---

SURGERY NOTES FOR MBBS - COMPREHENSIVE STUDY GUIDE

---

TOPIC 1: FLUIDS IN SURGERY

1.1 Body Water Composition (Know This Cold)

• Adult male: 60% of total body weight
• Adult female: 50% (more adipose tissue, less muscle mass)
• Neonates: 80% (decreases to ~65% by age 1)
• Obese individuals: adjust down 10-20%
• Malnourished individuals: adjust up 10%
• Fat and bone have LOW water content; muscle and solid organs have HIGH water content

---

1.2 Osmolality and Starling's Law

Serum Osmolality = 2([Na⁺] + [K⁺]) + BUN/2.8 + Glucose/18

Jv ∝ K[(Pc - Pi) - σ(πc - πi)]

• Net fluid OUT at arteriolar end (high hydrostatic pressure)
• Net fluid IN at venous end (pressure drops, oncotic pressure dominates)
• Albumin (large protein) cannot cross capillary wall - this generates oncotic pressure that pulls fluid back in

• ADH (vasopressin): Released by posterior pituitary in response to hyperosmolality OR decreased plasma volume. Promotes water reabsorption via aquaporins in distal collecting tubule.
• RAAS: Renal hypoperfusion → Renin → Angiotensin I → II → Aldosterone → Na⁺ reabsorption → volume expansion
• ANP (Atrial Natriuretic Peptide): Released in response to atrial stretch; promotes Na⁺ and water excretion

---

1.3 Types of IV Fluids

• Isotonic saline: stays in ECF (1/4 remains in plasma = 250 mL)
• 5% Dextrose: distributes throughout TBW (only 83 mL remains in plasma - very poor expander)

• Albumin (4%, 5%, 20%, 25%): Natural colloid; useful in hypoalbuminaemia
• Gelatin solutions (Haemaccel, Gelofusine): Bovine-derived; may cause anaphylaxis
• Hydroxyethyl starch (Hetastarch, Voluven): Concern over coagulopathy and renal impairment in sepsis
• Dextran: Rarely used now; impairs cross-matching

Key Principle: Colloids stay intravascular longer than crystalloids but are more expensive. Current evidence (SAFE trial, CRISTAL trial) does NOT show clear benefit of colloids over crystalloids in most ICU patients.

---

1.4 Fluid Therapy in Surgical Patients

4 mL/kg/hr for first 10 kg + 2 mL/kg/hr for next 10 kg + 1 mL/kg/hr for remainder

• First 10 kg: 40 mL/hr
• Next 10 kg: 20 mL/hr
• Remaining 50 kg: 50 mL/hr
• Total: 110 mL/hr ≈ 2500 mL/day

• Correct pre-existing deficits (dehydration, vomiting, diarrhoea, bowel prep losses)
• Identify electrolyte abnormalities and correct before elective surgery
• Prolonged fasting deficit = hourly maintenance rate × hours of fasting

• Replace ongoing surgical losses (blood, third-space shifts, evaporative losses)
• Third space losses: 4-8 mL/kg/hr for major abdominal procedures
• Aim for urine output > 0.5 mL/kg/hr
• Balanced salt solutions (LR/Hartmann's) preferred over large volumes of 0.9% NaCl (risk of hyperchloraemic metabolic acidosis)

• Continue maintenance + replace ongoing losses (drains, NG aspirate, stoma output)
• Re-assess frequently - fluid status can change rapidly
• ERAS (Enhanced Recovery After Surgery) protocols promote early oral intake and goal-directed fluid therapy to avoid both under- and over-resuscitation

---

1.5 Electrolyte Abnormalities in Surgical Patients

Sodium Disorders

• Mild: 130-135; Moderate: 120-130; Severe: <120
• Causes: SIADH, GI losses (vomiting/NG suction), renal losses, diuretics, hypotonic fluid overload

• Acute, symptomatic (seizures, coma): 100 mL of 3% hypertonic saline over 10 min, repeat if needed
• Rate of correction: maximum 6 mEq/L in first 24 hours (to avoid central pontine myelinolysis)
• Chronic asymptomatic: correct gradually with fluid restriction ± furosemide

EXAM TRAP: Rapid correction of chronic hyponatremia causes central pontine myelinolysis (osmotic demyelination syndrome) - irreversible spastic quadriparesis and pseudobulbar palsy.

• Causes: Inadequate water intake, excessive sodium administration, diabetes insipidus, osmotic diuresis
• Treatment: Replace free water deficit slowly (correct over 48-72 hrs, max 10-12 mEq/L per day)
• Free water deficit = TBW × (measured Na / 140 - 1)

Potassium Disorders

• Causes: GI losses (vomiting, diarrhoea, prolonged NG suction), diuretics, alkalosis, insulin
• ECG changes: U waves, flat T waves, prolonged QT
• Correction: Oral if mild; IV KCl if severe - NEVER give bolus IV potassium (causes cardiac arrest)
• Max IV rate: 20 mEq/hr with monitoring

• Causes: Renal failure, acidosis, tissue destruction (burns, rhabdomyolysis), massive transfusion
• ECG changes: Peaked T waves → widened QRS → sine wave → VF
• Emergency treatment: Calcium gluconate (membrane stabilisation) → Insulin + 50% Dextrose (shift K into cells) → Salbutamol nebuliser → Sodium bicarbonate if acidotic → Resonium (excretion) → Dialysis if refractory

---

TOPIC 2: RESUSCITATION IN SURGERY

2.1 Classification of Haemorrhagic Shock (ATLS Classes)

Memory tip: "Lost 40% = Lost the plot" - Class IV patients are lethargic/unconscious with near-absent urine output.

• Adult: approximately 70 mL/kg (~5 L for 70 kg adult)
• Child: 80 mL/kg
• Neonate: 90 mL/kg

---

2.2 Initial Resuscitation Approach (ABCDE)

1. IV access: Two large-bore (14-16G) peripheral IV cannulae in antecubital fossa
2. Blood samples: Cross-match, FBC, U&E, LFT, clotting, ABG, lactate
3. Initial fluid bolus:
   • Adults: 500 mL crystalloid (LR/0.9% NaCl) bolus, reassess
   • In trauma: consider permissive hypotension (target SBP 80-90 mmHg) until surgical haemostasis achieved - aggressive fluid resuscitation before controlling haemorrhage worsens outcome
4. Urine catheter: Monitor urine output (target >0.5 mL/kg/hr in adults, >1 mL/kg/hr in children)

---

2.3 Damage Control Resuscitation

• Activated when patient needs >10 units RBC in 24 hours OR replacement of >50% blood volume in 3 hours
• Goal: Deliver products in 1:1:1 ratio (RBC : FFP : Platelets)
• This approximates whole blood and prevents dilutional coagulopathy
• For every unit of RBC, also give 1 unit FFP (plasma) and aim for 1 therapeutic platelet dose per 6 units RBC

1. Hypothermia - impairs enzyme function in coagulation cascade
2. Acidosis - inhibits clotting factor function
3. Coagulopathy - dilutional and consumptive

• HR < 100, SBP > 90
• Urine output > 0.5 mL/kg/hr
• Base deficit improving (target < -6)
• Lactate normalising (normal < 2 mmol/L)
• Temperature > 36°C
• pH > 7.35

• Target SBP 80-90 mmHg in penetrating truncal injuries with uncontrolled haemorrhage
• Rationale: Aggressive fluid resuscitation before haemostasis is achieved displaces clots, dilutes coagulation factors, and worsens hypothermia
• Exception: NOT used in patients with traumatic brain injury (need MAP ≥ 80 to maintain cerebral perfusion pressure)

---

2.4 Special Resuscitation Contexts

• 30 mL/kg crystalloid in first 3 hours
• Reassess with clinical markers after each bolus (HR, BP, capillary refill, UO)
• If persistent hypotension despite fluids: Start noradrenaline (vasopressor)
• Target MAP ≥ 65 mmHg
• Lactate-guided resuscitation: clear lactate within 6 hours

• DO NOT give large fluid boluses - risks pulmonary oedema
• Small cautious 250 mL boluses with clinical reassessment
• Inotropes (dobutamine) ± vasopressors (noradrenaline)

4 mL × body weight (kg) × % TBSA burned over 24 hours

• Give half in first 8 hours (from time of burn, NOT from time of admission)
• Give remaining half over next 16 hours
• Use Hartmann's / LR solution (NOT saline - too much chloride)

---

TOPIC 3: SUTURES

3.1 Classification of Sutures

By Absorbability:

---

3.2 Suture Characteristics

• Monofilament: Single strand; smooth passage through tissue; lower infection risk (bacteria cannot harbour within); BUT more memory (springs back), harder to handle, more throws needed for knot security
• Multifilament (Braided): Multiple strands; better handling and knot security; BUT bacteria can harbour in interstices - avoid in infected wounds

• USP system: 0, 1, 2 (thickest) down to 2-0, 3-0...10-0 (finest)
• The more zeros, the finer/thinner the suture
• Skin closure: typically 2-0 to 4-0
• Fascia/abdominal wall: 0 or 1
• Vascular/ophthalmic: 7-0 to 10-0

• Fascia takes months to fully heal; hence slow-absorbing sutures (PDS) preferred for fascial closure
• Polyglactin (Vicryl) half-life ~3 weeks; PDS half-life ~6 weeks

---

3.3 Suture Needles

• Cutting needle: Triangular cross-section with cutting edge on inner curve - used for tough tissues (skin, fascia)
• Reverse cutting: Cutting edge on OUTER curve - better for skin; less risk of suture tearing through
• Round-bodied (tapered): Needle tip tapers to a point without cutting edges - used for bowel, vessels, peritoneum (tissues that must not be cut/torn)
• Blunt needle: For parenchymal organs (liver, kidney); reduces needlestick injury

• 3/8 circle: most common for skin
• 1/2 circle: used in body cavities with limited space

---

3.4 Wound Closure Techniques

• Faster; better distributes tension
• If one part breaks, entire closure is compromised

• Horizontal mattress: Everting; good for areas under tension; good blood supply
• Vertical mattress: Closes dead space; used in areas of high tension

• Recommended method: Continuous slowly absorbable monofilament (PDS or Maxon)
• 4:1 suture-to-wound length ratio (small bites 5 mm, advances 5 mm between bites)
• Peritoneum does NOT need to be closed separately in most cases
• Retention sutures (interrupted through all layers): Used in high-risk cases (cachectic, immunosuppressed, previously failed closure, intra-abdominal sepsis)

---

3.5 Other Wound Closure Methods

---

TOPIC 4: HAEMOSTASIS IN SURGERY

4.1 The Normal Coagulation Cascade

1. Vessel injury → exposure of subendothelial collagen
2. vWF bridges between collagen and platelet GP-Ib receptors (platelet adhesion)
3. Platelets activate and release granule contents (ADP, thromboxane A2, serotonin) → more platelet recruitment
4. Platelets bind each other via fibrinogen bridges to GP-IIb/IIIa receptors (platelet aggregation)
5. Unstable platelet plug forms

• Tissue Factor (Factor III, released by damaged endothelium) + Factor VIIa → activates Factor X
• Measured by PT/INR

• Factor XII (Hageman factor) activated by contact with collagen → XI → IX → VIII → X
• Measured by aPTT

• Factor Xa + Factor Va + phospholipid + Ca²⁺ (prothrombinase complex) → Prothrombin → Thrombin
• Thrombin cleaves Fibrinogen → Fibrin
• Factor XIII cross-links fibrin → stable clot

• Plasminogen → Plasmin (activated by t-PA from endothelium)
• Plasmin degrades fibrin → D-dimers (elevated in DVT/PE/DIC/recent surgery)

---

4.2 Surgical Haemostasis Methods

Mechanical Methods:

• Direct pressure: First-line for most bleeding; apply sustained pressure for 5-10 minutes
• Ligation: Tie off the bleeding vessel; gold standard for major vessels
• Suture ligation (transfixion): Suture passed through the vessel then tied; more secure
• Surgical clips (haemostatic clips): Quick; titanium or absorbable polymers; used laparoscopically
• Staples/linear cutters (GIA): Simultaneous cutting and stapling; bowel anastomosis
• Packing: Gauze packing used as temporising measure in damage control surgery; removed at relook (24-48 hrs)
• Tourniquet: For limb surgery/trauma; apply proximal to injury; note time applied

Energy-Based Methods:

• Monopolar diathermy (electrocautery): Current passes from probe through patient to grounding pad; produces tissue destruction and seals vessels; most common intraoperative haemostatic tool. CUT mode - high frequency sinusoidal current cuts. COAG mode - interrupted current coagulates.
• Bipolar diathermy: Current passes only between the two tips of the instrument; safer near nerves and in wet fields; less tissue damage
• Argon beam coagulator: Non-contact; useful for diffuse oozing from liver/spleen surfaces
• Laser: Used in endoscopic surgery
• Ultrasonic dissectors (Harmonic scalpel, CUSA): Use vibration (55,000 Hz) to seal and cut tissue; less smoke; no electrical current through patient; useful near nerves
• LigaSure/vessel-sealing devices: Combine pressure and bipolar energy to denature collagen and elastin and seal vessels up to 7 mm diameter

Chemical/Topical Haemostat Methods:

• Bone wax: Impedes bleeding from bone surfaces (e.g., sternum, skull); non-absorbable, impairs osteogenesis
• Oxidised cellulose (Surgicel): Absorbable; promotes platelet aggregation; used on liver/spleen surfaces
• Gelatin sponge (Gelfoam): Absorbable; absorbs blood and promotes clotting
• Thrombin: Applied topically; activates fibrinogen directly; combined with gelatin for greater effect
• Fibrin glue/sealant: Combination of fibrinogen + thrombin; creates fibrin clot immediately; used in parenchymal bleeding, anastomoses
• Tranexamic acid: Antifibrinolytic; blocks plasminogen → plasmin; given IV in major haemorrhage and trauma; CRASH-2 trial showed mortality benefit when given within 3 hours of injury

Risk Factors for Intraoperative Haemorrhage:

• Liver disease (reduced synthesis of clotting factors - vitamin K-dependent: II, VII, IX, X)
• Anticoagulants: warfarin, heparin, DOACs (dabigatran, rivaroxaban, apixaban)
• Antiplatelet drugs: aspirin, clopidogrel
• Inflammatory conditions: acute cholecystitis, diverticulitis
• Haemophilia, von Willebrand disease
• Thrombocytopenia

---

4.3 Pre-operative Assessment of Haemostasis

• PT/INR: Tests extrinsic + common pathway (Factors II, V, VII, X, Fibrinogen)
  • Normal PT: 11-13 seconds; INR: 0.8-1.2
  • Elevated in: warfarin use, liver disease, Vitamin K deficiency
• aPTT: Tests intrinsic + common pathway (Factors VIII, IX, XI, XII, plus common)
  • Normal: 25-35 seconds
  • Elevated in: heparin, haemophilia A (Factor VIII deficiency), haemophilia B (Factor IX deficiency)
• Fibrinogen: Normal 2-4 g/L; low in DIC, massive haemorrhage
• Platelet count: Adequate haemostasis with >80,000/μL; target >100,000 before surgery; target >50,000 if bleeding
• Bleeding time: Tests platelet function; prolonged in thrombocytopenia and platelet dysfunction (e.g., aspirin use)
• Thromboelastography (TEG)/ROTEM: Viscoelastic whole-blood tests; provides real-time picture of entire clot formation and lysis; increasingly used to guide blood product administration in massive haemorrhage

---

4.4 Reversal of Anticoagulation Before Surgery

---

TOPIC 5: BLOOD AND BLOOD TRANSFUSIONS

5.1 Blood Products Available

---

5.2 Blood Groups

• Group O = Universal Donor (no ABO antigens to react with recipient antibodies)
• Group AB = Universal Recipient (no circulating antibodies to react with donor antigens)
• ABO antibodies are naturally occurring (IgM) - no prior sensitisation needed

• Rh(D) antigen present in ~85% of population
• Rh-positive: D antigen present
• Rh-negative: D antigen absent
• Anti-D antibodies are NOT naturally occurring - form after exposure (transfusion or pregnancy)
• Rh-negative women given Rh-positive blood may develop anti-D antibodies
• Subsequent pregnancies: anti-D crosses placenta → haemolytic disease of the newborn (HDN)
• Prevention: Anti-D immunoglobulin (Rhogam) given to Rh-negative mothers after sensitising event

• O Negative: given to females of childbearing age (prevents Rh sensitisation)
• O Positive: given to males or post-menopausal females in extremis

---

5.3 Pre-Transfusion Testing

• Recipient serum + donor red cells
• Tests for ABO compatibility + any other clinically significant antibodies
• Takes 45 minutes
• Most reliable compatibility testing

• ABO/Rh matched only (no full cross-match)
• Ready in 10-15 minutes

Safety Check: Two healthcare staff MUST check patient identifiers against blood product label before administration. Most ABO incompatibility transfusion deaths are due to clerical/identification errors.

---

5.4 Indications for Transfusion

• < 100,000/μL: before neurosurgery or ophthalmic surgery
• < 50,000/μL: before most other surgery or with active bleeding
• < 10,000/μL: prophylactic transfusion in stable patients

---

5.5 Complications of Blood Transfusion

Immunological Complications:

• Most dangerous transfusion complication
• Cause: ABO incompatibility (usually clerical error)
• Timing: Within minutes of starting transfusion
• Features: Fever, rigors, back/loin pain, haemoglobinuria (red/dark urine), hypotension, DIC, renal failure
• Management: STOP transfusion IMMEDIATELY → give IV fluids → maintain urine output → notify blood bank → send residual blood + patient sample for recheck
• Can be fatal

• Most common transfusion reaction
• Cause: Recipient antibodies against donor leukocytes
• Features: Fever (+1°C), chills, mild discomfort - NO haemolysis
• Prevented by leukodepletion (leucoreduction)
• Management: Slow or stop transfusion; paracetamol; restart slowly if no other reaction signs

• Cause: Recipient antibodies against donor plasma proteins (often IgA deficiency)
• Features: Urticaria, itching, rarely anaphylaxis
• Management: Antihistamines; adrenaline for anaphylaxis; wash red cells or use IgA-deficient blood for future transfusions

• Cause: Donor antibodies against recipient HLA/neutrophil antigens → neutrophil activation in lungs
• Features: Acute respiratory distress, hypoxia, bilateral pulmonary infiltrates - within 6 hours
• Most fatal transfusion complication (with AHTR)
• Management: Supportive; ventilatory support

• Cause: Fluid volume overload, especially in elderly/cardiac patients
• Features: Pulmonary oedema, dyspnoea, hypertension
• Management: Slow infusion rate; diuretics; consider smaller volumes

Infective Complications:

• Bacterial contamination: Usually from faulty storage; presents as septic shock
• Viral transmission: Hepatitis B, Hepatitis C, HIV, CMV (very rare now with screening)
• Parasitic: Malaria (donor in endemic area)
• Blood is screened for HIV, HCV, HBV, HTLV, CMV, syphilis, malaria (in endemic regions)

Complications of Massive Transfusion:

• Coagulopathy: Dilution of platelets and coagulation factors → treat with FFP + platelets in 1:1:1 ratio
• Hypocalcaemia: Citrate in stored blood chelates calcium → metabolic manifestations, tetany, impaired cardiac contractility → give 10 mL 10% calcium gluconate IV for every 4-6 units
• Hyperkalaemia: K⁺ leaks from stored RBCs → risk of cardiac arrhythmia, especially if blood given rapidly
• Hypokalaemia: Later, as K⁺ shifts back intracellularly; monitor closely
• Hypothermia: Cold blood → impairs coagulation and cardiac function → use blood warmer; active warming
• Metabolic Alkalosis (late): Citrate metabolised to bicarbonate
• Acid-Base: Initially metabolic acidosis from citrate + haemorrhage; later alkalosis as liver metabolises citrate
• Iron Overload: With repeated long-term transfusions (e.g., thalassaemia); each unit contains ~250 mg elemental iron → haemosiderosis

---

5.6 Alternatives to Allogeneic Blood Transfusion (Patient Blood Management)

• Pre-operative autologous donation (PAD): Patient donates own blood weeks before surgery; stored and returned if needed; less common now
• Intraoperative cell salvage (autotransfusion): Blood lost during surgery is collected, washed, and re-infused; NOT suitable for cancer surgery (risk of tumour cell re-infusion) or infected fields
• Acute normovolaemic haemodilution (ANH): Blood removed pre-operatively, replaced with crystalloid/colloid; re-infused at end of operation

• Erythropoietin (EPO): Stimulates RBC production; used pre-operatively to boost Hb
• Tranexamic acid: Antifibrinolytic; reduces bleeding and transfusion requirements
• Desmopressin (DDAVP): Releases vWF from endothelium; used in mild haemophilia A and vWD
• Vitamin K: For warfarin reversal; takes 6-12 hours to work
• Recombinant Factor VIIa (rFVIIa): For life-threatening haemorrhage not responding to other measures; very expensive

---

QUICK REVISION SUMMARY TABLE

---

HIGH-YIELD MNEMONICS

"1972" = Factors II, VII, IX, X (remember as "2, 7, 9, 10")

"HAC" = Hypothermia, Acidosis, Coagulopathy

"FAITH" = Febrile reaction, Allergic reaction, Incompatibility (haemolytic), Transfusion-related lung injury (TRALI), Hepatitis/HIV/infections

Think in 15% steps: <15% Class I → 15-30% Class II → 30-40% Class III → >40% Class IV

"The Two-Thirds Rule": ICF = 2/3 of TBW; ECF = 1/3; Plasma = 1/4 of ECF

---

---