoma → Granulation → Callus → Remodelling → Modelling)
€ Factors:
™ “A TOP Bone Heals Faster”
 (Age, Type, Open fracture, Pathoanatomy, Bone type)
€ Complications:
™ D-N-M (Delayed Union, Non-Union, Malunion)

Reference: Essential Orthopaedics, J. Maheshwari, 5th Edition, Page no. 10.

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MedEd FARRE: Surgery

75. Define fat embolism syndrome. Discuss its pathogenesis, clinical features,
diagnosis, and management. (5 Marks)

Answer:

FAT EMBOLISM SYNDROME (FES)

Definition
€ Fat Embolism Syndrome (FES) is a severe complication following fractures,
particularly in long bones or major trauma. It is characterized by the occlusion of
small blood vessels by fat globules, leading to systemic dysfunction.

Pathogenesis
1. Release of free fatty acids:
™ Fat globules originate from bone marrow or adipose tissue, particularly
following major or multiple fractures.
™ Lipases act on neutral fats, releasing free fatty acids, inducing toxic vasculitis.

2. Platelet-fibrin thrombosis:
™ Platelet aggregation occurs alongside fibrin formation.
™ This leads to small pulmonary vessel obstruction.

Clinical Features
€ Symptoms usually appear 24–48 hours after the injury. The manifestations can be
divided into pulmonary, cerebral, and cutaneous features:
1. Pulmonary symptoms:
™ Tachypnea (Rapid breathing).
™ Hypoxia (Low oxygen levels).
™ Respiratory distress.

2. Cerebral symptoms:
™ Drowsiness
™ Restlessness and disorientation.
™ Progression to coma in severe cases.

3. Cutaneous symptoms:
™ Petechial rash, especially on:
 Neck
 Anterior axillary folds
 Chest
 Conjunctiva

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 Orthopedics

4. Other signs:
™ Tachycardia (Increased heart rate).

™ Fever in some cases.

Diagnosis of FES

Clinical suspicion:
€ Patients with multiple or major fractures.

€ Development of respiratory and neurological symptoms within 24–48 hours.

Diagnostic tools:

Parameter Finding

Sputum/Urine Analysis € Fat globules detected in sputum or urine.

Chest X-ray € Patchy pulmonary infiltration, resembling a

"snowstorm.”

Retinal Exam € Signs of retinal artery emboli, such as striate

hemorrhages and exudates.

Arterial Blood Gas € Partial pressure of oxygen (PaO₂) < 50 mmHg,

indicating severe hypoxia.

Management of Fat Embolism Syndrome

€ The management of FES is primarily supportive and aims to stabilize the patient while
minimizing further complications.

Treatment measures:

Intervention Description
Respiratory Support € 100% oxygen therapy.
€ Assisted ventilation for severe hypoxia or respiratory
failure.
Heparinisation € Reduces the risk of thrombosis and improves circulation.
Corticosteroids € Reduces inflammation caused by vasculitis and
systemic immune response.
Intravenous Therapy € Low molecular weight dextran (e.g., Lomodex-20) to
improve blood flow.
€ Dextrose with 5% alcohol to emulsify fat globules (Used
by some).

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MedEd FARRE: Surgery

Key Learning Tips

To make this content easily memorable:
1. Acronyms for features:
™ FES Triad: Respiratory (Tachypnea), Neurological (Drowsiness), Skin (Petechial
Rash).
™ Pulmonary + Cerebral + Rash: Core signs to identify FES.

2. Mnemonic for diagnosis: “SCORE”:

™ S: Sputum/Urine (Fat globules).
™ C: Chest X-ray (Snowstorm appearance).
™ O: Oxygen levels (PaO₂ < 50 mmHg).
™ R: Retinal artery emboli (Striate hemorrhages).
™ E: Early suspicion (Multiple fractures).

Reference: Essential Orthopaedics, J. Maheshwari, 5th Edition, Page no. 43.

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 Orthopedics

76. What is compartment syndrome? Discuss its causes, pathophysiology, clinical

features, and management, including surgical interventions. (5 Marks)

Answer:

COMPARTMENT SYNDROME

Definition
€ A rise in pressure within a confined space (Compartment) formed by bones,
fascia, and interosseous membranes, leading to reduced blood supply to muscles
and nerves leading to ischemia and necrosis.

Causes:
1. Primary causes:
™ Any injury causing muscle edema.
™ Fracture hematoma: Bleeding within the compartment from fractures.
™ Ischemia-related muscle swelling leading to further edema.

2. Common triggering injuries:

™ Supracondylar fractures of the humerus
™ Forearm bone fractures
™ Closed tibial fractures
™ Crush injuries (Legs or forearm)

Pathophysiology
The condition is initiated by trauma or another factor increasing compartment
pressure. The sequence is as follows:

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MedEd FARRE: Surgery

1. Initial events:
™ Trauma → Muscle ischemia (Reduced blood flow)
™ Ischemia causes histamine release, increasing capillary permeability.

2. Cycle of worsening pressure:

™ Increased capillary permeability → Intramuscular edema → Venous occlusion
™ Venous occlusion → Raised intracompartmental pressure → Further ischemia

3. Outcome:
™ Tissue ischemia causes muscle necrosis and nerve damage.
™ Necrotic muscle heals with fibrosis, resulting in contractures and functional
impairment.
™ Severe cases may lead to gangrene or permanent disability.

Clinical Features
1. Symptoms:
™ Pain: Severe pain disproportionate to the injury. Not relieved by analgesics.
™ Pain on Stretching: Stretching of muscles in the compartment (e.g., Passive
extension of fingers in the flexor compartment) causes sharp pain (Positive stretch
test).

2. Signs:
™ Tense, swollen compartment: Feels tight and firm on palpation.
™ Sensory Changes:
 Hypoesthesia or anesthesia over the affected area (Nerves compressed).
™ Muscle Weakness: Weakness or inability to move the limb actively.

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 Orthopedics

3. Late Features:
™ Absent pulses (May remain normal early but disappear as the condition worsens).

™ Tissue necrosis, gangrene, or permanent deformity.

Diagnosis

1. Clinical Diagnosis:
™ Based on high suspicion in patients with injuries known to cause compartment
syndrome.
™ Symptoms: Severe pain, tight compartments, and sensory deficits.

2. Stretch Test:
™ Passive movement of joints opposite to the muscle’s action elicits sharp pain (Early
indicator).

3. Compartment Pressure Monitoring:

™ A pressure exceeding 40 mmHg within the compartment is diagnostic.

Management
€ Management of compartment syndrome is aimed at preventing further tissue damage
and restoring normal blood supply

1. Conservative measures:
™ Limb Elevation: To reduce edema and venous congestion.

™ Active Finger/Toe Movements: Helps promote circulation and reduces swelling.

2. Definitive surgical treatment:

™ Fasciotomy:

 The deep fascia is cut longitudinally to release pressure.

 Example: Fasciotomy of the forearm for upper limb compartment syndrome.

™ Fibulectomy:

 In the leg, the middle third of the fibula is excised to decompress all compartments.

Complications
1. Ischemic contractures:
™ Necrotic muscles heal with fibrosis, causing joint stiffness and deformity.

™ Example: Volkmann’s ischemic contracture in the forearm.

2. Nerve damage:
™ Permanent sensory and motor deficits due to prolonged ischemia.

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 MedEd FARRE: Surgery

3. Gangrene:
™ Necrosis progressing to tissue death

4. Limb Amputation:
™ In extreme cases, to prevent systemic infection or sepsis.

Key Points
€ 5 Ps of Compartment Syndrome: Pain, Pallor, Paresthesia, Paralysis, Pulselessness.
€ Stretch Test: Earliest diagnostic tool.
€ Pressure >40 mmHg: Confirms diagnosis
€ Fasciotomy Saves Limbs: Always perform early if suspected.

Reference: Essential Orthopaedics, J. Maheshwari, 5th Edition, Page no. 47.

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77. Define Volkmann’s ischemic contracture. Explain its etiology, classification,

pathophysiology, clinical features and management strategies. (5 Marks)

Answer:

VOLKMANN’S ISCHEMIC CONTRACTURE (VIC)

Definition:
€ Volkmann’s Ischemic Contracture (VIC) is a sequela of untreated or severe
Volkmann’s ischemia, where the muscles of the forearm are replaced by fibrous
tissue due to prolonged ischemia.
€ This fibrous tissue contracts, pulling the wrist and fingers into permanent flexion
deformity.
€ Severe cases may involve sensory loss and motor paralysis in the forearm and hand
if nerves are affected.

Etiology
€ Primary cause:
™ Ischemia due to compartment syndrome or tight external bandages, which
compress the forearm muscles and blood vessels.
€ Triggering factors:
™ Improper management of supracondylar fractures of the humerus.
™ Application of tight splints or plaster casts.
™ Trauma or injuries causing increased compartmental pressure in the forearm.

Classification
Based on the severity and extent of contracture:

Grade Description Features

Mild Limited contracture Slight wrist and finger flexion deformity.

Moderate Moderate Wrist and finger flexion deformity with muscle

contracture fibrosis.

Severe Extensive contracture Severe deformity with bony abnormalities and

nerve loss.

Pathophysiology
1. Compartment syndrome:
™ Increased compartmental pressure in the forearm leads to decreased blood
supply (Ischemia) to the flexor muscles.

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MedEd FARRE: Surgery

2. Muscle necrosis:
™ Prolonged ischemia results in irreversible muscle necrosis and replacement of
muscle tissue with inelastic fibrous tissue.

3. Deformity formation:
™ Fibrous tissue shortens, leading to flexion deformity of the wrist and fingers.

4. Neurological impairment:
™ Nerve involvement causes sensory and motor loss in severe cases.

Clinical Features

1. Deformity:
™ Permanent flexion deformity of the wrist and fingers.

2. Volkmann’s sign:
™ Key diagnostic sign: Fingers can only be fully extended at the interphalangeal
joints when the wrist is flexed.

(a)

(b)
(a) Volkmann’s Ischaemic Contracture (VIC)
(b) Volkmann’s sign

3. Muscle atrophy:
™ Marked wasting of forearm muscles.

4. Skin and nail changes:

™ Dry, scaly skin over the forearm and hand.

™ Atrophic nails due to lack of blood supply.

5. Neurological symptoms:
™ Sensory loss (Hypoesthesia/anesthesia) and motor paralysis in severe cases.

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 Orthopedics

Management Strategies
1. Acute phase (Volkmann’s Ischemia)
™ Immediate removal of any external splints, casts, or bandages causing compression.
™ Elevate the forearm to relieve pressure.
™ Encourage movement of the fingers to improve blood flow.
™ If no improvement within 2 hours, perform a fasciotomy to release pressure by
cutting the fascia around the affected muscles.

2. Established volkmann’s ischemic contracture

Management depends on the severity of the deformity:

Severity Treatment Approach

Mild Deformity € Passive stretching using a turn-buckle splint (Volkmann’s

splint).

Moderate Deformity € Soft tissue sliding operations (e.g., Maxpage operation),

releasing flexor muscles from their origin.

Severe Deformity € Bone surgeries, such as forearm bone shortening or

carpal bone excision, may be required.

Rehabilitation
€ Postoperative physical therapy is essential to regain strength and function.
€ Early mobilization and regular exercises prevent recurrence and improve outcomes.

Reference: Essential Orthopaedics, J. Maheshwari, 5th Edition, Page no. 102.

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78. Explain the causes, clinical presentation, diagnostic methods, and management
of ulnar nerve palsy. (5 Marks)

Answer:

ULNAR NERVE PALSY

€ Ulnar nerve palsy refers to the functional impairment of the ulnar nerve, affecting
motor and sensory functions.

Anatomy of the Ulnar Nerve

Understanding the anatomy aids in locating the lesion:

1. In the arm:
™ Originates from the medial cord of the brachial plexus.

™ Runs medial to the axillary artery and posterior to the medial epicondyle.

2. In the forearm:
™ Passes between the two heads of the flexor carpi ulnaris.

™ Supplies the flexor carpi ulnaris and medial half of the flexor digitorum profundus.

3. At the wrist:
™ Divides into superficial and deep branches to supply the hypothenar muscles
and intrinsic hand muscles.

Causes of Ulnar Nerve Palsy

Ulnar nerve palsy can result from various injuries or conditions affecting the nerve
along its anatomical course:

1. High ulnar nerve palsy (Injury proximal to the elbow):

™ Causes:

 Fractures of the medial epicondyle.

 Elbow dislocations or prolonged compression at the elbow.

 Compression or stretching from repetitive movements or trauma.

™ Effect:

 Paralysis of all muscles supplied by the ulnar nerve in the forearm and hand.

2. Low ulnar nerve palsy (Injury distal to the forearm):

™ Causes:

 Fractures of the wrist or compressive neuropathy near the Guyon’s canal.

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 Orthopedics

™ Effect:
 Sparing of forearm muscles with paralysis restricted to the hand muscles.

Clinical Presentation
A. Motor deficits:

1. High ulnar nerve palsy:

™ Paralysis of:
 Flexor carpi ulnaris.
 Medial half of the flexor digitorum profundus.
 All intrinsic hand muscles supplied by the ulnar nerve (Hypothenar muscles,
interossei, adductor pollicis, and medial two lumbricals).

2. Low ulnar nerve palsy:

™ Paralysis of only intrinsic hand muscles supplied by the ulnar nerve.

B. Sensory deficits:
™ Loss of sensation in the skin over the medial side of the hand (Little finger
and medial half of the ring finger).
™ Sensory deficit remains the same for both high and low ulnar nerve palsy.

C. Characteristic deformities:
™ Claw Hand: Hyperextension at the metacarpophalangeal joints and flexion at
the interphalangeal joints of the fourth and fifth fingers due to loss of lumbricals
and interossei function.

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Diagnostic Methods

1. Flexor carpi ulnaris test:

™ The patient attempts to flex the wrist against gravity.

™ The hand deviates towards the radial side if the flexor carpi ulnaris is paralyzed.

2. Abductor digiti minimi test:

™ The patient abducts the little finger against resistance.

™ Weakness indicates ulnar nerve damage.

3. Interossei function tests:

™ Egawa’s test:

 The patient keeps the hand flat on a table and moves the middle finger side-
to-side.
 Inability to do so indicates paralysis of the dorsal interossei.
™ Card test:

 A card is inserted between extended fingers. The patient is asked to grip it

tightly.
 Weakness indicates impaired palmar interossei function.

4. Froment’s sign (Book test):

™ The patient grips a book between the thumb and index finger.

™ A positive sign is when the patient compensates by flexing the thumb’s

interphalangeal joint, indicating adductor pollicis paralysis.

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 Orthopedics

Management
A. Conservative treatment:

1. Immobilization: Resting the affected limb using splints.

2. Medications:
™ Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) to reduce pain and inflammation.

3. Physiotherapy:
™ Strengthening exercises for unaffected muscles.
™ Preventing contractures with range-of-motion exercises.

B. Surgical rreatment:

1. Nerve decompression:
™ Relieves pressure at the site of entrapment (e.g., Medial epicondyle or Guyon’s
canal).

2. Nerve transposition:
™ Relocates the ulnar nerve to a less vulnerable position.

3. Tendon transfers:
™ Restores lost motor function in chronic or severe cases.

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Summary of Key Details

Aspect Details
Causes High (Above elbow): fractures/dislocations; Low (Wrist):
compression/fractures.
Motor High: paralysis of forearm + hand muscles; Low: paralysis of
Impairment hand muscles.
Sensory Loss of sensation in the medial hand (Ring and little finger).
Impairment
Deformities Claw hand deformity (Hyperextension + flexion of medial fingers).
Tests Egawa’s test, card test, Froment’s sign.
Management Rest, physiotherapy, nerve decompression, or tendon transfer.
Reference: Essential Orthopaedics, J. Maheshwari, 5th Edition, Page no. 67.

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 Orthopedics

79. a) Compare ulnar and radial nerve palsies.  (5 Marks)

b) Describe the etiology, clinical features, diagnostic approach, and treatment

of radial nerve palsy.

Answer:

COMPARISON OF ULNAR AND RADIAL NERVE PALSIES

Feature Ulnar Nerve Palsy Radial Nerve Palsy

Anatomy € Arises from the medial cord € Continuation of the

of the brachial plexus. posterior cord of the
brachial plexus.

Motor Deficits € Paralysis of intrinsic € Paralysis of triceps,

hand muscles (Lumbricals, brachioradialis, wrist
interossei) leads to claw extensors, and finger
hand. extensors results in wrist
and finger drop.

Sensory Deficits € Loss of sensation in the € Loss of sensation in the

medial 1.5 fingers and posterior arm, forearm,
adjacent palm. and dorsal hand (Except
fingertips).

Clinical Features € Claw hand due to unopposed € Wrist drop and inability
action of extensors to extend fingers at the
and hyperextension of metacarpophalangeal joints
metacarpophalangeal joints. (Finger drop).

Etiology € Fractures of the medial € Fractures (Humeral shaft,

epicondyle, cubital tunnel radial groove), prolonged
compression, or trauma. compression, or penetrating
injuries.

Special Tests € Froment’s sign: Weak € Testing muscle strength

pinch grip due to thumb of triceps, brachioradialis,
compensation. and wrist extensors.

Treatment € Splinting, physical therapy, € Splinting, physiotherapy,

or surgical decompression for or surgical intervention in
severe cases. severe cases of entrapment
or nerve rupture.

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MedEd FARRE: Surgery

RADIAL NERVE PALSY

Etiology
1. High radial nerve palsy:
™ Occurs in the radial groove (Mid-shaft humeral fractures, compression from prolonged
pressure).
™ Muscles Affected: Triceps (Sometimes spared), brachioradialis, wrist extensors,
and finger extensors.
™ Results in wrist drop and partial or complete loss of finger extension.

2. Low radial nerve palsy:

™ Occurs near the elbow (e.g., Radial head fractures, forearm trauma).
™ Muscles Affected: Brachioradialis and distal forearm extensors like extensor carpi
radialis longus and brevis.
™ Wrist extension remains partially functional.

Clinical Features
1. Motor deficits:
™ Triceps: Inability to extend the elbow fully against resistance, especially noticeable
in high radial nerve palsy.
™ Brachioradialis: Weak elbow flexion in mid-pronation when tested against
resistance.
™ Wrist Extensors: Inability to extend the wrist leads to wrist drop, a hallmark of
radial nerve palsy.
™ Finger Extensors: Finger drop with the inability to extend metacarpophalangeal
joints.
™ Extensor Pollicis Longus: Inability to extend the thumb at the interphalangeal
joint.
2. Sensory deficits:
™ Numbness or loss of sensation in the radial nerve distribution:
 Posterior arm and forearm.
 Dorsal aspect of the hand (Excluding the fingertips).

Diagnostic Approach
1. History:
™ Look for trauma, fractures (Humerus), or prolonged compression (e.g., Crutch use,
tourniquet injury).
2. Clinical examination:
™ Motor Tests: Evaluate affected muscles.
 Triceps: Resistance during elbow extension.

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 Orthopedics

 Brachioradialis: Resistance during elbow flexion in mid-pronation.

 Wrist Extensors: Resistance to wrist extension.
 Finger Extensors: Attempted extension of fingers at metacarpophalangeal joints.
™ Sensory Tests: Assess loss of sensation on the posterior aspect of the arm, forearm,
and hand dorsum.
3. Imaging studies:
™ X-ray to identify fractures of the humerus or elbow.
™ MRI for soft tissue or nerve compression causes.

Treatment
A. Non-surgical management:
1. Splinting:
 Use a wrist cock-up splint to prevent wrist drop and provide functional support.

2. Physical Therapy:

 Strengthening exercises to maintain muscle function and prevent atrophy.
 Electrical stimulation may be used to promote muscle recovery.

B. Surgical management:
1. Indications: Severe injuries (Nerve laceration, prolonged compression, or non-
healing fractures).
2. Procedures:

 Nerve decompression for entrapment syndromes.
 Nerve repair or grafting for severe damage.

Tips for Easy Learning

1. Mnemonic for high vs. Low radial palsy:
™ High: “Wrist and finger issues but triceps spared.”
™ Low: “Wrist extension spared, distal muscles weak.”

2. Key clinical signs:

™ Wrist drop = hallmark of radial nerve palsy.
™ Claw hand = typical of ulnar nerve palsy.

Reference: Essential Orthopaedics, J. Maheshwari, 5th Edition, Page no. 65.

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 Radiology
69. What is MRCP? Discuss it briefly. (5 Marks)

Answer:

MRCP

€ MRCP stands for Magnetic Resonance Cholangiopancreatography.

€ It is a non-invasive imaging technique used to visualize the biliary tree, pancreatic
ducts, liver, gallbladder, and surrounding structures.
€ MRCP is performed using Magnetic Resonance Imaging (MRI) and is highly
effective in diagnosing disorders of the biliary and pancreatic systems.

Key Features
1. Purpose:
™ Provides detailed imaging of the biliary tree and pancreatic ducts.
™ Helps in diagnosing conditions like:
 Obstruction (e.g., By stones or tumors)
 Strictures (Narrowing of ducts)
 Congenital anomalies (e.g., Biliary atresia)
 Inflammatory diseases (e.g., Pancreatitis)
 MedEd FARRE: Surgery

2. Advantages:
™ Non-invasive: Unlike ERCP, it does not require insertion of an endoscope or
cannulation of ducts.
™ Radiation-free: Utilizes magnetic fields instead of ionizing radiation.
™ Contrast-free in most cases: Does not depend on iodine-based contrast agents,
making it safer for individuals with renal insufficiency or allergies.
™ Ability to identify intrahepatic and extrahepatic abnormalities.

3. Procedure:
™ Patients are positioned in an MRI scanner.
™ Utilizes T2-weighted sequences to differentiate fluid-filled structures (Like bile
and pancreatic ducts) from surrounding tissues.
™ Duration: Typically lasts 15–30 minutes, with minimal patient preparation required.

Clinical Applications
€ Biliary Obstruction: To identify and locate stones (Choledocholithiasis) or tumors
causing blockages.
€ Pancreatitis Evaluation: To detect ductal disruptions, strictures, or pseudocysts.
€ Congenital Anomalies: For conditions like biliary atresia or choledochal cysts.
€ Pre-surgical Planning: Provides clear ductal anatomy before biliary or pancreatic
surgeries.
€ Post-surgical Monitoring: Assesses complications like leaks or strictures after
procedures like cholecystectomy or transplantations.

Limitations
€ Motion artifacts: Breath-holding may be challenging for some patients.
€ Small lesion detection: May not identify very small stones or strictures.
€ MRI contraindications: Not suitable for patients with metallic implants,
claustrophobia, or severe obesity.
Reference: Grainger & Allison’s Diagnostic Radiology, 7th Edition, Page no. 1598.

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 Radiology

70. a) W
 hat is ERCP? Enumerate the indications and complications with a brief
note of procedure of ERCP.

b) Differentiate between MRCP and ERCP. (5 Marks)

Answer:

ERCP

€ Endoscopic Retrograde Cholangiopancreatography (ERCP) is a diagnostic and

therapeutic procedure used to visualize the bile ducts, pancreatic ducts, and
gallbladder.
€ Combines endoscopy and fluoroscopy to identify and treat conditions affecting the
hepatobiliary and pancreatic systems.

Indications of ERCP
1. Diagnostic indications:
™ Suspected choledocholithiasis (Bile duct stones).
™ Evaluation of biliary strictures or obstructions.
™ Suspected pancreatic ductal abnormalities.
™ Detection of biliary or pancreatic malignancies.

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2. Therapeutic indications:
™ Removal of bile duct stones.
™ Placement of stents in biliary or pancreatic ducts.
™ Treatment of biliary leaks.
™ Management of cholangitis or pancreatitis due to duct obstruction.

Complications of ERCP
1. Common complications:
™ Pancreatitis (Most frequent)
™ Bleeding post-sphincterotomy
™ Infection such as cholangitis

2. Less common complications:

™ Perforation of the duodenum or biliary ducts.
™ Adverse reactions to sedation or contrast agents.

Procedure of ERCP
1. Preparation:
™ The patient fasts for at least 6–8 hours before the procedure.
™ Sedation or general anesthesia is administered.

2. Procedure:
™ A duodenoscope is advanced through the mouth to the duodenum.
™ A catheter is passed into the bile or pancreatic ducts under fluoroscopic guidance.
™ Contrast dye is injected to obtain radiographic images.
™ Therapeutic interventions, such as stone removal or stenting, are performed if
needed.
3. Post-procedure care:
™ Monitor for signs of complications such as pain or fever.
™ Patients are observed for a few hours to ensure recovery from sedation.

DIFFERENCES BETWEEN MRCP AND ERCP

Feature MRCP ERCP

Full form Magnetic Resonance Endoscopic Retrograde

Cholangio pancreatography Cholangio pancreatography

Nature Non-invasive imaging technique Invasive diagnostic and

therapeutic procedure

Purpose Purely diagnostic to visualize Both diagnostic and

biliary and pancreatic ducts therapeutic

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 Radiology

Procedure Uses MRI technology with Uses endoscope and

contrast (If needed) fluoroscopy with contrast dye

Sedation No sedation required Sedation or general anesthesia

is required

Complications Minimal risk (Contrast reaction Risk of complications like

in rare cases) pancreatitis, bleeding, or
infection

Therapeutic None Can perform interventions like

ability stone removal, stenting

Indications Initial evaluation of biliary or When therapeutic intervention

pancreatic diseases or detailed imaging is needed

Reference: Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, 11th Edition,
Page no. 1448-1451.

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71. What is Intravenous Pyelography (IVP)? Describe its indications, contraindi-

cations and procedures. (5 Marks)

Answer:

INTRAVENOUS PYELOGRAPHY (IVP)

€ Intravenous Pyelography (IVP), also referred to as Intravenous Urogram (IVU), is

a diagnostic imaging technique used to study the kidneys, ureters, and bladder.
It involves the injection of a radiopaque contrast dye into a vein to visualize the
urinary tract using X-ray imaging.

Indications of IVP

1. Congenital abnormalities:
™ Polycystic kidney

™ Horseshoe kidney

™ Single kidney or duplication of kidneys and ureters.

2. Hydronephrosis:
™ Identification of renal dilation or obstruction.

3. Obstruction:
™ Detection at the pelviureteric junction or along the ureters.

™ Identifying causes like primary obstructed megaureter.

4. Renal stones:
™ Evaluation of renal, ureteric, or bladder stones.

5. Tumors and tuberculosis:

™ Identification of renal malignancies or tuberculosis lesions.

Contraindications of IVP

1. Iodine allergy: Test dose of contrast must be administered beforehand.

2. Renal failure: Inefficiency of kidneys to excrete the dye.

3. Multiple myeloma: Dye precipitation worsens obstruction, causing anuria.

4. Hyperuricemia: Uric acid crystals block renal tubules.

5. Sickle cell anemia: Risk of triggering a sickle cell crisis.

6. Dehydration: Increases nephrotoxicity risk from the contrast.

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 Radiology

Procedure for IVP

Preparation:
€ Dietary guidelines:
™ A fat-free, non-residual diet is recommended for 2–3 days before the procedure
to minimize bowel gas shadows.
™ Administration of dimol tablets (3 times daily for 2–3 days) to clear intestinal gas.
€ Fasting and hydration:
™ Patients are required to fast for 6 hours before the procedure.
€ Radiological contrast agent:
™ 45% sodium diatrizoate (20–40 mL) is injected intravenously, usually via the
median cubital vein.

Requirements before IVP:

1. Renal function evaluation:
™ Serum creatinine (0.5–2.0 mg%) must be tested for safety.
™ Urea is less reliable due to hydration variations.

2. Preliminary imaging:
™ Plain X-ray of Kidneys, Ureters and Bladder (KUB) is taken to differentiate between
renal and gall stones.

Precautions while injecting dye:

€ Administer dye slowly to avoid reactions.
€ Monitor for extravasation of dye at the injection site.
€ In allergic patients, premedication with bronchodilators or hydrocortisone (100 mg
IV) may be administered.
€ Antihistamines should be used in case of skin rash or urticaria.

Radiography
1. Nephrogram phase:
™ Images taken 2–5 minutes post-injection to outline kidney structure.

2. Pelvicalyceal system:
™ Visualized 5 minutes post-injection.

3. Bladder and ureters:

™ Detected 15–20 minutes post-injection

4. Post-void imaging:
™ To detect any residual contrast in the bladder.
™ Abdominal compression may be applied for better pyelogram visibility.

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MedEd FARRE: Surgery

Uses of IVP in Surgery

Intraoperative one-shot IV pyelogram:
€ Used during urological injuries where instability prevents prolonged imaging.
€ 2 mg/kg IV contrast is administered approximately 10 minutes before intraoperative
imaging to evaluate ureters and kidneys.

Key Imaging Observations During IVP

1. Normal findings:
™ Clear visualization of kidneys, ureters, and bladder.
™ No blockages or anatomical variations.

2. Pathological findings:
™ Hydronephrosis
™ Double ureter
™ Evidence of bowel gas interference

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Reference: Manipal Manual of Surgery, 4th Edition, Page no. 924.

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MedEd FARRE: Surgery

72. State imaging approach in a patient with blunt abdominal trauma. What is
FAST? Discuss the role of FAST in evaluation of trauma patients. (5 Marks)

Answer:

BLUNT ABDOMINAL TRAUMA - IMAGING APPROACH

Blunt Abdominal Trauma (BAT) can result in significant internal injuries. Early
detection and proper imaging are crucial for managing such cases. The imaging approach
depends on the patient’s hemodynamic status.

Steps in Imaging Approach

1. Primary survey and initial stabilization:
™ ABCs (Airway, Breathing, Circulation) are prioritized.
™ Begin with Focused Assessment with Sonography for Trauma (FAST) to assess
for internal bleeding.
2. Stable patients:
™ FAST is often the initial imaging.
™ Followed by a contrast-enhanced CT scan to evaluate:
 Solid organ injuries
 Retroperitoneal hematomas
 Active bleeding

3. Unstable patients:
™ Perform FAST to confirm intra-abdominal bleeding.
™ Positive FAST findings with instability usually require emergency laparotomy.

4. Other imaging modalities:

™ X-ray: For chest and pelvis to assess for fractures.
™ MRI: Rarely used but beneficial for specific cases like pediatric injuries.
™ DPA/DPL (Diagnostic Peritoneal Aspiration/Lavage):
 Used in inconclusive FAST or unavailability of advanced imaging.

FAST

Definition
€ FAST (Focused Assessment with Sonography for Trauma) is a bedside ultrasound
technique used to detect free fluid (Blood) in trauma patients, indicating internal
hemorrhage.

Key Areas Scanned

1. Perihepatic area (Morrison’s pouch)
2. Perisplenic area

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 Radiology

3. Pelvic cavity (Pouch of Douglas/retrovesical pouch)

4. Pericardial sac

eFAST (Extended FAST)

€ Includes evaluation of the pleural spaces to detect pneumothorax or hemothorax.

Indications for FAST

€ Hemodynamically unstable trauma patients.
€ Suspected internal bleeding.
€ Monitoring during ongoing resuscitation.

Role of FAST in Evaluation of Trauma Patients

Advantages of FAST:
1. Speed: Can be performed in 2–5 minutes.
2. Non-invasive: No exposure to radiation.
3. Portability: Useful in bedside or prehospital settings.
4. Dynamic Monitoring: Assists in assessing response to treatment.
Clinical utility:
1. Unstable patients:
™ Identifies intraperitoneal or pericardial fluid quickly.
™ Guides immediate surgical intervention if necessary.

2. Stable patients:
™ Determines if further imaging (e.g., CT) is required.
™ Helps rule out life-threatening injuries.

3. Monitoring in resuscitation:
™ Tracks fluid accumulation and hemorrhage progression.

Limitations of FAST
1. Operator-dependent results
2. Limited in detecting:
™ Retroperitoneal injuries (e.g., Pancreas, kidneys).
™ Hollow organ injuries (e.g., Bowel perforation).

3. May produce false negatives for small fluid volumes.

Reference: Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9th Edition,
Page no. 228–232.

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 Thorax
61. Write a short note on Flail chest. (5 Marks)

Answer:

FLAIL CHEST
€ Flail chest is a life-threatening condition caused by severe chest injuries leading
to instability in the chest wall. This condition significantly impairs breathing and can
result in respiratory failure if not treated promptly.

Features
€ Flail chest occurs when four or more ribs are fractured at two or more places,
leading to the detachment of a portion of the rib cage from the chest wall.
€ This creates a paradoxical movement of the chest:

™ Inspiration: The detached segment moves inward due to negative pressure.

™ Expiration: The segment moves outward

€ Paradoxical respiration leads to:

™ Hypoventilation

™ Carbon dioxide retention

™ Respiratory failure

Causes
€ Severe blunt trauma to the chest, such as:

™ Road traffic accidents

™ Falls from a height

™ Crush injuries

™ Assault with blunt objects

Clinical Presentation
€ Localized swelling, tenderness, and deformity over the chest wall

€ Difficulty breathing and painful respiration

€ Symptoms of hypoxia due to impaired oxygenation

MedEd FARRE: Surgery

Types of Flail Chest

Type Description
Anterior Flail Fracture at the costochondral junction on both
sides of the sternum
Posterior Flail Fracture of the ribs in the posterior chest wall
Lateral Flail Fracture along the shaft of the ribs

Treatment Options
1. Commonly Used Procedures:
™ Anterior flail:
 Stabilized using a seagull-shaped prosthesis to fix flail segments
™ Posterior flail:
 No treatment is needed as the scapula naturally supports flail segments
™ Lateral flail:
 Chest wall stabilization
 Reduction of respiratory dead space
 Treatment of pulmonary contusions
 Pain management using epidural analgesia or intercostal nerve blocks

2. Advanced and Rare Methods:

™ Surgical Stabilization:
 Rarely performed; involves osteofixation or open reduction
™ Internal pneumatic fixation:
 Positive pressure ventilation with intubation for at least 1 week to stabilize flail
segments
™ Physiologic stabilization:
 Use of IPPV (Intermittent Positive Pressure Ventilation) to:
Š Reduce rib deformities
Š Improve oxygenation and pulmonary function

Special Case – “Stove-In Chest”

™ A localized, severe blunt injury causing depression of a portion of the chest wall.
™ Managed similarly to flail chest & Thoracotomy may be required for internal
injuries.

Complications
™ Pneumonia due to impaired lung expansion
™ Atelectasis from incomplete lung inflation

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 Thorax

™ Respiratory failure, if oxygenation is not adequately managed

™ ARDS (Acute Respiratory Distress Syndrome) in severe cases

Key Points to Remember

™ Flail chest impairs ventilation and gas exchange, requiring urgent intervention.
™ Stabilization of the chest wall and adequate pain relief are critical.
™ Advanced methods like internal pneumatic fixation may be lifesaving in severe
cases.
™ Early detection and management of complications like pneumonia and ARDS are
crucial to improve outcomes.

Reference: Manipal Manual of Surgery, 4th Edition, Page no. 1010.

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62. Write a note on thoracic outlet syndrome. What is the cervical rib? Discuss its
management.

Answer:

THORACIC OUTLET SYNDROME (TOS)

€ Thoracic Outlet Syndrome (TOS) refers to B group of disorders caused by the

compression of the neurovascular bundle (Brachial plexus, subclavian artery, and
vein) as it exits the thoracic outlet.
€ Compression occurs between the scalene muscles, 1st rib, and clavicle.

Anatomy of the Thoracic Outlet

€ The thoracic outlet is bounded by:

™ Anteriorly: Manubrium of the sternum

™ Laterally: First rib

™ Posteriorly: Vertebrae of the spine

€ Key structures at risk:

™ Brachial plexus

™ Subclavian artery and vein

Etiology
€ Common causes of compression include:

1. Cervical rib (Most common structural anomaly)

2. Anomalies of the first rib

3. Hypertrophy of muscles (e.g., Subclavius or pectoralis minor)

4. Fibrous bands tethering the neurovascular structures

5. Post-traumatic changes (e.g., Callus formation in clavicular fractures)

Pathophysiology
€ Arterial compression:

™ Leads to stenosis, followed by post-stenotic dilatation

™ Turbulence results in thrombus formation, which can embolize, causing distal

ischemia
€ Neurological compression:

™ Pressure on the C8 and T1 roots

™ Results in sensory and motor deficits

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 Thorax

Clinical Features
1. Neurological symptoms (Most common):
™ Tingling or numbness, especially in the ulnar nerve distribution (C8, T1)
™ Weakness of hand muscles, impacting fine motor skills
™ Wasting of intrinsic hand muscles
™ Special tests:
 Card Test: Difficulty gripping a card due to weakness

 Froment’s Sign: Compensatory thumb flexion to pinch

2. Vascular symptoms:
™ Arterial compression:
 Pain resembling claudication
 Ischemic changes like splinter hemorrhages, cold fingers, and ischemic ulcers
™ Venous compression:
 Swelling of the arm
 Cyanosis or visible venous collaterals

3. Postural symptoms:
™ Aggravated by certain postures or arm elevation
™ Positive EAST (Elevated Arm Stress Test):
 Symptoms reproduce after arm elevation for 3 minutes

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MedEd FARRE: Surgery

Investigations
1. X-ray: Detects cervical ribs or bony abnormalities of the first rib
2. MRI: Identifies soft tissue anomalies or herniated discs
3. Duplex Ultrasonography: Evaluates blood flow to detect stenosis, thrombus, or
aneurysms
4. CT Angiography: Visualizes vascular compression or dilatation

Management of Thoracic Outlet Syndrome

Management depends on the severity and type of compression (Neurological
vs. vascular).
1. Conservative Treatment: Indicated for mild or early symptoms
™ Techniques:
 Posture correction:
Š Strengthening of shoulder girdle muscles
Š Avoidance of repetitive overhead movements

 Physical therapy:
Š Stretching exercises for the scalene and pectoralis muscles

2. Surgical Treatment: Indicated in persistent symptoms or vascular complications

™ Procedures:
 Cervical rib excision:
Š Removal of cervical rib along with its periosteum to prevent recurrence

 Scalenectomy:
Š Resection of hypertrophied scalenus muscles

 Subclavian artery repair:

Š Removal of thrombus or aneurysmal segment

 Sympathectomy:
Š Performed for vascular symptoms resistant to other treatments

CERVICAL RIB

€ A cervical rib is an extra rib arising from the 7th cervical vertebra. It is more
common in females and typically occurs on the right side.

Types of Cervical Ribs

1. Type I: Free bony mass, not connected to any structure
2. Type II: Complete rib attaching to the manubrium

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3. Type III: Incomplete rib (Partly bone, partly fibrous)

4. Type IV: Fibrous band only, not visible on X-rays
Pathophysiology of Cervical Rib
€ Compression of the neurovascular structures occurs at the thoracic outlet, leading to:
€ Neurological symptoms: Weakness, tingling, or atrophy of hand muscles
€ Vascular symptoms: Ischemia due to embolism, thrombosis, or arterial stenosis

Management of Cervical Rib

1. Conservative treatment:
™ Postural correction
™ Physiotherapy to relieve symptoms

2. Surgical treatment:
™ Extrapleural excision of the cervical rib
™ Removal of any fibrous bands or hypertrophied scalene muscles
™ Sympathectomy if ischemia persists
™ Repair of the subclavian artery in case of thrombus or aneurysm

Mnemonic for Causes of TOS : “CERVICAL”

™ C: Cervical Rib
™ E: Enlarged first rib
™ R: Repetitive trauma
™ V: Vascular anomalies
™ I: Idiopathic fibrous bands
™ C: Callus from fractures
™ A: Anomalous muscles
™ L: Lumps/tumors

Quick Table: Comparison of Neurological vs. Vascular TOS

Feature Neurological TOS Vascular TOS

Cause Compression of brachial plexus Compression of subclavian
artery/vein
Symptoms Tingling, numbness, muscle atrophy Claudication, cold extremities
Special Tests Froment’s sign, Card test Absent pulses, cyanosis
Management Physical therapy, scalenectomy Rib excision, artery repair
Reference: Manipal Manual of Surgery, 4th Edition, Page no. 100.

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63. Write a note on pneumothorax.

Answer:

PNEUMOTHORAX

Definition
€ Pneumothorax is the presence of air within the pleural cavity, resulting in lung
collapse and impaired ventilation. It is a frequent complication of chest trauma
and requires timely diagnosis and management to prevent fatal consequences.

Classification of Pneumothorax
1. Simple Pneumothorax:
™ Caused by air entering the pleural cavity, leading to partial or complete lung
collapse.
™ It may occur spontaneously or due to trauma.

2. Open pneumothorax (“Sucking chest wound”):

™ Air enters and escapes through a chest wall defect, creating a “sucking” sound
with each breath.

3. Tension Pneumothorax:
™ Most dangerous form, where air continues to accumulate in the pleural cavity
with each breath but cannot escape.
™ Results in increased intrapleural pressure, mediastinal shift, and significant
compromise of venous return and cardiac output.

Causes of Pneumothorax
1. Chest Trauma: Penetrating or blunt injury.
2. Rib Fractures: Subcutaneous emphysema and lung injury are indicators.
3. Iatrogenic Causes: Post-procedural complications like central line placement or
thoracic surgeries.

Pathophysiology
€ Injury to the lung or chest wall allows air to enter the pleural cavity, collapsing
the lung.
€ In tension pneumothorax, trapped air compresses the heart and great vessels,
reducing venous return, leading to:
™ Hypotension
™ Hypoxia
™ Cardiac arrest (In extreme cases)

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Clinical Features: The “5 Ts”

€ To diagnose pneumothorax, focus on the following key signs:

Feature Details
Tachypnoea Rapid, shallow breathing due to reduced lung function.
Tachycardia Increased heart rate as a compensatory mechanism.
Tympanic percussion Hollow drum-like sound on the affected side.
Total absence of No air movement on auscultation.
breath sounds
Tracheal shift Mediastinum shifts to the opposite side in tension
pneumothorax.
€ Additional findings include cyanosis, hypotension, and distended neck veins in
tension pneumothorax.

Diagnostic Imaging
1. Chest X-ray:
™ Visible collapse of the lung.

™ Mediastinal shift in tension pneumothorax.

2. Key observations:
™ Large bullae can mimic pneumothorax on X-ray.

™ Bilateral pneumothorax is a surgical emergency.

Management of Pneumothorax
1. General Management for All Types
™ Oxygen therapy to maintain adequate oxygenation.

™ Analgesics for pain control.

2. Specific Management for Tension Pneumothorax

™ Do not wait for imaging to confirm diagnosis.

™ Immediate thoracocentesis: Insert a needle at the second intercostal space,

midclavicular line to relieve tension.
™ Follow with Intercostal Chest Tube (ICT) insertion.

Complications
1. Untreated Tension Pneumothorax:
™ Hypoxia, hypotension, and eventual cardiac arrest.

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2. Failure to Adequately Drain Hemothorax:

™ Leads to fibrothorax and empyema.

Indications for Thoracotomy

€ Persistent bleeding: 1000 mL initially or >100 mL/hour for 4 hours.
€ Clotted hemothorax seen on imaging despite ICT placement.

Comparison of Types of Pneumothorax

Type Key Features Management

Closed Air in pleural space, no Observation, chest tube for large air leaks.
wound.
Open Sucking chest wound. Chest wound closure, ICT insertion.
Tension Life-threatening, Needle thoracocentesis followed by a chest
mediastinal shift. tube connected to an underwater seal system.

Remembering Key Points - FASTHUG

To manage pneumothorax in critically ill patients, use the mnemonic FASTHUG:

Letter Action
F Feeding (Usually enteral)
A Analgesia for pain relief.
S Sedation and neurological check.
T Thromboembolism prophylaxis.
H Head elevation (20–30°).
U Ulcer prophylaxis.
G Glucose control
Reference: Manipal Manual Of Surgery, 4th Edition, Page no. 1010.

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64. Write a note on intercostal drainage using a chest tube.

Answer:

INTERCOSTAL DRAINAGE (ICD) USING CHEST TUBE

Definition
€ Intercostal Drainage (ICD) with a chest tube is a procedure used to remove air,
blood, or fluid from the pleural cavity, allowing the lung to re-expand. It is commonly
used in conditions such as pneumothorax, hemothorax, and empyema.

Steps for Chest Tube Insertion

1. Preparation:
™ Position the Patient: Supine with the head elevated at 20–30°.
™ Select the Triangle of Safety:
 Above the level of the nipples.
 Anterior to the midaxillary line.
 Below and lateral to the pectoralis major muscle.

2. Administer Local Anesthesia:

™ Infiltrate local anesthetic to the parietal pleura.

3. Incision and Tube Placement:

™ Make a 2–3 cm incision parallel to the ribs.
™ Use blunt dissection with finger and artery forceps to reach the pleura (Separate
the intercostal muscles).
™ Insert the tube obliquely, making a short tunnel to minimize leaks.
™ Fix the tube with good sutures and a vertical mattress suture for wound closure.

4. Connection to Underwater Seal:

™ Attach the chest tube to an underwater seal system to ensure unidirectional
flow.

Precautions (Ten Commandments of Using ICT-ICD)

Precaution Details
Triangle of Safety Ensure insertion within the triangle to prevent damage
to vital structures.
Direct Tube Direct the tube towards the apex in pneumothorax and
hemothorax.
Empyema Cases Direct the tube towards the base for empyema drainage.

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Ensure Holes Confirm all holes are within the thoracic cavity.
Connect to Underwater To allow proper drainage.
Seal
Observe Fluid Column Check movement of fluid with respiration.
Post-Insertion X-ray To confirm the correct position of the tube.
Prevent Tube Kinking Avoid bends that can block drainage.
Avoid Clamping in Leak Do not clamp the tube if air leakage is present.
Keep Below Patient Level Always keep the drainage system below patient level to
prevent backflow.

ICT Removal
€ Ensure lung expansion with no drainage (Less than 100 mL for 24 hours).
€ Confirm via chest X-ray.
€ Clamp the tube for 24 hours before removal.
€ Remove the tube after ensuring lung stability.

Indications for Chest Tube Insertion

€ Pneumothorax: Air in pleural space.
€ Hemothorax: Blood in pleural space.
€ Empyema: Pus in pleural cavity.
€ Trauma: Rib fractures with lung injury.

Complications and Prevention

1. Complications:
™ Tube dislodgement.
™ Infection
™ Subcutaneous emphysema.

2. Prevention:
™ Secure tube with sutures.
™ Ensure proper placement and monitoring.

Management of Lung Lacerations

™ Minor Lacerations: Treat with intercostal chest tube.
™ Major Lacerations: May require thoracotomy and repair.

Reference: Manipal Manual Of Surgery, 4th Edition, Page no. 1013.

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65. Write a note on hemothorax

Answer:

HEMOTHORAX

Definition
€ Hemothorax is the accumulation of blood in the pleural cavity, often resulting
from trauma to the chest. It can lead to respiratory compromise and requires prompt
management.

Causes
€ Injury to Major Vessels:
™ Internal mammary artery
™ Intercostal arteries

™ Vascular lung adhesions

Clinical Features
€ Signs and symptoms:

™ Reduced chest expansion on the affected side.

™ Dullness to percussion

™ Absent breath sounds on the affected side.

™ Hemothorax may be delayed or recur after several days.

€ Radiological findings:

™ May be missed on chest X-ray in the supine position.

™ Appears as opacification of the affected side.

Management
1. Initial management:
€ Insert an Intercostal Chest Tube (ICT):
™ Location:

 Second intercostal space (Anterior midclavicular line) for pneumothorax.

 Sixth intercostal space (Midaxillary line) for hemothorax.

™ Triangle of Safety:
 Above the nipples

 Anterior to the midaxillary line.

 Below and lateral to the pectoralis major muscle.

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™ Procedure:
 Infiltrate local anesthetic up to the parietal pleura.
 Make a 2–3 cm incision parallel to the ribs.
 Insert the chest tube with a trocar into the pleural cavity.
 Connect the chest tube to an underwater seal for effective drainage.

2. Indications for thoracotomy:

™ Initial drainage > 1000 mL.
™ Persistent bleeding > 100 mL/hour for 4 hours.
™ Clotted hemothorax (opacity persisting on chest X-ray despite ICT insertion).
™ Features of shock or ongoing hemodynamic instability.

Complications
€ Inadequate drainage may result in:
™ Residual Clotted Hemothorax.
™ Empyema.
™ Late Fibrothorax.

Reference: Manipal Manual Of Surgery, 4th Edition, Page no. 1013.

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